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Adv Patho > exam_2_20150304202951 > Flashcards

exam_2_20150304202951 Flashcards

1
Q

What is the purpose of the pericardium?

A

it is a fibroserous sac that encloses the heart and protects it from friction

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2
Q

What is the pressure in the Right and Left atria normally?

A

Right 4-8 mmHgLeft 4-12 mmHg

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3
Q

Which of the ventricles has lower pressure?

A

The RV is lower pressure 25/8LF is high pressure 90-130

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4
Q

How many semilunar cusps does the pulmonary and aortic valves have?

A

aortic=3 valve cuspspulmonic=3 semilunar cusps

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5
Q

What is the purpose of the chord tendineae?

A

tendinous attachments from papillary mm to tricuspid and mitral valves that helps to prevent eversion of valves into the atria during systole

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6
Q

What do sacromeres contain?

A

actin and myosin

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7
Q

What are the thick and thin filaments of a muscle called?

A

Actin=thinMyosin=thick

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8
Q

What do troponin and tropomysin regulate?

A

they regulate the cross bridging of actin and myosin

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9
Q

What is the sarcolemma, sarcoplasma, T tubules and sarcoplasmic reticulum?

A

sarcolemma=membrane that surrounds the myocytesarcoplasma=intracellular fluid which contains super abundance of mitochondriat-tubles=transmit action potential rapidly from sarcolemma to all myofibrils inside the fiber to citrate all the myofibril of one fiber simultaneouslysarcoplasmic reticulum=stores calcium ions

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10
Q

What is the purpose of intercalated discs?

A

they enable electrical impulses to spread quickly in a continuous cell to cell fashion

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11
Q

What supplies the heart with blood?

A

left anterior descending arteryleft circumflex arteryright coronary artery

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12
Q

75% of coronary perfusion is during…

A

diastole

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13
Q

What happens to the smaller blood vessels during contractions and how does the heart receive O2 during contractions?

A

the vessels are compressed during systole decreasing blood flow and oxygen is supplied by myoglobin (a protein in muscle that stores O2 and releases it in hypoxia during the period of systolic compression)

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14
Q

There is one capillary per…

A

fiber

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15
Q

What is the normal oxygen extraction?

A

70-75%

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16
Q

Formular for MAP

A

(2D+S)/3

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17
Q

How to calculate pulse pressure?

A

BP 136/84Pulse Pressure: 136-84=52

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18
Q

What is Laplace’s Law?

A

T=P x r/WT=tension of vessel wall that opposes the distending pressure inside the vesselP=intraluminal pressureR=vessel radiusW=wall thicknessinternal pressure expands the easel until it is balanced by wall tensionthe larger the radius, the greater the tension needed to balance a particular pressurewall tension is inversely related to wall thickness (the thicker the vessel wall the lower the tension)walls hypertrophy to reduce wall stress

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19
Q

How do you calculate cardiac output?

A

CO= HRxSVSV=preload, afterload, and contractility

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20
Q

What is the Frank-Starling Curve?

A

increase preload stretches fibers causing more forceful contraction->increased SV->increased COmyocardial fibers reach a point of stretch beyond which it cannot contract and SV and CO decrease

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21
Q

What are the factors of stroke volume (SV)?

A

preload: streching force that acts on cardiac muscle before contraction (diastole)afterload: resistance that must be overcome by ventricles in order to open semilunar valves and propel bloodcontractility: the hearts contractile forceincrease in contractility is caused by SNS, inotropic drugs, increase in cytoplasmic Ca

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22
Q

Normal ejection fraction (EF)…

A

60-70%percentage of preload volume ejected from the LV per beat

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23
Q

Extrinsic Control of HR

A

Vagus nerve (PNS)superior, middle, and inferior cardiac nerves (SNS) increase contractile force by facilitating influx of Ca into myocytes Norepinephrine Alpha adrenergic Beta adrenergic (B1) Epinephrine beta adrenergic B1 beta adrenergic B2

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24
Q

What are the effects of the B1 beta adrenergic receptor sites?

A

effected by norepinephrine and epinephrineincrease SA node discharge increase HR

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25
Q

What is the effect of the alpha adrenergic receptor sites?

A

effected by norepinephrinevasoconstriction

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26
Q

What is the effect of B2 adrenergic receptor sites?

A

effected by epinephrinecauses vasodilation

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27
Q

Intrinsic Controle of HR

A

central: thalamus/hypothalamus, diencephalon, cerebral cortexrelfex: baroreceptors, arterial chemoreceptors, bainbridge reflex, respiratory reflex

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28
Q

positive inotrophic means…

A

increased force of myocardial contraction

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29
Q

Action potential Fast response (ventricular and atrial myocytes)Phase 0

A

rapid Na=depolarization 20-30 mV

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30
Q

Action potential Fast response (ventricular and atrial myocytes)Phase 1

A

closing of Na channels=slight repolarization

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31
Q

Action potential Fast response(ventricular and atrial myocytes)Phase 2

A

influx of ca and some Na influx, efflux K=plateau

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32
Q

Action potential Fast response(ventricular and atrial myocytes)Phase 3

A

inactivation of Ca channels; heaviest K efflux=repolarization to RMP

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33
Q

Action potential Fast response(ventricular and atrial myocytes)Phase 4

A

rest

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34
Q

When is there absolute refractory during cardiac cycle?

A

phases 1,2, and part of 3 the cell cannot be depolarized again

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35
Q

When is there relative refractory period?

A

phase 3 and continues to phase 4 when the cell may be able to depolarize again

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36
Q

Action potential Slow response(pacemaker cells)Phase 0

A

slo Ca and Na influx for initial depolarization +20mV

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37
Q

Action potential Slow response(pacemaker cells)Phase 2-3

A

gradual efflux of K with drop off of Na and Ca currents depolarized to “R” MP

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38
Q

Action potential Slow response(pacemaker cells)Phase 4

A

spontaneous decreasing K efflux allos depolarization to threshold

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39
Q

What does the P wave signify?

