Cardiovascular Flashcards

1
Q

Virchow’s Triad

A

3 categories likely to contribute to thrombosis

  1. Stasis of bloodflow
  2. Endothelial injury
  3. Hypercoagulability
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2
Q

Arteriolosclerosis (affects what? assoc. w/ what?)

A

Affects arterioles

Associated w/ hypertension & diabetes

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3
Q

Monckeberg’s arteriosclerosis

A

Medial calcific sclerosis - calcifications in the muscular wall (tunica media) of arteries

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4
Q

Hyaline arteriosclerosis

A

Thickening of arteries via deposition of hyaline

Associated w/ hypertension & diabetes

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5
Q

Hyperplastic arteriosclerosis

A

Narrowing of the lumen of arteries (thickened BM & mm)

Associated w/ malignant hypertension

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6
Q

Atherosclerosis

A

Affects larger arteries

Formation of intimal lesions (atheromas)

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7
Q

Death rate of atherosclerosis & common cause of the death

A

50% death rate

25% due to MI

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8
Q

Risk factors to arteriosclerosis

A
Male
40-60 y.o.
Genetics
Hypercholesterolemia
Diabetes (2x risk)
Hypertension
Smoking
Inflammation (CRP levels)
Hyperhomocysteinemia
Lipoprotein (a) levels
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9
Q

Hyperhomocysteinemia

A

High homocysteine levels due to deficiencies of vitamin B6, folic acid (vitamin B9), and vitamin B12

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10
Q

Steps in arterial plaque formation

A
  1. Accumulation of excess lipoproteins (LDL+Chol.) in subendothelial vessel wall
  2. Monocyte adhesion occurs at site of accumulation and the monocytes ingest lipid to become foam cells
  3. FGF and PDGF secreted by the endothelium and other cytokines released by foam cells recruit s.m. cell proliferation
  4. Plaque is fully developed w/ collagen cap & lipid core
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11
Q

Fatty streaks

A

Non-pathological
Appear in children
May progress to atheromas
Reversible

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12
Q

Common place to detect atheromas

A

Bifurcation of carotid a.

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13
Q

Are atheromas reversible?

A

No

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14
Q

Normal BP

A

<140/90

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15
Q

Mild Hypertension BP

A

<159/104

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16
Q

Moderate/Severe Hypertension BP

A

> 160/106

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17
Q

Hypertension affects what % of the US population?

A

20-30%

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18
Q

Concentric L ventricle hypertrophy

A

Compensated (normal cardiac output)

Outside dimensions are the same (hypertrophy on inside)

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19
Q

L ventricle hypertrophy with ventricular dilation

A

Decompensated

Dec. contractility, dilation, CHF

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20
Q

Complications of hypertension

A
Concentric LVH
LVH & ventricular dilation
Retinal injury
Nephrosclerosis
Dissecting hematoma of aorta
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21
Q

Malignant hypertension BP

A

> 200/140

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22
Q

Malignant hypertension complications

A

Cerebral edema/hemorrhage/encephalopathy
Papilledema
Renal failure

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23
Q

Malignant hypertension prognosis

A

5 year life expectancy

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24
Q

CHF compensatory mechanisms

A

Activating neurohumoral systems (release NE)
Frank-Starling Mechanism
Myocardial hypertrophy

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25
Q

Frank-Starling mechanism

A

Inc. end-diastolic filling volume to contract more forcefully

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26
Q

Which side of the heart is more likely to fail?

A

Left

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27
Q

Causes of L side heart failure

A
IHD
Hypertension
Myocarditis
Cardiomyopathy
Valvular disease
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28
Q

Causes of R side heart failure

A

L side heart failure
Pulmonary hypertension
Septal defects w/ L-R shunts
Valvular disease

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29
Q

Symptoms of L side heart failure

A

Dyspnea
Chronic cough
Orthopnea
Cerebral hypoxia

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30
Q

Symptoms of R side heart failure

A

Congestion of liver & spleen (nutmeg liver)
Edema (pitting) of subcutaneous tissues
Cerebral hypoxia

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31
Q

How common is CHD?

