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Block 4 - Cardio > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

0
Q

What is forward and backward heart failure?

A

Forward - inadequate cardiac output

Backward - congestion of venous circulation, normally accompanies forward

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1
Q

What is low output vs. high output failure?

A

Low - heart unable to pump all blood delivered to it from veins
High - heart pumps enough blood but for non cardiac reason delivery of nutrients and oxygen to tissue is not adequate

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2
Q

What are the three compensatory mechanisms employed during heart failure?

A
  1. Activation of neurohormonal systems - release of NE increases HR and contractility, activation of RAAS increases peripheral resistance and blood volume, atria secrete ANP in response to distension which produces vasodilation, natriuresis, and diuresis
  2. Frank starling mechanism - increased stretch of myocytes increases contractility by increasing number of myosin heads that can attach to actin in sarcomere
  3. Myocardial hypertrophy - pressure overload leads to concentric hypertrophy (increase in cell diameter), volume overload leads to eccentric hypertrophy (increase in cell length)
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3
Q

What are the four main causes of left sided heart failure?

A

Ischemic heart disease
Systemic hypertension
Mitral or aortic valve disease
Primary diseases of myocardium

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4
Q

What are the main causes of right sided heart failure?

A

Left sided heart failure

Diseases of pulmonary parenchyma or vasculature

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5
Q

What are the clinical findings in left sided heart failure?

A

Predominantly pulmonary symptoms

Dyspnea, cough, pulm venous congestion, leakage of fluid and RBCs into alveoli

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6
Q

What is the morphology of left sided heart failure?

A

Pulm congestion and edema
Hemosiderin in macrophages in alveoli = heart failure cells
Dependent upon underlying disease process

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7
Q

What are the clinical findings in right sided heart failure?

A

Peripheral edema, ascites, hepatosplenomegaly, pleural effusions, dependent pitting edema

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8
Q

What is the morphology of right sided heart failure?

A

Hepatosplenomegaly with nutmeg liver
Pleural effusions
Pedal edema

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9
Q

What are the two forms of hypertension?

A

Systemic - entire body except lungs

Pulmonary (cor pulmonale) - only increase in BP is in pulm vasculature

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10
Q

What are the criteria for pathologic diagnosis of hypertensive heart disease?

A

Left ventricular hypertrophy with no other identified cause and a history of or evidence of hypertension (hyaline arteriosclerosis)

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11
Q

What are the clinical findings in systemic hypertensive heart disease?

A

Left ventricular hypertrophy without dilation

Ischemic heart disease, progressive renal failure, cerebral vascular hemorrhage, heart failure

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12
Q

What are the criteria for pathologic diagnosis of cor pulmonale?

A

Right ventricular hypertrophy and dilation

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13
Q

What are the two forms of cor pulmonale?

A

Acute - follows thromboemboli that obstruct >50% of vasculature
Chronic - prolonged pressure overload on right ventricle

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14
Q

What are the causes of cor pulmonale?

A

Diseases of pulmonary parenchyma - COPD, CF, fibrosis, pneumoconiosis
Diseases of pulm vessels - recurrent thromboemboli, pulm arteritis
Disorders affecting chest movement - kyphoscoliosis, obesity
Disorders inducing pulm arterial constriction - metabolic acidosis, hypoxemia

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15
Q

What are the four clinical syndromes composing the general category of ischemic heart disease?

A

Angina pectoris (stable, unstable, prinzmetal)
Acute MI
Chronic ischemic heart disease
Sudden cardiac death

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16
Q

What is the most common underlying cause of ischemic heart disease?

A

Coronary artery atherosclerosis

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17
Q

Other than growth, what acute changes in a plaque can contribute to obstruction of vessel?

A

Vasospasm of vessel
Hemorrhage into plaque
Thrombosis

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18
Q

What three conditions are comprised by the term acute coronary syndrome?

A

Unstable angina
Acute MI
sudden cardiac death

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19
Q

What is an acute plaque change?

A

Rupture, fissuring, or ulceration of plaque will expose lipid core to the blood - very thrombogenic
Plaque of certain size can become neovascularized & hemorrhage

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20
Q

What are vulnerable plaques?

A

Thin fibrous cap (<6.5 micrometer) and thick core less stable and more likely to rupture

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21
Q

Besides cap and core, what are other factors affecting the stability of a plaque?

