Renal

Front 1

where is ADH released?

Back 1

Posterior pituitary

Front 2

Causes of diabetic insipidus

Back 2

1. Central (malignant, trauma, infiltration, sheehan's)
2. Nephrogenic ( Amyloidosis, drug toxicity, UTI, Sickle cell nephropathy)
3. gestational (placental vasopressinase)

Front 3

Diffentials for polyuria

Back 3

Diabetes insipidus - hypernatremic polyuria
primary polydipsia- hyponatremic polyuria

Front 4

How to differentiate primary polyuria and diabetes insipidus

Back 4

water deprivation test
1. in PP will cause increase in urine osmolality to >600
2. In DI urine osmolality will remain below 200

Front 5

How to differntiate between the different DIs?

Back 5

Administer desmopressin
1. IN Central and gestational DI- will cause a rise in urine osmolality to >600
2. Urine osmolality remains low in nephrogenic DI

Front 6

Fluid management (choice) in hypernatremia

Back 6

Treat shock if present: bolus of isotonic saline is acceptable.
In absence of shock, avoid isotonic saline due to risk of cerebral edema
Hypotonic saline ie 4% dextrose favourable

Front 7

How to correct hepernatremia?

Back 7

1. Aim for no more than a drop of 10 mmol/L per day to avoid cerebral edema
2. Adjust fluid therapy by calculating totaal water defecit
= Total Body water {0.6x weight} x {(serum sodium/target sodium)-1}

Front 8

Symptoms of methanol poisoning

Back 8

visual impairment/blindness, mydriasis or an afferent pupil defect, abdominal pain (pancreatitis)
Renal toxicity from formic acid
Secondary parkinsonism from putaminal injury

Front 9

Symptoms of ethylene glycol poisoning

Back 9

flank pain or oliguria from calcium oxalate precipitation
renal failure, cardiac failure and pulmonary edema
seizures, coma

Front 10

What is the protective mechanism of ethanol on methanol and ethylene glycol poisoning?

Back 10

It inhibits alcohol dehydrogenase, preventing the breakdown of parent alcohol to toxic metabolites.
seizures, coma

Front 11

Treatment of alcohol poisoning

Back 11

Fomepizole - competitive inhibitor of alcohol dehydrogenase
hemodialysis
Sodium bicarbonate infusion to maintain pH >7.3 until hemodialysis can be initialised

Pyridoxine and thiamine for EG poisoning and folic acid for methanol to metabolise parent alcohol to non-toxic compounds

Front 12

associations for minimal change disease, likelihood of progressing to CKD

Back 12

Associated with atopic disease
Progression to CKD is rare

Front 13

Treatment for minimal change disease and prognosis

Back 13

Prednisolone.
Up to 70% will achieve complete remission, however relapses are common
25-30% will have corticoid resistant/dependent disease

Front 14

stages of diabetic nephropathy (mainly for T1 but also applies to T2, but nephropathy might occur earlier and progress quicker)

Back 14

1. Hyperfiltration
2. Microalbuminaemia
3. Overt Proteinuric
4. Progressive
5. ESKD (GFR< 15ml/min/1.73m2)