EXAMINATION - Weebly  · Web viewINSPECTION. General look of the patient. i. Cyanosed ii. Breathless iii. Air hunger. iv. Pursed lip breathing (COPD) v. Pink puffer (Emphysema) vi.

EXAMINATIONINSPECTION

General look of the patienti. Cyanosed ii. Breathless iii. Air hungeriv. Pursed lip breathing (COPD) v. Pink puffer (Emphysema)

vi. Blue Bloaters (chronic Bronchitis) Inspection of Chest

Respiratory rate Shape of the chest (Elliptical- Normal, Barrel, Funnel, Ricketic, Pigeon shape) Movement of chest Symmetry of Chest (Symmetrical, Asymmetrical) Types of Respiration (Abdomino-thoracic or Thoraco-abdominal) Visible Apex Beat In drawing of Ribs Tracheal Tug Supraclavicular Fossae Prominent Veins, Scar, Pigmentation

PALPATION Trachea (Normally it is centrally placed) if not then

Pull (Fibrosis, Collapse) Push (Pleural Effusion, Pneumothorax, Malignancy) Trail Sign is +ve in COPD

Chest Expansion (Normal expansion is 3-5 cm) Decreased in (Fibrosis, Collapse, Pleural effusion, Pneumothorax, Consolidation)

Vocal Fremitus (Tactile Fremitus) Increased in (Consolidation, Cavitation, Collapse with Patent Bronchus) Decreased in (Pleural Effusion, Pneumothorax, Fibrosis, Collapse with Obs:

Bronchus) Apex Beat

Displaced in (Collapse, Pleural Effusion, Pneumothorax, Fibrosis) Tenderness

Hypertrophic Pulmonary Osteoarthropathy (Bronchogenic Carcinoma) Teitz Syndrome (Costo-chondritis) Fracture of Rib

PERCUSSION Normal percussion note is RESONANT Hyper-Resonant (Emphysema, Pneumothorax) Dull (Consolidation, Fibrosis, Collapse) Stony Dull (Pleural effusion) We do Tidal Percussion for the movement of Diaphragm

AUSCULTATION Normal Breathing is “Vesicular Breathing”

Inspiration is longer than Expiration Inspiration is harsher than Expiration No gap b/w Inspiration & Expiration

Bronchial Breathing (Consolidation, Fibrosis, Collapse) Expiration is longer than Inspiration Marked gap b/w Inspiration & Expiration

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Plural Rub (Pleuritis) Pericardial Rub (Pericarditis) Pleuro-Pericarditis Crepitations (Fine in Pulmonary edema, Coarse in TB & Pneumonia) Wheeze (Asthma, COPD) Vocal Resonance

Increased in (Consolidation, Cavitation, Collapse with Patent Bronchus) Decreased in (Pleural Effusion, Pneumothorax, Fibrosis, Collapse with Obs:

Bronchus)

PNEUMONIADef: Acute inflammatory consolidation of lung parenchyma.CLASSIFICATION OF PNEUMONIAANATOMICAL

Lobar Pneumonia Segmental / Lobular Pneumonia Broncho pneumonia

HISTOLOGICAL Typical Pneumonia Atypical Pneumonia

PATHOLOGICAL (Causative Organism) Bacterial Pneumonia

i. Streptococcal Pneumonia ii. H-influenzaiii. Staphylococcal Aureus iv. Klebsellav. Moraxella Catarrhalis vi. Pseudomonasvii. E-coli viii. Anaerobesix. Mycoplasma x. Coxiella Burnettixi. Rickettsia xii. Legionella

Viral Pneumoniai. Adeno virus ii. Coxsackie Virusiii. Influenza virus A, B etc….

Parasites (Loeffler’s Pneumonia)i. Ascaris Lumbricoides ii. Toxicoraiii. Paragonimus Westermeni

Fungal Pneumoniai. Aspergilloma

Lipid Pneumonia (Bronchogenic Carcinoma)CLINICAL CLASSIFICATION

Community Acquired Pneumonia (Pneumonia which occur in previously healthy or within 48 hours of hospitalization)

Hospital Acquired Pneumonia (After 48 hours of hospitalization)(E-Coli, Klebsella, Pseudomonas, Staphylococcus Aureus)

C/F Fever (high grade) with Chills Cough initially dry then productive (initially Mucoid then Purulent) Dysponea, Chest pain