A

Collagen remodeling

Adrenergic stimulation - through development of hypertension or vasospasm

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22
Q

What are three factors affecting development of ischemic heart disease?

A

Inflammation
Thrombus - can organize (directly increasing size of plaque) or stimulate migration of smooth muscles in (indirect)
Vasoconstriction - stimulated by adrenergic agonists, thromboxane, and imbalance between vasoconstrictors and dilator

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23
Q

What is angina pectoris?

A

Chest pain due to non-sustained and reversible myocardial ischemia
3 types - stable, unstable, prinzmetal

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24
Q

What is stable angina?

A

Chest pain with exertion but not rest
Pain is constant
Crushing or squeezing
Due to fixed (no acute change) plaque with >75% stenosis

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25
Q

What is prinzmetal angina?

A

Chest pain at rest

Due to vasospasm of a vessel that can be normal or have atherosclerosis

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26
Q

What is unstable angina?

A 
Not constant - occurs with increasing frequency and intensity
Can occur at rest
Still crushing or squeezing 
Due to an acute plaque change
Reversible but Pre-infarction angina
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27
Q

What are the two possibilities when only a portion of the myocardium is affected by an MI?

A

Obstruction was not complete

Infarct only due to atherosclerosis with no acute plaque change in combo with increased myocardial demand

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28
Q

What are the functional, biochemical, and morphological changes that occur in the myocardium following ischemia?

A

Functional - loss of contractility and electrical instability
Biochemical - loss of ATP and glycogen
Morphological - ultra structural (cell swelling), microscopic (necrosis), gross (infarct)

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29
Q

How does an infarct evolve?

A

Starts in subendocardium and takes 3-6 hrs to reach epicardium
20-40 minutes to cause irreversible injury
If heart is working, more area damaged
Collateral circulation can develop if evolves slowly

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30
Q

Where do most infarcts occur?

A

Left ventricle or inter ventricular septum

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31
Q

What is trans mural or subendocardial infarct?

A

Trans mural involves >50% of wall (STEMI)

Subendocardial involves <50% of wall (NSTEMI)

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32
Q

What is the timing of the gross appearance of MIs?

A

Before 12 hrs nothing seen

After 2 months, all dense scars

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33
Q

What is the timing of the morphological appearance of MIs?

A

4 hrs - coagulative necrosis begins
12 hrs to 3 days - neutrophilic infiltrate
3 days - macrophages enter
7-10 days - granulation tissue
10-14 days - collagen deposition, increases until 2 months

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34
Q

How do infarcts heal?

A

From the outside in

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35
Q

What happens microscopically with reperfusion?

A

Hemorrhage because of damaged leaky vessels

Contraction band necrosis - calcium enters damaged cells and promotes intense contraction

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36
Q

What are EKG abnormalities associated with MIs?

A

Q waves indicate transmural infarct
St segment abnormalities
T wave inversion indicates myocardial repolarization abnormalities

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37
Q

How are lab values used to diagnose an MI?

A

CK-MB/total CK ratio is high
Troponin I is elevated - can be detected longer after infarct than CK-MB - preferred marker but not completely specific for MI

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38
Q

What are complications of MIs?

A

Contractile dysfunction - hypotension, pulm congestion and edema
Cardiogenic shock - from loss >40% of LV
arrhythmias - sinus bradycardia, heart block, v tach,v fib
Myocardial rupture - 3 days after
Pericarditis - 2-3 days after transmural MI
infarct expansion
Mural thrombus - can embolize
Ventricular aneurysm - rarely rupture but thrombi can form
Papillary muscle dysfunction

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39
Q

What is the morphology of chronic ischemic heart disease?

A

Dilated and hypertrophied heart
Coronary artery atherosclerosis
Might be fibrous scars in myocardium
Microscopically - hypertrophy, fibrosis, subendocardial vacuolization

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40
Q

What is sudden cardiac death?

A

Death occurring without symptoms or within 1-24 hrs from symptom onset
Most common cause is atherosclerosis

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41
Q

What are the three man vascular congenital anomalies?

A

Berry aneurysm - outpouchings of vessel walls located in circle of Willis, not present at birth - expansion of congenital wall weakness
Arteriovenous fistulae - bypass capillaries, remain unused and increase work of heart –> high output failure
Fibromuscular dysplasia - thickening of wall of muscular arteries, in renal arteries leads to secondary HT

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42
Q

What is the pathogenesis of arteriosclerosis?