A

6-8 : 1,000

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32
Q

Causes of CHD

A

Environmental factors

Chromosomal abnormalities

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33
Q

Types of non-cyanotic CHD

A

ASD
VSD
PDA

34
Q

ASD

A

Atrial septal defect - 2nd most common type of non-cyanotic CHD

35
Q

VSD

A

Ventricular septal defect - Most common form of non-cyanotic CHD
Occurs in 4 : 1,000

36
Q

PDA

A

Patent ductus arteriosus - Connects aorta & pulmonary a., should normally close within a few days of birth

37
Q

Types of cyanotic CHD

A

Tertalogy of Fallot

Transposition of great arteries

38
Q

Anomalies of Tetralogy of Fallot

A
  1. VSD
  2. Overriding of VSD by aorta
  3. Narrowed RV outflow
  4. RV hypertrophy
39
Q

Primary cause of IHD

A

atherosclerosis

40
Q

Causes of IHD

A

Atherosclerosis (>75% narrowing)
Hypertension (Inc. myocardial O2 demand)
Hypotension/shock (Dec. BV)
Pneumonia (Dec. oxygenation)
Anemia (Dec. O2 carrying capacity)

41
Q

Clinical types of IHD

A

Angina pectoris
MI
Chronic IHD w/ CHF
Sudden cardiac death

42
Q

Angina pectoris (cause & types)

A

Caused by transient, reversible myocardial ischemia

  1. Stable - predictable pain relieved via rest or sublingual NG
  2. Unstable - Inc. freq./duration, happens w/ no/minimal exertion
43
Q

Cases of IHD annually and death rate

A
  1. 5 mil cases annually

0. 5 mil die

44
Q

How long must ischemia last to cause irreversible myocyte injury & cell death

A

20-40 min

45
Q

How long after a death via MI can an autopsy reveal the cause?

A

12-24 hours after death

46
Q

Symptoms of MI

A
Chest pain
SOB
Nausea/vomiting
Diaphoresis (sweat)
Low-grade fever
47
Q

Diaphoresis

A

Sweating profusely

48
Q

Tests for MI

A

ECG/EKG

Test for inc. in serum proteins (troponin, CPK-MB) from damaged cardiac myocytes

49
Q

Tx for MI

A

Coronary stents
CABG
Streptokinase

50
Q

Most common cause of sudden cardiac death

A

IHD (80-90%)

51
Q

Causes of sudden cardiac death in young px

A

Congenital coronary artery abnormalities
Aortic valve stensosis
Myocardial hypertrophy

52
Q

Types of cardiac myopathies

A

Primary - Disease solely confined to heart mm.

Secondary - Myocardium is involved as part of a systemic disorder

53
Q

3 patterns of cardiomyopathies

A
  1. Dilated
  2. Hypertrophic
  3. Restrictive
54
Q

Characteristics of dilated cardiomyopathy

A

Primary/Secondary/Genetic(20-50%)/Acquired
Poor ventricle contractility
Nonspecific histology (fibrosis & hypertrophy)

55
Q

Characteristics of hypertrophic cardiomyopathy

A

Genetic (AD)/Missense point mutation
Stiff ventricles cause inadequate filling (diastolic dysfxn)
Histology = myocyte disarray w/ fibrosis

56
Q

Characteristics of restrictive cardiomyopathy

A

Idiopathic/Secondary to radiation fibrosis, amyloidosis, sarcoidosis, hemochromatosis
Stiff ventricles cause inadequate filling (diastolic dysfxn)

57
Q

Myocarditis causes

A

Pyogenic bacteria
Viruses - Coxsackie A&B
Parasites - Chagas disease
Hypersensitivity - Perivascular infl. w/ eosinophils

58
Q

Mitral valve stenosis (cause, occurance, features)

A

Result of ARF(acute rheumatic fever) - Secondary to Group A beta-hemolytic streptococcal pharyngitis
Occurance - 80% children/20% adults
Features - Arthritis, carditis, rash, subcutaneous nodules

59
Q

Rheumatic carditis features

A

Pericarditis - Fibrinous
Endocarditis - Sterile vegetations
Myocardtiis - Aschoff bodies
Recurrent ARF -> fibrosis & mitral valve stenosis

60
Q

Aschoff bodies

A

Granulomatous inflammation seen in rheumatic fever - consists of mononuclear cells & fibroblasts

61
Q

Causes of mitral valve regurgitation

A

IHD
IE
Floppy mitral valve (MV prolapse)

62
Q

MV prolapse features

A
Isolated or part of Marfan syndrome
Myxomatous degeneration (weakening of CT)
Complications in 3% px - endocarditis, thromboemboli, atrial fibrillation, sudden death
63
Q

Aortic valve stenosis (causes)

A

Chronic rheumatic valvular disease
Advanced age (70-80 y.o.)
Congenital bicuspid valve (40-50 y.o.)

