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Finals > Renal > Flashcards

Renal Flashcards

1
Q

what is AKI?

A

it is an acute drop in renal function
a rise in Cr >25mmol/L in 48h or >50% in 7 days
UO<0.5ml for 6 hours

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2
Q

what are the risk factors for AKI?

A

CKD, HF, DM, liver disease, increasing age, cognitive impairment, nephrotoxins, contrast

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3
Q

what are the three causes for AKI?

A

pre-renal
renal intrinsic
post renal

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4
Q

how is AKI investigated?

A

urinalysis - blood, protein, leucocytes, nitrates, glucose
U&Es

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5
Q

what is the management of AKI?

A

prevention, fluids, r/v drugs, relieve obstruction, dialysis

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6
Q

what are the complications of AKI?

A

hyperkalaemia, fluid overload, HF, PO, MA, uraemia, pericarditis, encephalopathy

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7
Q

how is renal transplant completed?

A

kidneys are left in place, donor kidney anastomosed with patient pelvic vessels and places in abdomen

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8
Q

what are some complications of renal transplant?

A

transplant rejection - acute and chronic
IHS, T2DM
infection
NHL
skin cancer

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9
Q

what is CKD?

A

it is a chronic reduction in renal function
DM, HTN, age, glomerulonephritis. PCKD, drugs

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10
Q

what are the risk factors for CKD?

A

increasing age, HTN, DM, smoking

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11
Q

how does CKD present?

A

pruritis, decreased appetite, nausea, cramps, oedema, neuropathy, pallor, HTN

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12
Q

how is CKD managed?

A

slow progression, treat complications

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13
Q

how is CKD investigated?

A

eGFR, urinary ACR, USS kidneys

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14
Q

what are the indications for dialysis?

A

acidosis, electrolytes, abnormalities, intoxication, oedema, uraemia symptoms

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15
Q

what dialysis options are there?

A

haemodialysis, continuous ambulatory peritoneal automated, peritoneal

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16
Q

how is haemodialysis carried out?

A

tunnelled cuffed catheter or AV fistula (preferred)

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17
Q

what are some complications of peritoneal complications?

A

SBP, sclerosis, failure, weight gain ,psychosocial

18
Q

summarise nephrotic syndrome?

A

proteinuria, oedema, thrombosis, HTN, hypercholesterolaemia - mostly caused by minimal change in children or FSG in adults
management - steroids in children or manage complications and treat cause

19
Q

how is glomerulonephritis treated generally?

A

immunosuppressants such as steroids, and BP control with ACEi and ARBs

20
Q

what is the presentation of nephritic syndrome?

A

haematuria, proteinuria, oliguria, fluid retention

21
Q

what is diabetic nephropathy?

A

most common cause of glomerular pathology due to chronic hyperglycaemia, results in scarring, proteinuria, investigated with ACR and U&Es, and managed with managing BP, BM, ACEi

22
Q

what is interstitial kidney disease?

A

it is AKI and HTN due to tubule and interstitial inflammation - caused by hypersensitivity
it presents with rash, fever and eosinophilia
treated with steroids or by treating cause

23
Q

summarise acute tubular necrosis?

A

damage to the epithelial cells of tubules causing AKI
caused by ischaemia and toxins
takes 7-21 days for the cells to regenerate
investigation - urinalysis - muddy brown casts, renal tubular epithelial cells present
mx - supportive with IVF, r/v drugs, treat complications

24
Q

what is renal tubular acidosis?

A

it is metabolic acidosis in the kidneys due to a tubular pathology

25
Q

describe T1 and T2 renal tubular acidosis?

A

type 1 - distal tubule cannot excrete H+ - FTT, hyperventilation, CKS, osteomalacia, increased K, increased urinary pH, MA - treated with oral HCO3-
Type 2 - proximal tubule cannot reabsorb HCO3- - increased urinary pH, MA, decreased K - treat with oral HCO3-

26
Q

describe type 3 and 4 renal tubular acidosis?

A

type 3 - combination of type 1 and 2
type 4 - reduced aldosterone - increased K, Cl, MA, decreased urinary pH - treat with NaHCO3 and fludrocortisone

27
Q

what is PCKD?

A

it is a genetic condition with fluid filled cysts and significant impairment of the function

28
Q

how does PCKD present?

A

with hepatic, pancreatic, prostatic and ovarian cysts, cerebral aneurysms, valve disease, aortic root dilatation, loin pain, HTN, CVD, haematuria, renal stones
renal failure underdevelopment of lungs, flat nasal bridge, low set ears (autosomal recessive)

29
Q

how is PCKD investigated?

A

USS, genetic testing

30
Q

how is PCKD managed?

A

tolvaptan to slow development of cysts, treat complications - antihypertensives, analgesia, dialysis, ABx and drainage, avoid NSAIDs and contact sports, regular monitoring, angiograms for cerebral aneurysms

31
Q

what are some causes of hyperkalaemia?

A

AKI, CKD, rhabdomyolysis, adrenal insufficiency, tumour lysis syndrome, drugs, K supplementation

32
Q

how is hyperkalaemia investigated?

A

bloods, ECG

33
Q

what are the signs of hyperkalaemia on ECG?

A

tall tented T waves, flattened absent P waves, broad QRS

34
Q

how is hyperkalaemia managed?

A

<6 and stable - monitoring and change diet and drugs
> 6 and ECG changes or >6.5 - insulin and dextrose - 10 U or actrapid in 50mls of 50% dextrose
10ml of 10% calcium gluconate
neb salbutamol, IV fluids, oral calcium resonium, NaHCO3, dialysis

35
Q

what is rhabdomyolysis?

A

when the skeletal muscle tissue breaks down and releases products into the blood and is from overuse or injury
myocytes undergo apoptosis - K, P, CK and myoglobin release - increased K and AKI

36
Q

how does rhabdomyolysis present?

A

muscle aches, pains, oedema, fatigue, confusion, red or brown urine

37
Q

how is rhabdomyolysis investigated?

A

CK, myoglobinurea, U&Es

38
Q

how is rhabdomyolysis managed?

A

IV fluids, IV NaHCO3, IV mannitol

39
Q

what is haemolytic uraemic syndrome?

A

thrombosis in small vessels usually due to shiga toxin resulting in haemolytic anaemia, AKI and thrombocytopenia

40
Q

how does HUS present?

A

gastroenteritis (usually treated with ABx and loperamide) followed by decreased UO, haematuria, abdo pain, lethargy, irritability, confusion, HTN, bruising

41
Q

How is HUS managed?

A

It is self limiting but an emergency so requires admission for supportive treatment with anti hypertensives, blood transfusions and dialysis

Finals (16 decks)

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