Vascular Disorders

Front 1

Explain endothelial injury in atherosclerosis -

Back 1

a. Major risk factors: smoking (direct damage & LDL oxidation), HTN (pressure), high cholesterol, DM (non-enzymatic glycosylation)
b. Minor risk factors: obesity, gender, sedentary lifestyle, family history, stress, high triglycerides, hyperhomocystinemia, autoimmune vasculitis
c. Response of injured endothelial cells: ↓vasodilatory substances & ↑vasoconstrictor substances, upregulate adhesion molecules, ↓antithrombotic and anti-adhesion substances

Front 2

Explain fatty streak formation in pathology of atherosclerosis -

Back 2

Fatty streak formation begins in childhood and builds up over time

a. Macrophages & platelets can adhere to endothelium due to above
b. Foam cells (macrophages that ingest oxidized LDL) build up to fatty streak
c. Oxidized LDL inhibits nitrous oxide and stimulates cytokine release
d. Cytokines attract the immune system causing further damage & stimulate smooth muscle cells and fibroblasts to move from media to intima

Front 3

Explain fibrous plaque (atheroma) formation -

Back 3

fibrous cap over a lipid core
a. Fibrous cap: smooth muscle cells proliferate and fibroblasts lay down connective tissue to form a cap
b. Lipid cord: made of foam cells, cholesterol clefts, cell debris
c. Result: narrowing of vessel lumen with calcification in advanced stages
i. Stable plaque: thick fibrous cap that is unlikely to rupture, often more than 70% occlusion
ii. Unstable plaque: thin fibrous cap with large lipid core that is highly likely to rupture and result in clot formation, often 40-70% occlusion

Front 4

Complications of atherosclerosis -

Back 4

1) Coronary artery disease
a. Stable cap usually results in stable angina
b. Unstable plaque may result in acute coronary syndromes
2) Peripheral vascular disease
3) Aortic disease (aneurysms, dissection, etc)
4) TIA, strokes
5) Ischemic colitis
6) Renal artery stenosis

Front 5

PP of chronic PAD -

Back 5

occlusion of blood supply to extremities (usually lower), from atherosclerotic plaque formation

Front 6

Presentation of chronic PAD -

Back 6

depends on degree of involvement and presence of collateral blood flow
o Intermittent claudication: reproducible leg pain that occurs with exertion and always relieved with rest
o Rest pain: leg pain that is present at rest and worse when lying flat, usually improving with letting the legs hang down
o Ulceration/gangrene: a result of critical limb ischemia due to poor perfusion
o May also have muscle atrophy, pallor, hair loss, distal cyanosis

Front 7

Location of chronic PAD -

Back 7

o Aortoiliac: Leriche’s syndrome (claudication of buttocks, male impotence)
• Rule out OA of back, pseudoclaudication (lumbar spine compression)
o Femoropopliteal disease: leg/calf claudication

Front 8

Dx of chronic PAD -

Back 8

o Clinical diagnosis, poor distal pulses, auscultation of bruits
o Ankle-brachial index (ABI): ratio of ankle to brachial systolic BP, normal 0.9-1.0
o Doppler ultrasound: measures flow
o Angiography

Front 9

Tx of chronic PAD -

Back 9

o Risk factor modification: smoking cessation, exercise (develop collaterals), diet
o Medical therapy: ASA, Pentoxyphyllin, Cilostazol
• β-blockers may worsen symptoms
o Interventional therapy: percutaneous transluminal angioplasty, stenting, bypass graft, endarterectomy, amputation
• Note: only indicated if symptoms causes significant disability

Front 10

PP of acute PAD -

Back 10

embolization from heart or cholesterol atheroembolism, usually affecting distal digits

Front 11

Presentation of acute PAD -

Back 11

6 P’s – pain, pallor, pulselessness, paralysis, paresthesia, poikilothermia

Front 12

Dx/Tx of acute PAD -

Back 12

similar to chronic, but more aggressive

Front 13

PP of aortic aneurysms -

Back 13

cystic medial degeneration weakens the aortic wall, giving >50% dilatation involving all 3 layers; different locations have different etiologies
o Ascending: Marfan’s gives aneurysms at the root
o Arch: Syphilis (pathologically looks like a tree bark)
o Descending/Abdominal: often associated with atherosclerosis (major risk factors include HTN, smoking, hypercholesterolemia)
• Majority present below the renal arteries (no vasa vasorum = no blood supply resulting in a weaker aorta)

Front 14

Presentation of aortic aneurysms -

Back 14

usually asymptomatic; AAA – pulsatile abdominal mass, abdominal bruit
o If AAA rupture: hypotension, tearing abdominal pain, pulsatile abdominal mass

Front 15

Dx of Aortic Aneurysm -

Back 15

abdominal ultrasound for screening (men 65+ with TOB history or a relative with a history of AAA), CT for precise anatomy

Front 16

Tx of Aortic Aneurysm -

Back 16

o Medical therapy if <5.5cm: smoking cessation, antihypertensives (specifically β-blockers), statins
o Elective surgery if >5.5cm
o Emergent surgery has 50% mortality

Front 17

PP of Aortic dissection -

Back 17

disruption of intima allows blood to enter the media, creating a false lumen, which can propagate proximally or distally

o Most often associated with severe HTN (one of your hypertensive emergencies)
o Other risks: inflammatory vasculitis, connective tissue d/o, aortic valve dysfunction, trauma, cocaine

Front 18

Presentation of Aortic dissection

Back 18

sudden tearing pain in chest radiating to back, asymmetric pulses/BP

Front 19

Dx/Tx of Aortic dissection

Back 19

• Diagnosis: CXR (widened mediastinum), CTA
• Treatment: depends on classification
o Ascending: SURGICAL EMERGENCY. AHHHHH!!!
o Descending: medical management for BP control (Labetolol, Nitroprusside)

Front 20

Consequences of proximal aortic dissection?

Back 20

Leads to aortic valves, coronary arteries and pericardium

Front 21

Mcc Aortic aneurysm?

Back 21

Descending aortic aneurysm

Front 22

Arteritis and associations with aortic dz - Marfan's and Ehler's Danlos -

Back 22

Marfan’s syndrome: autosomal dominant mutation in fibrillin-1 gene on chromosome 15
• Aortic root dilation/aneurysms, mitral valve prolapse, euchonoid proportions, superior subluxation (dislocation) of the lens in the eye

Ehler’s Danlos: defect in type III collagen (skin, vessels)
• Spontaneous aortic rupture, stretchy skin, MVP

Front 23

PP of chronic venous insufficiency/stasis -

Back 23

inability to veins to adequately return blood to heart, resulting in stasis
o Obstruction: mechanical block due to tumor, cysts, aneurysms
o Thrombosis: usually manifests more acutely if DVT; superficial phlebitis may cause chronic varicose veins
o Valvular dysfunction: veins normally have valves that prevent blood from flowing downwards with gravity; exercise aids with the function of valves
• Due to immobility, estrogen, 2° to DVT, hereditary
o Pressure dysfunction: imbalance between hydrostatic and oncotic pressure draws transudate out of the venous system
• Often due to right heart failure, cirrhosis, kidney dysfunction
• Transudate pits when palpated (impression of finger stays)

Front 24

Presentation of chronic venous insufficiency/stasis -

Back 24

swelling, dry itchy skin, reddish brown discoloration (hemosiderin staining), weeping of transudate, ulcers

Front 25

Dx of chronic venous insufficiency/stasis -

Tx?

Back 25

o Palpable cord if varicose veins
o Trendelenberg test: looks at filling of veins with and after a tourniquet is placed
o Doppler ultrasound, Venography, CT/MR imaging

Treatment: elevation, NSAIDs/analgesics, compression stockings, surgery

Front 26

DVT PP =

Back 26

thrombosis is usually secondary to Virchow’s triad
o Stasis: long trips, bed rest, incompetent valves
o Endothelial injury: injury to lower extremities
o Hypercoaguable state: malignancy, pregnancy, OCP, genetic abnormalities (Protein C/S deficiency, Factor V Leiden, Antithrombin III mutation, hyperhomocysteinemia, prothrombin mutation)

Front 27

DVT Presentation

Back 27

pain, swelling, erythema
o Pulmonary embolus → SOB, fever, pleuritic pain, tachy, hemoptysis
o Stroke if PFO

Front 28

Dx of DVT

Back 28

o Physical exam: palpation of calves, Homan’s sign (50% sensitivity/specificity)
o Doppler ultrasound
o Spiral CT or V/Q scan if suspect PE

Front 29

Tx/Prevention of DVT

Back 29

• Treatment: anticoagulation, elevation/compression, IVC filter if anticoagulation is contraindicated
• Prevention: early ambulation > Heparin/LMWH > pneumatic compression

Front 30

Phlegmasia alba dolens -

Back 30

milk leg of pregnancy
compression of L. common iliac artery against pelvic rim of enlarged uterus
Also common in malignancy

NO ischemia
DVT -> Sudden occlusion of deep venous system

Rely upon superficial venous drainage

Front 31

Phelgmasia cerulea dolens -

now called HIT -

Back 31

extensive thrombotic occlusion of MAJOR and COLLAT veins.

Alba -> cerulea.

Gangrene and ISCHEMIA
Swelling, cyanosis