A

spread of excitation over the atria

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40
Q

What does the QRS wave signify?

A

spread of excitation over the ventricles

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41
Q

What does the T wave signify?

A

spread of depolarization over the ventricles

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42
Q

Process of Excitation-Contraction Coupling

A

action potential is conducted from cell to cell through intercalated discsaction potential is spread into the interior of the cell via T tubulesCa begins to enter cell and the beginning of Ca influx triggers more Ca from the sarcoplasmic reticulum via Ca channelsCa binds to protein troponinthe Ca-torponin complex interacts with tropomyosin to unblock active sites between the actin and myosin filaments=>allows cross bridgingat end of systole, Ca influx ceases and sarcoplasmic reticulum is no longer stimulated to release Casarcoplasmic reticulum avidly takes up Ca via an ATP-energized Ca pumpCa binding to troponin stops and this stops the tropomyosin to again block the sites for interaction between the actin and myosin filaments*Relaxation occurs

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43
Q

What is the effect of Ca on the force of action potentials in the cardiac myocytes?

A

the greater the amount of Ca in the cytoplasm the greater the force and the lesser amount of Ca in the cytoplasm the lesser the degree of force

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44
Q

What blocks the site of interaction between the actin and myosin filaments in the cardiac myocyte?

A

tropomyosin

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45
Q

What causes the tropomyosin (attached to actin filament) to expose the binding site for myosin?

A

Ca*Ca binds to troponin C which causes the tropomyosin to expose the actin binding site and ATP is split to allow energy for myosin to then bind to actin

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46
Q

What are the causes of Congenital heart disease?

A

it occurs in 1% of live birthsetiology: unknown 90% Rubella, genetic (chromosome 13, 15, 18, 21, 22), Turner syndrome, abnormalities in transcription factors

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47
Q

What are the types of congenital heart disease?

A
  1. left to right shunts: blood flow from the L to R and eventually causes pulmonary HTN, atrial septal defects, ventricular septal defects, parent ductus arteriosus 2. R to L shunt: cause unO2 blood from R to L and will cause cyanosis at or near time of birth: Tetralogy of Fallot, transposition of the great arteries3. obstructive lesions: pulmonic valve stenosis, aortic valve stenosis or atresia, coarctation of the aorta
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48
Q

What type of arrhythmia is caused by depolarization during the relative refractory period (i.e. late phase 3 or phase 4)?

A

tachycardia

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49
Q

How does myocardial ischemia cause arrythmias?

A

can cause tachycardia because it alters the action potential of myocardial cells because it disrupts the Na/K pump*major reason for PVC’s or V tach that initiate ventricular fibrillation

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50
Q

What is reentry phenomena?

A

occurs when a propagator impulse fails to die out after normal activation of the heart and persists to re-excite the heart after the refractory period as ended; responsible for Afib, flutter, AV reentry, extra nodal bypass tract, Vtach

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51
Q

Sudden cardiac death

A

V fib (heart quivers; no cardiac output)Asystole

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52
Q

Etiology of CAD

A
  1. athersclerotic most common 2. valvular disease, myocardial hypertrophy and aortic dissection3. coronary spasm: circulating adrenergic agonist, locally released platelet contents, impaired secretion of endothelial cell relaxing factors (nitric oxide) relative to contracting factors (endothelin)4. thrombus5. hypotension, increased HR, congenital abnormalities, vasculitis, vegetative emboli6. increased demand by HTN, increased HR, increased blood volume, LVH, thyrotoxicosis
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53
Q

Three types of coronary syndromes:

A

angina, MI, sudden cardiac death

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54
Q

types of angina

A

Stable Angina: no cell necrosis, no usually associated with plaque disruption, pain short 3 to no more than 30 minutes, relieved by rest or nitroUnstable Angina: sudden change in plaque morphology or increased stenosis, pain that occurs with progressively increasing frequency, more prolonged in durationVariant Angina: coronary artery spasm, occurs at rest,

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55
Q

how does a thrombus form from plaque fissuring or stenosis?

A

fissuring: exposure of plaque to sub endothelial collagen and necrotic plaque contents cause formation of thrombus with variable thrombotic occlusion stenosis: increased stenosis from size of plaque increasing

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56
Q

Patho of MI

A
  1. coronary artery occlusion from thrombosis plaque fissuing/erosion; primary prolonged vasospasm; emboli; hypotension superimposed on an unchanged obstruction; decreased O2 carrying capacity of blood
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57
Q

MI Response Times

A

within 20 minutes potentially reversibleafter 20-40 minutes irreversible myocyte injury within 3-6 hours the extent is largely complete

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58
Q

What irreversible damage by MI is non-Q wave?

A

subendocardial: limited to inner 1/3-1/2 of ventricular wallthe subendocardium is the least well perfused resin and left ventricular myocardial pressure is greatest near the endocardium

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59
Q

What is intramural refer to in MI?

A

within the wall, the term intramural refers to microinfarcts

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60
Q

What irreversible damage by MI is represented by Q wave?

A

transmural: full thickness

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61
Q

What are types of repercussion in the cases of MI?

A
  • thrombolysis, CABG, angioplasty* decreases area of injury and reverses ischemiamay also injure cells and increase apoptosis because O2 utilization by cell is impaired, O2 being delivered to cell from ROS and this causes damage as it draws leukocytes even after flow as been restored may leave cells poorly contractile for a few hours up to 1-2 days because of hypoxi and inflammation caused by hypoxia causes release of myocardial depressant factors that is derived from combined release of TNFa and IL-1
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62
Q

What is the usual location of MI?

