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