A

Endothelial injury leads to smooth muscle cells migrating into intima - start secreting ECM
Thickening and loss of elasticity of vessel wall (esp intima)

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43
Q

What are the three different forms of arteriosclerosis?

A

Atherosclerosis
Arteriosclerosis - hyaline, hyperplastic
Monckeberg medial calcification

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44
Q

What is monckeberg medial calcification?

A

Calcified deposits in media of muscular arteries (often radial or ulnar) in individuals over age of 50
Rarely causes stenosis of vessel

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45
Q

What are causes of intimal thickening?

A

Anything damaging intima - it is a nonspecific change

Infection, trauma, inflammation, toxins, etc.

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46
Q

What are the three categories of risk factors for atherosclerosis?

A

Major and modifiable
Major and non-modifiable
Those of uncertain risk

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47
Q

What is the pathogenesis of atherosclerosis?

A

Endothelial dysfunction results in:
Adhesion of monocytes that produce ROS that oxidize LDL - macrophages ingest this leading to accumulation
T cells release gamma interferon which causes smooth muscle cells to enter intima - FGF and TGF-alpha
Smooth muscle cells proliferate and secrete ECM (collagen)
Platelet adhesion and thrombosis

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48
Q

What can cause injury to the endothelium?

A

Toxins in cigarette smoke
Hemodynamic disturbances - plaques commonly occur at points of altered flow like bifurcations and Ostia, laminar flow induces protective genes
Hypercholesterolemia
Infectious agents

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49
Q

What are some major, non-modifiable risk factors for atherosclerosis?

A

Increasing age
Male sex (until menopause)
Family history - increases risk, but multifactorial

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50
Q

What are some major and modifiable risk factors for atherosclerosis?

A

Smoking
Diabetes
Hypercholesterolemia
HT

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51
Q

What are “other” risk factors for atherosclerosis?

A

Elevated c reactive protein - acute inflammation reactant, acts as a marker
Lipoprotein a - competitively inhibits plasminogen
Metabolic syndrome
Hyperhomocysteinemia
Elevated pro coagulants

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52
Q

What is the morphology of atherosclerosis?

A

Fatty streaks - linear, slight intimal elevations filled with lipid laden foam cells, can appear in aorta as young as 1
Plaque - smooth muscle cells, T cells, and macrophages in shoulder, ECM, and lipid

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53
Q

What are acute complications of atherosclerosis?

A 
Rupture
Ulcer
Erosion
Hemorrhage 
Embolism
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54
Q

What are chronic complications of atherosclerosis?

A

Slow increase in stenosis of vessel

Aneurysm from weakened media

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55
Q

What is claudication?

A

Atherosclerosis in vessels of lower extremities produces ischemia of muscles with exercise (walking) that causes this pain
Pain ceases with cessation of exercise

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56
Q

What is essential (primary) hypertension?

A

Systemic hypertension not due to identifiable cause
90-95% of cases
Due to multiple genetic and environmental factors that reduce renal sodium excretion and/or produce vasoconstriction

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57
Q

What are some causes of secondary hypertension?

A

Most commonly renal causes - Ren art stenosis, chronic disease, acute glomerulonephritis
Endocrine causes - Aldo secreting tumor, pheochromocytoma
Cardiovascular diseases - coarctation, RA stenosis, polyarteritis n.
Neurologic causes - increased intracranial pressure, stress

58
Q

What is benign hypertension?

A

Longer duration

Capable of long life unless acute complication occurs

59
Q

What is malignant hypertension?

A

Acute and marked increase in BP associated with renal failure and other symptoms
Can cause death in 1-2 yrs if untreated

60
Q

What is the morphology of systemic hypertension?

A

Hyaline arteriosclerosis - acellular and eosinophilic thickening of wall due to leakage of plasma proteins and overproduction of ECM, seen in benign HT
hyperplastic arteriosclerosis - cellular, concentric, thickening of arterioles wall = onion skin, seen in malignant HT
Cardiac hypertrophy and granular kidney

61
Q

What is an aneurysm?

A

Localized abnormal dilation of blood vessel wall or wall of heart

62
Q

When does a dissection occur?

A

Tear in intima of vessel allows blood to dissect into media which is often weakened by another disease process

63
Q

What is a true vs. false aneurysm?