A

40-50% are LAD (left anterior descending) artery

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63
Q

What are the markers for MI?

A
  1. creatine kinase (CK) specifically the myocardial isoform CK-MB2. troponin 1 and troponin T: after MI both are detectable within 2-4 hrs with levels peaking at 48 hr and persist for 7-10 days (***more reliable to dx MI because last so long)
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64
Q

What causes the systemic response during MI?

A

release of catecholamines and angiotensin II *anxious, fearful, weak, cold, clammy skin, acute confusion, stroke for 85+; hypo or hyper BP

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65
Q

Some causes of Acute Coronary Syndrome…

A

aka Sudden cardiac deathCADnonatherosclerotic cardiac diseases like hypertrophic cardiomyopathy*congenital abnormalitiesPatho: most often caused by lethal arrhythmia triggered by electrical irritability of myocardial cells not part of the conduction system

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66
Q

What is the etiology of LVSD?

A
  1. volume overload: regurgitant valves; high-output states (anemia, hyperthyroidism)2. pressure overload: systemic HTN; outflow obstruction (aortic stenosis, asymmetric septal hypertrophy)3. myocyte ischemia/loss of muscle: MI form CAD; connective tissue disease (SLE)4. loss of contractility: myocarditis; poisons (alcohol, cobalt, doxorubicin); infections (viral or bacterial); genetic mutations of cellular architecture or sacromere proteins5. restricted filling: mitral stenosis; pericardial disease (constrictive pericarditis, pericardial tamponade); infiltrative diseases (amyloidosis)
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67
Q

What causes diastolic dysfunction?

A

it is the inability for the ventricle to relax and fill with blood*diseases that decrease relaxation, decrease elastic recoil or increase stiffness of the ventricle *(left ventricle hypertrophy, myocardial fibrosis, deposition of amyloid, constrictive pericarditis)=> restrict filling

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68
Q

What causes right sided heart failure?

A

left sided heart failureright ventricular infarctionpulmonary disease including Cor Pulmonalecongenital heart disease*pulmonic or tricuspid valvular disease

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69
Q

How does heart failure trigger the SNS?

A

increased release of catecholamines= norep and epi to compensate for decreased CO=this causes increased HR and BP and cardiac contractility but causes increased work and O2 demand and can cause arrhythmias

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70
Q

How does heart failure trigger vasopressin secretion?

A

vasopressin release leads to vasoconstriction and reabsorption of water in the renal tubules to compensate for decreased CO=this increases the preload (LVEDP)= increases stretch=increases forcible contraction (Frank Starling Relationship)=and increases CO = but if it causes too much stretch it will result in decreased CO because actin and myosin will not connect effectively and can result in pulmonary edema which reduces oxygen supply and leads to myocellular hypoxia

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71
Q

How does heart failure activate the renin-angiotensin-aldosterone system?

A

reduced renal blood pressure triggers this system=aldosterone secretion leads to sodium and water reabsorption in the renal tubules=incresaed preload (LVEDP)=increased stretch=increased forcible contraction=increased CO= but will lead to too much stretch because the myosin and actin do not connect effectively which will cause decreased CO and lead to pulmonary edema and reduced oxygen supply and myocellular hypoxia

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72
Q

How does heart failure activate angiotensin II?

A

reduced blood flow triggers the renin-angiotensin-aldosterone system which results in renin stimulating the production of angiotensin II and angiotensin II stimulates production of aldosterone which leads to Na reabsorption and K excretionangiotensin II results in smooth muscle vasoconstrictionthis results in increased after load= inhibits NO release-stimulates fibroblasts proliferation

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73
Q

How does heart failure trigger release of atrial natruretic peptide (ANP) and brain natruretic peptide (BNP)?

A

these are stored in granules in atrial and ventricular cytoplasm*ANP is secreted from atrium and BNP is secreted from ventricle when stretched they inhibit secretion of renin, aldosterone and relax smooth muscle and inhibit Na and water absorptionserum BNP or precursor pro-BNP is used to monitor progression of HF

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74
Q

ANP is secreted from…

A

atriums

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75
Q

BNP is secreted from…

A

ventricles

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76
Q

What is the result of increased myocardial stretch?

A

results cells stretching, increased protein synthesis and number of sarcomeres and mitochondria increased size of myocyte with new sarcomeres increase wall thickness and or the lengthwise addition of new sarcomeres enlarge chamberthis will result in a larger distance between the capillaries which will alter the delivery of Ca=this will interfere with contractility, lead to ischemia of cells and trigger apoptosis *continued stress on the muscle will cause altered gene expression and re-expression of embryonic forms of myosin and troponin will occur and result in inability to contract normally

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77
Q

How does endothelin effect the heart during myocardial hypertrophy?

A

there is injury to the endothelial and this releases endothelin which causes vasoconstriction=decrease O2 supply

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78
Q

What happens when the myocyte is injured during myocardial hypertrophy?

A

injury to myocyte results in inflammatory response=cytokine release (TNFa and IL1TNFa promotes cardiac hypertrophy and apoptosisInterleukins promote cardiac remodeling and eventually induces contractile dysfunctionthis stimulates deposition of fibrous tissue and interstitial collagen which will cause chambers to be stiffapoptosis will result in decreased myocytes and increased work/stress on the remainder cells that will ultimately contribute to myocardial contractile failure

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79
Q

The similarities and differences of left sided HF and right sided HF manifestations:

A
  1. left sided HF: activates SNS(^HR)decreased COpulmonary congestion (dyspnea, orthopnea, crackles/wheezes, S3 and S4 sounds, displaced lateral apical pulse)increased BNP, LVhypertrophy, decreased EF2. right sided HF:poor EFJVDperipheral edemaascitieshepatomegaly, splenomegaly (from congestion)
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80
Q

What is Cor Pulmonale?

