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Clinical medicine > Cardiovascular disease > Flashcards

Cardiovascular disease Flashcards

1
Q

Aortic Aneurysm

A

a pathologic dilation of a segment of a blood vessel

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2
Q

True aneurysm involves

A

all three layers of the vessel wall

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3
Q

aortic aneurysm fusiform

A

affects entire circumference of a segment of a vessel

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4
Q

aortic aneurysm saccular

A

involves only a portion of the circumference

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5
Q

causes of aortic aneurysm

A

conditions that cause degradation or abnormal production of the structural components of the aortic wall, elastin and collagen

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6
Q

Specific causes of aortic aneurysm

A

degenerative disorders, genetic, developmental disease, vasculitis, infections, trauma

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7
Q

The most common pathologic condition associated with degenerative AA

A

atherosclerosis

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8
Q

Pearls of AA

A

atherosclerosis is most common cause, males are 8x more likely, screen AAA with u/s on males over 65, AAA and TAA, “male smoker with CAD, emphysema and renal impairment”

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9
Q

Thoracic aortic aneurysm most common

A

descending thoracic aorta

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10
Q

average growth of TAA

A

.1-.2 cm/year

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11
Q

Fear of TAA

A

risk of rupture, depends on size and symptoms, chest pain, sob, cough, hoarseness, dysphagia

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12
Q

CXR of TAA

A

widening of mediastinal shadow, displacement or compression of trachea or left main stem bronchus

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13
Q

ECHO of TAA

A

used to assess proximal ascending and descending thoracic aorta

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14
Q

CT of TAA

A

sensitive and specific, small aneurysms monitored this way every 6-12 months

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15
Q

Treatment of TAA

A

Beta-adrenergic blockers, control of HTN, operative repair on symptomatic pt with >5.5 cm ascending, 6 cm descending, diameter >1cm per year

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16
Q

Abdominal aortic aneurysm

A

occur more frequently in males, increase w/ age, usually asymptomatic, may be incidental in finding

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17
Q

Symptoms/signs of AAA

A

palpable, pulsatile, expansile, nontender mass, pain in chest, lower back or scrotum, if rupture cause acute pain (tearing) and hypotension

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18
Q

Diagnostic studies of AAA

A

abdominal xr (if not calcified will not show), abdominal u/s (best for measuring), CT w/ contrast and MRI

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19
Q

AAA treatment

A

operative repair that are rapid or symptomatic, or asymptomatic >5.5 cm, otherwise monitor

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20
Q

Mortality rate of aortic aneurysm dissection

A

90%

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21
Q

Predisposing factors of AAD

A

systemic HTN, marfans, loeys-dietz syndrome, inflammatory aortitis, congenital aortic valve anomalies, coarction of aorta, Hx of aortic trauma, 3rd trimester of pregnancy, weight lifting, cocaine

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22
Q

Clinical manifestations of AAD

A

after 60 yo, men 2:1, sudden onset of pain, diaphoresis, syncope, dypnea, weakness

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23
Q

Diagnostic study of AAD

A

TEE, Ct, MRI, CXR

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24
Q

Treatment of AAD

A

admit to ICU, Beta blockers, sodium nitroprusside, surgical correction

25
Q

In-hospital mortality after surgery of AAD

A

15-25%

26
Q

Giant cell arteritis

A

systemic inflammatory condition of medium and large vessels, focal granulomatous lesions involving entire artery wall

27
Q

Giant cell arteritis pearls

A

occurs >50 yo, mean 79 yo, affects women more, coexists with polymyalgia rheumatica, can lead to blindness, unilateral temporal headache, jaw claudication

28
Q

Clinical manifestations of Giant cell arteritis

A

scalp tenderness, jaw claudication, throat pain, diplopia, elevated inflammatory markers, fever (15%), polymyalgia rheumatica

29
Q

diagnostic studies of giant cell arteritis

A

erythrocyte sedimentation rate elevated, c-reactive protein, normochromic normocytic anemia, thromboytosis, may have elevated ALP, temporal artery U/S, temporal artery biopsy

30
Q

Treatment of giant cell arteritis

A

high-dose prednisone, low dosse aspirin, treatment initiated immediately and not wait on biopsy results due to complicating factors such as blindness

