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Cardiovascular 3 > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

What is the 3 step pathogenesis to cause acute coronary syndromes (ACS)?

A

Unstable angina –> MI –> irreversible heart necrosis

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2
Q

What type of occlusion can cause a NSTEMI and NQMI?

A

Partial occlusive thrombus

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3
Q

Unlike unstable angina, what happens to the myocardium in a NSTEMI?

A

myocardial necrosis

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4
Q

So what type of occlusion leads to a STEMI or QwMI?

A

complete obstruction of coronary artery –> severe ischemia and necrosis

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5
Q

Which 2 important intrinsic chemical substances can cause plaque disruption, leading to rupture?

A

g-interferon, MMP

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6
Q

What is the main physical stress which can lead to plaque rupture?

A

BP

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7
Q

In atherosclerosis, there can be decreased amounts of NO and prostacyclin, which leads to what abnormality of the vessel?

A

Loss of vasodilation.

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8
Q

What 2 chemicals can over-run the vasodilators, causing a contractile events in endothelial dysfxn?

A

Thromboxane and serotonin

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9
Q

If you find a pt with ST depression and/or T-wave inversion, what can u use to differentiate a NSTEMI and unstable angina?

A

Serum biomarkers

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10
Q

Where do the serum markers come from to Dx a NSTEMI and STEMI?

A

Myocytes. They’re damaged so they leak em out.

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11
Q

These markers are absent in a healthy person, so detection of these markers is specific for myocyte damage.

A

Troponins (TnC, TnI)

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12
Q

When is the onset to serum troponin markers after MI?

A

they rise after 3-4 hours

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13
Q

When is the peak of serum troponin markers in an MI?

A

18-36 hours

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14
Q

This is the form of creatine kinase that is used as a cardiac marker for MI’s.

A

CK-MB

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15
Q

Besides the heart, where else in the body can u find CK-MB?

A

Small amts in the uterus, prostate, gut, diaphragm, and tongue.

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16
Q

In MI, how much greater is the CK-MB than the CK?

A

> 2.5%

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17
Q

When is the rise, peak, and return to normal for CK-MB during an MI?

A

rise 3-6 hours
peak at 24
fall to normal from 48-72 hours

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18
Q

What are the 3 drugs you can give to the potential STEMI/NSTEMI/UA patient to prevent ischemia?

A

B-blocker, Nitrates, +- Ca++ channel blocker

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19
Q

If a STEMI patient comes into ER, if you can’t do an emergent PCI within 90 minutes, what type of drug therapy should you give?

A

Fibrinolytic therapy

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20
Q

What is the score to asses risk in UA and NSTEMI?

A

TIMI score

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21
Q

If the UA or NSTEMI ranks high on the TIMI score, what is the appropriate management?

A

Invasive therapy (PCI or CABG)

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22
Q

Bradycardia, bronchospasm, decompensated HF, and hypoTN are contraindications to which drug that reduces the sympathetic drive of the heart?

A

B-blockers

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23
Q

If B-blockers and nitrates don’t work, which class of drugs can you give to prevent ischemia by decreasing HR and contractility?

A

CCB

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24
Q

Which antithrombolytic is given with aspirin to block the P2Y12 ADP receptor to reduce CV mortality, recurrent cardiac events, and strokes?

A

Clipidogrel

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25
Q

Which thieopyridine deriviative also blocks the P2Y12 ADP receptor to further reduce coronary events in ACS pts who undergo PCI?

A

Plasurgel

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26
Q

Abciximab, eptifibate and tirofiban are of which class of drugs that blocks the final common pathway of platelet aggregation to decrease adverse coronary events in pts undergoing PCI?

A

Glycoprotein IIb/IIIa receptor antagonists

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27
Q

This anticoagulant binds to antithrombin, which increases the potency of the plasma protein in the inactivation of the clotting forming thrombin.

A

UFH

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28
Q

How do u measure the dose adjustments when using UFH?

A

aPTT

test question lol

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29
Q

This anticoagulant interacts with antithrombin but prefers to inhibit coagulation factor Xa, is more predictible than UFH, and given via 1 or 2 subQ injections (rahter than IV).

