Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Renal 15 Renovasc.
Leonard: Renovascular Disease
| Question | Answer |
|---|---|
| Hypertensive Nephrosclerosis | Does not typically lead to significant renal impairment *Often asymptomatic* *Accounts for 1/3 of ESRD* Most prevalent in African-Americans (leading cause of ESRD) |
| Pathologic findings of hypertensive nephrosclerosis | Atrophic kidneys -Granular surface |
| What would you see with light microscopy? | Prominent changes in the subcortical area Tubular atrophy (due to dysfunction of glomeruli) |
| Appearance of the arteries | Larger arteries: intimal fibrosis Smaller arteries: medial fibrosis/sclerosis Arterioles: hyaline thickening of the walls (amorphic pink) |
| Malignant hypertension | *Diastolic pressures >120-130* Accompanied by ocular changes: Retinal vascular changes, papilledema, renal dysfunction |
| Etiology of Malignant Hypertension | Now well understood Develops de novo in some cases |
| Clinical findings for Malignant Hypertension | M>W, ~ 40s *Headache, dizziness visual disturbances* Progressive renal dysfxn |
| Pathology of MH | Kidneys vary in size Surface is mottled red/yellow with scattered *infarcts* *Fibrinoid necrosis, marked hyaline sclerosis, hyperplastic arteritis* |
| What's seen with LM? | Fibrinoid necrosis *Onion skin lesion* |
| Renal artery stenosis | *can be reversed* with reestablishment of lumen |
| What might you see clinically with RAS? | Mild-moderate HTN +/- briuts |
| Etiology of RAS | Increased activity of RAAS #1 cause is athrosclerosis |
| Fibromuscular dysplasia | Fibrosis of the arterial wall with resultant stenosis *Medial fibroplasia* Areas of thickening altering with atrophy *String of beads" pattern. |
| Thrombotic Microangiopathies | Systemic thromubus formation through out *small vessels* |
| Clinical features of Thrombotic Microanhiopathies. | Hemolytic anemia, thrombocytopenia, HTN, renal failure |
| Lab findings for TM. | *Schistocytes* in peripheral blood smear Normal coagtimes or normal/slightly elevated FPS |
| Causes of TM. | Endothelial damage with leakage of plasma into subendothelial tissues |
| Categories of TM causes | Infection Drugs Autoimmune disease Malignant HTN Pregnancy and postpatrum depression |
| Morphology of TM | Somewhat similar to malignant HTN *arteriolar fibroid necrosis* Collapsing of glomeruli, necrosis or glomerular capillary congestion |
| Two forms of Hemolytic Uremic Syndrome (HUS) | Typical (diarrhea +) Atypical (diarrhea -) |
| Typical HUS | Ingestion of food contaminated with *bacteria* Generally E.coli Kids > adults Sudden onset of a GI bleed, oliguria and hematuria |
| Atypical HUS | *Inherited mutations* of complement proteins *Acquired* anti-phopholipid antibodies Seen in adults Worse prognosis |
| Classical pentad of symptoms for Thrombotic Thrombocytopenia Purpura (TTP) | Fever Neurologic symptoms Microangiopathic hemolytic anemia Thrombocytopenia ARF |
| TTP is caused by ____ or a genetic defect resulting in ____ | *Antibiotics* *Decreased fxn of ADAMTS13* |
| What does ADAMTS13 do, and what does its absence result in? | ADAMTS13 normally cleaves large multimers of vWF Lack of this results in large vWF multimers autoinducing platelet aggregation |
| Renal Vasculitides | Diseases that affect small, medium, and large vessels in the kidney |
| Where do small-vessel vasculitis attack? | Glomeruli Arterioles Interlobular arteries |
| When can you see preeclampsia? | 3rd trimester of pregnancy |
| Symptoms of preeclampsia | HTN proteinuria edema |
| Eclampsia | HTN Proteinuria Edema *Seizures* |
| Sickle cell nephropathy | From sickle cell dz or trait |
| Sickle cell nephropathy clinical findings | hematuria Diminished concentrating ability of the kidney |
| Etiology/pathology of Sickle cell nephropathy | Medullary interstitium is hypertonic and hypoxic Promotes sickling of RBCs Vascular occlusion with hypoxia *papillary necrosis* FSGS may develope |
| Tx for Sickle cell nephropathy | Improve oxygenation Red cell exchange |
| Renal embolization | Reason for the majority of renal infarcts |
| Sources of renal emboli | **************** Cardiac Mural thrombi Cardiac vavlular vegetations Complicated atherosclerotic plaques **************** |
| Renal embolization results in... | *wedge-shaped* cortical infarcts |
Created by:
bcriss
Popular Medical sets