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CPR 2 Exam 1 > Hillard Cardiac Pathology Part 1 > Flashcards

Hillard Cardiac Pathology Part 1 Flashcards

1
Q

what is the most common cause of ischemic heart disease?

A

atherosclerosis

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2
Q

What is the most sensitive and specific biomarkers of myocardial damage?

A
  • Troponin T cTnT
  • Troponin I cTnI
  • Both rise as they are released from dead/dying myocytes occurs as early as 3 hours
  • can have heart attack prior to troponin levels rise- need to perform serial troponins
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3
Q

after a MI when does CK-MB return to normal?

A

48-72 hours

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4
Q

After a MI when do cTnI and cTnT return to normal?

A

>5 days

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5
Q

What does the LAD supply?

A
  • Apex of heart
  • LV anterior wall
  • Anterior ⅔ of septum
  • apex anterior
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6
Q

What does the Left circumflex artery supply?

A
  • LV lateral wall
  • LV lateral
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7
Q

What does the right coronary artery supply?

A
  • RV free wall
  • LV posterior wall
  • Posterior ⅓ of septum
  • Posterior and right
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8
Q

How do infarctions occur (move)?

A

Inside of tissue to the outside

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9
Q

How long after a MI until you see waviness of fibers at the border on light microscopy?

A
  • ½ to 4 hours
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10
Q

When do you see early coagulation necrosis, edema, and hemorrhage on light microscopy after a MI?

A
  • 4-12 hours
  • Occasionally can grossly see dark mottling
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11
Q

When do you see ongoing coagulation necrosis, pyknosis of nuclei, myocyte hypereosinophilia, marginal contraction band necrosis and early neutrophilic infiltrate after an MI on light microscopy?

(also note grossly dark mottling)

A
  • 12-24 hours
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12
Q

When do you see coagulation necrosis with loss of nuceli and striations with a brisk interstitial infiltrate of neutrophils after an MI on light microscopy?

(grossly see mottling with a yellow tan infarct center)

A

1-3 days

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13
Q

How long after an MI, until you see the beginning disintegration of dead myofibers with dying neutrophils & early phagocytosis of dead cells by macrophages at the infarct border on light microscopy?

(grossly see hyperemic border with central yellow tan softening)

A

3-7 days

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14
Q

How long after an MI until you see well developed phagocytosis of dead cells, with granulation tissue at the margins on light microscopy?

(grossly see maximally yellow tan and soft with depressed red tan margins)

A

7-10 days

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15
Q

How long after an MI until you see well established granulation tissue with new blood vessels and collagen deposition on light microscopy?

(grossly see red grey depressed infarcted borders)

A

10-14 days

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16
Q

How long after an MI until you see increased collagen deposition with decreased cellularity?

(grossly see grey white scar)

A

2-8 weeks

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17
Q

How long after an MI until you see a dense collagenous scar on light microscopy?

(grossly scar is complete)

A

>2 months

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18
Q
A
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19
Q

Day 3 through 1-2 weeks

A

nothing

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20
Q

What are the early complications of MI?

A
  • Arrhythmia and contractile dysfunction
  • first 24 hrs
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21
Q

What are the intermediate complications of MI?

A
  • Rupture of the septal wall or papillary muscles
  • Acute fibrinous pericarditis
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22
Q

Here is what a rupture of different areas of the heat looks like grossly.

A

This occurs around 3 days

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23
Q

What are the late complications of MI?

A
  • Chronic pericarditis (Dressler Syndrome)
  • Ventricular aneurysm
  • Continued risk of HF and life threatening arrhythmias
  • CHF
  • occurs after 2 weeks
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24
Q

What is the most common COD within the first 24 hours of MI?

A
  • Arrhythmias- particularly Ventricular arrhythmia
  • This leads to dysfunction of the contraction of the heart leading to cardiogenic shock
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25
Q

What are the risk factors for myocardial rupture? What kind of infarct is usually needed?

A
  • Increased age
  • First MI
  • absence of LV hypertrophy
  • Transmural infarct 2-4 days post MI
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26
Q

What is Dressler syndrome?

A
  • Fibrinous pericarditis caused by immune response against myocardial proteins in the blood
  • Leading to Fever pleuritic pain, and pericardial effusion
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27
Q

How does a ventricular aneurysm occur?

A
  • after large transmural infarct with expansion on a thin walled scar leading to the aneurysm
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28
Q

What is angina pectoris?

A
  • transient recurrent chest pain induced by myocardial ischemia insufficient to induce MI
    • Stable angina
    • Prinzmetal variant angina
    • Unstable angina
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29
Q

What is stable angina? What relieves it and agitates it?

A
  • stenotic occlusion of coronary artery
  • Substernal pressure, squeezing, burning
  • Relieved by rest or vasodilators
  • Induced by physical activity and stress
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30
Q

What is the Prinzmetal variant angina?