31
Q

Peripheral artery disease

A

cliniccal disorder in which there is a stenosis in the aorta or the arteries of the limbs

32
Q

PAD Pearls

A

> 40 yo, most common result of atherosclerosis, intermittent claudication, hair loss, absent distal pulses, erectile dysfunction

33
Q

Causes of PAD

A

thrombosis, embolism, vasculitis, fibromuscular dysplasia, entrapment, cystic adventitial disease, trauma

34
Q

Risk factors of PAD

A

Smoker, diabetes, hypercholesterolema, hypertension, renal insufficiency

35
Q

Clinical manifestations of PAD

A

50% symptomatic, intermittent claudication, pain, sense of fatigue in muscle, relieved by rest

36
Q

best relief of claudication

A

exercise

37
Q

Physical findings of PAD

A

decreased or absent pulses distal to obstruction, bruits, muscle atrophy, hair loss, thickened nails, smooth shiny skin, reduced temp, pallor, cyanosis, edema, pallor at soles of feet upon elevation

38
Q

Diagnostic studies of PAD

A

Ankle brachial index, doppler u/s, angiography, elevated homocysteine

39
Q

Treatment of PAD

A

Aggressive risk of modification, stop smokiing, control other ailments, BB, ACEi, statins, exercise, antiplatelet therapy

40
Q

Phlebitis/thrombophlebitis

A

involves partial or complete occlusion of a vein and inflammatory changes, greater saphenous most involved

41
Q

Virchow triad

A

associated with phlebitis, includes stasis, vascular injury, hypercoagulability

42
Q

Clinical manifestation of phlebitis

A

dull pain, redness, tenderness, localized, palpable cord, subsides in 1-2 weeks, urgent treatment

43
Q

Clinical pearls of phlebitis

A

verchow triad, pain to touch/move, great saphenous affected, staph most common infection

44
Q

Treatment of local phlebitis

A

local heat, NSAIDs

45
Q

Treatment of septic superficial thrombophlebitis

A

urgent tx with heparin, antibiotics, augmentin combo, rocefin

46
Q

Risk factors of varicose veins

A

obesity, family hx, prolonged sitting, history of phlebitis

47
Q

Clinical manifestations of varicose veins

A

dull ache or pressure sensation in legs after prolonged standing, legs heavy, relieved when elevated, mild ankle edema, ulceration near ankle, spider veins

48
Q

Treatment of varicose veins

A

leg elevation, avoid prolonged standing, elastic support hose, exercise, sometimes endovenous radiofrequency, laser ablation, compression sclerotherapy, surgical stripping

49
Q

Venous insufficiency

A

may result from DVT and or valvular incompetence, after DVT, valves become thickened and contracted, so can’t support flow

50
Q

Clinical manifestations of venous insufficiency

A

c/o dull ache in leg that worsens with prolonged standing an resolves with elevation, increased leg circumference, edema, superficial varicosity, erythema, dermatitis, skin ulceration

51
Q

Treatment of venous insufficiency

A

avoid prolonged standing, elevate legs, compression hose, stasis dermatitis and ulceration: wet compresses with hydrocortisone cream (SD)

52
Q

The “never event”

A

DVT, venous thrombosis

53
Q

Prothrombotic states, most common autosomal dominant genetic mutation

A

Factor V Leiden: causes resistance to activated protein C, activates clotting factor V, VIII; prothrombin gene mutation: increases plasma prothrombin concentration

54
Q

predisposing factors of DVT

A

increased homocysteine, cancer, COPD, obesity, smoking, pregnancy, surgery, trauma etc

55
Q

Clinical manifestation of DVT

A

cramp in lower calf that persists for days and becomes worse, swelling and tenderness of femoral vein, unable to walk, if very swollen not likely DVT

56
Q

diagnostic study of DVT

A

D-dimer: rises due to breakdown of fibrin, useful rule out test; duplex venous u/s: relies on loss of vein compressibility, study of choice, venography is most accurate method

57
Q

Treatment of DVT

A

elevate feet, leg exercises, compression hose, anticoagulation with enoxaprin (LMWH) or unfractionated heparin with warfarin, 3-6 months

58
Q

Management of DVT

A

warfarin, 5 mg; overlap UFH or LMWH for 5 days, INR 2.5, IVC filters

Clinical medicine (19 decks)

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