64
Q

AV regurgitation (causes)

A

Valve cusp destruction (IE, rheumatic carditis)
Weakened valve cusps (Marfans)
Dilation of aortic root

65
Q

Infective endocarditis (predisposing factors)

A
Valvular disease
IV drug abuse
Intracardiac shunts
Prosthetic valves
Immune suppression
Diabetes
66
Q

Infective endocarditis (features)

A
Fever
Fatigue
Anemia
Myalgia/arthralgia
Heart murmur
Roth spots (retinal)
Splinter hemorrhages (nail bed)
67
Q

Acute endocarditis (features)

A
SHORT duration
VIRULENT organism
LARGE vegetations
PROMINENT tissue destruction
Previously NORMAL valve
68
Q

Subacute endocarditis (features)

A
LONG duration
LOW VIRULENCE organism
SMALL vegetations
LESS tissue destruction
Previously ABNORMAL valve
69
Q

Infective endocarditis (complications)

A
Rupture of chordae tendinae
Valvular regurgitation
Contiguous spread of infection
Thromboembolism
Septic emboli w/ abscesses
70
Q

Vasculitis (causes)

A
Infection
Immunologic mechanisms
Radiation
Trauma
Caustic substances
71
Q

Vasculitis classifications

A
  1. Large vessel - Giant cell … Takayasu arteritis
  2. Med. vessel - Polyarteritis nodosa … Kawasaki disease
  3. Small vessel - Microscopic polyangiitis … Wegener granulomatosis
72
Q

Giant cell (temporal) arteritis (cause, features, tx)

A
LARGE VESSEL VASCULITIS
Unknown cause
Rare <50 y.o.
Tenderness @ temples, Stiff shoulders/neck, Visual disturbances
Granulomatous infl., Intimal fibrosis
Tx - corticosteroids
73
Q

Takayasu arteritis (cause, features)

A
LARGE VESSEL VASCULITIS
Unknown cause
), visual disturbances
Involves aortic arch & branches
Granulomatous infl., Intimal fibrosis
74
Q

Polyarteritis nodosa (cause, features)

A

MEDIUM VESSEL VASCULITIS
Unknown cause (once thought to be assoc. w/ Hep B)
Acute relapsing chronic fever, melena, hematuria, abdominal pain, hypertension
KIDNEY>HEART>LIVER>GI

75
Q

Kawasaki disease (Mucocutaneous lymph node syndrome) (cause, features)

A

MEDIUM VESSEL VASCULITIS
Antiendothelial Ab triggered by viral infxn
Infants & children < 4 y.o.
Mucous membrane erythema, fever, skin rash, lymphadenopathy (usually self-limited)

76
Q

Microscopic polyangiitis (cause, features, triggers)

A

SMALL VESSEL VASCULITIS
MPO-ANCA
Skin rash, other organs affected, fibrinoid necrosis, karyorrhexis of pmn’s
Triggers - drugs, bacteria, foreign/tumor proteins

77
Q

Melena

A

tarry stool appearance

78
Q

Wegener granulomatosis (cause, features)

A

SMALL VESSEL VASCULITIS
PR3-ANCA
Strawberry gingivitis
Sinusitis, pneumonitis, renal failure, glomerulonephritis
Affects kidneys & LR tract
Fibrinoid necrosis, necrotizing granulomas

79
Q

Beurger disease (Thromboangiitis obliterans) (cause, features)

A

Endothelial injury from smoking
<35 y.o.
Pain of extremities, ischemic ulcers, gangrene
Vasculitis w/ thrombosis

80
Q

Dissecting aortic hematoma (predisposing conditions, complications, pathology)

A

Hypertension, Marfan’s
Rupture (hemorrhage), branch obstruction, sudden death
Intimal tear btwn. mid & outer 1/3 of media
Affecting ascending aorta is HIGH RISK of death (Type A)