Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

cardiovasc > cv 2 > Flashcards

cv 2 Flashcards

1
Q

stroke mechanism

A

atheroembolization from carotid birfucation lesion (below jaw)

OR

thromboembolization from left atrial appendage in a-fib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MI mechanism

A

plaque rupture from a non-occlusive thrombosis -> occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

DVT, PE mechanisms

A

venous thromboembolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Venous vs Arterial thrombi

A

venous: fibrin rich, areas of stasis, env+genetic predispositions TX: Anticoag
arterial: platelet rich, areas of high flow, atheroscerlosis/anti-phospholipid Abs/trauma, TX: Antiplatelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Peripheral arterial dz mechanism

A

claudication: stable plaque with >70% diameter reduction

acute limb ischemia: obstructs blood flow w/o prior development of collateral flow, can be atheroembol or thromboembol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Vasospastic disorders

A

Raynauds, pernio; causes dysfxnal endothelium contributing to start of thrombus :(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

N.O formed from

A

L-arginine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CK-MB rise, peak, fall

A

4-6 hrs, 18 hrs, 2-4 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

C-Troponin I rise, peak, fall

A

4-6 hrs, 12 hrs, 3-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

C-Troponin T rise, peak, fall

A

4-6 hrs, 12-48 hrs, 7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acute Coronary syndrome can be one of these 3

A

UA, NSTEMI, STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

does unstable angina present with biomarkers?

A

no you fuckin nerd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Agitated saline/microbubbles purpose

A

use with echo to determine if there’s a shunt - inject into vein, should only see it go into RIGHT side of heart as it should be breathed out, if seen in left you got problems homie

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

pharmacologic stress test chemicals

A

dobutamine/dipyridamole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when is a stress test have good Dx value, vs bad Dx value?

A

Good: Left main or 3 vessel coronary artery dz

bad: 2 or 1 vessel CAD (and then its better if LAD>RCA>CIRC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is M mode

A

records movement of heart muscle on a 2D axis in an echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

is RA, RV more anterior or posterior

A

anterior, left side is more posterior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

pt is sensitive to radiation, what imaging test should you order

A

MRI, dweeb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ANP vs BNP vs CNP

A

ANP in atria, 28 AA

BNP in ventricles, 32 AA released with stretch (correlates with LVEDV+P; can be ^ in renal insuff and old, women
-GOOD NEGATIVE predictive value

CNP in endothelium, 53 or 22 AA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why would troponin remain elevated, even in HF

A

renal failure - cleared by kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

at what level of stenosis do you get Sx

A

> 70% diameter reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

at what level of stenosis do you become unstable

A

> 90% diameter reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

mechanism of reperfusion injury

A

blood flow restored after ischemia, typically hemorrhagic because you’re pushing blood back through damaged microvasculature ya goofball; so will get accel. infl. and fibrosis
(as well as get mitochondrial dysfxn, myofibril hypercontracture, cytoskeletal dmg, cell death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what’s the R coronary supply

A

posterior LV, septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what’s the L circumflex supply

A

lateral LV wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

CHANGES IN MI:

0-30 min:
1-2 hrs:
4-12 hrs:
18-24 hrs: 
24-72 hrs: 
4-7 days: 
10 days:
4-8 weeks:
A

0-30 min: REVERSIBLE changes, structural and biochemical

1-2 hrs: irreversible - swollen mitochondria, release of intracellular proteins

4-12 hrs: wavy fibers - (You should have no trouble telling these heart fibers are dead, because the nuclei are gone. The extra-dark pink staining of the cytoplasm also indicates necrosis. As the still-beating live heart pulls at the dead portion, it makes some of the fibers crumpled or “wavy”)

18-24 hrs: coag necrosis, neutrophilic infiltrate, dark discoloration -> worry about damage to nodal tissue/creation of arrhythymias

