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2/117

6 II 666 6F

85? #*;(A'#"

Pyru

vatetranslocase

Malateaspartateshuttle

G3Pshuttle(brain)

Cytosol

Outer membrane

#E>

NADH

NADH

NADH

GTPFADH2

Pyruvate

Vit B1

NADH FADH2

NADH NAD+FADH FAD+

Succinate fumarate

H+

H+

H+

H+

H+

H+

CoQe- e- e- e-

O2

Cyt Ccopper

F1

FoH+

H+

+ regulators: ADP,

NADH, FADH2,

- regulators

RotenoneAmytaldemerol

AntimycinACO, cyanideAzide, H2S

oligomycin

2Semester 1 Mini 3 Fall 2010 TVL


3/117

SMOLANOFF OXIDATIVE PHOSPHORYLATION Mitochondria

Matrix: decarboxylation of pyruvate

TCA cycle FA oxidation

Inner Mitochondrial Membrane: Oxidative

phosphorylation

Outer mitochondrial membrane: permeable

Electron carriers: Flavins, Iron Sulfurcomplexes, Quinones, Cytochrome, Copper

ions

Complex II: Succinate Dehydrogenase pair of e- from FADH2 (enter complex II) = 2 ATP

pair of e- from NADH (enter complex I)= 3 ATP

both transfer e- to coenzyme Q

Diffusable Carriers: Coenzyme Q: isoprenoid molecule (repeating units

of unsaturated Carbon atoms). Q10 is potentantioxidant.

Cytochrome C: heme containing. Transfer e-

between complex III and IV. It cannot bind Oxygen!

Complex IV: Cytochrome Oxidase Can bind oxygen (final e- acceptor) to form water

Reduction potential : Oxygen is strongest

oxidant. NAD + is weakest.

Malate Aspartate Shuttle: active in Liver and

Heart

NADH and NAD+ are impermeable (cannot be

physically transported). So malate is being shuttledin to be reoxidized to oxaloacetate while NAD+

being converted into NADH.

Produce 3 ATP

G3P shuttle: active in brain

Form FADH from FAD. Dihydroxyacetone

phosphate G3P

Difference in cytosolic and mitochondrial G3P DH

enzyme Producing 2 ATP

Inhibitors of OxPhos

Complex I: Rotenone (roots of trees) not readilyabsorbed by human. Amytal and demerol(barbituate)

Complex III:Antimycin A (antibiotic). Strep.Blocks e- flow from cyt bc1.

Complex IV: CO, H2S, Azide, Cyanide ATP Synthase: Oligomycin: binds to protein of Fo

complex. Block flow of H+ and block ATP synthesis

Uncoupler: 2,4 DNP and pentachlorophenol .Transport H+ into mitochondria @ sites other than

Fo channel. Gradient is dissipated and heat is

generated (no ATP)

Endogenous couplers: thermogenin(found in brown fat). Thermogenin =

Uncoupling Protein (UCP)

3

Semester

1Mini3Fall2010TVL


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Dehydrogenasewill produce

3 NADH and

1 FADH2 for ATPin ETC

Glucose

PyruvateLactate Acetyl CoA

+

Oxaloacetate

Ketone bodies Lipid synthesis cholesterol

Pyruvate

translocase

PDHcomplex

citrate

isocitrate

keto gluterate

succinyl-coA

succinate

fumerate

malate

Biotin = B vitamin

+

malatedehydrogenase

commited step

cannot go back

4

Semester

1Mini3Fall2010TVL


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SMOLANOFF - TCA Acetyl coA + oxaloacetate Citrate

Citrate synthase: Highly Exergonic. It can be regulated in

other metabolic pathway (PFK1)

Citrate isocitrate

Aconitase: has an iron center. Deficiency in iron willaffect aconitase. Flouroacetate (rat killer) is a potent

inhibitor of aconitase. It is converted to acetyl coA which

becomes flourocitrate which will inhibit aconitase.

Isocitrate -glutarate

Isocitrate DH: first CO2 released, NADH produced. First

commited step

-glutarate succinyl CoA

-glutarate DH: E3 subunit of this is same as in

PDH complex. Mutation in E3 will affect both PDHs.

NADH produce

Succinyl CoA succinate

Succ coA synthase: thiokinase. Substrate level rxn.

Exergonic. GTP produced. Succ CoA leave pathway forheme synthesis

Succinate fumarate

Succinate DH: FADH2 produced. Succinate is complex II

of ETC.

Fumarate L-malate (fumarase)

L-malate OxaloacetateMalate DH: 3rd molecule of NADH.

Ca2+ signal activates

isocitrate DH

ketoglutarate DH

PDH complex Anaplerotic Reaction: enzyme catalyzed

reaction that can replenish the supply of

intermediates in TCA cycle.

Pyruvate Carboxylase: replenishoxaloacetate to TCA. acetyl CoA

stimulates pyruvate carboxylase. Biotin activate and transfer CO2

also. Avadin (found in raw egg

whites) binds biotin so this will

decrease pyruvate carboxylase

function hypoglycemia

Methylmalonyl CoA mutase:replenish succinyl coA for TCA cyclefrom odd chains Fas.

B12 is coenzyme. Vitamin B12

deficiency will have build up of

(methymalonic acid, odd chain FA

into myelin sheat Pernicious

anemia, and no succinyl coA so noTCA)

Control of TCA

5

Semester

1Mini3Fall2010TVL


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HIGH YIELD

Biotin: B vitamin

inhibited by Avadin (raw egg whites)

Patient has been a lot of raw egg whites

and comes in with these symptoms.

What is the mechanism?Avadin binding with Biotin

Aneupleurotic reaction Citrate : can go to sterol or FA synthesis.

Oxaloacetate: replensih by aspartate.

Alpha keto glutarate: replensihed by glutamate

To make neurotransmitter(GABA and

glutamate) Succinyl CoA (below)

Pyruvate carboxylase

Aconitase: inhibited by flouroacetate (rat

poison) Succinyl coA:

Pyruvate

Dehydrogenase 48:23

odd chain FA Propranyl CoA

Methyl Malonyl CoA

Succinyl coA

Heme

vitamin B12

EFFECTS OF TCA intermediates

6

Semester

1Mini3Fall2010TVL

MOLANOFF


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MOLANOFF - Pyruvate Dehydrogenase Deficiency: cause congenital lactic

acidosis (inability to convert pyruvate to acetyl coA so default,

lactate! Problems with brain . Three forms (severe, moderate, mild).

Severe above: lactic acidosis death

Moderate: motor retardation, damages to cerebral cortex

death

Mild: episodic inability to coordinate voluntary muscles (ataxia)after carb rich meals.

Treatment:

High Fat, Low carb diet

Dichloroacetate (DCA): block kinase subunit of E1 PDH in active form.

Beri Beri:. Neurologic and cardiovascular disorder. Seen inmalnourished individuals. deficiency in thiamine: unable to oxidize

pyruvate. Therefore there will be increased pyruvate or alanine inblood (alanine is interconvertible by transamination)

: Resulting from Thiamine Deficiency.Neuropsychiatric syndrome. Triad of:

Ophthalmoplegia: weakness/paralysis of eye movements

Ataxia: unsteady gait

Sudden onset of confusion

--Sometimes nystagmus: rapid, repetitious, rhythmic

involuntary eye movements.

Korsakoff psychosis: resulting from thiamine deficiency.

Persistent deficits in learning and memory (anterograde and

retrograde amnesia)

Confabulation: making up plausible stories w/o intentions when oneactually cant recall what happened.

Wernicke-korsakoff syndrome(in alcoholics). Too much alcohol + too little thiamine will produce

hemorrhages in mammillary bodies in the brain. Treatment: Must give IV thiamine first before giving IV glucose.

Removes e- from acetyl coA to form NADH andFADH2

Isocitrate DH

Alpha Ketoglutarate DH

Succinate DH

Fumarase

Stages of Cellular Respiration: generating acetyl coA(from pyruvate irreversible), acoA oxidized to yieldNADH, FADH, then lastly, e- transferred to O2 via

respiratory chain.

Pyruvate enter mitochondria via pyruvatetranslocase

PYRUVATE DEHYDROGENASE PATHWAY Product of this reaction: CO2, Acetyl coA, NADH

E1: has two subnits (kinase, phosphatase).Kinase phosphorylate @ serine residue to

inactivate. Phosphatase will activate.

Activation is Ca2+ dependent. THIamine

E2: arsenic

treatments of syphilis and trypanosomiasis. This

inactivate E2.

E3

Allosteric regulation: ATP, NADH, acetyl coA, and

presence of long chain FA inhibit. High ratio of for

example: NADH/NAD ATP/ADP acetylcoA/ coA will

promote phosphorylation (inactivation)

Covalent modification: Mg2+ ATP dependentkinase inactivate E1. Mg2+ and Ca2+ dependentphosphatase activate E1.

7

Semester1Mini3Fall2010TVL

Arsenic inactivates E2


8/117

BELLOT OBS/RES DISEASE

Difficult with deflating the lungs due to narrowing of airways and

reduced elastic recoil of the lungs. (emphysema)

Decreased FEV1. FEV1/FVC = 40%

Emphysema (COPD): irreversible overinflation of air to spacesdistal to terminal bronchioles with destructions of walls bullous formation.

Bullous formation: emphysema eventually will producecyst like space that will bulge out. Lung surfaces will be

destroyed and cyst expansion rupture

Pneumothorax.

