Flashcards in RENAL Deck (17)
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1
- 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
2
what drugs cause fanconi
ifosfamide
cisplatin
tenofovir
expired tetracycline
3
reabsoprtive defect in the thick ascending loop
autosomal recessive
presents like loop diuretics
Barrter Syndrome
4
reabsoprtive defect of NaCL in the DCT
similar to affects of thiazides
autosomal recessive
leads to hypokalemia, hypomagnesemia
Gitelman syndrome
5
gain of function mutation that increases sodium reabsorption in the CT presents like hyperaldoseteronism
BUT aldosterone is barley detectable
Liddle SYndrome
6
SIADH has a deficiency in what
11B-hydroxysteroid DH
7
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
8
licorice can cause
SIADH , blocks 11B-hydroxysteroid
9
what is interesting about SIADH
there are low aldositeron levels because this is not what is doing the stimulation
10
what cytokines are made by TH1 cells
IL-2 and IFN gamma. leads to stimulation of t cells and macrophages
11
UTI tx
amoxiccilin
12
neonatal infection tx
ampicillin combined with gentamicin
13
syphillis tx
penicillin g
14
pseudomonas tx
pipercillin or tmicracillin
15
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
16
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
17