EXAMINATIONInspection

Increased Respiratory Rate

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Decreased Chest Movement on the affected sidePalpation

Chest expansion reduced Increased Vocal Fremitus Trachea may be deviated to opposite side if pleural effusion

Percussion Note is DULL

Auscultation Bronchial Breathing Some times Crepitations

INVESTIGATION1. Chest X-ray:

Consolidation (Opacity) in Lobar / Segmental Patchy infiltration in Bilateral Bronchopneumonia Para pneumonic Effusion

2. Blood CP: Increased WBC Raised ESR

3. Sputum for Microscopy4. Sputum for Culture5. Serology

Ab (against Mycoplasma, Rickettsia, Chlamydia, Legionella etc…) Immunoflouresence Ab Coombs Test

ATYPICAL PNEUMONIAIn this case extra pulmonary are more common.i. Low grade fever ii. Head ache iii. Nausea iv. Vomitingv. Diarrhea vi. Myalgia vii. Arthralgia viii. Dry Cough TREATMENT OF PNEUMONIAEmpirical therapy (out patient treatment) for 14 days

Amoxycillin + Clavilumic Acid (Augmentin 625mg 1+0+1) OR Cefaclor (Ceclor 500mg) OR Cefuraxime axetil (Zinacef 250mg 1 x OD) OR Clarithromycin (Klaricid) OR Ofloxacin (Oflobid) OR Levofloxacin (Xeflox, Novidate).

CRITERIA FOR HOSPITALIZATION Extreme of Age (>65 years or <05 years) Co morbidity (IHD, DM, CLD, COPD, AIDS, Renal Failure etc…) Seriously ill patients Not responding to empirical therapy Leucopoenia If we found these signs

o Tachycardia >140 beats/ mino Tachypenia >30 breaths/ mino PaO2 <60cm of H2O

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TREATMENT Bed Rest Proper Nutrition Anti Pyretic O2 inhalation if require Empirical Therapy (out patient treatment) but all in the form of injections.

COMPLICATIONS OF PNEUMONIA

Pulmonary Complications Extra Pulmonary Complication Lung Abscess Sinusitis Bronchiectasis Meningitis Cavitation Otitis Media Collapse Endocarditis Respiratory Failure Precipitate Cardiac Failure Pleural effusion Precipitate Atrial Fibrillation Empyema ATN Pleuritis Septicemia

COPDChronic Bronchitis EmphysemaChronic Bronchitis: Chronic persistent productive cough for more than 3 months in consecutive 2

years is called chronic Bronchitis. Emphysema: Permanent dilation of Respiratory Unit (below the level of terminal

bronchiole) because of destruction of wall of it.Risk factors:

Active Smoking >10pack year (20 cigarettes per day till 10 years)

Passive Pollution Free Radicals Alpha 1 Anti trypsin deficiency (Pi ZZ) genotype

Symptoms Persistent Cough, some times turbid, productive usually in morning time. Dysponea

Signs (on inspection) Barrel shaped chest Pink puffer / Blue bloaters Pursed Lip Breathing Accessory muscle use during respiration In drawing of ribs Prominent Supra Clavicular Fossa Tracheal tug may be seen RR may be increased

On Palpation Tracheal tug (trail sign) Apex beat may be displaced

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On Percussion Hyper resonant

On Auscultation NVB with may be prolong expiration There may be Wheeze There may be Crepitations

INVESTIGATION1. Chest x-ray

Hyper translucent Lung folds Widening of intercostal spaces Flattening of diaphragm Tubular Heart Emphysematous Bullae

2. Pulmonary Function Test (Spirometry) FEV1 = <80% FEV1 / FVC = <70%

3. Blood CP Polycythemia ESR (may be raised) C-reactive Protein Raised

4. ECG

P- Pulmonale5. Sputum DR & Culture

Infections6. ABGS

For Severity Alpha 1 Anti trypsin deficiency Alpha 1 Anti trypsin Level

MANAGEMENT Cessation of smoking

First Ask then Advice then Assess then Augment then Assist 5 years complete cessation is equal to non-smokers.

