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Cardiovascular > Pathology of Ischemic CV Disease > Flashcards

Pathology of Ischemic CV Disease Flashcards

1
Q

Heart disease is secondary to many things. Name 4 of the more common ones, and two less common.

A
  1. valve abnormalities 2. coronary atherosclerosis 3. hypertension 4. congenital anomalies 1. Primary Idiopathic Cardiomyopathy 2. Specific heart muscle disease (myocarditis, sarcoidosis, amyloidosis, hemochromatosis, etc.)
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2
Q

What is Ischemic Heart Disease (IHD)?

A

IHD is a variety of syndromes when myocardial O2 requirement exceeds cardiac blood supply

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3
Q

What is the greatest cause (accounting for >90%) of IHD cases?

A

Obstructive Coronary Atherosclerosis

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4
Q

Symptomatic IHD (stable angina) is typically associated with increased oxygen demand in the presence of >____% coronary atherosclerotic obstruction.

A

70%

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5
Q

>____% stenosis can lead to symptoms even at rest (unstable angina)

A

90%

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6
Q

Myocardial ischemia depends on the extent and severity of the coronary artery stenosis AND the +/- of _________

A

exacerbating factors

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7
Q

Name 3 exacerbating factors of coronary atherosclerosis.

A
  1. Coronary artery vasospasm 2. Platelet aggregation +/- coronary vasospasm 3. Hypotensive episode (e.g. shock, massive hemorrhage in the presence of critically stenosed coronary artery)
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8
Q

What 2 harmful things does coronary artery vasospasm cause?

A

Directly compromises lumen and increases local mechanical shear forces which may contribute to plaque rupture

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9
Q

What are 6 less frequent causes of myocardial ischemia (IHD)?

A
  1. increased myocardial O2 demand (increased HR, HTN) 2. Decreased blood volume (hypotension) 3. Decreased oxygenation (pneumonia) 4. Decreased O2 carrying capacity (anemia) 5. Arteritis (inflammation narrows lumen) 6. Cocaine Abuse (mechanism is vasospasm)
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10
Q

What is Chronic Ischemic Heart Disease?

A

Chronic Ischemic Heart Disease is when there is progressive cardiac decompensation following an acute infarct or multiple small ischemic events with development of contractile impairment due to replacement of myocardium by fibrous tissue (non contractile)

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11
Q

What is the difference between stable and vulnerable plaques?

A

Stable plaques have densely collagenized thickened fibrous caps with minimal inflammation and small atheromatous/lipid cores. Vulnerable plaques are non-obstructive plaques prone to rupture or superimposed acute thrombus. These are thin fibrous caps which are unable to withstand circumferential stress. Large lipid core composed of extracellular lipid released by macrophage cell death.

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12
Q

What are 4 things that happen with vulnerable plaque?

A
  1. Increased plaque inflammation (macrophages/T cells degrade ECM by phagocytosis or proteolytic enzyme secretion and weaken the thin fibrous plaque) 2. Vascular remodeling which is associated with plaque inflammation 3. Vasa vasorum neovascularization of the plaque starts to provide oxygen and remove lipid but fails (lacks supporting cells) red blood cell extravasation, inflammation, and hemorrhage which can lead to luminal narrowing. 4. Intra plaque hemorrhage associated with extravasation of red blood cells with their breakdown and further tissue damage.
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13
Q

What are erosion type plaques?

A

These are heterogenous but in general have little inflammation, often no calcification and an eroded/missing endothelial layer at the plaque-thrombus interface.

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14
Q

What kind of patients are erosion type plaques more common in?

A

Females

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15
Q

What is the most common cause of myocardial infarction?

A

>90% are due to acute coronary artery thrombus superimposed on severe atherosclerosis with plaque rupture.

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16
Q

Where do myocardial infarcts start?

A

Typically, in the subendocardial region. This is because this is the most poorly perfused and hence more vulnerable region

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17
Q

If myocardial infarcts start in the subendocardial region, where do they progress to?

A

They progress outwards towards the epicardial region over several hours. Interventions may limit the progression.

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18
Q

What has a more detrimental effect? Myocardial ischemia due to hypoxia AND low blood flow or just hypoxia alone?

A

Hypoxia and low blood flow together have a more detrimental effect due to the added detrimental metabolic problems.

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19
Q

What are the 4 determinants of the extent of myocardial infarction?

