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Cardio Week 4 > ICL 4.5: Pathology of Acute Coronary Syndromes > Flashcards

ICL 4.5: Pathology of Acute Coronary Syndromes Flashcards

1
Q

what are hematoxylin bodies?

A

naked nuclei

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2
Q

septic infarct

A

infectious endocarditis embolism from the friable vegetations

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3
Q

what is ischemic heart disease?

A

it’s an imbalance between the supply/perfusion and the demand of the heart for oxygenated blood

this imbalance usually occursd due to reduced blood flow due to obstructive atherosclerosis of the coronary arteries (coronary artery disease)

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4
Q

what are the clinical manifestations of ischemic heart disease?

A
  1. MI (tissue death)
  2. angina (no necrosis)
  3. chronic ischemic heart disease with CHF
  4. sudden cardiac death
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5
Q

what are the pathological causes of ischemic heart disease?

A
  1. reduced coronary flow (atherosclerosis)
  2. increased myocardial demand (hypertrophy)
  3. reduced availability of o2 in the blood
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6
Q

how common is ischemic heart disease?

A

leading cause of death in the US with 500,000 deaths a year

there has been a decline in cases due to:
1. lifestyle modifactions

  1. elmiinating risk factors like smoking, hyperlipidemia, HTN
  2. technology has allowed for early diagnosis
  3. advanced therapies like angioplasty, stents, and CABGs
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7
Q

what is the pathogenesis of ischemic heart disease?

A

reduced coronary perfusion relative to myocardial demand

this can be caused by:
1. acute plaque change

  1. inflammation
  2. thrombosis
  3. vasoconstriction
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8
Q

how can acute plaque change cause ischemic heart disease?

A
  1. acute plaque change is rupture/fissuring exposing the highly thrombogenic plaque constituents

changes in plaques are triggered by stress, abrupt changes in BP, adrenergic stimulation, or increased platelets reactivity

  1. erosion/ulceration exposing the thrombogenic subedothelial BM to blood
  2. hemorrhage in the atheroma which leads to expanding its volume
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9
Q

how can inflammation cause ischemic heart disease?

A

inflammation plays a huge role in atherosclerosis which then plays a role in ischemic heart disease

endothelial cells interaction with circulation leucocytes leads to accumulation of t cells and macrophages in the arterial wall

macrophages then release chemical mediators which leads to atherosclerosis and eventually ischemia

**high sensitivity CRP is the major acute phase reactant and predicts the risk of coronary heart disease!! it’s a marker of atherosclerosis

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10
Q

how can thrombosis cause ischemic heart disease?

A

thrombosis in a partially occluded artery leads to complete occlusion of the coronary arteries

thrombosis can also embolize!

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11
Q

how can vasoconstriction cause ischemic heart disease? what are 3 causes of vasoconstriction?

A

vasoconstriction leads to disruption of plaques and ischemia

causes of vasoconstriction:
1. circulating adrenergic agonists

  1. locally released platelet contents
  2. impaired secretion of endothelial cell relaxing factors
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12
Q

what are the consequences of myocardial ischemia?

A
  1. stable angina
  2. unstable angina
  3. MI
  4. sudden cardiac death
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13
Q

what is stable angina?

A

results from an increase in myocardial oxygen demand

no plaque disruption

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14
Q

what is unstable angina?

A

plaque disruption

results in thrombosis and vasoconstriction

severe but transient reduction in blood flow which is why it doesnt cause necrosis

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15
Q

what is an MI?

A
  1. acute plaque change
  2. abrupt thrombotic occlusion
  3. myocardial necrosis
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16
Q

what is sudden cardiac death?

A
  1. regional myocardial ischemia

2. fatal ventricular arrhythmia

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17
Q

what is the coronary artery pathology in ischemic heart disease?

A

STABLE ANGINA
stenoses, no plaque disruption, no plaque associated thrombus

UNSTABLE ANGINA
some stenoses, frequent plaque disruption, nonocclusive plaque associated thrombus

TRANSMURAL MI
some stenoses, frequent plaque disruption, occlusive plaque associated thrombus

SUBENDOCARDIAL ENFARCT
variable stenoses, variable plaque disruption, variable plaque associated thrombus

SUDDEN DEATH
usually severe stenoses, frequent plaque disruption, small platelet aggregates or thrombi

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18
Q

what is angina pectoris?

A

it’s transient ischemia with paroxysmal pain and no necrosis

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19
Q

what type of pain do you feel with ischemia?

A

pressure pain

this is things like MI or angina

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20
Q

what pain do you feel with pericarditis pain?

A

pins and needles

stabbing pain

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21
Q

what pain do you feel with dissecting aneurysms or cardiac tamponade?

A

tearing my chest apart and radiating pain to the back

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22
Q

what are the 3 types of angina?

