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Cardiology > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

90% result from plaque rupture which leads to thrombus formation

A

Acute Coronary Syndromes

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2
Q

Plaque rupture leads to exposure of

A

Thrombogenic CT

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3
Q

Begins within seconds and we see platelet plug formation as platelets adhere to subendothelial collagen

A

Primary Hemostasis

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4
Q

Exposure to tissue factor citrates the clotting cascade, ultimately activating thrombin which forms a fibrin clot

A

Secondary hemostasis

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5
Q

Platelet plug formation

A

Primary hemostasis

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6
Q

Clotting cascade

A

Secondary Hemostasis

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7
Q

Irreversibly binds thrombin and other factors and it activity is modulated by heparin sulfate

A

Antithrombin

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8
Q

Inactivate factors Va and VIIIa which are important in accelerating the coagulation cascade

A

Protein C and S and thrombomodulin

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9
Q

Negative feedback inhibitor for the extrinsic coagulation pathway

A

Tissue Factor Pathway Inhibitor (TFPI)

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10
Q

Released by endothelial cells in response to thrombus formation and it converts plasminogen to plasmin

A

Tissue Plasminogen Activator (tPA)

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11
Q

Degrades fibrin clots

A

Plasmin

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12
Q

Inhibits cyclic AMP formation, thereby decreasing platelet activation and aggregation

A

Prostacyclin

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13
Q

Nitric Oxide inhibits

A

Platelet activation

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14
Q

Decreases the vasodilatory and antithrombic properties

A

Coronary thrombosis

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15
Q

Small plaque ruptures with low thrombus burden may get incorporated into the vessel wall and increase

A

Stenosis

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16
Q

Involves the full thickness of the myocardium as a result of prolonged, completely occluded vessels (STEMI)

-Endocardium to epicardium

A

Transmural Infarction

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17
Q

Only a partial thickness infarction and typically the subendocardium is the most susceptible

A

Subendocardial infarction

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18
Q

In a myocardial infarction, a more proximal occlusion results in a

A

Greater territory of infarction

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19
Q

A rapid shift from aerobic or anaerobic metabolism, leading to the accumulation of lactic acid and thus lower pH

A

Myocardial Infarction

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20
Q

During an infarct, we see decreased myocardial function in as early as

A

2 Minutes

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21
Q

In an infarction, we see irreversible cell injury after

A

20 Minutes

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22
Q

We can see myocardial edema due to increased vascular permeability and an interstitial oncotic pressure rise from leaked proteins in

A

4-12 hours

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23
Q

Interstitial edema separating myocardial cells give the histologic characteristic of an MI which is

A

Wavy Myofibers

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24
Q

In an MI, sarcomeres are contracted and consolidated, seen at infarct borders. This histologic characteristic is called

A

Contraction bands

-Seen at infarct borders

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25
Q

In24-48 hours post infarction, histologically we can see

A

Inflammatory cells and coagulation necrosis

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26
Q

Start at about 4 hours after infarct

A

Inflammatory Cells

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27
Q

Charcterized by pyknotic or shrinking nuclei and bland eosinophilia cytoplasm

-Seen 18-24 hours

A

Coagulation Necrosis

28
Q

5 days following an MI, neutrophils are replaced by macrophages that remove necrotic connective tissue and dead cells. This is known as

A

Yellow Softening

29
Q

This causes thinning and dilation of the infarcted zone, which can result in

A

Myocardial wall rupture

30
Q

We see granulation tissue with neovascularization and mild chronic inflammation at

A

10 days post MI

31
Q

At 10 days post MI, we see

A

Lymphocytes and Fibroblasts

32
Q

1-2 months following an MI, we see dense

A

Dense fibrosis

33
Q

Abnormal wall motion of the affected area

A

Systolic Dysfunction

34
Q

We see a rise in LVEDP due to both systolic and diastolic dysfunction in an

A

MI

35
Q

Chronically ischemic tissue due to severe stenosis that then becomes an MI

A

Ischemic preconditioning

36
Q

Patients with recent angina that precedes an MI have less

A

Morbidity and mortality

37
Q

The infarcted tissue becomes thin and dilated, so infarct expansion without further myocyte death can

A

Occur

38
Q

Non-infarcted tissue can dilate to compensate for cardiac output. This can also lead to continued

A

LV enlargement and HF

39
Q

ACE inhibitors and ARBs may help to decrease

A

Ventricular remodeling

40
Q

Left-sided substernal pain that radiates to jaw or arm. May be more intense than angina pain or last longer

A

Acute MI

41
Q

The physical exam for a patient with ACS is mainly just symptoms of

A

Congestive Heart Failure

42
Q

Shows T-wave inversion or ST depression

A

Unstable angina

43
Q

Shows T-wave inversion or ST depression

A

NSTEMI

44
Q

Shows ST segment elevation

A

STEMI

45
Q

A proximal RCA occlusion will show up in EKG leads involving the

A

RV branches

46
Q

We can perform a right sides EKG to check for

A

RV infarct

47
Q

An isolated posterior infarct typically involves the distal

-Supplies the posterior part of the LV located just beneath the AV sulcus

A

Left Circumflex Artery

48
Q

Shows tall R waves in V1-V3, with ST depressions and upright T waves

A

Posterior infarct

49
Q

To catch a posterior infarct, we can place

A

Posterior leads

50
Q

Most often, a posterior infarct will be combined with an

A

Inferior (RCA) or lateral (proximal LCx) infarct

51
Q

Shows ST elevation in inferior leads with tall R waves and ST depression seen in anterior leads

A

Inferno-posterior Infarct

52
Q

An inferno-posterior infarct is confirmed with

A

Posterior leads

53
Q

Protein that controls interaction between actin and myosin

A

Troponin

54
Q

Very specific to cardiac tissue

A

Troponin I and Troponin T

55
Q

Is not specific to cardiac tissue

A

Troponin C

56
Q

Begins to rise 3-4 hours after symptoms and peak at 18-36 hours

A

Cardiac Troponin

57
Q

How long after an MI are cardiac troponins detectable for?

A

10 days

58
Q

Begins to rise 3-8 hours after symptoms and returns to normal 48-72 hours

A

CK-MB

59
Q

Used for anti-ischemic therapy because they reduce myocardial oxygen demand

A

Beta-blockers

60
Q

What are three things used for anti-ischemic therapy?

A

Beta-blockers, Nitrates, and Ca2+ channel blockers

61
Q

Re-occlusion of the artery. More common in patients treated with tPA than PCI but can also happen with PCI

A

Recurrent Ischemia

62
Q

Severely decreased cardiac output which is a vicious cycle as hypotension leads to worsening of coronary perfusion

A

Cardiogenic Shock

63
Q

Leads to profound hypotension and right sided heart failure

A

Right Ventricular Infarct

64
Q

Acute inflammation post MI can cause acute

-Pain, fevers, and a friction rub

A

Pericarditis

65
Q

Delayed pericarditis after an MI due to an immune process against damaged myocardial tissue

A

Dresser syndrome

66
Q

We may see pericardial effusion and elevated inflammatory markers with

A

Dressler Syndrome

67
Q

Can form in the area of blood stasis due to the MI

A

Thromboembolism

Cardiology (27 decks)

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