renal

Question 1

what happens to urine osmolality and urine sodium in pre-renal disease

Answer 1

• K still ftns to concentrate urine and retain sodium
• urine osmolality HIGH >500 mOsm/kg
• urine sodium LOW

Question 2

mx of hyperkalaemia

Answer 2

BNF - If K+ > 6.5 mmol/l or if there are ECG changes:
1.Administer 10 ml 10% CALCIUM GLUCONATE by slow IV injection titrated to ECG response
2.Give 10 U ACTRAPID in 50 ml of 50% GLUCOSE over 10-15 MINS
2.Consider use of nebulised salbutamol
4.Consider correcting acidosis with sodium bicarbonate infusion
Nb. to remove potassium from body –> calcium resonium, loop diuretics, dialysis

Question 3

HLA matching for renal transplant what is most imp

Answer 3

DR>B>A

Question 4

RF for AKI

Answer 4

1. CKD
2. Other organ failure/chronic disease eg HF, liver failure, DM
3. hx of AKI
4. use of drugs with nephrotoxic potential eg NSAIDs, aminoglycosides, ACEi, ARBs + Diuretics in past week
5. use of iodinated contrast agents in the past week
6. age 65Y+

Question 5

Drugs safe to continue in AKI

Answer 5

• paracetamol
• warfarin
• statins
• aspirin (at CARDIOPROTECTIVE DOSE 75mg od)
• clopi
• beta blockers

Question 6

drugs that should be stopped in AKI as may worsen renal function

Answer 6

1. NSAIDs (except aspirin at 75mg)
2. Aminogylcosides
3. ACEi
4. ARB
5. Diuretics

Question 7

drugs that may need to be stopped in AKI as increased risk of toxicity (but won’t WORSEN AKI itself)

Answer 7

Metformin - stop if eGFR <45ml/min due to risk of lactic acidosis
Lithium
DIgoxin

Question 8

Adult PKD extra renal features

Answer 8

Extra-renal manifestations

• LIVER CYSTS (70% - the commonest extra-renal manifestation): may cause hepatomegaly
• BERRY ANEURYSMS (8%): rupture can cause SAH
• CV system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
• CYSTS in OTHER ORGANS: pancreas, spleen; very rarely: thyroid, oesophagus, ovary

Question 9

what is the max rate of potassium infusion via peripheral line

Answer 9

10 mmol / hour

-rates above 20 mmol / hour require cardiac monitoring

Question 10

gold std for bladder cancer diagnossi

Answer 10

CYSTOSCOPY

-recommended in all pts with sx suggestive of bladder C

Question 11

KDIGO criteria stage 1

Answer 11

1. Increase in creatinine to 1.5-1.9 times baseline, or
2. Increase in creatinine by ≥26.5 µmol/L, or
3. Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours

Question 12

KDIGO criteria stage 3

Answer 12

1.Increase in creatinine to ≥ 3.0 times baseline, or
2.Increase in creatinine to ≥353.6 µmol/L or
3.Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
4.The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2

Question 13

what happens in acute tubular necrosis to urine osmolality and urine sodium

Answer 13

ATN = most common cause of renal AKI

• the K no longer FTNs to concentrate urine + retain sodium SO –>
• urine osmolality LOW
• urine sodium HIGH

Question 14

how is post renal AKI identified usually

Answer 14

due to obstruction of urinary tract –> identified with hydronephrosis on renal US

Question 15

what rate should maintenance fluids be prescribed

Answer 15

30 ml/kg/24h

Question 16

diabetic nephropathy screening

Answer 16

• all pts screened anually using ACR
• early morning specimen
• ACR>2.5 = microalbuminuria

Question 17

diabetic nephropathy mx

Answer 17

1. dietary protein restriction
2. tight glycaemic control
3. BP aim for <130/80
4. ACEi or ARB should be started if ACR of 3mg/mmol +
5. control dyslipidaemia eg statins

Question 18

4x causes of transient or spurious non-visible haematuria

Answer 18

1-UTI
2-menstruation
3-vigorous exercise (this normally settles after around 3 days)
4-sexual intercourse

Question 19

causes of persistent, non-visible haematuria

Answer 19

1. cancer (bladder , renal, prostate)
2. stones
3. BPH
4. prostatitis
5. urethritis e.g. Chlamydia
6. renal causes: IgA nephropathy, thin basement membrane disease

