Brainscape's Knowledge GenomeTM

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


See full index

Cardiology > Lectures 23-24: Acute Coronary Syndrome > Flashcards

Lectures 23-24: Acute Coronary Syndrome Flashcards

1
Q

Critical parts of coagulation cascade

A

Tissue factor liberated due to plaque rupture + Factor VII –> Factor Xa, turns prothrombin –> thrombin, turns fibrinogen –> fibrin –> MESH CLOT

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

Where is Factor Xa in the coagulation cascade?

A

Intersection of ex and intrinsinc pathways

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

How do we inhibit clots? Where do these proteins arise?

A

Antithrombin (inhibits thrombin w/ heparan on endothelial cells); Protein C/S/thrombomodulin; Tissue Factor Pathway Inhibitor; ALL FROM ENDOTHELIAL CELLS

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

How do we destroy clots? Relation to endothelial cells?

A

Lysis via plasmin, converted from plasminogen by TPA, which is secreted by endothelial cells

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

Interaction between endothelium and platelets (healthy, 2 main ways)

A

Inhibit platelet aggregation via NO, PGI and conversion of ADP into Adenosine; promote vasodilation

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

What does an activated platelet do?

A

Aggregate due to factor release (ADP) and FIBRIN linking via glycoproteins (IIb-IIIa) on platelet surfaces

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

Why do plaques rupture?

A

Chemical factors (cytokines, enzymes), physical stresses (high blood pressure, emotional upset)

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

Hypokinesis

A

Reduced contraction

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

Akinesis

A

Loss of contraction

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

Dyskinesis

A

Outwad bulging during contraction

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

Why is there diastolic dysfunction during MI?

A

Relaxation is a process that requires ATP, leads to reduced compliance and increase filling pressure

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

What is ischemic preconditioning?

A

Increased ischemic threshold with continued exercise is protective against MI

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

Define ventricular remodeling

A

Changes in cardiac size, shape, structure, physiology which can be pathological

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

Early remodeling occurs where and includes

A

At site of injury, infarction zone thinning and elongation

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

Late remodeling occurs where and includes

A

Diffuse process with hypertrophied myocytes and increased interstitial collagen

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

What does a remodeled heart look like (late)

A

Spherical

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

Early/late remodeling: good or bad?

A

Early may be adaptive by increasing stroke volume in setting of decreased CO; late is bad because of hypertrophy and pathological shape

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

How do we prevent remodeling?

A
  1. Early reperfusion (prevent large infarct); 2. Medical therapy (ACE-I, ARBs, beta-blockers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Type 1 and 2 of MIs

A

Type 1: classic plaque rupture; Type 2: supply-demand inbalance w/ no plaque rupture (anemia)

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

Q wave MI

A

Transmural

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

Non-Q wave MI

A

Subendocardial

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

Type 3 MI

A

Cardiac death

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

Type 4/5 MI

A

Revascularization process

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

Some nonatherosclerotic causes of acute MI and patient profile

A

Young OR no coronary risk factors: valve problems, inflammatory disorders (vasculitis), peripartum female, cocaine abuse

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

How does cocaine abuse cause acute MI?

A

Vasospasm decreases O2 supply, increased HR/inotropy increases O2 demand AND chronic abuse increases atherosclerosis risk

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

First step of flow chart of ischemic discomfrot at rest

A

ST segment elevation

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

Ischemic discomfort at rest can ultimately be due to…

A

Unstable angina, Non-Q-wave MI, Q-wave MI

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

A non-occlusive thrombus can cause either…what’s the difference between these two outcomes?

A

Unstable angina or Non-ST elevation myocardial infarction (NSTEMI); NSTEMI causes necrosis while unstable angina does NOT

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

An occlusive thrombus causes…

A

ST-elevation myocardial infarction (STEMI)

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

Comparing unstable angina to MI

A

Severe, longer duration chest pain compared to stable angina not improved with rest; large sympathetic response (diaphoresis, nausea, tachycardia, cool skin); shortness of breath

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

Physical findings of MI (4)

A

S4 (atrial contraction into a concompliant LV), S3 (volume overload), systolic murmur (rupture or papillary dysfunction), low grade fever (inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Some items on MI differential

A

Pericarditis (painful with inspiration), aortic dissection (ripping pain, look for BP asymmetry), PE, GI problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why BP assymetry on aortic dissection?

A

If dissection is proximal to subclavian, you will get different BPs in right arm vs left arm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What might you see on EKG for unstable angina/NSTEMI? How can you differentiate NSTEMI from USA?

A

T wave inversion or ST Depression OR normal; biomarkers elevated in NSTEMI

35
Q

For STEMI, discuss EKG and biomarkers

A

ST segment elevated, biomarkers elevated

36
Q

Lateral wall leads, what artery?

A

I, aVL, V5, V6; Left circumflex

37
Q

Inferior wall leads, what artery?

A

II, III, aVF; Right coronary

38
Q

Anteroseptum leads, what artery?

A

V1 - V4; LAD

39
Q

Overtime, an unreated ST segment elevation MI will evolve into what on EKG?

A

Q wave; absence of electrical force in that segment

40
Q

3 biomarkers of myocardial necrosis

A

Troponin core complex (TnI and TnC); creatine kinase myocardial band (CK-MB), and myoglobin

41
Q

Discuss positive troponin test and MI?

A

Elevated cTnI (cardiac troponin) is NECESSARY but NOT sufficient for diagnosis of cardiac MI

42
Q

When are cTnI levels highest?

A

Begin to rise within 3-4 hours and pea at about 1 day, slow deline

43
Q

What is CK?