Types of Emphysema (characteristic

Panacinar: uniform elargement of acinus Centriacinar: sparing the peripheral alveoli, only central

parts of acinus enlarge

Pathogenesis: imablance between proteases and protease

inhibitors (alpha 1 antitrypsin). Cause by increase proteolytic

enzyme (elastase). Smoking recruits PNLs and macrophagewhich releases proteaase and therefore inactivate alpha-1-antitrypsin.

Death in severe cases Cor-pulmonale (chronic heart failure).Pink puffer

Chronic Bronchitis (COPD): persistent cough with sputum(mucous) for @ least 3 months. Hypertrophy of mucous glands.

Reed Index: measure thickness of mucous layers compare toepithelium layer. In chronic cases, squamous cell metaplasia

Blue Bloater

Bronchial Asthma

Bronchiectasis

Difficult to expand the lungs upon inspiration due to reduced

TLC (chest wall disorder, fibrosis)

Decreased FVC. FEV1/FVC = 80% (greater than

normal)

In common, having diffuse inflammation of alveolar wall.

Pathogenesis: injury to alveolar epithelium (initial) inflammation (early acute) diffuse interstitial fibrosis (late)

Looks like honeycomb lung (similar to emphysema) but

microscopically, you will see thickening of alveolar wallsdue to collagen (Trichome stain)

Diffuse interstital Lung disease due to occupational andenvironemntal causes (exposure to certain inorganic dusts)

Pneumoconioses:

Coal workers pneumoconiosis and absestosis

1. Anthracosis: harmless (towndwellers)

2. Simple CWP (coal worker pneumo): aggregatesforming coal macules but not massive destruction.

Masks protection can prevent.

3. Progressive massive fibrosis CWP: severescarring. Upper respiratory zone affected more

respiratory insufficiency. Silicosis: inhalation of silica dense nodular fibrosis

(macrophage activation release fibrogenic factors).

Histologically: whorls of collagenous fibrous scars.

Abestosis: Fibrous silicates (found in ceiling typesinsulators, roofing). Asbetos induce cytokines release

fibrogenesis increased risk of bronchogenic carcinoma

and pleural mesothelioma . Two form with amphibole

being less common but much more pathogenic. Described

Obstructive

Restrictive

8

Semester1Mini3Fall2010TVLALPHA1 ANTI DEFICIENCY -

EMPHYSEMA PANACINAR

not a lot of sputum

blue

dilation of bronchial treeSepentine, curly, more

common not very pathogenic

stiff straight


9/117

BELLOT OBS/RES DISEASE

Lunglobules

seen inpulmonary

edema

Bullous form rypture= pneumothorax

REED INDEX

Terminal Respiratory Unit = acinus. Part of lungs that

contain terminal bronchiole, respiratory bronchiole, alveolar

duct and sacs.

Lobule is a cluster of 3-5 terminal respiratory units.

Normally, we cannot see lobule on the peripheral

surface. In abnormality (pulmonary edema), stretching

of the lung out we will see these structures

9



10/117

Coal Worker

Pneumoconioses

Silicosis

Asbestos10



11/117

BELLOT VASCULAR LUNG

DISEASECongenital Anomalies

STRUCTURAL : Arrested development of the lungstructures. Structural defect such as hypoplasia (fully

formed bronchus but failure of alveoli to develop reduce in size)

Other anomalies: tracheo-esophageal fistula

(very likely leading to pneumonia) quick death in

infants

CONGENITAL CYSTS: these are mostlybronchogenic and has mucinous secretion. Oftenlead to infection (lung abcess).

BRONCHOPULMONARY SEQUESTRATION: lunglobes/segments without connection to airways. Has its

own vascular supply (from aortic branches)

Extralobar (mediastinal masses): outside main

lung

Intralobar (mass within lung): most of the timemistaken for cancer when discovered @ adult age.

Atelectasis: incomplete expansion of the lungs orcollapse. This will reduce oxygenation and increase

infection. Can shift mediastinum to other side.

RESORPTION: complete bronchial obstruction due to

secretions (asthma, chronic bronchitis), neoplasms.

May shift mediastinum to same side

COMPRESSIVE: caused by fluid (hemothorax) or air in

pleural cavity which will compress. Mediastinum mayshift to other side

PATCHY

Pulmonary Edema: caused by hemodynamicdisturbances

HEMODYNAMIC: increase hydrostatic pressure

Left Heart Failure

Hypoalbuminemia decrease oncotic pressure

MICROVASCULAR INJURY: infection, gases,aspiration, drugs, DIC (diseminated intravascular

coagulation) and ARDS

ARDS: adult respiratory distress syndrome akaDiffuse alveolar damage (DAD). Pulmonaryedema lead to presence of hyaline membranehypoxemia. Mortality is 50%. Fibrosis develop and

T2 pneumocyte proliferation. Causes: severe

infections, O2 toxicity, and gastric aspiration. This is

not related to surfactants!

PULMONARY EMBOLISM; Due tothromboembolus (most arise from deep veins of legs)

Post mortem sticky and shiny

Pre mortem not shiny; adherent to endothelial surface

Saddle of pulmonary artery

Large Emboli: cause sudden death or CHF. Massive chest

pain and die before your eyes.

Small Emboli: may cause pulmonary hemorrhage orinfarction. (Fat, air BM particles, amniotic fluid)

Multiple Emboli will cause pulmonary hypertension corpulmonale. Treatment with fibrinolysis.

In lung, organizations of structures (collagen formation)

will cause permanent damage11



12/117

BELLOT VASCULAR LUNG DISEASE

PULMONARYHYPERTENSION

Mean pulmonary pressure

increase to ! or more of

systemic p (normally 1/8th ).

Caused by COPD, Leftsided HF, and recurrent

pulm embolism. Effects:

Large arteries

atheroslcerosis

Medisum sized/small muscular

arteries intimal fibrosis and

hypertrophy of tissue of

media

PLEURAL EFFUSIONS: Fluidor something that is effused

into pleural space

Exudate: Caused by reaction

to something (infection).

Pneumonia will precipitatea reaction on pleural

pleural infected fluid

accumulate

Transudate: Caused by

hemodynamic (thin, watery)

12



13/117

Structural

(Hydroplasia)

Brocho ulmonar se uestration

ATELECLASIS

13



14/117

EDEMA

Shiny stretched out pleurawith prominent lobular

markings

Caused by:

Left heart failure14



15/117

ADULT RESPIRATORYDISTRESS SYNDROME

PULMONARY HYPERTENSION

Thickening arteriole walls

15



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PULMONARY EMBOLUS

16



17/117

HEART

Surfaces

Anterior or Sternocostal: R.Ventricle Stab wound to middle sternum @ T4/T5

Diaphragmatic: L. Ventricle(some R.vent)

Pulmonary: L. Ventricle

Costodiaphragmatic Recess:

lowest extent of pleural cavity

Insertion of needle for

thoracocentesis

@ midclavicular line: rib 6-8 @ midaxillary line: rib 8-10

@ paravertebral line: rib 10-12

17



18/117

IMPROVEMENTS IN HEALTH CARE CH 5

Reasons for process:

process analysis helps

identify which parts ofthe system are

important to measure

provides a common

picture, a shared model

for an improvement

team

process analysis helps

generate hypotheses

for change

Literacy

18



19/117

CARDIAC INDEX

Cardiac index (CI) relates cardiac performanceto the size of the individual

The normal range of cardiac index is 2.6 - 4.2

L/min per square meter.

If the CI falls below 1.8 L/min, the patient may be

in cardiogenic shock.

Cardiac Index (CI) = Body Surface Area (BSA)

Cardiac Output (CO)

19



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alveo

SHAMS RESPIRATORY EQUATIONS

DeadSpace

Minuteventlation

Alveolar ventilation

Alveolar O2 by using

Respiratory quotient

R = ratio of CO2

production to O2

production

R = rate of CO2production

rate of O2 consump

Partial pressure of O2 @ high altitude

20



21/117

SHAMS RESPIRATORY PHYSIO

Dead space: Anatomical: segments of airway of the first 16

generation. Gas exchange does not take

place. Conducting zone (150mL)

Physiological: some area of alveolar regions

that does not participate in gas exchange.

Gas exchange: From branch generation 17-23.

Tidal volume is 2/3 of 500mL. (-150mL for ds)

Residual Volume: Volume @

end of maximal expiration (after

max expiration, the lung is not

empty and will contain about1.5L of air.

Expiratory Reserve Volume:

Volume @ end of normal

expiration (1.5 + 1.5 = 3L).

Along with this volume + 1.5 of

Residual Volume. So considerthis extra volume along with RV

Tidal Volume: Volume of air we

breath in and out normally (.5L)

Inspiratory Reserve Volume:

Volume we are able to inhale

extra after normal inspiration ifwe give maximal inspiratory

effort (2.5L)

Intro and morphology

Lung Volumes

SpirometercannotmeasureRV!

Lung Capacities

Inspiratory Capacity: IRV + TV

Functional Residual Volume: RV + ERV

Vital Capacity: TV, ERV, IRV largest breath

that can be taken

Total Lung Capacity: All four volumes21


DS (1/3 500ml)


22/117

IC (inspiratory capacity) = IRV + TVFRC (Functional Residual Capacity) = ERV + RVVC (vital capacity) = IRV + ERV + TV

TLC (Total Lung capacity) = IRV + ERV + TV + RV

22

Semester1

Mini3Fall2010TVL


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SHAMS PHYSIO

1. Lung volumes and lung capacities that

cannot be measured with a simple

spirometer include the residual volume, the

functional residual capacity, and the total

lung capacity,. These can be determined by

helium dilution or the body plethysmograph.

2. Alveolar ventilation is the volume of fresh

(nondead space) gas entering therespiratory zone per minute.