A

right ventricular hypertrophy, dilation and possibly failure secondary to disorders of the lungs or pulmonary vasculature that produce pulmonary HTN

81
Q

What occurs from Cor Pulmonale?

A

it can result in right ventricular hypertrophy and dilation, and right atrial dilation from pulmonary HTN increasing the after load of the right ventricle

82
Q

What heart sounds are effected by Cor Pulmonale?

A

persistent split of S2, pulmonic valve murmur, tricuspid valve murmur

83
Q

What is the etiology of aortic stenosis?

A
  1. rheumatic heart disease *rheumatic fever=strep bacteria=Type III hypersensitivity response Ag/Ab complexes deposited on endothelium and endocardium valves2. congenitally defective valves 3. degenerative: age(60-70 y/o), fibrosis and calcification
84
Q

What results from aortic stenosis?

A

increases the after load in the LV*the obstruction leads to LV hypertrophy, stiff, fatigue, dilates, ischemia, failure**Manifestations are similar as LHF

85
Q

What heart sound is heard with aortic stenosis?

A

mid-systolic murmur, S4

86
Q

How does aortic/cardiac enlargement lead to aortic insufficiency?

A

if heart enlarges the valve ring dilates and the cusps can no lunger close tightly

87
Q

What heart sound is heard from aortic insufficiency?

A

S3, diastolic murmur (early rumble throughout and extends to systole)

88
Q

Rheumatic fever is common cause in…

A

aortic valve stenosis, aortic insufficiency and mitral valve stenosis and mitral insufficiency

89
Q

Mitral valve stenosis will result in…

A

increased LA pressure, hypertrophy, and dilation

90
Q

What will be heard on a patient with a mitral valve stenosis?

A

diastolic murmur, opening snap

91
Q

What will be heard in a patient with mitral insufficiency?

A

pansystolic regurgitant murmur, S3 (in failure, chronic)

92
Q

Long term effects on heart with mitral insufficiency…

A

LVEDP, LV hypertrophy after LA hypertrophy, A-fib

93
Q

What is the intrinsic primary cause of cardiomyopathies?

A

HF(secondary cause is acquired by disease)

94
Q

Main cause of dilated cardiomyopathy…

A

primary 50% idiopathic, other factors: alcohol, pregnancy, viral, bacterial, autoimmunesecondary: ischemia, valvular, HTN, CHF

95
Q

Etiology of hypertrophic cardiomyopathy (HCM)…

A

primary: genetic mutation to proteins that encode sarcomere secondary: Hypertensive heard disease, aortic stenosis

96
Q

What is the pathology of HCM primary etiology?

A

sarcomere proliferation thus myocyte hypertrophy, fibroblast (synthesis collagen matrix) proliferation with collagen deposition=this often leads to thickening of septumcan lead to Afib

97
Q

Etiology of restricted cardiomyopathy…

A

primary: idiopathic, amyloidosis(deposition of insoluble proteins in extracellular spaces), radiationsecondary: pericardial constriction

98
Q

Does restrictive CMP lead to hypertrophy?

A

No, the ventricular cavity remains normal size, but interstitial fibrosis occurs decreasing CO and increasing LVEDP

99
Q

Difference between acute pericarditis and pericardial effusion and constrictive pericarditis…

A

acute pericarditis results in inflamed and roughened membrane and may result in exudatespericardial effusion is an accumulation of serous, inflammatory exudate or blood in the pericardial cavityconstrictive pericarditis results when normal tissue is replaced by fibrous tissue, scar and calcification

100
Q

Manifestations of pericarditis and pericardial effusion and constrictive pericarditis…

A

pericarditis: can mimic MI pain, worse with breathing, friction rub, pericardial effusion and constrictive pericarditis: SOB, JVD, hepatomegaly, ascites, muffled heart sounds, cardiac tamponade

101
Q

What is cardiac/or pericardial tamponade?

A

*physical signs that arise from the limited filling of the ventricleThree classic signs: Beck’s Triad1. hypotension2. elevated jugular venous pressure3. muffled heart soundspt may have decreased systemic pressure with inspiration(paradoxic pulse or pulsus paradoxes)increased R sided heart pressure,results in restriction=hypotension, decreased SV, CO Low BP may be late sign

102
Q

What is the three elements of pathology of endocartitis?

A
  1. damaged endocaridial tissue2. seeding of blood with microbes and attachmentattachment of microbes to valve are facilitated by the coexistence of damaged endocardial tissue((normally valves are fibrotic without soft tissue matrix and vascular supply so leukocytes cannot protect them and defense is only bactericidal activity of serum and continuous flow inhibits attachment))3. bacterial proliferation and vegetative formationbacterial colonies from within aggregates of fibrin and platelets become progressively more enmeshed in tight fibrin networks protected from hosts self-defense mechanismkeep growing *sequelae=destruction of underlying cardiac tissues because inflammatory process and can result in systemic emboli, tissue fibrosis and calcification
103
Q

What are the manifestations of endocarditis?

A

IL-1 and TNFa symptoms(fever, wt loss, fatige)murmur 90% havecardiac complicationsglomerularnephritis secondary to trapping of Ab/Ag complexes (similar to type III hypersensitivity)

104
Q

What is nonbacterial thrombotic endocarditis?

A

masses of sterile fibrin, platelets, and other blood components on cardiac valves cause damage to valves and cause hyper coagulable states, embolize and become medium for bacterial colonization

105
Q

What types of arteries are more likely to contribute to physiological resistance to blood flow?

A

small arterioles: have more smooth muscle innervation(large=aorta, more elation and fibers)(medium=muscular, renal arteries)

106
Q

How many layers do capillaries have?

A

sigle endothelial layer for easy exchange of diffusable substances

107
Q

What are the three layers of vascular walls?

