Acute Coronary Syndromes

Question 1

90% result from plaque rupture which leads to thrombus formation

Answer 1

Acute Coronary Syndromes

Question 2

Plaque rupture leads to exposure of

Answer 2

Thrombogenic CT

Question 3

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

Answer 3

Primary Hemostasis

Question 4

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

Answer 4

Secondary hemostasis

Question 5

Platelet plug formation

Answer 5

Primary hemostasis

Question 6

Clotting cascade

Answer 6

Secondary Hemostasis

Question 7

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

Answer 7

Antithrombin

Question 8

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

Answer 8

Protein C and S and thrombomodulin

Question 9

Negative feedback inhibitor for the extrinsic coagulation pathway

Answer 9

Tissue Factor Pathway Inhibitor (TFPI)

Question 10

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

Answer 10

Tissue Plasminogen Activator (tPA)

Question 11

Degrades fibrin clots

Answer 11

Plasmin

Question 12

Inhibits cyclic AMP formation, thereby decreasing platelet activation and aggregation

Answer 12

Prostacyclin

Question 13

Nitric Oxide inhibits

Answer 13

Platelet activation

Question 14

Decreases the vasodilatory and antithrombic properties

Answer 14

Coronary thrombosis

Question 15

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

Answer 15

Stenosis

Question 16

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

-Endocardium to epicardium

Answer 16

Transmural Infarction

Question 17

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

Answer 17

Subendocardial infarction

Question 18

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

Answer 18

Greater territory of infarction

Question 19

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

Answer 19

Myocardial Infarction

Question 20

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

Answer 20

2 Minutes

Question 21

In an infarction, we see irreversible cell injury after

Answer 21

20 Minutes

Question 22

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

Answer 22

4-12 hours

Question 23

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

Answer 23

Wavy Myofibers

Question 24

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

Answer 24

Contraction bands

-Seen at infarct borders

Question 25

In24-48 hours post infarction, histologically we can see

Answer 25

Inflammatory cells and coagulation necrosis

Question 26

Start at about 4 hours after infarct

Answer 26

Inflammatory Cells

Question 27

Charcterized by pyknotic or shrinking nuclei and bland eosinophilia cytoplasm -Seen 18-24 hours

Answer 27

Coagulation Necrosis

Question 28

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

Answer 28

Yellow Softening

Question 29

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

Answer 29

Myocardial wall rupture

Question 30

We see granulation tissue with neovascularization and mild chronic inflammation at

Answer 30

10 days post MI

Question 31

At 10 days post MI, we see

Answer 31

Lymphocytes and Fibroblasts

Question 32

1-2 months following an MI, we see dense

Answer 32

Dense fibrosis

Question 33

Abnormal wall motion of the affected area

Answer 33

Systolic Dysfunction

Question 34

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

Answer 34

MI

Question 35

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

Answer 35

Ischemic preconditioning

Question 36

Patients with recent angina that precedes an MI have less

Answer 36

Morbidity and mortality

Question 37

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

Answer 37

Occur

Question 38

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

Answer 38

LV enlargement and HF

Question 39

ACE inhibitors and ARBs may help to decrease

Answer 39

Ventricular remodeling

Question 40

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

Answer 40

Acute MI

Question 41

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

Answer 41

Congestive Heart Failure

Question 42

Shows T-wave inversion or ST depression

Answer 42

Unstable angina

Question 43

Shows T-wave inversion or ST depression

Answer 43

NSTEMI

Question 44

Shows ST segment elevation

Answer 44

STEMI

Question 45

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

Answer 45

RV branches

Question 46

We can perform a right sides EKG to check for

Answer 46

RV infarct

Question 47

An isolated posterior infarct typically involves the distal -Supplies the posterior part of the LV located just beneath the AV sulcus

Answer 47

Left Circumflex Artery

Question 48

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

Answer 48

Posterior infarct

Question 49

To catch a posterior infarct, we can place

Answer 49

Posterior leads

Question 50

Most often, a posterior infarct will be combined with an

Answer 50

Inferior (RCA) or lateral (proximal LCx) infarct

Question 51

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

Answer 51

Inferno-posterior Infarct

Question 52

An inferno-posterior infarct is confirmed with

Answer 52

Posterior leads

Question 53

Protein that controls interaction between actin and myosin

Answer 53

Troponin

Question 54

Very specific to cardiac tissue

Answer 54

Troponin I and Troponin T

Question 55

Is not specific to cardiac tissue

Answer 55

Troponin C

Question 56

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

Answer 56

Cardiac Troponin

Question 57

How long after an MI are cardiac troponins detectable for?

Answer 57

10 days

Question 58

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

Answer 58

CK-MB

Question 59

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

Answer 59

Beta-blockers

Question 60

What are three things used for anti-ischemic therapy?

Answer 60

Beta-blockers, Nitrates, and Ca2+ channel blockers

Question 61

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

Answer 61

Recurrent Ischemia

Question 62

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

Answer 62

Cardiogenic Shock

Question 63

Leads to profound hypotension and right sided heart failure

Answer 63

Right Ventricular Infarct

Question 64

Acute inflammation post MI can cause acute -Pain, fevers, and a friction rub

Answer 64

Pericarditis

Question 65

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

Answer 65

Dresser syndrome

Question 66

We may see pericardial effusion and elevated inflammatory markers with

Answer 66

Dressler Syndrome

Question 67

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

Answer 67

Thromboembolism