A

True - dilation involve all three layers of wall

False - hematoma outside wall due to damage

64
Q

What are the different shapes of an aneurysm?

A

Saccular - eccentric outpouching of wall of vessel involving only segment of wall
Fusiform - generalized, concentric dilation of vessel wall
Mycotic - from infections

65
Q

What are common and less common causes of aneurysm?

A

Common - atherosclerosis and cystic medial degeneration

Other - infections (syphilis), trauma

66
Q

What is an AAA?

A

True, sac ulnar aneurysm
Usually just distal to renal arteries
Most often due to atherosclerosis

67
Q

What is the pathogenesis of an AAA?

A

Weakening of wall - inflammation and oxidative stress
Matrix mellanoproteinases and inhibitors - digest wall
Necrosis from plaques impairing delivery of nutrients

68
Q

What is the clinical course of an AAA?

A 
Rupture and hemorrhage 
Obstruct branch vessel --> ischemic injury
Emboli
Compression of adjacent structure
Abdominal mass
69
Q

What is the treatment of an AAA?

A

At 5 cm, risk of rupture greatly increases - these and bigger are treated with excision or graft placement

70
Q

What are causes of thoracic aortic aneurysms?

A

Syphilis
Bicuspid aortic valve
Marfans syndrome
Vasculitis (giant cell arteritis, Takayasu arteritis)

71
Q

What are the complications of a thoracic aortic aneurysm?

A

Pressure on mediastinal structures - lungs, esophagus, airway
Persistent cough - recurrent laryngeal nerves
Valvular (aortic) insufficiency
Aortic rupture

72
Q

What is the main cause of aortic dissection?

A

Hypertension

Can also occur in Marfans and pregnancy

73
Q

What is the pathogenesis of the development of an aortic dissection?

A

Increased BP on aortic wall comprises vasa vasorum and thus oxygen and nutrient delivery to wall

74
Q

What are the clinical complications of an aortic dissection?

A

Sharp, excruciating pain
High mortality
Aortic insufficiency if hemorrhage extends to valve ring
MI if coronary artery compressed

75
Q

What are the two main mechanisms by which vasculitis occurs?

A

Immune mediated - immune complex associated, antineutrophil cytoplasmic antibodies cause them to degranulate (c-ANCA - cytoplasmic against proteinase3, p-ANCA - perinuclear against myeloperoxidase), anti-endothelial antibodies
Infections

76
Q

What are the different forms of vasculitis?

A

Large vessel: giant cell (temporal arteritis), Takayasu arteritis
Medium vessels: polyarteritis nodosa, Kawasaki disease
Small cell: microscopic polyarteritis, wegener granulomatosis

77
Q

How do you differentiate between giant cell (temporal) and Takayasu arteritis?

A

Affect aorta and branch vessels
Have granulomas
Giant cell symptoms - facial pain, headache, visual disturbances
Takayasu symptoms - pulseless disease, ocular and neurologic
Giant cell in >50 years old
Takayasu in <50 years old

78
Q

What is polyarteritis nodosa?

A

Small and medium sized vessels (renal and visceral, not pulm)
Segmental and transmural necrotizing inflammation, temporally dissimilar lesions
Varied clinical presentation
30% have HBsAg-HBsAb immune complexes, no ANCA association

79
Q

What is Kawasaki disease?

A

Coronary arteries
Transmural inflammation, less fibrinous necrosis than PAN
Affects infants and children
Acute - conjunctival and oral erythema, edema of hands and feet, rash, cervical lymph node enlargement, coronary arteritis
Chronic - coronary artery ectasia and aneurysm
Delayed type hypersensitivy with formation of autoantibodies to endothelial cells

80
Q

What is microscopic polyarteritis?

A

Capillaries, arterioles, venules
Segmental and transmural necrotizing inflammation
Temporally similar lesions - unlike PAN
lung commonly involved - unlike PAN
Involves skin, brain, heart, GI tract, kidney
P-ANCA antibodies in most

81
Q

What is wegener granulomatosis?

A

Small vessels
Characteristic triad is acute necrotizing granulomas of upper respiratory tract, necrotizing or granulomatous vasculitis (lungs), and focal necrotizing or crescentic glomerulonephritis
Male more affected than females, 40 years old, chronic pneumonitis and sinusitis, renal disease
C-ANCA antibodies in most

82
Q

What is churg-Strauss syndrome (allergic granulomatosis and angiitis)?

