Renal

Question 1

what is AKI?

Answer 1

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

Question 2

what are the risk factors for AKI?

Answer 2

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

Question 3

what are the three causes for AKI?

Answer 3

pre-renal
renal intrinsic
post renal

Question 4

how is AKI investigated?

Answer 4

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

Question 5

what is the management of AKI?

Answer 5

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

Question 6

what are the complications of AKI?

Answer 6

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

Question 7

how is renal transplant completed?

Answer 7

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

Question 8

what are some complications of renal transplant?

Answer 8

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

Question 9

what is CKD?

Answer 9

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

Question 10

what are the risk factors for CKD?

Answer 10

increasing age, HTN, DM, smoking

Question 11

how does CKD present?

Answer 11

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

Question 12

how is CKD managed?

Answer 12

slow progression, treat complications

Question 13

how is CKD investigated?

Answer 13

eGFR, urinary ACR, USS kidneys

Question 14

what are the indications for dialysis?

Answer 14

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

Question 15

what dialysis options are there?

Answer 15

haemodialysis, continuous ambulatory peritoneal automated, peritoneal

Question 16

how is haemodialysis carried out?

Answer 16

tunnelled cuffed catheter or AV fistula (preferred)

Question 17

what are some complications of peritoneal complications?

Answer 17

SBP, sclerosis, failure, weight gain ,psychosocial

Question 18

summarise nephrotic syndrome?

Answer 18

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

Question 19

how is glomerulonephritis treated generally?

Answer 19

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

Question 20

what is the presentation of nephritic syndrome?

Answer 20

haematuria, proteinuria, oliguria, fluid retention

Question 21

what is diabetic nephropathy?

Answer 21

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

Question 22

what is interstitial kidney disease?

Answer 22

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

Question 23

summarise acute tubular necrosis?

Answer 23

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

Question 24

what is renal tubular acidosis?

Answer 24

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

Question 25

describe T1 and T2 renal tubular acidosis?

Answer 25

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-

Question 26

describe type 3 and 4 renal tubular acidosis?

Answer 26

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

Question 27

what is PCKD?

Answer 27

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

Question 28

how does PCKD present?

Answer 28

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)

Question 29

how is PCKD investigated?

Answer 29

USS, genetic testing

Question 30

how is PCKD managed?

Answer 30

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

Question 31

what are some causes of hyperkalaemia?

Answer 31

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

Question 32

how is hyperkalaemia investigated?

Answer 32

bloods, ECG

Question 33

what are the signs of hyperkalaemia on ECG?

Answer 33

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

Question 34

how is hyperkalaemia managed?

Answer 34

<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

Question 35

what is rhabdomyolysis?

Answer 35

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

Question 36

how does rhabdomyolysis present?

Answer 36

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

Question 37

how is rhabdomyolysis investigated?

Answer 37

CK, myoglobinurea, U&Es

Question 38

how is rhabdomyolysis managed?

Answer 38

IV fluids, IV NaHCO3, IV mannitol

Question 39

what is haemolytic uraemic syndrome?

Answer 39

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

Question 40

how does HUS present?

Answer 40

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

Question 41

How is HUS managed?

Answer 41

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