3. The anatomic dead space is the volume of

the conducting airways.

4. The physiologic dead space is the volume

of lung that does not eliminate CO2. It is

either greater or equal to anatomic dead

space

5. By a restrictive lung disease all lung

volumes and lung capacities are

proportionally smaller than normal. So ratio

is normal

6. By an obstructive lung disease residual

volume and functional residual capacity are

larger than normal and particularly

FRC/TLC is increased compared to normal.

Lowest Compliance of RS is @ TLC

(high volume) and @RV (low volume)

Highest Compliance of RS is @ FRC(resting volume) where transmural P =

0. Here the RS is recoiling towards

resting volume (FRC)

FRC:

Inspiration- moving away from FRC = active

process

Expiration normal expiration movingtowards FRC = passive

Maximal inspiration is restricted by the

lungs while maximal expiration is

restricted by chest wall.

Key concept lungvolumes

Compliance

23

Semester1

Mini3Fall2010TVL


24/117


25/117

EXERCISE-INDUCED CHANGES IN CARDIAC OUTPUT

A lot of arteriolar resistance at rest resides in skeletal muscle.

the vasodilation occurring there during exercise almost compensates for the elevation incardiac output.

So MAP does not change much during exercise (may increase ~ 15-30 mmHg).

So you want to constrict everything first, then later as you really need it, you can vasodilateonly the area that is need most.

Activity SANS Systemic

vasoconstriction TPR

Massive vasodilation in

exercising muscles (local

control; metabolic theory)

Overall

reduction

in TPR

cardiac output

MAPSANS effect

TPR

Localmechanismwins

25

Semester1

Mini3Fall2010TVL


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MALIK BP COMPETENCIES

Pulsus paradoxus: weakening ofpulse during inspiration. Here there

is more volume coming into the

heart during inspiration

26

Semester1

Mini3Fall2010TVL


27/117

EPIDEMIOLOGY:

Four levels of disease prevention:

Primordial: Avoid social, economic,patterns of living that could elevate

risk of disease.

Ex.Lung cancer: Increasing

taxes, make smoking

unattractive

Primary: Eliminating risk factors,increasing resistance of person to

disease

Ex. Stop/prevent cigaretsmoking, vaccines for kids.

Secondary: target persons who areearly in disease progress to prevent

progression.

Ex. Tb skin test, screening for

breast cancer, pap smear

Tertiary: target person who havedisease, stop/halt progression,

minimize complication, and

rehabilitate

Ex. Follow up w/ patient with

COPD and maintain daily living.

Pandemic: occuring over very wide area. @least two geographical regions (continent)

Ex. Europe and America, not US and

canada

Tuberculosis: Droplet infection (cough,sneeze) vs latent infection (several months,

years)

Screening: secondary prevention. Validitymeasured by:

Sensitivity: able to identify person who have

the disease

Specificity: able to identify person who

DONT

Syndromic surveillance: based on reportingdiff categories of clinical presentations (signs

and symptoms) rather than diagnoses from lab

test.

Ex: Fever and respiratory syndrome (anthrax) vs fever

and diahrea (cholera). Prevention of bioterrorism

Anthrax: 3 forms (cutaneous, inhalation, GI)

Pandemic Influenza: AIDS kill 25mil/25 years.Influenza 25mil/25 weeks!

Failed containment: pandemic containmentwill delay disease transmission and peak.

27

Semester1

Mini3Fall2010TVL


28/117

VALIDITY CALCULATIONS

Reference (Gold Standard)Test

Positive Negative

ScreeningTest

Positive a b

Negative c d

#)*/ S&,%?%B/, U #)*/ =/(0?%B/, U0 2V0',/ S&,%?%B/, U . V0',/ =/(0?%B/, U 6

P/4,%?%B%?9 U S)&+&)?%&4 &3 ?)*/ S&,%?%B/, 6&))/6?'9 %2/4?%3%/2U 0R-0W67

P+/6%3%6%?9 U S)&+&)?%&4 &3 ?)*/ 4/(0?%B/, 6&))/6?'9 %2/4?%3%/2 U 2R-.W27

S&,%?%B/ S)/2%6?%B/ X0'*/ U 0R-0W.7 =/(0?%B/ S)/2%6?%B/ X0'*/ U 2R-6W2728

Semester1

Mini3Fall2010TVL

DEVELOPMENT OF RESPIRATORY SYSTEM YIN


29/117

DEVELOPMENT OF RESPIRATORY SYSTEM-YIN

Week 4, respiratory diverticulum (lung bud) appearas outgrowth of foregut (cranial segment of primitive

gut tube)

Epithelium of internal lining of larynx, trach, bronch, lungs =

endoderm. Endoderm also line phar arches.

Cartilaginous, muscular, CT components = splanchnicmesoderm

Very cranial part of gut tube = pharynx (phar pouches)

Esoph atresia w or w/o tracheoesoph fistulas Abnormal partitioning of esoph and trachea by

tracheoesoph septum infant cannot swallow

amniotic fluid (polyhydromnios = too much amniotic fluidin cavity)

vomitting.

VACTERL association: vertebral and renalanomalies, anal and esoph atresia, cardiac and limbdefects, tracheoesoph fistula.

LARYNX Epithelium (endoderm) but cart/muscle from

mesenchyme of 4th and 6th pharyngeal arches

Sup laryngeal nerve innervate 4th archderivatives (thyroid)

Recurrent laryngeal nerve innervate 6th archderivatives (cricoid)

TRACHEA, BRONCHI, LUNG

Lung buds trachea + 2 lateral

bronchial buds.

Splanchnic mesoderm parietal pleura

Somatic mesoderm visceral pleura Diaphragm begin @ Septum

transversum.

Initially, lung will grow into pericardio-

peritoneal canal. Then pleural pericardial

folds appear grow from sides towards

midline fuse then separation of

thoracic and peritoneal cavity. Epithelial-mesenchymal interactions

regulate branching bt endoderm of lung

bud and splanchnic mesoderm

Congenital Diaphragmatic Hernia:pleuroperiotneal folds fail to form properly (on

left), foramen of Bochdalek develops in

posterolateral region of diaphragm smallbowel loops present in thoracic cavity

hinders lungs formation (pulmonaryhypoplasia). Degree of pul hypoplasiadetermines survival.

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DEVELOP OF RESP SYSTEM - YIN

Maturation of lungs

Pseudoglandular period (w 5-16):

branching form terminal bronchiole, norespiratory bron yet! No survival

Canalicular period (w 16-26): Terminal

bronch respiratory bronch alveolar

ducts but no connection to blood yet. No

respiration!

Terminal sac period (w 26 to birth):Cuboidal resp epi thin, flat. Now

associated w/ blood. Primitive alveoli

forms (terminal sacs). Respiration.

@28th week, T2 pneumocytes appear

surfactant

Alveolar period (8th

m to childhood):Terminal sac (alveoli) increase. T1

pneumocytes become thinner. Growth of

lung after birth is due to increase in # of

resp bronchioles and alveoli. 1/6th alveoli

formed @ birth. The rest during 1st 10

years of life.

Fetal Breathing movements: before birth

cause aspiration of amniotic fluid.

Important for stimulating lungdevelopment and conditioning respiratory

muscles. Without surfactants =

atelecstasis.

Respiratory distress syndrome (RDS): aka

hyaline membrane disease due to

insufficient surfactant (only hyaline

membranes and laminar bodies remain)

alveoli collapse during expiration.

Common cause of death of premature

infant. Treatment: glucocorticoids to

stimulate production of surfactant

Ectopic lung lobes: arise from trachea or

esophagus

Congenital cysts of lung: formed by dilation

of terminal or larger bronchi

honeycomb appearance on radiograph.

Poor drainage and chronic infections!30

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C C I


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CARDIOPATHIES AND CARDIAC ION

CHANNELOPATHIES - SANDS

Hypertrophic: common 1/500.Hypertrophy in ansence of an increased

external load. Impaired diastolic

function. Septum involvement. Diseaseof the Sarcomere. Genes involve: Beta myosin Heavy chain

Cardiac Troponin T

Cardiac Myosin binding protein

These gene will make sarcomere more

sensitive to Ca2+ overworking

hypertrophy

Dilated: LV enlargement and systolic

dysfunction. Mutation of gene will makeyou less sensitive to Ca2+ less ATP

weaker muscle dilated Disease ofcardiac cytoskeleton

Glycogen: Result from defects in genes ofmetabolism associated with lysosome

glycogen deposition will disrupt function

Pompe: inherited lysosomal acid -1,4-glucosidase deficiency. Recessive

Danon: lysosome associated membraneprotein (LAMP2). X linked

Fabry: lysosome hydrolase Galactosidase A(GLA) deficiency

PRKAG2: encodes subunit of AMP-activatedprotein kinase (AMPK)

Restrictive: normal or decreased volume ofboth ventricles. Bi atrial enlargement.

Mutations in cardiac Troponin I

Arrhythmogenic RV: Right ventricle lossof myocytes with fatty or fibrofatty tissue

replacement. Disease of desmosomes(plakoglobin, desmoplakin, plakophilin,

desmogelin, desmocollin)

CARDIOPATHIES

Types of cardiopathies

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SANDS - CHANNELOPATHIES

Cardiac Action potential: mediated by ion channels. Maintenance of normal rhythm is dependent

upon movments of ions

Channelopathy: due to mutations in genes coding for specific ion channels Long QT syndrome: repolarization disorder increase risk of ventricular tachyarrhythmias

(in child hood: torsades de pointes).