A
  1. stable
  2. unstable
  3. prinzmetal
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23
Q

what is the cause and effect of stable angina?

A

cause = chronic coronary stenosis of an atherosclerotic coronary artery

effects = pain on exertion

24
Q

what is the cause and effect of unstable angina?

A

cause = disruption of plaque with superimposed partial thrombosis

effect = pain at rest and on exertion for prolonged period

25
Q

what is the cause and effect of prinzmetal angina?

A

cause = coronary artery spasm

effect = pain at rest

26
Q

A 55-year-old male, obese banker develops sudden crushing chest pain after a Board Dinner

The pain radiates to his left shoulder. His friends drive him to the emergency room upon arrival, he is found to be diaphoretic and his blood pressure is 80/40

The patient has been a heavy smoker for 40 years

A

obese, crushing chest pain, radiates to the left shoulder, diaphoretic, heavy smoker, stress from Board dinner

patient is in shock 80/40 BP and sweaty because the heart isn’t pumping properly

27
Q

what are the risk factors for MI?

A
  1. HTN
  2. DM
  3. hyperlipidemia
  4. obesity
  5. smoking

10% < 40 years old

45% < 65 years old

28
Q

what is the pathogenesis of MI?

A

sudden change in a plaque

platelet adhesions and aggregation and release of serotonin and platelet factors 3-4 = vasospasm mediated by factors released from platelets

activation of extrinsic coagulation pathway

occlusion of coronary artery by the newly formed thrombus

BUT 10% of transmural MI have no thrombus and are caused by vasospasm, emboli,or disorders of intramural coronary vessels so just because you don’t find a thrombus doesn’t mean your coronary artery hasn’t been occluded

29
Q

what part of the heart is damaged when the LAD is occluded?

A
  1. anterior wall of the LV

2. anterior septum

30
Q

what part of the heart is damaged when the RCA is occluded?

A
  1. posterior wall of LV
  2. posterior septum
  3. papillary muscles –> can cause arrhythmia
31
Q

what part of the heart is damaged when the LCX is occluded?

A

lateral wall of LV

32
Q

what is a transmural MI?

A

necrosis of the full thickness of the ventricular wall

this usually happens in an area of the heart that is perfused by a single coronary artery and there’s coronary atherosclerosis, plaque disruption or a thrombus

33
Q

what is a subendocardial MI?

A

necrosis of 1/3 to 1/2 of the ventricular wall

this usually happens in an area of the heart that is perfused by more than one coronary artery

usually caused by shock, HTN or a transient thrombus

34
Q

what is the evolution of morphological changes in an MI?

A

0-1 hr: relaxation of myofibrils, glycogen loss, mitochondrial swelling –> reversible injury

4 hrs: variable waviness of fibers at the border, sarcolemmal disruption, mitochondrial amorphous densities

4-12 hrs: dark mottling, early coagulation necrosis, edema, hemorrhage

12-24 hrs: dark mottling, ongoing coagulation necrosis, pyknosis of nuclei, myocyte hypereosinophilia, marginal contraction band necrosis, early neutrophilic infiltrate

1-3 days: mottling with yellow-tan infarct center, coagulation necrosis, loss of nuclei and attractions, brisk interstitial infiltrate of neutrophils

3-7 days: hyperemic border, ventral yellow-tan softening, beginning disintegration of dead myofibers with dying neutrophils, early phagocytosis of dead cells by macrophages at infarct border

7-10 days: maximally yellow-tan and sot with depressed red-tan margins, well-developed phagocytosis of dead cells, granulation tissue at margins forms

10-14 days: red-grey depressed infarct borders, well-established granulation tissue with new blood vessels and collagen deposition

2-8 weeks: gray-white scar progressive from border toward core of infarct, increased collagen deposition with decreased cellularity

2+ months: scarring complete, dense collagenous scar

35
Q

what is coagulative necrosis?

A

denaturation of proteins inside the cell

so you can still see the cell but there’s fading of the nucleus because the cell is dying

36
Q

what is the summary of evolution of morphological changes in an MI?**

A

4 hours: no changes that we can see

12-14 hours: dark mottling, neutrophils begin to invade, coagulation necrosis

1-3 days: neutrophils everywhere, inflammatory cascade has begun

3-7 days: yellow-tan softening meaning coagulation necrosis, neutrophils are gone, macrophages have come in

5-7 days is the most vulnerable time for the myocardium to rupture and cause a tamponade that could kill the patient

10-14 days: well established granulation tissue

2-8 weeks: scar

37
Q

what is granulation tissue composed of?

A
  1. collagen
  2. fibroblasts
  3. blood vessels
  4. monocytes
38
Q

a 50 year old male one week post acute mI present with sharp chest pain which increases with inspiration. his troponin levels are coming down.

CK MB normal, myoglobin normal

diagnosis?
tests?