24-72 hrs: maximum neutrophil infiltrate, yellow pallor

4-7 days: macrophages w/ disintegration of necrotic myocytes

10 days: granulation tissue with many blood vessels, plump fibroblasts, collagen

4-8 weeks: fibrosis - worry about this because it’s weaker than the wall of myocardian, can rupture/aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Htn causes __ hypertrophy

A

concentric (pressure overload), sarcomeres added in parallel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Pulm htn often due to

A

COPD. less often CF, chest disorders kyphoscoliosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Aneurysms are

A

weakening of vessel wall -> dilation of vessel wall, due to systemic dz (vasculitis), developmental (berrry aneurysm); infxn, congenital (Marfans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Berry aneurysms

A

congenital defects in tunica media at bifurcation of cerebral vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Aortic dissection

A

intimal tear of aorta, followed by blood dissects into media
blood can then dissect back into lumen (double-barrel aorta), or pericardial sac (tamponade)

32
Q

Medium vessel vasculites (Chapel Hill classification)

A

Polyarteritis Nodosa: kidneys, GI, heart. P-ANCA

Kawasaki’s: coronary arteries, young Asians

33
Q

Small vessel vasculites (Chapel Hill classification)

A

Wegener’s granulomatosis: idiopathic, upper+lower resp. tracts and kidneys. C-ANCA

Churg-strauss - asthma+eosinophilia, mostly in lungs

Leukocytoclastic/hypersenstivitiy: drugs, infxns

34
Q

Large vessel vasculitis (Chapel Hill classification)

A

Giant cell/temporal arteritis: segmental chronic granulomatous vasculitis of temporal A., +/- opthalmic A.

35
Q

Heparin

A

binds AT III to inhibit 2, 9, 10, 11, 12, 13; IV or SC, avoid IM, monitor with aPTT. bleeding, hard on thrombocytopenics

USE: prevent hypercoagulability following vasc. injury/venous stasis, can be adjunct in Tx of coronary occlusion in UA/acute MI

faster than LWMH, safer for renal insuff. (reticuloendothelial elim.)

36
Q

LWMH (Enoxaprin)

A

bind AT III to inhibit 10 only; IV or SC, avoid IM, no monitoring. bleeding, less bad on thrombocytopenics

longer acting than heparin and less variable response, less thrombocytopenia, first order renal elim.

37
Q

Fondaparinux

A

binds AT III to inhibit 10 only; SC, NO thrombocytopenia, renal elim.

38
Q

Protamine

A

reversal of Heparin; incomplete reversal of LWMH (Enoxaparin)

39
Q

Warfarin/Coumadin

A

blocks liver synthesis of vit-K -> no gamma-carboxylation so blocks 2, 7, 9, 10, C, S (note that C has shortest t1/2 so get early PROcoag effect)

USE: a-fib, prophylaxis of venous thromboembolism

Oral OD, 99% protein bound, CYP450 met.

monitor with aPTT, see max effect in 3-5 days. if INR creeps up, administer vit K orally, if major bleed, give vit K IV, and stop that shit

gotta worry about Abx (kill vit K microorganisms), ASA, avoid in preg.

40
Q

Dabigatran

A

direct inhibition of Da Big one, thrombin/factor 2

USE: lower risk of stroke and systemic embolism in patients w/ non-valve a-fib

(poor, polar prodrug) Oral BID, renally dose, needs dessicant container

reversal w/ Praxbind

no monitoring really, can monitor w/ ECT but expensive and hard to find

faster than warfarin

41
Q

Rivaroxaban/Xarelto, Apixaban/Eliquis, Edoxaban/Savaysa

A

Direct factor 10 inhibitors (Xa is in the name)

USE: lower risk of stroke, systemic embolism in pt w/ non-valve a-fib

Oral, renally dose Edoxaban, CYP3A4 Rivaroxaban

no reversal agent, no monitoring at all, shorter-acting than warfarin

42
Q

ASA

A

Irreversibly inhibit COX1 so less TXA2 is made, biggest effect on circulating platelets as opposed to tissue endothelials

