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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
In-hospital mortality after surgery of AAD
15-25%
26
Giant cell arteritis
systemic inflammatory condition of medium and large vessels, focal granulomatous lesions involving entire artery wall
27
Giant cell arteritis pearls
occurs >50 yo, mean 79 yo, affects women more, coexists with polymyalgia rheumatica, can lead to blindness, unilateral temporal headache, jaw claudication
28
Clinical manifestations of Giant cell arteritis
scalp tenderness, jaw claudication, throat pain, diplopia, elevated inflammatory markers, fever (15%), polymyalgia rheumatica
29
diagnostic studies of giant cell arteritis
erythrocyte sedimentation rate elevated, c-reactive protein, normochromic normocytic anemia, thromboytosis, may have elevated ALP, temporal artery U/S, temporal artery biopsy
30
Treatment of giant cell arteritis
high-dose prednisone, low dosse aspirin, treatment initiated immediately and not wait on biopsy results due to complicating factors such as blindness
31
Peripheral artery disease
cliniccal disorder in which there is a stenosis in the aorta or the arteries of the limbs
32
PAD Pearls
>40 yo, most common result of atherosclerosis, intermittent claudication, hair loss, absent distal pulses, erectile dysfunction
33
Causes of PAD
thrombosis, embolism, vasculitis, fibromuscular dysplasia, entrapment, cystic adventitial disease, trauma
34
Risk factors of PAD
Smoker, diabetes, hypercholesterolema, hypertension, renal insufficiency
35
Clinical manifestations of PAD
50% symptomatic, intermittent claudication, pain, sense of fatigue in muscle, relieved by rest
36
best relief of claudication
exercise
37
Physical findings of PAD
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
Diagnostic studies of PAD
Ankle brachial index, doppler u/s, angiography, elevated homocysteine
39
Treatment of PAD
Aggressive risk of modification, stop smokiing, control other ailments, BB, ACEi, statins, exercise, antiplatelet therapy
40
Phlebitis/thrombophlebitis
involves partial or complete occlusion of a vein and inflammatory changes, greater saphenous most involved
41
Virchow triad
associated with phlebitis, includes stasis, vascular injury, hypercoagulability
42
Clinical manifestation of phlebitis
dull pain, redness, tenderness, localized, palpable cord, subsides in 1-2 weeks, urgent treatment
43
Clinical pearls of phlebitis
verchow triad, pain to touch/move, great saphenous affected, staph most common infection
44
Treatment of local phlebitis
local heat, NSAIDs
45
Treatment of septic superficial thrombophlebitis
urgent tx with heparin, antibiotics, augmentin combo, rocefin
46
Risk factors of varicose veins
obesity, family hx, prolonged sitting, history of phlebitis
47
Clinical manifestations of varicose veins
dull ache or pressure sensation in legs after prolonged standing, legs heavy, relieved when elevated, mild ankle edema, ulceration near ankle, spider veins
48
Treatment of varicose veins
leg elevation, avoid prolonged standing, elastic support hose, exercise, sometimes endovenous radiofrequency, laser ablation, compression sclerotherapy, surgical stripping
49
Venous insufficiency
may result from DVT and or valvular incompetence, after DVT, valves become thickened and contracted, so can't support flow
50
Clinical manifestations of venous insufficiency
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
Treatment of venous insufficiency
avoid prolonged standing, elevate legs, compression hose, stasis dermatitis and ulceration: wet compresses with hydrocortisone cream (SD)
52
The "never event"
DVT, venous thrombosis
53
Prothrombotic states, most common autosomal dominant genetic mutation
Factor V Leiden: causes resistance to activated protein C, activates clotting factor V, VIII; prothrombin gene mutation: increases plasma prothrombin concentration
54
predisposing factors of DVT
increased homocysteine, cancer, COPD, obesity, smoking, pregnancy, surgery, trauma etc
55
Clinical manifestation of DVT
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
diagnostic study of DVT
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
Treatment of DVT
elevate feet, leg exercises, compression hose, anticoagulation with enoxaprin (LMWH) or unfractionated heparin with warfarin, 3-6 months
58
Management of DVT
warfarin, 5 mg; overlap UFH or LMWH for 5 days, INR 2.5, IVC filters

Clinical medicine (19 decks)

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