A
  1. Site of occlusion (proximal or distal) 2. Duration of ischemia 3. Extent of any collateral circulation (there is more collateral circulation in the outer myocardium which is another reason that subendocardial area is more susceptible to infarct) 4. Metabolic needs of the myocardium
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20
Q

What is myocardial infarction reperfusion injury?

A

This is injury that occurs to myocytes following restoration of blood flow

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21
Q

What are 5 causes of reperfusion injury?

A
  1. Mitochondrial dysfunction 2. Influx of calcium causing myofibril hypercontracture with cytoskeletal damage and cell death 3. Free radicals damage membrane proteins and phospholipids 4. Leukocyte aggregation 5. Platelet and complement activation
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22
Q

Which part(s) of the heart are the most common sites for myocardial infarction?

A

LV and septum. Only 1-3% involve RV alone. This is because LV has a larger mass, higher workload, and oxygen demand.

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23
Q

For myocardial infarcts, what is the time frame in which ultrastructural and biochemical changes are reversible?

A

0-30 minutes

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24
Q

For myocardial infarcts, what is the time frame in which ultrastructural and biochemical changes begin to be irreversible?

A

1-2 hours

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25
Q

What are 3 examples of reversible ultrastructural/biochemical changes?

A
  1. mitochondrial swelling 2. sarcoplasmic edema 3. loss of glycogen
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26
Q

What are 3 examples of irreversible ultrastructural/biochemical changes?

A
  1. sarcolemmal disruption 2. release of intracellular proteins 3. ion gradient disruption
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27
Q

When looking at macroscopic and light microscopy, what findings do you expect to see after 4-12 hours of infarction?

A

Wavy fibers (non contractile ischemic fibers stretched with each systole)

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28
Q

When looking at macroscopic and light microscopy, what findings do you expect to see after 18-24 hours of infarction?

A

Coagulation necrosis, neutrophils, pallor, and contraction bands at edge of infarct

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29
Q

When looking at macroscopic and light microscopy, what findings do you expect to see after 24-72 hours of infarction?

A

Maximum coagulation necrosis and neutrophils

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30
Q

When looking at macroscopic and light microscopy, what findings do you expect to see after 4-7 days of infarction?

A

Macrophages with disintegration of the myocytes (maximal softening). Pallor with hyperemic border

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31
Q

When looking at macroscopic and light microscopy, what findings do you expect to see after 10 days of infarction?

A

Granulation tissue. Yellow, soft with dark border.

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32
Q

When looking at macroscopic and light microscopy, what findings do you expect to see after 4-8 weeks of infarction?

A

Fibrosis. Firm and gray.

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33
Q

What is this picture of?

A

Fibrosis

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34
Q

What is this a picture of?

A

Granulation tissue and a lot of vascularity trying to rebuild

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35
Q

Of all who have MIs, how many have sudden cardiac death and don’t even make it to the hospital?

A

25%

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36
Q

Out of all the MI cases that are treated at the hospital, how many (percentage) will have complications? And what are 4 of the complications?

A

80-90%

  1. Arrhythmias
  2. LV failure with pulmonary edema
  3. Cardiogenic shock (if >40% LV infarct)
  4. Pericarditis (chest pain, friction rub)
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37
Q

What is this a picture of? (hint: lung)

A

This is a normal lung with clear alveolar spaces

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38
Q

What is this a picture of? (hint: lung)

A

This is a patient with severe left heart failure with pulmonary edema.

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39
Q

What is papillary muscle dysfunction?

A

Papillary muscle dysfunction is infarction or rupture of the papillary muscle which results in valve incompetence. This causes the valves to not close properly and results in regurgitation and heart murmur.

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40
Q

How can rupture of the LV free wall or septum occur after MI? What is the time frame after an MI that this can occur?

A

LV free wall or septum rupture can occur within the first 3 weeks, usually within 2-10 days post infarction. This happens around the 4-7 days period where macrophages disintegrate the myocytes (maximal softening)

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41
Q

Thrombus is a dangerous complication of MI. Explain.

A

Thrombus can form when there are transmural infarcts. The thrombus forms right against the area that is infarcted. During contractions, the area that had infarct won’t be contracting which allows thrombus to form. Parts of the thrombus can break off and cause stroke, kidney infarct, etc (thromboembolus)

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42
Q

For thrombus complication in MI, is it acute or can it happen later on too?