To reduce Dysponea Theophylline Ipratropium bromide B2 Agonist (sos short term)

Anti inflammatory Corticosteroids

If infection then give antibiotics L.T.O.T: (Severely ill)

O2 for 15 hrs in 24 hrsCOMPLICATIONS

Pneumothorax Fibrosis Collapse Pulmonary HTN

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Cor- Pulmonale Type II Respiratory Failure (hypoxemia + hypercapnia)

TUBERCULOSISDef: Chronic grnulomatous inflammation with caseous necrosis caused by Acid Fast Bacilli.CAUSATIVE ORGANISM (Obligate Aerobes)

1. Mycobacterium tuberculosis Typical2. Mycobacterium Bovis3. Mycobacterium Avium Intercellularis4. Mycobacterium Cheloni5. Mycobacterium fortuitum Atypical6. Mycobacterium Marinum7. Mycobacterium Gastrae

SITE:Primary sites:

i. Lung ii. Intestine iii. Lymph nodesiv. Tonsils v. Skin

Secondariesi. TB Meningitis ii. Tuberculoma (Brain) iii. TB Serositisiv. Genito urinary TB v. TB Osteomyelitis vi. TB Adrenal Glandsvii. Lupus Vulgaris (skin) etc…

PRIMARY TUBERCULOSIS In non immune person who is not previous infected It can lead to Miliary TB Usually A symptomatic Calcification cause buried of Mycobacterium We see GHON FOCUS (sub plural parenchyma around interlobar fissure) We also see GHON COMPLEX (ghon focus + hillar Lymph node involvement)

SECONDARY TUBERCULOSIS Because of re-infection OR re-activation of previous lesion. Symptomatic Usually lung apex involve Cavitation

SYMPTOMS Low grade fever Night sweats Anorexia Wt: loss Lethargic Chronic cough with sputum If long standing TB then Hemoptysis If TB complicated then Pleuritis, Pleural effusion, Pneumothorax, and Chest pain.

W.H.O CATEGORIZATION OF TB

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Category I: New cases smear +ve with pulmonary parenchymal involvement Smear –ve with severely parenchymal disease Severe extra pulmonary TB (eg. TB Meningitis)

Category II: Defaulters Re RX

RelapseCategory III:

Extra pulmonary TBCategory IV:

Drug resistant MDR Chronic cases

Some important definitions New Cases: Patients who never taken ATT before OR if taken then less then 4 weeks.

Smear Positive: Consecutive 3 samples of sputum for AFB. Out of them 2 are positive OR if one is positive + chest X-ray shows active lesion.

Smear Negative: Only chest X-ray shows active pulmonary lesion.

Relapse: patient has completed ATT course and declared as a cure patient but now again he come with active lesion.

Drug Resistant: Patient has taken regular ATT for 5 months but still he is smear positive.

Multiple Drug Resistant: Patient is resistant for RIFAMPICIN + ISONIAZID.

Chronic Cases: Complete 8 months therapy but not declared as a cure.

INVESTIGATION1. Chest X-ray:

Consolidation 2. Sputum for AFB

Total 03 samples, 01 sample every morning for 03 days before breakfast. 3. Sputum Culture Sensitivity4. PCR5. Biopsy6. Tuberculin Skin Test {PPD} (Montoux Test)

> 15 mm suggestive of TB 10-15 mm doubtful Sensitivity & Specifity is low 05-10 mm unlikely

TREATMENTCategory I

Initial Regimen

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Give initial regimen for 02 months, which include (Rifampicin + Isoniazid + Ethambutol + Pyrizinamide)

Then go for Sputum AFB

If Sputum –ve if Sputum +ve

Then continue initial regime for 1 month more

Then start maintenance therapy then start maintenance therapy

Maintenance Regimen (continuation phase)

Rifampicin + Ethambutol (for 6 months)OR

Rifampicin + Isoniazid (for 4 months)

Total regimen duration for ATT in Category I{08 months if continuation with Rifampicin + Ethambutol}

OR{06 months if continuation with Rifampicin + Isoniazid}

Category IIInitial Regimen

Give initial regimen for 02 months with 05 drugs(Rifampicin + Isoniazid + Ethambutol + Pyrizinamide + Streptomycin)

Then go for Sputum AFB

If Sputum –ve if Sputum +ve

Then give 4 drugs for 01 month then continue initial regime for 1 month more{R H E Z} {R H E Z + S}

Now again go for sputum AFB

Then start maintenance therapy then start maintenance therapyMaintenance Regimen (continuation phase)

Rifampicin + Ethambutol + Isoniazid (for 5 months)In category II go for Sputum AFB

At the end of 02 months At the end of 03 months At the end of 05 months

Category IIIInitial Regimen

Give initial regimen for 02 months, which include (Rifampicin + Isoniazid + Ethambutol + Pyrizinamide)

