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51 Cards in this Set

  • Front
  • Back

Types of Large Vessel Vasculitis

1) Temporal Giant Cell Arteritis

2) Takayasu Arteritis

Types of Medium Vessel Vasculitis

1) Polyarteritis Nodosa

2) Kawasaki Disease

3) Buerger Disease

Types of Small Vessel Vasculitis

1) Wegener Granulomatosis (Granulomas w/ Polyangiitis)

2) Microscopic Polyangiitis

3) Churg-Strauss Syndrome

4)Henoch-Schonlein Purpura

MOST COMMON vasculitis in older adults

Temporal Giant Cell Arteritis

(>50) usually affects Females

Temporal Arteritis clinical symptoms?

Affects large branches of carotid artery leading to headache (temporal artery), and visual disturbances(ophthalmic artery) and jaw claudication

Some pts. have flu like symptoms w/ joint/muscle pain = polymyalgia rheumatica -> Elevated ESR (>100)

Vascular lesions are SEGMENTAL so a negative biopsy does NOT exclude disease

What is at risk to be damaged if Giant Cell Arteritis is not treated?

How is it Tx?

Ophthalmic Nerve ischemic damage causing blindness

Tx. w/ corticosteroids

Takayasu Arteritis:

type of arteritis?


Granulomatous vasculitis, classically involves aortic arch at branch points

Young Asian females < 50 years old

How does Takayasu Arteritis present? How is it treated?

  • visual and neurologic symptoms with weak or absent pulse in upper extremities ("pulseless disease")
  • ESR elevated

Tx. w/ corticosteroids

Polyarteritis Nodosa

  • Necrotizing vasculitis of MULTIPLE ARTERIES (Poly-arteritis)

  • Multiple Arteries -> Involvement of MOST Organs (BUT LUNGS Spared)

  • young adults

Polyarteritis Nodosa clinical symptoms? Classic finding? a/w?

Depends on Arteries Involved

  • Hypertension if Renal artery involvement,

  • Abdominal pain with melena (Mesenteric artery involvement)

  • Neurologic symptoms & Skin Lesions

  • HBs (Hep B Surface Ag often found in these pts.)

  • 'String of Pearls' appearance on imaging
Diseases associated with 'String of pearls'

Polyarteritis Nodosa
Fibromuscular Dysplasia

What drug treats Polyarteritis Nodosa vasculitis?

1) Corticosteroids (stop Inflammation)

2) Cyclophosphamide

FATAL if NOT Treated

Kawasaki Disease demographic

Asian children < 4 years old

Kawasaki Disease presentation

Non-specific symptoms:



Erythymatous Rash on palms and soles

Lymphadenopathy of Cervical Lymph nodes

Which artery is commonly involved in Kawasaki?

Coronary Artery; risk of

(1) thrombosis with MI

(2) aneursym with rupture

Kawasaki Disease treatment

1) Aspirin

2) IVIG (IVIG reduces vasculitis in KD by suppressing the marked immune activation associated with this disease b/c it upregulates Suppressor Tcells that block release of IFN-Gamma/IL-1 & TNF that drive the pathophysiology of Kawasaki's)

Buerger Disease HY associations

SMOKING disease

Tx = STOP Smoking

presents with Necrotizing vasculitis involving Digits (Fingers & Toes). Associated with Raynauds (vaso-spasm of blood vessels going to digits) (Turn White (b/c blood supply cut off)->Blue (b/c tissue becomes cyanotic)->Red (when blood flow returns after smasm ends)) ->autoamputation of digits w/out Tx.

Wegener's Granulomatosis

  • Necrotizing granulomatous vasculitis involving nasopharynx, lungs and kidneys.
  • c-ANCA positive
  • Treatment is Cyclophosphamide
  • large necrotizing granulomas with adjacent necrotizing vasculitis on biopsy

Classic presentation in Wegener's granulomatosis

Middle aged male with sinusitis or nasopharyngeal ulceration, hemoptysis with bilateral nodular lung infiltrates, and hematuria due to rapidly progressive glomerulonephritis

Wegener's Granulomatosis


Microscopic Polyangiitis


1) Both involve multiple (Poly-angitis)

2) Both involve Lung & Kidney

3) Tx. Cyclophosphamide & Corticosteroids

4) Relapses are common

Different: Unlilke Wegener's Granulomatosis, Microscopic Polyangitis has:

1) No Nasopharyngeal involvment or granulomas

2) serum p-ANCA (p-ANCA levels correlate w/ severity of Dz.) NOT c-ANCA

Microscopic Polyangiitis vs. Churg-Strauss Syndrome


1) Involves multiple organ systems

2) Involve LUNGS -> particularly LUNGS (Churg-Strauss)

3) p-ANCA +

Different: Unlike Microscopic Polyangitis, Churg-Strauss has:

1)Necrotizing Granulomatous Vasculitis w/

2) Eosinophils (peripheral eosinophilia) leading to...

3) Asthma

4) Involves Heart

Churg-Strauss presents with Asthma, Granulomas and peripheral eosinophilia.