A

LMWH (like enoxapirin)

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30
Q

This anticoagulant also blocks factor Xa but has less bleeding complications than LMWH.

A

Fondaparinux

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31
Q

This anticoagulant is a direct thrombin inhibitor and has superior clinical outcomes compared to the combo of UFH + GP IIb/IIIa receptor blocker.

A

Bivalarudin

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32
Q

How many of these factors must you have to begin antithrombolytic therapy?

a. Age >65 y/o
b. > 3 risk factors for CAD
c. Known coronary stenosis of >50% by prior angiography
d. ST segment deviations of the ECG at presentation
e. At least 2 anginal episodes in prior 24 hrs
f. Use of aspirin in prior 7 days
g. Elevated serum troponin or CK-MB

A

3

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33
Q

So if a pt comes into the ER with a total coronary artery occlusion and a STEMI, you give drugs like ASA, UFH, B-blockers, and nitrates, but that doesn’t actually treat the condition- it just stalls it. Which class of drugs must you give to treat the thrumbus to reperfuse the heart?

A

Fibrinolytics

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34
Q

This class of fibrinolytics work by stimualting the natural fibrinolytic system of the body, which transforms the inactive plasminogen into plasmin, which lyses fibrin clots.

A

tissue-type Plasminogen activators

35
Q

So if you give a fibronolytic (like t-PA) within 2 hours of STEMI Sx, what is the % decrease in mortality compared to those who receive it 6 hours later?

A

50%

36
Q

Boom. You give the t-PA. Sx disappear, ST segments go back to baseline, markers peak earlier than normally. How can you prevent immediate vessel reocclusion?

A

Antithrombotics (ASA, UFH or LMWH, and clopidogrel)

37
Q

Obviously t-PA can cause a lot of bleeding. Which pt’s is t-PA a contraindication?

A

PUD, bleeding disorders, recent stroke, recovering from recent surgery

38
Q

If you have the access, what is the alternative therapy to fibrinolytics to treat pts with acute STEMIs?

A

PCI

39
Q

If you can get the PCI done within 90 mins, what is the optinal flow rate of the newly opened coronary vessels?

A

95%

40
Q

True or False: the contraindications for PCI are the same as those for giving fibrinolytics.

A

True

41
Q

The most important of post-MI outcome is the extent of damage to which part of the heart?

A

LV

42
Q

What are the 4 classes of drugs u send the pt home with after they are treated for ACS?

A

ASA, B-blocker, Statin, and an ACEi (if the pt has a LV contractile dysfxn)

43
Q

True or False: episodes of V-fib that occur during the first 48 hours of MI are often related to TRANSIENT electrical activity.

A

True!

44
Q

This is the condition when blood demand to a portion of the heart is higher than the supply of oxygenated blood.

A

Ischemic Heart Disease (IHD)

45
Q

What is the main culprit in IHD?

A

Atherosclerotic plaque occluding the coronary arteries.

46
Q

True or False: IHD is the leading cause of death worldwide, killing 500k Muricans/year.

A

True

47
Q

If an atherosclerotic plaque isnt the culprit causing the narrowing of the arterial lumen, what can be the other 2 causes to cause IHD?

A

thombosis and vasospasm

48
Q

True or False: Angina is substernal recurrent chest pain that is from ischemia leading to necrosis.

A

False. It doesnt lead to necrosis.

49
Q

This type of angina is the most common, caused by exertion or stress, and relieved at rest.

A

Stable/typical

50
Q

This type of angina has a pattern of increasing frequent pain of prolonged duration with less and less exertion to trigger it.

A

Unstable/crescendo

51
Q

This type of angina is caused by coronary artery spasm and occurs at rest.

A

Prinzmetal

52
Q

This is the most important form of IHD, where there is death of cardiac muscle due to prolonged severe ischemia.

A

MI

53
Q

After what time after ischemia do the cells show myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling?

A

just 60 seconds.

Thats just nutty. Like a…. nevermind.

54
Q

However, these changes to myocytes after 60s are reversible, right?

A

Yes.

55
Q

So when does myocytes have irrversible damage after ischemia?

A

2-4 hours

56
Q

Give me 1 patient with all the risk factors for an MI. DO IT.

