Renal Flashcards
Type 1 and 2 hepatorenal syndromes and Hx associations
Type I is acute and rapid decline over couple of weeks if that, poor prognosis. Follows acute event like upper GI bleed.
Type II is a slower gradual decline in renal function, often associated with refractory ascites.
Mx of hepatorenal syndromes
Vasopressin analogies like terlipressin, cause vasoconstriction to the splanchnic circulation.
Presentation of salicylate (aspirin) poisoning
Nausea, vom, headache, tinnitus
What overdose does naloxone treat?
Opioid overdose
Blood gas pattern for aspirin poisoning + mx
Initially hyperventilate and get respiratory alk- charcoal.
After 24 hours if severe, develop metabolic acidosis with raised anion gap- IV sodium bicarb.
Minor OD- supportive mx
Side effect of lithium on kidneys
Nephrogenic D.Insipidus (insensitivity to ADH). Develop polyuria, polydipsia and high-normal Na.
What is an acceptable fall in GFR and rise in creatinine in CKD patients being treated with ACE i’s?
Decrease in GFR up to 25%
Rise in creatinine up to 30%
These changes can be expected due to the drugs causing a small decrease in filtration pressure.
Pathology and complications of CKD
1) Low Vit.D- hydroxylation step occurs in kidneys usually. So get low Ca due to low vit.D and raised phosphate.
2) Raised phosphate- kidneys usually excrete phosphate. The raised phosphate drags Ca from bones = osteomalacia.
3) Secondary hyperparathyroidism (low Ca, Vit D and raised phosphate)
Mx of mineral bone disease in CKD
Aim: reduce PTH and phosphate
Reduced dietary intake of PO4 = first line
Phosphate binders.
Vit D (calcitriol, alfacalcidol)
How do you diagnose CKD?
Stages 1-2: GFR + supporting evidence (albuminuria on A:Cr, imaging or histological abnormalities)
Stages 3-5: GFR alone = sufficient.
What syndrome does minimal change glomerulonephritis cause?
Nephrotic syndrome
Cause and mx of minimal change disease
Majority = idiopathic. Mx = pred (renal biopsy if unresponsive)
Why does anaemia occur in CKD?
Reduced EPO level, toxic effects of uraemia on bone marrow caused reduced erythropoeisis.
Reduced absorption of iron.
Type of anaemia and mx in CKD
Normocytic, normochromic anaemia. Usually occurs when GFR < 30.
Mx: iron studies then EPO if likely to benefit.
Complication of anaemia in CKD
LVH
Tx and mechanisms for hyperkalaemia
Initially IV calcium gluconate: stabilises cardiac membrane
Insulin/dextrose infusion: ST shifts K from extracellular to intracellular compartment.
Calcium resonium: excretion of K. Most effective as enema.
How does nephrotic syndrome predispose to thromboses?
Loss of antithrombin-III, proteins C and S.
Associated rise in fibrinogen.
Triad of nephrotic syndrome
Proteinuria
Hypoalbuminia
Oedema
When should you not give Haartmann’s?
Any patient with hyperkalaemia
E.g. in the context of AKI
Fluid resus
500ml bolus of crystalloid over 15 mins.
What is the risk of using large volumes of 0.9% saline?
Hyperchloraemic metabolic acidosis
What do you need to consider when prescribing fluids in heart failure?
Too much fluid will precipitate pulmonary oedema.
How do you calculate anion gap?
Na - (Cl + HCO3).
Normal = 10-18
High anion gap occurs if excessive H accumulation or impaired H excretion.
Why does raised anion gap occur?
Anything that raises lactate, ketones, urea (renal failure). Salicylate poisoning.
2 causes of Diabetes Insipidus
1) Cranial DI: deficiency of ADH
2) Nephrogenic DI: insensitivity to ADH
Mx for 2 types of DI
Cranial: synthetic vasopressin = desmopressin.
Renal: Chlorothiazide- thiazide diuretic causes more sodium to be released into the urine. Breaks polydipsia poyluria cycle.
When does haemolytic uraemic syndrome usually occur?
Following exposure to toxin. E.g. after infective diarrhoea like GE.
Features of HUS in investigations
Normocytic anaemia, thrombocytopenia and AKI following diarrhoeal illness.
Inv: FBC, Us and Es, stool culture (usually E.coli)
Presentation of HUS with mx
Fatigue, pale, petechiae.
Supportive mx.
Triad for Alport’s syndrome
Sensorineural hearing loss
Renal failure
Ocular abnormalities
Suspect in children.
Signs of overload
Crackles
Ascites
Tachpynoea
Oliguria
Typical presentation of IgA nephropathy
Macroscopic haematuria only, in young boys 1-2 DAYS after an URTI.
Typical presentation of post-streptococcal glomerulonephritis
Haematuria, proteinuria and low complement 1-2 WEEKS after an URTI.
Haematuria can occur but proteinuria is the main sx.
A patient with CKD develops a raised A:Cr. What drug should be started?
ACE-inhibitor
Renal US findings for CKD
bilateral shrunken kidneys
Renal US findings for chronic diabetic nephropathy
normal/large kidneys
How do you calculate routine IV maintenance fluids for kids/young people?
Holliday-segal formula
First 10kg = 100ml per kg
Second 10kg = 50ml per kg
Subsequent kg = 20ml per kg
Above equation is sufficient if no underlying disease, otherwise more accurate calculation required.
Most common viral infection following solid organ transplant + mx
CMV
Ganciclovir
Post op problems following renal transplant
ATN
Vascular thrombosis
Urine leakage
UTI
What’s the recommended K requirement when prescribing fluids?
1mmol/kg/day