USE: STEMI, UA/NSTEMI, PCI, secondary prevention of MI or stroke

Antiplatelet agent. Oral. care for GI bleed, N/V

43
Q

Clopidogrel/Plavix, Ticagrelor, other -grel names

A

Irreversible inhibit platelet ADP receptor to block aggregation

USE: STEMI, NSTEMI, PCI, all w/ ASA

Plavix is Oral OD, CYP450 met: Avoid if pt. taking PPIs as PPIs block Plavix

Ticagrelor is NOT CYP450 and is reversible inhibition, but Oral BID

44
Q

Dipyridamole

A

Inhibits phosophodiesterase -> increased cAMP levels -> better anti-agg effects of PGI2

USE: secondary prevention of ischemic stroke w/ ASA

Oral TID

45
Q

Abciximab (human monoclonal antibody), Tirofiban (non-peptide)

A

GPIIb/IIIa receptor antagonists on platelets, blocking all platelet aggregation, most legit blocking

USE: PCI w/ ASA + ADP antag

IV

46
Q

Alteplase, Reteplase, Tenectaplase

A

All activate plasmin via tPA activation (t,p,a is in name)

Alteplase is selective for EXISTING clots (All teh clots)

USE: Acute MI - prompt use with adjunctive drugs (Betas, ACEI, ASA), as well as DVT, pulm. emboli

47
Q

Friedewald formula (calculate LDL)

A

LDL = total chol. - HDL - (TG/5)

TG/5 is estimate for vLDL, but only if TG

48
Q

average LDL

A

130 mg/dL, though majority of CHD occurs in pt. around here, though increasing does increase risk

49
Q

Exogenous lipoprotein

A

eat fat, intestines package to chylomicron w/ B-48, goes to lymph then vasc., fat gets hydrolyzed by lipoprotein lipase
Free fatty acid goes to use/storage, chylomicron remant recycled by liver into bile

50
Q

Endogenous lipoprotein

A

liver packages chol + TGs into vLDL, HDL turns into triglycerides and FFAs (use+strorage), becomes intermediate density LP which looks like chylomicron remnant and some goes to liver while the rest has lipoprotein lipase turn it into LDL w/ B-100, goes to LDL receptor at liver

51
Q

HDL metabolism

A

nascent HDL (no lipids) adds cholesterol ester to become mature HDL, either goes to liver OR CETP transfers cholesterol + triglycerides to LDL which is cleared DIFFERENTLY than via LDL receptor

52
Q

decreasing preload and decreasing afterload will change…

A

preload will increase diastolic filling (less pressure against walls, less compression of veins),; afterload decreases O2 demand

53
Q

Tx of stable angina (vasodilators)

A

beta-blockers, nitrates, Ca++ channel blockers (decrease demand)

54
Q

Tx of unstable angina (vasodilators)

A

antithrombotics first, beta-blockers, nitrates, Ca++ channel blockers (decrease demand and increase supply)

55
Q

Tx of variant angina (eg caused by Raynauds)

A

Ca++ channel blockers, nitrates (prevent vasospasm)

56
Q

Nitrates

A

NO -> PKG -> guanylate cyclase -> increase cGMP -> increase myosin LC phosphatase activity -> myocyte relaxation; mostly venous

USE: acute angina, prophylaxis for stable angina

sublingual, but poor oral

isosorbide = chronic; nitroglycerin stat = acute

Adverse rxn: extension of vasodilation, so headaches, orthostatic hypotension, flushing, and CAN build tolerance - so intermittent period is necessary

57
Q

Ca++ channel blockers

Verapimil, Diltiazem, Nifedipine

A

block L-types in cardiac or VSMCs, decreasing vasoconstriction (mostly arteriole) and inotrophy, HR

Nifedipine (DHPR) is most VSMC selective and most vasodilation, though can cause reflex tachycardia via activation of sympathetic baroreceptors

Diltiazem is next most VSMC selective, Verapimil is least, and most selective for myocytes

USE: vasospastic angina, stable angina

Adverse rxn: cardiac depression (bradycardia, CHF) - less likely with DHPR due to selectivity, hypotension, edema, flushing

58
Q

Ranolazine/Ranexa

A

Inhibits late Na+ current which prevents NCX from exchanging more Ca++ in and prevents Ca++ overload - often happens in ischemia

USE: ischemia or hypertrophy ONLY, no vasodilatory effect

P-glycoprotein substrate, CYP3A4 met.