A

Small vessels
Transmural necrotizing inflammation
Allergic rhinitis, asthma, peripheral eosinophilia, coronary arteritis is more common and renal disease less common than wegener
Half have p-ANCA antibodies

83
Q

What is buerger disease (thromboangiitis obliterans)?

A

Medium and small vessels esp tibial and radial arteries
Segmental and acute chronic vasculitis, with luminal thromboses and micro abscesses
Begins before 35 yrs almost entirely in heavy smokers
Phlebitis with pain leads to ulceration of toes, feet, fingers
Due to toxicity of tobacco or idiosyncratic immune response

84
Q

What is raynaud phenomenon?

A

Condition due to exaggerated vasoconstriction of arterioles and arteries in digits
Fingers appear white at constriction, blue distal to it, and red proximal

85
Q

What is primary raynaud phenomenon?

A

Common in young women
Vasoconstriction due to cold or emotion
Benign with rare ulceration and atrophy

86
Q

What is secondary raynaud phenomenon?

A

Vasoconstriction associated with another underlying disease process like SLE or atherosclerosis

87
Q

What is cardiac raynaud?

A

Excessive constriction of heart vessels leads to infarction

Can result in SCD or ischemic dilated cm

88
Q

What are varicose veins?

A

Dilated veins produced by increased intraluminal pressure or loss of vessel wall support
In legs - associated with stasis
Esophageal - due to cirrhosis of liver
Hemorrhoids - due to prolonged pelvic vascular congestion

89
Q

What is thrombophlebitis?

A

Inflammation and thrombosis of veins
Risk factor are immobility, factor v Leiden and other hypercoagulable states, CHF, neoplasia, pregnancy, obesity
Can embolize

90
Q

What is lymphangitis?

A

Inflammation of lymphatics

Often bacterial in origin

91
Q

What are the three types of hemangiomas?

A

Cavernous - more common in deeper organs, do not regress
Capillary - more common in skin, tend to regress, common in infants and children
Pyogenic granuloma - proliferating capillaries, chronic inflammatory infiltrates, and edema (exuberant granulation tissue) - often follow trauma and on skin, gingiva (of pregnant females)
These are all benign

92
Q

What are other benign vascular tumors in addition to hemangioma?

A

Lymphangiomas
Glomus tumor - painful, from modified smooth muscle cells of glomus body, common on distal parts of digits under nails
Vascular ectasia - dilation of Pre existing vessel, includes hereditary hemorrhagic telangiectasia = osler weber rendu with dilated capillaries and veins in skin and oral mucous membranes
Bacillary angiomatosis - skin, bone, and brain due to infection with bartonella, in immunocompromised

93
Q

What is an intermediate grade malignant tumor?

A

Kaposi sarcoma:
Chronic - lower extremities, not associated with HIV
Lymphadenopathic - aggressive involving internal organs, not associated with HIV
Transplant associated - Aggressive
Aids associated - skin or viscera
Due to infection with HHV-8
Patches, then plaques, then nodules
Microscopic angulated blood vessels and spindle cells with extravasated RBCs

94
Q

What is an angiosarcoma?

A

Range from well to poorly differentiated
Hepatic arises in background of vinyl chloride use, arsenical pesticides, thorotrast
Most arise after axillary node dissection for breast cancer

95
Q

Are stenosis and regurgitation acute or chronic?

A

Stenosis - almost always chronic

Regurgitation - acute or chronic

96
Q

What are causes of aortic stenosis?

A

Degenerative calcific tricuspid valve
Calcification of congenital bicuspid
Chronic rheumatic valvulitis

97
Q

What are causes of aortic regurgitation?

A 
Chronic rheumatic valvulitis 
Infective endocarditis
Syphilitic aortitis
Rheumatoid arthritis
Marfan
98
Q

What are causes of mitral stenosis?

A

Chronic rheumatic valvulitis

99
Q

What are causes of mitral regurgitation?

A 
Chronic rheumatic valvulitis
Infective endocarditis
Myxomatous valve
Fen phen induced valvular fibrosis 
Rupture of papillary muscle or chordae tendinae 
Left ventricular enlargement 
Calcification of mitral ring
100
Q

What is the age of onset of symptoms of aortic stenosis?

A

Tricuspid: 70-80 yrs
Bicuspid: 40-50 yrs

101
Q

What are the three main clinical features of aortic stenosis?