Question 20

spurious causes of red/orange urine, where blood is not present on dipstick

Answer 20

foods - beetroot, rhubarb

drugs - rifampicin, doxorubicin

Question 21

what is the definition of non-visible haematuria

Answer 21

microscopic or dipstick positive haematuria

-found in 2.5% population

Question 22

painless visible haematuria is most likely whata

Answer 22

TCC of bladder

Question 23

urgent referral 2WW to urology

Answer 23

age >45Y +

• unexplained visible haematuria without UTI, or
• visible haematuria that persists or recurs after successful tx of UTI

age>60Y +
-have unexplained non-visible haematuria + either dysuria or a raised WCC on bloods

Question 24

non-urgent referral to urology indications

Answer 24

age >60Y with recurretn or persistent unexplained UTI
-since the Ix (or not) of non-visible haematuria is so common, in general –> pts <40Y with normal renal ftn, no proteinuria + who are normotensive DO NOT need to be referred + may be Mx in primary care

Question 25

what happens to anion gap in DKA, septic shock + methanol poisoning

Answer 25

RAISED - as they lead to dev of anion that is not incl in calclulation of anion gap - Septic shock --> lactic acidosis - DKA --> raised ketones - methanol poisoning --> rise in formic acid

Question 26

alport syndrome inheritance + features

Answer 26

X-linked dominant pattern - MICROSCOPIC HAEMATURIA - PROGRESSIVE RENAL FAILURE - bilateral SN DEAFNESS - LENTICONUS: protrusion of the lens surface into the anterior chamber - RETINITIS PIGMENTOSA - RENAL BIOPSY: splitting of -lamina densa seen on electron microscopy

Question 27

what is the screening test for PCKD

Answer 27

Ultrasound scan

Question 28

CKD 2x basic problems

Answer 28

- 1 alpha hydroxylation normally occurs in the Kidneys --> CKD leads to LOW VIT D - Kidneys normally excrete phosphate --> CKD leads to HIGH PHOSPHATE

Question 29

CKD 3x further problems due to low vit D + high phosphate

Answer 29

1-high phosphate levels 'drags' calcium from the bones --> OSTEOMALACIA 2-LOW CALCIUM: due to lack of Vit D, high phosphate 3-SECONDARY HYPERPARATHYROIDISM: due to low calcium, high phosphate + low vit D

Question 30

how to mx high phosphate in CKD

Answer 30

=aim is to reduce phosphate and parathyroid hormone levels. 1-reduced dietary intake of phosphate is the 1st-line mx 2-phosphate binders 3-vitamin D: alfacalcidol, calcitriol 4-parathyroidectomy may be needed in some cases PHOSPHATE BINDERS =aluminium-based binders are less comm used now =Ca-based binders problems include hypercalcemia + vasc calcification =sevelamer a non-calcium based binder

Question 31

what type of DI can hereditary haemochromatosis cause

Answer 31

CRANIAL DI

Question 32

what happens in urea: creatinine ration in pre renal disease

Answer 32

RAISED serum urea: creatinine ratio

Question 33

HSP prognosis

Answer 33

usu excellent with full renal recovery, esp in children without renal invovlement -around 1/3 pts have relapses

Question 34

mnemonic for kidney functions x 7

Answer 34

``` A - WET - BED Acid-base balance Water balance Electrolyte disturbance Toxin removal BP control EPO production Vitamin D metabolism ```

Question 35

Mx of CKD - based on ftns x5

Answer 35

1. Modify RF - antihypetensives, good glycaemic control 2. FLUID BALANCE - fluid + salt restriction 3. ANAEMIA - EPO stimulating agents 4. HYPOCALCAEMIA - phosphate binders, activated Vit D replacement (alpha calcidol) 5. RRT - PD, HD, Renal transplant - for stage 5 disease (eGFR<15)

Question 36

Cx of AV fistula

Answer 36

Pain, infection, bleeding | Thrombosis, stenosis, aneurysm, steal syndrome, high output HF

Question 37

Cx of Tesio line

Answer 37

Sepsis, PERITONITIS, DIC, Fluid overload, DDS = cerebral oedema