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Then go for Sputum AFB

If Sputum –ve if Sputum +ve

Then continue initial regime for 1 month more

Then start maintenance therapy then start maintenance therapy

Maintenance Regimen (continuation phase)

Rifampicin + Ethambutol (for 6 months)OR

Rifampicin + Isoniazid (for 4 months)

Category IVIn this case we treat with one of the following drug or combination of 2 or 3 drugs

1. Ofloxacin (Market name: - Oflobid)2. Amakacin (Market name: - Gracil, Amakin)3. Kanamycin4. Cycloserine5. Ethionamide 6. Rifabutin7. 5 Amino salicylic Acid8. Capreomycin9. Levofloxacin (Market name: - Novidat, xeflox, leflox)

INDICATION OF STEROIDS IN T.B

1. Disseminated T.B (Miliary)2. Extensive Pulmonary parenchymal lesion3. If Rashes Developed4. Drug Resistant5. TB Meningitis6. Genito urinary TB

T.B IN PREGNANCYIn case of T.B in pregnancy we can give all the drugs except “STREPTOMYCIN” because it cross the placental barrier & can Cause

Vestibular Damage VIII cranial nerve lesion Renal failure both Mother & Baby (Fetus) Abortion Still Death

DESCRIPTION OF INDIVIDUAL DRUGSISONIAZID

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Mechanism of Action: - It inhibit Mycotic Acid present in the wall of Mycobacteria, so it is BACTERICIDAL

Indications: Treatment of T.B Prophylaxis of T.B

Side Effects: Hepatotoxicity (Jaundice) Peripheral Neuropathy Hypersensitivity Reaction

Dose:5 mg /kg /dayMax: 300 mg / day before breakfast

RIFAMPICIN

Mechanism of Action: - Inhibits DNA dependent RNA polymeraseIndications:

Treatment of T.B Prophylaxis of T.B

Side Effects: Hepatotoxicity (Jaundice) Skin Rashes Hypersensitivity Reaction Flu Syndrome (fever, Rhino rhea, Cough) Abdominal Pain, Diarrhea Discoloration of Urine Cause Enzyme Induction

Dose:10 mg /kg /day before breakfast

ETHAMBUTOL

Mechanism of Action: - UnclearIndications:

Treatment of T.B Prophylaxis of T.B

Side Effects: Retinobulbar Neuritis (Should not given to Children) Colour Blindness Hepatitis Hypersensitivity Reaction

Dose:15-25 mg /kg /day before breakfast

PYRIZINAMIDESide Effects:

Hyperurecemia

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Gont Hepatitis

Dose:15-30 mg /kg /day before breakfast

STREPTOMYCINDose:

15 mg /kg /day I/M injection

DOT THERAPY (Directly Observed Therapy)This is the observing therapy, which is for checking the patients that he is taken medicine properly or not & see the improvement in the patient’s health after taking medicine and it is done by

1. Close Family Member2. Patient himself come to nearby health facility unit3. Any respectable member of society.

COMPLICATIONS OF T.B

Pulmonary Complications Extra Pulmonary Complication Consolidation T.B Meningitis Bronchiectasis Fluctynular Conjunctivitis Fibrosis Lupus Vulgaris (skin) Collapse T.B Pericarditis Cavitation T.B Lymph Nodes Pleural effusion Pott’s Disease Pneumothorax TB Osteomyelitis Respiratory Failure Infertility

ASTHMADef: Chronic inflammatory reversible process of Airway in which there is episodic attacks of

breathlessness, cough, and wheeze & chest tightness.

Cardiac Asthma Bronchial Asthma 1. Central chest pain radiating to shoulder not radiate to shoulder, neck, arm etc…

Neck & arm etc… 2. No attacks when exposed to dust H/o of attack when exposed to dust, pollen, cold 3. Occurs usually at night & during exertion Usually attacks in Morning & Evening

At daytime. 4. Because of Pulmonary edema Bilateral Wheeze with NVB with prolong expiration

Crepitations.

TYPES OF ASTHMA:1. Extrinsic Asthma (Atopic)

Patient is hypersensitive to exogenous Allergens.

