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PKD, ARF, CRF
Clinical Medicine-II
| Question | Answer |
|---|---|
| In recessive and dominant PKD, where do the cysts evolve from | R: renal collecting ducts, D: arise anywhere in the nephron |
| What is the MC inherited renal dz in infancy and childhood | Autosomal recessive PKD |
| Where is the mutation for recessive | defect on chromosome 6P 21 |
| What is a common feature of recessive PKD | infants have a problem w/ free water excretion leading to hyponatremia |
| What is the difference b/w autosomal dominant PKD and chronic KD | PKD causes progressive kidney enlargement |
| Is this 100% genetic | there are genes that code for this, but mutations are common that lead to PKD as well |
| What two factors of PKD would show slower progression | PKD 2 and females |
| Why do PKD pts do so well on dialysis alone | they can still excrete free water (urine), but have trouble filtering |
| Clinical features of PKD | most are asymptomatic, pain once the kidneys get large, UTI’s and stones, Hematuria (50%), HTN (60%), intracerebral aneurysm |
| What can happen with these cysts? | can get infected, must be drained |
| How do we dx PKD | US, (CT and MRI not usually used, but MRI can detect change in kidney vol) |
| Tx for PKD | none. Dialysis, and trxp. Control HTN and Lipids to prevent progression, tx pain |
| What is the worst thing a pt could do to worsen ANY kidney dz | smoking |
| What is goal tx of BP with PKD | 130/80 (low enough to not have hypotension sxs) must individualize care |
| What are some extra renal manifestations, and RFs w/ this | liver cysts, RF: females exposed to estrogen: preggo, and oral contraceptives |
| Besides the liver cysts, what else can PKD precipitate | cerebral aneurisms |
| What is rhabdomyolysis | stressed skeletal muscle that releases its contents (creatnine kinase) of muscle into the extracellular fluid that could cause kidney damage |
| Where do we see rhabdo | intense athletes (marathons), military, crush syndrome |
| Causes of Rhabdo | physical trauma, ↑physical activity-szs, movement d/o’s, compromised flow to muscle→necrosis leads to release of CK, Drugs, Toxins, ↑↓temps, infectious causes and bites |
| What drugs may cause Rhabdo | HMG co-A reductase inhibitors (statins) |
| Toxins that may cause rhabdo | ethanol, CO, snake venom |
| Dx of rhabdo | pink urine, ↑CK: >10-20,000, evidence of renal failure, |
| Tx of rhabdo | maintain hydration, forced mannitol-alkaline diuresis (can use Lasix? But must be certain they are hydrated 1st) |
| What is mannitol | a osmotic diuretic |
| 25 yo runner running 50mile race, feeling fatigue, muscle pain, stops to urinate and has red urine, dx? | rhabdomyolysis |
| Dx of urine that is red | it is red, but has no blood cells, red d/t myoglobin |
| Pt goes into acute renal failure in ICU what is the mortality rate | 40-90%! |
| 3 major categories of acute renal injury | pre-renal, intra-renal, post-renal (need to be able to tell the diff) |
| What are causes of pre-renal renal failure | anything that may reduce renal perfusion: vol depletion, hypotension, CHF, arrhythmias,, intrarenal vasoconstriction? hypercalcemia, hepatorenal syndrome |
| What are some drugs that may ↑intrarenal vasoconstriction | ACEi, NSAIDS, AmphoB, cyclosporine/tacrolimus, radiographic contrast |
| What are intrarenal failure causes | any damage to the kidney parynchema, vascular, tubular, glomerular, interstitial damages |
| Is cortical and tubular necrosis reversible | cortical: usually bilaterally do not recovery, tubular, can regetnerate tubules and kidney fxn returns |
| What is acute interstitial nephritis | allergic rxn in the kidney. Eosinophils in urine and or blood, commonly d/t an abx (tx is prednisone and stopping offending agent) |
| Post renal causes | Obstruction: prostatic hypertrophy, nerogenic bladder, intraureteral obstruction, extrauretral obstruction: tumors, retroperitoneal fibrosis |
| Any female that has bilateral obstruction of the kidneys has what | a carcinoma until proven otherwise |
| Functionally, urine outpul tell that required to maintain solute balance | Oliguric, <400ml/24hrs |
| Complete obstruction of urine, major vascular catastrophy, commonly severe ATN | anuric <100ml/24hrs |
| When is oliguria seen | more common w/ obstruction, prerenal azotemia |
| When is nonoliguric more common | intrarenal causes, nephrotoxic ATN, acute GN, AIN |
| Dysgeusia | altered taste sensation |
| Hiccups | singultus |
| Signs of chronic dz | pre-exisiting illness, uremic sx, small echogenic kidneys by US |
| What is a significant lab test for ARF | FENA and BUN |
| What does a BUN/Creatinine ration >20/1 suggest | prerenal or obstruction |
| Fxns of kidney | ↑ calcium absorption: calcitriol, Stimulates RBC production, Regulates BP and electrolytes: renin |
| Classifications of acute renal failure | sudden, rapid ↓ urine output, usually reversible, tubular cell death with regeneration |
| Classifications of chronic renalfaiure | progressive, not reversible, nephron loss, can lose ~75% renal fxn prior to having sxs |
| What ↑ as kidney fxns ↓ | uraemia |
| Stages of CDK | Stage 1-5 |
| Kidney damage w/ nl or ↑ GFR | Stage 1 GFR >90 |
| Severe ↓ GFR | stage 4 15-29 |
| Kidney failure | stage 5, <15 or dialysis |
| Kidney damage w/ mild ↓ GFR | stage 2, 60-89 |
| Mod ↓ GFR | stage 3, 30-59 |
| Causes of CKD | DM, HTN, GN, PKD, obstructions, infections |
| What may progress CKD | sustaining primary dz, HTN, intraglomerular HTN, proteinuria, nephrocalcinosis, Dyslipidemia, |
| What should all CKD pts be on | lipid lowering agent , and ACEi (if they can be) (statins: have a factor that help the kidney “deal” with CKD) |
| how can we slow pregoression of CKD | control HTN, diet, anemia, ca++ and PO3, lipids, obesity, smoking |
| Sxs CKD | often asymptomatic, lethargy, anorexia, vomiting, HTN/HF, unexplained anemia |
| Tx of metabolic acidosis | oral Na+ bicarb |
| MC cause of renal failure | DM |
| What are two types of dialysis | hemodialysis, peritoneal dialysis (thru abdomen) |
| Questions | Not done :D |
Created by:
becker15
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