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Pathology -- Cardiology > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

Three ways a heart might have inadequate O2 delivery (broad)

A

Decreased Perfusion
Other oxygenation causes
Inadequate O2 secondary to increased demand

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2
Q

Causes of decreased perfusion of the heart (5)

A 
Progressive stenosis
Thromboembolus
Vasospasm
Vasculitis
Hypovolemia
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3
Q

Non-perfusion oxygenation issues (5)

A 
Anemia
CO
Congenital Heart Disease
Asphyxia
Lung Disease
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4
Q

Once stenosis reaches _____%, there is a decreased ability to meet the demand

A

75%

severe/fatal usually requires a 70% reduction in diameter

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5
Q

Where is the most severe narrowing typically?

A

The proximal 2cm

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6
Q

Thrombus formation usually results from

A

rupture or fissure of plaque with platelet aggregation, release of thromboxane

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7
Q

Vasospasm is associated with…

A

Adrenergic stimulation, local factors (NO, endothelin, platelet factors), HTN/Platelet Activity

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8
Q

Two types of coronary vessels

A

Epicardial (Conductance Vessels – get athero)

Intramyocardial (Resistance Vessels - autoregulation and flow)

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9
Q

How does hypoxia kill muscle cells

A

Switch to anerobic glycolysis, lactate buildup, lowered pH, impaired membrane fxn lets K leak and Na in

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10
Q

Injury becomes permanent after…

A

20-40 minutes

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11
Q

Irreversible Injury to the heart…whats that like

A

Necrosis and permanent loss of functional myocardium

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12
Q

What is acute ischemic heart disease

A

blockage of flow in a coronary vessel leads an entire region of myocardium to become necrotic (MI)

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13
Q

What is chronic ischemic heart disease

A

Ischemia leading to loss f individual myocytes and diffuse fibrosis, resulting in myocarfial dysfunction and eventually heart failure

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14
Q

Morphology of reversible injury

A

Stunned Myocytes

Mitochondrial swelling, Relaxation of myofibrils, distortion of cristae

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15
Q

Morphology of irreversible injury (in chronic)

A

Chronic loss of myocytes, esp. in subendocardial
Coagulative necrosis + Apoptosis
Area becomes fibrotic
Subendocardial band of infarcted myo at watershed

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16
Q

Morphology of acute ischemia (MI) - Gross

A

Early – Pallor with hyperemic border
3-7 days: hyperemic border with central, yellow-brown softening. Possibly hemorrhage.
Eventual replacement w/ red-brown, depressed, scarred area.
Eventually gray and fiber like

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17
Q

Phases of color of a post-MI heart

A

White–> Yellow Brown –> Red-Brown –> Gray

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18
Q

Morphology of acute ischemia (MI) – Microscopic

A

Necrosis of Myocytes
Inflammation, Infiltration w/ Inflamm cells
Clean up of necrotic debris
Replacement of myocardium w/ scar tissue

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19
Q

Morphology of reperfusion injury?

A

Presence of contraction bands in damaged myocytes.

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20
Q

Two main symptoms of cardiac ischemia?

A

Chest Pain + Diaphoresis

21
Q

Describe the chest pain of an MI

A

Crushing Pain over sternum
Radiates to left arm/back
NOT sharp or fluctuating

22
Q

Describe MI diaphoresis

A

Shortness of Breath, Sweating, Nausea

23
Q

Three serum enzymes associated with ischemic heart

A

Troponin I/T
Creatinine kinase (MB isoenzyme)
Lactic dehydrogenase

24
Q

Whats the deal with troponin?

A

Cardio specific/Sensitive
Increase w/ CMB, elevated up to 7 days
Most sensitive/specific

25
Q

Whats the deal w/ CK-MB

A

Highly specific and sensitive
Peaks at 12-24 hrs. Down quickly after.
Indicator of repeat infarct

26
Q

Whats the deal with lactic dehydrogenase

A

Indicator of tissue damage that rises form 24h to 3-6 days. Stays up for weeks.
Nonspecific and basically useless.

27
Q

Aside from symptoms and enzymes, how else might you diagnose an MI

A

EKG

Leukocytosis + Elevated ESR

28
Q

The triad of symptoms associated with ischemic heart disease…

A

Systemic HTN
LVH
CAD

29
Q

Most important clinical correlation with ischemic heart?

A

atherosclerosis

30
Q

Difference between Stable, Unstable, and Prinzmetal’s angina

A

S – Relieves with rest+nitro
U – Not relieved with rest+mitro
P – Caused by vasospasm (ex. from cocaine)

31
Q

How do chronic heart disease patients tend to present?>

A

History of angina/MI in last 5-10 years

Cardiac decompensation from slow myocardial atrophy

32
Q

Pathophysiology of Chronic ischemic heart disease?

A

Progressive injury resulting in eventual CHF

Diffuse atherosclerosis w/ myocardial fibrosis + patchy scars

33
Q

Most MIs are precipitated by…

A

Rupture of atherosclerotic plaque and thrombus formation

Sometimes from thromboemboli

34
Q

Characteristic unique histological feature of MI

A

Inflammation delayed by 24-48 hours

35
Q

MI sign at first few hours…

A

Acute Cell Injury –> Necrosis

36
Q

First visual sign of inflammation?

A

Edema occurs at margin within first 24 hours

37
Q

Hallmarks of coagulative necrosis

A

Loss of nuclei and hypereosinophilic fibers

38
Q

In the 2-4 days following the day of MI….

A

Neutrophils migrate into necrotic area, cellular infiltrate becomes prominent
Afterwards macrophages get in

39
Q

What’s going on with the heart 4-5 days following MI

A

Highest risk of rupture

40
Q

Early complications of MI

A

Dysfunctional Heart Muscle
Arrythmia
Extensions of Infarct

41
Q

Late complications of MI (5)

A 
Aneurysm/Dilation
Ventricular Rupture
Mural Thrombus
Pericardial effusion/Pericarditis
Papillary Muscle Infarct with Mitral Insufficiency
42
Q

How does ischemia show up on an EKG?

A

Inverted T Wave

Displacement of ST

43
Q

Transient ST depression suggests…

A

subendocardial ischemia

44
Q

Transient ST elevation suggests…

A

Transmural ischemia

45
Q

Whats unique about an EKG after infarction?

A

Q waves/Loss of R waves
ST changes
Q wave, non-Q infarction

46
Q

Angiography perfusion study indicated in…

A

Chronic Stable or Unstable Angina (symptoms despite therapy)
Patients w/ troublesome symptoms that occlude diagnosis
Patients with severe ischemia

47
Q

Treatment of Angina

A

Lifestyle changes/Treat risk factors
Treat underlying conditions
Drugs – Nitrates, b-blockers, calcium channel blockers
Prevent thrombosis – aspirin, platelet adhesion blockers

48
Q

Treatment of MI

A

Diagnose+Increase oxygenation
Aspirin
Anti-arrythmics
Reestablish bloodflow (Angiography, PCI, Fibrinolysis)

49
Q

Fibrinolysis is most effective in…

A

the first 30 minutes

Pathology -- Cardiology (13 decks)

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