Adverse rxn: can prolong QT interval because inhibits phase 3 K+ outward current

59
Q

Beta blockers (-olol)

B1: metoprolol, atenolol (at lower doses is selective)

B1, B2: propanolol (pro: was before the good shit)

A

Blocks B1 in heart (vs B2 in lung, blood vessels), decreasing HR, inotropy and thus O2 demand, no vasodilatory at all

USE: first-line for stable angina

AVOID: asthma, peripheral vasc dz, bradycardia

Adverse rxn: abrupt withdrawal can cause oversympathetic activity

60
Q

4 scenarios for statin Tx indication

A
  1. PT w/ known clinical ASCVD (prev MI, TIA, angina)
  2. LDL > 190 mg/dL (recall avg is 130)
  3. PT w/ DM, age>40, LDL>70
  4. 10 yr. ASCVD risk >7.5% (det. by M>F, age, race, total chol, BP, DM, smoker)

Moderate risk? get into FHx, CRP (>2), LDL>160, coronary calcium score

61
Q

atheroprotective diets

A

DASH diet, mediterranean diet (more veg, fruit, whole grains, less fats)

62
Q

aPTT measures + NL values

A

intrinsic pathway; NL is 25-35 sec

63
Q

PT measures + NL values

A

extrinsic pathway; NL is 10-15 sec

64
Q

INR is

A

(Pt. PT/mean NL PT) ^ some number

65
Q

Thrombin Time

A

measures thrombin inhibition, used to measure Dabigatran toxicity

66
Q

Fatty streak formation

A

damaged endothelium can’t keep shit out so LDL accumulates in the INTIMA, apolipoprotein B gets oxidized and monocytes are recruited, become macrophages, phagocytose LDL, they lose mobility and as they eat more and more LDL via a mutated receptor mechanism (not the normal way they do things), they become foam cells in the intima

67
Q

Fibrous plaque formation

A

Foam cells, platelets, and epi cells release growth factors which cause smooth muscle and fibroblasts to move in and grow; smooth muscle deposits connective tissue

68
Q

Plaque progression

A

Plaque grows and central region becomes necrotic as all this infl. shit accumulates, while the fibrous cap is chilling. as it grows can occlude artery, and can rupture (esp. if calcified) via stressors, releasing it’s pro-infl. factors and causing thrombus, or can even be reabsorbed into intima to form bigger plaque

69
Q

Stable vs. Vulnerable Plaque

A

Stable will have a thick fibrous cap, calcified, low lipid content, and less infl. content, less apoptosis.
Vulnerable is the exact opposite…

Plaques often form in the abdominal aorta

70
Q

Normal endothelium provides

A

Protective surface with anti-inflammatory and anti-thrombogenic qualities

71
Q

Familial hypercholesterolemia

A

mutated LDL receptor causes increased LDL in blood

72
Q

Cardiac supply determined by:

A

prevent hypotension (maintain diastolic perfusion pressure)
increase diastolic time (slow rate)
decrease coronary resistance (vasodilate)
increase O2 content (Tx anemia, hypoxemia)

73
Q

Cardiac demand determined by:

A

lower systolic BP (lower need for work)
lower heart rate
lower wall tension (decrease preload) T=(Pr)/(wall thickness)
lower inotropy

74
Q

Most important mechanism for coronary vasoregulation

A

Autoregulation: dilate to increase blood flow or constrict to decrease, mainly via local metabolites (adenosine)

75
Q

The heart receives blood during

A

diastole you fuckin lamer

76
Q

When doing an angiography, you stick two catheters in, one in front of the stenosis and one past it, and then you dilate resistance vessels with

A

adenosine. R=(nL)/r^4

cardiovasc (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions