Renal Flashcards

1
Q

Type 1 and 2 hepatorenal syndromes and Hx associations

A

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.

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2
Q

Mx of hepatorenal syndromes

A

Vasopressin analogies like terlipressin, cause vasoconstriction to the splanchnic circulation.

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3
Q

Presentation of salicylate (aspirin) poisoning

A

Nausea, vom, headache, tinnitus

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4
Q

What overdose does naloxone treat?

A

Opioid overdose

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5
Q

Blood gas pattern for aspirin poisoning + mx

A

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

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6
Q

Side effect of lithium on kidneys

A

Nephrogenic D.Insipidus (insensitivity to ADH). Develop polyuria, polydipsia and high-normal Na.

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7
Q

What is an acceptable fall in GFR and rise in creatinine in CKD patients being treated with ACE i’s?

A

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.

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8
Q

Pathology and complications of CKD

A

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)

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9
Q

Mx of mineral bone disease in CKD

A

Aim: reduce PTH and phosphate
Reduced dietary intake of PO4 = first line
Phosphate binders.
Vit D (calcitriol, alfacalcidol)

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10
Q

How do you diagnose CKD?

A

Stages 1-2: GFR + supporting evidence (albuminuria on A:Cr, imaging or histological abnormalities)

Stages 3-5: GFR alone = sufficient.

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11
Q

What syndrome does minimal change glomerulonephritis cause?

A

Nephrotic syndrome

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12
Q

Cause and mx of minimal change disease

A
Majority = idiopathic.
Mx = pred (renal biopsy if unresponsive)
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13
Q

Why does anaemia occur in CKD?

A

Reduced EPO level, toxic effects of uraemia on bone marrow caused reduced erythropoeisis.
Reduced absorption of iron.

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14
Q

Type of anaemia and mx in CKD

A

Normocytic, normochromic anaemia. Usually occurs when GFR < 30.

Mx: iron studies then EPO if likely to benefit.

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15
Q

Complication of anaemia in CKD

A

LVH

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16
Q

Tx and mechanisms for hyperkalaemia

A

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.

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17
Q

How does nephrotic syndrome predispose to thromboses?

A

Loss of antithrombin-III, proteins C and S.

Associated rise in fibrinogen.

18
Q

Triad of nephrotic syndrome

A

Proteinuria
Hypoalbuminia
Oedema

19
Q

When should you not give Haartmann’s?

A

Any patient with hyperkalaemia

E.g. in the context of AKI

20
Q

Fluid resus

A

500ml bolus of crystalloid over 15 mins.

21
Q

What is the risk of using large volumes of 0.9% saline?

A

Hyperchloraemic metabolic acidosis

22
Q

What do you need to consider when prescribing fluids in heart failure?

A

Too much fluid will precipitate pulmonary oedema.

23
Q

How do you calculate anion gap?

A

Na - (Cl + HCO3).
Normal = 10-18
High anion gap occurs if excessive H accumulation or impaired H excretion.

24
Q

Why does raised anion gap occur?

A

Anything that raises lactate, ketones, urea (renal failure). Salicylate poisoning.

25
Q

2 causes of Diabetes Insipidus

A

1) Cranial DI: deficiency of ADH

2) Nephrogenic DI: insensitivity to ADH

26
Q

Mx for 2 types of DI

A

Cranial: synthetic vasopressin = desmopressin.
Renal: Chlorothiazide- thiazide diuretic causes more sodium to be released into the urine. Breaks polydipsia poyluria cycle.

27
Q

When does haemolytic uraemic syndrome usually occur?

A

Following exposure to toxin. E.g. after infective diarrhoea like GE.

28
Q

Features of HUS in investigations

A

Normocytic anaemia, thrombocytopenia and AKI following diarrhoeal illness.

Inv: FBC, Us and Es, stool culture (usually E.coli)

29
Q

Presentation of HUS with mx

A

Fatigue, pale, petechiae.

Supportive mx.

30
Q

Triad for Alport’s syndrome

A

Sensorineural hearing loss
Renal failure
Ocular abnormalities

Suspect in children.

31
Q

Signs of overload

A

Crackles
Ascites
Tachpynoea
Oliguria

32
Q

Typical presentation of IgA nephropathy

A

Macroscopic haematuria only, in young boys 1-2 DAYS after an URTI.

33
Q

Typical presentation of post-streptococcal glomerulonephritis

A

Haematuria, proteinuria and low complement 1-2 WEEKS after an URTI.
Haematuria can occur but proteinuria is the main sx.

34
Q

A patient with CKD develops a raised A:Cr. What drug should be started?

A

ACE-inhibitor

35
Q

Renal US findings for CKD

A

bilateral shrunken kidneys

36
Q

Renal US findings for chronic diabetic nephropathy

A

normal/large kidneys

37
Q

How do you calculate routine IV maintenance fluids for kids/young people?

A

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.

38
Q

Most common viral infection following solid organ transplant + mx

A

CMV

Ganciclovir

39
Q

Post op problems following renal transplant

A

ATN
Vascular thrombosis
Urine leakage
UTI

40
Q

What’s the recommended K requirement when prescribing fluids?

A

1mmol/kg/day