A

sharp pain = pericardium pain

fibrinous pericarditis because it’s post MI! uremia and RF also cause fibrinous pericarditis

Dressler syndrome! occurs usually 10 days after MI and it’s a fibrinous pericarditis –> you’ll hear a friction rub because the damaged pericarditis is exposed to the immune system and when the antibodies eventually develop against the pericardium, they’ll attack it and cause a pericarditis

39
Q

what are the non-specific lab findings you’ll see post-MI?

A
  1. increased ESR

2. increased WBCs (neutrophils)

40
Q

how do creatinine kinase levels change post MI?

A

CKMB starts to go up at 4 hours post-MI but peaks at 12 hours

by 72 hours it’s back to baseline

41
Q

how do myoglobin levels change post MI?

A

myoglobin starts to go up 2-4 hours post-MI but peaks at 9-12 hours

it’s back to baseline by 24-36 hours

42
Q

what do myoglobin levels tell you about an MI?

A

myoglobin levels provide you information about:

  1. size of the infarct
  2. type of MI

transmural will have higher myoglobin than subendocardial

43
Q

what are the advantages of measuring troponin-i levels post-MI?

A

Troponin-i is a cardiac marker that is truly cardiac specific, unlike CK-MB and Total CK.

Troponin-i, has a specificity of 99.4% vs. CK-MB which has a specificity of 92.8%.

Troponin-i, unlike other cardiac markers, will not show elevation in trauma or other disease states

troponin > 0.5 indicates an MI

44
Q

how do troponin levels change post MI?

A

troponin-i starts to elevate 4-6 hours after onset of chest pain and remains elevated for 6-9 days after onset of chest pain

the fact that it remains elevated for 6-9 days will lend itself as a useful tool in diagnosis of those patients who present to the E.D. much later

troponin-i, due to the above facts, will eventually eliminate the need for Total-CK, CK-MB and LD Iso-enzymes

LDH is present in various tissues including the heart and during an MI, LDH-1 which is in the heart, the levels increase but now that we have troponin-i we don’t need to measure LDH1

45
Q

what are the complication of MI?

A
  1. cariogenic shock and sudden death –> you go into shock because the necrotic heart fails and doesn’t pump so you have poor perfusion and the BP goes down due to pump failure
  2. contractile dysfunction –> heart failure
  3. arrhythmia if there’s papillary muscle rupture
  4. ruptured myocardium –> cardiac tamponade
  5. pericarditis
  6. mural thrombus
  7. ventricular aneurysm
  8. rupture of papillary muscles
46
Q

how would a patient with cardiac tamponade present?

A

they can’t pump their heart because it’s being compressed by heart so you can’t feel their pulse BUT if you do an EKG though you can see electrical signals = pulsus paradoxicus

might also see distention of the jugular veins

47
Q

what happens when the papillary muscles rupture?

A
  1. arrhythmias

2. mitral valve regurgitation

48
Q

what is chronic ischemic heart disease?

A

aka ischemic cardiomyopathy

it’s a condition of the elderly who develop progressive heart failure as a result of ischemic myocardial damage

49
Q

what are the predisposing factors to chronic ischemic heart disease?

A
  1. post-infarction

2. severe atherosclerosis without infarction but have myocardial dysfunction

50
Q

what things can cause sudden cardiac death?

A
  1. acute myocardial ischemic arrhythmias
  2. congenital anomalies
  3. aortic stenosis
  4. mitral prolapse
  5. myocarditis
  6. cardiomyopathies
  7. hypertensive heart
  8. cocaine (vasoconstriction)
51
Q

A 45 year old football coach is rushed to the ER after he collapses at the end of the game.
He is not responsive and has no pulse. EKG reveals abnormal electric signals.

diagnosis?

A

cardiac tamponade

pulsus paradoxicus

52
Q

51 year old executive for a shipping company has been feeling some chest pain over the last year, particular after climbing up the stairs to the office. he had a cholesterol level of 250 and HDL of 25. his fasting glucose is 145. he smokes half pack of cigarettes a day. he’s overweight. he is admitted to the hospital after onset of severe chest pain that was substernal and described as crushing. he died 12 hours after admission

differential?

what was responsible for his symptoms?

A

acute MI!

pain with exercise = stable angina –> crushing pain = ischemic heart pain aka MI

risk factors = high cholesterol, low HDL, smoker, obese, sedentary lifestyle, DM

anginas pain due to poor perfusion of the myocardium secondary to coronary artery occlusion

53
Q

when do neutrophils first appear in an MI?

A

1 day

54
Q

when do macrophages first appear in an MI?

A

3-5 days

55
Q

what is the most vulnerable time for a ruptured myocardium post-MI?

A

5-7 days

56
Q

verrucus endocarditis

A

RF

57
Q

people with pancreatic cancer and develop marantic endocarditis?

A

Trousseu’s sign

Cardio Week 4 (16 decks)

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