Copy of Board Questions

Pulmonary

Total amount of air in the lungs at the end of normal expiration

Total amount of air in a fully expanded lung

Define Residual Volume, RV

How do you calculate the A-a gradient?

Difference in partial pressure of Oxygen, PO2, between the alveolar PO2 and arterial PO2 PAO2=FiO2(713) - arterial PCO2/0.8

What causes an A-a gradient and how is it useful in differentiating causes of hypoxemia?

A-a gradient is caused by a mismatch between ventilation and perfusion. Hypoxemia of pulmonary origin causes an increased A-a gradient (>30). Hypoxemia of extrapulmonary origin has a normal A-a gradient.

What are some causes of ventilation defects?

Impaired O2 delivery to the alveoli for gas exchange, e.g. from airway collapse due to respiratory distress syndrome or atelectasis.

What are some causes of perfusion defects?

Decreased or absent blood flow to the alveoli, e.g. pulmonary embolus

What are some causes of diffusion defects?

O2 cannot diffuse across alveolar-capillary interface, e.g. pulmonary fibrosis or pulmonary edema. Causes decreased DLCO

What are some causes of shunting?

A shunt is technically blood going from right to left because of heart issues, e.g. right to left shunting from tetralogy of fallot.

What are some causes of hypoxemia with a normal A-a gradient?

Depression of the respiratory center in the medulla (barbiturates, brain injury); upper airway obstruction (epiglottitis, croup); Chest bellows dysfunction (paralyzed diaphragm, ALS with degeneration of anterior horn cells).

Define Functional Residual Capacity, FRC (Refer to Pulmonary attachment 1).Define Total Lung Capacity, TLC

Volume of air left over in the lung after maximal expiration: FRC-ERV

Define Tidal Volume, TV Volume of air that enters/exits the lungs during normal respiration

Total amount of air expelled after maximal inspiration

70-80%

Amount of air forcibly expelled at the end of normal expiration

They're at the bifurcation of airways, larynx and distal esophagus

Postnasal discharge

Define Forced Vital Capacity, FVCDefine Forced Expiratory Volume, 1 second, FEV1

Amount of air expelled from the lungs in 1 second after maximal inspiration

What is the normal FEV1/FVC?Define Expiratory Reserve Volume, ERV

Describe spirometry in restrictive lung disease

TLC decreased, RV decreased, FEV1 decreased, FVC decreased, FEV1/FVC normal to increased, PaO2 decreased, A-a gradient increased (if disease of lungs, not just restriction of chest wall

Describe spirometry in obstructive lung disease

TLC increased, RV increased, FEV1 decreased, FVC decreased, FEV1/FVC decreased, PaO2 decreased, A-a gradient increased

Define Dyspnea and list some causes.

Difficulty breathing. Can be due to stimulation of J receptors causing decrease in full inspiration. Also decreased compliance, e.g. interstitial fibrosis; increased airway resistance, e.g. chronic bronchiti; chest bellows disease, e.g. obesity; kyphoscoliosis, interstitial inflammation or fluid accumulation, e.g. left sided heart failure.

Where are cough receptors located?What is the most common cause of cough with a normal CXR?What causes nocturnal cough?

GERD from acid refluxing into the bronchial tree at night. Bronchial asthma due to airway constriction

What drugs cause cough?

What causes productive cough?

Chronic bronchitis, usually associated with smoking cigarettes. Typical bacterial pneumonia. BronchiectasisACE inhibitors-inhibit degradation of bradykinin which causes mucosal swelling and irritation in the tracheobronchial tree. Aspirin causes increases in Leukotriene C, D and E4 which are all bronchoconstrictors

Define hemoptysis and the mechanisms.

Coughing up blood-tinged sputum. Caused by parenchymal necrosis and/or bronchial/pulmonary vessel damage.

What are some causes of hemoptysis?

Chronic bronchitis (most common), pneumonia, bronchogenic carcinoma, tuberculosis, bronchiectasis, aspergilloma (fungus in a cavitary lesion)

Define tachypnea and list the causes.

Rapid, shallow breathing, more than 20 breaths/minute. Causes are restrictive lung disease, pleuritic chest pain, pulmonary embolus with infarction (tachypnea is the key finding)

Define tracheal shift and list the mechanism.

shift of trachea from large changes in pleural fluid volume. Causes are pressure in contralateral lung, large tension pneumothorax, large pleural effusion; decreased volume in ipsalateral lung, large spontaneous pneumothorax, resorption atelectasis.

What is vocal tactile fremitus?

Palpable thrill (vibration) transmitted through the chest when the patient says "99," or "E"

What causes decreased tactile fremitus?

Emphysema or asthma with increased AP diameter from increased total lung capacity.

What causes increased tactile fremitus?

Sound travels better through fluid/solid so any type of lung consolidation, pneumonia, etc.

What causes absent tactile fremitus?

Atelectasis/collapse of airways, fluid/effusion, air in pleural space (pneumothorax)

What causes dull and hyperresonant percussion?

Dull percussion comes from pleural effusions, lung consolidations, atelectasis. Hyperresonant percussion comes from pneumothorax, asthma or emphysema

What is the origin and mechanism of normal breath sounds?

Normal breath sounds come from the trachea and are caused by air velocity and turbulence inducing vibrations in airway walls

Where does laminar air flow start?

Terminal bronchioles where the increased surface area converts turbulent to laminar flow

What are tubular breath sounds?

Sound like air blowing through a tube-this is normal over the trachea but is always abnormal over the bronchi. Causes a loud, high pitched sound with a tubular or hollow quality. Expiration is longer than inspiration. Means that there is consolidation or patent but partially collapsed bronchi

What are vesicular breath sounds?

Tracheal sounds that are modified in the alveoli. Inspiratory to expiratory ratio is 3:1. Diminished in emphysema and asthma due to increased AP diameter. Absent in pneumothorax, atelectasis or effusion

What are bronchovesicular breath sounds?

Normal breath sounds over the main bronchi with an equal inspiratory and expiratory ratio.

What are crackles and how are they caused?

Extra sounds, usually inspiratory, that sound like (you guessed it), crackles! Early and midinspiratory crackles are due to secretions in proximal large to medium sized airways. These clear with coughing. Late inspiratory crackles are due to reopening of distal airways partially occluded by increased interstitial pressure (fluid, transudate, pus). These do not clear with coughing and vary from fine to course

What is a flow volume loop?

What is wheezing and how is it caused?

High pitched musical sound usually in expiration. Caused by inflammation of segmental bronchi and small airways by asthma or chronic bronchitis; pulmonary edema constricting airway (cardiac asthma); pulmonary infarction (release of TXA from platelets in the embolus causes bronchoconstriction

What are Rhonchi and how are they caused?

Low pitched snoring sounds during inspiration or expiration. Due to secretions in large airways (bronchus or trachea). Usually clear with coughing, common in chronic bronchitis

What is inspiratory stridor and how is it caused?

High pitched inspiratory sound. Indicates upper airway obstruction. Caused by epiglottitis (H. Influenzae), croup (parainfluenza)

What is a pleural friction rub and how is it caused?

Two inflamed surfaces (pleural and parietal) rubbing against each other. Usually happens at the end of inspiration and beginning of expirations when things are changing direction. Caused by pleuritis due to cancer, infarction, pneumonia, serositis (SLE). Disappears with alrge effusion bc separates layers and stays with holding breath.

What does grunting in a newborn mean?

Newborns should not grunt after 24 hours. It's a sign of respiratory distress syndrome.

What is bronchophony and egophony?

Caused by alveolar consolidations. Spoken numbers, syllables are heard more distinctly through stethoscope. Egophany is when the patient says E and you hear an A through the stethoscope.Plot of inspiratory and expiratory flow rate(L/sec) versus lung volume(L)

Begins at point A, RV and goes to point B, TLC

Vital Capacity

TLC is decreased, RV is decreased. AKA right shifted curve.

What is Choanal Atresia?

What is a Nasal Polyp?

Excessive snoring with intervals of breath cessation (apnea)

Where is maximal inspiration on the diagram? (see Pulmonary attachment 2 for following)

Define Peak Expiratory Flow (PEF)

Begins at point B, TLC, and goes to point C, PEF. Occurs early in expiratory phase of loop due to elastic recoil of the lungs with low resistance and large caliber. Slope decreases to point A as resistance increases and airways get smaller.

What is the volume between points B and C?Describe the flow-volume loop in obstructive lung disease.

TLC is increased and RV is increased. AKA left shifted curve. Decreased PEF. Can have concavity at C from mucus plugs or collapsed airways.

Describe the flow-volume loop in restrictive lung disease.

Unilateral or bilateral bony septum between the nose and pharynx. Newborn urns cyanotic on breast feeding but crying causes them to pink up again

Non-neoplastic tumefactions which develop as a response to chronic inflammation. Allergic polyps are the most common and are most often seen in asults with IgE mediated allergies. Also associated with aspirin and other NSAIDs b/c Cyclooxegenase block increases Leukotrienes whcih results in bronchoconstriction. Oten associated with CF

Define Obstructive Sleep Apnea

Define Laryngeal Carcinoma.

What causes obstructive sleep apnea?

Most commonly a result of obesity causing the pharyngeal muscles to collapse under the weight of the tissue. Can also result from tonsilar hypertrophy or nasal septum deviation.

What is the pathogenesis and clinical findings in sleep apnea?

Airway obstruction causes CO2 retention resulting in hypoxemia. Decreased PO2 and O2 saturation during apnea with increase in PCO2. See excessive snoring with apneic periods and excessive daytime somnolence. Can cause pulmonary arterial hypertension leading to Right Ventricular Hypertrophy and polycythemia secondary to hypoxemia.

Define Sinusitis and describe its causes.

Inflammation of the sinuses, most often maxillary or ethmoid sinuses. Caused by URI blocking drainage of sinuses into nasal cavity. Can be caused by a deviated nasal septum, allergic rhinitis, barotrauma, or cigarettes. Pathogens implicated are rhinovirus, strep pneumoniae, anaerobes (chronic sinusitis), systemic fungi (diabetics due to Mucor species).

What is a Nasopharyngeal Carcinoma?

Most common malignant tumor of the nasopharynx, more common in males and increased incidence in the Chinese and African populations. Closely related to EBV. Often causes squamous cell carcinoma or undifferentiated cancers which can metastasize to cervical lymph nodes.

Carcinoma most commonly located on the true vocal cords. Mostly keratinizing squamous cell carcinomas, mostly in med. Related to cigarette smoking, alcohol (synergistic with cigarettes), HPV 6 and 11 and squamous papillomas and papillomatosis. Persistent hoarseness from cervical lymphadenopathy is common.

What is Atelectasis?

Loss of lung volume due to inadequate expansion of the airspaces (collapse). Collapse happens because of lack of air and distal resorption of air through pores of Kohn in the alveolar walls. May see ipsilateral elevation of the diaphragm and tracheal deviation. Treat with incentive spirometry, CPAP or PEEP.

What is resorption atelectasis?

Airway obstruction in bronchiols, segmental bronchi or bronchi, by thick secretions which prevents air from reaching the alveoli. Can be caused by mucus or mucopruluent plug after surgery, aspiration of foreign material or centrally located bronchogenic carcinoma.

What is compression atelectasis?

Air or fluid in the pleural cavity under increased pressure collapses small airways beneath the pleura.

What is atelectasis due to loss of surfactant?

Synthesized by Type II pneumocytes starting in the 28th week of gestation. Stored in lamellar bodies. Major component is phosphatidylcholine (lecithin). Synthesis is increased by cortisol and thyroxine but decreased by insulin. Surfactant reduces surface tension so airways don't collapse. Without surfactant, airways can collapse causing atelectasis.

What is Respiratory Distress Syndrome?

Decreased surfactant in lungs results in atelectasis and respiratory distress from massive intrapulmonary shunting. Collapsed alveoli are lined by hyaline membranes (from protein leaking out of damaged alveoli). Causes respiratory difficulty, grunting, tachypnea, intercostal retractions and hypoxemia with respiratory acidosis.

What are complications of respiratory distress syndrome?

Superoxide radicals from O2 therapy can cause blindness (retinopathy of prematurity) and damage to small airways (bronchopulonary dysplasia). Can cause intraventricular hemorrhage, patent ductus arteriosus from hypoxemia, necrotizing enterocolitis from intestinal ischemia (allows entry of gut bacteria into intestinal walls) and hypoglycemia leading to seizures and neuronal damage.

What is Pulmonary Edema and what are the causes?

Collection of fluid. Can be due to Starling forces from left sided heart failure, volume overload or mitral stenosis. This produces transudate. Can be exudate from microvascular or alveolar injury resulting from infection. Can be from aspiration, drugs, high altitude or ARDS.

What is Acute Respiratory Distress Syndrome, ARDS?

Noncardiogenic pulmonary edema from acute alveolar-capillary damage. Caused by direct injury to the lungs or systemic disease. Risk factors are gram (-) sepsis, gastric aspiration, severe trauma and shock, diffuse pulmonary infections (SARS, hantavirus), Heroin, smoke inhalation, acute pancreatitis, cardiopulmonary bypass, DIC, amniotic fluid or fat embolism.

What is the pathogenesis of ARDS?

Acute damage to alveolar capillary walls and epithelial cells results in alveolar macrophages releasing cytokines. Capillary damage and chemotactic factors allow neutrophils and exudate to leak producing hyaline membranes. Neutrophils damage Type I and II pneumocytes, reducing surfactant and causing atelectasis.

What are clinical signs/symptoms of ARDS?

Dyspnea/tachypnea, late inspiratory crackles, severe hypoxemia not responsive to 100% O2, increased pulmonary wedge pressure, increased A-a gradient, bilateral infiltrates and consolidations.

What are the subtypes of Pneumonia?

Community acquired which can be typical or atypical and hospital acquired, aka nosocomial.

Describe the pathogenesis of typical pneumonia.

Most caused by bacterial pathogens, particularly Strep Pneumoniae. Pathogenesis is via inhalation of aerosol from infected person or aspiratin of nasopharyngeal flora while sleeping.

Describe the pathogenesis of bronchopneumonia.

Begins as acute bronchitis and spreads locally into the lungs, usually lower lobes or right middle lobes. Causes patchy consolidations and may have microabscesses.

Describe clinical findings in lobar pneumonia.

Complete or almost complete consolidation of a lobe of the lung. Can be complicated by lung abscesses, empyema or sepsis. See sudden onset of fever with productive cough, chest pain, tachycardia, dullness to percussion, increased tactile fremitus, late inspiratory crackles, bronchial breath sounds, bronchophany and egophany.

Describe clinical findings in atypical pneumonia.

Usually caused by mycoplasma pneumoniae, also chlamydophilia pneumoniae, RSV, influenzavirus, and adenovirus. Contracted by inhalation of droplets. Causes patchy, mononuclear infiltrate but the alveolar spaces are usually free of exudate. Insidious onset with nonproductive cough, low grade fever, chest pain, flu like symptoms including pharyngitis, laryngitis, myalgia and headache. No consolidation.

Describe clinical findings in nosocomial pneumonia.

Happens in patients with severe underlying disease, immunosuppresion, or who are on antibiotic therapy. Respirators are the most common source of infection. Usually gram (-) bacteria, often pseudomonas, E coli, or gram (+) like staph aureus. In immunocompromised, can be opportunistics like CMV, Pneumocystis Jirovecis, Aspergillus-fumigatus.

Acute chest syndrome: fever with pleuritis

Describe pneumonia from Tuberculosis.

From inhalation of Mycobacterium Tuberculosis. Infects phagosomes of alveolar macrophages and produces a protein that prevents fusion of the lysosome with the phagosome. Strict aerobe, acid fast. Cord factor is major virulence factor. Drug resistance by mutations in mycolic acid or catalase peroxidase (activates Isoniazid).

Describe Primary TB Infection.

Subpleural location, usually upper part of lower lobes or lower part of upper lobes. Causes Ghon focus (caseous necrosis) in periphery and Ghon complex in hilar lymph nodes. Produces a calcified granuloma or area of scar tissue

Describe Secondary TB Infection.

Due to reactivation of primary TB. Usually involves apices in upper lobes b/c increased V/Q ratio. Causes cavitary lesions from release of cytokines by T Cells. Causes fever, drenching night sweats, weight loss. May cause miliary TB with invasion into bronchus, lymphatics or extrapulmonary sites like the kidney. Spread to vertebra is called Pott's disease.

Describe pneumonia from Mycobacterium Avium Intracellulare

Atypical mycobacterium causing atypical pneumonia in AIDS patients. Happens when CD4+ T Cell count falls below 50 cells/mm3. Often disseminates and co-occurs with systemic fungal infection.

What is the most common cause of the common cold?

Rhinovirus, transmitted by hand to nose/eye contact. Less common are coronavirus, adenovirus, influenza C and coxsackievirus

What does Coxsackievirus cause?

What is the most common viral cause of atypical pneumonia and bronchiolitis in children and otitis media in older children?

Respiratory Syncitial Virus. Occurs in late fall and winter. Can give Palivizumab to high risk kids (passive immunity)

What is the most common viral cause of laryngotracheobronchitis (croup) in infants?

Parainfluenza. Causes inspiratory stridor from sunmucosal edema obstructing the upper airway. Anterior CXR shows steeple sign in anterior neck.

What is the most common viral cause of pneumonia in immunocompromised hosts?

Cytomegalovirus. Enlarged alveolar macrophages/pneumocytes with basophilic inclusions surrounded by a halo.

What can happen with aspirin ingestion when a child has influenza?

Reye's Syndrome. Causes fatty liver, severe encephalopathy, palmar rash, comiting, lethargy and stupor.

What are signs and symptoms of Rubeola infection?

Measles. Fever, cough, conjunctivitis and excessive nasal mucous. Koplik spots in the mouth precede rash. Warthin-Finkeldey multinucleated giant cells are characteristic

What are signs and symptoms of SARS

Infects lower respiratory tract and then spreads systemically thus severe respiratory infection and systemic symptoms.

What is Hantavirus pulmonary syndrome?

Transmission is via inhalation of urine/feces from deer mice in SW US. Causes ARDS, hemorrhage and renal failure.

What is the second most common (bacterial) cause of atypical pneumonia?

Chlamydophilia pneumoniae. Has a seroepidemiologic association with coronary artery disease. Treat with doxycycline.

What is a common bacterial cause of newborn pneumonia?

Chlamydia trachomatis from passage through infected birth canal. Afrebile with staccato cough, conjunctivitis and wheezing. Treat with erythromycin.

What is the most common baterial cause of atypical pneumonia?

Mycoplasma Pneumoniae. Insidious onset with low grade fever. Can cause bullous myringitis(inflamed Tympanic membrane), cold autoimmune hemolytic anemia from anti-IgM antibodies.

Describe the signs and symptoms of Coxiella Burnetti infection

Atypical pneumonia, myocarditis, granulomatous hepatitis. Associated with dairy farmers and vetrinarians.

What is the most common cause of community acquired lobar pneumonia?

Strep pneumoniae. Rapid onset, productive cough and signs of lobar consolidation. Can test with urine screen.

What are signs/symptoms of pneumonia from Staph Aureus?

Commonly superimposed on measles or influenza pneumonia or in CF or IV drug users. Hemorrhagic pulmonary edema, yellow sputum, abscess formation and tension pneumatocysts (intrapleural blebs) which can rupture and produce tension pneumothorax.

Describe signs and symptoms of infection with Corynebacterium Diptheriae.

Causes toxin-induced pseudomembranous inflammation producing a shaggy gray membrane in the oropharynx and trachea. Can cause toxic myocarditis from impaired B oxidation of fatty acids in the heart.

What are signs and symptoms of infection with Bacillus Anthracis?

Cutaneous anthrax initially looks like a scab but swells to form a black scab (eschar) with an area of central necrosis. Pulmonary anthrax causes necrotizing pneumonia, meningitis, splenomegaly and systemic dissemination.

What are signs and symptoms of Actinomyces infection?

Normal flora in tonsils and adenoids. Can produce draining sinuses in the jaw, chest cavity and abdomen. Pus contains yellow specks (sulfur granules) which contain the bacteria.

What are signs and symptoms of Nocardia infection?

Granulomatous microabscesses in the lungs. Often disseminates to CNS and kidneys.

What are signs and symptoms of infection with Bordatella Pertussis?

Produces whooping cough-inspiratory whoop between coughing fits. Catarrhal phase is 1-2 weeks and involves mild coughing, rhinorrhea and conjunctivitis. Paroxysmal phase lasts 2-5 weeks and involves coughing in succession followed by inspiratory whoop and absolute lymphocytosis (20,000-50,000). Convalescent pahse lasts 1-2 weeks or more and involves a slow decline in lymphocytosis and coughing. Can cause hemorrhage into skin, conjunctiva, bronchus, brain or rectal prolapse from coughing. Also otitis media and meningoencephalitis.

What are signs and symptoms of infection with H. Influenzae?

Common cause of sinusitis, otitis media, conjunctivitis, epiglottitis with inspiratory stridor. Swelling of epiglottis produces a thumbprint sign on lateral xray of the neck. Can cause COPD exacerbation.

What are signs and symptoms of Moraxella Catarrhalis infection?

Causes typical pneumonia, especially in the elderly. Causes acute COPD exacerbation, chronic bronchitis, sinusitis and otitis media.

What are signs and symptoms of infection with Pseudomonas Aeruginosa?

Green sputum (pyocyanin), nosocomial pneumonia and pneumonia in CF patients. Often associated with infarction from vessel invasion.

What are signs and symptoms of Klebsiella Pneumoniae infection?

Most common gram negative that causes lobar pneumonia and typical pneumonia in nursing home patients and alcoholics. Associated with blood tinged, thick, mucoid sputum, lobar consolidations and abscesses.

What are signs and symptoms of infection with Legionella Pneumophila?

Pneumonia associated with high fever, dry cough, flu like symptoms. May produce tubulointerstitial disease with destruction of the JG apparatus leading to hyporeninemic hypoaldosteronism (type IV renal tubular acidosis-hyponatremia, hyperkalemia, metabolic acidosis). Urine antigen is an excellent screen.

