Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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 |
|
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)
|
|
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? demographic? |
Granulomatous vasculitis, classically involves aortic arch at branch points
Young Asian females < 50 years old |
|
How does Takayasu Arteritis present? How is it treated?
|
Tx. w/ corticosteroids |
|
Polyarteritis Nodosa |
|
|
Polyarteritis Nodosa clinical symptoms? Classic finding? a/w? |
Depends on Arteries Involved
|
|
Diseases associated with 'String of pearls'
|
Polyarteritis Nodosa |
|
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: Fever Conjunctivitis 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 |
|
Wegener's Granulomatosis |
|
|
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 vs. Microscopic Polyangiitis |
Same 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 |
Same 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. |
|
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 |
|
Atherosclerosis |
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 |
|
Hemangioma |
Benign tumor comprised of blood vessels; commonly present at birth and regresses during childhood; often involves skin and liver |
|
Angiosarcoma |
|
|
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 |