Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardio > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

(62 cards)

Start Studying
1
Q

What do endothelial cells start to express when exposed to inflammatory mediators?

A

Tissue factor

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

Intrinsic pathway

A

Contact activation pathway
Factor XII converted into XIIa, which turns factor XI into XIa, which IX into IXa, which complexes with factor VIIIa.

This complex converts factor X into factor Xa. Xa and Va convert prothrombin into thrombin. Thrombin converts fibrinogen into fibrin. And we have a cross linked fibrin clot

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

Extrinsic pathway

A

Factor VII converted to VIIa by trauma. Simultaneously Tissue factor exposed due to trauma. VIIa and Tissue factor cleave X to Xa.

Xa, along with Va, convert prothrombin to thrombin, which converts fibrinogen to fibrin.

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

Antithrombin

A

Plasma protein that inactivates thrombin

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

Protein C/thrombomodulin

A

Thrombin receptor on endothelial cells so its unable to cleave fibrinogen to fibrin

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

Tissue factor pathways inhibitor (TFPI)

A

Yeah its pretty much what it sounds like

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

Mechanisms of clot lysis

A

Blood clots initiate the secretion of TPA from endothelial cells, which converts plasminogen to plasmin. Plasmin degrades fibrin clots.

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

How do plaques adhere to injured epithelium

A

Bind to von Willibrand factor and collagen.

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

Thromboxane A2

A

Pro-thrombotic factor that binds to platelets

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

ADP

A

Causes platelet aggregation

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

How does endothelium prevent the actions of ADP?

A

Turns it into adenosine.

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

Two factors released by endothelial cells that prevent platelet aggregation and increase blood flow

A

Prostacyclin and NO. Also convert ADP.

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

How does prostacyclin and NO induce vasodilation prevent thrombus formation?

A

Because increased blood flow prevents contact between procoagulant factors.

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

Major cause of coronary artery thrombosis?

A

Plaque rupture

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

Two chemical factors that destabilize fibrous caps?

A

MMP (matrix metalloproteinase)

T-lymphocyte cytokines that inhibit collagen synthesis

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

Most prone part of cap to rupture?

A

Shoulder of cap due to stress. Can also rupture because of myocardial contraction or high intraluminal blood pressure

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

When do MIs usually occur

A

Early morning hours because physiologic stress is highest. High BP, high blood viscosity, high sympathetic tone

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

What is the first step in coronary thrombogenesis?

A

Dysfunction of the endothelium. Vasoconstriction becomes the favored state. Thromboxane and serotonin will promote vasoconstriction.

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

Functional sequellae of MI

A 
Impaired contractility (systolic dysfunction)
Impaired relaxation (diastolic dysfunction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do MIs cause systolic dysfunction

A

Hypokinesis (reduced contraction) or Akinesis, or dyskinesis (bulging out during contraction)

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

How do MIs cause diastolic dysfunction

A

Reduced compliance because its energy dependent too.

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

Stunned myocardium

A

Reversible injury to myocytes after MI. Contractile function is restored days to weeks later.

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

Ischemic preconditioning

A

Episodes of ischemia actually make tissue resistant to subsequent episodes. This occurs during stable angina.

