Vascular Disease and Syncope Flashcards

1
Q

Aortic aneurysm

A

Defined as more than 50% dilatation of all 3 layers of the aortic wall. Aortic aneurysms are most commonly associated with atherosclerosis. Most are abdominal, and more than 90% originate below the renal arteries.

AA is more with athero. AD is more with HTN.

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2
Q

History and physical for AA

A

1) usually asymptomatic and discovered incidentally on exam or radiologic study
2) Risk factors are: HTN, high cholesterol, other vascular disease, positive family history, smoking, gender (males), and age
3) Exam demonstrates a pulsatile abdominal mass or abdominal bruits
4) Ruptured aneurysm leads to hypotension and severe, tearing abdominal pain that radiates to back

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3
Q

Dx of AA

A

1) All men 65-75 years of age with a history of smoking should be screened once by US for AAA
2) Abdominal US is used for diagnosis or to follow an aneurysm over time
3) CT with contrast may be useful to determine the precise anatomy

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4
Q

Tx of AA

A

1) In asymptomatic patients, monitoring is appropriate for lesions less than 5cm
2) Surgical repair is indicated if the lesion is more than 5.5cm (abdominal), more than 6cm (thoracic) or smaller but rapidly enlarging
3) Emergency surgery for symptomatic or ruptured aneurysms

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5
Q

Aortic dissection

A

Defined as transverse tear in the intima of a vessel that results in blood entering media, creating a false lumen and leading to a hematoma that propagates longitudinally.

Most commonly secondary to HTN. The most common sites of origin are above the aortic valve and distal to the left subclavian artery.

Most often occurs at 40-60 years of age, with greater frequency in men

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6
Q

History and physical for aortic dissection

A

1) Presents with sudden tearing/ripping pain in anterior chest (ascending) or back (descending)
2) Patients are typically hypertensive. If a patient is hypotensive, consider pericardial tamponade, hypovolemia from blood loss or other cardiopulmonary etiologies
3) Signs of pericarditis or percardial tamponade may be seen
4) Asymmetric pulses and BP measurements are indicative of aortic dissection
5) A murmur of aortic regurgitation may be heard if the aortic valve is involved with a proximal dissection
6) Neuro deficits may be seen if aortic arch or spinal arteries are involved

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7
Q

Dx of aortic dissection

A

1) CTA is gold standard. MRA can be used if contrast CT is contraindicated
2) TEE can provide details of the thoracic aorta, the proximal coronary arteries, the origins of arch vessels, the presence of a pericardial effusion, and aortic valve integrity
3) The stanford system classifies any dissection proximal to L subclavian as type A and all others as type B

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8
Q

Tx of aortic dissection

A

1) Monitor and medically manage BP and heart rate as necessary. Avoid thrombolytics. Begin B-blockade after starting vasodilators to rpevent reflex tachy
2) If the dissection involves the ascending aorta, it is a surgical emergency. Descending can often be managed with BP and HR control

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9
Q

DVT

A

Clot formation in the large veins of the extremities or pelvis

Classic Virchow triad of risk factors includes venous stasis (from plane flights, bed rest, incompetent venous valves in lower extremities), endothelial trauma (surgery, injury to lower extremities), and hypercoagulable states (malignancy, OCP use, pregnancy)

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10
Q

History and physical of DVT

A

1) Presents with unilateral lower extremity pain and swelling
2) Homan’s sign is calf tenderness with passive foot dorsiflexion (poor sensitivity and specificity for DVT)

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11
Q

Diagnosis of DVT

A

Doppler US; a spiral CT or V/Q scan may be used to evaluate for PE

A negative D-dimer can be used to rule out possibility of PE in low risk patients

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12
Q

Treatment of DVT

A

1) Anticoagulate with IV unfractionated heparin or SQ low-molecular weight heparin followed by PO warfarin for a total of 3-6 months
2) In patients with contraindications for anticoagulation, IVC filters should be placed
3) Hospitalized patients should receive DVT ppx consisting of exercise as tolerated, anti-thromboembolic stocking, and SQH or LMWH

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13
Q

Peripheral arterial disease

A

Defined as a restriction of the blood supply to the extremities by atherosclerosic plaque. The lower extremities are most commonly affected.