A

Enzyme involved in generation of ATP

44
Q

Describe kinetics of elevated CK in MI

A

Rises and peaks faster (24 hours) but clears faster

45
Q

Why is using both CK-MB and cTnI helpful?

A

If they had multiple MIs in short period of time, CK-MB would be high again (though cTnI might not have fallen)

46
Q

Goal of STEMI treatment

A

IMMEDIATE RESTORATION OF BLOOD FLOW TO OCCLUDED VESSEL

47
Q

Approaches to NSTEMI

A

Conservative vs invasive approaches

48
Q

Anti-ischemic drug classes (3)

A

Beta-blockers, nitrates, Ca2+ channel blockers

49
Q

Beta-blockers do what in context of ACS?

A

Relieve ischemic pain, reduce infarct size, and life threatening arrhythmias –> mortality benefit

50
Q

What categories of patients do we NOT give nitrates to?

A

Hypotensive and STEMI patients with inferior MI/RV infarction (must fill RV to allow for heart function)

51
Q

Are Ca2+ channel blockers used in ACS?

A

Not really, no mortality benefits

52
Q

Anti-thrombotic therapy: drug classes and why it works

A

Inhibit thrombin reduces platelet aggregation proliferation (but do not reduce size); includes antiplatelets and anticoagulants

53
Q

Anti-platelet therapy drugs and mechanism

A

Aspirin (COX inhibitor), Clopidogrel (blocks ADP at P2Y12 receptor), Anti GPIIb-IIIa (binds fibrinogen)

54
Q

What do statins due in setting of ACS?

A

Stabilize plaque

55
Q

Who gets aspirin?

A

Any patient with acute MI

56
Q

Two P2Y12 ADP receptor blockers

A

Clopidogrel and prasugrel

57
Q

Clopidogrel is indicated in…What’s a problem with clopidogrel?

A

All patients with USA/NSTEMI unless surgery planned; substantial variability in response

58
Q

Prasugrel is different from clopidogrel how?

A

More consistent effect at inhibition of platelets with increased risk of bleeding

59
Q

Describe GPIIb-IIIA receptor antagonists

A

Very potent because they inhibit the final common pathway of platelet aggregation so platelets CANNOT aggregate

60
Q

T/F: GPIIb-IIIA receptor antagonists are commonly prescribed

A

False! Use is declining

61
Q

Anti-coagulation therapy drugs do what? Name drugs

A

Inhibit some step of coagulation cascade; heparin, direct thrombin inhibitors (bivalirudin), factor Xa inhibitor (now a major target)

62
Q

Descibe mechanisms and delivery of two types of heparin

A

Unfractioned heparin (IV, must test levels): binds antithrombin which binds both factor Xa and thrombin; Low molecular weight heparin (SQ, don’t have to check levels) only binds factor Xa

63
Q

USA/NSTEMI conservative approach vs invasive approach

A

Medications alone until sx worsen vs urgent cardiac catheterization with revascularization if indicated

64
Q

How do we decide to use conservative or invasive approach?

A

TIMI risk score calculator (higher than 2-3 will benefit from aggressive treatments)

65
Q

What do we do to reperfuse STEMI?

A

Fibrinolysis vs mechanical revasularization (PCI or CABG)

66
Q

What does fibrinolysis refer to?

A

Medical therapy to enzymatically break down fibrin clot

67
Q

Fibrinolytic agent that is still used today

A

tPA

68
Q

Compare primary PCI vs fibrinolysis for STEMI

A

PPCI is better for flow and reduced risk of hemorrhage (compared to fibrinolysis) –> generally favor PCI

69
Q

When is fibrinolysis preferred?

A

Early presentation (

70
Q

When is invasive strategy preferred? (5)

A

Skilled PCI lab available, high STEMI risk (shock), fibrinolysis contraindicated (risk of bleeding), late presentation (>3 hours, lytic therapy won’t work), diagnosis of STEMI is in doubt

71
Q

Additional therapies for STEMI patients…

A

Antiplatelets, anticoagulants

72
Q

Do you give GBIIb-IIIa inhibitors if lytics are chosen for STEMI patients?

A

NOPE, no role for them

73
Q

What other drugs do we give to MI patients?

A

ACE-I (prevent remodeling), statins (stabilize plaque and eventually lower atherosclerosis), prolonged anticoagulation (in certain patients)

74
Q

When would be prescribe LT anticoagulation?

A

LV thrombus, Afib

75
Q

MI complications: electrical

A

Vfib, supraventricular arrhythmias (brady and tachycardias), conduction blocks

76
Q

MI complications: mechanical

A

Left: pulmonary congestion; Right: JVD and hypotension

77
Q

T/F: MIs can cause sytolic and dystolic dysfunctions

A

True!

78
Q

What arrhythmia are we particularly concerned about with MI?

A

V fib! Can cause SCD

79
Q

You’ve occluded the RCA…consequence…treatment…

A

Damage to right ventricle –> JVD –> hypotension (cannot get blood into R ventricle) –> treatment is volume to get blood into right ventricle

80
Q

Posterior wall MI has what kind of EKG?

A

Will demonstrate ST depression in anterior leads (as opposed to ST elevation)

81
Q

Other MI complications (3)

A

LV aneurysm: true and pseudoaneurysm; papillary muscle rupture; pericarditis

82
Q

What is a pseudoaneurysm. Treatment?

A

Essentially a mycocardial rupture that is contained by sac; surgical emergency

83
Q

What can a papillary muscle rupture cause? Treatment?

A

Severe mitral regurgitation and death; surgery

84
Q

Two flavors of pericarditis

A

Acute (due to inflammation) vs later, called Dressler syndrome (autoimmune system may be involved)

Cardiology (22 decks)

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