A
  • Episodic coronary artery spasm relieved with vasodilators
  • Unrelated to Physical activity HR or BP
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31
Q

What is unstable angina?

A
  • Present at rest and/or has increased frequency and duration (Crescendo pattern)
  • Acute chest pain with activity and rest is caused by a ruptured plaque with non occlusive thrombus
  • Chest pain worsening over days to weeks but not occuring at rest is caused by progressive occlusion
32
Q

Helpful chart to angina

A
33
Q

What causes arrhythmias?

A
  • ischemic heart disease (#1)
  • cardiomyopathies
  • myocarditis
  • valvular disease
  • familial congenital disorders
34
Q

What is sick sinus syndrome?

A
  • SA node is damaged leading to bradycardia
35
Q

What is A. fib? What is the risk?

A
  • myocytes depolarize independently and sporadically with variable transmission in the AV node
  • Irregularly irregular
  • Can cause thrombus formation leading to an increased risk of thromboembolism
36
Q

First degree heart block?

A

prolonged PR interval

37
Q

Second degree heart block?

A

Intermittenet transmission

38
Q

3rd degree heart block?

A

complete heart failure

39
Q

What are hereditary channelopathies?

A

Voltage gated ion channels are abnormal causing arrhythmogenic disease

40
Q

What is the most common hereditary channel disorder cause of sudden death after exertion?

A

Long QT syndrome, K or Na dysfunction

41
Q

What is Torsades de pointes on EKG?

A

Long QT syndrome

42
Q

In younger patients what causes sudden cardiac death?

A
  • Drug abuse
  • Hereditary conduction abnormalities
  • Hypertrophic or dilated cardiomyopathy
  • Myocardial hypertrophy
  • Mhyocarditis
  • Mitral valve prolapse
43
Q

___ is overwhelmingly the most common cause of sudden death due to ischemia induced arrhythmias.

A

Coronary artery disease is overwhelmingly the most common cause of sudden death due to ischemia induced arrhythmias.

44
Q

What condition does concentric left ventricular hypertrophy occur in? What are the two complications of this?

A

Hypertension

  • there is no addition of capillaries to supply the increase in muscle so we have an increased oxygen demand which can eventually lead to systolic dysfunction
  • This can also lead to diastolic dysfunction as the left ventricle become stiffer and looses its ability to completely relax. Left ventricle will not fill to capacity and will pump out less blood overall.
45
Q

What are the changes seen in A B C and D

A

A. Marked concentric left vent hypertrophy due to pressure overload, associated with hypertension or significant aortic stenosis

B. Left is same as A, Right is dilated hypertrophy seen with volume overloaded heart

C. normal

D. Enlarged myocyte nucleus consistent with myocyte hypertrophy

46
Q

Left sided heart failure is divided into two categories. Describe them.

A
  • Systolic failure leading to decreased ejection fraction, caused by Ischemic heart disease, HTN, aortic stenosis, dilated cardiomyopathy
  • Diastolic failure leading to a normal ejection fraction but lower total volume due to less filling, caused by HTN, aortic stenosis, hypertrophic cardiomyopathy, restrictive cardiomyopathy
47
Q

What causes R. sided heart failure?

A

Left sided heart failure is the most common cause and Cor Pulmonale is next

48
Q

What are the clinical effects of LHF due to?

A
  • Pulmonary congestion/edema
  • Decreased tissue perfusion
49
Q

What are the signs/sx of left sided heart failure?

A
  • Paroxysmal nocturnal dyspnea
  • Cough, crackles, wheezes, tachypnea
  • Cyanosis
  • Exertional dyspnea
  • Tachycardia
  • Orthopena
50
Q

What does this indicate?

A

Left sided heart failure, however Kerly B lines are not only seen in Left sided CHF

51
Q

What causes R. side heart failure?

A
  • Left heart fails and there is back flow causing Pulmonary hypertension, the pressure gradient is too much for right ventricle and fluid backs up into the right atrium and then the systemic system.
52
Q

Signs and symptoms of R. sided heart failure?

A
  • Exertional dyspnea
  • Ascites
  • Hepatosplenomegaly
  • Distended jugular veins
  • Dependent edema
  • Effusions involving peritoneal pleural and pericardial spaces
53
Q

What causes an isolated right sided heart failure?

A
  • Parenchymal lung disease is the most common cause
  • Lung thrombi
  • Primary pulmonary htn (rare)
    • pushing against increased pressure gradient, right heart eventually fails and fluid backs up into venous system
54
Q

What does this indicate?

A

Right sided heart failure

55
Q

What happens with a chronic pericardial effusion?

A
  • slow accumulation of fluid <500 mL typically asymptomatic effusion
  • See globular enlarged heart on CXR
  • Ex: serous effusion seen in CHF
56
Q

What happens in an acute pericardial effusion?