A
  1. intima=single layer of endothelial cells, connective tissue, elastic tissue2. Media=smooth muscle cells, contains elastin, myosin, actin, Ca binding to calmodulin, O2 nutrients provided by diffusion of lumen 3. adventitia (externally)=connective tissue, nerve fibers, vasovasorum
108
Q

What are the functions of vascular smooth muscle?

A

constrict or dilatesyntheisize collagen, elastin, proteoglycans(extracellular matrix ECM),elaboration of growth factors and cytokinesproliferation and migration to the intima

109
Q

How does blood flow normally in a vein?

A

normally blood flow is laminar

110
Q

What is myogenic response?

A

the tendency of smooth muscle cells in arteries to contract in response to stretch

111
Q

What substances are secreted by endothelium?

A
  1. endothelia’s and angiotensin converting enzymes cause vasoconstriction2. prostacyclin (PG12 prostaglandin) and NO promote vasodilation
112
Q

How is NO produced by the endothelium?

A
  1. Things that promote NO production: shearing of tissue, stress, Ach, bradykinin, substance P, vasoactive intestinal polypeptide (VIP)2. Things necessary for production: Ca and arginine
113
Q

What does NO react with to produce constant vascular smooth muscle cells to relax?

A

cGMP

114
Q

What mediators are released when there is injury to the vessel wall?

A

thromboxane and leukotrines cause vasoconstrictionprostaglandins cause vasodilation

115
Q

Which hormones are principle vasodilators in circulation?

A

Kininsproduced in inflammation and by other tissuesinactivated by kininase II (angiotenin-converting enzyme)*inhibition of ACE for the treatment of HTN or HF allows higher plasma and tissue kinins which results in vasodilationex: bradykinin

116
Q

What are the effects of ANP and BNP?

A

increases glomerular filtration rateantagonize angiotensin IIvasodilate

117
Q

How does the peripheral nervous system regulate vascular resistance?

A

Constrition:central control: baroreceptors (vagus nerve nucleus in medulla, vasomotor cell bodies in medulla)SNS: alpha adrenergic receptors, maintains steady state of tonic activity and further vasoconstrictspulmonary reflexDilation:cholinergic neurons innervating blood vessels in skeletal muscleB2 adrenergic

118
Q

What are the types of arteriosclerosis?

A

arteriosclerosis: effects small arteries and arterioles; associated with HTN and DMMonckleberg medical calcific sclerosis: calcium deposists in muscular arteries; usually does not narrow vessel lumenatherosclerosis: slowly progessivwe abnormal fibrous thickening and hardening of arterial vessel walls

119
Q

What causes thickening of arterial vessel walls in atherosclerosis?

A

lipid depositionsmooth muscle cell proliferationsynthesis of extracellular matrix in the intma

120
Q

what is hyperhomocysteinemia?

A

plasma homocysteine is a significant source of ROS that can cause endothelial dysfunction and damage and it interferes with NO action

121
Q

Patho of lipids

A

LDL accumulates in arterial intima usually at points that they branch and where increased permeability is; they produce ROS that directly impairs endothelial cell function; intimal LDL is oxidized and given the scavenger receptor which is a chemotactic for circulating monocytes, this causes the monocytes/macrophages to ingest them, this inhibits NO production by endothelial cells, and oxidized LDL is cytotoxic to endothelial cells and smooth muscle cells (this stimulates movement of the smooth muscle cell (SMC) to intima)

122
Q

Patho of inflammation on oxidized lipids…

A

*macrophages take up oxidized LDL through special scavenger receptors to become foam cells secrete IL1 and TNa and other cytokines which continue the inflammatory processelaborate growth factors->stimulate smooth muscle cell proliferation

123
Q

Patho of immune system on atherosclerosis…

A

T cells are recruited to site by chemoattractants and interact with macrophages and release pro inflammatory cytokinesB cells produce IgM and IgG antibodies against oxidized lipoprotiens

124
Q

Patho of role of platelets on atherosclerosis…

A

elaborate growth factors particularly PDGF which stimulates smooth muscle cell proliferationparticipate in clotting cascase

125
Q

Patho of role of SMC proliferation…

A

migrate from media to intima and proliferatesynthesize and deposit collagen, elastin, and glycoprotiens (exctracellular matrix)take up oxidized LDL and become foam cellsMigrate over the fatty streak to form a cap over lesion

126
Q

What are the types of lesions formed in atherosclerosis?

A

*initial fatty streak formed by SMC proliferation fibrofatty plaque (atherosclerotic): it is elevated and protrudes into lumen and can cause destruction of the media layerComplicated lesion

127
Q

What is the fibrous cap made up of?

A

smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization

128
Q

What is the necrotic center made up of?

A

cell debris, cholesterol crystals, foam cells, calcium

129
Q

What occurs from a complicated lesion?

A

it is a patchy or massive calcificationfocal rupture/ulceration of luminal surface can cause exposure of thrombogenic substances that induce thrombus formation and discharge of debris-microemboli (cholesterol emboli or atheroemboli)*hemorrhage superimposed thrombusatrophy of media

130
Q

Patho of primary/essential HTN…

A

having reduced renal sodium excretion in the presence of normal arterial pressure will cause increased water reabsorption by the kidneys to increase fluid volume to increase CO and cause peripheral vasoconstriction problems with the renin angiotensin aldosterone system: genetic d/o, allele variation, results in arterial smooth muscle remodeling and HTNfunctional vasoconstriction: sedentary lifestyle (^Na diet=increased water retention), stress, smoking (causes structural thickening of the arterial walls)defects in vascular smooth muscle growth and structure: genetic( increased wall thickness)*altered SNS function

131
Q

What is the most common etiology of aneurysms?

A

atherosclerosis: causes arterial wall thinning through destruction of medial layer of vascular wall and compromises nutrient/oxygen supply to the arterial wall

132
Q

Where is the area effected by a dissecting aneurysm?