What are signs and symptoms of infection with Yersinia Pestis?

The plague!!! Macrophages cannot kill bacteria due to protection by V and W antigens so you get really sick. Bubonic causes infected lymph node which enlarge and mat together and drain to the surface (buboes). Pneumonic and septicemic are just what they sound like. Treat with gentamicin and doxycycline (pneumonic) or gentamicin and streptomycin (bubonic)

What are signs and symptoms of infection with Cryptococcus Neoformans?

Granulomatous inflammation with caseation. Acquired from pigeon feces.

What are signs and symptoms of infection with Aspergillus Fumigatus?

Aspergilloma-fungus ball that develops in a prior cavitary lesion and cause massive hemoptysis. Allergic bronchopulmonary aspergillosis-type I and III hypersensitivity. IgE increase, eosinophilia, intense inflammation of airways and mucous plugs in terminal bronchioles resulting in bronchiectasis and interstitial lung disease. Vessel invasion with hemorrhagic infarctions and necrotizing bronchopneumonia.

What are signs and symptoms of infection with Mucor species?

Happens to diabetic and immunosuppressed patients. Vessel invasion producing hemorrhagic infarcts in the lungs. Invades the frontal lobes when there is diabetic ketoacidosis (rhinocerebral mucormycosis).

What are signs and symptoms of infection with Coccidoides Immitis?

Contracted by inhaling arthrospores in dust in arid areas (increased after earthquakes). Causes flu-like symptoms and erythema nodosum and granulomatous inflammation of the lungs with caseous necrosis.

What are signs and symptoms of infection with Histoplasma Capsulatum?

Most common systemic fungal infection, endemic in Ohio and Mississippi river valleys. Causes granulomatous inflammation with caseous necrosis, simulating TB. Produces coin lesions, consolidations, milary spread and cavitation. Causes marked dystrophic calcification of granulomas and multiple calcifications in the spleen.

What are signs and symptoms of infection with Blastomyces Dermatitidis?

Male dominant disease, common in Great lakes, central and southern US. Causes skin disease that simulates squamous cell carcinoma and lung disease with granulomatous inflammation and caseous necrosis.

What are signs and symptoms of infection with Pneumocystis Jiroveci?

Cysts and trophozoites attach to Type I pneumocytes. Most common AIDS-defining infection, CD4+ count <200. Fever, dyspnea and severe hypoxemia, diffuse intra-alveolar foamy exudates with cup chaped cysts (under silver or Giemsa stain). Diffuse alveolar and interstitial infiltrates.

What are the common causes of lung abscesses?

Aspiration of oropharyngeal material. Risk factors are alcoholism, loss of consciousness and recent dental work. Can also be a complication of pneumonia, a result of septic embolism or from an obstructive lung neoplasia.

What are the most common pathogens in lung abscesses?

Aerobic and anaerobic streptococci, staph species, prevotella, fusobacterium

What is Hampton's Hump? Wedge shaped area of consolidation/infarction from PE

Where are most lung abscesses due to aspiration located?

Right side because the bronchi going to the right lobes are more direct (straight) so it's easier to aspirate crap into there. Usually in the upper portion of the right lower lobe, but it depends on the position of the person when they aspirated.

What are clinical findings in a lung abscess?

Spiking fever with productive cough and foul smelling sputum. CXR shows cavitation with an air/fluid level.

What is the pathophysiology of a pulmonary thromboembolism?

Venous clot, most commonly from the femoral vein. Risk factors are Virchow's triad-stasis of blood flow, hypercoagulable states and trauma to the vessel. Clot breaks off and goes to the lung-size of the embolus determines what it will block. Large embolus blocks major vessels (saddle embolus) while small emboli occlude medium and small vessels.

What are consequences of pulmonary thromboembolism?

Increase in pulmonary artery pressure, decreased flow to pulmonary parenchyma which can cause hemorrhagic infarct, see a red-blue, raised, wedge shaped area that extends to the pleural surface. Fibrinous exudate on the pleural surface and hemorrhagic pleural effusion.

What are clinical signs of pulmonary thromboembolism?

Sudden increase in PA pressure which can cause right ventricular failure, sudden onset of dyspnea and tachypnea, fever, pleuritic chest pain, plueral friction rub, pleural effusion, expiratory wheezing from release of TXA2 from platelets.

What are lab findings of pulmonary thromboembolism?

Respiratory alkalosis (PCO2<33mmHg), PaO2<80 mmHg, increased A-a gradient, increased D-Dimer

Define Pulmonary Hypertension

Mean pulmonary artery pressure >25 mmHg at rest or >30mmHg with exercise.

What causes primary pulmonary hypertension?

Mutation associated with TGF-B resulting in vascular hyperreactivity with proliferation of smooth muscle

What causes secondary pulmonary hypertension?

Endothelial cell dysfunction, e.g. loss of vasodilation (NO), increase in vasoconstriction (endothelin). Hypoxemia and respiratory acidosis stimulate vasoconstriction of pulmonary arteries resulting in smooth muscle hyperplasia and hypertrophy. Any sort of lung disease that results in chronic hypoxemia or chronic respiratory acidosis can do this, e.g. high altitude, chronic bronchitis, sleep apnea, loss of pulmonary vasculature from emphysema or recurrent PE, left to right shunting/volume overload, mitral stenosis resulting in volume overload.

What are clinical findings of pulmonary hypertension?

Exertional dyspnea (common), chest pain, tapering of arteries on CXR, accentuated P2, left parasternal heave or other signs of right ventricular hypertrophy.

How do you treat pulmonary hypertension?

Diuretics, O2, vasodilators-Ca channel blockers, prostanoids, endothelin receptor antagonists, lung transplant

What is Goodpasture's Syndrome?

Pulmonary hemorrhage with hemoptysis often preceding renal failure. Autoantibodies to Type IV collagen in basement membrane of lung and glomerulus.

What are common causes of restrictive lung disease?

Chest wall disorders with normal lungs, e.g. kyphoscoliosis, pleural disease like mesothelioma or obesity. Acute or chronic interstitial lung diseases, e.g. ARDS, pneumoconiosis or other fibrosing disorders, granulomatous diseases like amyloidosis or sarcoidosis.

What is the pathogenesis of interstitial fibrosis?

Elveolitis-leukocytes release cytokines which stimulate fibrosis. Causes functional loss of type I/II pneumocytes and capillaries (decreased DLCO), and decreased expansion of lung parenchyma during inspiration. Increased elasticity to recoil on expiration is increased.

What is a pneumoconiosis?

What is silicosis?

What are clinical findings in restrictive lung disease?

dry cough and exertional dyspnea, late inspiratory crackles in lower lung fields, potential cor pulmonale, equal decreases on PFT's.

Inhalation of mineral dust into the lungs leading to interstitial fibrosis. Can be silica, asbestos, beryllium or others.

Describe Coal Worker's Pneumoconiosis.

"I think I've got the black lung pop…" Coal dust, aka aanthracotic pigment comes from coal mines, large cities, second hand smoke, etc. Deposits in alveolar macrophages creating "dust cells." Fibrotic opacities smaller than 1 cm in upper lobes and coal deposits adjacent to respiratory bronchioles producing centriacinar emphysema- simple CWP. Complicated CWP involves large fibrotic opacities, crippling lung disease (black lung), may have cor pulmonale or large cavitating rheumatoid nodules (Caplan Syndrome). No increase in TB or primary lung cancers.Common occupational disease from quartz/silicon dioxide, foundries, sandblasting and working in mines. Quartz is fibrogenic and deposits in the upper lungs, activates and is cytolytic to alveolar macrophages. Macrophages release cytokines resulting in fibrosis.

Describe clinical findings in silicosis.

Ground glass appearance on CXR or nodular opacities in more advanced disease (concentric layers of collagen w/wo central cavitation). Dystrophic calcification of lymph nodes. Can cause cor pulmonale or Caplan syndrome and increased risk of lung cancer and TB.

What is Berylliosis?

What is Sarcoidosis?

How do asbestos related diseases occur?

Serpentine asbestos-interstitial fibrosis and lung cancer; amphilobe asbestos-interstitial fibrosis, lung cancer and mesothelioma. Deposits in respiratory bronchioles, alveolar ducts and alveoli. Comes from insulating pipes, naval shipyards, roofing material, ceiling tiles, old floor tiles and demolition of old buildings.

What is the pathogenesis of asbestos related disease?

Fibers are coated in iron and protein (ferruginous bodies) which are then pahgocytosed, coated with ferritin and look golden and beaded in sputum or distal small airways. Causes calcified pleural plaques which don't predispose to mesothelioma, diffuse interstitial fibrosis, primary bronchogenic carcinoma (esp if smoker), malignant mesothelioma of the pleura arising from serosal cells of the pleura. Can cause cor pulmonale or Caplan syndrome.

Beryllium exposure from nuclear and aerospace industry causes diffuse interstitial fibrosis with noncaseating granulomas. Increased risk for cor pulmonale and primary lung cancer.

Multisystem granulomatous disease of unknown origin. Common in Black women and nonsmokers and causes 25% of chronic interstitial lung disease. Granulomas in mediastinal/hilar lymph nodes and interstitium. Granulomas contain multinucleated giant cells, laminated calcium concretions (Schaumann bodies) and stellate inclusions (asteroid bodies). Dyspnea is the most common symptom.

What are other clinical signs in Sarcoidosis?

Nodular lesions containing granulomas, violaceous rash on the nose and cheeks (lupus pernio), erythema nodosum-painful nodules on lower extremities, inflammation of subcutaneous fat. Eye lesions produce uveitis, blurry vision, glaucoma and corneal opacities. Can ahve granulomatous hepatitis, enlarged salivary and lacrimal glands, diabetes insipidus, and granulomas in the bone marrow and spleen. See increased ACE, hypercalcemia (increased 1-alpha hydroxylase in granulomas), polyclonal gammopathy, and cutaneous anergy of skin antigens like Candida (due to consumption of CD4+ T cells in granulomas)

What is idiopathic pulmonary fibrosis?

Idiopathic means the doctor is an idiot!!! Repeated cycles of alveolitis, release of cytokines producing interstitial fibrosis, alveolar fibrosis leading to proximal dilation of small airways giving the lung a honeycomb appearance. See fever, dyspnea on exertion, chronic, nonproductive cough, and late inspiratory crackles.

What collagen vascular diseases cause lung disease?

Systemic Lupus causes interstitial disease in 50% of patients and pleuritis with effusion (serositis). Rheumatoid Arthritis can cause rheumatoid nodules (if with a pneumoconiosis, Caplan's syndrome).

What is hypersensitivity pneumonitis?

Extrinsic allergic alveolitis associated with exposure to known inhaled antigen. Does not involve IgE or have eosinophilia.

What is Farmer's Lung?

What is Silo Filler's Disease?

What is Byssinosis?

What is Emphysema?

What causes Emphysema?

Exposure to thermophilic actinomyces (Saccharopolyspora rectivirgula) in moldy hay causes precipitating IgG antibodies which combine with inhaled antigens to form immune complexes. Type III hypersensitivity. Immune complexes deposit in lung and cause inflammation which chronically causes granulomatous inflammation (type IV hypersensitivity).

Inhalation of gases (oxides of nitrogen) from plant material causes an immediate hypersensitivity reaction associated with dyspnea.

Contact with cotton, linen and hemp in textile factories causes exposure to gram negative endotoxin growing on the cotton. Causes dyspnea on exposure to cotton, linen or hemp. Disease occurs on returning to work-Monday Morning Blues (cyanosis)

What drugs are associated with interstitial fibrosis?

Amiodarone, Bleomycin and Busulfan, Cyclophosphamide, Methotrexate and methysergide, nitrosurea and nitrofurantoin.

What is obstructive lung disease?

Obstruction to airflow out of the lungs. Usually loss of elastic recoil or obstruction of airways.Permanent enlargement of all or part of the respiratory unit-respiratory bronchioles, alveolar ducts and alveoli. Smoking is the most common cause. Also can be from Alpha-1 Antitrypsin deficiency

What is the pathogenesis of Emphysema?

Increased compliance and decreased elasticity (C=V/P). There can be an imbalance between elastase and anti-elastases (A1AT), or an imbalance between oxidants and antioxidants. Elastase and oxidants all derive from macrophages so chronic inflammation results in tissue destruction. Smoking produces a functional A1AT deficiency.

What is Chronic Bronchitis?

What is the normal function of elastic fibers in the lung?

Fibers attach to the outside of the walls of small airways and provide radial traction to keep the lumen open. Destruction causes loss of radial traction and small airway collapse, especially on expiration.

Where is the site of obstruction in emphysema?

During expiration, the distal terminal bronchioles collapse preventing egress of air. Trapped air distends parts of the respiratory unit that have no elastic tissue. Trapped air increases TLC and RV

What type of Emphysema is most common in smokers?

Centriacinar/Centrilobular. Mostly apical segments of upper lobes, distal terminal bronchioles and respiratory bronchioles lose elastic tissue.

What type of Emphysema is most common in Alpha-1 Antitrypsin deficiency?

Panacinar emphysema. Autosomal dominant disorder. MM phenotype is normal, Homozygous ZZ phenotype causes disease. Primarily affects the lower lobes. Tissue destruction happens in distal terminal bronchioles and all parts of the respiratory units. See absent alpha-1 globulin peak in serum protein electrophoresis. Dyspnea is sever and occurs early, causes pink puffers. Frequently coexists with chronic bronchitis.

What are 2 non-obstructive types of Emphysema?

Paraseptal emphysema-localized to the subpleura and targets alveolar ducts and alveoli. Increased incidence of spontaneous pneumothorax from rupture of subpleural blebs. Irregular Emphysema-localized disease associated with scar tissue.Productive cough for at least 3 months. Most commonly from smoking and Cystic Fibrosis.

What is the pathogenesis of chronic bronchitis?

Hypersecretion of mucous in bronchi, obstruction to airflow in the terminal bronchioles, proximal to the obstruction seen in emphysema. Causes irreversible fibrosis of terminal bronchioles.

What is Asthma?

What is Extrinsic Asthma?

What changes are seen in the bronchi with chronic bronchitis?

Hypersecretion of submucosal mucus-secreting glands in the trachea and bronchi are responsible for sputum overproduction. Acute inflammation with neutrophils are superimposed on chronic inflammation. Causes loss of ciliated epithelium resulting in squamous metaplasia. Mucus plugs can block the exodus of CO2. GOblet cell metaplasia is seen with hypertrophy of mucus secreting glands, fibrosis and narrowing of the airway.

What are clinical findings of chronic bronchitis?

Productive cough, dyspnea late in the disease, cyanosis of skin and membranes, decreased SaO2 from hypoxemia. These patients are called Blue Bloaters. Tend to be stocky or obese, have expiratory wheezing and siliant rhonchi and often cor pulmonale. Also have chronic respiratory acidosis with increased bicarb to compensate.Episodic and reversible obstructive airway disease. Primarily targets bronchi and terminal bronchioles.

Type I hypersensitivity reaction with exposure to extrinsic allergens, typically in children with atopic family history. Initial sensitization to inhaled allergens stimulates induction of Th2 cells which release IL-4 and IL-5. IL-4 facilitates isotype switching to IgE and IL-5 stimulates production and maturation of eosinophils. Inflammatory mediators like histamine facilitate bronchoconstriction, mucus production and influx of leukocytes. Later Eotaxin is released which recruits eosinophils. Eosinophils release major basic protein which damages epithelial cells and produces airway constriction.

What are other chemical mediators involved in Extrinsic Asthma?

Leukotriene C, D, E4 cause prolonged bronchoconstriction. Acetylcholine causes airway muscle contraction.

What is Intrinsic Asthma?

What is Bronchiectasis?

What are some histologic changes in Extrinsic Asthma?

Thickening of the basement membrane, edema and mixed inflammatory infiltrate, hypertrophy of submucosal glands and hypertrophy/hyperplasia of smooth muscle cells. Also see spiral shaped mucus plugs which contain old epithelial cells-Curschmann Spirals. This is a pathologic effect of major basic protein. Crystalline granules in eosinophils coalesce to form Charcot-Leyden crystals.

What are clinical findings in Extrinsic Asthma?

Episodic wheezing, nocturnal cough, increased AP diameter from air trapping. Initially have respiratory alkalosis but may turn into respiratory acidosis if bronchospasm is not relieved.Nonimmune asthma caused by virus-induced respiratory infection, or air pollutants.

Permanent dilation of bronchi and bronchioles due to destruction of cartilage and elastic tissue by chronic necrotizing infections.

What are some causes of Bronchiectasis?

Cystic Fibrosis, Infection (TB, adenovirus, staph, HiB), bronchial obstruction (bronchogenic carcinoma), Primary ciliary dyskinesia (absent dynein arm in cilia aka Kartagener's Syndrome), Allergic Bronchopulmonary Aspergillosis.

What are some clinical findings in Bronchiectasis?

Cough productive of massive amounts of sputum, hemoptysis, digital clubbing, cor pulmonale, crowded bronchial markings that extend to lung periphery.

What is Cystic Fibrosis?

Primary breast cancer, colon cancer and renal cell carcinoma.

Autosomal Recessive disease. Three nucleotide deletion on chromosome 7(should be phenylalanine) resulting in defective CF transmembrane conductance regulator (CFTR) for chloride ions. Defective protein is degraded in the Golgiso there is decreased reabsorption of Na+ and Cl- from sweat glands, but decreased secretion of Na and Cl into luminal secretions. This results in dehydrated body secretions which are thick and easily infected.

What are clinical findings in CF?

Nasal polyps, heat exhaustion, respiratory infections/failure, cor pulmonale, pneumothorax, malabsorption, type I diabetes from pancreatic destruction, infertility in males (atresia of vas deferens), meconium ileus, rectail prolapse from straining, gallstones from thick bile and secondary biliary cirrhosis.

What are risk factors for lung cancer?

Smoking, Radon gas (uranium mining), asbestos, metal exposure-chromium, cadmium, beryllium, arsenic- secondhand smoke, ionizing radiation, air pollution, prior TB

What are some features of adenocarcinoma?

Most common tumor, weakest smoking association, tends to be peripherally located bc filters in cigarettes remove large carcinogens leaving the small ones that can move peripherally.

What are some features of squamous cell carcinoma?

2nd most common tumor, greatest smoking association. Tends to be centrally located (mainstem bronchus)

What are common sites for metastasis?

Hilar lymph nodes (most common), adrenal glands, liver, brain, bone

Which cancers are most commonly responsible for lung metastasis?

What is a Pancoast tumor?

Where in the lung do tumors commonly metastasize?

Parenchyma, pleura and pleural space (pleural effusions), lymphatics (causes severe dyspnea)

What are common findings in primary lung cancer?

Cough, weight loss, chest pain, hemoptysis, dyspnea, superior vena cava syndrome

Superior sulcus tumor. Usually a primary squamous cancer located at the extreme apex of the lung. Causes desctruction of superior cervical sympathetic ganglion producing Horner's syndrome.

What are some paraneoplastic changes associated with lung cancers?

Digital clubbing from reactive periosteal changes in underlying bone. Muscle weakness (Eaton Lambert Syndrome). Ectopic hormone secretion (ACTH)

What are the common causes of mediastinal masses?

Usually metastatic primary lung cancer in older patients, usually a primary disease in younger patients. Neurogenic tumors (posterior mediastinum)- neuroblastoma (malignant in children), ganglioneuroma (benign in adults). Thymomas, pericardial cysts, malignant lymphomas (anterior mediastinum, usually nodular sclerosing Hodgkin's in a woman), teratomas-usually benign, in anterior mediastinum.

What are some symptoms of Thymoma?

Thymoma is usually benign (70%) neoplastic epithelial tissue. Most patients have systemic symptoms of Myesthenia Gravis. Most commonly have follicular B cell hyperplasia in the thymus (that's where antiacetylcholine antibodies are synthesized). Also can have hypogammaglobulinemia, RBC aplasia and increased incidence of other autoimmune diseases.

Describe a transudate

Describe an exudate Protein-rich and cell-rich fluid from increased vessel permeability.

Describe Chylous fluid

Describe Pseudochylous fluid

What is the etiology of pleural effusions?

Increased hydrostatic pressure in visceral pleura (CHF), decreased oncotic pressure (nephrotic syndrome), obstruction of lymphatic drainage from pleura (lung cancer), increased vessel permeability of pleural capillaries (pulmonary infarction, pneumonia), metastasis to the pleura (metastatic breast cancer).Ultrafiltrate of plasma from disturbances in Starling pressures (CHF, nephrotic syndrome)

Indicates interruption of the thoracic duct. Turbid, milky appearance. Can be from malignancy, trauma (iatrogenic) or too many chylomicronsTurbid, milky appearance from increased inflammation with necrotic debris. Most often from rheumatoid lung disease.

How do you distinguish between exudate and transudate?

Ratio of pleural fluid protein and LDH to serum protein and LDH. PF protein/serum protein <0.5 is transudate, >0.5 is exudate. PF LDH/serum LDH <0.6 is transudate, >0.6 is exudate. PF LDH <200 U/L is transudate, >200 U/L is exudate

How does a spontaneous pneumothorax happen?

Commonly seen in tall, thin young men, 20-40 yrs old, increased risk with smoking. Can be caused by rupture of apical subpleural blebs (secondary to high negative intrapleural pressure), COPD, Marfan syndrome, scuba diving, insertion of a subclavian catheter. Loss of negative intrapleural pressure causes collapse of lung. Sudden onset of dyspnea with pleuritic chest pain.

What is the pathogenesis of a Tension Pneumothorax?

Penetrating trauma to the lungs, rupture of tension pneumocytes. Flap like tear in pleura allows air into pleural cavity but prevents its release resulting in increasing positive intrapleural pressure. This results in compression atelectasis. Sudden onset of severe dyspnea and plueritic chest pain, can cause trachea and mediastinal structures to deviate to contralateral side. Can cause compromised venous return to the heart.