They BOTH have lung involvement, both express p-ANCA.

Henoch-Schonlein Purpura

Vasculitis due to IgA Immune complex deposition

Presents with palpable purpura on buttocks and legs, GI pain and bleeding, and hematuria (IgA nephropathy); usually occurs following UTI

Henoch-Schonlein Purpura demographic

most common vasculitis in children

Important cause of stenosis in young females?

fibromuscular dysplasia (frequently involves renal artery) - developmental defect of blood vessel wall, resulting in irregular thickening of large and medium sized arteries

Primary HTN

HTN of unknown etiology (95% of cases)

Secondary HTN

due to identifiable etiology (ie renal artery stenosis, atherosclerosis, fibromuscular dysplasia)

Malignant HTN

severe elevation in BP ( >180/120 mm Hg):

1. may arise from preexisting benign HTN or de novo

2. presents with acute end-orange damage (eg acute renal failure, headache, and papilledema) and is medical emergency


thickening of INTIMA, affects medium/large sized arteries (abdominal aorta, coronary artery, popliteal artery, internal carotid artery)

Complications of atherosclerosis

1. Stenosis of medium-sized vessels leadings to peripheral vascular disease, angina, ischemic bowel disease

2. Plaque rupture with thrombosis resulting in MI and stroke

3. Plaque rupture with embolization

4. Aneurysm

Hyaline arteriosclerosis

caused by proteins leaking into vessel wall, producing vascular thickening; proteins are seen as pink hyaline on microoscopy

Causes of hyaline arteriosclerosis

long standing benign HTN or diabetes

Hyperplastic arteriolosclerosis

thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin' appearance) due to malignant HTN

What does hyperplastic arteriosclerosis lead to?

reduced vessel caliber with end-organ ischemia; may lead to fibrinoid necrosis of vessel wall with hemorrhage; classically causes acute renal failure with 'flea-bitten' apperance

Complications of aortic dissection

Obstruction of branching arteries results in end-organ ischemia

Most common cause of death due to aortic dissection
pericardial tamponade
Classically causes thoracic aneurysm
tertiary syphilis which causes endartertis of the vaso vasorum resulting in 'tree barkin' of the aorta.
Major complication of thoracic aneurysm

dilation of the aortic valve root, resulting in regurgitation; other complications include compression of mediastinal strucutres (eg airway or esophagus) and thrombosis/embolism

Monckeberg medial calcific sclerosis

calcification of media of muscular arteries; nonobstructive; not clinically significant (incidental finding on X ray)

Aortic dissection

Intimal tear with dissection of blood through media of aortic wall; occurs in proximal 10 cm of aorta with preexisting weakness of media

Causes of aortic dissection

1. HTN (most common)

2. Inherited defects of connective tissue (Margan or Ehlers-Danlos syndrome)

Kaposi's Sarcoma demographic

Older Eastern European males -- tumor remains localized to skin

AIDS and Transplant patients -- tumor spreads early.

Abdominal aortic aneurysm

Balloon-like dilation of abdominal aorta; usually arises below renal arteries but above aortic bifurcation

Causes of abdominal aortic aneurysm

Atheroslcerosis; classically seen in male smokers >60 with hypertension


Benign tumor comprised of blood vessels; commonly present at birth and regresses during childhood; often involves skin and liver


  • Malignant proliferation of endothelial cells; highly aggressive
  • Common sites: skin, breast, liver

What is liver angiosarcoma associated with?

exposure to polyvinyl chloride, arsenic, and Thorotrast

Kaposi sarcoma

Malignant proliferation of endothelial cells; associated with HHV-8

How does Kaposi sarcoma present?

Purple patches, plaques, nodules on skin; may also involve visceral organs

Modifiable Risk factors for Atherosclerosis

1) HTN

2) Hypercholesteremia

3) Smoking

4) Diabetes

All these drive Pathophysiology fo Atherosclerosis

Non-Modifieable Risk factors for Atherosclerosis

1) Age - # of lesions Incr. w/ age

2) Gender - Males >> than pre-menopausal Females (b/c estrogen protective)

3) Genetics - Family History highly predictive od risk

Pathogenesis of Atherosclerosis

Intima is Endothelial cells sitting on BM

1) Lipid Invasion of Intima = Endothelial damage allows lipids to interact w/ BM

2) The lipids are oxidized

3) Oxidized lipids Phagocytosed by Macrophages (Macrophages called in to clear these oxidized lipids)

4) Collection of Macrophages filled with lipids are now in Intima = FATTY STREAK - yellow streaks running along large blood vessels - already seen in teenagers

5) Macrophages activate Inflammation, followed by healing-> Fibromuscular cap

6) Each bout of inflamamtion, brings more lipids into the intima->more lipid laden Macrophages->More inflmmation. Therefore the atherosclerotic plaque continues to grow if there is Increased inflmmation and LDL cholesterol in blood

7) Fibromuscular cap is part of the Healing Process, as deposition of ECM (granulation tissue), proliferation of smooth muscle (both can be done by fribroblasts)

8) As the plaque expands, it increasingly occludes blood flow