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14 Cards in this Set
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- Back
Renal System-Renovascular Disease by Leonard
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Renal System-Renovascular Disease by Leonard
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Benign HTN...clinical features...who gets it most?
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Does not typically lead to significant renal impairment
-Often asymptomatic -Small proportion of people with mild-moderate hypertensive disease develop renal insufficiency -Because so many people have “benign hypertension,” if accounts for ~ 1/3 of cases of ESRD Most prevalent in African-Americans -Leading cause of ESRD |
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Benign HTN...pathology...what do the kidneys look like?
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Atrophic kidneys, usually bilaterally
-Granular surface of “fixed” capsule; thinned cortex LM: changes most prominent in subcortical area -Varying degrees of glomerular damage: capillary walls thickened to globally sclerotic glomerulus -Tubular atrophy (due to dysfunction of glomeruli) |
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Malignant Hypertension... what is it, who gets it, pathology..
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-Diastolic pressures over 130 mm Hg; retinal vascular changes, papilledema, renal dysfunction
Clinical:M>W; ~ 40’s; headache, dizziness, visual disturbances; progressive renal dysfunction/failure Pathology: Kidneys vary in size: small to large (edema) -Cut surface is mottled red/yellow, with scattered infarcts -Fibrinoid necrosis, marked hyaline sclerosis, hyperplastic arteritis |
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Renal Artery Stenosis is permanent, right? Clinical and Etiology, please.
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Can be reversed with reestablishment of lumen (Surgical revascularization, angioplasty, nephrectomy)
Clinical: Mild-moderate hypertension +/- bruit over main renal artery; Dx by imaging -Elevation of renal vein renin from affected side Etiology:Increased activity of Renin, angiotensin II, aldosterone Causes: #1 – atherosclerosis; also vasculitis, fibromuscular dysplasia |
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What the heck is Fibromuscular Dysplasia? WHat do you see on angiogram?
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Fibrosis of arterial wall with resultant stenosis
-Can affect intima, media, or and region of vessel wall from intima to adventitia E.g., medial fibroplasia (most common; 66% of cases) Areas of thickening (e.g., medial) alternating with areas of atrophy -“String of beads” pattern on angiogram |
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Thrombotic Microangiopathies, what is it and the clinical and laboratory features
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Systemic thrombus formation through small vessels (capillaries, arterioles) leading to ischemia
Clinical: Microangiopathic hemolytic anemia, thrombocytopenia, hypertension, renal failure Laboratory: Schistocytes (fragmented RBCs) in peripheral smear Normal coagulation times; normal or slightly elevated FSPs |
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Thrombotic Microangiopathies Causes
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Common pathogenesis: endothelial damage with leakage of plasma proteins into subendothelial tissues; promotion thrombosis (various mechanisms)
-Both reduce vascular lumen and result in ischemia |
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Thrombotic Microangiopathies Morphology...what does it look like?
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-Some similarity to malignancy hypertensive nephropathy
-Arteriolar fibrinoid necrosis -Edematous expansion of arteriolar intima -Collapsing of glomeruli, necrosis or glomerular capillary congestion -Vascular thrombosis |
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So what are the two forms of Hemolytic Uremic Syndrome (HUS)?
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Typical (epidemic, classic, diarrhea-positive)
-Associated most often with ingestion of food contaminated with bacteria – Shiga-like toxin Atypical (diarrhea-negative, non-endemic) -Inherited mutations in complement system proteins Acquired: anti-phospholipid antibodies; associated with: pregnancy, oral contraceptives, chemotherapy, radiation therapy, autoimmune vasculitides. Occurs in Adults. -Worse prognosis |
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What is the classic pentad of clinical symptoms of Thrombotic Thrombocytopenia Purpura (TTP)
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-Fever
-neurologic symptoms, -microangiopathic hemolytic anemia, -thrombocytopenia, -ARF |
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What has a decreased function, and what causes it in TTP
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Usually caused by antibodies (autoimmune, drug-induced) or a genetic defect that result in decreased function of ADAMTS13
-ADAMTS13 protease normally cleaves large multimers of vWF -Persistent very large vWF promotes platelet aggregation |
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Sickle cell nephropathy
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Form sickle cell disease (homozygous) or trait (heterozygous)
Clinical: hematuria, diminished concentrating ability Etiology/Pathology: -Medullary interstitium (supplied by vasa recta) is hypertonic and relatively hypoxic: promotes sickling of RBCs with aberrant Hb -Vascular occlusion of these vessels with hypoxic infarction of papilla and medulla – papillary necrosis -Glomeruli are congested with sickle cells -FSGS may develop in some |
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Common sources and morphologic appearance of embolic kidney disease?
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Sources of emboli:
Cardiac mural thrombi (ventricular wall dyskinesia from prior MI; atrial fib) Cardiac valvular vegetations (infected, noninfected) Complicated atherosclerotic plaques Responsible for majority of cases of renal infarcts -Interlobar and arcuate arteries -Result in wedge-shaped cortical infarcts |