ReproductiveWhat vein drains the ovaries/testes?

Ovary/Testis drains to the para-aortic lymph nodes.

Connects ovaries to the lateral pelvic wall and contains the ovarian vessels.

Connects the cervix to the side wall of the pelvis and contains the uterine vessels.

Contains the Uterine fundus to the labia majora but carries no structures.

Derivative of the Gubernaculum. Travels through the round inguinal canal.

Connects the ovary to the uterus and does not contain any structures.

Becomes the Glans Penis or Clitoris

Becomes the shaft of the penis or the labia minora

Scrotum and Labia majora

Sympathetic nervous system via the hypogastric nerve

Visceral and somatic via the pudendal nerve

Acrosome, head, nucleus, neck, middle piece, tail

Maintain the germ pool and produce primary spermatocytes

Left Gonadal vein to the left renal vein to the IVC. Right ovary/testis drains to right gonadal vein straight to the IVC.

What is the lymphatic drainage of the Ovaries/Testes?Where does lymph from the vagina/vulva/scrotum drain to?

Distal 1/3 of the vagina/vulva/scrotum drains to the superficial lymph nodes. Proximal 2/3 of vagina/uterus drains to the obturator, external iliac and hypogastric lymph nodes

What does the suspensory ligament of the ovaries connect?What does the Cardinal ligament connect?What does the Round ligament of the uterus connect?What is the round ligament of the uterus derive from?What does the Broad Ligament connects?

Connects the uterus, fallopian tubes, and ovaries to the pelvic side wall. Contains the ovaries, fallopian tubes, and round ligaments of the uterus.

What does the Ligament of the ovary connect?What does the Genital Tubercle become?What does the Urogenital Fold become?What does the labioscrotal swelling become?What is the pathway of sperm during ejaculation?

(SEVEN UP) Seminiferous tubules to epididymis to vas deferens to ejaculatory ducts (nothing) to urethra to the penis

What is the autonomic innervation causing an erection?

Erection-Parasympathetic nervous system (pelvic nerve). Nitric oxide increases cGMP which causes smooth muscle relaxation which causes vasodilation and is proerectile. Also Norepinephrine causes an increase in Calcium which causes smooth muscle contraction which causes vasoconstriction and is antierectile.

What is the autonomic innervation causing Sperm Emission?What is the autonomic innervation causing Ejaculation?What are the different parts of the sperm?Where do the different parts of the sperm come from?

Acrosome-Golgi apparatus, Flagellum/Tail-Centrioles, Middle Piece-contains the mitochondria, Head and nucleus come from the nucleus.

What is the function of spermatogonia?

What is the function of Sertoli Cells?

What is the function of Leydig Cells? Secrete testosterone

What is the composition of Semen?

What is spermiogenesis?

What are the common Androgens? Testosterone (Testes), Dihydrotestosterone (Converted peripherally) and Androstendione (Adrenal)

5 Alpha reductase converts Testosterone to DHT.

Development of genitalia (external) and breast, and female fat distribution.

Secrete inhibin which inhibits FSH. Secrete Androgen Binding Protein to maintain the level of testosterone. Form tight junctions between adjacent Sertoli Cells to form the blood-testis barrier, isolating gametes from immune attack. Support and nourish spermatozoa. Regulate spermatogenesis. Produce Anti-Mullerian hormone.

Seminal Vesicle Products(fructose, ascorbic acid, prostaglandins, phosphorylcholine, flavins), Prostate Products (Zinc, citrate acid, phospholipids, acid phosphatase, fibrinolysin), Sperm

Describe the general process of spermatogenesis

Spermatogenesis begins at puberty with spermatogonia. Full development takes 2 months. Occurs in seminiferous tubules. Produces spermatids that undergo spermiogenesis to form mature spermatozoaMaturation of sperm as they lose their cytoplasmic contents, gain an acrosomal cap and become mature spermatozoa

Describe the process of spermatogenesis.

Spermatogonium (diploid 2N) copies genome to make Primary spermatid (Diploid 4N). Primary spermatocyte divides into 2 secondary spermatocytes (Haploid 2N). The Secondary spermatids divide again to produce 4 spermatids (Haploid, 1N). These undergo spermiogenesis to form mature spermatozoa

Describe the hormonal regulation of Spermatogenesis.

Hypothalamus releases GnRH which causes FSH and LH release from the anterior pituitary. LH stimulates testosterone release from Leydig cells which release testosterone into the seminiferous tubules and the blood. FSH stimulates Sertoli cells to produce Androgen Binding Protein and Inhibin. Testosterone from the Leydig cells stimulates spermatogenesis and stimulates the Sertoli Cells to nurse the Spermatozoa. Inhibin from the Sertoli cells feeds back and downregulates FSH release. Testosterone from Leydig cells feeds back and downregulates LH production and GnRH release.

What are the functions of Testosterone in development?

Differentiation of the Epididymis, Vas deferens and seminal vesicles. Growth spurt of the penis, the seminal vesicles, sperm, muscle, and red blood cell growth. Deepening of voice, closing of epiphyseal plates (via estrogen converted from testosterone) and Libido.

What is the function of Dihydrotestosterone in development?

In early differentiation it causes development of the penis, scrotum and prostate. In later/pubertal development it causes prostate growth and sebaceous gland activity.

How is testosterone converted to DHT?What are the sources of Estrogen in a woman?

Ovary makes 17 Beta estradiol, Placenta makes estriol and blood/peripheral tissues can aromatize androgens to estrogen.

What is the function of Estrogen in development?

50 fold increase in estradiol and estrone. 1000 fold increase in estriol indicates fetal well being.

What is the source of Progesterone? Corpus Luteum, placenta, adrenal cortex and testes (in men obviously)

Ovulation!!!

What is the function of Progesterone?

When is follicular growth fastest? 2nd week of the proliferative phase.

Estrogen

What maintains the endometrium? ProgesteroneWhat defines Oligomenorrhea? Cycle greater than 35 daysWhat defines Polymenorrhea? Cycle less than 21 daysWhat defines Metorrhagia? Frequent but irregular menstruationWhat defines Menometrorrhagia? Heavy, irregular menstruation

What are the typical functions of estrogen beyond development?

Growth of the follicle, endometrial proliferation, increased myometrial excitability. Upregulates LH, FSH and estrogen receptors and thus upregulates itself. Feedback inhibition of LH and FSH and then the LH surge. Stimulates prolactin secretion but blocks its action at the breast. Increases transport of proteins, Steroid hormone binding globulin synthesis, increases HDL and decreases LDL.

How much do estrogens increase in pregnancy?

Describe the hormonal regulation of estrogen.

Pulsatile GnRH from the Hypothalamus causes release of FSH and LH from the anterior pituitary. FSH stimulates the granulosa cells of the ovaries to increase Aromatase which can then convert androstendione to estrogen. LH acts on the Theca cells to upregulate Desmolase which convert cholesterol to androstendione. The androstendione goes to the granulosa cells to be converted to estrogen.

What does elevation of progesterone indicate?

Stimulation of endometrial glandular secretions and spiral artery development. Maintains pregnancy. Decreases myometrial excitability. Increases production of thick cervical mucous, which inhibits sperm entry into the uterus. Increases body temperature (hence why you take your temp), inhibits gonadotropins (LH and FSH), relaxes uterine smooth muscle (prevents contraction) and decreases estrogen receptor expressivity.

What happens during the proliferative/follicular phase of a woman's cycle?

Granulosa cells respond to FSH and stimulate growth of 10-20 follicles. LH responsive Theca cells stimulate growth of the corpus luteum and produce androgens which are converted to estrogen by granulosa cells (to stimulate the developing follicle). Estrogen encourages growth of the endometrium and provides positive feedback to the anterior pituitary to stimulate release of more FSH/LH leading to the midcycle gonadotropin surge. About 1 week before ovulation, one follicle becomes dominant meaning that it becomes more responsive to FSH. The follicle secretes lots of inhibin which downregulates FSH and causes atresia of the other follicles.

What stimulates endometrial proliferation?

What is Mittelschmerz? Blood from ruptured follicles which can cause peritoneal irritation that mimics appendicitis.

What is the process of oogenesis?

How is lactation induces after labor? The decrease in maternal steroids induces lactation.

PRL induces and maintains lactation and decreases reproductive function.

Describe the hormonal changes during a woman's cycle (see Reproductive Attachment 1).

During the follicular phase, both estrogen and progesterone are low. FSH is fairly low as is LH initially. LH spikes about halfway through the follicular phase which increases estrogen above its threshold. Estrogen feeds back onto LH which causes it to spike along with an estrogen spike. FSH is also increased and has a small spike along with the LH spike. This causes ovulation and begins the secretory/luteal phase. LH and FSH then drop. Estrogen increases again but Progesterone increases a lot throughout the whole phase thus maintaining the lining of the endometrium. Everything drops when entering the menstrual phase which allows the endometrial llining to shed.

Describe the maturation of the Follicle (see Reproductive Attachment 2).

A primordial follicle consists of an oocyte surrounded by a single layer of squamuos granulosa cells. The granulosa cells enlarge and become cuboidal turning the follicle into a primary follicle. The primary follicle then enlarges and the granulosa cells form more than one layer. The Zona Pellucida then forms around the oocyte. The structure becomes a secondary follicle when fluid filled vesicles develop among the granulosa cells and a well developed capsule, Theca layer, becomes apparent around the granulosa cells. The Theca has both internal and external layers. It becomes a mature follicle when the vesicles form a single antrum. At full maturity, the oocyte is located in the cumulus mass.

What happens to the follicle during ovulation?

During ovulation, the oocyte is released with some granulosa cells called the corona radiata. The remaining granulosa cells divide rapidly and enlarge to form the corpus luteum which makes progesterone for the remainder of the cycle or the beginning of pregnancy. The corpus luteum then degenerates to form the corpus albicans and eventually becomes fibrotic.

What hormonal changes are seen during ovulation?

Increased estrogen, increased GnRH and increased GnRH receptors on anterior pituitary, estrogen surge precedes LH surge. Increased temperature from increased progesterone.

When does oogenesis begin and when is it completed?

Primary oocytes begin Meiosis I during fetal life but don't complete Meiosis I until just before ovulation. Thus Meiosis I is arrested in Prophase for years until ovulation. Meiosis II arrests in metaphase until fertilization. If there is no fertilization, the secondary oocyte degenerates.Begins with a diploid Oogonium (2N) which replicates (interphase) to become a diploid primary oocyte (4N). The Primary oocyte then arrests in Prophase I until ovulation. During ovulation it divides to become a secondary haploid oocyte (2N) and a polar body which degenerates. It arrests in Metaphase II here until fertilization. The secondary Oocyte divides again to become a Haploid Ovum (1N) and another polar body that degenerates.

Where does Fertilization most commonly happen?

Most commonly happens in the upper end of the Fallopian tube (the ampulla). Typically within a day after ovulation.

When does implantation into the wall of the uterus typically occur?

6 days after fertilization. The trophoblast secretes Beta-HCG which is detectable in the blood 1 week after conception and in urine (home test) 2 weeks after conception.

How is milk production maintained after birth?

Suckling increases nerve stimulation which increases oxytocin and prolactin production thus maintaining milk production.

What is the role of Prolactin in the female?

Helps with milk letdown and may be involved with uterine contractions.Where is hCG made? Syncytiotrophoblast of the placenta.

What is the function of hCG?How is pregnancy detected? hCG is used to detect pregnancy because it appears early in the urine.

HHAVOC-Hirsutism, Hot flashes, Atrophy of the Vagina, Osteoporosis, Coronary artery disease

What is Klinefelter's Syndrome?

What is Turner's Syndrome?

Describe a double Y male 47 (XYY). Phenotypically normal, very tall, severe acne, antisocial behavior in 1-2%, normal fertility.

Increased testosterone and increased LH (female phenotype I think)

Increased testosterone but decreased LH from negative feedback

Decreased testosterone and increased LH from gonadal failure and lack of feedback.

Decreased testosterone and decreased LH from pituitary failure not stimulating the gonads.What is pseudohermaphroditism? Disagreement between the phenotypic (external genitalia) and gonadal (testes vs ovaries) sex.

What is the role of Oxytocin in the female?

Maintains corpus luteum (thus progesterone) for the first trimester by acting LH. The Placenta synthesizes its own estriol and progesterone during the 2nd and 3rd trimester and the corpus luteum degenerates.

What changes in hCG are there in pathologic states?

hCG is elevated in Hydatidiform moles, Choriocarcinoma, Gestational trophoblastic tumors (and other tumors I think)

What hormonal changes are seen in menopause?

Decreased Estrogen production due to age linked decline in follicles. Significantly increased FSH, increased LH, increased GnRH. Average age of onset is 51, earlier in smokers. Usually preceded by a few years of irregular periods.

What is the main source of Estrogen after menopause?

Estrone from peripheral conversion of androgens. Increased androgens can cause hirsutism (that's why your grandma has a mustache)

What are some symptoms of menopause?

47 (XXY). Causes testicular atrophy, eunuchoid body shape, tall, long extremities, gynecomastia, female hair distribution. May cause developmental delay. Usually a Barr body is present (inactive X chromosome)

How does Klinefelter's Syndrome cause infertility?

Dysgenesis of seminiferous tubules causes decreased inhibin which leads to increased FSH. Abnormal Leydig cell function causes decreased testosterone and increased LH and estrogen.45 (XO). Causes short stature, ovarian dysgenesis (streak ovaries), shield chest, bicuspid aortic valve, webbing of the neck from cystic hygroma, preductal coarctation of the aorta, no Barr body and primary amenorrhea.

What hormonal changes would you see with a defective androgen receptor?

What hormonal changes would you see with a Testosterone-secreting tumor, or exogenous steroids

What hormonal changes would you see with primary hypogonadism?What hormonal changes would you see with Hypogonadotropic hypogonadism?

What is a male pseudohermaphrodite?What is a true hermaphrodite? (46, XX or 47, XXY). Both ovaries and testicular tissue present. Ambiguous genitalia. Very rare.

What is 5 alpha reductase deficiency?

What is a Hyaditiform Mole?

What is a complete Hyaditiform Mole?

What is pre-eclampsia? Combination of hypertension, proteinuria and edema.What is eclampsia? Pre-eclampsia + Seizures

Pre-existing hypertension, diabetes, chronic renal disease and autoimmune disorders.

What is HELLP Syndrome? Hemolysis, Elevated LFT's, Low Platelets from Pre-eclampsia

What is Abruptio Placentae?

What is a female pseudohermaphrodite?

46 (XX). Ovaries are present but the external genitalia are virilized or ambiguous. It's due to excessive or inappropriate androgen exposure during early gestation. Usually congenital adrenal hyperpasia or exogenous androgen administration.46 (XY). Testes are present but external genitalia are female or ambiguous. The most common reason is androgen insensitivity syndrome aka testicular feminization.

What is Androgen Insensitivity Syndrome?

Defect in androgen receptors resulting in normal-appearing female. Female external genitalia with a rudimentary vagina. Uterus, uterine tubes are generally absent. No sexual hair. Testes are often found in the labia majora and must be surgically removed to prevent malignancy. Increased testosterone (although no response), increased estrogen and LH

Inability to convert testosterone to DHT. Ambiguous genitalia until puberty when the massive testosterone increase causes masculinization and increased growth of the external genitalia. Testosterone/estrogen levels are normal; LH is normal or increased. Internal genitalia are normal.Cystic Swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast) that presents with abnormal vaginal bleeding. Most common cause of Choriocarcinoma. See increased Beta-hCG, a honeycombed uterus, looks like a cluster of grapes (if a cluster of grapes is totally disgusting looking). See an abnormally enlarged uterus. 2 sperm with a completely empty egg. Classically have a snowstorm appearance with no fetus during first sonogram. Moles can lead to uterine rupture. Treat with dilitation and curettage and methotrexate. Monitor Beta-hCG.

What characteristics are seen in a complete mole?

Karyotype is 46,XX or 46, XY. Massively increased hCG, increased uterine size, 2% convert to adenocarcinoma, no fetal parts, 2 sperm +empty egg, 15-20% form malignant trophoblastic disease.

What characteristics are seen in a partial mole?

Karyotype is 69,XXY, slightly increased hCG, no change in uterine size, rare for it to convert to choriocarcinoma, 2 sperm+1 egg, risk of malignancy is less than 5%

What are some common causes of recurrent miscarriages?

during the 1st weeks- low progesterone levels (no response to Beta-hCG, 1st trimester-chromosomal abnormalities, 2nd trimester-bicornate uterus

What are some risk factors for pre-eclampsia?What is the pathogenesis of Pre-eclampsia?

Caused by placental ischemia due to impaired vasodilation or spiral arteries, resulting in increased vascular tone. May be an issue with implantation.

What are some clinical features of Pre-eclampsia?

Headache, blurred vision, abdominal pain, edema of the face and extremities, altered mentation, hyperreflexia. Lab findings include thrombocytopenia and hyperuricemia.

How do you treat Pre-Eclampsia or Eclampsia?

Delivery of the fetus as soon as it's viable. Otherwise bed rest, salt restriction, and monitoring/treatment of hypertension. Treatment is IV magnesium sulfate and diazepam to prevent seizures of eclampsia.Premature detachment of the the placenta from the implantation site. Fetal death and DIC may occur. Increase in risk with smoking, hypertension and cocaine use.

What is Placenta Acreta?What is Placenta Increta? Just like Placenta Acreta but extends further into the myometrium.

What is Placenta Percreta?

What is Placenta Previa?

What is an Ectopic Pregnancy?

May cause postpartum hemorrhage.

What is Polyhydramnios?

What is Oligohydramnios?

What is Potter's Syndrome?

HPV 16 and 18

Multiple sexual partners, smoking, early sexual intercourse, HIV infection

What is a Koilocyte?

What is Endometriosis?

Severe menstrual-related pain.

Defective decidual layer allows the placenta to attach to the myometrium. No separation of the placenta after birth. May cause massive bleeding after delivery. Associated with prior C-Section. Acreta does not penetrate the entirety of the myometrium.

The worst form of Placenta Acreta which involves the placenta extending all the way through the myometrium to the serosa. The placenta may then attach to other organs like the bladder or rectum.Attachment of the placenta to the lower uterine segment. May then occlude the internal os (so baby can't get out). Associated with multiparity and prior C-Section.

Pregnancy that isn't in the uterus. Most often in the Fallopian tubes. Suspect with increased hCG and sudden lower abdominal pain. Confirm with ultrasound. May be clinically mistaken for appendicitis.

What is the problem with retained placental tissue?

What are some risk factors associated with ectopic pregnancy?

History of infertility, Salpingitis/PID, ruptured appendix (at any point), prior tubal surgery or any lower abdominal surgery, endometriosis.Greater than 1.5-2 Liters of amniotic fluid. Associated with esophageal and duodenal atresia, causing inability to swallow amniotic fluid. Also associated with anencephaly.

Less than 0.5 Liters of amniotic fluid. Associated with placental insufficiency, bilateral renal agenesis or posterior urethral valves (in men) and thus an inability to excrete urine. Can cause Potter's syndrome.Atypical appearance of the fetus in the womb as a result of oligohydramnios. Causes clubbed feet, pulmonary hypoplasia and cranial anomalies.

Describe Dysplasia and Carcinoma in Situ of the cervix.

Disordered epithelial growth. Begins at the basal layer of the squamo-columnar junction and extends outward. Classified as CIN I, CIN II or CIN III (Carcinoma in Situ), depending on the extent of the dysplasia.

What virus is associated with Cervical dysplasia?What risk factors are associated with cervical dysplasia?

Describe invasice carcinoma of the cervix

Pretty much the cervical cancer gone really nasty. Often squamous cell carcinoma. Papsmear can catch cervical dysplasia (koilocytes) before it becomes invasive carcinoma. Lateral invasion can block ureters causinf renal failure.Cervical cell infected with HPV that is undergoing dysplasia. See large nuclei and large ring of cytoplasm. See Attachment 3 for some pics.

Non-neoplastic endometrial glands/stroma in an abnormal location outside the uterus. Characterized by cyclic bleeding from the ectopic endometrial tissue resulting in blood filled "chocolate cysts." Does anyone else want to puke right now? Often in the ovary or on the peritoneum.

How does Endometriosis manifest clinically?

Often causes infertility, possibly due to retrograde mentrual flow or ascending infection. What is Adenomyosis? Endometrium within the myometrium

What is Endometrial Hyperplasia?

What is Endometrial Carcinoma?

Describe a Leiomyoma?

What is a Leiomyosarcoma?

Incidence- Endometrial>Ovarian>Cervical. Worst Prognosis- Ovarian>Cervical>Endometrial

What is premature Ovarian failure?

What is Polycystic Ovarian Syndrome?

Increased LH and FSH and increased Testosterone.

What is a Follicular Cyst?What is a Corpus Luteum cyst? Hemorrhage into persistent corpus luteum. Commonly regresses spontaneously.

What is a Theca Lutein Cyst?

What are possible complications of Endometriosis?

Abnormal endometrial gland proliferaton usually caused by excess estrogen stimulation. Associated with increased risk for endometrial carcinoma.

How does Endometrial Hyperplasia manifest clinically and what are some risk factors?

Postmenopausal vaginal bleeding. Risk factors are anovulatory cycles, hormone replacement therapy, polycystic ovarian syndrome and granulosa cell tumors.Most common gynecologic malignancy, usually between 55 and 65 years of age. Usually a progression of endometrial hyperplasia so presents with vaginal bleeding after menopause. Risk factors are prolonged estrogen exposure without progesterone, obesity, diabetes, hypertension, nulliparity and late menopause. The more it's invaded the myometrium, the worse the prognosis.

Most common cause of all tumors in females. Essentially a Fibroid. Often causes multiple tumors with well demarcated borders. This is a benign smooth muscle tumor and malignant transformation is very rare. Mostly occurs between 20-40 years old and is often asymptomatic. may cause abnormal uterine bleeding or result in miscarriage. If bleeding is severe it may cause Iron deficiency anemia. See a whorled pattern of smooth muscle bundles (doesn't become Leiomyosarcoma). See attachment 4 for a picture.

Bulky, irregularly shaped tumor with areas of necrosis and hemorrhage. Nasty tumor. Typically arises de novo, not from a Leiomyoma. Highly aggressive tumor with a tendency to recur. May protrude out of the cervix and bleed (yuck!). More common in middle aged women and African American women.

What is the epidemiology of gynecologic tumors?

Premature atresia of ovarian follicles in women of reproductive age. Presents with signs of menopause after puberty but before age 40. See decreased estrogen but increased LH and FSH b/c no feedback.

what are the most common causes of anovulation?

Polycystic ovarian syndrome, obesity, Asherman's Syndrome (adhesions), HPO axis abnormalities, premature ovarian failure, hyperprolactinemia, thyroid disorders, eating disorders, Cushing Syndrome and adrenal insufficiency

Increased LH production leading to anovulation, hyperandrogenism due to deranged steroid synthesis by theca cells. Enlarged bilateral cystic ovaries manifest clinically with amenorrhea, infertility, obesity and hirsutism. Associated with insulin resistance, increased risk of endometrial cancer. Treatment is weight loss, OCP, gonadotropin analogs, clomiphene or surgery.

What hormonal changes do you see in PCOS?

Distention of a ruptured Grafian Follicle. May be associated with hyperestrinism and endometrial hyperplasia.

Commonly bilateral or multiple cysts. Due to gonadotropin stimulation. Associated with choriocarcinoma and moles.

What is a Chocolate Cyst? Blood-containing cyst from ovarian endometriosis. Varies with the menstrual cycle.

Most common in adolescents

What is a Dysgerminoma?

What is a Choriocarcinoma?

What is a teratoma?

What is a serous cystadenoma?

Makes up about 50% of ovarian tumors, malignant and frequently bilateral.

What is a Mucinous Cystadenoma? Multilobular cyst lined by mucus-secreting epithelium. Benign. Intestine-like tissue.

What is a Brenner tumor? Benign tumor that looks like the bladder.What is a Fibroma? Bundles of spindle shaped fibroblasts.

What is Meigs' Syndrome?

What is a Granulosa Cell Tumor?

What is a Krukenberg tumor? GI Malignancy that metastasizes to the ovaries, causing a mucin-secreting signet cell adenocarcinoma.

Secondary to squamous cell carcinoma of the cervix.

Affects women who had exposure to DES in utero.

Affects girls < 4 years of age. Spindle shaped tumor cells that are desmin positive.

Rare. Present with pain in the labia majora. Can result from previous infection.

What age group most commonly gets Ovarian Cell Tumors?

Malignant, equivalent to a male seminoma, but rarer (1% vs 30%). Sheets of uniform cells with hCG and LDH.Rare but malignant. Can develop during pregnancy in mother or the baby. Large, hyperchromatic syncitiotrophoblastic cells. Increased frequency of theca-lutein cysts. Along with moles, comprise spectrum of gestational trophoblastic neoplasia. hCG is the tumor marker.

What is a yolk sac (endodermal sinus) tumor?

Aggressive malignancy in the ovaries (testes in boys) and sacrococcygeal area of young children. These are yellow, friable, solid masses. 50% have Schiller Duval bodies that resemble glomeruli. Alpha fetoprotein is the tumor marker.

90% of ovarian germ cell tumors. Contain cells from 2-3 germ layers. Mature teratomas/Dermoid cysts are the most frequent benign ovarian tumors/teratomas. Immature teratomas are aggressively malignant. Struma Ovarii contain functional thyroid tissue. Can present as hyperthyroidism.Makes up about 20% of ovarian tumors. Frequently bilateral, lined with Fallopian tube-like epithelium. Benign.

What is a serous cystadenocarcinoma?

What is a Mucinous Cystadenocarcinoma?

Malignant! Pseudomyxoma peritonei- intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor.

Associated with Fibromas. Triad of ovarian fibroma, ascites and hydrothorax. Causes pulling sensation in the groin.

Secretes estrogen-causes precocious puberty. Can cause endometrial hyperplasia or carcinoma in adults. See Call-Exner bodies-small follicles filled with eosinophilic secretions. Abnormal uterine bleeding.

What causes squamous cell carcinoma of the vagina?What predisposes to Clear Cell Adenocarcinoma?Who is affected by Sarcoma Botryoides (variant of Rhabdomyosarcoma)

How do Bartholin's gland cyst present?

What is an Intraductal Papilloma?

What is a Phyllodes Tumor?

What is invasive ductal carcinoma?

What is an invasive Lobular tumor? Malignant breast tumor, often multiple and often bilateral. See an orderly row of cells.

Malignant tumor with a good prognosis. See fleshy, cellular, lymphatic infiltrate.

Subtype of DCIS. See ductal caseous necrosis.

What is Paget's disease?

What is Fibrocystic disease?

What is acute mastitis?

What is Fat Necrosis?

What is Gynecomastia?

What is a Fibroadenoma of the breast?Small, mobile, firm mass with sharp edges. Most common tumor in those <25 years. See increasing siza and tenderness with increasing estrogen such as during menstruation. Not a precursor to breast cancer.Small tumor that grows in lactiferous ducts. Typically beneath areola. See serous or bloody nipple discharge. Slight (1.5-2X) increased risk for breast carcinoma.Large bulky mass of connective tissue and cysts with "Leaf like projections." Most common in the 6th decade. Some may become malignant.

How do malignant breast tumors arise and when/where are they most common?

Common postmenopause. Arise from mammary duct epithelium or lobular glands. Overexpression of estrogen/progesterone receptors on erb-B2 (HER-2 and EGF Receptor) is common. Affects therapy and prognosis. Axillary lymph node involvement is the single most important prognostic factor.

What are some risk factors for malignant breast tumors?

Risk factors are increased estrogen exposure. Increased total number of menstrual cycles, older age at 1st live birth, obesity (adipose tissue serves as a major source of estrogen in post-menopausal women by converting androstenedione to estrone).

What is a Ductal Carcinom in Situ (DCIS)?

Malignant tumor of the breast that fills the ductal lumen. Arises from ductal hyperplasia. Early malignancy without basement membrane penetration.Worst and most invasive ductal carcinoma but also most common. Forms firm, fibrous, rock hard masses with sharp margins and small, glandular duct like cells.

What is a medullary tumor of the breast?What is a comedocarcinoma of the breast?What is an inflammatory tumor of the breast?

Nasty, malignant tumor with a 50% 5 year survival. See dermal lymphatic invasion by breast carcinoma. See Peau d'orange-breast skin looks like orange peel.Eczematous patches on nipples. Paget cells are large cells in the epidermis with clear halo around them. May also be seen on the vulva. Suggests an underlying carcinoma.Most common cause of breast lumps after age 25. Presents with premenstrual breast pain and multiple lesions, often bilaterally. See a fluctuation in size of the mass. Usually does not indicate increased risk of carcinomas.

What are the histologic subtypes of Fibrocystic disease?

Fibrosis-hyperplasia of breast stroma. Cystic-fluid filled, blue dome. Ductal dilation. Sclerosing adenosis-increases acini and intralobular fibrosis. Associated with calcifications. Epithelial hyperplasia-increase in number of epithelial cell layers in terminal duct lobule. Increases risk of carcinoma with atypical cells. Occurs in women >30 years of age.Breast abscess. During breast feeding. Increases risk of bacterial infection through cracks in the nipple. Staph Aureus is the most common pathogen.A benign, painless lump. Forms as a result of injury to breast tissue. Up to 50% of patients may not report trauma.Results from hyperestrogenism (cirrhosis, testicular tumor, puberty, old age), Klinefelter's syndrome or drugs (estrogen, marijuana, heroin, psychoactive drugs, Spironolactone, Digitalis, Cimetidine, Alcohol, Ketoconazole).

Nipple, Lactiferous sinus, major duct, terminal duct, lobules. All surrounded by stroma

How does prostatitis present? Dysuria, frequency, urgency, low back pain.

What are causes of acute prostatitis? Usually bacterial, especially E. Coli

May be bacterial or abacterial.

How do you treat BPH? Use alpha antagonists like Terazosin, tamulosin, which cause relaxation of smooth muscle.

What is Prostatic adenocarcinoma?

What is cryptorchidism?

95% of all testicular tumors. May present as a mixed germ cell tumor.

What is a Seminoma?

What is an embryonal carcinoma?

What is a Choriocarcinoma in a man?What is a teratoma in a man? Similar to females except that mature teratomas in men are usually malignant.

5% of all testicular tumors, most of which are benign.

What is the order of structures in the breast starting at the nipple?

What tumors occur at each of these structures?

Nipple-Paget's disease, breast abscesses. Lactiferous sinus-Intraductal papilloma, breast abscess, mastitis. Major duct-Fibrocystic change, ductal cancer. Terminal ducts-Tubular carcinoma. Lobules-lobular carcinoma, sclerosing adenitis. Stroma-Fibroadenoma, phyllodes tumor.

What are causes of chronic prostatitis?

What is Benign Prostatic Hyperplasia (BPH)?

Hyperplasia (not hypertrophy) of the prostate gland. May be due to an age related increase in estradiol with possible sensitization of the prostate to the growth-promoting effects of DHT. Characterized by a nodular enlargement of the periurethral (lateral and middle) lobes, which compress the urethra into a vertical slit. Often present with increased frequency of urination, nocturia, difficulaty starting and stopping the stream of urine and dysuria. May lead to distention and hypertrophy of the bladder, hydronephrosis and UTI's. Not considered premalignant. Do see increased free PSA but not rapidly increasing like in cancer.

Common in men >50. Arises most frequently from the posterior lobe of the prostate(peripheral zone) and is most commonly diagnosed by digital rectal exam and prostate biopsy. Prostatic acid phosphatase and PSA are the most useful tmor markers. See increased total PSA with decreased fraction of free PSA. Osteoblastic metastases in bone may develop in later stages and appears as lower back pain and an increase in serum alkaline phosphatase and PSA.

Undescended testis. Lack of spermatogenesis due to increased body temperature. Also associated with increased risk of germ cell tumors. Prematurity increases the risk of cryptorchidism.

How common are testicular germ cell tumors?

Malignant, painless, homogenous testicular enlargement. Most common testicular tumor, mostly affecting males age 15-35. See large cells in lobules with watery cytoplasm and a fried egg appearance. These are radiosensitive, only metastasize late and have a great prognosis.

Malignant, painful tumor with a worse prognosis than a seminoma. Often glandular or papillary morphology. Can differentiate and become other tumors and is associated with increased AFP and hCG.

What is a yolk sac (endodermal sinus) tumor in a man?

Yellow, mucinous tumor analagous to an ovarian yolk sac tumor. See Schiller Duval bodies which resemble primitive glomeruli.Malignant, hCG secreting tumor. Has distinct syncytiotrophoblastic and cytotrophoblastic elements. Causes hematogenous metastases.

How common are testicular non-germ cell tumors?

What is a Leydig Cell Tumor?What is a Sertoli Cell Tumor? Androblastoma from the sex cord stroma.What is testicular lymphoma? Most common testicular cancer in older men. It's pretty much lymphoma in the testicles.

What is a tunica vaginalis lesion? A lesion in the serous covering of the testis. Presents as testicular masses that can be transilluminated.What is a Variocele? Dilated vein in pampinoform plexus which can result in infertility. Looks like a bag of worms.What is a Hydrocele? Increased fluid secondary to incomplete fusion of the processus vaginalisWhat is a spermatocele? Dilated epididymal duct

What is Bowen's Disease?Qhat is Erythroplasia of Queyrat? Red, velvety plaques, usually involving the glans penis. Otherwise similar to Bowen's disease.What is Bowenoid papulosis? Multiple papular lesions. Affects younger men but isn't usually invasive

What is Peyronie's Disease? Bent penis due to acquired fibrous tissue formation.

When does Blastocyst hatching occur? When the blastocyst enters the endometrial cavity, about 5 days after fertilization.What is the Zona Pellucida? Non-cellular, porous layer of glycoproteins around the oocyte.

Apposition, Adhesion and InvasionWhat is the Decidua Basalis? Decidua that forms underneath the embryoWhat is the Decidua Capsularis? Capsule of decidua over the embryoWhat is the Decidua Paritalis? Other decidua lining the uterine cavity

Both are increased but plasma is increased more than RBC. This results in a dilutional effect in hematocrit.

May be due to decreased CO2 stimulating the respiratory center and causing subjective shortness of breath.

Androgen producing tumor which causes gynecomastia in men, precocious puberty in boys. Contains Reinke crystals and is golden brown in color.

Gray, solitary, crusty plaque, usually on the shaft of the penis or on the scrotum. Peak incidence is in the 5th decade of life. Progresses to invasive squamous cell carcinoma in <10% of cases.

What is Squamous Cell Carcinoma of the penis?

Essentially like any other SCC, just on the penis. Commonly associated with HPV and lack of circumcision. More common in Asia, Africa and South America.

What changes are seen in Decidualization?

Glycogen and lipid accumulation, extra-cellular matrix changes, prolactin and IGF binding proteins increased, COX-2 increase which increases PGE2, and influx od dedidual NK cells.

What proteins characterize preimplantation of the embryo?

Early pregnancy factor, Platelet activating factor, human Chorionic Gonadotropin, Matrix Metalloproteinases and Inhibitors of Matrix Metalloproteinases, Heparin binding-EGF like growth factor receptors

What are the three stages of implantation?

What happens to RBC and Plasma volume and mass in pregnancy?

What happens to GFR and Creatinine Clearance during pregnancy?

Creatinine clearance is increased. GFR increases fairly significantly. Increased clearance of creatinine and urea results in serum creatinine and urea that are really low. Thus normal creatinine and urea are problematic.

Why does respiratory alkalosis happen during pregnancy?

Estrogen and progesterone both stimulate the respiratory center. Greater tidal volume and increased respiration rate also cause increased minute ventilation, thus more CO2 is blown off. Thus respiratory alkalosis from decreased PaCO2

Why do women get dyspnea during pregnancy?

What defines menopause? No menses for one year after age 40.

Increase in LH and FSH from a drop in estrogen (LH) and progesterone (FSH)

What is Hirsutism? Excess hair in normal hair-bearing areas.What is virilization? Hirsutism plus male secondary sex characteristics

Increased muscle mass, acne, enlarged clitoris

What causes virilization or hirsutism?

What is Polycystic Ovarian Syndrome?

Menstrual irregularities, mostly oligomenorrhea and often hirsutism, infertility or obesity.

Why are Thyroxin and Cortisol increased in pregnancy?

hCG simulates TSH since they share the same alpha subunit. Thus it stimulates T4 secretion during the first 10 weeks. Estrogen promotes growth of the pituitary and the thyroid and synthesis of thyroid binding globulin. Thus T4 and cortisol are increased but free T4 and cortisol are the same.

What are the physiologic causes of menopause?

Waxing and waning of estrogen levels from decreased ovarian function. Depletion of granulosa and thecal cells. Lack of response to gonadotropins. Increased LH stimulates androgen production in stromal cells (thus hirsutism)

What are non-physiologic causes of menopause?

Surgical removal or radiation of ovaries. Turner syndrome. Family history of early menopause and left handedness (seriously???)

What is the average age of menopause and how is age at menopause determined?

Average age is 51. The age at which it's determined is genetically determined, but smokers reach menopause early and peri-menopause is mid-to late 40's.

What are some clinical findings in menopause?

Secondary amenorrhea, hot flushes, night sweats, atrophic vaginitis with pruritis, burning, bleeding and dyspareunia. Also see mood swings, anxiety, depression, insomnia, decreased libido, urinary incontinence, headaches, tiredness, lethargy, and osteoporosis with increased risk of Colle's and vertebral fractures.

What are some labroratory findings in menopause?What are some treatment options for symptomatic menopause? Estrogen replacement, progestins added if the uterus is still present to prevent endometrial adenocarcinoma. What are risks of long term hormone replacement?

Thromboembolism, Coronary heart disease, stroke, slightly increased risk for breast cancer, increased risk for dementia in women over 65.

What are male secondary sex characteristics?

Both caused by increased androgens of either ovarian or adrenal origin. In the ovaries, the androgen is testosterone, in the adrenals it's DHEA-S

What are some causes of virilization and hirsutism?

Polycystic ovary syndrome, idiopathic causes, adrenogenital syndrome, insuline resistance, drugs like androgenic progestins, phenytoin, cyclosporin, minoxidil. Can also be from ovarian tumors like a leydig or sertoli-leydig cell tumor, adrenal tumors producing Cushing syndrome, decreased steroid hormone binding globulin from obesity and hypothyroidism.

Syndrome that occurs around menarche. See increased synthesis of LH and decreased synthesis of FSH. Increased LH increases androgen synthesis resulting most often in hirsutism. Androgens are then aromatized to estrogen in adipose cells increasing the risk of endometrial carcinoma. The increased estrogen feeds back positively on LH and negatively on FSH. Suppression of FSH causes follicle degeneration resulting in fluid accumulating and producing subcortical cysts that then enlarge the ovaries.

What are clinical findings in polycystic ovarian syndrome?

What are some lab findings in PCOS? LH:FSH ratio >2. Increased serum testosterone and androstendione. Increased serum estrogen.

What is the treatment in PCOS?

What is Menorrhagia?

What is Dysmenorrhea?

NSAID's, OCP, nifedipine, magnesium sulfate

Essentially deal with the underlying disease.

Menorrhagia, Hypomenorrhea, Metrorrhagia, Menometrorrhagia, Oligomenorrhea, Polymenorrhea

Anovulatory cycle in 90% of cases but less than 10% due to anovulation during reproductive years.

What is Primary Amenorrhea?What is Secondary Amenorrhea? Absence of menses for 3 months, most commonly due t pregnancy.

Anovulatory dysfunctional uterine bleeding, Von Willebrand's disease

Weight reduction in obese women. Low dose OCP's or medroxyprogesterone to suppress steroidogenesis and LH. Can use Spironolactone if OCP's are unacceptable to block androgen receptors on the hair follicle. LH-releasing hormone analogs inhibit ovarian androgen production.Loss of blood >80 mL per period. It's likely if sheets are stained despite heavy protection. Excessive passage of clots indicates that plasmin does not have enough time to dissolve clot.

Painful menses, occuring in approximately 50% of women. Primary type occurs in ovulatory cycles due to increased prostaglandin PGF-2alpha. See increased uterine contractions from increased prostaglandins. The secondary type is from endometriosis, adenomyosis, leiomyomas, or cervical stenosis.

What is the treatment for Primary Dysmenorrhea?What is the treatment for secondart Dysmenorrhea?What is dysfunctional uterine bleeding? Abnormal uterine bleeding that is unrelated to an anatomic cause. Note that this is a diagnosis of exclusion. What are some types of dysfunctional uterine bleeding?What is most common cause of irregular bleeding?What causes anovulatory dysfunctional uterine bleeding?

Excessive estrogen stimulation relative to progesterone resulting in an absent secretory phase. It produces excessive endometrial hyperplasia and excessive bleeding.

What causes ovulatory dysfunctional uterine bleeding?

Inadequate luteal phase resulting in inadequate maturation of the corpus luteum. This causes inadequate synthesis of progesterone and delay in the development of the secretory phase. May see decreased 17-OH progesterone .

How do you treat ovulatory dysfunctional uterine bleeding?

If the follicle size is normal, supplement progesterone. If the follicle size is inadequate, give clomiphene sulfate.Absence of menses by age 16. Most cases are due to constitutional delay with a family history of delayed menses.

What are some causes of amenorrhea?

Hypothalamic or pituitary dysfunction resulting in decreased LH and FSH which results in decreased estrogen and progesterone. Ovarian disorders cause problems in synthesis of estrogen or progesterone.

What are causes of abnormal vaginal bleeding in a pre-pubertal girl?

Vulvovaginitis, poor hygeine, infection, gonrrhea, sexual abuse, foreign bodies, embryonal rhabdomyosarcoma

What are some causes of abnormal vaginal bleeding between menarche and 20 years?

Anovulatory dysfunctional uterine bleeding, endometrial hyperplasia, cancer.

Entirely covered by the chorionic plate. The chorionic villi vessels converge with the umbillical cord. What covers the chorion? Chorion is covered with amnion

Contains cotyledons covered by decidua basalis.

Where do the chorionic villi project? Into the intervillous space

What lines the chorionic villi? Trophoblastic tissue

Syncytiotrophoblast.

Synthesizes hCG, and HPL which directly correlates with placental mass and has anti-insulin activity.

Cytotrophoblastic tissue

One umbillical vein and two umbillical arteries. The vein carries the oxygenated blood in this case

Ascending infections, often from premature rupture of membranes

What is Funisitis? Infection of the umbillical cordWhat is Placentitis? Infection of the placentaWhat is chorioamnionitis? Infection of the fetal membranes

Neonatal sepsis and meningitis. Treat with Cefoxitin or Ticaricillin-ClavulanateWhat is Placenta Previa? Implantation over cervical os. Previous C Section is major risk factor

How does Placenta Previa present?

How do you diagnose Placenta Previa?

What are some causes of abnormal vaginal bleeding between ages 20-40?

Pregnancy and related complications, ovulatory dysfunctional uterine bleeding, PID, hypothyroidism, submucosal leiomyomas, adenomyosis, endometrial polyp, endometriosis

What are some causes of abnormal vaginal bleeding after age 40?What part of the placenta covers the fetal surface?

What covers the maternal surface of the placenta?

What does the intervillous space contain?

Maternal blood that delivers oxygen and nutrients and spiral arteries from the uterus that empty into the space

What forms the outside layer of the trophoblast?What does the Syncytiotrophoblast do?What forms the inside layer of the trophoblast?How many vessels are contained in the umbillical cord?What risks are related to a single umbillical artery?

Increased incidence of congenital anomalies, defects including cardiovascular defects, trisomy 18 and esophageal atresia.