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(Ag - Ab reaction) Type-I Allergy2. Intrinsic Asthma

Hyper responsive Airway to endogenous substance(Viral Fever, Emotions)

3. Chronic AsthmaChronic persistent Asthma, which is episodic for 6 months

4. Occupational Asthma

CLINICAL CLASSIFICATION

1. Mild Asthma Dysponea on activity Patient can complete sentence during attack On auscultation wheeze during end of expiration

2. Moderate Asthma Dysponea on talking Can complete phrase On auscultation wheeze during whole expiration

3. Severe Asthma Dysponea on rest Speak only single word with difficulty On auscultation wheeze during all phase of respiration

Status AsthmaticusSevere Asthma + Tachycardia > 120/ min + pulsus Paradoxus + RR >30 /min +Use of Accessory Muscle +Cyanosed

INVESTIGATION1. Pulmonary Function Test (gold standard)

FEV1 = <80 % this shows Obstructive pattern.

FEV1 / FVC = <70%Now give Beta 2 Agonist inhalation (inhaler, nebulizer)So if FEV1 & FEV1 / FEC ratio becomes normal after giving Beta 2 Agonist so Asthma is Confirmed

Means Reversibility Test is +ve2. Chest X-ray

Usually Normal3. Blood CP

Esinophilia4. Ig E Level

Increased in Atopic Asthma5. Other Lab Investigations

Curshman’s Spirals Present in Sputum OR Exfoliated Pseudostatified Epithelium Charcot Laden Crystals: - These are the protein liberated from esinophils & mast cells

6. If a patient is in Acute Severe Asthma & is Cyanosed then send ABGS.

TREATMENT STEP UP THERAPY: - Previous Concept that start Anti Asthmatic RX with low dose

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STEP DOWN THERAPY: - New concept start RX according to the level of severity.

STEP I: Occasional Use of Broncho dilators (Beta 2 Agonist)STEP II: Regular Inhaled Corticosteroids (15 – 30 mg / day) with Beta 2 AgonistSTEP III: High Dose Inhaled Steroids ( 1 mg /kg of body wt / day)STEP IV: High Dose Inhaled Steroids with Regular BronchodilatorSTEP V: High Dose Inhaled Steroids with Regular Bronchodilator & Oral steroid

TREATMENT OF MILD ASTHMA

Intermittent -------------- Step I Persistent -------------- Step II

TREATMENT OF MODERATE ASTHMA

Step III & Step IV Therapy

TREATMENT OF SEVERE ASTHMA

Step V Therapy

MEDICATIONS1. Short Term Relievers 2. LONG TERM CONTROLLERS

Beta 2 agonist Long Acting Steroids (see Above)Methyl xanthenes derivates Mast Cell Stabilizing Agents

(Cromolyn Sodium, Nedocromil)Ipratropium bromide Leukotrine Inhibitors

(Montelukast, Zafirlukast, Zileuton)Short Acting Steroids Long Acting B2 Agonist

Desensitization

BETA 2 AGONIST i. Albuterol

ii. Procaterol Short Actingiii. Terbuteroliv. Salbutamolv. Salmeterol

vi. Formetrol Long Acting

Mechanism of Action: - These Drugs act on B2 receptors that causes Bronchial dilationSIDE EFFECTS: - Tremors, Tachycardia, Hyperglycemia, Insomnia, Wild goose chase

METHYL XANTHENES DERIVATES i. Theophylline

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Mechanism of Action: - 5’ diestrase Enzymes Inhibitions so therefore CAMP level increased, which cause relaxation of Bronchiole Smooth Muscle.

SIDE EFFECTS: - Hyperkalemia, Cardiac Arrhythmias

IPRATROPIUM BROMIDE It is Anticholinergic drug

SIDE EFFECTS: - Constipation, Anorexia, Urinary Retention, Dry mouth

GLUCO – CORTICOSTEROIDS i. Hydro cortisone

ii. Prednisoloneiii. Dexamethasoneiv. Beclomethasonev. Fludrocortisone

Mechanism of Action: - Anti inflammatory & it inhibits the gene for cycloxgenase pathway.SIDE EFFECTS: - Truncal Obesity, HTN, Paper Money Skin, Lemon on Stick

Abdominal Striae, Brittle Hair, Osteoporosis, Cataract, GlaucomaPseudo tumor cerebri, Hyperglycemia, Secondary Diabetes etc…

COMPLICATIONS Hypoxemia (type I Respiratory Failure) Pulmonary HTN Cor Pulmonale Airway Infection Acute Severe Asthma