A
  • Less than one week, 200-300 mL of fluid rapidly accumulates causing Cardiac tamponade (hypotension and death)
  • Caused by hemopericardium, trauma, ruptured MI, aortic dissection
57
Q

What are classic signs and symptoms of pericarditis?

A
  • Pleuritic and position dependent chest pain
  • Pericardial friction rub
  • fever
  • EKG change
  • Pericardial effusion
58
Q

What is the most common type of pericarditis?

A
  • Fibrinous and Serofibrinous pericarditis
    • Fibrinous inflammatory exudate with a variable amount of fluid
59
Q

When is fibrinous or serofibrinous pericarditis seen?

A
  • first 1-3 days after acute MI
  • Weeks later with Dressler’s syndrome (autoimmune)
  • Uremia can lead to this, it is increase in urea seen in CKD with elevate BUN
60
Q

What causes serous pericarditis?

A
  • viral or noninfectious inflammatory diseases
61
Q

What is purulent or suppurative pericarditis?

A

Active infection caused by microbes

62
Q

What is caseous pericarditis?

A
  • TB in origin occasionally fungal
63
Q

Hemorrhagic pericarditis?

A

Caused by malignant neoplasm also trauma

64
Q

Constrictive pericarditis?

A
  • heart is encased in dense fibrous or fibrocalcific scar that limits diastolic expansion and CO, features mimic restrictive cardiomyopathy
65
Q

What is the most common malignant tumor in the heart?

A

Angiosarcoma

66
Q

What is the number one cardiac tumor in adults?

A

Myxoma

67
Q

Most common cardiac tumor in kids and infants?

A

Rhabdomyoma

68
Q

What are cardiac myxomas?

A
  • Stromal tumor of mesenchymal origin
  • Typically seen on the left atrium beginning in the septal region of fossa ovalis
  • “Ball valve” obstruction mechanical damage
  • Secrete IL-6 leading to fever and malaise
  • Ausculation sounds like Plop
69
Q

What are the myxoma associate familial syndromes?

A
  • McCune Albright Syndrome
    • polyostotic fibrous dysplasia, cafe au lait spots, endocrine abnormalities, myxomas GNAS1 mutation
  • Carney complex:
    • skin changes, endocrine dysfunction, mycomas PRKAR1A mutation
70
Q

Describe cardiac lipomas?

A
  • Localized mass composed of mature lobulated fat
  • occurs throughout the heart
71
Q

What is a papillary fibroelastoma?

A
  • Typically incidental
  • “sea anemone like” lesion
  • Located on valves
  • resembles Lambl Excrescences
72
Q

What are rhabdomyomas?

A
  • Most common primary benign tumor (hamartoma) of pediatric heart
  • 50% sporadic mutations
  • 50% associated with tuberous sclerosis with mutations in TSC1 and TSC2
  • Firm grey white well circumscribed masses
  • Larage vacuolated cells called spider cells
73
Q

What is an allograft rejection heart transplant?

A
  • Cell mediated rejection: T cell lymphocytic response, first month to several years after
  • Ab mediated: first month to several years after
  • Allograft vasculopathy:
    • many years later, progressive, diffusely stenosing intimal proliferation
    • 50% develop in five years & in virtually all patients by 10 yrs
    • Silent MI: denervated transplanted heart no angina
74
Q

ChaComplications of heart transplants?

A
  • Infection
  • Malignancy
    • skin cancers
    • EBV positive lymphoproliferative disorder, with T cell immuno suppression
75
Q

Changes in the aging heart?

A
  • Reduction in compliance and elasticity in vessels and heart
  • Fibrous mitral valve
  • Calcific deposits
  • Lambl excrescences
  • Left ventricle cavity size decreases
  • Atrial dilation occurs
  • Atherosclerotic changes
76
Q

Changes with aging in epicardial and myocardial heart?

A
  • Increase in epicardial fat
  • Lipofucin granules ( not pathologic)
  • Basophilic degeneration (not pathologic)
  • Myocyte loss
  • amyloid deposition ( transthyretin) can result in senile amyloidosis (heart failure)
77
Q

Evolution of microscopic changes in a MI.

A
  • ½ -4 hr wavy fibers
  • 4-12 hr early coagulation encrosis, edema
  • 12-24 hr ongoing coagulation necrosis, pyknosis, hypereosinophilia, contraction band necrosis
  • 1-3 days coagulation necrosis loss nuclei
  • 3-7 days beginning disintegration of dead myofibers early phagocytosis by macrophages
  • 7-10 days well dev phagocytosis dead cells & granulation tissue at margins
  • 10-14 days established granulation tissue with blood vessels & collagen tissue
  • 2-8 wk increased collagen deposition decreased cellularity
  • >2 mo dense collagenous scar

CPR 2 Exam 1 (21 decks)

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