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Clin Pathology > Cardiology part 2 slide 173-287 > Flashcards

Cardiology part 2 slide 173-287 Flashcards

1
Q

what is the most common symptom assoc. with CAD

A

CP

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2
Q

if pain only occurs with exertion and is stable over a period of time is classified as

A

Stable angina

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3
Q

if chest pain occurs at rest this is known as

A

unstable angina

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4
Q

if cp persists without interruption for prolonged periods and irreversible myocyte damage has occurred is indicative of

A

myocardial infarction

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5
Q

does chest pain worsen with deep breath?

A

no

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6
Q

CAD can be assoc. with what other symptoms?

A

sob, diaphoresis, n/v

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7
Q

what is the etiology of CAD (4)

which is most common?

A

atherosclerosis***, spasm, emboli, congenital

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8
Q

the heart is responsible for what percentage of the body’s resting oxygen consumption?

A

7%

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9
Q

what occurs when there is either increased demand for oxygen relative to maximal arterial supply or an absolute reduction in oxygen supply

A

cellular ischemia

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10
Q

fatty streaks in arterial walls are found mainly in areas exposed to increased ______ ____ like bending points and bifurcations and are thought to arise from _____________________

A

shear stress;

isolated macrophage foam cell

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11
Q

which cells regenerate (remodel) to re-cover the exposed intima

A

endothelial cells

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12
Q

at rest, pt have ischemia due to arterial lumen decreasing to what percentage?
what about during exercise?

A

90% at rest

50% with exercise

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13
Q

what causes plt accumulation and occlusion? and how long can these episodes last?

A

fissuring of the atherosclerotic plaque

-10-20 min

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14
Q

what has an important role in clinical presentation for artheroscleorsis??

A

plaque composition mediated by inflammation*

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15
Q

how many seconds does it take for cells to fall to zero after coronary artery occlusion?

A

60 seconds

the longer the worse

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16
Q

what occurs within seconds even BEFORE depletion of high energy phosphates occur

A

dysfxn of myocardial relaxation and contraction

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17
Q

how long does it take for an inerreversible injury to occur if perfusion is not restored

A

40-60 min

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18
Q

which vasoconstrictive factors release cause vasoconstriction and decrease flow?

A

thromboxane A, or serotonin

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19
Q

explained “stunned” myocardium

A

ischemia after 1 hr taking 1 month to restore ventricular function

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20
Q

what is the live vest vs AICD implantation

A

life vest would be after a stunned myocardium to monitor heart, after 3 months check it and if ef when up to 60-65% then it can be taken off
aicd implan- I think if its when tissue of affected area does not go back to normal and need defib to monitor heart

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21
Q

what is the actual trigger for nerve stimulation seen in chest pain

A

adenosine

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22
Q

chest pain that worsens with deep inspiration is indicative of

A

pericarditis

due to inflammation in pericardium

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23
Q

what is the pericarditis sound

A

friction rub “to and fro” and high pitched squeaking sound

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24
Q

continual inflammation of the pericardium leads to fibrosis and development of ______ pericarditis

A

constrictive pericarditis

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25
Q

define kussmaul sign

A

inappropriate increase in the RAP and jugular venous pulsation level with inspiration

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26
Q

what are etiologies of pericarditis

A

infections, collagen vascular disease, neoplasm, metabolic, injury, idipathic

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27
Q

deposition of calcium in pericarditis indicates

A

scarring

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28
Q

where is “to and fro” rub most commonly heard? and why

A

in CP with pericarditis

- diastolic components merge, between visceral and parietal pericardial

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29
Q

what occurs during the filling of the ventricles in pericarditis known as a diastolic knock?

A

early filling occurs but the filling suddenly stops by the non elastic thickened pericardium makes v wave more prominent on ekg

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30
Q

during pericarditis, does the systemic venous pressure increase or decrease

A

INCREASES bc blood entering heart is limited so increasing RA pressure

Normally: inspiration there’s a decrease in pressure to allow filling
bUT this is prevented due to the inflammation

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31
Q

pericardial effusion and tamponade define

A

too much fluid in pericardial space

- sudden filling of heart limits ventricular filling (tamponade)

32
Q

what are the Becks Triad

what dz has this

A
  • hypotension
  • elevated JVP
  • muffled heart sounds
  • pericardial effusion and temponade
33
Q

what causes pericardial effusion

A

any cause of pericarditis

34
Q

what are the names of the layers of the arterial vessels and what are they made up of

A

adventitia- outer layer of connective tissue
media- middle layer of smooth muscle
intima- containing the layer of endothelial cells

35
Q

resistance vessels vs capacitance vessels

A

resistance vessels: arteries

capacitance: venues and veins–> walls distend

36
Q

what is the smooth muscle surrounding the capillary openings called

A

precapillary sphincters

37
Q

arterioles is to ___ as veins is to oncotic

A

hydrostatic

38
Q

prostacyclin is produced by ___ and thromboxane A2 is produced by ____

A
  • endothelial cells

thrombi: platelets

39
Q

prostacyclin promotes ____ where as thromboxane causes plt aggregation and vasoconstriction

A

vasodilation

40
Q

nitric oxide is a potent ___

A

dilator

41
Q

NO produces cGMP which in turn mediates ____

A

relaxation of vascular smooth muscle –> vasodilation

42
Q

due to vasodilation from NO, it leads to ___

A

hyperemia

43
Q

what is the most potent vasoconstrictor

A

endothelia-1 ET1

44
Q

what are the principal vasoconstrictors vs principal vasodilators

A

constrict: norepinephrine and epi
dilators: vasoactive peptide, kinins, natriuretic peptides

45
Q

what are bradykinin and Lysyl-bradykinin

A

vasodilators

46
Q

what type of vasodilator is used as a marker to see if there’s an improvement of Heart Failure after natriuresis

A

BNP- brain natriuretic peptide

— if bnp levels are elevated its consisted with HF so if it shows that it is going down then less likely to have HF

47
Q

a discharge of noradrenergic vasomotor nerves lead to ___ of BP and inhibits effect of ____ stimulation which ____ CO

A

inc

vagal; dec

48
Q

C-reactive protein are a marker for ____

A

inflammation or plaques

49
Q

whenever you see foam cells think ____

A

LDL - fatty streaks

50
Q

explain pathogenesis of atherosclerosis in terms of foam cells, endothelial, and thrombosis

A

smooth –> foam –> endothelial cells (plaque) –> rupture –> pltl aggrgt –> block blood flow (thrombosis)

51
Q

chylomicrons

A

protein coat of cholesterol and triglycerides in intestinal epithelial cells

52
Q

thrombotic strokes are due to

A

blockage of cerebral circulation

53
Q

intermittent claudication is seen in

A

circulation of legs –> pain and fatigue when walking

54
Q

where do you see frank gangrene

A

in extremities in atherosclerosis

55
Q

what main body parts do clot formation and obstruction occur

A

brain, kidney, heart

56
Q

how is progression of atherosclerosis less rapid in premenopausal women than in men

A

ESTROGEN- increases cholesterol removal

57
Q

homocysteine levels are associated with

A

accelerated atherosclerosis / inflammation

58
Q

diabetes, smoking, nephrotic syndrome, and hypothyroidism is seen in acceleration of

A

atherosclerosis

59
Q

is HTN a syndrome or disease

A

syndrome

60
Q

renal artery constriction increases blood pressure which in turn activates —-

A

RAS system - false HTN

its really due to the obstruction of blood flow

61
Q

pill HTN

A

normally renin secretion is dcreased to compensate but this compensation is inadequate and BP is high

62
Q

conns disease ( hyperaldosteronism)

A

tumor in adrenal that secretes large amounts of aldosterone aka Na retention and inc fluid and HTN

63
Q

pheochromocytoma- excess secretion of catecholamines leads to

A

increase secretion of norepinephrine and inc pressure

64
Q

three main causes of HTN

A

sugar, cholesterol, BP, and diet and smoking play a role

65
Q

**which type of shock causes warmth of the skin

A

Distributive Shock due to vasodilation***

66
Q

hypovolemic shock

A

inadequate volume to fill vascular system — stab wound loosing blood like crazy

67
Q

distributive shock (3 types)

A
  • anaphylactic (allergies)
  • neurogenic (head and spine injuries, loss of activity)
  • septic shock
68
Q

cariogenic shock

A

inadequate pumping of the heart – usually LV infarct

69
Q

obstructive shock

A

Pumonary/vascular

-right sided heart failure –> PE, pulm HTN

70
Q

virchows triad seen in thrombosis

A
  • endothelial damage (Abnl vessel wall)
  • abnl blood flow
  • inc coag of blood
71
Q

canalization

A

new lumen form within the thrombus

72
Q

embolization

A

part of thrombus becomes dislodged and travels distal to site of formation and can produce obstruction

73
Q

thromboembolism from left side of heart vs right side of heart

A

left side: stroke (goes to aorta to cerebral artery)

right side: PE (DVT to right side to pulmonary)

74
Q

Deep Vein Thrombosis location and etiology and S&S

A

begin in the lower extremities and pelvis
etiology: virchows triad
S&S: edema, heat to site, Homan’s sign

75
Q

etiology of Peripheral apertural disease (PAD)

A

atherosclerosis

76
Q

6 Ps in PAD

A 
pain
pallor
pulselessness
paresthesia's
poikilothermic
paralysis

Clin Pathology (8 decks)

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