Late Cyanosis

Exhaustion of Respiratory Muscle

Respiratory Arrest

Death

BRONCHOGENIC CARCINOMARisk Factors

1. Smoking 2. News paper worker3. Mine Worker4. Pollution5. Uv Rays / Radiotherapy6. Asbestosis7. H/o Head & Neck Tumors8. Fibrosis

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TYPES Central: - Small cell Carcinoma & Squamous

Cell Carcinoma Peripheral: - Adeno Carcinoma, Large Cell

Carcinoma & Broncho alveolar CaC/F

Clinical feature of tumor itself Clinical feature because of Pressure symptoms Clinical feature because of paraneoplastic Syndrome Clinical feature because of Metastasis

Clinical feature of tumor itself Chronic cough, Hemoptysis Purulent sputum Weight loss Anorexia Cachexia (generalized muscle wasting) Dysponea (if pleural effusion) Chest Pain (if Pneumothorax)

Clinical feature because of Pressure symptoms Dysphagia (pressure on esophagus) Hoarseness of voice (compression over recurrent laryngeal nerve) Superior Vena Cava Syndrome (dusky face & prominent Neck Vein) Vagus Nerve Involvement (Tachy arrhythmias) Pan coast Syndrome (if tumor is of Apical part of lung then medial & lateral cord of Brachial

plexus are compressed so Medial part of upper limb with upper lateral part of the limb with shoulder pain)

Horner’s Syndrome (if sympathetic trunk is involved which is present in the carotid sheath so leading to Partial Ptosis, Anhydrosis on the affected side, Miosis enophthalmous)

Ribs Fracture (Rib Osteoporosis)

Paraneoplastic SyndromeDef: - Symptoms complex apart from Cachexia related to certain substance, which are released

from tumor cells.Squamous Cell Carcinoma

1. PTH Gamma Peptide (Hyperparathyroidism) C/f: - Depression, Behavioral Changes, Constipation, Peptic Ulcer, Kidney stone,

Polyuria, Pancreatitis etc…2. Ectopic ACTH released

Cushing Syndrome with Pigmentation3. Lambert Eaton Myasthenic Syndrome

Myasthenia Gravis Lambert Eaton Myasthenic SyndromeI Autoimmune Disease Paraneoplastic SyndromeII As the day passes weakness of Muscle As the Activity is performed Weakness

Progresses reducedIII EMG shows “Decremental Waves” EMG shows “Incremental Waves”

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4. Trousseaus’ Sign Hypercogulability because of formation of clotting factors like substance

Small Cell Carcinoma ACTH (Cushing Syndrome) ADH (Syndrome of inappropriate ADH secretion) Decreased Urination Volume overload Dilutional electrolyte Imbalance

Clinical feature because of Metastasis

SITES Lymph Nodes Brain Adrenal gland Liver Bone

Lymph Nodes: - Large palpable, hard, fixed to skin & underlying structure, Non- mobile, May be Ulcerated, May compress adjacent Viscera etc…

Brain: - Fits---> Seizure-----> Coma -----> Death

Adrenal gland: - Addison’s disease

Liver: - Jaundice, Carcinomatous Cirrhosis, Liver Failure, Hepatic Encephalopathy, Coma, and Death

Bone: - Decreased density if bone, Bone Fracture etc…

INVESTIGATION1. Biopsy (Trans bronchial)

2. Chest X-ray Consolidation Fibrosis Mediasternal widening Trachea shifted Collapse Rib Erosions Bronchogram Pattern

3. Sputum Cytology

4. CT Scan (Chest, Brain, Abdomen) To know the extent of tumor & Metastasis

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5. Other Lab Investigations Blood CP (Polycythemia, Increased ESR >100) LFTS (may be deranged, PT & APTT may be prolonged)

TREATMENT

Small Cell Carcinoma ChemotherapySquamous Cell Carcinoma Radiotherapy followed by ChemotherapyLarge Cell Carcinoma Very Resistant to treatmentAdeno Carcinoma Chemotherapy

STAGING

Stage 0 Ca in situStage I Only Tissue InvolvementStage II Tissue Involved + 1 Lymph Node involve

A (more than 3 tissue involvement & 2 Lymph nodes)Stage III

B (> 3 tissue involvement & 3 Lymph Nodes)

Stage IV Metastasis

RX According to Stage

If Stage I & Stage II ---------- Surgery followed by specific treatment of particular Ca.Stage III A ---------- may be benefited from SurgeryStage III B & Stage IV ---------- Chemotherapy & Radiotherapy & Palliative treatment.