A

there is a tear in the intimal layer

133
Q

What is the definition of shock?

A

an abnormality of the circulatory system in which there is inadequate tissue perfusion due to a relatively inadequate cardiac output.

134
Q

Major categories of shock:

A
  1. hypovolemia2. distributive=inappropriate vasodilation3. cardiogenic=impairment to the heart such that blood flow to tissues is no longer adequate to meet metabolic demands4. obstructive=obstruction of blood flow in the lungs or heart *massive pulmonary edema, tension pneumothorax, cardiac tamponade
135
Q

Types of hypovolemic shock:

A
  1. hemorrhagic shock2. traumatic shock: due to loss of blood and tissue damage that releases free radicals and initiates massive inflammatory response: increased serum K and increased myoglobin->causes kidney damage3. surgical shock: due to a combination of external hemorrhage, bleeding into injured tissue, and dehydration4. burn shock: due to massive loss of plasma from the skin surfaces
136
Q

Types of disruptive shock:

A
  1. anaphylactic shock: type I hypersensitivity releases large amounts of histamine, producitng marked vasodliation=hypotension2. septic shock: lipopolysaccharides are released from bacterial cell wall when cell walls are degraded=>results in massive endothelial cell injury=>excessive releases of NO and prostaglandin results in arterial and venous vasodilation=> hypovolemia results when there is loss of plasma into peripheral tissues=> maldistribution of blood flow to vital organs3. neurogenic shock: increased autonomic activity that results in vasodilation and pooling of blood int he veins
137
Q

Patho of shock…

A

*inadequate tissue perfusion=>anaerobic metabolism and production of lactic acid=>lactic acidosis depresses myocardium and decreases peripheral vascular responsiveness to catecholamines (epi and norep)=>hypoxic cell injury and death result=>blood flow is slowed and clotting cascade is activated=>cells soak up water and further depleted intravascular volume=>lysosomal enzymes leak out and destroy neighbor cells

138
Q

Condition in which the valves of the veins do not function adequately and there is a decrease in return of blood moving form the legs upward to the trunk of the body.

A

chronic vein insufficiency

139
Q

Patho of chronic venous insufficiency…

A

increased prolonged intraluminal pressure causes dilation, valves become incompetent and further dilation and venous stasis results (varicose veins, thrombosis, edema)valvular damage and defects in venous wall permit back flow and result in regurgitation and this causes increased pressure from a large volume of blood under the influence of gravity and results in more dilation and venous stasis (varicose veins, thrombosis, edema)

140
Q

What are the long term effects of venous insufficiency?

A

trophic skin changes, dermatitis and ulceration d/t hypoxia of cells from outward pressure of edema on tissue

141
Q

What is Virchow’s triad?

A

stasis of blood flowendothelial injuryhypercoagulability (venous thromboembolism)

142
Q

Classes of HF

A

I without limitationII slight limitation, comfortable at restIII marked limitation in activityIV inability to carry on activity without sx

143
Q

Semilunar valves closing signifies…

A

diastole

144
Q

Atrial-ventricular vavles closing signifies…

A

beginning of systole

145
Q

What cells secrete mucus in the respiratory system?

A

goblet cells and submucosa cells

146
Q

What are the areas of respiratory exchange?

A

bronchioles, alveolar ducts and alveoli

147
Q

What occurs to type II alveolar cells when type I are injured?

A

alveolar type II switch roles** I provide structure and repair alveolar epithelium** II secrete surfactant

148
Q

Where are the mesenchymal cells located and what do they secrete?

A

located in the interstitial space of the alveolar-capillary space and secrete fibroblasts and a few leukocytes

149
Q

What do the neurons and chemoreceptors in the pons and medulla respond to front he arterial blood?

A

they response to changes in he PaCO2 and the pHthey maintain rhythmic respirations

150
Q

What is the efferent innervation of the respiratory system?

A

PSN=vagalSNS=B2 receptors nonadrenergic, noncholinergic (NANC)

151
Q

What chemoreceptors in the periphery respond to low PaCO2?

A

carotid bodies and aortic bodies

152
Q

What regulates capillary flow?

A

The arterioles regulate capillary flow

153
Q

Because the lymphatics only extend to the terminal respiratory bronchioles, what pressure helps to expel fluid from lungs?

A

intrapleural pressure during inspiration (creates greater negative pressure)

154
Q

Where is the principle site of airway resistance?

A

the medium sized bronchi and larger bronchiolesthe alveoli have low resistance

155
Q

What happens when there is decreased O2 in an alveoli?

A

this causes alveolar capillary vasoconstriction to help shunt the blood to another alveoli with greater O2. if more alveoli are without much O2 this will cause general vasoconstriction and results in pulmonary HTN

156
Q

Why does ventilation and perfusion not match?

A

because there is greater negative pressure in the apex of the lung and less negative pressure in the base of the lungthis results in less compliance in the apex because the alveoli are already expanded to a certain degree and there is greater compliance in the base of the lungs because those alveoli are able to expand much morebecause there is greater negative pressure and less compliance in the apex this helps to shunt/distribute air to the base of the lungs

157
Q

When you have a low ventilation perfusion ratio (V/Q) what occurs in the heart?

A

perfusion is normal but ventilation is impaired <0.8*it is also called right to left shunt as blood is being pumped from the right side of the heart to the left side without being oxygenated

158
Q

What is a normal V/Q ration?

A

alveolar ventilation is about 4L/min and pulmonary artery blood flow is about 5L/min (4/5=0.8)

159
Q

What is hight V/Q ration?

A

> 0.8 ventilation remains normal but perfusion is impaired *have a greater dead space

160
Q

What is dead space, alveolar dead space and physiological dead space?