Mutation in K channel subunits prolong AP repolarization

Mutation in SCN5A (Na channel) increase inward Na+ current

Short QT syndrome: high rate of sudden death. SQTS repolarization is hastened by gain of function

Brugada syndrome: ST elevation in R. Precordial lead. Risk of sudden cardiac death.Effects on Na curent are opposite in LQTS.

Cardiac Conduction Disease/Sinus Node dysfunction: Loss of function mutation incardiac Na channel complex (SCN5A and SCN5B) cardiac conduction disease.

Mutation in SCN5A: loss of Na channelAR form of sick sinus syndrome

Mutation in HCN4: which encodes cardiac pacemaker channel cause AD sinus nodedysfunction

Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT and PVT triggered by adrenergic stimuli.

Autosomal dominant: Mutation in ryanodine receptor channel

Autosomal Recessive: Mutation in CASQ2 : encodes calsequestrin.

Cardiac disease due to loss of Calcium regulation 32

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BERGERON PULMONARY DEFENSE MECHANISM


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BERGERON PULMONARY DEFENSE MECHANISM Normal microbiota interfere with pathogens by competing for space, for nutrients, and also

produce antibacterial substances (lactic acid, H2O2, bacteriocins)

Cell mediated immunity: use to kill infectious particle inside cell

Humoral Immunity: Antibody produced to kill outside infectious particle. ring: lymphoid tissue around entrance of airway. Formed by tonsils and adenoids

Secreted Immunoglobulins:

IgG: abundant in blood and plasma

IgA: most abundant because it is found in mucosal.

J chain in polymeric Ab (IgM and IgA) is a tag used by epithelial cells to grab Ab frominside(basolateral side) to be trancytosed to outside

Secreted IgA: neutralize toxins and interfere with pathogen adhesion. Immunodeficiency inIgA can be replaced by IgM (also secretory)

Macrophages: resident in lamina propria. Phagocytotic. APC(alveolar macrophage also)

Secrete IL-10: avoid inflammation

Secrete IL-8: recruit neutrophil.

Macrophage killing mechanism: Phagocytosis, Reactive O2 species (ROS), antimicrobialCationic peptides/proteins.

Neutrophils: recruited when pathogen is too large/virulent.

Neutrophil Killing mechanism: Opsonin-enhanced phagocytosis, ROS, AC P/P

Intraepithelial T-lymphocytes: already activated CD8 T cells. Destroy infected epi cell rightaway.

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PHARMACOLOGY AZIM ANGINA


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PHARMACOLOGY -AZIM

Goal: less than 140/90 and 130/80 (diabetic)

Receptors:

PARASYM - M1: nerve -M2: heart (atria) -M3: in periphery -

M4, M5: brain

SYMPA - Beta 1: renal

Management: lifestyle modification 1st then drugs!

Thiazide diuretics: Hydrochlorothiazide. Inhibit Na reabsorptionin distal tubules water loss (K+ and H+ also). AE: Hypokalemia

ACE inhibitor: Captopril. Inhibit ACEnzyme (no Angiotensin II, nobradykinin break down vasodilation) AE: Hyperkalemia!

Angiotensin II Receptor blocker (ARBS): Valsartan. Block AngioII receptor type I. NO vasoconstriction, no aldosterone release.

Does not cause dry cough (not involved with bradykinin)

Beta Blocker: Propanalol. Beta Adrenergic receptor blocker.

Ca2+ channel blocker: Nifedipine. Inhibit Ca entry from L-typechannel (smooth muscle and myocardium). Cause orthostatic

hypotension (dilate vein), hypersensitivities, unstable angina.

Form of Ischemia

Chronic stable: most common. Exercise or Chronic

narrowowing of c.arteries due to atherosclerosis.

Alleviated by rest

Unstable: dangerous, transient formation and dissolution

of blood clot because no NO or prostacyclin produced.

Vasospastic (Variant): from coronary spasm.

Temporarily reduce blood flow. Caused by emotional

stress (increase sympa)

Organic nitrates Nitroglycerin (glyceryl trinitrate),Isosorbide dinitrate

Nitroglycerine: Converted to NOincrease cGMP

inactivate MLCK smooth muscle relaxation.

Lower dose: decrease preload. Higher load:

decrease afterload. Adverse effect: headache.

Calcium channel blockers Nifedipine, Diltiazem,Verapamil

Beta blockers Propranolol, Timolol

HYPERTENSION

ANGINA

Myocardial Infarction

Levine Sign: sign of Myocardial infarction (caused byischemia)

STEMI ST elevation MI

First thing: full dose of aspirin or alteplase or tissue

plasminogen activator ask pt to take deep breath give thrombolytic agent catherization

Anti-arrythmic drugs

Class 1: Na channel blockers. Qunidine,Procalnamide, Lidocaine Class 2: Beta-blockers act on phase 4 and phase 0.Class 3: K channel blockersAll these act to increase refractory period

Heart Failure: reduce pumping efficiencyof heart

Drugs: similar drugs for hypertension + cardiacglycosides and aldosterone antagonist.

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AZIM - TUTOR

Nifedipine: Ca2+ channel blocker.Acute hypertensive situationDO NOT GIVE.

Vasodilation block Ca2+ in smooth

muscle orthostatic hypotension.

Short half life. 2 hours, so give

enough drugs Drug approve to treat ecclempsia and

not any other acute hypertensive.

Thiazide Diuretics: give 1st thing totreat hypertension

CaptoprilACE inhibitor. Low BP, kidney will secrete

renin. B1 receptor.

ACE is found in lungs.

ACE inhibitor also block

bradykinin breakdown.

Valsartan: block receptor for

Angiotensin II. Beta blockers: Propanalol

Dont withdraw quickly. If

you block beta receptors,

heart will make more

overexpress. If you w/d

quickly, tons of beta

receptors, HR will go up

heart attack!

Also its not specific, so it

acts on all Betas (B1 and

B2) pulmonary spasm Nitroglycerin: for chronic

stable heart failure.

HIGH YIELDS

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MOORE CIRCULATORY

SYSTEM

Veins

Have smooth muscles

that run longitudinallyin adventitia. When

constrict, help moveblood up.

Artery

Muscular artery:

characterized by

internal elastic lamina.

Capillary: has pericytes to act the role of sm muscle.

Sinusoidal

Liver, BM, spleen hematopoeitic

organ

Irregular blood pools/channel which conform toshape of structure which they are located

Incomplete basement membrane, discontinuous.

Interchange of material is faciliated by cap wall

structure

No Diaphragms

Fenestrated

Kidney, intestine, endocrine glands

tissue with rapid interchange of

substance occurs

Ultrathin diaphragm (ex in renal glommerulus)

Continuous (somatic)

Muscle, CT, exocrine, nervous tissue

Absence of fenstrae. Tight Junction (leaker due

do less sealing strands)

Allow for diapedesis of leukocytes.

Numerous pinocytotic vesicles

Lymph Has anchoring fibers which help attach to nearby

tissue (prevent collapse of lumen)

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MOORE RESPIRATORY SYSTEM Nasal Cavity


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MOORE- RESPIRATORY SYSTEM Conduction Portion consist of everything until Respiratory

bronchioles (here is respiratory portion)

Conducts Air

Conditions Air: vibrissae (small hairs) to remove matter

Produce speech when air passed through larynx

Carries stimuli for sense of smell (olfactory mucosae)

Respiratory Portion: Res bronchiole, alv ducts & sacs,alveoli. Function in gas exchange (respiration)

: Immotile Cilia Syndrome

Lack of dynein in cilia cilia fail to function. Flagella

also nonfunctional. Male sterility

Cilia cannot clear airways of mucus mucus collects

bacteria growth and infection

Odorant: chemical compound that has a smell/odor (must be

volatile and in high concentration) to interact with olfactory

receptors. Organic + inorganic compounds. A single odorant

molecule may bind to number of olfactory receptors. Wide

range of diff odor receptors (only 400 functional. Like

immune system, olf receptor is able to detect/distinguish bt

infinite # of odorant molecules. Receptor will activates olfactory type G protein on inside of neuron (7

transmembrane domain) act on ion channels. Glomeruli = synapse of

axons of olfactory neurons and dendrites of mitral cells. Glomerulus

receives input of 2000 olf neurons. Humans (5mil receptors) Dog (250

mil)!

Gland: beneath olfactory epithelium. These areserous secreting glands. A solvent dissolve odoroussubstance

y Vestibule: stratified squamous epi. Contains

vibrissae (hair that trap particulates). Contains

sebaceous and sweat glands. Nasal conchae(turbinates) to swirl air as it passes throughwarm, moisten, and cleaned

Respiratory Portion: posteriorly is lined byrespiratory epi (characteristic epi ofrespiratory system!) This is ciliated pseudostrat

columnar epi with goblet cells (secrete mucus).

Mucus sweep up debris and beat in one

direction.

Olfactory Epithelium: responsible for smell.Pseudostratified columnar epi. Superior aspect

of nasal septum/concha. Smell (sensual

pleasure, warnings of danger, identify food,

mates, and predators).

Respiratory Epithelium cell types:

Ciliated columnar: most abundant. Hasnumerous mitochondria (ATP!)

Mucous goblet cells: Secrete mucous Brush cell: Columnar. Contains microvili on

apical surface. Sensory receptors (has afferent

nerve endings on basal surfaces)

Basal cells (stem cells): differentiation capacity

Small granule cells (enteroendocrine):secrete bombesin/serotonin to regulate airway

smooth muscle tone, blood flow and secretion.

