Renal 2 Flashcards
what pH imbalance does renal tubular acidosis cause
metabolic acidosis
what is type 1 renal tubular acidosis
failure of DCT to excrete H+
what is type 2 renal tubular acidosis
failure of DCT to reabsorb bicarbonate ion
what is type 3 renal tubular acidosis
a mix of type 1 and 2
failure of the DCT to excrete H+ and the PCT to rabsorb bicarbonate
what is type 4 renal tubular acidosis
low aldosterone causes hyperkalemia
this causes a lack of ammonia production, alongside H+ being excreted in the urine
urine pH and blood K+ in renal tubular acidosis type 1
urine pH= high
blood K+= hypokalemia
urine pH and blood K+ in renal tubular acidosis type 2
urine pH= high
blood K+= hypokalemia
urine pH and blood K+ in renal tubular acidosis type 4
urine pH= low
blood K+= hyperkalemia
renal tubular acidosis management
type 1 and 2= bicarbonate
type 4= treat cause and replace aldosterone with fludrocortisone, can also use bicarbonate
HUS triad
autoimmune haemolytic anaemia
thrombocytopenia
AKI
HUS is triggered by
e coli 0157
shiga toxin
what happens in HUS
thrombi in small blood vessels throughout the body
HUS timeline
gastroenteritis (diarrhoea which turns bloody in 3 days)
a week after features of HUS develop
what is released in rhabdomyolysis
myoglobin
potassium
creatine kinase
phosphate
what electrolyte imbalance in most dangerous is rhabdomyolysis
hyperkaelmia
rhabdomyolysis mx
IV fluids
treating hyperkalemia
main diagnostic test for rhabdomyolysis and result
creatine kinase
raised to 1000-10000
moderate hyperkalemia
6-6.5
severe hyperkalemia
over 6.5
hyperkalemia what happens to p waves
flattened
hyperkalemia what happens to PR interval
prolonged
hyperkalemia what happens to QRS complexes
wide
medications that cause hyperkalemia
acei
arb
aldosterone antagonists
nsaids
hyperkalemia mx
30ml 10% calcium gluconate
10 units insulin with 50ml 50% glucose
10 10 10 50 50
adjuncts include
nebulised salbutamol
calcium resonium
types of polycystic kidney disease
autosomal dominant
autosomal recessive
what type of polycystic kidney disease is more severe
how does this manifest
autosomal recessive
causes oligohydramnios in utero, this leads to pulmonary hypoplasia so babies have resp failure at birth
what can slow the development of autosomal dominant polycystic kidney disease
tolvaptan
KDIGO stage 1 AKI rise in creatinine
1.5-1.9x baseline
KDIGO stage 2 AKI rise in creatinine
2-2.9x baseline
KDIGO stage 3 AKI rise in creatinine
above 3x baseline
KDIGO stage 1 AKI urine output reduction
<0.5ml/kg/hr for 6 hours or more
KDIGO stage 2 AKI urine output reduction
<0.5ml/kg/hr for 12 hours or more
KDIGO stage 3 AKI urine output reduction
<0.3ml/kg/hr for 24 hours or more