Clinical manifestations depend on the vessels involved, the extent and rate of obstruction, and the presence of collateral blood flow

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14
Q

PAD history and physical

A

1) Presents with intermittent claudication (reproducible leg pain that occurs with walking and is relieved with rest). As the disease progresses, pain occurs at rest and affects the distal extremities. Dorsal foot ulcerations may develop secondary to poor perfusion. A painful, numb foot is characteristic of critical limb ischemia.
2) Aortoiliac disease: Buttock claudication. Reduced femoral pulses. Male impotence (Leriche’s syndrome).
3) Femoropopliteal disease: Calf claudications. Reduced pulses below the femoral artery
4) Acute ischemia: Most commonly caused by embolization from heart; acute occlusions commonly occur at bifurcations distal to the last palpable pulse. 6 Ps. May also be secondary to cholesterol atheroembolism (blue toe syndrome)
5) Chronic ischemia: Lac of blood perfusion leads to muscle atrophy, pallor, cyanosis, hair loss, and gangrene/necrosis

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15
Q

Diagnosis of PAD

A

1) Measurement of ankle and brachial systolic BP (ankle-brachial index) can provide objective evidence of atherosclerosis (rest pain usually occurs with ABI less than 0.4). A very high ABI can indicate calcification of the arteries
2) Doppler US helps identify stenosis and occlusion. Normal ankle doppler readings are over 90% of brachial readings
3) Arteriography and digital subtraction angio are needed for surgical eval

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16
Q

Treatment of PAD

A

1) Control underlying conditions (DM, tobacco) and institute careful hygiene and foot care. Exercise helps develop collateral circulation
2) ASA, cilostazol, and thromboxane inhibitors may improve symptoms; anti-coagulants may prevent clots
3) Angioplasty and stenting have a variable success rate that is dependent on the area of occlusion
4) Surgery (arterial bypass) or amputation can be employed when conservative treatment fails

17
Q

6 Ps of acute ischemia

A
Pain
Pallor
Paralysis 
Pulse deficit
Paresthesias 
Poikilothermia
18
Q

Lymphedema

A

Disruption of lymphatic circulation that results in peripheral edema and chronic infection of the extremities. It is often a complication of surgery involving lymph node dissection.

In underdeveloped countries, parasitic infection can lead to lymphatic obstruction. Congenital malformations of the lymphatic system (Milroy’s Disease) can present with lymphedema in childhood

19
Q

History and physical for lymphedema

A

1) Postmastectomy patients present with unexplained swelling of the upper extremity
2) Immigrants present with progressive swelling of the lower extremities bilaterally with no cardiac abnormalities (ie filariasis)
3) Children present with progressive, bilateral swelling of the extremities

20
Q

Dx of lymphedema

A

Diagnosis is clinical Rule out other causes of edema, such as cardiac and metabolic disorders

21
Q

Tx of lymphedema

A

1) Directed at symptom management, including exercise, massage therapy and pressure garments to mobilize and limit fluid accumulation
2) Diuretics are ineffective and relatively contraindicated
3) Maintain vigilance for cellulitis with prompt gram positive antibiotic coverage for infection

22
Q

Syncope

A

A sudden, temporary LOC and postural tone secondary to cerebral hypoperfusion. Etiologies are either cardiac or not.

1) Cardiac - valvular lesions, arrhythmias, PE, cardiac tamponade, aortic dissection

Cardiac syncope is associated with 1 year sudden cardiac death rates up to 40%

2) Not - orthostatic/hypovolemic hypotension, neurologic (TIA, stroke), metabolic abnormalities, neurocardiogenic syndromes (vasovagal/micturition syncope), psychiatric

23
Q

History and physical of syncope

A

1) Triggers, prodromal symptoms and associated symptoms should be investigated
2) Cardiac causes of syncope are typically associated with very brief or absent prodromal symptoms, a history of exertion, lack of association with changes in position and/or a history of cardiac disease

24
Q

Dx of syncope

A

Depending on the suspected etiology, Holter monitors or event recorders (arrhythmias), echo (structural abnormalities), stress tests (ischemia), and tilt-table testing (neurally mediated syncope) can be useful.

25
Q

Tx of syncope

A

Tailored to the etiology; commonly B-blockers for rate control