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MOORE RESPIRATORY SYSTEM Olfactory Epi cell types:

Olfactory receptor cells : neurons havemodified immotile cilia on surfaces containing

odorant receptor proteins and single axon. These

are bipolar neurons (centrally located nucleus with2 cytoplasmic processes dendritic, proximal).

Dendritic side has immotile cilia on its surface.These cells are the only neurons in the nervoussystem exposed directly to external environment.

Supporting cells (sustenacular): support andhold the neurons in place. These provide physical

and metabolic support to olfactory cells.

Cytoplasmic has accumulations of yellow-brown

pigments

Basal cells: generates/replace apoptosedolfactory neurons (last only 1 month) andsustenacular cells

Pathway of entry to brain for certain micro-

brain eatingamoeba throughcribiform plate of ethmoid bone (holes).

Direct connection to brain.

Metaplasia: reversible replacement of onedifferentiated cell type with another mature

diff cell type. Tissue can return to normal if

stimulus is removed. Metaplasia is not

directly carcinogenic.

Dysplasia: abnormality of development.Expansion of immature cells and decrease #

of mature cells. Indicative of early neoplastic

rocess.

PHARYNX: @ nasal cavity, end @ larynx. Threeportion (naso, oro, laryngeal)

Nasal :respiratory epi

Oral and laryngeal: Stratified squamous Epi (toughest epi, towithstand friction)

EPIGLOTTIS: has core of elastic cartilage During respiration: vertical position for flow of air

During swallowing: horizontal, closing laryngeal

LARYNX: voice box (phonation and preventing entryof food into respiratory system). Walls has hyalinecartilage (cricoid and thyroid) and elastic cartilage(epiglottis). Larynx has 2 folds (false vocal cords) and

(true vocal cords) separated by laryngeal ventricle.The bigger the vocal folds (longer, relaxed) the deeper

the pitch of sound (male)

True Vocal cords has: Strat squamous epi, vocal ligament,vocal muscle

False vocal folds has: respiratory epi, lamina propria. This isthe superior portion.

TRACHEA: from larynx to bifurcation. Lined by

respiratory epi. Has C shaped rings of hyalinecartilage connected by smooth muscle. C end face

esophagus. Three layers:

Mucosa: pseudostrat ciliated columnar epi. Thick basallamina. Lamina propria rich in elastic fibers and lymphocytes.

Submucosa: Denser CT. Seromucous glands.

Adventitia: has fibroelastic CT. Most prominant feature=

hyaline cartilage C rings and intervening fibrous CT.

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MOORE RESPIRATORY SYSTEM


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MOORE RESPIRATORY SYSTEM BRONCHI: Extrapulmonary bronchI are similar to trachea

(Cshaped rings). Intrapulmonary bronchi: irregular plates ofhyaline cartilage. This is the point where bronchi enter lungs.

Smooth muscle is present. (parasym causes contraction,

sympa cause relaxation)

BRONCHIOLES: distal airway. Site where ciliated epi ceased.(terminal and respiratory) No cartilaginous support. Pseudostrat colum pseudostrat

cuboidal. Thick layer of smooth muscle.

Has Clara cells: dome shape, short microvilli. As bronchiole

size decreases, clara cells increase.

Functions of Clara Cells:

Protect bronchiolar epi by secreting secretory protein(CCSP), a component of lung surfactant. Also

glycosaminoglycans to prevent adhesion to pollutants.These decrease inflam response

To detoxify harmful substance: lots of cytochrome P450. (lotsof smooth ER)

Divide/differentiate to form both ciliated and non ciliated epi.But ciliated cells in respiratory epi is from basal cells not clara!

Asthma: spasmic dyspnea with wheezing due to prolongedcontraction of smooth muscle of bronchioles. Treatment (steroids

and B2 agonists) will relax smooth muscle.

Dyspnea: SOB, difficulty/distress in breathing.

Emphysema: COPD enlargement of air space, destruction ofinteralveolar wall. Smoking is main culprit stimulatedestruction/synthesis of elastic fibers and components of septum.Leads to fewer, larger alveoli. Difficulty in exhaling.

RespiratoryDistress Syndrome: in newborn immatureinfants (before7 months) who produce insufficient surfactant. Treat

with synthetic surfactant or glucocorticoid (stimulate T2pneumocytes).

RESPIRATORY BRONCHIOLES: Transition zone. Involve in both conduction and gas

exchange.

Key distinguish: any breaks in the wall.

To distinguish between duct and sac: duct contains

knobs of smooth muscle. Walls of ducts btoppening of sac is supported by elastic, collagen,

smooth muscle fibers. Alveolar sac occur at

termination of alveolar duct.

ALVEOLI: a wall between twoo alveoli(interalveolar wall). This is site of gas exchange.Has CT, elastic fibers and capillaries.

T1 pneumocyte is for gas exchange. Simple squamous.Line the majority of alveolar surfaces 95%. Joined by tightjunction

T2 pneumocyte: secrete surfactant from lamellar bodies.Larger, more spread out. Divide give rise to T1. Simple

cuboidal.

Blood Air Barrier: layers/components Alveolar epi cell (T1 cells process)

Basal lamina of T1 Basal lamina of cap endothelium

Endothelial cells of capillary

Alveolar Macrophage: dust cell In air space + interalveolar septum to scavenger for

particulates.

Alveolar Pores: Pores of Kohn found w/iinteralveolar septum. This will equalize pressure w/i

alveoli

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CARDIAC VS SMOOTH MUSCLE

Cardiac

Sarcomere (same crossbridges as skeletal muscle)

T-tubules : Diads @ Z-line

Requires external Ca2+

Ca2+ go through DHAPchannel bind to RyRReceptor Sr release Ca2+

Getting rid of Ca2+ SERCA (same as skeletal)

ATP dependent. PumpCa2+ back to SR

PMCA Ca2+ ATPase. Pump out of

cell

Ca2+/3Na+ exchanger

Pump out of cell

Smooth Muscle

No sarcomere (littletropomyosin)

No T-Tubules

Reduced SR

Ca2+ from channels of SRand calveolae For contractions

For RyR open SR

Ca2+ bind calmodulin complex activate MLCK

phosphorylates myosinhead

MLC-phosphatase removephosphate group stopcontraction

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HEART BLOCK

Normal QRS

Lengthened P-R interval

Mobitz Type 1

Dropped QRS

Lengthened P-R interval witheach beat.

Mobitz Type 2

Unpredictable loss of AV

conduction

2:1 block ( 2 P-R interval to 1

QRS)

1st degree (incomplete)

2nd degree Heart Block

3rd degree Heart Block

No AV node conduction (purkinje

take over)

Biphasic P wave2 peak QRS

Inverted T wave

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CARDIAC FORMULAS

SeriesRTOT = R1 + R2 + R3 + R4

ParallelRTOT = 1/(1/R1 + 1/R2 + 1/R3 + 1/R4)

Pulse pressure = Psys - Pdias

dias + 1/3 (Pulse Pressure)

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SHEAKLEY- CARDIAC TENSION CURVE

Which two points aremaking the totaltension @ point X?

Point A Point D

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CARDIAC

Beta Receptors

Increase cAMP

activate pKA

Increase HR

Increase contractility

Beta Blockers

Decrease HR

Decrease contractility

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SVC= 3rd costal cartilage

IVC = 5th costal cartilage

Papillary muscles

1. anterior

2. posterior3. septal

Moderator Band = septomarginal trabeculae

Coronary sinus = Thebesian vein

Stab wound in front of chest would beRight Ventricle

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Where to Listen for Valve


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Where to Listen for ValveSound

Pulmonary Valve: (1)

-Over the medial end of the left 2nd

intercostal space

Aortic Valve: (2)-Over the medial end of the right2nd intercostal space

Tricuspid Valve: (3) -Just to the left of the lower part ofthe sternum near the 5th intercostalspace

Mitral Valve: (4)-Over the apex of the heart in theleft 5th intercostal space at themidclavicular line

12

3 4

aortic pulmon

These are the sounds,

not the actual projection

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HEART DOMINANCE CRITERIA -- WHICH EVER ONE SUPPLIES THE

POSTERIOR INTERVENTRICULAR BRANCH

RCA branches Right Marginal

SA nodal

AV nodal

Posterior Interventricularbranch

RCA supplies RA

RV (most)

Diaphragmatic surface ofLV

Posterior 1/3 of AVseptum 60% SA node

80% AV node

LCA branches Circumflex branch form

marginal branch

Anterior interventricularaka Left anteriordescending (LAD) form diagonal branch

LCA supplies LA

LV (most)

Apex

Anterior 2/3 AV septum 40% SA node

20% AV node

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THORACIC UDDIN

T2 Jugular notch T4, T5 Sternal Angle

T10 Xiphoid

STERNAL ANGLE At rib #2

T4-T5

Bifurcation of trachea (carina)

Aortic arch Ascending branch end

Descending begins

Division between superior andinferior mediastinum

Arch of azygous vein

Crossing over of thoracic duct

L. Vagus N. give rise to L.Recurrent Laryngeal N.

Junction of upper 1/3 (skeletal m)

lower 1/3 (smooth m) ofesophagus

Ligamentum arteriosum(ductus arteriosus in neonate =shunt) 50

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THORACIC - LEVELS

Types of Ribs

True Ribs (1-7)

False Ribs (8-10)

attached through costal

cartilage Floating ribs (11-12)