A
  1. dead space: area in the lungs that is filled with air but does not participate in gas exchange2. alveolar dead space: unit of air in gas exchange but is not being perfused3. physiological dead space: total volume of gas that does not participate in gas exchange
161
Q

Which diffuses faster, oxygen or carbon dioxide?

A

CO2 diffuses 20x faster than O2

162
Q

What causes shift to right or left of the oxyhemoglobin dissociation curve?

A

shift to right: high pH, low blood temp, low PaCO2 increase affinity of hgb for O2shift to lef: low pH, higher blood ten;, high PaCO2 decrease affinity of hgb for O2

163
Q

What is the Aa gradient?

A

the difference between the alveolar and arterial PO2

164
Q

What is the etiology of hypoxemia?

A
  1. high V/Q (poor perfusion / well ventilated)ex PE2. low V/Q (good perfusion / poor ventilation)atelecatasis, pneumonia, ARDS
165
Q

What is the etiology of hypercapnia?

A

depression of resp centers by drugsdiseases of medulla, spinal conducting pathways, neuromuscular junction or resp musclesthoracic cage abnormalitieslarge airway obstructionincreased work of breathingphysiological dead space i.e. emphysema

166
Q

What are the non respiratory bronchioles?

A

respiratory bronchiolesalveoli ducts alveoli

167
Q

A deficiency of alpha 1-antitrypsin results in what disease?

A

emphysema

168
Q

Patho of emphysema…

A
  1. protease: a small amount of protease enzymes are normally secreted by alveolar macrophages and by neutrophils sequestered in pulmonary capillariesthey digest/destroy elastic fibers in the alveolar interstitial tissueinflammation: neutorphils and macrophages increase their release of proteases and recruit more neutrophils and macrophages to the site 2. a1-antitrypsin (protease inhibitor); smoking and other irritants damage inhibitors of protease resulting in damaged cartilage(gene expression chromosome 14)(expressed in liver as well)3. Oxidative stress: free radicals react with proteins and in this case react with a1-antitrypsin and inhibit its action4. Smoking: promotes secretion of protease and produces ROS=>larger alveoli, more compliance but less recoil, destruction of alveolar capillary walls=>decreased resp exchange
169
Q

Classifications of emphysema…

A
  1. centriacinar (centrilobular): most common in smokers: resp bronchioles are effected2. panacinar (panlobular): genetic anitrypsin deficiency and affects alveolar ducts then resp bronchioles3. distal acinar (paraseptal): distal part of the acini are affected
170
Q

What pulmonary function tests associated with emphysema?

A

reduced FEV1 (forced expiratory volume in 1 sec)FEV1/FVC (forced vital capacity)=FEV1% ratio

171
Q

What is emphysema?

A

chronic obstructive airway disease*characterized by an abnormal permanent enlargement of air spaces distal to the non respiratory bronchioles with destruction of their walls and without obvious fibrosis

172
Q

What is chronic bronchitis?

A

inflammatory process in the larger airways with mucosal thickening from hypertrophy and hyperplasia of mucus glandsairway narrowing occurs as result of mucus gland hyper secretion and secondary to infection

173
Q

Patho of chronic bronchitis…

A

irritant produces inflammationvasodilation and edema of airway infiltration of inflammatory cells hypersecretion of mucus=>ongoing results in hypertrophy and hyperplasia of submucosal glands in the larger airways and goblet cells in the bronchi and bronchiolesimpaired airway clearance results in infectionresults in bronchiolar wall fibrosis from inflammation

174
Q

Clinical manifestations of chronic bronchitis…

A

*productive cough, thick purulent sputum, wheezes/crackles, hypoxemia, *increased Reid index

175
Q

What is a normal Reid index?

A

*ratio of the submucosal gland layer thickness to the bronchial wall (normal <0.4)indicates chronic bronchitis

176
Q

What are the pulmonary function values associated with chronic bronchitis?

A

increased RVdecreased expiratory flow Reduced FEV1 and FEV1/FVC (FEV1% ratio)

177
Q

Etiology of asthma…

A
  1. atopic: genetic predisposition to type I hypersensitivity or atophy usually begins in childhoodfamily hx2. non atopic:pulmonary infection/viruses, environmental, stress or exercise
178
Q

What is asthma?

A

chronic inflammatory disorder characterized by chronic bronchial inflammation, bronchial hyperreactivity and bronchial smooth muscle cell hypertrophy leading to intermittent and reversible obstruction

179
Q

Patho of atopic sensitization of asthma…

A

inflammatory response stimulates Th2 to secrete IL4 and IL 5 and IL 13IL4->Bcells produce IgEIL5->activates eosinophilsIL13->stimulates mucous production=>acute response lasts 10-15 minutes to 60 minutes as the mast cells on the resp mucosal surface are activated to release histamine, PAF (platelet activating factor), and AA=>these substances are metabolized to produce protsaglandins and leukotrienes->this opens intercellular junctions allowing penetration of antigen to mucosal mast cells=>vasodilation and increased permeability results from activation of more mast cells stimulating autonomic receptors that results in bronchoconstriction and edema=>smooth muscle contraction from activation of vagal nerve receptors and release of leukotrienes and recruitment of additional inflammatory cells =>late phase lasts 2-24 hours brining eosinophils that injure bronchial and bronchiolar epithelium->enhances penetration of antigen to submucosal mast cells and cytokines are secreted that stimulate growth and activation of mast cells, eosinophils, more leukocytes, promotion of IgE production in B cells and proliferation of smooth muscle

180
Q

What is the V/Q ratio of asthma?

A

low V/Q ratio

181
Q

What are the pulmonary function test values in asthma?

A

during active attacks: increased RV, increased TLC, reduced FEV1 and FEV1/FVCBronchial hyperresponsiveness test: 20% decrease in FEV1 in response to provoking factor and 20% increase in FEV1 to response to a bronchodilator

182
Q

What is pleural effusion?