A

It can be acute or also happen later on.

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43
Q

How can a ventricular aneurysm happen as a complication of MI?

A

When part of the ventricular wall has infarct, it no longer contracts. So, during contraction, the other parts of the ventricle are exerting force but the infarcted area of the wall is only fibrous tissue. This part of the wall gets pressure pushed on it from the other parts of the wall pushing blood and it starts to stretch and buldge out. This is ventricular aneurysm. The main complication of this is thrombus and thromboembolism. This is because static blood gets stuck in the area of the aneurysm and can break off.

44
Q

What is the most dangerous part about ventricular aneurysm?

A

Thrombus and thromboembolus.

45
Q

What is re-stenosis and how does this happen in interventional therapy?

A

Re-stenosis is when atherosclerotic plaques develop after interventional therapy. Angioplasties cause endothelial damage and tears in the atherosclerotic plaque and the media which can result in intimal hyperplasia +/- superimposed thrombus with re-stenosis.

Transplanted saphenous veins used in coronary artery bypass operations undergo adaptive and reparative changes including intimal hyperplasia, focal muscle hypertrophy, and advventitial scarring with atherosclerotic plaques developing after several years.

46
Q

In HTN heart disease, there is pressure overload which results in what physical finding?

A

In HTN heart disease, the pressure overload causes new sarcomeres to be added parallel to the long axis of the myocyte. This increase the diameter of the muscle fibers resulting in concentric hypertrophy where the increased thickness is the same all around the heart.

47
Q

With HTN heart disease, patients are prone to ischemic injury. Why?

A

With HTN heart disease, there is an increase in the ventricle wall thickness with increased oxygen requirement. This makes the heart more vulnerable to ischemic injury since the myocardial capillary bed does not expand to compensate for the increased myocardial mass.

48
Q

What is HTN heart disease?

A

HTN heart disease is left ventricular hypertrophy in the presense of clinical HTN and in the absence of other causitive factors.

Sustained LV pressure overload leads to concentric LV hypertrophy which, after a certain point, is no longer compensatory because increased mass causes increased diffusion distances which decrease oxygen perfusion (more prone to ischemia)

49
Q

Patients with HTN are predisposed to ______.

A

Atherosclerosis

50
Q

While HTN can be asymptomatic, what are 3 possible symptoms that patients might present with?

A

Headache, dizziness, renal/cerebrovascular complications

51
Q

What is primary essential idiopathic hypertension?

A

Primary essential idiopathic hypertension is hypertension where there is no identifialbe cause. This accounts for 95% of hypertensive patients. Causes are likely genetic

52
Q

What is the most common kind of HTN?

A

Primary essential idiopathic hypertension. 95%

53
Q

Name 3 types of secondary hypertension and include subtypes if possible.

A
  1. Renal (renal artery stenosis, chronic renal disease)
  2. Endocrine (phaeochromocytoma, adrenal cortical adenoma, cortical tumors)
  3. Vascular (aortic coarctation)
54
Q

What is Cor Pulmonale? What are some diseases that can cause it?

A

Cor Pulmonale is RV hypertrophy/failure due to pulmonary hypertension associated with structural/functional lung abnormalities.

Caused by chronic obstructive airways disease, diffuse interstitial fibrosis, cystic fibrosis, pulmonary emboli, kyhoscoliosis.

55
Q

What are aneurysms?

A

Aneurysms are localized congenitall or acquired vessel dilation secondary to weakening of the wall

56
Q

What are 3 systemic diseases that can cause aneurysms?

A
  1. Atherosclerosis
  2. HTN
  3. Vasculitis
57
Q

What is the congenital disease that can cause aneurysms?

A

Marfan Sndrome (defective synthesis of protein fibrillin)

58
Q

How can infection cause aneurysm?

A

Mycotic aneurysms secondary to septic emboli from infective endocarditis; extension from adjacent infection

59
Q

What are 4 complications of aneurysms?

A
  1. Stenosis or occlusion of vessel branches adjacent to aneurysm resulting in ischemia/infarction
  2. Stasis with thromboembolism
  3. Impinge on adjacent structures (e.g. ureter)
  4. Rupture
60
Q

Are aneurysms symptomatic?

A

No. They are typically asymptomatic but can present with abdominal/chest pain and symptoms of complications (acute ischemic pain)

61
Q

What is a berry aneurysm?