T8

IVC

Phrenic nerve

T 10

Esophagus

Vagus nerve T 12

A aorta

A azygous vein

T Thoracic duct

OPENINGS OF DIAPHRAGM

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SIBSONS FASCIA

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-


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INTERCOSTAL MUSCLES

THORACOCENTESIS

Layers punctured: Skin

superficial fascia

deep fascia

external intercostalmuscle

internal intercostal muscle

innermost intercostalmuscle

endothoracic fascia

parietal pleura

pleural cavity

PARASTERNAL NERVE BLOCKT5-T6 Skin

Superficial fascia

Deep fascia

External intercostal membrane

Internal intercostal muscle

Innermost intercostal membrane

Endothoracic fascia Parietal pleura

Posterior

anterior

external

Internal

Innermost

Dash = tendon

Solid = muscle

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MUSCLES OF RESPIRATION

INSPIRATION:

diaphragm

Serratus Posterior Superior

External Intercostals

Levator Costorum

FORCED INSPIRATION

External Intercostals

Scalene

Sternocleidomastoid

EXPIRATION Passive

FORCED EXPIRATION:

Internal Intercostals

Abdominal

Serratus Posterior Inferior

Internal

inferior 54

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Right Lung


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LUNGS

3 lobes

Superior (@ 2nd rib)

Middle (@ 4th rib)

Inferior (@ 6th

rib) 2 Fissures

Horizontal

Obligue (@ 5th rib)

Has 10 tertiary bronchii

Left Lung

2 lobes

Superior

Inferior

1 fissure

Features

Cardiac Notch

Fissure

Has 8 tertiary bronchii

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BRONCHIOPULMONARY SEGMENTS

Right Lung (10) Superior Lobe

A pical

P osterior

A anterior

Middle Lobe L ateral

M edial

Inferior Lobe P osterior

A anterior

L ateral

M edial S uperior

Left Lung (8) Superior Lobe

A piocposterior (apical + Posterior)

S uperior lingular

I nferior lingular

A nterior lingular

Inferior Lobe Anteromedial basal (anterior + medial)

Lateral basal

Posterior basal

Superior

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THORAX

Thoracocenthesis

Purpose: to remove fluid pus or blood


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THORAX Knife wound to chest wall above

clavicle may damage:

Subclavian artery

Lower trunk of brachial plexus

(ulnar, median)

Cervical pleura

Apex of lung pneumothorax

Projection of diaphragm on chest

wall

Right dome arch superiorly to

upper border of 5th rib

(midclavicular line)

Left dome arch superiorly to

lower border of rib @midclavicular line

Thoracic Outlet syndrome

Anomalous cervical rib compress

Lower trunk of brachial plexus

Subclavian artery

Purpose: to remove fluid pus or blood

from thoracic cavity

Need is inserted in upright position,

superior to rib, 9th intercostal space,midaxillary line.

Pericardiocenthesis

Point of insertion: 5th and 6thintercostal space near sternum

(infrasternal angle)

(bare area) = pleural notch area.=area of cardiac dullness

Careful not to puncture internal thoracic

artery and branches

Intercostal nerve block

To alleveiate pain associated with ribfracture or Herpes zoster.

Needle inserted @ posterior angle of

rib, lower border of rib to bathe nerve in

anesthetic

Must block several intercostal nerve @

one time.

Pleurodesis : a surgical procedure to fuseparietal and visceral pleura together (2nd

atelectasis) with an irritating agent. This is

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Can Lovers Live In

Village Cottages:

C - Type 1

(chylomicrons)

L - Type IIa (LDL)

L - Type IIb (LDL and

VLDL)

I - Type III (IDL and

VLDL)

V - Type IV (VLDL)

C - Type V

(Chylomicrons and

VLDL)

Type IIb through V all

have increased VLDL

Hope that helps!

)&**0 ) *& &


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!"#$%#$& "'(%)*+&$*#,(

+-./01 +.13 456 7 8.45139:

,;;9. &.413


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SUPERIOR MEDIASTINUM Angle of Louie (T4/T5) =

separation of superior and inferior

mediastinum

Superior Mediastinum boundary Superior Boundary

Thoracic inlet

Anterior boundarymanubrium

Posterior boundary

Thoracic vertebrae T1-T4 Inferior boundary imaginary

line (T4/T5)

Superior Vena Cava Syndrome: tumors,cysts, or enlarged structures compressing

the SVC.

Symptoms: Facial and arm edema.

Large Neck veins and dyspnea.

Important collateral circulation:

AZYGOUS VEINS, internal thoracic,lateral thoracic, and esophageal.

Aneurysm of Ascending Aorta: walls ofaorta are subjected to strong thrust of

blood. Aneurysm may develop.

Symptoms: chest pain and alsoradiation to back. Difficulty

swallowing (trachea and esop

compressed) and breathing.

Coarctation of Aorta: abnormalnarrowing of arch of aorta (post or pre

ductal). Post ductal coarctation has good

collateral circulation through

intercostal and internal thoracicarteries. 61

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POSTERIOR MEDIASTINUM - UDDIN


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POSTERIOR MEDIASTINUM UDDIN The 3 BIRDS in Posterior

Mediastinum

Systems of Vein

Hemiazygous vein crosses to

join azygous @ T9

Accessory Hemiazygous crosses

to join azygous @ T7 or T8

Thoracic Duct

Drains Left side of body, head,

neck, and lower limbs

Originate from cisterna chyli

@ T4 (T5) sternal angle, itdeviates to the LEFT.

CHYLOTHORAX lymph inthoracic cavity caused by

laceration of thoracic duct

(vulnerable during surgery)

because it is thin walled and

colorless

Sympathetic Trunk (THORACIC): supply

viscera inferior to diaphragm

Greater from T5-T9 celiac ganglion

Lesser From T10-T11 aorticorenalganglion

Least From T12 prevertebral

ganglion

Esophageal plexus: @ esophagus

Left Vagus Nerve form anterior plexus

Right Vagus Nerve form posterior plexus.

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Clinical Relevance:


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Mediastinal Mass Lesions:

Thymoma:(1) Neoplasm of thymus-Invasive thymoma is frequently associated

with symptoms due to local compression

such as super vena cava syndrome

Lymphoma:(2) Neoplasm of lymphoid

tissue

Germ Cell Tumors:(3) -Some germ cells which fail to complete the

migration give rise to anterior mediastinal

tumors

Neurilemoma:(4) -Neurofibroma -

Ganglioneuroma -

Schwann Cell Tumors

Mediastinal cysts (5) pericardial cysts,bronchogenic cysts, enteric cysts, thymic

cysts & thoracic duct cysts------ all of these

lesions can produce compressivesymptoms

(1)

(2)

(2)(3)

(4)

(5)

(5)

(5)

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Phases:


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(1) Passive ventricular

filling

(2) Active ventricular

filling(3) Atrial contraction

phase

(4) Isovolumetric

contraction

(5) 1st phase of ejection

(rapid ejection)

(6) Reduced ventricular

ejection

(7) Isovolumetric

relaxation

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CARDIAC MECHANICS The Fast response (non-pacemaker) action potential is

seen incontractile muscle cells

(atrial and ventricular) and iscommonly divided into five phases. The start of the actionpotential looks like the start of an action potential in a nerveor skeletal muscle cell. However, shortly after the membranebegins to repolarize, there is a long plateau phase whichdiffers from that of nervous tissue or skeletal muscle.

Phase 0 (depolarization) - produced by the opening offast voltage-dependant Na+ channels (Na+ influx).

Phase 1 (early repolarization) - produced by theclosure of fast voltage-dependant Na+ channels and the

opening of voltage-dependant K+ channels (efflux ofK+).

Phase 2 (plateau) - produced by the opening ofvoltage-dependant slow L-type Ca++ channels (influx ofCa++); the downward slope during this phase isproduced by opening of slow delayed rectifier K+

channels.

Phase 3 (rapid repolarization) - produced by theclosure of L-type Ca2+ channels and the opening of

several K+ channels (efflux of K+); slow delayedrectifier, rapid delayed rectifier, and inward rectifier.

Phase 4 (resting membrane potential) bothdelayed K+ rectifier channels close, but the inward K+

rectifier channels (efflux of K+) remain open andmaintain the resting membrane potential.

The Slow response (pacemaker) action potential isproduced by conduction cells(SA node and AV node).These cells have no true resting membrane potential,and generate regular, spontaneous (automatic) actionpotentials due to the phase 4 pacemaker potentialdescribed below.

Phase 0 (slow depolarization) - produced by theopening of voltage-dependant slow L-type Ca++

channels (influx of Ca++).

Phase 3 (repolarization) - produced by the

closure of L-type Ca++ channels and opening of K+channels.

Phase 4 (pacemaker potential) - due to theclosure of K+ channels and the opening of funnychannels (Na+ influx), T-type Ca++ channels and L-type Ca++ channels (Ca++ influx).

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CARDIAC

Conduction pathway

SA node L + R atria

(fast) AV node

(slow) bundle of His

L + R bundlebranches purkinje

fibers ventricular

muscles

Venous pressurewaves

A wave: due to atrial

contraction (no valve so

wave can travel back tojugular vein

C wave: due to bulging

of tricuspid valve back

during ventricular

systole V wave: due to the filing

of R.A (maximal

volume) 67

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SHEAKLEY VALVULAR DISORDERS AND MURMURSA ti St i


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Aortic Stenosis:

increase afterload, increase

ESV, decrease in SV, S4

heard, concentric hypertrophy,

Mitral Stenosis: decrease EDV, SV, CO.

Decrease afterload, diastolic

murmur due to turbulent bf

through stenosed valve

Aortic Regurge:

increase EDV --> eccentrichypertrophy (S3) Diastolic

murmur. Will progress to

increase ESV (due to largve

SV build up)

Mitral regurge:

Systolic murmur (as bloodejected back to atrium in

systole). Decreased afterload.