A

Angina
Syncope
CHF

102
Q

What is the pathogenesis of myxomatous mitral valve?

A

Unknown
Chromosomes 16, 11 and 13 have been linked to prolapse
Associated with syndromes with defects in connective tissue
Women affected much more than men

103
Q

What is the morphology of myxomatous mitral valve?

A

Ballooning of leaflets that are large, thick and rubbery

Chordae tendinae are long and can rupture

104
Q

What are the clinical features of myxomatous mitral valve/mitral valve prolapse?

A

Mid systolic click
Can develop regurgitation
Risk for SCD due to ventricular arrhythmia

105
Q

How does acute rheumatic fever develop?

A

Due to antibodies against m proteins of group a strep that cross react with glycoproteins in human body

106
Q

What are the clinical manifestations of acute rheumatic fever?

A

Arthritis that moves from joint to joint

Carditis - peri, myo, or endo

107
Q

How is acute rheumatic fever diagnosed?

A

Evidence of previous strep infection and two or more of jones criteria:
Carditis, migratory polyarthritis, subcutaneous nodules, erythema marginatum, Sydenham chorea

108
Q

What is chronic rheumatic fever characterized by?

A

Scarring of valve

Most often mitral, then aortic

109
Q

What is the morphology of acute rheumatic fever?

A

Aschoff bodies - zone of degenerating, hypereosinophilic material infiltrated by t lymphocytes, with large macrophages, called anitschkov cells with wavy ribbon-like chromatin

110
Q

What is the morphology of chronic rheumatic fever?

A

Mitral valve - thick leaflets, thick, fused, and shortened chordae tendinae, fusion of commissures, stenosis –> LA dilation and mural thrombi
Aortic valve - fusion at all commissures, cusps can be thickened and fibrotic

111
Q

What are the different forms of infective endocarditis?

A

Acute - rapid, highly virulent organism, often damages previously normal valve, high mortality
Subacute - prolonged course, previously abnormal valve, less virulent organism, harder to diagnose because less symptoms

112
Q

What is the pathogenesis of infective endocarditis?

A

Jet streams produced by an abnormal valve allow for platelet-fibrin deposits to form on valves
These are infected by bacteria
Vegetarians are friable because only bacteria and fibrin holding them together

113
Q

What patients are most at risk for infective endocarditis?

A

Patients with neutropenia, immunodeficiency, malignancy, diabetes, or history of drug and alcohol use

114
Q

What are the three main complications of infective endocarditis?

A

Glomerulonephritis
Septicemia
Embolization

115
Q

What kind of bacteria infects normal as opposed to abnormal valves most commonly?

A

Normal - s. aureus

Abnormal - viridans strep

116
Q

What is marantic endocarditis/non bacterial thrombotic endocarditis?

A

Sterile vegetations (fibrin, platelets, blood components) found on normal valves
Can organize into strands of fibrous tissue = Lambl excrescences
Occurs in setting of hypercoagulable states (sepsis with DIC, malignancy esp mucinous adenocarcinoma)
Damage to valve minimal, but vegetations can embolize

117
Q

What are the two separations of cardiomyopathies?

A

Primary - disease confined to heart muscle

Secondary - disease part of more widespread, multi-organ disorder

118
Q

What are the three main types of cardiomyopathies?

A

Dilated - impaired systolic function

Hypertrophic and restrictive - impaired diastolic

119
Q

Which cardiomyopathy cannot be diagnosed microscopically?

A

Dilated

120
Q

What are the main causes of dilated cardiomyopathy?

A

Viral infections - coxsackie b or enteroviruses
Alcohol use
Genetic abnormalities - mutations in lamins A and C and beta myosin heavy chain, dystrophin, alpha cardiac actin
Peripartum state - combo of pregnancy induced hypertension, volume overload, and underlying cardiac defect

121
Q

What are the clinical features of dilated cardiomyopathy?

A

CHF from dilation of LV
Mitral insufficiency
Abnormal cardiac rhythms
Emboli from mural thrombi

122
Q

What can be seen microscopically in HCM?

A

Myofiber disarray
Fibrosis
Sclerosis of blood vessels
Hypertrophy without dilation

123
Q

What is the pathogenesis of HCM?

A

Mutations in sarcomeric proteins
Mostly beta myosin heavy chain, also myosin binding protein c and troponin t
Inefficient contraction may trigger hypertrophy

124
Q

What are the clinical features of HCM?