A

Berry aneurysms are congenital defects in the tunica media of arteries at the bifurcation of cerebral vessels. They are the most common cause of spontaneous subarachnoid hemorrhage.

62
Q

Can a patient have multiple berry aneurysms?

A

Yes, in about 25% of cases, there are multiple berry aneurysms

63
Q

What are symptoms of berry aneurysms?

A

Sudden onset of severe headache

64
Q

Berry aneurysms is associated with another disease. What is it?

A

Polycystic renal disease

65
Q

What is the most common type of aneurysm?

A

Atherosclerotic aneurysm

66
Q

How does atherosclerosis cause aneurysms?

A

Atherosclerotic plaque compresses the underlying tunica media causing degeration and thinning of the wall. Inflammation mediates ECM degradation further weakening the wall

67
Q

What age and gender of patient is most commonly affected by atherosclerotic aneurysms?

A

Elderly males

68
Q

Which part of the aorta is a common site of atherosclerotic aneurysm?

A

Lower abdominal aorta below the renal arteries

69
Q

What are symptoms of atherosclerotic aneurysms?

A

Typically asymptomatic. Sometimes in thin patients you can palpate the pulsing mass.

70
Q

Aortic aneurysm at which level of the aorta can compress ureter?

A

The lowest part of the aorta that is below the kidneys.

71
Q

What is vessel dissection and where does it most frequently happen?

A

Vessel dissection is when the blood dissects into the tunica media of the vessel wall. In the majority of cases, a tunica intima defect allows the blood to dissect into the wall. This most commonly happens in the Aorta.

72
Q

What are 3 outcomes of vessel dissection?

A
  1. Dissection goes into the wall and out into the mediastinum. This can rupture and bleed into the mediastinum or retroperitoneum
  2. The vessel dissection can progress from the aorta back into the pericardial cavity which can cause tamponade
  3. The vessel dissection can be double barrelled and go from one part of the aorta to another.
73
Q

What are symptoms of vessel dissection?

A

Sudden onset of severe chest pain radiating to the back

74
Q

What can vessel dissection cause?

A

Hypotension and shock

75
Q

What does vessel dissection look like on a CT scan?

A

Double lumen

76
Q

Who is most likely to get vessel dissection?

A

Men age 40-60 w/ HTN, or younger patients with Marfan syndrome

77
Q

What is vasculitis? what vessels can it be found in?

A

Inflammatory process involving vessels with damage to the vessel wall. There are cases where there are only a few vessels involved and there are also cases where there is widespread vascular involvement.

78
Q

What happens to vessels in vasculitis? (5 things)

A
  1. Narrowing of the lumen
  2. Destruction of the internal elastic lamina
  3. Fibrosis
  4. Thrombosis with ischemia, infarction
  5. Aneurysm formation
79
Q

What is vasculitis classification based on? (4 things)

A
  1. Size of blood vessels involved
  2. Anatomic site
  3. Histologic characteristics (e.g. granulomatous inflammation, eosinophils)
  4. Clinical features and serologic tests
80
Q

What is infectious vasculitis?

A

Direct invasion of arteries by bacteria or fungi especially aspergillus/mucor

81
Q

What is Giant Cell (temporal) arteritis?

A

Segmental granulomatous inflammation of branches of the carotid arteries especially the temporal artery with fragmentation of the internal elastic lamina (sometimes involves the opthalmic artery)

82
Q

What is the most common type of arteritis?

A

Giant Cell (temporal) Arteritis

83
Q

How can Giant Cell (temporal) Arteritis cause blindness?

A

This happens if the segmental granulomatous inflammation takes place in the opthalmic artery. This is a medical emergency and if not treated, patients can go permanently blind.

84
Q

Which patients (age and gender) are most prone to temporal (giant cell) arteritis?

A

Elderly females

85
Q

What are symptoms of temporal (giant cell) arteritis?

A

Headache, localized tenderness, visual symptoms (blindness)

86
Q

How do you diagnose temporal (giant cell) arteritis?

A

Patient greater than 50 years old, clinical symptoms (headache, localized tenderness, visual symptoms), Erythrocyte sedimentation rate, and biopsy.

Elevated ESR is a positive finding

87
Q

How do you treat temporal (giant cell) arteritis?