A

type of restrictive pulmonary problem*excess liquid (greater than 15 cc) in pleural space makes it difficult to set up pressure gradient for inspiration1. transudate: high fluidity less protein than exudate2. exudate: higher amounts of protein and cells in effusion than transudate3. hemothorax: blood in pleural space4. chylothorax: lymphatic drainage in pleural space5. emphysema: pus in pleural space

183
Q

What happens when there is air in the pleural space?

A

pneumothorax: creates a positive pressure in pleural space restricting air from coming in=> collapse lung

184
Q

What are the key manifestation in restrictive pulmonary diseases?

A

SOB, chest paindecreased chest movement on effected sidedecreased normal breath sounds on effected sidepleural friction rub

185
Q

Patho of interstitial lung disease…

A

injury=>infiltration of inflammatory cells and production of fibrous tissue leads to reduced compliance and hypoxiaactivation of leukocytes accumulate within the alveolar walls and spaces releasing pro-inflammatory cytokinesleukocytes secrete protease that injure cells and degrade connective tissueformation of free radicals injure cells and macrophages activate fibroblasts/proliferationtype I cells are damaged and apoptise and type II take their place which decreases surfactant production thus resulting in increased inflammatory cell recruitment and secretion of fibrogenic cytokines=>widespread fibrosis, vascular injury, non-uniform alveolar distortion and destruction, decreased lung compliance and increased lung elastic recoil

186
Q

What happens to type I and type II cells in interstitial lung disease?

A

type I epithelial cells are injured and results in release of cytokines and TGF-B1 that induces fibroblastic and myofibroblastic proliferationthey are then apoptised and type II cells replace themtype II cells now change and decrease producing surfactant and try to maintain structure of alveoli. the decrease in surfactant results in=recruitment of inflammatory cells, secretion of fibrogenic cytokines

187
Q

What happens when their is increased proliferation of fibroblasts?

A

increased collagen and elastin deposition

188
Q

What are the pulmonary function test values with interstitial lung disease?

A

decreased TLC, FVC, RVnormal or increased FEV1/FVC

189
Q

Types of atelectasis…

A
  1. reabsorption atelectasis from airway obstruction2. compression atelectasis from external pressure created by fluid, blood, air, tumors, within the pleural/thoracic cavity or by abd content3. contraction atelectasis from fibrotic changes/increased elastic coil
190
Q

What is pulmonary edema?

A

excess fluid in the extravascular space of the lungEtiology:increased pulmonary after and capillary hydrostatic pressuresdecreased plasma colloid oncotic pressure (Starling’s Law)increased pulmonary capillary endothelial permeabilityincreased alveolar epithelium permeability*reduced lymphatic clearance

191
Q

What is Starling’s Law of the capillaries?

A

flow of fluid moves form plasma into interstitial then pack to plasma at venal end and remaining fluid is absorbed by the lymphatics 1. capillary hydrostatic pressure and interstitial oncotic pressure forcing fluid out of capillaries while interstitial hydrostatic pressure and capillary oncotic pressure are pulling fluid in

192
Q

What are the stages of accumulation in pulmonary edema?

A

*increased interstitial fluid and pressure *altered alveolar epithelial permeability because of this pressure fluid accumulates in alveolisurfactant disrupted(fluid accumulates in the basal regions initially because of hydrostatic pressure is greater in these sites)

193
Q

Patho of RDS…

A

Pathway 1. circulating toxins and systemic shock cause damage to capillary endothelium; increases permeability of capillaries; fluids and proteins and blood cells leak into the pulmonary interstitium and alveoliPathway 2. inhaled toxins cause alveolar epithelium damage; fluids, proteins and blood cells leak into the pulmonary interstitium into the alveoli and results in alveolar floodinginflammation-neutrophils/macs-ROS-proteases-cytokines-fibroblast activitydamage to type I and II cells-loss of surfactanthyaline membrane formation(fibrin rich edema fluid mixed with necrotic epithelial cells)diffuse interstitital and intra-alveolar fibrosis

194
Q

What is the red heaptization/consolidation and the gray hepatization that occurs in pneumonia?

A

red hepatozation/consolidation: alveoli fill with red blood cells, leukocytes, fibrin, edematous fluid, other exudatesred cell lysis/disintegration, persistence of finbrinosuppurative exudate in the consolidated alveoli

195
Q

What occurs in pneumonia?

A

infection of the lung with accumulation of inflammatory exudate in airways/alveoliIn acute-community acquired: inflammatory response extends to alveoli but is confined to the alveolar septa and pulmonary interstitial; the alveolar septa become widened, edematous, and infiltrated with inflammatory cells

196
Q

Patho of TB…

A

deposition o the TB in upper lobes, replication with inflammatory response, endocytosis by macs, *CD4 differentiate to Th1 and Th2 Th1 secrete IFN cytokine that activates macsmacs express iNOS (oxidative destruction), ROS (antibacterial effect) secrete TNF (recruits more monocytes)

197
Q

What occur at first with the TB infection and macrophages?

A

macs are unable to kill initially because the bacteria are able to stop them through endosomal arrest

198
Q

What are the commonly deleted or inactivated tumor suppressor genes in lung carcinoma?

A

p53, 3p, (both small and non small cell CA) RB mutation (small cell CA) , p16 (non small cell CA),

199
Q

Lung Carcinoma

A
  1. squamous cell : more central bronchi, spread locally, 2. adenocarcinoma: glandular epthelium-bronchial derived or bronchiolo-alveolar; grow slowly and from smaller masses and tend to metastasize quickly3. small cell: derived from neuorendocrine cells4. large cell: undifferentiated, larger cell and nuclei

Adv Patho (11 decks)

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