RENAL Flashcards
(17 cards)
- generalized reabsorption defect in the PCT
- increased excretion of all amino acids, glucose, bicarb, and phosphate
- can cause metabolic acidosis
- due to wilson disease, tyrosinemia, and cystinosis
fanconi syndorme
what drugs cause fanconi
ifosfamide
cisplatin
tenofovir
expired tetracycline
reabsoprtive defect in the thick ascending loop
autosomal recessive
presents like loop diuretics
Barrter Syndrome
reabsoprtive defect of NaCL in the DCT
similar to affects of thiazides
autosomal recessive
leads to hypokalemia, hypomagnesemia
Gitelman syndrome
gain of function mutation that increases sodium reabsorption in the CT presents like hyperaldoseteronism
BUT aldosterone is barley detectable
Liddle SYndrome
SIADH has a deficiency in what
11B-hydroxysteroid DH
normal function of 11B-hydroxysteroid DH
usually turns cortisol into cortisone which is the inactive mineralocorticoid receptor, so without this enzyme then there is an overstimulation of the mineralocorticoid receptors causing HTN
licorice can cause
SIADH , blocks 11B-hydroxysteroid
what is interesting about SIADH
there are low aldositeron levels because this is not what is doing the stimulation
what cytokines are made by TH1 cells
IL-2 and IFN gamma. leads to stimulation of t cells and macrophages
UTI tx
amoxiccilin
neonatal infection tx
ampicillin combined with gentamicin
syphillis tx
penicillin g
pseudomonas tx
pipercillin or tmicracillin
describe what is seen in Distal renal Tubular Acidosis ( Type 1)
- hypokalemia
- urine ph > 5.5
- impaired H+ excretion by alpha intercalated cells
- no new HCO3- is generated
- metabolic acidosis
what is going on in proximal renal tubular acidosis Type 2
- HCO3- is not reabsorbed back into the body
- metabolic acidosis
- hypokalemia
- urine ph is
type 4 - Hyperkalemic Renal Tubular Acidosis ?
- low aldosterone
- impaired ammonium excretion
- urine ph