A

a 60 year old ham planet with a previous MI, who’s a smoker, has HTN and dyslipidemia, diabetic, lazy, stressed about being lazy, drug user, and who’s family also has a Hx of MI’s as well.

You said all that, right?

57
Q

Which one of these causes ST elevation: transmural infarcts or subendocardial infarcts

A

Transmural infarcts

Food for thought: is an “in-fart” the thing when your bowel grumbles?

58
Q

True or False: transmural infarcts are the most common form of infarct and involve the full thickness of the ventricular wall.

A

True

59
Q

How much of the wall does a subendocardial MI involve?

A

limited to inner 1/3-1/2 of ventricular wall

60
Q

Why is the subendocardial zone the most vulnerable to any reduction in coronary flow?

A

it’s one of the least perfused region of the myocardium

61
Q

This is the time span after an MI when reversible injury occurs.

A

0-0.5 hours

62
Q

This is the time span after an MI when there is no gross features, and there is viarable waviness of fibers at the border.

A

0.5-4 hours

63
Q

This is the time span after an MI when there is dark mottling of the heart, and u can see early coagulation necrosis, edema, and hemorrhage.

A

4-12 hours

64
Q

This is the time span after an MI when you see dark mottling, ongoing coagulation necrosis, pykinosis, myocyte hypereosinophilia, marginal contraction band necrosis, early neurtophilic infiltrate

A

12-24 hours

65
Q

This is the time span after an MI when there is mottling with yellow-ran infarct, coagulation necrosis with LOSS OF NUCLEI and striatins, and brisk interstitial infiltrate of neutrophils

A

1-3 days

66
Q

At 3-7 days after an MI, there is a hyperemic border with central yellow-tan softening, and what happens to the dead myocytes?

A

the dead ones disintegrate by phagocytosis from myocytes

67
Q

When does granulation tissue begin to form after an MI?

A

7-10 days

68
Q

During the 7-10 day period after an MI, there is well established granulation tissue, which brings about the appearance of what 2 things?

A
  1. new blood vessels

2. collagen deposition

69
Q

Ok so the granulation tissue is set and we’re trying to rebuild the heart, but it usually doesnt happen to like how it was. What happens during the 2-8 week span to decreased cellularity?

A

increased collagen deposition

70
Q

After what time is the scarring of the heart complete with the formation of a dense collagenous scar?

A

> 2 months

71
Q

This may be obvious, but what is the best way to limit and stop MI damage?

A

Reperfusion

72
Q

BUT WAIT. There are problems with FURTHER injurying tissue after a certain period of ischemia. When is it important to reperfuse the area after an MI?

A

before 4 hours

73
Q

This is the syndrome when the MI knocks out LV function, leading to pump failure, which has a 70% mortality rate.

A

Cardiogenic shock

74
Q

True or False: the size, area, and thickness of the infarct is DIRECTLY related to MI complications.

A

True

75
Q

This is the condition that results when the myocardium becomes soft and weak from the necrotic and inflammed destruction.

A

Myocardial rupture

literally your heart explodes lol

76
Q

Where is the most common location of myocardial rupture?

A

Ventricular free wall

77
Q

If your ventricular free wall ruptures, where does blood accumulate? What is the condition resulting from this?

A

Hemopericardium –> cardiac tamponade

Once again, if like gives you tampons, you make tamponade.

78
Q

This is a complication of an MI where fiberous or fibrohemorrhagic formations of the pericardium develops around the 2nd or 3rd day.

A

Pericarditis (dressler syndrome)

79
Q

Which other chamber can have an infarction when there is ischemic injury to the adjacent chambers?

A

RV

80
Q

True or False: infarcts can spread to adjacent tissues from weakening of the necrotic muscle.

A

True

81
Q

This is a complication of an MI when the combination of a local abnormality in contractility (causing stasis) and endocardial damage can result in a specific formation.

A

Mural thrombus

82
Q

This is a complication of an MI when the ventricals can buldge as a result of a complication of large transmural infarcts.

A

Ventricular aneurysm

83
Q

The dysfunction of these muscles is a complication of an MI, resulting in mitral regurgitation.

A

Papillary muscles

Cardiovascular 3 (8 decks)

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