What causes most placental infections?

How should you treat a placental infection even if culture is negative?

Treat prophylactically with IV Ampicillin+Erythromycin followed by PO amoxicillin and erythromycin. If culture positive you can give IV penicillin or ampicillin

What complications might arise from chorioamnionitis?

Painless vaginal bleeding, usually second or third trimester. The uterus is soft and non-tender and fetal distress is usually not present.Do not do a pelvic exam. Transabdominal ultrasound localizes the placenta and transvaginal ultrasound confirms placenta previa.

What is Abruptio Placentae?

What are risks for abruptio placentae?

What is Placenta Acreta?

What is Velamentous insertion?

Increased risk of hemorrhage if they are detached.

Diabetes mellitus, Rh hemolytic disease of the newborn, congenital syphilis

Monochorionic and monoamniotic although they can have dichorionic placentas

Twin Twin Transfusion syndrome.What is Preeclampsia? Toxemia of pregnancy

Premature aging of the placenta, multiple placental infarctions, spiral arteries show atherosclerosis

What is a Hyaditiform Mole? Benign tumor of the chorionic villus from an empty egg and 2 sperm or an egg and 2 sperm.

What is a complete Hyaditiform Mole?

Premature separation of the placenta due to formation of a retroplacental clot. This separates the placenta from the implantation site. This is most common cause of late pregnancy bleedingHypertension, smoking, cocaine, advanced maternal age, trauma, chorioamnionitis, premature membrane rupture, previous abruptio placentae.

What are the clinical signs of abruptio placentae?

Painful uterine bleeding, forceful uterine contractions or signs of preterm labor, usually see evidence of fetal distressDirect implantation into muscle without intervening decidua. Causes great risk for hemorrhage during delivery, commonly requiring surgery to control bleeding. Often requires hysterectomy.Umbilical cord inserts away from the placental edge-the vessels pass to the placenta through the membranes between the amnion and chorion. Causes increased risk for hemorrhage if the vessels are torn. Deliver by C Section to avoid vessel tear.

What risks do accessory lobes of the placenta pose?

What can cause an enlarged placenta?What type of placentas do Monozygotic twins have?

What risks are associated with monochorionic, diamnionic placentas?

What are risk factors for Preeclampsia?

First pregnancy, more common in women <20 years and >35 years, history of previous preeclampsia, positive family history, multiple gestations, african american, thrombocytosis, obesity

What is the pathogenesis of Pre-eclampsia?

Abnormal placentation causing mechanical or functional obstruction of the spiral arteries. The abnormal trophoblastic tissue invades the spiral arteries. Imbalance favors vasoconstriction over vasodilation (decreased PGE2 and NO, increased TXA2, Ang II and increased sensitivity to Ang II)

What are pathologic findings in Pre-Eclampsia?

What are clinical findings in Pre-Eclampsia?

Hypertension, proteinuria from leaky capillaries (increased inflammation), dependent pitting edema from loss of albumin, weight gain, seizures in eclampsia, swollen endothelial cells in glomerular capillaries producing oliguria.

What are some other symptoms in Pre-Eclampsia?

Right upper quadrant pain and hepatomegaly, periportal necrosis with increased transaminases, HELLP syndrome

The entire placenta is neoplastic. Dilated swollen villi without fetal blood vessels. No embryo is present. Ovum 46, XX, lacking maternal chromosomes. The chromosomesare derived from the father, either 2 sperm or duplicated 23X sperm in the ovum

Which type of Mole has an increased risk of Choriocarcinoma?

Complete mole. Presents with painless vaginal bleeding in fourth, fifth month of pregnancy. Causes severe vomiting, pre-eclampsia, uterus that is too large for gestational age, increased hCG for gestational age, and snowstorm appearance on ultrasound.

What is a partial Hyaditiform Mole?

What is a Choriocarcinoma?

Lungs and vagina-hemorrhagic lesions

Swallowed and recycled by the fetus.

What is Polyhydramnios?

What is Oligohydramnios?

Where is estriol made in pregnancy? Derived from fetal adrenal gland (DHEA-S) which is aromatized by the placenta.

Fetal adrenal cortex converts pregnenolone from the placenta to DHEA-S.

Hydroxylates DHEA-S to 16-OH-DHEA-S

What does decreased estriol indicate? Sign of fetal-maternal-placental dysfunction

Decreased urine estriol, decreased AFP, increased serum Beta-hCG

Upper outer quadrant-thus cancer is most commonly located in this location. Also underneath the nipple.

Estrogen stimulates ductal and alveolar growth. Progesterone stimulates alveolar differentiation.

Not all villi are neoplastic or dilated? Embryo is present but this is triploid. Egg with 23X is fertilized by 23X and 23Y sperm. (Not that if the embryo is doubled, it's not considered a mole). This has a low risk of choriocarcinoma.malignant tumor composed of syncytiotrophoblast and cytotrophoblast without chorionic villi. Risks are complete mole, spontaneous abortion and normal pregnancy

Where does Choriocarcinoma metastasize?What is the composition of amniotic fluid?

Predominantly fetal urine, initially plasma ultra-filtrate from mom. High salt content causes ferning when dried on a slide-good sign of premature rupture of amniotic sac.

What is the quantity of amniotic flud maintained?

Excessive amniotic fluid. Causes are tracheoesophageal fistula, duodenal atresia, maternal diabetes-maternal hyperglycemia causes fetal hyperglycemia resulting in fetal polyuria.Decreased amount of amniotic fluid. Caused by juvenile polycystic kidney disease, fetal genitourinary obstruction, uteroplacental insufficiency and premature rupture of membranes.

What can Alpha Fetoprotein indicate in pregnancy?

Increased maternal AFP indicates open neural tube defects (often related to Folate deficiency). Decreased maternal AFP can indicate Down syndrome.

What does the Lecithin to Sphingomyelin ratio indicate?

Lecithin is synthesized by type II Pneumocytes which decreases alveolar tension to prevent atelectasis. L:S ratio >2 indicates adequate surfactant.

What can increase surfactant production in the fetus?

Cortisol and thryroxine increase surfactant synthesis. Maternal administration of glucocorticoids can increase surfactant if the baby must be delivered before term. Insulin inhibits surfactant synthesis.

What part of estriol synthesis does the fetal adrenal cortex control?What does the fetal liver do in estriol synthesis?What does the maternal placenta do in estriol synthesis?

Initially converts LDL to pregnenolone for fetal processing. Placental sulfatase then cleaves off the sulfate from 16-OH-DHEA-S and converts it to free unbound estriol via aromatase.

What does the maternal liver do to estriol?

Conjugates it to estriol sulfate and estriol glucosiduronate which is then excreted in the maternal urine and bile.

What is the triad of markers in Down syndrome?What is the most high density location of breast tissue?What effects do sex hormones have on the breast during the menstrual cycle?

What hormones affect lactation?

Axillary lymph nodes

Internal mammary lymph nodes.

Mechanical stimulation of the nipple from prolonged suckling or sexual intercourse.

What causes Bloody nipple discharge? Intraductal papilloma, ductal cancer

Acute mastitis due to Staph A., usually related to breast feeding

Mammary duct ectasia (plasma cell mastitis)

Fibrocystic changeWhat is Mondor's disease? Superficial thromboplebitis of veins overlying the breast, presenting as a palpable, painful cord.

What is Fibrocystic change?

What is sclerosing adenosis?

What is Ductal Hyperplasia?

What is traumatic fat necrosis?

What is a Phyllodes tumor?

What is an Intraductal Papilloma?

Prolactin-stimulates and maintains lactogenesis. Oxytocin-released by the suckling reflex which causes expulsion of milk into the ducts.

Where do outer quadrant breast cancers drain?Where do inner quadrant breast cancers drain?What are normal causes of Galactorrhea?What are pathologic causes of Galactorrhea?

Prolactinoma, primary hypothyroidism (decreased T4 causes increased TRH which stimulates PRL), drugs like OCP's, phenothiazines, methyldopa, H2-Receptor blockers and angiolytics.

What causes prululent nipple discharge?What causes Green-Brown nipple discharge?What is the most common cause of Breast Pain?

Most common painful breast mass in women <50 years old. Causes distortion of normal cyclic breast changes. Some cysts have hemorrhage into the cyst fluid-called blue-domed cysts. Vary in size with the menstrual cycle but have no malignant potentialProliferation of small ductules/acini in the lobule-pattern is often confused with infiltrating ductal cancer. Often contains microcalcifications.

Ducts are estrogen sensitive. See papillary proliferation called papillomatosis, apocrine metaplasia (change to sweat producing glands), and atypical ductal hyperplasia (increased risk for carcinoma)

What is Mammary duct ectasia/plasma cell mastitis?

Main ducts fill up with debris causing dilation, rupture and inflammation. Results in greenish-brown nipple discharge. May result in skin and nipple retraction stiulating cancer but no increased risk for breast cancer.Trauma to breast tissue. Microscopic findings are lipid-laden macrophages with foreign body giant cells, fibrosis and dystrophic calcification. See a painless indurated mass which is painful in the acute stage and may produce skin retraction stimulating cancer.

What is a Fibroadenoma of the breast?

Most common breast tumor in women <35 years. Discrete movable, painless or painful mass. It's a benign tumor derived from the stroma which proliferates and compresses the ducts. The duct epithelium is not neoplastic. Estrogen sensitive so increases in size during pregnancy. May spontaneously involute during menopause.Bulky tumor derived from stromal cells. Most commonly benign but can be malignant in some cases-see hypercellular stroma with signs of mitoses in malignancy. Lobulated tumor with cystic spaces containing leaf-like extensions.Most common cause of bloody nipple discharge in women <50. Develops in the lactiferous ducts or sinuses. No increased risk for cancer.

BRCA 1 and BRCA 2, Li-Fraumeni, RAS oncogene, ERBB2, RB suppressor gene

Breast feeding, moderate or vigorous physical training, healthy body weight.

ER/PR expression generally confers a good prognosis whereas ERB2/NEU has a poor prognosis if amplified.

What is Infiltrating Ductal Carcinoma?

What is Paget's disease?

What is Invasive Lobular Carcinoma? Invasive mass of neoplastic cells arranged in a linear fashion or in concentric circles.

What is Tubular Carcinoma? Invasive mass that develops in terminal ductules. Increased incidence of cancer in the opposite breast.

Invasive mass that usually occurs in older women. Neoplastic cells surrounded by extracellular mucin.

What is Gynecomastia?

What are risk factors for breast cancer?

Prolonged estrogen stimulation, genetic susceptibility, especially if first generation relatives. Prolonged estrogen stimulation from either early menarche or late menopause or nulliparity.

What are some genetic markers for breast cancer?What decreases risk for breast cancer?What are clinical findings in breast cancer?

Painless mass in the breast, usually the upper outer quadrant. Skin or nipple retraction, painless axillary lymphadenopathy, hepatomegaly and bone pain if there are metastases.

What is the primary screening test for breast cancer?

Mammography-detects 80-90% of non-palpable breast masses. Does not distinguish benign from malignant lesions. Can identify microcalcifications and spiculated masses with or without microcalcification.

Where do microcalcifications most commonly occur?

Ductal carcinoma in situ, and sclerosing adenosis. Five or more microcalcifications that are punctate, microlinear or branching all suggest malignancy

How is estrogen and progesterone receptor expression related to prognosis?What is a Ductal Carcinom in Situ (DCIS)?

Nonpalpable mass. Forms a cribiform pattern (seive like) or comodo like pattern (necrotic center). Commonly contains microcalcifications which allow it to be detected on mammogram.

What is a Lobular Carcinoma in Situ (LCIS)?

Nonpalpable mass. Virtually always an incidental finding on breast biopsy for something else. Not identifiable on mammography. Lobules are distended with bland neoplastic cells. Usually ER/PR positive. Increased incidence of cancer in the opposite breast, that isn't LCIS.Malignant, invasive breast tumor. Has a stellate morphology. Indurated, gray-white tumor. 1/3 have ERB2 amplification conferring poor prognosis. These look gritty on cut section and have reactive desmoplasia causing induration.Extension of DCIS into the lactiferrous ducts and skin of the nipple producing a rash with or without nipple retraction. Palpable mass often present, see Paget's cells as well.

What is Medullary Carcinoma of the breast?

Invasive tumor associated with BRCA1 mutations. Bluky, soft tumor with large cells and a lymphoid infiltrate. Most are ER/PR negative.

What is inflammatory carcinoma of the breast?

Invasive tumor that presents with erythematous breast with dimpling of the skin like an orange peel from fixed opening of the sweat glands. Plugs of tumor block the lumen of dermal lymphatics causing localized lymphedema. Has a very poor prognosis.

What is a Colloid (Mucinous) Carcinoma?

Benign glandular proliferation in the male breast due to estrogen from increased enstrogens, decreased androgens or a defect in androgen receptors. Most often unilateral. Normal in newborns, puberty or the elderly.

Infection with Neisseria Gonorrhea

What is Lichen Sclerosis? Thinning of the epidermis with parchment appearing skin. Most commonly in post-menopausal women.

What is Lichen Simplex Chronicus?What is a Papillary Hidradenoma? Benign tumor of the apocrine sweat gland. Causes painful nodule on the labia majora.

HPV 16, smoking, immunodeficiency.

Melanoma cells, histologically similar to Paget cells except these are PAS negative.

What causes pathologic gynecomastia?

Cirrhosis causes an inability to metabolize estrogen or to metabolize 17-ketosteroids which are then aromatized to estrone. Genetic diseases like Klinefelter's and testicular feminization cuase gynecomastia. Drugs that displace estrogen from SHBG, such as spironolactone or ketoconazole or drugs with estrogen activity like DES or digoxin, or androgen blocking drugs like spironolactone or flutamide or that decrease androgen production like leuprolide. These all increase estrogen.

What is the most common cause of Bartholin gland abscesses?

White plaque like skin lesion (leukoplakia) due to squamous cell hyperplasia. Small risk for developing Squamous Cell Carcinoma.

What is Vulvar Intraepithelial Neoplasia?

Dysplasia of the vulva, ranging from mild to carcinoma in situ. Strong association with HPV 16 and high risk of developing squamous cell carcinoma

What are risk factors for squamous cell carcinoma of the vulva?

What is extramammary Paget's disease?

Red, crusted vulvar lesion. Intraepithelial adenocarcinoma derived from primitive epithelial progenitor cells. Malignant Paget cells contain mucin which is Periodic Acid Schiff positive. Spreads along the epithelium but rarely invades the dermis.

What is Malignant melanoma of the vulva?

What type of lesion results from infection with Calymmatobacterium Granulomatis?

Gram negative coccobacilli that causes granuloma inguinale. It's phagocytosed by macrophages forming Donovan bodies and results in creeping, raised sores that heal by scarring. Treat with bactrim or doxy.

What types of lesions result from infection with Candida Albicans?

Yeast and pseudohyphae which should be part of the normal vaginal flora. Causes vaginitis, pruritic vaginitis with a white discharge and fiery red mucosa. Risk factors are diabetes, antibiotics, pregnancy and OCP's

What type of lesion results form infection with Chlamydia Trachomatis?

STD-commonly coinfecting with Neisseria Gonorrhea. See red inclusions (reticulate bodies) in squamous cells which then divide and form elementary bodies which can reinfect other cells. Causes sterile pyuria, epididdmitis, proctitis (in males obviously) and urethritis, cervicitis, PID, perihepatitis (Fitz-Hugh Curtis), proctitis and bartholin gland abscesses (in females obviously). Can also cause conjunctivitis and pneumonia in a newborn.

What types of lesions result from infection with Chlamydia Trachomatis subspecies?

Lymphogranuloma venerum, papules with no ulceration, inguinal lymphadenitis with granulomatous microabscesses and draining sinuses. Lymphedema of the scrotum or vulva and possibly rectal strictures in women

What types of lesions are seen with infection by Gardnerella Vaginalis?

Gram negative rod that causes bacterial vaginosis. Most common vaginitis which presents with malodorous discharge. Organisms adhere to the squamous epithelium forming clue cells.

How do you treat HPV? Vaccine! Topical podophyllin, alpha-IFN injections and imiquimod cream

Septic arthritis in the knee, tenosynovitis of the hands and feet, pustules on the hands and feet

RPR or VDRL. Titers should decrease after treatment.

FTA-ABS which is positive with or without treatment

Absence of the upper vagina and uterus resulting in primary amenorrhea

What is a Gartner's Duct cyst? Remnant of the Wolffian/mesonephric duct which presents as a cyst on the lateral wall of the vagina.What is a Rhabdomyoma? Benign tumor of skeletal muscle in the vagina (can also be on the tongue or heart)

Necrotic, grape like mass protruding from the vagina, most often in girls <5 years

What is Vaginal Adenosis?

What types of lesions result from infection with Hemophilus Ducreyi?

Gram negative rod that causes Chancroid. Male dominant disease, often correlated with HIV. Causes painful genital warts and perianal ulcers with suppurative inguinal nodes which main have draining sinuses.

What types of lesions result from infection with HSV-2?

STD with the virus remaining latent in the sensory ganglia. Causes recurrent vesicles that ulcerate on the vulva, penis, cervix and perianal area. See multinucleated squamous cells on Tzanck prep

What types of lesions result from infection with HPV?

Types 6 and 11 associated with Condyloma Acuminata (warts)-fernlike or flat lesions in the genital area. Types 16 and 18 associated with dysplasia and squamous cell carcinoma. See koilocytes in squamous epithelium. Cells have wrinkled, pyknotic nuclei surrounded by a clear halo.

What types of lesions result from infection with Neisseria Gonorrhoeae?

Gram negative diplococcus that infects glandular transitional epithelium in sites similar to Chalmydia. Causes prululent lesions and urethritis. Can cause ectopic pregnancy, male sterility, disseminated gonococcemia, septic arthritis, and Fitz Hugh Curtis.

What are signs of disseminated Gonococcemia?

What types of lesions result from infection with Treponema Pallidum?

Gram negative spirochete that causes syphillis. Primary syphillis presents with a solitary, painless, indurated chancre on the penis, labia or mouth. Secondary presents with a maculopapular rash on the trunk, palms and soles along with generalized lymphadenopathy, condylomata lata (flat lesions) and alopecia. Tertiary syphillis presents with neurosyphillis, aortitis and gummas.

What are the non-specific screening tests for Syphillis?What are the confirmatory tests for Syphillis?What is the Jarisch-Herxheimer reaction?

Intensification of rash in primary or secondary syphillis after proteins are released from the dead organisms following penicillin treatment

what types of lesion results from infection with Trichamonas Vaginalis?

Flagellated protozoan with jerky motility which produces vaginitis, cervicitis and urethritis. Causes a strawberry colored cervix and fiery red vaginal mucosa with greenish, frothy discahrge.

What is Rokitansky-Kuster Hauser Syndrome?

What is an Embryonal Rhabdomyosarcoma?

What is clear cell adenocarcinoma of the vagina?

Adenocarcinoma of the vaginal wall (pretty self explanatory). Occurs in women with DES exposure since DES inhibits mullerian differentiation-tubes, uterus, cervix and upper third of the vaginaPrecursor lesion for squamous cell carcinoma. Produces red, superficial ulcerations in the upper portion of the vagina

Endocervix and exocervix. The exocervix begins at the cervical osWhat lines the exocervix? squamous epitheliumWhat lines endocervical glands? Mucus secreting columnar cells

What is acute cervicitis?

What causes chronic cervicitis? Essentially persistence of acute cervicitisWhat is follicular cervicitis? Pronounced lymphoid infiltrate with germinal centers caused by Chlamydia Trachomatis.

Screening test for squamous dysplasia and cancer. Evaluate the hormone status of the patient.

Adequate estrogen

Adequate progesterone

Lack of estrogen and progesterone.

What is a Cervical Polyp?

What is CIN I? Mild dysplasia involving the lower third of the epitheliumWhat is CIN II? Moderate dysplasia involving the lower 2/3 of the epitheliumWhat is CIN III? Severe dysplasia to carcinoma in situ involving the full thickness of the epithelium

Abnormal vaginal bleeding, often post coital, malodorous discharge

What are some other DES related abnormalities?

Abnormally shaped uterus that thwarts implantation (T shape). Cervical incompetence which can cause recurrent miscarriage.

What is vaginal squamous cell carcinoma?

It's what it sounds like. That said, primary SCC is associated with HPV 16. Most of these are actually extensions of cervical SCC into the vagina.

What does the cervix actually consist of?

How does the endocervical epithelium transform into the exocervical epithelium?

Endocervical epithelium migrates down to the exocervix where exposure to the acid pH of the vagina causes squamous metaplasia. This area is called the transformation zone and is the most likely location for squamous dysplasia and cancer.

What is the pathogenesis of a Nabothian cyst?

Metaplastic squamous cells block endocervical gland orifices resulting in obstruction to outflow of mucus. This is a normal finding however.Acute inflammation is often present in the transformation zone, however pathologic acute inflammation may be due to infection-Chlamydia, Neisseria, Trichomonas, Candida, HSV, HPV.

What are clinical findings in acute cervicitis?

Vaginal discharge, pelvic pain, dyspareunia, pain on palpation (chandelier sign), easy bleeding and erythematous or exudative cervical os.

What is the purpose of a Cervical Pap test?What do superficial squamous cells indicate on Pap?What do intermediate squamous cells on Pap indicate?What do parabasal cells on Pap indicate?What types of cells are seen on Pap from a non-pregnant and pregnant woman?

Non-pregnant: 70% superficial, 30% intermediate squamous cells. Pregnant: 100% intermediate squamous cells from progesterone effect.Non-neoplastic polyp that protrudes from the cervical os. Arises from the endocervix, most commonly in perimenopausal or multigravida women.

Describe Cervical Intraepithelial Neoplasia, CIN

Most cases associated with HPV which produces koilocytes in squamous cells. Associated with early age of sexual intercourse, multipe high-risk partners, high risk HPV types, smoking, OCP's and immunodeficiency.

What is the epidemiology of cervical cancer?

Least common GYN cancer with higher incidence in developing countries. Most are squamous cell carcinomas with the same risk factors as CIN

What are clinical findings in cervical cancer?

What is the sequence to menarche? Breast budding (Thelarche), growth spurt, pubic hair, axillary hair, menarche (mean age is 12.8 years).When does ovulation occur? Between days 14 and 16

Progesterone

What changes occur after fertilization?What initiates menses? Drop-off in serum estrogen and progesterone signalling endometrial cells to undergo apoptosis.

What are the functions of FSH?

What are the functions of LH?

Where does Estradiol come from? Aromatized testosterone in granulosa cells. Primary estrogen in non-pregnant women.Where does Estrone come from? Weak estrogen produced during menopause from adipose cell aromatization of androstendione

Where does Estriol come from?

Equal derivation from ovaries and adrenal cortex

Almost exclusively from the adrenal cortex

SHBG preferentially binds testosterone over estrogen thus lack of SHBG can cause hirsutism in women.

What is acute endometritis?

What are some characteristics of cervical cancer?

Cancer often extends down into the vagna and out into the lateral wall of the cervix and vagina. May infiltrate the bladder wall and obstruct the uterus causing postrenal azotemia and possibly death. May metastasize distantly, e.g. to the lungs.

What mediates the secretory phase of the cycle?

Fertilization usually occurs in the ampullary portion of the Fallopian tube. The fertilized egg spends 3 days there, 2 days in the uterine cavity and then implants in the endometrial mucosa on day 21. There is an exaggerated secretory phase in pregnancy called the Arias-Stella phenomenon.

Prepares the follicle of the month, increases aromatase synthesis in the granulosa cells, increased synthesis of LH receptors.

Increases synthesis of 17-ketosteroids in the theca interna (DHEA and androstenedione). Convert DHEA to androstenedione and androstenedione to testosterone. Increase aromatization of testosterone. (Obviously LH isn't doing these things directly but it uprgulates necessary enzymes)

What hormonal changes are seen in pregnancy?

Human chorionic gonadotropin-synthesized in the syncytiotrophoblast lining the chorionic villus. hCG acts as an LH analog and maintains the corpus luteum to produce progesterone.

What is in Oral Contraceptive Pills and how do they work?

Mixture of estrogens and progestins which then prevent the midcycle LH surge and ovulation. Progestin arrests the proliferative phase and cause gland atrophy and also inhibit LH directly. OCP's also render the cervical mucus hostile to sperm and alter Fallopian tube motility.

End product of estradiol metabolism. Primary estrogen of pregnancy derived from fetal adrenal, placenta and maternal liver.

Where does androstendione come from in a woman?Where does DHEA come from in a woman?Where does testosterone come from in a woman?

derived from conversion of androstenedione to testosterone in the ovaries and adrenal glands. Can be converted to DHT peripherally.

What is Sex Hormone Binding Globulin?

Binding protein for both estrogen and testosterone, mostly synthesized in the liver. Androgens, obesity and hypothyroidism all decrease SHBG

What does SHBG have a greater affinity for?

Acute inflammation of the endometrium, most commonly as a result of bacterial infection following delivery or miscarriage. Group B strep, staph a, bacteroides, C. trachomatis, N. Gonorrhoeae, E Coli.

Fever, uterine tenderness, prululent or foul vaginal discharge and abdominal pain.

What causes chronic endometritis? Retained placenta, gonorrhea, IUD (with infection)

Like all chronic inflammatory conditions, you see plasma cells

What is Adenomyosis?

Menorrhagia, dysmenorrhea or pelvic pain

What is Endometriosis?

What is an endometrial polyp?

Common cause of menorrhagia, spotting in between periods or after menopause

What is a Hyatid Cyst of Morgagni? Cystic mullerian remnant most often in the fibriated end of the tube. May undergo torsion causing pain.

What is pelvic inflammatory disease?

What are some risk factors for PID? Multiple sex partners, vaginal douching, prior PID, unprotected sex

What is ectopic pregnancy?

Most occur in the broad ampullary region below the fimbriae.

What are clinical findings in acute endometritis?

What is the key histologic finding in chronic endometritis?

Invagination of the stratum basalis into the myometrium. See glands and stroma thickening in the myometrium and general enlargement of the uterus.

What are clinical findings in adenomyosis?

Functioning endometrial glands and stroma located outside the uterus causing cyclic bleeding of gland and stromal implants. Essentially reverse menses through the Fallopian tube allows inplantation of viable endometrial cells. Can also be from vascular spread. Most common sites are ovaries, rectal pouch, Fallopian tubes and intestines.

What are clinical findings in Endometriosis?

Dysmenorrhea, abnormal bleeding, painful stooling during menses, intestinal obstruction and bleeding during menses, increased risk for ectopic pregnancy and enlargement of the ovaries with blood filled cystsBenign polyp on the endometrium that enlarges with estrogen stimulation. Does not progress to endometrial carcinoma but it can protrude through the cervix into the vagina.

What are clinical findings of an endometrial polyp?

Inflammation in the pelvis, often due to N. Gonorrhoeae or C. Trachomatis. See Fallopian tubes that are filled with pus or see hydrosalpinx (clear fluid in Fallopian tube). Causes fever, lower abdominal pain, cervical motion tenderness, abnormal uterine bleeding, vaginal discharge, mucopurulent discharge in the cervical os, and right upper quadrant pain (FHC Syndrome)

What is Salpingitis Isthmica Nodosa (SIN)?

Invagination of the mucosa of the tube into muscle (tubal diverticulosis). Produces nodules in the tube that narrow the lumen. Most likely a result of infection and can result in infertility and ectopic pregnancy.

Pregnancy that isn't in the uterus. Most often in the Fallopian tubes. Suspect with increased hCG and sudden lower abdominal pain. Confirm with ultrasound. May be clinically mistaken for appendicitis.

What are risk factors for ectopic pregnancy?

Scarring from previous PID, Endometriosis, Altered tubal motility (SIN), progestin only pill, previous tubal ligation, prior abdominal surgery.

Where in the tubes do ectopic pregnancies most commonly implant?

What is Oophoritis? Inflammation of the ovary, possible as a result of mumps or PID.

What is stromal hyperthecosis?

How can ovarian tumors be classified?

Increased CA-125- only in surface derived tumors

What is a Serous Ovarian tumor?

What is an endometroid tumor? Malignant tumor associated with endometrial carcinoma. Commonly bilateralWhat is a Brenner tumor? Usually a benign tumor that contains Walthard's rests (traditional-like epithelium)

What is a cystic teratoma?

What is a Thecoma-Fibroma? Benign tumor associated with Meigs' syndrome (ascited, right sided pleural effusions). Commonly calcify.

What is a Granulosa-Theca cell tumor? Low grade malignant tumor which produces estrogen and contains Call-Exner bodies

What is a Sertoli-Leydig cell tumor? Benign tumor that produces androgens. Pure leydig cell tumors contain cells with crystals of Reinke.

What are some clinical findings in ectopic pregnancy?

Sudden onset of lower abdominal pain and tenderness, usually about 6 weeks after LMP, adnexal tenderness, peritoneal signs, abnormal uterine bleeding, hypovolemic shock as a result of intraperitoneal hemorrhage.

How do you diagnose ectopic pregnancy?

Beta hCG is a good screening test but a positive hCG doesn't mean that there is an ectopic pregnancy. Vaginal ultrasound showing an amniotic sac is confirmatory.

Bilateral ovarian enlargement from hypercellular ovarian stroma. Stroma have vacuolated (leutenized) stromal hilar cells which synthesize excess androgens. May cause hirsutism or virilization. Associated with obesity, acanthosis nigracans, insulin resistance, and hypertension.

What are risk factors for Ovarian cancer?

Nulliparity-increased number of ovulatory cycles increases risk, also causes increased risk for surface-derived ovarian tumors. Genetic factors are BRCA1 and BRCA2 suppressor gene mutations, Lynch syndrome, Turner syndrome (dysgerminoma), Peutz-Jeghers syndrome (sex cord tumors with annular tubules), history of breast cancer, postmenopausal estrogen replacement, obesitycancers are similar to those seen in the testicle, not many are malignant. Sex cord stromal tumors-derive from stromal cells, may be hormone producing, most are benign. Metastases-most commonly from breast, and stomach (Krukenberg tumors)

What are some clinical findings in Ovarian tumors?

Abdominal enlargement from fluid. Malignant ascites may cause induration in the rectal pouch on digital rectal exam and intestinal obstruction with colicky pain. Palpable ovarian mass in postmenopausal woman, malignant pleural effusion, torsion and infarction (cystic teratomas), signs of hyperestrinism in estrogen secreting tumors or virilization in androgen secreting tumors.

What is a common tumor marker of malignant ovarian tumors?

Most common group of primary benign and malignant tumors, many are bilateral. Cysts are lined by ciliated cells (like Fallopian tubes). A Serous Cystadenoma is benign. A Serous Cystadenocarcinoma is malignant and has psammoma bodies and dystrophic calcification.

What is a Mucinous tumor of the ovary?

Cysts lined by mucus-secreting cells (like endocervical cells). Cause large multi-nucleated tumors. Seeding of tumor produces pseudomyxoma peritonei. A mucinous cystadenoma is benign and may be associated with Brenner tumors. A mucinous cystadenocarcinoma is malignant.

Most common benign germ cell tumor. See ectodermal differentiation (hair, sebaceous glands, teeth) mostly found in a nipple like structure called Rokitansky Tubercle. A Struma Ovarii subtype has functioning thyroid tissue

What is a Gonadoblastoma?What is a Krukenberg tumor? Metastasis to the ovary. Contains signet ring cells from hematogenous spread of gastric cancer.

Malignant tumor with a mixture of germ cells (dysgerminoma) and sex-cord stromal cells. Associated with abnormal sexual development. May calcify

Renal

What is the pronephros? First kidney. Nonfunctional and disappears by week 4

What is the mesonephros?What is the metanephros? Forms the definitive kidney

What is Potter's Sequence?

Patent Urachus results in Urachal fistula at birth

What does the urinary system derive from?

Intermediate mesoderm of the posterior wall of the abdominal cavity.

How many sets of kidneys are there?

Three sets of kidneys-pronephros, mesonephros and metanephros

Forms after the pronephros and forms the mesonephric/Wolffian duct. That eventually connects the mesonephros to the cloaca and forms adult genital structures.

What is the excretory system of the kidneys derived from?

Primary ureteric bud. Becomes the glomerulus, Bowman's capsule, Loop of Henle, Distal Collecting tubule and collecting system

What are the collecting ducts of the kidney derived from?

Outgrowth of the Mesonephric duct which joins the metanephros to form the ureteric bud. Forms the major and minor calyces, renal pelvis and ureters.

What adult structure does the Allantois become?

Allantois goes to Urachus and becomes the Median umbilical ligament. Don't confuse this with the medial umbilical ligament which is a remnant of the umbilical artery.

Malformation of the Ureteric Bud which results in bilateral renal agenesis. Results in oligohydramnios/Potter's syndrome

What are the limb deformities in Potter's Syndrome?

Clubfoot, flipper hands, hyperextensible joints, and compressed thorax

What are the facial deformities in Potter's Syndrome?

Sloping forehead, flattened nose, recessed chin, low floppy ears. Results from compression of the fetus against the wall of the the amniotic sac.

Why does Pulmonary Hypoplasia result from Potter's Syndrome?

Fetal lungs mature through swallowing of amnion which allows the lungs to expand. Thus decreased amnion causes decreased expansion of the lungs.

What can occur if the allantois fails to obliterate?

Urinary bladder and urethra

Wat causes a pelvic kidney?

What is a Horseshoe kidney?

What does the urogenital sinus become?

During development, the embryologic kidneys must ascend and pass under the umbilical arteries. If a kidney can't pass, it remains in the pelvis

How do pelvic kidneys present?

Obstructive hydronephrosis and vesicoureteric reflux. May have pain or infection.

Kidneys are pushed close together while ascending under the umbilical arteries. Causes the lower poles to fuse which causes it to look like a horseshoe and get trapped underneath the inferior mesenteric artery. Associated with Turner's

What is the most common presentation of horseshoe kidney?

Most are asymptomatic but can present with UTI followed by obstructive hematuria or abdominal pain. Predisposes to nephrolithiasis

What is required for definitive diagnosis of Horseshoe kidney?

IV pyelogram shows rotated calyces but doesn't show the isthmus. Need a Dimercaptosuccinic Acid Scan (DMSA)

What is the origin and insertion, innervation, blood supply and action of the Psoas major muscle?

Origin-vertebral column (T12-L5), insertion-lesser trochanter of the femur. Innervation-Ventral rami of L1-3. Blood supply-mucular branches of the medial femoral and circumflex artery. Actions-flex thigh and trunk and laterally rotate the hip.

What is the origin and insertion, innervation, blood supply and action of the Psoas minor muscle?

Origin-Vertebral column (T12-L1), insertion-pectinate line. Innervation-Anterior rami of lumbar nerves L1-2. Actions-with the Psoas major, flexes the trunk at the hip and stabilizes the thigh

What is the origin and insertion, innervation, blood supply and action of the Iliacus muscle?

Origin-Iliac fossa, insertion-lesser trochanter of the femur. Innervation-femoral nerve L3-4. Blood supply-Muscular branches of the medial femoral circumflex artery. Actions-powerful hip flexor and lateral rotator

What is the origin and insertion, innervation, blood supply and action of the Quadratus Lumborum muscle?

Origin-Transverse process of L3-5, insertion-lower border of the 12th rib. Innervation-Ventral branches of T12 and L1-4. Action-extends and laterally flexes vertebral column.

Renal arteries which branch off the abdominal aorta

Renal veins drain into the IVC

Which structures are retroperitoneal?

Pancreas (except tail), Duodenum (second, third and fourth parts), ascending and descending colon, aorta, IVC, rectum, adrenal glands, and since this is the renal section-the kidneys!!!

Where are the kidneys located?

Located at T12-L3 on the left and slightly lower on the right, embedded in Gerota's Fascia.

Where do the ureters pass in relation to the uterine artery or vas deferens?

Water goes under the bridge. Pass across the bifurcation of the common iliac and pass under the uterine arteries or vas deferens and then join the bladder on the posteroinferior side.

What is the arterial supply to the kidneys?What is the venous return from the kidneys?What is unique about the Left Renal Vein?

It also drains blood from the left gonad and is longer than the right renal vein since it must cross the IVC

What are the structures of the Renal filtration system in the order in which filtrate would pass through?

Glomerulus surrounded by Bowman's capsule then proximal convoluted tubule the the straight portion of the proximal tubule, then thick descending, the Loop of Henle, then thick ascending limb, then the distal collecting tubule followed by the collecting duct.

What is the direction of urinary drainage out of the kidneys?

Renal pyramids to the renal papillae to the minor calyces to the major calyces

What types of epithelium line the Urethra?

Transitional epithelium as it exits the bladder, then stratified columnar epithelium followed by stratified squamous epithelium.

What are the anatomic divisions of the male urethra?

Prostatic, Membranous (surrounded by striated muscle forming the voluntary external urethral sphincter), Bulbous then Pendulous (surrounded by Littre's glands. Does that mean it swings like a pendulum? Just wondering

What are the anatomic divisions of the female urethra?

Much shorter so not really divided. Lined by stratified squamous and pseudostratified columnar epithelium. At the mid-portion it's surrounded by the striated muscle of the voluntary external urethral sphincter. Also surrounded by Littre's glands

What is the glomerulus?

What is Bowman's capsule?

Lined by simple cuboidal epithelium without a brush border

Lined by columnar epithelium

What comprises a Renal Corpuscle?

Primary filtering component, comprised of the glomerulus and Bowman's capsuleCollection of dilated capillaries with a fenestrated endothelium, which emerge from the afferent arteriole and drain into the efferent arterioleDouble-walled epithelial capsule enclosing the glomerulus. Consists of visceral and parietal layers with urinary space in between. Visceral layer filters the blood while the parietal layer covers the outside and is continuous with the proximal convoluted tubules.

What is special about the visceral layer of Bowman's capsule?

Specialized filtration lining that is made of Podocytes resting on a basement membrane, primary processes and foot processes.

Is the basement membrane of the Glomerulus charged?

Yes! It's a fused basement membrane full of heparan sulfate which gives it a negative charge and makes it more impenetrable to things like albumin that are also negatively charged.

Describe the histology of the Proximal Convoluted Tubule

Lined by simple cuboidal epithelium with a microvilli brush border. Interdigitations between the cells prevent loss of fluid and solutes

Describe the histology of the Loop of Henle

Specialized system for absorption and secretion of electrolytes. Consists of the thick descending, thin descending, thin ascending and thick ascending loops (see more about transport later)

Describe the histology of the Distal Convoluted TubuleDescribe the histology of the collecting tubule

Lined by simple cuboidal epithelium. Transports urine from the functional nephron to the hilum

Describe the histology of the Collecting Ducts

What doe Juxtamedullary nephrons do?

Exceptionally long Loops of Henle allow them to set up a hypertonic gradient in the kidney, regulating the production of concentrated urine

What is the Macula Densa?

What is the Juxtaglomerular Apparatus?

Consists of macula densa cells in the proximal portion of the distal tubule and juxtaglomerular cells in the afferent and efferent arterioles. Controls GFR in response to BP in the afferent arterioles. JG cells secrete Renin leading to increased angiotensin II and aldosterone in response to decreased renal blood pressure, decreases sodium delivery to the distal tubule and increases sympathetic tone (Beta 1).Group of epithelial cells in the distal tubules that contact the afferent and efferent arterioles (JGA). Cells are sensitive to sodium concentration and rates of flow through the Distal Convoluted Tubule. Regulates GFR through locally active hormones.

What are Juxtaglomerular cells?

Specialized myoepithelial cells located on the afferent arterioles which act as baroreceptors. Monitor BP and maintain GFR through Renin release

What are extraglomerular mesangial cells?

Contractile cells with receptors for angiotensin II and natriuretic factor allowing them to regulate glomerular flow.

What types of cells line the bladder?

Transitional epithelium-can stretch and thin as it's distended. Smooth muscle in 3 layers arranged in multiple dimensions which evevntually become three distinct layers at the bladder's neck. Innermost is the involuntary sphincter.

Walk through a Darrow-Yannet Diagram (see following questions as well)

Diagram shows volume of ICF and ECF in the body. Osmolarity should be equal between ICF and ECF. Normovolemia is 42 liters total with 28L in the ICF. See Attachment 1 and walk through the diagram.

What are clinical implications of Water deprivation?

ICF decreased, ECF increased, osm increased. Technically volume contraction and hypotonic but water more contracted that solute.

What are the clinical implications of Diarrhea?

No change in ICF, ECF decreased, no change in osm. Essenitally volume and solute contraction but equal contraction.

What are the clinical implications of Adrenal Insufficiency?

ICF increased, ECF decreased, Osm decreased. Volume and solute contracted because not holding onto water and salt

What is Renal Clearance?

What does is mean if Cx<GFR? Net tubular reabsorption of X

What does it mean if Cx>GFR? Net tubular secretion of X.

What does it mean if Cx=GFR? Neither secretion or reabsorption of X

What are the clinical implications of Infusion of isotonic NaCl?

ICF unchanged, ECF increased, osm unchanged. Giving increasing amounts of fluid and solute so volume expansion.

What are the clinical implications of high NaCl intake?

ICF decreased, ECF increased, osm increased. Volume expansion but solute pulls water into ECF

What are the clinical implications of SIADH?

ICF increased, ECF increased, osm decreased. Holding onto water and salt but water in excess of salt.Cx=UxV/Px Volume of plasma from which the substance is completely cleared per unit of time. C-clearance of X, U-urine concentration of X, V-urine flow rate, P-plasma concentration of X. (mL/minute)

How is Inulin used to calculate GFR?

Inulin can be used because it is freely filtered and neither reabsorbed nor secreted. GFR=Uinulin *V/Pinulin = Cinulin

How are Creatinine Clearance and GFR related?

Creatinine Clearance is an approximate measure of GFR. Slightly overestimates GFR because there is moderate secretion of creatinine by the renal tubules.

What is the Clearance ratio (with Inulin)?

Clearance Ratio=Cx/Cinulin. 1 if equal to inulin. <1 means that clearance is less than inulin so either not filtered or filtered and reabsorbed. >1 means that clearance is more than inulin so filtered and excreted/activelly pumped.

What forms the Glomerular Filtration Barrier?

Fenestrated capillary endothelium. Glomerular basement membrane-composed of type IV and V collagen, laminin, heparan sulfate. Three layers-Lamina rara interna, lamina densa and lamina rara externa. Epithelial layer consists of podocytes which help form a barrier.

How can you estimate Effective Renal Plasma Flow (ERPF)?

Estimate using PAH clearance because it's filtered and actively secreted in the proximal tubule-thus all PAH is excreted. ERPF=UPAH *V/PPAH = CPAH

Decreased RPF, Decreased GFR, No change in filtration fraction

Decreased RPF, Increased GFR, increased filtration fraction

No change in RPF, decreased GFR and filtration fraction

No change in RPF, decreased GFR, decreased filtration fraction

What is Filtration Fraction?

How do you estimate Renal Blood Flow?

RBF=RPF/(1-Hct). Note that ERPF underestimates RPF by about 10% so RBF is overestimated.

What is Dopamine's effect on the nephron?

Dopamine dilates the vessels and suppresses sodium reabsorption in the proximal tubule by inhibiting the action of the basolateral Na/K ATPase. Released directly by the proximal tubule in response to an increase in BP resulting in decreased RBF and GFR.

How does Afferent arteiole constriction affect RPF, GFR and Filtration Fraction?

How does Efferent arteiole constriction affect RPF, GFR and Filtration Fraction?

How does increased Plasma protein affect RPF, GFR and Filtration Fraction?

How does decreased plasma protein affect RPF, GFR and Filtration Fraction?

No change in RPF, increased GFR and increased filtration fraction

How does constriction of the ureter affect RPF, GFR and Filtration Fraction?

Describe autoregulation of blood flow in the kidneys

Two autoregulatory mechanisms-stretch/myogenic and tubuloglomerular feedback. Stretch-when BP increases, arterioles are stretched leading to vasoconstriction in the afferent arteriole thus maintaining constant RBF. Tubuloglomerular feedback- increased arterial pressure leads to increased RBF and increased flow to the distal tubule which is sensed by the macula densa. This results in constriction of the afferent arteriole, attenuating RBF.

Fraction of plasma filtered across the membrane of the glomerular capillaries. FF=GFR/RPF. Normal FF is about 20%

What is Filtered Load? GFR * Plasma concentration.

What is Free Water Clearance?

How does ADH affect Ch2o?

Excretion rate= V*Ux

Reabsorption=Filtered-Excreted

Secretion=Excreted-Filtered

How are amino acids cleared?

What is Hartnup's Disease?

Define the Nephron.

Ability to dilute urine. Free water (Ch2o)= V-Cosm (Cosm=Uosm*V/Posm)

Where does free water clearance occur?

Thick ascending limb and early distal tubule. NaCl is reabsorbed without reabsorption/permeability to H2O. ADH causes retention of free water so Ch2o<0. Concentrated urine

How can you calculate Excretion rate?How can you calculate Reabsorption?How can you calculate Secretion?

How is glucose reabsorbed and how does it go wrong?

Should be completely reabsorbed in the proximal tubule by Na/Glucose cotransport. At a plasma glucose >160-200 mg/dL you start to see glucosuria because the transport is being overwhelmed. At 350 mg/dL, all transporters are fully saturated so clinical glucosuria developsShouldn't be cleared. Na dependent transporters in the proximal tubules reabsorb amino acids with multiple carrier systems. Deficiency of neutral amino acid (tryptophan) transporter. Causes Pellagra.Unit composed of the glomerulus, through which fluid is filtered, and the tubular system where filtered fluid is modified through the reabsorption and secretion of various solutes to produce urine.

How do tubules of the nephron maintain low intracellular Na and the Na gradient across the tube?

Na/K ATPase on the basolateral membrane maintains the Na gradient from the lumen to the cell.

Describe transport across the luminal and basolateral side of the Proximal Tubule (see attachment 2).

The proximal tubule is the major site of reabsorption, based on the transmembrane Na gradient. Reabsorbs all filtered glucose and amino acids via cotransport with Na. Reabsorbs most bicarb, sodium, chloride and water. Isotonic absorption. Generates and secretes ammonia which buffers secreted H. Na and H are exchanged, Cl is absorbed in exchange for bicarb.

How is bicarb regulated/excreted in the Proximal tubule?

CO2 and H2O cross the membrane and are made into bicarb by carbonic anhydrase. That is excreted and then made into CO2 and H2O again.

How do Angiotensin II and Atrial Natriuretic Peptide act on the Proximal tubule?

Ang II stimulates Na reabsorption which ANP blocks Na reabsorption.

How does Parathyroid hormone affect excretion/absorption?

PTH inhibits Na/Phosphate cotransport resulting in phosphate excretion.

Describe transport across the Loop of Henle.

Thin descending loop absorbs about 20% of filtered water but no solute via medullary hypertonicity. Thin ascending limb is impermeable to water and has no significant reabsorption. Thick ascending limb is the diluting segment of the tubular system. Actively absorbs Na, K and Cl (NK2Cl). This induces the paracellular absorption of Mg and Ca because K leaks back into the lumen creating a positive charge in the lumen. It's impermeable to H2O so it dilutes urine.

Describe transport across the distal convoluted tubule.

Impermeable to water and urea. Early distal tubule actively reabsorbs Na and Cl making urine hypotonic. PTH increases Ca/Na exchange thus increasing Ca absorption.

Describe transport across the late distal tubule and collecting ducts.

Principle cells reabsorb Na and H2O and secrete K via the Na/K ATPase. Intercalated cells secrete H and reabsorb K and HCO3.

How does Aldosterone affect the collecting ducts?

Inserts more Na channels on the luminal side increasing Na reabsorption.

How does ADH affect the collecting tubules?

Acts at V2 receptors and inserts aquaporins H2O channels into the luminal side.

What is the Vasa Recta?

What does it mean if TF/P=1 Solute and water are reabsorbed at equal rates

What does it mean if TF/P<1 Solute is reabsorbed more quickly than water.

What is the function of ANP?

What is the function of ADH?

What is Erythropoietin?

What is 1, 25-(OH)2 Vitamin D?

U shaped capillaries which are freely permeable to H2O and solutes except protein. Situated close to the Loop of Henle. Enables the cortico-medullary osmolar concentration gradient. Preserves hyperosmolarity of renal medulla to maintain absorption.

What does it mean if Tubular Fluid (TF)/Plasma (P) >1?

Solute is being reabsorbed more slowly than water or there is net secretion of solute.

What is the function of Angiotensin II?

Affects baroreceptors, limits reflex bradycardia which would normally accompany pressors. Constricts efferent arterioles-increased FF to maintain GFR in low volume states. Increases proximal tubule Na/H activity and can stimulate thirst in the hypothalamus.Released from the atria in response to low volume. Relaxes vascular smooth muscle via cGMP resulting in increased GFR and decreased renin.

Regulates osmolarity and responds to low blood volume which takes precedence over osmolarity. Increases H2O channel insertion in principle cells resulting in H2O reabsorption.

What is the function of Aldosterone?

Increases Na channel, increases Na/K pump insertion in principle cells, enhances K and H excretion creating a favorable Na gradient for Na and H2O reabsorption. Primarily regulates blood volume.Glycoprotein hormone that stimulates RBC production in response to hypoxia. Released from endothelial cells of peritubular capillaries. Epo receptors are on proerythroblasts which mature in response.Active Vitamin D. Proximal tubule cells convert 25-OH-Vitamin D to the dihydroxy form. This increases intestinal reabsorption of both calcium and phosphate.

What is Renin?

How does Parathyroid Hormone affect the kidney's endocrine function?

PTH directly acts on the kidney to increase renal calcium reabsorption and decrease renal phosphate excretion. Also stimulates proximal tubule cells to make 1, 25 dihydroxycholicalciferol. Secreted by JG cells in response to increased renal arterial pressure and increased renal sympathetic discharge (Beta 1 effect). Stimulates Angiotensin

What do prostaglandins do in the kidney?

Paracrine secretion of PGE2 vasodilates the afferent arterioles to increase GFR. NSAIDs can cause acute renal failure by inhibiting PGE thus preventing the arterioles to vasodilate to maintain GFR.

Where do each of the above hormones act on the kidney? (this rehashes all the functions as well)

ANP is secreted in response to increased atrial pressure. Causes increased GFR and increased Na filtration. Acts right at the beginning of proximal convoluted tubule. PTH is secreted in response to decreased plasma Ca, increased plasma PO4 or decreased plasma vitamin D. Causes increased Ca reabsorption in the distal convoluted tubule, decreased PO4 reabsorption at the proximal convoluted tubule, increased Vitamin D production and increased Ca and PO4 absorption from gut. Renin is released from the JGA and acts on the distal convoluted tubule. Ang II is synthesized in response to decreased BP and causes the efferent arteriole constriction thus increasing GFR and FF but with compensatory Na reabsorption. ADH is secreted in response to increased plasma osmolarity and decreased blood volume. Binds receptors on principal cells causing increased aquaporins. Acts on collecting ducts. Aldosterone is secreted in response to decreased blood volume and increased plasma K, resulting in increased Na reabsorption and increased Kand H secretion. Acts on collecting duct.

What causes K shift out of cells?

Insulin deficiency (decreased Na/K ATPase), Beta Adrenergic antagonists (decreased Na/K ATPase), Acidosis or severe exercise (K/H exchange), Hyperosmolarity, Digitalis (blocks Na/K ATPase), Cell lysis

What causes K shift into cells?

What is normal pH of blood? About 7.4

What is metabolic acidosis? Decreased Bicarb. Compensation by hyperventilation

What is metabolic alkalosis? Increased bicarb. Compensation by hypoventilation.

What is Winter's Formula?

PCO2 increases 0.7 mmHg for every 1 mEq/L HCO3

What is respiratory acidosis?

What is respiratory alkalosis? Decreased PCO2. Compensate with less bicarb reabsorption.

Diarrhea, Glue sniffing, Renal Tubular Acidosis, Hyperchloremia

Diuretic use, vomiting, antacid use, hyperaldosteronism.

Insulin (increased Na/K ATPase), Beta Adrenergic agonists (increased Na/K ATPase), Alkalosis (K/H exchanger), Hypo-osmolarity.

Respiratory compensation in response to metabolic acidosis. PCO2=1.5 (HCO3) +8 (+/-2)

How much should PCO2 increase when bicarb increases?

Increased PCO2. Compensation with increased bicarb absorption

What are some causes of Respiratory Acidosis?

Hypoventilation-Airway obstruction, acute lung disease, chronic lung disease, opiods/narcotics, weak respiratory muscles.

What are some causes of Anion Gap Metabolic Acidosis?

MUDPILES-Methanol, Uremia, Diabetic Ketoacidosis, Paraldehyde or Phenformin, Iron tablets or INH, Lactic Acidosis, Ethylene glycol, Salicylates

What are some causes of non-Anion Gap Metabolic Acidosis?What are some causes of Respiratory Alkalosis?

Hyperventilation-(early) high altitude exposure, Aspirin ingestion (early)

What are some causes of Metabolic Alkalosis?

What is Type 1 (Distal) Renal Tubular Acidosis?

Defect in the collecting tubule's ability to excrete H. Associated with hypokalemia and risk for Ca containing kidney stones.

What is Type 2 (proximal) Renal Tubular Acidosis?

Defect in proximal tubule HCO3 reabsorption. Associated with hypokalemia and hypophosphatemic rickets.

Na- (HCO3 + Cl) normal =10-12

Why does an anion gap occur?

What is a delta delta?

What is Type 4 (hyperkalemic) Renal Tubular Acidosis?

Hyperaldosteronism or lack of collecting tubule response to aldosterone causes hyperkalemia- inhibition of ammonia excretion in proximal tubule. Leads to decreased urine pH due to decreased buffering capacity.

How does Aldosterone act on the Late Distal Tubule?

Stimulated Mineralocorticoid receptors on Principal Cells. This increases their permeability to sodium and potassium by adding Na channels and increases enzymes of the citric acid cycle thus increasing ATP to pump Na/K out the basolateral side. Also stimulated alpha-intercalated cells to secrete more H, thus regulating plasma HCO3 and acid-base balance.

How do you calculate the anion gap?

Secondary to a loss of bicarb or an excess of acid. Essentially there's a lot of something in the blood that's neither Na, HCO3 or Cl that isn't being accounted for so there's a gap in the math.Comparison of change in anion gap to change in bicarbonate. Can tell you what there is in excess if there is a mixed acid base disorder.

How do you calculate a delta delta?

Change in anion gap = AG-12. Change in Bicarb = 24-measured HCO3. Delta delta is ratio of the two

How do you interpret a delta delta?

AG>HCO3 - Metabolic alkalosis + metabolic acidosis. AG<HCO3 -Wide AG + non AG metabolic acidosis. Equal-wide anion gap metabolic acidosis.

How much should CO2 rise in response to increased bicarb?

For every 10 mmol/L rise in HCO3, PCO2 should increase 6mmHg

What are the general functions of the Kidneys?

Excretes harmful waste (urea, creatinine, uric acid, etc.), Maintains acid-base homeostasis, Reabsorbs essential substances, Regulates water and sodium metabolism, Maintains vascular tone, Produces erythropoeitin, Maintains calcium homeostasis.

What is Proteinuria? Protein >150 mg/24 hours or >30 mg/dL via dipstick.

What is Functional Proteinuria?

What is Overflow proteinuria?

What is Serum BUN?

What is hematuria and what are some common causes?

Blood in the urine. Causes fro, the upper urinary tract- renal stone, glomerulonephritis (dysmorphic RBC's), Renal cell carcinoma. Causes from the lower urinary tract- Infection, transitional cell carcinoma, benign prostatic hyperplasia. Drug related causes-anticoagulants, cyclophosphamide (hemorrhagic cystitis and risk for transitional cell carcinoma)

What are diagnostic tests for proteinuria?

Dipstick-detects albumin only. Sulfosalicylic acid-detects albumin and globulins.Protein <2g/24 hour, not associated with renal disease. Causes are fever, exercise, CHF.

What is Orthostatic Proteinuria?

Postural-only occurs when standing. First void in the morning has no protein but subsequent during the day does have protein. No association with renal disease.

Variable protein loss with LMW proteins. Essentially the amount filtered is greater than the tubular reabsorption. Causes are multiple myeloma with Bence Jones proteinuria, Hemoglobinuria from intravascular hemolysis, myoglobinuria from crush injuries, McArdle's glycogenosis and increases in serum creatine kinase.

BUN is a normal end product of amino acid and pyrimidine metabolism that is produced by the liver in the urea cycle. It is filtered in the kidneys and partially reabsorbed in the proximal tubule (amount reabsorbed is flow dependent).

What does serum BUN depend on?

GFR, protein content of the diet, proximal tubule reabsorption and the functional status of the urea cycle.

What are some causes of increased BUN?

Decreased cardiac output (decreased GFR), increased protein intake/breakdown, increased tissue catabolism (burns, surgery, etc), acute glomerulonephritis, acute or chronic renal failure, postrenal disease.

What are some causes of decreased BUN?

Increased plasma volume (pregnancy, SIADH, etc), decreased urea synthesis (cirrhosis, Reye syndrome, fulminant liver failure), decreased protein intake (Kwashiorkor, starvation gluconeogenesis in kideys)

What is Serum Creatinine?What is Azotemia? Increased serum BUN and creatinine

97-137 mL/minute. Less than 100 mL/minute is abnormal.

Concentrated urine, Bilirubinemia, Increased UBG, Vitamins

Metabolic end product of creatine in muscle. Filtered in the kidneys and not reabsorbed or secreted. Serum concentration varies with age and muscle mass.

What is a normal Serum BUN: Creatinine ratio?

15. Urea is filtered and partly reabsorbed whereas Creatinine is filtered entirely. BUN:Cr ratio depends on changes-can be prerenal, renal or postrenal

What is Prerenal Azotemia and what are some causes?

Increased BUN and creatinine caused by something before the kidneys. Most common cause is decreased cardiac output/hypoperfusion of the kidneys decreasing GFR. BUN:Cr >15 because proportionately more Urea is reabsorbed from the low flow rate.

What is Renal Azotemia and what are some causes?

Increased BUN and Cr from parenchymal damage to the kidneys. Some causes are Acute Tubular Necrosis and Chronic Renal Failure. BUN:Cr <15. Both are filtered, there is extrarenal loss of urea and urea may not be reabsorbed as well.

What is Postrenal Azotemia and what are some causes?

Increased BUN and Cr from urinary obstruction below the kidneys. Prostate hyperplasia, blockage or ureters by stones or cancer. Serum BUN:Cr ratio >15. Obstruction to flow decreases GFR resulting in back diffusion of urea (not Cr) into blood and a disproportionate increase in BUN.

What is a normal Cr Clearance?

What are some causes of increased Cr Clearance?

Normal pregnancy (Increased plasma volume means increased GFR), early diabetic glomerulopathy (constricted efferent arteriole from hyaline sclerosis causing increased GFR)

What are some causes of decreased CR Clearance?

Elderly people (decreasing GFR with age), Acute and Chronic Renal disease (ARF from tubular sclerosis, CRF from diabetic glomerulopathy)

What does dark yellow color indicate in Urinalysis?

What does Red or Pink color indicate in Urinalysis?

Hematuria, hemoglobinuria, myoglobinurua, drugs (phenazopyridine), porphyria

First sign of diabetic nephropathy

Bilirubinuria may indicate hepatitis or obstructive jaundice

Nitrites produced by nitrate reducing uropathogens.

What does smoky-colored urine indicate?

Acid pH converts Hb to hematin. Common in nephritic glomerulonephritis

What does black urine after exposure to light indicate?

Alkaptonuria. Deficiency of homogentisate oxidase resulting in buildup of homogentisic acid

What does clarity of the urine indicate?

Cloudy urine with alkaline pH is normal, probably from phosphates. Cloudy urine with acid pH is normal probably from uric acid. Otherwise, bacteria, WBC's, Hb, myoglobin

What does the specific gravity of the urine indicate?

Urine concentration and dilution. SG>1.023 indicates urine concentration and excludes intrinsic renal disease. Hypotonic <1.015. Fixed SG (1.008-1.010) may indicate a lack of concentration and dilution possibly renal failure.

What does the pH of the urine indicate?

Determined by diet and acid base status of person. Vegan often have alkaline pH, meat eaters have acidic pH. An alkaline pH plus strong ammonia smell indicates a urease producing pathogen.

What does glucose indicate in the urine?

Increased serum glucose means glucosuria and DM. Normal serum glucose and glucosuria can happen in normal pregnancy, benign glucosuria

What does microalbuminuria indicate?

What do ketones in the urine indicate?

Acetone and acetoacetic acid. Ketonuria from DKA, starvation, ketogenic diets, pregnancy and isopropyl alcohol poisoning

What does bilirubin in the urine indicate?

What does Urobilinogen indicate?

Trace amounts are normal. No UBG with increased urine bilirubin may be obstructive jaundice. Increased UBG with absent urine bilirubin means extravascular hemolytic anemia. Increased UBG with increased urine bilirubin means hepatitis

What does blood in the urine indicate?

Hematuria from renal stone, hemoglobinuria from intravascular hemolytic anemia, myoglobinuria from increased serum creatine kinase and crush injuries.

What do nitrites in the urine indicate?

What is a hyaline cast?

What is a RBC Cast?

What is a WBC cast?

What is a renal tubular cast?

What is a fatty cast? Cast of cells with lots of lipid. Indicates nephrotic syndrome

What is a Waxy/Broad cast? Refractile, acellular cast seen in chronic renal failure.

What does Leukocyte Esterase in the urine indicate?

Esterase in neutrophiles (pyuria). Infections from urethritis, cystitis, pyelonephritis. Sterile pyuria-Chalmydia trachomatis urethritis, TB, drug induced interstitial nephritis

What do cells in the urine indicate?

Bacteria-UTI, RBC's-hematuria from renal stones, cancer, glomerulonephritis. Dysmorphic RBC's-hematuria of glomerular origin. Neutrophils-pyuria from UTI or sterile pyuria. Oval fat bodies-renal tubular cells with lipids (nephrotic syndrome)

What do casts indicate in the urine?

Casts are formed in tubular lumens in the kidney and are composed of a protein matrix with entrapped cells, debris or protein leaking through the glomeruli. Proves renal origin of the disease.Acellular, ghost like cast containing protein. Only significant if there is accompanying proteinuriaNepritic type of glomerulonephritis resulting in a cast made of RBC'sCast of WBC's indicating acute pyelonephritis, acute tubulointerstitial nephritisCast of a sloughed off renal tubule. Indicates acute tubular necrosis

What types of crystals can be seen in the urine and what do they indicate?

Calcium oxalate crystals-pure vegan diet, ethylene glycol poisoning, calcium oxalate stone. Uric acid crystals-hyperuricemia from gout or massive cell destruction after chemotherapy. Triple phosphate crystals-sign of UTI from urease producing pathogens like Proteus. Cystine crystals-hexagonal crystals seen in Cystinuria

Describe the blood supply to the kidney.

Renal cortex receives 90% of the blood supply. Medulla is relatively ischemic from reduced blood supply. Renal vessels are all end arteries with no collateral circulation so occlusion of any branch produces infarction. Afferent blood flow is controlled by renal-derived PGE2 and renin. Efferent blood flow is controlled by ATH (vasoconstrictor)

Heparan Sulfate

What is Renal Dysplasia?

What is minimal change disease?

Loss of charge of the glomerular basement membrane which produces selective proteinuria.

What protein produces the charge on the glomerular basement membrane?

What are some causes of GBM thickening?

Deposition of immunocomplexes such as in membranous glomerulopathy. Increased synthesis of Type IV Collagen such as in DM.

What do Visceral Epithelial Cells do in the glomerulus?

Production of the GBM. Contain podocytes and slit pores between podocytes which serve as a distal barrier to prevent protein loss in the urine. Podocytes fuse in nephrotic syndrome, no matter what the cause.

What do Mesangial Cells do in the glomerulus?

Support the glomerular capillary. Can release inflammatory mediators and proliferate-IgA glomerulopathy has mesangial immune complex deposits.

What do parietal epithelial cells do in the glomerulus?

Lining cells of Bowman's capsule. Proliferation causes crescents that encroach upon and destroy the glomerulus.

Most common cystic disease in children. See abnormal development of one or both kidneys with abnormal structures persisting in the kidneys (cartilage, immature collecting ductules). Present as enlarged, cystic, unilateral or bilateral flank mass. May lead to chronic renal failure.

What is Juvenile Polycystic Kidney Disease?

AR disease. Bilateral cystic disease with cysts involving all parts of the nephron in the cortex and medulla. Bilaterally palpable kidneys.

What other types of conditions are seen in Juvenile Polycystic Kidney Disease?

Cysts present in liver. Associated with congenital hepatic fibrosis which leads to portal hypertension. Also associated with oligohydramnios and Potter's Syndrome.

What is Adult Polycystic Kidney Disease?

AD disease with defect on chr 16. Bilateral cystic disease with the cysts involving all parts of the cortex and medulla. Develop chronic renal failure a lot of the time.

Only a few glomeruli are abnormal

All glomeruli are abnormal

>100 nuclei in affected glomeruli

Thick GBM, no proliferative change

Thick GBM, hypercellular glomeruli

Fibrosis involving only a segment of the involved glomerulus

Involves glomeruli and other organs, e.g. SLE

What other conditions are associated with Adult PKD?

Cysts may be present in the liver, pancreas and spleen. Also have intracerebral Berry aneurysms. May cause hemorrhage if hypertension results in rupture, intracerebral hemorrhage and lacunar infarcts. Other associations are sigmoid diverticulosis, hematuria, mitral valve prolapse, and risk for developing renal cell carcinoma.

What is Medullary Sponge Disease?

Multiple cysts in the collecting ducts present in the medulla. See striations in the papillary ducts of the medulla (swiss cheese appearance). Recurrent UTI's, hematuria and renal stones.

What is Acquired Polycystic Kidney Disease?

Most commonly caused by renal dialysis. Tubules become obstructed by interstitial fibrosis or oxalate crystals. Small risk for renal cell carcinoma.

What are simple retention cysts?

Most common adult renal cyst. Derived from tubular obstruction. May cause hematuria and may resemble renal cell carcinoma. Needle aspiration will distinguish it from RCC

What is Focal Glomerulonephritis?What is Diffuse Glomerulonephritis?What is Proliferative Glomerulonephritis?What is Membranous Glomerulonephropathy?

What is Membranoproliferative Glomerulonephritis?What is Focal Segmental Glomerulosclerosis?What is Crescentic Glomerulonephritis?

Proliferation of the parietal cells around the glomerulus (in Bowman's Space, thus forming a crescent)

What is Primary Glomerular Disease?

Involves only glomeruli and no other target organs. Essentially something like minimal change disease.

What is Secondary Glomerular Disease?

Ya, definitely do that :-)

Anti GBM antibodies attack the glomerular basement membrane

Look at Golijan page 400 and go through all the histologyWhat does a Linear pattern indicate on Immunofluorescence?

Antibodies line upagainst evenly distributed antigens in the GBM. Think Goodpasture's Syndrome

What does a Granular or Lumpy Bumpy appearance indicate on Immunofluorescence?

Think immunocomplex deposits in the glomerulus forming lumps of Ig. Not attached to the GBM.

What do immune complexes look like on Electron Microscopy?

Electron dense giving them a dark color. Subendothelial are trapped between the endothelial cell and GBM. Subepithelial has passed through the GBM but is stuck in the podocytes. Intramembranous is within the GBM and Mesangial is within the mesangium.

How does Type III Immune complex disease cause glomerular disease?

Circulate and deposit in glomeruli or develop in situ. Immune complexes then activate complement, procude C5a which is chemotactic to neutrophils which attack the GBM.

How does something like Goodpasture's Disease cause glomerular damage?

How does T Cell production of cytokines damage the GBM?

Cytokines cause the GBM to lose its negative charge. Cytokines also damage podocytes causing them to fuse.

What are clinical manifestations of glomerular disease?

Nephritic syndrome, nephrotic syndrome and chronic glomerulonephritis

Describe the pathophysiology of Nephritic Syndrome?

Glomerular injury primarily occurs due to neutrophils which damage See hypertension from salt retention, periorbital puffiness from salt retention, oliguria (decreased GFR from inflamed glomeruli) and Hematuria. The hematuria features dysmorphic RBC with irregular membranes from inflamed glomeruli with IC deposition. Often see neutrophils in the sediment, especially if immune complex. RBC casts are a key finding, and occasionally there are WBC casts.

Henoch Schonlein Purpura

What are some lab findings in Nephritic syndrome?

Proteinuria>150mg/day but less than 3.5 g/day. Azotemia with BUN:Cr ratio >15 because tubular function is intact in acute glomerulonephritis

What is IgA Nephropathy (Berger's Disease)?

Most common nephropathy, mostly nephritic. Increased mucosal synthesis and decreased clearance of IgA with increased serum IgA. Produces Focal Proliferative Glomerulopathy. Also see Mesangial IgA immune complex deposits with granular immunofluorescence. IC's activate the alternative complement pathway.

What does Berger's disease often immitate?What happens after a URI in Berger's disease?

Episodic hematuria and hypertension following URI because of increased IgA deposits.

What is Post-Streptococcal Glomerulonephritis?

Most common type of post-infectious glomerulonephritis, usually after group A strep infection of skin (scarlet fever) or pharunx. Subepithelial immune complex deposits with granular immunofluorescence. IC's activate the alternative complement pathway. See a diffuse proliferative pattern with neutrophilic infiltrate.

How does Post-Streptococcal Glomerulonephritis present?

Hematuria, 1-3 weeks following group A strep infection by a nephritogenic strain (never produces rheumatic fever). Causes periorbital edema from sodium retention not hypoalbuminemia, transient, sometimes severe hypertension.

What lab tests are indicative of Post-Strep Glomerulonephritis?

Increased DNAase B titers. ASO is degraded by oil in the skin and is thus not increased. Streptozyme test is positive (anti-DNAase B, ASO, anti-AH and anti-NAD antibodies).

What is Diffuse Proliferative Glomerulonephritis?

Most common type of glomerular disease in SLE. Subendothelial IC deposits with granular immunofluorescence. DNA-anti-DNA IC's activate the classical complement pathway. See "wire looping of capillaries" as well as neutrophil infiltration with hyaline thrombi in capillary lumens.

What does the serum ANA test look like in Diffuse Proliferative Glomerulonephritis?

Serum ANA has a rim pattern, corresponding to the presence of anti-ds DNA antibodies

Corticosteroids and Cyclophosphamide

80% are HLA-BR2 positive

What is Nephrotic Syndrome?

How do you treat Diffuse Proliferative Glomerulonephritis?

What is Rapidly progressive Crescentic Glomerulonephritis?

Clinical syndrome that may be either primary or secondary disease. See a rapid loss of renal function that progresses to acute renal failure within weeks. May or may not be associated with crescent formation.

Which diseases are associated with Rapidly Progressive Crescentic Glomerulonephritis?

Goodpasture's syndrome, microscopic polyarteritis (p-ANCA), Wegener's granulomatosis (c-ANCA)

What HLA type is common in Goodpasture's syndrome?

How do you treat Goodpasture's syndrome?

Plasma exchange to remove antibodies, immunosuppressive therapy with steroids and cyclophosphamide or renal transplantGlomerular injury due to cytokines not neutrophils. Cytokines released from T Cells destroy the negative charge of the membrane thus allowing protein leak. They also cause the podocytes to fuse together.

What are the key findings in nephrotic syndrome?

Proteinuria >3.5 g/24 hr, pitting edema and ascited due to hypoalbuminemia. Increased risk for spontaneous peritonitis from strep pneumoniae. Sometiems there is hypertension from salt retention. Hypercoagulability due to loss of Antithrombin III causing potential for renal vein thrombosis. Hypercholesterolemia from increased synthesis (after albumin loss). Hypogammaglobulinemia from protein loss. Fatty casts with maltese crosses and oval fat bodies.

What type f kidney disease does Diabetic Glomerulopathy cause?

Nephrotic syndrome with Nodular Glomerulosclerosis (Kimmelstiel-Wilson disease). Risk factors are poor glycemic control, hypertension and high correlation with coexisting diabetic retinopathy.

Microalbuminuria

Renal papillary necrosis and acute or chronic pyelonephritis

What is renal amyloidosis?

What is Alport's Syndrome?

What is the pathogenesis of Diabetic Glomerulopathy?

Nonenzymatic glycosylation of the GBM, also affecting the tubule basement membranes. Results in increased vessel and tubular permeability to proteins. NEG of the afferent and efferent arterioles also results in hyaline arteriolosclerosis (efferent first). There is also osmotic damage to the glomerular capillary endothelium because glucose is converted to sorbitol by aldolase reductase resulting in an osmotic gradient. Selective hyaline arteriolosclerosis of the efferent arterioles results in increased GFR and causes hyperfiltration damage to the mesangium.

What is Diabetic Microangiopathy?

Increased Type IV collagen deposition in the GBM, tubular basement membrane and mesangium results in a microangiopathic state.

What microscopic changes are seen in Diabetic Glomerulopathy?

Fusion of podocytes, afferent and efferent hyaline arteriolosclerosis, nodular masses of type IV collagen and trapped proteins in the mesangium

What lab values are significant in Diabetic Glomerulopathy?

Are there any other diseases of the kidney associated with Diabetic Glomerulopathy?

Amyloid deposits in the kidney secondary to primary or secondary amyloidosisX-Linked recessive (sometimes AR or AD) mutations in A chains of type IV collagen in the GBM. Lipid accumulates in VEC's producing foam cells. Also see sensorineural hearing loss and ocular abnormalities

What is Thin Basement Membrane Disease?

Benign familial hematuria. AD disorder with extremely thin basement membranes in the setting of normal renal functin. See mild proteinuria and persistent microscopic hematuria

Shrunken kidenys with glomerular sclerosis and tubular atrophy

What is Acute Renal Failure?

What are the common causes of Chronic Glomerulonephritis?

Rapidly progressive glomerulonephritis, focal segmental glomerulosclerosis, type I membranoproliferative glomerulonephritis, membranous glomerulopathy, type IV diffuse proliferative glomerulonephritis in SLE, IgA nephropathy.

What are gross and microscopic findings in chronic glomerulonephritis?

What is ischemic Acute Tubular Necrosis?

Most often caused by prerenal azotemia due to hypovolemia. Ischemia damages endothelial cells decreasing vasodilators and increasing vasoconstrictors, thus worsening the situation and further decreasing GFR. Ischemia also damages tubular cells which then detach into the lumen, cause obstruction and produce pigmented renal tubular cell casts. The casts further obstruct the lumen increasing tubular pressure, decreasing GFR and pushing fluid into the interstitium resulting in oliguria.

What segments of the nephron are damaged in ischemic ATN?

Straight segment of the Proximal tubule (part of the degree most susceptible to hypoxia), Medullary segment of the thick ascending limb (location of the NK2C transporter), and the Tubular basement membrane (interferes with renal tubular cell regeneration)

What is Nephrotoxic Acute Tubular Necrosis?

ATN from nephrotoxic substances. Aminoglycosides are most common, radiocontrast agents and heavy metal poisoning are also causes. Most commonly see oliguria, occasionally polyuria. This primarily damages proximal tubule while the tubular basement membrane is intact. Also see pigmented renal tubular cell casts, hyperkalemia and anion gap metabolic acidosis, increased BUN and Cr with ratio of BUN:Cr <15. Often have issues with hypokalemia in the diuresis phase.

What is the epidemiology of Acute Tubular Necrosis?

10% of ICU patients, 40% iatrogenic, 20% of patients with sepsis and >50% of patients with septic shockAcute suppression of renal function developing in 24 hours, accompanied by oliguria or anuria. Most commonly caused by ATN.

What is RPGN? Rapidly progressive glomerular nephritis

What is Oliguria? Urine output <400 mL/day or less than 20 mL/hr.

How do you calculate a FENa? FENa = (Una * PCr)/(PNa * Ucr) *100

Tubular dysfunction. Good predictor of ATN

What are some causes of Acute Renal Failure?

Postrenal obstruction, vascular disease (malignant htn), RPGN, drugs, DIC, urate nephropathy.

How do you treat Acute Renal Failure?

Treat prerenal azotemia-volume expansion if hypovolemic to increase renal blood flow. Low dose dopamine. Fenoldopam (dopamine Alpha-1-receptor agonist), Dialysis

What is Tubulointerstitial Nephritis?

Acute or chronic inflammation of tubules and interstitium. May be caused by acute pyelonephritis, drugs, infections (legionaire's, leptospirosis), SLE, lead poisoning, Urate nephropathy and multiple myeloma.

What are common causes of acute pyelonephritis?

E Coli is most common followed by Enterococcus. Risk factors are indwelling catheter, obstruction, medullary sponge kidney, DM, pregnancy and sickle cell

How does vesicoureteral reflux cause pyelonephritis?

Intravesical portion of the ureter is not compressed during micturition so urine refluxes up. Causes ascending infection into the renal pelvis and parenchyma.

What are common causes of Oliguria?

Prerenal azotemia, acute glomerulonephritis, acute tubular necrosis/renal azotemia, and postural azotemia.

What does decreased Urine Osm indicate?

Urine osm <350 mOsm/kg indicates poor concentrating ability and thus tubular dysfunction

What does a FENa less than 1% indicate?

Sodium filtration closely mimics creatinine filtration. FENa less than 1% means good tubular function

What does a FENa greater than 2% indicate?

What can UNa tell you about tubular function?

UNa<20 mEq/L indicates good tubular function aka you're not dumping salt like crazy. UNa >40 mEq/L indicates poor tubular function aka you're not reabsorbing salt.

How do you distinguish postrenal azotemia from ATN?

ATN usually presents with pigmented tubular casts. In postrenal azotemia, the sediment is usually normal.

Hematogenous spread of the infection to the kidneys.

Hypertension

What is Analgesic Nephritis?

What should you suspect if there is staph a. cultured in the urine?What are gross and microscopic findings in pyelonephritis?

Grayish white areas of abscess formation in the cortex and medulla. Microabscesses form in the tubular lumens and interstitium.

What are the clinical and lab findings in pyelonephritis?

Clinical-spiking fever, flank pain, frequency and dysuria. Lab-WBC casts, pyuria, bacteruria, hematuria

What are complications of Acute Pyelonephritis?

Chronic Pyelonephritis, Perinephric Abscess, Renal Papillary necrosis, septicemia with endotoxic shock

What are pathological findings in Chroninc Pyelonephritis?

U shaped cortical scars overlying a blunt calyx, visible on IV pyelogram.

What pathological findings are seen in obstructive Chronic Pyelonephritis?

Uniform dilation of the calyces and diffuse thinning of cortical tissue.

What are microscopic findings of Chronic Pyelonephritis?

Chromic inflammation with scarring of the glomeruli. Tubular atrophy-tubules contain eosinophilic material resembling thyroid tissue (thyroidization)

What can reflux nephropathy cause in children?

What drugs are associated with acute drug induced ATN?

Penicillin esp. methicillin. Rifampin, sulfonamides, NSAIDs, diuretics

What is the pathogenesis of Drug induced ATN?

Combination of Type I and IV hypersensitivity. Abrupt onset of fever, oliguria and rash that resolves with withdrawal of the drug. Causes tubular disease with a BUN:Cr <15, eosinophilia and eosinophiluria

Chronic drug induced Tubulointerstitial nephritis. Chronic use of Acetominophen with Aspirin because Acetominophen causes free radical damage while aspirin inhibits renal synthesis of PGE2 leaving AT II unopposed.

What is Urate Nephropathy?

Nuclear acid-fast inclusions in the proximal tubule

What is Renal Osteodystrophy?

What are complications of Analgesic Nephritis?

Renal papillary necrosis-sloughing of renal papillae producing gross hematuria, proteinuria and colicky flank pain. Ring defect where papillae used to reside. Hypertension, CRF and Renal pelvic and bladder transitional cell carcinomas.Deposition of Urate crystals in the tubules and interstitium. May be caused by massive release of purines (often after chemo), lead poisoning or gout.

How does lead poisoning cause Urate Nephropathy?

Decreased excretion of uric acid from the lead. Also direct toxic effects cause TIN

What is seen microscopically in Urate Nephropathy resulting from lead poisoning?

How does Multiple Myeloma cause renal disease?

Bence Jones light proteins are toxic to the tubular epithelium and result in tubular casts. Casts obstruct the lumen and incite a foreign body giant cel reaction of the tubules and interstitium, leading to renal failure. Nephrocalcinosis from bone breakdown/hypercalcemia also causes metastatic calcification of the basement membrane collecting tubules. Finally, BJ proteins may be converted to amyloid and cause primary amyloidosis resulting in nephrotic syndrome.

What are hematologic findings in Chronic Renal Failure?

Normocytic anemia with low corrected reticulocyte count. Due to decreased Erythropoietin production. Also see qualitative platelet defects.

Chronic kidney disease-mineral bone disorder. Osteitis fibrosia cystica due to hypovitaminosis D. Causes hypocalcemia which then stimulates the production of PTH-secondary hyperparathyroidism. Hyperparathyroidism causes bone resorption causing cystic lesions in the bone. Hemorrhage into cysts caused brown discoloration.

What are some complications of Renal Osteodystrophy?

Osteomalacia from decreased mineralization of the osteoid. Osteoporosis from loss of organic bone mass and minerals (often due to chronic metabolic acidosis because excess H is buffered by bone minerals).

Reduce proteinuria and treat hypertension.

What are some cardiovascular findings in Chronic Renal Failure?

Hypertension from salt retention, hemorrhagic fibrinous pericarditis, CHF and accelerated atherosclerosis.

What are some other clinical consequences of Chronic Renal Failure?

Hemorrhagic gastritis and uremic frost (urea crystals deposit on the skin). Also hyperkalemia and anion-gap metabolic acidosis.

Why does renal failure cause hypocalcemia?

Hypovitaminosis D from decreased 1-Alpha Hydroxylase and thus decreased reabsorption of calcium from the small intestines. Also hyperphosphatemia from decreased renal excretion drives calcium into bone and soft tissue.

Why is there increased Serum Cystatin C?

Cystatin in a Cysteine protease inhibitor produces by the nucleus of all cells. It should be filtered by the glomerulus but not secreted so it's a good marker of renal function.

What is seen on urinalysis in Chronic Kidney Failure?

Fixed specific gravity because no concentrating ability, free water clearance is 0, waxy/broad casts are present.

Why do you give ACE inhibitors in kidney disease?

What is benign nephrosclerosis?

Common renal disease in essential hypertension caused by hyaline arteriolosclerosis of arterioles in the renal cortex. Results in tubular atrophy, interstitial fibrosis and glomerular sclerosis. See small kidneys with a finely granular cortical surface.

What is Malignany Hypertension?

Sudden onset of accelerated hypertension with end organ damage. Risk factors are pre-existing BNS, Hemolytic Uremic syndrome, thrombotic thrombocytopenic purpura and systemic sclerosis

What microscopic changes are seen in Malignant Hypertension?

Fibrinoid necrosis and necrotizing arteriolotis and glomerulitis with pinpoint hemorrhages on the cortical surface. Also hyperplastic arteriolosclerosis (onion skin lesions) with smooth muscle hyperplasia and reduplication of the basement membrane.

What are clinical findings in Malignant Hypertension?

Hypertensive encephalopathy-cerebral edema, papilledema, retinopathy with flame hemorhages and potential for an intracerebral bleed.

What causes Renal infarction?

Renal stones, retroperitoneal fibrosis, cervical cancer and BPH

What causes Urolithiasis?

What is a calcium stone?

Embolization from thrombi in the left heart, atheroembolic renal disease, vasculitis especially polyarteritis nodosa.

What is the gross and microscopic appearance of a renal infarction?

Irregular wedge-shaped pale infarct in the renal cortex. Old infarct have a V shape from scar tissue.

What is Diffuse cortical necrosis?

Complication of obstetric emergencies. Due to DIC in the renal cortex which results in fibrin clots in arterioles and glomerular capillaries and bilateral, diffuse, pale infarcts of the renal cortex. See anuria in a pregnant woman followed by ARF.

What are some causes of Hydronephrosis?

What are some clinical findings of hydronephrosis?

Compression atrophy of the renal medulla and cortex and dilated ureters and renal pelvis

Hypercalcuria in the absence of hypercalcemia (absorptive hypercalcuria), decreased urine volume, reduced urine citrate (citrate chelates calcium), primary hyperparathyroidism, diet high in dairy (contains phosphates or oxalate), and urinary infections due to urease producers (proteus)Calcium oxalate stone-from vegans or people with Crohn's. Calcium Phosphate stone-dairy products and distal renal tubular acidosis.

What is a Magnesium Ammonium Phosphate stone?

Struvite stone causing a Staghorn calculus. Associated with urease producing bugs. Urine is alkaline and smells like ammonia.

How do you treat a calcium stone?

Most pass. Can give hydrochlorothiazide which increases renal tubule reabsorption of calcium. Cellulose phosphate binds calcium in the intestine.

How do you treat a Uric Acid stone?

Allopurinol, increase urinary pH to make the stone soluble. Cotreat chemo patients with allopurinol to prevent urate nephropathy.

How do you treat a struvite stone?

Surgical removal because of size. Antibiotic to eliminate urease producer.

What is an Angiomyolipoma?

What is Renal Pelvic Cancer?

What is a Wilm's Tumor?

Hamartoma composed of blood vessels, smooth muscle and adipose cells. Associated with tuberous sclerosis causing mental retardation and multisystem hamartomas.

What are risks for Renal Cell Carcinoma?

Smoking, Von Hippel-Lindau, Adult PKD, obesity, asbestos and lead exposure, and gasoline or petroleum product exposure.

What is Von Hippel Lindau disease?

AD disease with defect on chr 3. Increased VEGF causes hemangiobalstomas of the cerebellum and retina and bilateral renal cell carcinomas.

What are some gross and microscopic findings in Clear Cell renal carcinoma?

Upper pole mass with cysts and hemorrhage composed of clear cells that contain lipids and glycogen. Tendency for renal vein invasion and invasion into the IVC and right heart.

What are clinical signs of clear cell renal carcinoma?

Hematuria, abdominal mass, flank pain, hypertension, triad of hematuria, abdominal mass and flank pain. Constitutional symptoms. Left sided variocele from blocking of left renal vein.

What hormonal changes are seen in renal clear cell carcinoma?

EPO is elevated causing secondary polycythemia. PTH-related protein produces hypercalcemia.Transitional cell carcinoma. Risk factors are smoking, Phenacetin abuse, aromatic amines (aniline dyes), cyclophosphamide.

AD tumor with the defect on chromosome 11. WAGR Syndrome-wilms tumor, aniridia (absent iris), genital abnormalities, retardation. Beckwith-Wiedmann syndrome-wilms tumor with enlarged body organs, hemihypertrophy of extremities.

Where do Wilm's tumors come from?

Large necrotic gray tumors derived from mesonephric mesoderm, containing abortive glomeruli and tubules with primitive blastemal cells and rhabdomyoblasts.

How does a Wilm's tumor present?

Unilateral palpable mass in a child with hypertension (renin secretion). Metastasis to the lungs.