PLEURAL EFFUSIONDef: Abnormal collection of fluid in the pleural cavity is called Pleural effusion.

Normally 15 ml is present in the pleural space.Types of Fluid:

Transudates Exudates s Chylous Hemorrhagic

TRANSUDATIVE CAUSE Liver Cirrhosis Protein losing Enteropathy HypoAlbuminemia Nephrotic Syndrome Malnutrition CCF Constrictive Pericarditis Cardiac Causes Cardiac Temponade Peritoneal Dialysis Myxedema

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EXUDATIVE CAUSES (Inflammation) Para pneumonic Effusion (Empyema) T.B Malignancy Connective tissue disorder Pulmonary Embolism Rickettsia, Chlamydia Infection Meig’s Syndrome (Ovarian Fibroma + Rt Sided Pleural Effusion) Viral Infections Fungal infections Parasitic infections Dressler’s syndrome (shoulder pain, fever, pleuropericardial effusion)

CHYLOUS EFFUSION: (Milky white lymph accumulation) Lymph Node enlargement & compression over lymphatic draining the pleural cavity T.B Malignancy Sarcoidosis Milroy’s disease

HEMORRHAGIC EFFUSION Trauma Tumor Esophageal rupture Acute Pancreatitis

C/F Exertional Dysponea Cough Restlessness Chest pain Wt: loss Wasting May be fever etc…

INVESTIGATIONS1. Clinical Examination

Chest movement reduced Trachea may be shifted Vocal Fremitus decreased Percussion note is Stony Dull Breath Sounds Diminished

2. Chest X-ray Loss of Costopherinic angle (initially) Loss of Lung Field (Massive Effusion)

3. Chest U /s (for loculated effusion)

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4. Diagnostic Thoracentesis Aspirate pleural fluid for the diagnosis of cause of effusion.

LIGHT’S CRITERIA (modified) for Exudates Pleural fluid LDH > 200 units Pleural fluid proteins / serum proteins ratio > 0.5 Pleural fluid LDH / serum LDH ratio >0.6 Serum effusion Albumin gradient <1.2

5. Biopsy (pleural) for Malignancy6. Sputum for AFB / Culture for T.B

Other things which help in Diagnosis

1. Pleural fluid Glucose Reduced Para pneumonic Effusion T.B Malignancy

2. Decreased PH < 7.3 (pleural Fluid) Para pneumonic Effusion T.B Malignancy Acute Pancreatitis Esophageal Rupture

TREATMENTLIGHT’S CRITERIA

Transudative Effusion Exudative Effusion

Give RX of Cause Aspirate (not more then 1 liter) Frusimide ACE inhibitor O2 then Give RX of Cause

If T.B then ATTObserve for 03 days If Pneumonia then Antibiotic

Etc…

If no relief then go for Chest U/sFor Loculated Effusion

If No relief then we inject Streprokinase

If Recurrent Effusion then do Then Aspirate Pleurodesis (Complete Adhesion

of Perital & Visceral Pleura by Tetracycline, Talk)

WHEN DO INTUBATION If frank pus in Pleural Aspirate Pleural Fluid PH < 7.1 – 7.2 If Pleural LDH > 1000 units

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If Pleural Glucose <60 mg/ dl

RESTRICTIVE LUNG DISEASES

Obstructive Lung Disease Restrictive Lung Disease

1. Chronic Bronchitis + Emphysema Asbestosis, Sarcoidosis, Pneumoconiosis, ARDS, Pulmonary HTN etc…

2. Pathology id Airway Obstruction Pathology shows Interestial Hypertrophy & Hyperplasia so Airway dimension is reduced

3. FEV1 Reduced FEV1 Usually Normal

4. FVC usually Normal FVC Reduced

5. FEV1 / FVC ratio Decreased FEV1 / FVC ratio Increased

SARCOIDOSIS

Def: Autoimmune disease involving multisystem & is non-Caseating grnulomatous inflammation and is associated with other autoimmune disease.

i.e. Scleroderma, Sjogram Syndrome, Hashimoto Thyroidosis etc…

C/F Exertional Dysponea May be Cough Fatigability Lethargic

Initially it involves Lung Hillar Lymphadenopathy Montoux Test –ve Pulmonary Nodules Pulmonary Fibrosis

& Then Multi system involvement EYES, BLOOD VESSEL, SKIN etc…

DIAGNOSIS Calcium Increased Kidney Stone Pulmonary Nodule Increased ACE enzyme level in blood Erythema Nodosum on skin (usually at Shin)

TREATMENTImmunosuppresin ( usually we give Corticosteroids)

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PNEUMOCONIOSIS Asbestosis Silicosis Coal Worker Pneumoconiosis Baggasosis Bissinosis

C/F Dysponea ---- Cough ------ Sputum------ Resp: Distress ------ Inc: Chances of Malignancy

Cor Pulmonale

DIAGNOSIS1. First of all take Occupational history2. Chest X-ray

ASBESTOSIS: - Pleural thickening, Pleural Plaque / Calcification, Lung fibrosis SILICOSIS: - Nodules usually in upper lobe, egg shape Calcification Coal worker pneumoconiosis: - fibrosis, may lead to Esophageal carcinoma

CAPLAN SYNDROME:Rheumatoid Arthritis + Pneumoconiosis

TREATMENT O2

No specific treatment

BRONCHIECTASISDef: - Permanent dilation of bronchi & Bronchioles above the level of terminal Bronchioles

Congenital Acquired

Immotile Sillia Syndrome Lung AbscessSevere Pneumonia

Kartegner’s Syndrome T.B(Dextrocardia, infertile sinusitis & Bronchiectasis) Malignancy

Fungal infectionCystic Fibrosis

C/F Cough Copious Sputum Rusty Smelling Recurrent infection of Airway Wheeze & Crackles

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INVESTIGATIONS It is not a disease. It is just a Complication of Disease

Chest X-ray CT Scan Bronchogram

TREATMENT Postural Drainage Steam Inhalation If fever give Antibiotic If Secretion Obstructs Airway then Bronchodilator Symptomatic relief by Expectorants

LUNG ABSCESSDef: - Pus containing cavity is called Abscess.

CAUSES Streptococci Staphylococci Klebsella Pseudomonas H- influenza E- coli Bacteroides

C/F Fever, cough with sputum Sputum of foul smelling Poor Dentition Wt: loss

DIAGNOSIS

Chest X-ray Thicken walled solitary cavity surround by consolidation & an air fluid level is presenting the cavity.

TREATMENT

Medical: - Antibiotics (I/v)

If not response to max: dose of antibiotic then do

U/S guided Drainage OR CT guided Drainage

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SLEEP APNEADef: Cessation of Air flow > 10 sec at least 10- 15 times/ hrs during sleep

Types

Obstructive Central

Usually in very obese ON DINE Curse

Pickwickian Syndrome in this central ventriculatory Even with proper ventilatory drive drive is inadequate

DIAGNOSIS Sleep Study (Polysomnography)

TREATMENT Continuous +ve Airway Pressure Uvulopalatopharyngoplasty (UPPP) Nasal septoplasty

ATELACTESISCollapse of lung

TYPES1. COMPRESSION ATELACTESIS

Pneumothorax Pleural effusion Malignancy

2. RESORPTION ATELACTESIS Foreign body Operational hematoma Tumor Mucous Plug

3. MICRO ATELACTESIS (Absent Surfactant) ARDS Acute Pancreatitis Heavy Smoke

4. BASAL ATELACTESIS Diaphragm move inadequately

C/F Dysponea Fever Tachycardia / palpitation

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SIGNS Trachea deviated Collapse with patent bronchus then vocal Fremitus increased Breath sounds decreased

DIAGNOSIS Chest X-ray

TREATMENTTreat the causeIf mucous plug / hematoma then do BRONCHOSCOPYIf compression Atelactesis then treat the pleural effusion & PneumothoraxIf Micro Atelactesis then give SURFACTANT

PULMONARY HTNDef: Pulmonary Arterial pressure is more than 30 mmHg

TYPES Primary pulmonary HTN Secondary pulmonary HTN

C/F Dysponea Orthopnea Chest pain

SIGNS P2 Loud Systolic ejection click Raised JVP Peripheral Cyanosis Bat Wing X-ray Appearance

INVESTIGATIONS Chest X-ray Echo ECG Pulmonary Function Test

TREATMENTOnce pulmonary HTN develops then HEART LUNG TRANSPLANTATIONOr we can give vasodilator (Ca++ blocker, Nitroglycerine, Hydralizine etc…)

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