S3 (chronic) because of high

EDV causing eccentric

hypertrophy70


Concentric hypertrophy:


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Thickened ventricular wall and unchanged or reduced ventricular

chamber diameter. Decreased ventricular compliance, S4 heart sound.

Due to increased afterload for an extended period of time (i.e. chronic

hypertension, aortic valve stenosis).

Eccentric (dilated) hypertrophy:

thickening of the ventricular wall and increased ventricular chamber

diameter. S3 heart sound. Volume overload

Due to volume overload (increased preload) for an extended period of

time, such as mitral valve regurgitation or aortic valve regurgitation.

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SHEAKLEY HEART SOUNDS


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SHEAKLEY HEART SOUNDS physiological heart sound

valve close S2 = aortic valve

close Split S1

right bundle branch block

Split S2

Normal if during inspiration, it gets

louder due to increase VR and delays

of pulmonic closure. Pathological if not accentuated during

inspiration

S3 : Valve affected will be heard

loudest there

Normal: in children and thin adults

Pathological: large volume entering

ventricle large EDV (aortic regurge,mitral regurge)

S4: Pathological! Coincides with

atrial contraction.

Heard in low compliance situation

(thick ventricular wall) = Concentric

hypertrophy due to (aortic stenosis

and hypertension)

Systolic murmurs:

S1 SSSSS- S2

Mitral Regurge

Aortic Stenosis

Diastolic Murmurs:

S1 S2 SSSSS

Mitral Stenosis

Aortic Regurge

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VALVES PATHOLOGY


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PATHOLOGY DR NINECongenital Heart Disease


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Types of Valvular pathology

Valve Annulus: imaginary line where the valve leaflet

embed into the muscle of the heart.

Valvular STENOSIS: Mitral and Aortic: most common. Pulmonary is almost

always congenital

Degenerative (old age, calcify) most common cause.

2nd cause: rheumatic heart disease, infection,

congenital

Signs for stenosis

Aortic :systolic murmurs, weakened

pulse, LV hypertrophy

Mitral: atrial fibrilation (due to dilatedatria causing improper electrical signal

conduction.

Valvular PROLAPSE:

weakened due to myxomatous degeneration.Papillary muscle rupture can also be 2nd cause.

Signs/symptoms for prolapse,

insufficiency, regurgitation: mid systolicclick with late systolic murmur.

ACYANOTIC

NO significant mixing of deoxygenated

blood in systemic circulation

Involve with LR shunt

Ventricular Septal Defect: mostcommon CHD (blood from LV RV

Holysystolic murmur

Eisenmenger Syndrome: diseaseprogression (over the years) to

pulmonary hypertension then RL

shunt. Seen in adults.

CYANOTIC

Significant mixing of deoxygenated

blood in systemic circulation

Involve RL shunt

Tetralogy of Fallot: common cyanoticCHD (Right to left shunt). Severity

depends upon pulmonic

stenosis/atresia.

P- pulmonary atresia

R RV hypertrophy

O overiding aorta

V - VSD

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DR.NUNN HEART DEVELOPMENT Left Atrium formation: developmentof veins for lung connection. Single puleino tgro th 4 branches


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Splanchnic mesoderm origin. Lateralbody/cranio-caudal foldings fuse to form single

definitive heart tube.

Primitive heart vessels: Viteline veins (d) from

yolk sac, Cardinal veins (d) from embryo, andUmbilical veins (o) from placenta.

Dorsal mesocardium degenerate transversepericardial sinus.

Flow: caudally cranially Sinus venosusprim

a prim vbulbous cordistruncus arteriosus

aortic sac

DEXTROCARDIA: heart tube shifting to the rightinstead of left. This is abnormal heart looping.

With sinus invertus, life compatible.

Right Atrium formation: from R.Primitiveatrium + R. Sinus venosus. Left Sinus horn

decrease in size while R. Sinus horn enlarges.

Left u,v,c vein by week 10, obliberated.

Remnants of Left sinus horn obligue vein +coronary sinus.

Smooth portion (sinus venarum) from

R.sinus horn of sinus venosus

Trabeculated portion: from R. Primitive

atrium.

Crista Terminalis: separate both internally

Sulcus terminalis: separate both externally

veinoutgrowth 4 branches

(L,R,S,I)outgrowth come back to form

primitive atrium.

Smooth part: from outgrowth of pulmonary

veins

Rough part: primitive L.atrium

Fetal circulation placenta straight to Left A and V (RL

shunt), some goes to lung for

development.

Atrial Septal Formation: Endocardialcushion is where septum will anchor.Septum primum osteum primum

osteum secundum. Then septum

secundum valve of foramen ovale.

After birth, high pressure blood from

pulmonary will rush down LA to close

valve. Now called fossa ovalis. ATRIAL SEPTAL DEFECT

Probe Patent Foramen Ovale: incomplete

sep pri and sec fusion. Most common

(1/4). No clinical importance

Premature closure of Foramen Ovale: Noblood from R LA. LV cannot fully

develop. Right side will hypertrophy.Death after birth.

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PRIMUM!!!!

Septum Secundum makes the

Foramen!

NUNN- HEART DEVELOPMENT


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NUNN HEART DEVELOPMENT VENTRICLE FORMATION:

Trabeculated portion = primitive ventricle

Smooth portion: LV (aortic vestibule) RV (conus

arteriosus)

SEPTUM FORMATION IN VENTRICLE:

Interventricular septum form. Consist of

Muscular septum: from myocardium. Form

expansion of heart muscle.

Membranous spetum: from fusion of 3 tissues

(endocardial cushion, muscular septum, aortico-

pulmonary septum)

VENTRICULAR SEPTAL DEFECTS: Mostsmall VSDs close spontaneously

Membraneous VSD: most prevalent.Associated with defects in aorticopulmonary

septum. Large VSD can cause LR shunt (due to

high pressure on L side) leading to pulmonaryhypertension/cardiac failure.

MuscularVSD: Less common. Swiss cheese

Common Ventricle (cor trilocularebiatriatrium): Failure of both membraneous and

musclar IV septum to fuse.

AV VALVES DEVELOPMENT: 5th 8th

week. Mesenchyme proliferation and

expansion at the AV orifice. Blood flow in

and kill some weak cells. Blood damage

cause reorientation to form valve, chordinae,

and muscle.

OUTFLOW TRACT PARTITIONING: Conus

cordis (cranial portion of bulbus cordis) +

truncus arteriosus partition. Neural crest cells

then form ridges spiral fashion aorta and

pulmonary trunk.

Persistent Truncus Arteriosus + ConusCordis: failure to partition results inmembraneous VSD. This leads to common

outflow for both ventricle. Cyanosis. Child die

w/i 2 years.

Transposition of Great Vessels: Wrongvessels with wrong chambers. (aorta receivingde02 blood!). Maternal risk increase with

rubella or viral illness during pregnancy. Spiralseptum formed straight not spiral. Cyanosis,

poor feeding, SOB.

Incompatible unless with accompanying shunt (patent

foramen ovale or patent ductus arteriosus)

Treatment: inject baby with prostaglandin. This keepsductus arteriosus open to allow mixing of blood

Tetralogy of Fallot: Abnormalities caused bysame primary defect. Anterior displacement of

aorticopulmonary septum leading to PROV.

Cyanosis. Depend on degree of pulmonic

stenosis.

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NUNN VASCULAR DEVELOPMENT


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Early Blood Vessel Formation: form from

splanchnic mesoderm (4th week). Vascular

Endothelial GF stimulates.

Vasculogenesis: form major vessels. Angiogenesis: Form minor vessels.

Angioblast: cells line cavity(endothelial lining)

Hemangioblast: Form blood cells.

AORTIC ARCHES: Developed with 5

pharyngeal arches. Mesenchymeembedded. Arise from aortic sac(cranially)and connects dorsally to dorsal aorta

1st arch: remnant = maxillary arteries

2nd arch: remnant = stapedial arteries

3rd arch: R+L common carotid

4th arch: Lpart of aortic arch RSubclavian artery (prox seg).R.Rlaryngeal Nerve loop under

6th arch: L ductus arteriosus +some L.pulmonary arteryL.Rlaryngeal Nerve loop under.R--

Right Pulmonary artery.

COARCTATION OF AORTA: constriction

of aorta.

Preductal (patent ductus arteriosus):

permit continuous blood flow. RL

shunt. RV hypertrophy and

pulmonary hypertension. Die

shortly after bith due to poor

collateral circulation.

Preductal (closed DA): increase

diastolic overload, LV hypertrophy.High mortality rate. Associated

with mitral valve malformation and

Congestive HF.

Postductal: most common type.

Collateral branches develop via

intercostal and thoracic arteries.Severity depends on stenosis and

collateral development. (see below)

Double aortic arch: Failure of R.dorsal

aorta to regress form vascular ring

that will constrict esophagus and

trachea.

77


forms R Pulmonary Artery!!! And some of the left

Forms DA

Forms prox R

****


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DR NUNN VASCULATURE DEVELOPMENT

Clinical case:coarctation of aorta

Post ductal constriction

Collateral circulation

Blood will bypass theroute of L subclavian

artery internal thoracic

anterior intercostal

artery posterior

intercostal artery

descending aorta

78


NUNN VASCULAR DEVELOPMENTVITELLINE ARTERIES: bv of yolk sac will regress

ABSENCE OF HEPATIC SEGMENT (ofIVC): failure to form. Blood from lower

drains through azygous/hemiazygous and


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VITELLINE ARTERIES: bv of yolk sac will regress adult remnant =

Celiac

superior mesenteric

inferior mesenteric arteries UMBILICAL ARTERIES: 5th week lose

connection to dorsal aorta. Remant

Proximal portion = internal iliac and superior

vesicle arteries

Distal = medial umbilical ligaments

VITELLINE VEIN:

Left regresses with L sinus horn

R.vitelline enlarges hepatic portion of IVC

UMBILICAL VEIN:

R.UV obliberated

Left persist. Ductus venosus forms in liver

(fetal shunt) to bypass liver sinusoids.