A

Steroids. Results in dramatic response

88
Q

What is polyarteritis nodosa? Which organs/systems does it affect? Which organ system does it not affect?

A

Acute segmental necrotizing vasculitis of small & medium size arteries with coexisting different stages of inflammation; +/- superimposed thrombosis (organ infarcts), microaneurysms (can rupture).

Affects Kidney (hematuria, hypertension, failure), GI tract (abdominal pain, melena), and Heart

NO lung involvment.

89
Q

What age and gender patient is more likely to get polyarteritis nodosa?

A

Middle aged males

90
Q

What is the pathogenetic mechanism of polyarteritis nodosa?

A

It is thought that immune complexes develop containing hepatitis B antigens that deposit in affected vessels with resultant inflammation and associated consequences. Hepatitis B surface antigen is positive in 30% of polyarteritis nodosa patients

91
Q

How do you treat Polyarteritis Nodosa?

A

Steroids and immunosuppressive drugs

92
Q

What is Kawasaki’s Disease?

A

Acute necrotizing vasculitis of medium sized vessels, targets the coronary arteries.

93
Q

What is the typical course of Kawasaki’s Disease? What patients typically present with it? Symptoms?

A

Kawasaki’s Disease is found usually in infants and chlidren. It is a self limited febrile illness. Symptoms are fever, conjunctivitis, oral erosions, skin rash, adenopathy, and rarely cardiac involvement (<1% develop coronary arteritis with thrombosis or aneurysms with an associated mortality.

94
Q

What is Wegener’s Granulomatosis? Which organs/systems are involved?

A

Wegener’s Granulomatosis is necrotizing granulomatous inflammation of small to medium sized vessels.

Involves upper and lower respiratory tract (chronic sinusitis, mucosal ulcers, pneumonitis) and Kidneys (focal/crescentic glomerulonephritis)

95
Q

Is wegener’s granulomatosis more commonly found in males or females?

A

males

96
Q

What is the suspected pathophysiology for Wegener’s Granulomatosis?

A

Cell mediated hypersensitivity response directed against inhaled infectious or environmental antigents (with resultant tissue damage)

97
Q

What is Churg Strauss Syndrome? Which age group of patients? Symptoms and organ systems?

A

Allergic type vasculitis which causes granulomatous necrotizing vasculitis of small arteries and veins. It’s more common in young adults and presents with fever, asthma, eosinophilia. It targets the lungs, spleen, heart, GI, and CNS.

98
Q

What is leukocytoclastic/hypersensitivity vasculitis?

A

It is a hypersensitivity to drugs or infections which involves arterioles, venules, and capillaries of the skin mucosa. Presents as palpable purpura on skin.

99
Q

What is granuloma pyogenicum?

A

It’s a benign vascular lesion which presents as a polypoid (polyp) granulation tissue nodule on skin or mucosa. May be associated with trauma or pregnancy and in pregnancy it usually disappears after delivery

100
Q

What is capillary hemangioma?

A

It is a benign neoplastic proliferation of the skin, mucosal surfaces, and occasionally deep organs. These happen typically in newborns and regress over time.

101
Q

What is cavernous hemangioma?

A

Cavernous hemangioma are larger than capillary hemangioma. It can happen on the skin, mucosa, or organs.

It may be associated with Von Hippel Lindau disease (autosomal dominant with visceral angiomas and renal cell carcinoma).

Distribution with the 5th cranial nerve may be associated with Sturge Weber Syndrome.

102
Q

What is angiosarcoma? Age and race? Organs/systems?

A

It’s a rare, malignant sarcoma involving the skin, soft tissue, breast, or liver. Typically effects elderly caucasians. May be associated with thorotrast, arsenic, polyvinyl chloride.

103
Q

Whati s Kaposi’s Sarcoma?

A

It is an intermediate grade tumor with skin, mucosa, or deep visceral involvement.

Associated with AIDS and HHV8 virus (herpes virus-8)

May start with skin/mucosal plaques/nodules and progress to involve internal organs.

104
Q

Name the benign vascular legions (3)

A
  1. Granuloma Pyogenicum
  2. Capillary Hemangioma
  3. Cavernous Hemangioma
105
Q

Name an intermediate grade vascular lesions

A

Kaposi Sarcoma

106
Q

Name a malignant vascular lesion

A

Angiosarcoma

Cardiovascular (22 decks)

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