Nephrology Flashcards
Calcium receptor agonist used for secondary hyperparathyroidism
Cinacalcet
Hypercalcemia of malignancy not responding to bisphosphonate
Denosumab
Morphine toxicity: signs
nausea, pruritus, somnolence, delirium, myoclonus
High clinical suspicion of drug induced AIN: Mx
- No further testing
- Discontinue drug
PSGN begins _ to _ days after pharyngitis
PSGN begins 10 to 14 days after pharyngitis
Normal albumin: creatinine ratio
MustKnow: Attending
CK: Intern
< 30
Fixable risk factors for diabetic nephropathy
Hypertension, hyperglycemia
Urine osmolality in polydipsia
< 100
BUN Creatinine ratio in volume depletion
> 20
In normal and uncomplicated renal disease: ~10:1.
BUN:Cr > 20:1 in hypovolemia because of the increase in urea reabsorption.
- ~ 40 to 50 percent of filtered urea is reabsorbed, most in the PCT, where it is passively linked to the reabsorption of Na and H20.
- Increase in proximal Na reabsorption in hypovolemia produces a parallel increase in urea reabsorption.
- Net effect is a fall in urea excretion and elevations in the BUN and the BUN/serum creatinine ratio, frequently to greater than 20:1.
- This selective rise in the BUN is called prerenal azotemia.
- The serum creatinine concentration will increase in this setting only if the degree of hypovolemia is severe enough to lower the GFR.
Hyaline cast: imply
Concentrated urine, diuretics, non-specific
Hyaline casts — Hyaline casts are only slightly more refractile than water and have a transparent, empty appearance.
Hyaline casts may be observed with small volumes of concentrated urine or with diuretic therapy and are generally nonspecific.
Frequency of the full triad of features (fever, rash, eosinophilia)
< 10%
PSGN features
- Hypertension
- Edema
- Hematuria
- Proteinuria
- Hypocomplementemia
- 2-3 weeks after infection
IgA nephropathy vs PSGN
PSGN: 2-3 weeks after infxn, IgA: concurrent, within 2-3 days
Alport syndrome
- Mutations in type IV collagen
- Typically X-linked dominant
- Progressive glomerular disease to ESRD
- Ocular abnormalities (eg, anterior lenticonus),
- sensorineural hearing loss
Alport syndrome: why glomerular disease/
Mutations in Type IV collagen which is an important component of GBM
Contrast nephropathy prophylaxis: IVF
NS for 7 hours
EKG abnormalities in hypokalemia and hypomagnesemia
- Hypokalemia: U waves, T-wave flattening
- Hypomag: QT prolongation
Cocaine intoxication: eye finding
Mydriasis
Cocaine intoxication: why is dialysis useless?
Cocaine is 90% protein bound
Ethylene glycol and methanol poisoning: Rx
Fomepizole
Profound metabolic acidosis
Methanol or ethylne glycol poisoning
Few conditions other than methanol and ethylene glycol intoxication present with a profound metabolic acidosis (serum bicarbonate less than 8 meq/L), and most of these conditions present in a characteristic fashion (eg, status epilepticus, profound shock, ischemic bowel) .
Serum HCO3 < 8: Signifies
Ethylene glycol or methanol poisoning
Few conditions other than methanol and ethylene glycol intoxication present with a profound metabolic acidosis (serum bicarbonate less than 8 meq/L), and most of these conditions present in a characteristic fashion (
- eg, status epilepticus,
- profound shock,
- ischemic bowel
CK greater than _ _ the normal limit is diagnostic of rhabdomyolysis
CK greater than 5 times the normal limit is diagnostic of rhabdomyolysis
AKI caused by rhabdo: CK is usually > 5K, often > 10K
Incontinence following radical prostatectomy: Rx1
Kegel
Tolteredine, oxybutinin: SideFx
Dry mouth, constipation, Drowsiness
Both anti-muscaranic agents, hence above SideFx
Oval fat bodies: why are they seen in nephrotic syndrome?
- There is heavy proteinuria (3.5 g/day).
- Lipoproteins are re-absorbed in the PCT.
- These PCT cells are desquamated.
- These are the oval fat bodies or lipid containing granular casts.
Muddy brown casts: Signify
ATN