Connects with Left UV IVC CARDINAL VEIN: anterior + posterior common

cardinal vein. These below will form IVC

Supracardinal v drain body wall

Subcardinal v drain kidney

Sacrocardinal v drain lower extremities

SVC form from R common cardinal vein + R.Anterior cardinal vein.

g yg yg

directly empty into IVC RA. This is still

okay

FETAL CIRCULATION: before birth

Ductus Venosus: shunt to bypass the liver

to end up directly in IVC RA. Some still go toliver for development

Foramen Ovale: Blood from placentalalready highly O2, why waste time through lung?

Directly go through foramen ovale to enter LA

systemic.

Ductus Arteriosus: No need to go throughlung. Straight from pulmonary trunk aorta.

FETAL CIRCULATION 1st breath, placental circulation cease.

Ductus arteriosus: localized increase in O2initiate constriction. Intima proliferation

ligamentum arteriosum

Foramen Ovale: Pressure changes in LAcloses hole. oval fossa

Umbical arteries remant medialumbilical ligament

Umbilicalveins Ligamentum teres(hepatic)

Ductus venosus ligamentum venosum

PATENT DUCTUS ARTERIOSUS: preterminfant common. Spontaneously close.

Remainder can be ligated with little risk.

Prostaglandin keeps patency

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1 7 7 F

REMNANTS DERIVED FROM


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12!2@8!476@07 76@07F=@2707

12@078!5=!62707 N03N0712!,67

R7/225D ?8!5!FS

?!2>6/8382!58 5!0@1078!5=!62707

70?=!62!/=7=@5=!61 F656336@=8!5=!4

8!5=!4

?2!583F=6@ !T F656336@=F=6@

!=@83F=6@ 70N18!,6@83F=6@

70?=!62!/=7=@5=!61 F65=336@=F=6@F=6@

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SELF DIRECTED LEARNING


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SELF DIRECTED LEARNING

Link the materialpresented here, withthe material in Dr your textbooks to writea paragraph on theeffects of

abnormalities 1, 2 and3 on the newborn

Incidence

Shunting of blood?

Effects on chambers?

Symptoms/signs

Prognosis

1

23

1

Aka common atrium

81



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LAVILLE-LIPOPROTEINS Apo A1

In chylomicron: a structural proteins,

making it soluble

In HDL: activates LCAT

Apo A2

In chylomicron: structural

In HDL: enhances hepatic lipase

activity Apo B48

Only in chylomicrons (edited from

ApoB100) in intestinal epithelium.

Lack the LDL receptors. Only forpacking exogenous fat

ApoB100 : One of the longest knownproteins in human

Ligand for LDL receptors, VLDL,and IDL as well

Apo C2: Activates lipoprotein lipase(found in adipose, skeletal and heart)

which help with our fat metabolism.

Apo C3: Inhibites lipoprotein lipase

Apo D: Only on HDL. Closelyassociated with LCAT

Apo E: Binds to BE receptor onhepatocytes. There are 5 different

alleles for Apo E. Necessary forclearance of lipo proteins. w/o hyperlipidemia. Need either E3 or E4

E2 homozygous = problem! hyperlipidemia. High chylomicron,

early onset of CHD (atheroslcerosis)

E4 homozygous = Alzheimer

Apo a: 19 alleles

Disulfide bond to Apo B100

(complex with LDL)

Strongly resembles plasminogen increase clots!

Double dose: High CHD (from LDL)

+ high thrombosis82

Semester1Mini3Fall2010TVLbinding domain

^

chylomicrons, HDL, IDL, VLDL

NOT HDL

NOT LDL

ame as

before

CETP - exclusively associated w/ HDL,

cholesterol ester transfer

Type 3

HyperlipidemiaHigh CE and

TG

LAVILLE-LIPOPROTEINS


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Chylomicron

High TGs content (exogenous fat

carrier)

Synthesize in small intestine.

Exchange with HDL for necessary

proteins. Once mature it goes to

membranes where Apo C will activate

LP lipase (fat leaves chylomicron to go

into tissues)

Form

Nascent: Apo B48

Mature: Apo B48, Apo E, Apo C2

Remnant: Apo 48 and Apo E

VLDL

Still high TGs, some cholesterol esters

Endogenous fat carriers Apo B100, Apo C2, Apo E

IDL

Chopped off C2 (no longer needed)

Has Apo B100, Apo E

Hepatic lipase will remove TGs from

here.

LDL

Low TG and high cholesterol content.

LDL takes cholesterol to tissue where Apo

B100 will be recognized by LDL receptors onthese tissue.

HDL

HDL2 and HDL3 (better, highest protein)

A reverse cholesterol transporter. Cleans

tissue of cholesterol take to liver

Liver has scavenger receptor (SRB1) HDL has no ligand for any receptors, it just

sit on membrane of any cell for cholesterol to

diffuse esterification (LCAT/ACAT)

transfer back to liver VLDL or IDL

LCAT : found in plasma

ACAT: found within cell

83


comes f rom VLDL, intermediate btwn VLDL

and LDL, high TG and CE

LAVILLE - LIPOPROTEINS


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LAVILLE LIPOPROTEINS

Thyroid Hormone: T3 helps bindingof LDL to receptors.

Lysosomal degradation amino

acids, fatty acids, and free

cholesterol release.

Cholesterol esterified by ACAT

(inside cell)

Activation of HMG-CoA Reducatase

(controlled on gene expression level)

Sterol Regulator Element Binding

Protein (SREBP): when a cell needs

cholesterol, these will be cleaved

from ER bind to sterol regulatory

element on gene for HMGcoAreductase cause

transcription/translation of HMGCoA

Reducatase cell synthesize

cholesterol.

This enzyme will synthesize

cholesterol from mevalonate. Insuliln activates while glucagon

(and statin drugs) inhibit activity.

Upregulation of LDL receptors

Amount of cholesterol going intothe cell is controlled by:

Regulation of intracellularCholesterol

LDL modification and FoamCells formation

LDL has lots of cholesterol esters

(polyunsaturated) oxidized

macrophages has scavengerreceptors (w/o subject to feedback

control) take up LDL into cells =

white foam cells FC release GF

smooth muscle cells migration in

artery layers fibrous

calcification ruptures

hemorrahges MI

84



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LAVILLE - LIPOPROTEIN

Type 1: abnormal LPL no clearance of chylo.Apo C defect. Epigastric pain, acute pancreatitis, low LDL, HDL

Type 2a: LDL receptors defect

reduced LDLclearance high LDL CAD/plagues. Most

common

Type 2b: increased LDL; delayed VLDLclearance. Associated with increase risk of CAD.Single gene disorder (hyper TG and cholesterol)

Type III: Apo E2 homozygous xanthomas

LP (VLDL, IDL, chylo) massive hyper TG and

cholesterol. Early onset

Type 4:Associated with T2diabetes. BelevatedVLDL production.

Wolman disease: defect in lysosomal

cholesterol ester hydrolase. Reduced LDLclearance CAD/plagues.

Abetalipoproteinemia(acanthocytosis): no chylomicrons,

VLDL, LDL due to defect in apo B

expression. Rare malabsorption of fat.

Familialhypobetalipoproteinemia: Apo B

gene mutation. Low LDL and

VLDL. Mild or no pathological

change Tangier and Fish Eye disease:

reduced HDL. Apo A1 and C3defiency

Inherited Hyperlipidemias InheritedHypolipoproteinemias

85

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ini3Fall2010TVL

increased

chylomicrons

deficianc

y in

Apoc2 Familial LPL deficiency or Fam

Hyperchylomicronemia

Familial Hypercholesterolemia

Familial Combine

Hyperlipidemia

Familial dysbetalipoproteinemia or broad beta disease

Fam Hyper Triglyceredemia

TYPE 5: Familial, elevated VLDL and chylomicrons,

Hypetrycliceride and Hypercholesterol, decreased LDL and

HDLHigh Plasma LDL

xanthomas

insulance

resistane, obesity,

alcohol.

turbid eyes

Rbc

distorted

shape

Can Lovers Live In Village Cottages:

C - Type 1 (chylomicrons)

L - Type IIa (LDL)

L - Type IIb (LDL and VLDL)


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Xanthelasmas: deposit of

fat underneath the

eyes, Arcus Senilis

Xanthomas on arm by the

elbow, achilles tendon

Fibrates: TG lowering drugs

Resins: act on metabolism ofbile acids for getting rid of

cholesterol. Resins bind BA inintestin and take it out in feces.

Niacin: action on VLDL:prevents release of FA from

adipose tissue FA will be

used for energy so there will beless storage, less TG syntehsis

from liver, less left for making

VLDL.

Signs ofhypercholesterolaemia

Lipid lowering drugs

86

Semester1M

ini3Fall2010TVL

yp ( )

I - Type III (IDL and VLDL)

V - Type IV (VLDL)

C - Type V (Chylomicrons and VLDL)

Type IIb through V all have increased VLDL

Hope that helps!

white ring around your

eye

Normal Intervals


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P-R Interval

0.120 - 0.200 sec 120 200 msec

3-5 bo

Study Product 1

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