A

Impaired diastolic filling –> reduced CO
increase in pulm pressure
Systolic ejection murmur
Ischemia

125
Q

What are the three main complications of HCM?

A

Arrhythmias
CHF
sudden death

126
Q

What is the morphology of restrictive cardiomyopathy?

A

Ventricles normal or slightly enlarged
No dilation
Microscopic changes depend on cause

127
Q

What is the pathogenesis of restrictive cardiomyopathy?

A

Reduction in ventricular compliance due to infiltrative process of myocardium cause impaired filling during diastole

128
Q

What are the causes of restrictive cardiomyopathy?

A 
Idiopathic
Amyloidosis
Hemochromatosis 
Sarcoidosis
Radiation fibrosis
Inborn errors of metabolism
129
Q

What are the two variants of restrictive cardiomyopathy?

A

Endomyocardial fibrosis - children and young adults in Africa and tropical areas, dense fibrosis of endocardium and subendocardium which causes reduced compliance
Loeffler endomyocarditis - dense endocardial fibrosis associated with peripheral eosinophilia, major basic protein from eosinophils may damage endocardium

130
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

Dilation of RV associated with thinning of wall and fibrosis
Can present with features of RHF or SCD
AD familial and linked to ch 14 in some cases

131
Q

According to the Dallas criteria, what is myocarditis defined by?

A

Inflammatory infiltrate (lymphocytes) and myocardial necrosis

132
Q

What are some causes of myocarditis?

A

Viral - coxsackie, ECHO, flu, HIV, CMV
Chlamydia and rickettsia
Bacteria - corynebacterium diphtheriae, borrelia
Fungi - candida
Protozoa - t. Cruzi, toxoplasmosis
Helminths - trichinosis
Immune mediated - post viral, post strep, SLE, drug hypersensitivity
Unknown - sarcoidosis and giant cell myocarditis

133
Q

What is the pathogenesis of myocarditis?

A

Most often caused by viruses esp coxsackie b
Direct cytotoxic effect on myocardium or induce cross reacting antibodies or body can mount response against viral damaged cells

134
Q

What are the different variants of myocarditis?

A

Lymphocyte myocarditis - mononuclear inflammatory infiltrate associated with myocyte necrosis, most commonly viral cause
Hypersensitivity myocarditis - eosinophils concentrated around vessels, prescription meds are cause
Giant cell myocarditis - prominent number of macrophages and multinucleated giant cells, high mortality rate

135
Q

What is the morphology of pericarditis (inflammatory infiltrate in pericardial sac)?

A

Exudate can be fibrinous (viral), fibrinopurulent (bacteria), fibrinohemorrhagic (malignancy)
First two are acute and can resolve but possibly with scars
Pericarditis + scars = chronic pericarditis
Fibrosis can impair diastole = constrictive pericarditis

136
Q

What are causes of pericarditis?

A

Viral, fungal, bacterial, post MI, uremia, rheumatic fever, SLE, Metastases

137
Q

What are clinical findings of pericarditis?

A

Atypical chest pain not related to exertion
Friction rub
Tamponade
SLE can cause fibrous band around heart

138
Q

What are the types of pericardial effusions?

A

Serous - CHF, hypoalbuminemia
Serosanguinous - trauma, malignancy, ruptured MI
chylous - lymphatic obstruction

139
Q

What are the clinical features of pericardial effusions?

A

Slow accumulation can tolerate larger amount (1-2 liters)

Rapid accumulation 250-300 ml can cause tamponade

140
Q

What is the most common neoplasm of the heart?

A

Metastases from lung, lymphoma, breast cancer, leukemia, melanoma, carcinoma of liver

141
Q

What are primary neoplasms of the heart?

A

Mostly benign
Order of frequency: myxoma, fibromas, lipomas, papillary fibroelastoma, rhabdomyomas (associated with tuberous sclerosis), angiosarcomas

142
Q

What are myxomas as neoplasm of the heart?

A

80% in left atrium usually near fossa ovalis
Can be sessile or pedunculated
Tumor is soft with prominent myxoid matrix and myxoma cells can can obstruct valves or cause embolism

143
Q

What are papillary fibroelastomas?

A

Resemble sea anemones
Occur on valves
Myxoid connective tissue surrounded by epithelium
Can fragment and embolize

Block 4 - Cardio (15 decks)

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