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

Remodeling definition and process

A

Process of ventricular reorganization after infarct. First the infarct zone will thin and elongate. This is also known as infarct expansion. Then spherical dilation will occur with increased interstitial collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Why is infarct expansion so dangerous?
Because its associated with higher mortality and a higher rate of complications like HF. Signs: new gallop sounds, new/worsening pulmonary congestion
26
What is the product that stimulates ventricular hypertrophy during late remodeling
Local ang II release
27
Nonatherosclerotic causes of ACS in young patients or somebody with no risk factors
Mechanical valves or infective endocarditis -- cause emboli that occlude coronaries. Inflammatory disorders like vasculitis Peripartum female (can have spontaneous coronary dissection) Cocaine abuse
28
How does cocaine abuse cause ACS?
Vasospasm decreases oxygen supply, increased HR + inotropy cause increased demand. Also associated with increased atherosclerosis.
29
Types of Myocardial Infarction
Type 1 -- classic case of plaque rupture Type 2 -- Supply/demand imbalance without plaque rupture Type 3 -- Cardiac death Type 4/5 -- MI in the setting of a revascularization procedure.
30
Types of type 2 MI
Vasospasm or endothelial dysfunction (prinzmetal/cocaine) Fixed atherosclerosis causing supply-demand imbalance Supply-demand balance alone (syndrome X)
31
Q-wave MI
Transmural infarction
32
Non q-wave MI.
Subendocardial ischemia -- few collaterals there and exposed to highest pressures from ventricle
33
Presentation of ACS?
Ischemic discomfort at rest
34
Sign of ACS
Either ST segment elevation or non ST segment elevation
35
Non ST segment elevation ACS
Can be unstable angina, Non-q wave MI, or even a Q wave MI (very rarely)
36
ST segment elevation ACS
Generally a q-wave MI, but sometimes (rare) can be a non-q wave MI.
37
Nonocclusive ruptured plaque leading to thrombus causes
Unstable angina, NSTEMI
38
Occlusive ruptured plaque leading to thrombus causes
STEMI.
39
Increasing severity of ACS
Unstable angina -> NSTEMI -> STEMI
40
Most critical distinction to make
NSTEMI or STEMI
41
Clinical symptoms of MI
``` Chest pain more severe, longer duration, with greater radiation than normal. Does not improve with rest or nitroglycerin. Sympathetic discharge (diaphoresis, tachycardia, nausea, clammy skin) Shortness of breath (LV volume rises, so backs up to lungs) ```
42
Who is likely to have an MI without symptoms?
Diabetics
43
Physical findings of MI
S4 (noncompliant LV) S3 (volume overload and systolic dysfunction) Systolic murmur (may come from papillary muscle dysfunction leading to MR) Fever
44
Why can an MI cause MR?
Because papillary muscle doesn't function properly.
45
Differential for MI
Pericarditis, pleuritis (pain w/inspiration and diffuse ST ele) Aortic dissection (ripping pain, BP asymmetry, widened mediastinum on CXR) PE Acute cholecystitis
46
ECG findings of USA or NSTEMI
T wave inversion, ST depression or normal
47
Are biomarkers elevated in USA?
No
48
Are biomarkers elevated in NSTEMI
yes
49
ECG evolution with STEMi
See slides
50
Definition of STEMI
Prolonged chest discomfort unrelieved by nitroglycerin with ST segment elevation on EKG and rise in cardiac markers
51
Definition of NSTEMI
Angina at rest for longer than 20 minutes without ST segment elevation but with cardiac biomarkers.
52
Pathophysiology of STEMI
Total or near total occlusion of coronary artery
53
Pathophys of NSTEMI
Abrupt decrease in myocardial O2, thrombus formation or an atherosclerotic plaque
54
Management of STEMI
Immediate reperfusion with a preferred door to balloon time of <90 minutes
55
Management of NSTEMI
Depends on TIMI score
56
Cardiac biomarkers
Troponin (T, I, or C) Creatine Kinase Myocardial Band (CK-MB) Myoglobin
57
Troponins
Control calcium mediated interactions between actin and myosin that are released into circulation from muscle and cytosolic reserves during necrosis. TNI and TNT are highly sensitive and specific for myocardial necrosis.
58
Where is troponin released from first?
Cytosolic pool, but if injury persists, then muscular pool
59
When do levels of troponin rise and peak?
Rise within 3-4 hours. Peak at 18-36 and decline slowly
60
Creatine Kinase
Enzyme involved in ATP generation. Found in heart (CK-MB) but also in muscle (MM) and brain (BB). Also in uterus prostate gut.
61
Kinetics of CK
Faster release and peak (24h) then cTn, returns to normal faster.
62
Can biomarkers be normal early in ACS?
Yes 100%.

Cardio (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions