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27 Cards in this Set

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314. What accounts for majority of Wegener’s deaths?
a. Renal disease.
315. How do you diagnose Wegener’s Granulomatosis?
a. CXR is abnormal: nodules or infiltrates.
b. Lab findings
i. Markedly ↑d ESR
ii. Anaemia (Normochromic, normocytic)
iii. Haematuria
iv. Positive c-ANCA in 90% of pts!!! sensitive and specific
v. Thrombocytopenia may be present.
316. What confirms diagnosis of Wegener’s Granulomatosis?
a. Open lung biopsy.
317. Prognosis of Wegener’s Granulomatosis?
a. Prognosis is poor w/o tx.
b. Most pts die w/I 1 yr after diagnosis.
318. Tx of Wegener’s Granulomatosis?
a. A combination of cyclophosphamide and corticosteroids can induce remissions in many pts, but a relapse may occur at any time.
b. Consider renal transplantation if the pt has end-stage renal disease (ESRD).
319. What distinguishes PAN from Wegener’s?!!!
a. There is no pulmonary involvement in PAN!!!
320. General characteristics of Polyarteritis Nodosa PAN?
a. Vasculitis of medium-sized vessels involving the nervous system and GI tract
321. With what conditions may PAN be associated!?!?
a. Hepatitis B
b. HIV
c. Drug reactions
322. Pathophys of PAN?
a. PMN invasion of all layers and fibrinoid necrosis
b. Plus resulting intimal proliferation
i. Leads to reduced luminal area, which results in ischaemia, infarction, and aneurysms.
323. Symptoms of PAN?
a. Early:
1. Fever
2. Weakness
3. Wt. loss
4. Myalgias
5. Arthralgias
6. Abdominal pain (bowel angina)
b. Other Findings:
1. HTN
2. Mononeuritic multiplex
3. Livedo reticularis
324. Diagnosis of PAN?
a. Made by biopsy of involved tissue
i. Or
b. Mesenteric angiography
c. ESR is usually elevated
d. Test for fecal occult blood.
325. What antibody may be present w/PAN?
a. P-ANCA.
326. Prognosis and tx of PAN?
a. Prognosis is poor, but is improved to a limited extend w/tx.
b. Start w/steroids.
c. If severe, add cyclophosphamide
327. Pathophys of Behçet’s syndrome?
a. Autoimmune, multisystem vasculitic disease; cause is unknown.
328. Clinical features of Behçet’s syndrome?
a. Recurrent oral and genital ulcerations (usually painful)
b. Arthritis- knees and ankles most common
c. Eye involvement- Uveitis, optic neuritis, iritis, conjunctivitis.
d. CNS involvement
e. Fever
f. Wt. loss
329. CNS sx of Behçet’s syndrome?
a. Meningoencephalitis
b. Intracranial HTN
330. How do you confirm diagnosis of Behçet’s syndrome?
a. Biopsy of involved tissue
b. lab tests are not helpful
331. Tx of Behçet’s syndrome?
a. Steroids, which are helpful.
332. In whom does Buerger’s Disease (Thromboangiitis Obliterans) primarily occur?
a. Occurs mostly in young men who smoke cigarettes.
333. Pathophys of Buerger’s Disease (Thromboangiitis Obliterans)?
a. Acute inflammation of small- and medium-sized arteries and veins, affecting arms and legs.
b. May lead to gangrene.
334. Clinical features of Buerger’s Disease (Thromboangiitis Obliterans)?
a. Ischaemic claudication
b. Cold, cyanotic, painful distal extremities
c. Paresthesias of distal extremities
d. Ulceration of digits.
335. Tx of Buerger’s Disease (Thromboangiitis Obliterans)?
a. Smoking cessation is mandatory to reduce progression!
336. Hypersensitivity vasculitis?
a. Small-vessel vasculitis that is a hypersensitivity reaction in response to a drug (PCN, sulfa drugs), infection, or other stimulus.
337. Presentation of Hypersensitivity vasculitis?
a. Skin is predominantly involved:
1. Palpable purpura, macules, or vesicles (common on lower extremities) can occur.
ii. Lesions can be painful.
b. Constitutional symptoms: fever, wt. loss, fatigue) may be present.
338. Diagnosis of Hypersensitivity vasculitis?
a. Biopsy of tissue.
339. Prognosis and treatment of Hypersensitivity vasculitis?
a. Prognosis is very good- spontaneous remissions are common.
b. Withdrawal of the offending agent and steroids are the treatments of choice.
340. Complete!
340. Complete!