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6th Year Endo/Haem/Misc MJ > renal > Flashcards

renal Flashcards

1
Q

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

A
  • K still ftns to concentrate urine and retain sodium
  • urine osmolality HIGH >500 mOsm/kg
  • urine sodium LOW
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2
Q

mx of hyperkalaemia

A

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

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3
Q

HLA matching for renal transplant what is most imp

A

DR>B>A

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4
Q

RF for AKI

A
  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+
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5
Q

Drugs safe to continue in AKI

A
  • paracetamol
  • warfarin
  • statins
  • aspirin (at CARDIOPROTECTIVE DOSE 75mg od)
  • clopi
  • beta blockers
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6
Q

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

A
  1. NSAIDs (except aspirin at 75mg)
  2. Aminogylcosides
  3. ACEi
  4. ARB
  5. Diuretics
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7
Q

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

A

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

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8
Q

Adult PKD extra renal features

A

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
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9
Q

what is the max rate of potassium infusion via peripheral line

A

10 mmol / hour

-rates above 20 mmol / hour require cardiac monitoring

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10
Q

gold std for bladder cancer diagnossi

A

CYSTOSCOPY

-recommended in all pts with sx suggestive of bladder C

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11
Q

KDIGO criteria stage 1

A
  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
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12
Q

KDIGO criteria stage 3

A

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

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13
Q

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

A

ATN = most common cause of renal AKI

  • the K no longer FTNs to concentrate urine + retain sodium SO –>
  • urine osmolality LOW
  • urine sodium HIGH
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14
Q

how is post renal AKI identified usually

A

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

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15
Q

what rate should maintenance fluids be prescribed

A

30 ml/kg/24h

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16
Q

diabetic nephropathy screening

A
  • all pts screened anually using ACR
  • early morning specimen
  • ACR>2.5 = microalbuminuria
17
Q

diabetic nephropathy mx

A
  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
18
Q

4x causes of transient or spurious non-visible haematuria

A

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

19
Q

causes of persistent, non-visible haematuria

A
  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
20
Q

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

A

foods - beetroot, rhubarb

drugs - rifampicin, doxorubicin

21
Q

what is the definition of non-visible haematuria

A

microscopic or dipstick positive haematuria

-found in 2.5% population

22
Q

painless visible haematuria is most likely whata

A

TCC of bladder

23
Q

urgent referral 2WW to urology

A

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

24
Q

non-urgent referral to urology indications

A

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

25
Q

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

A

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
26
Q

alport syndrome inheritance + features

A

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
27
Q

what is the screening test for PCKD

A

Ultrasound scan

28
Q

CKD 2x basic problems

A
  • 1 alpha hydroxylation normally occurs in the Kidneys –> CKD leads to LOW VIT D
  • Kidneys normally excrete phosphate –> CKD leads to HIGH PHOSPHATE
29
Q

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

A

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

30
Q

how to mx high phosphate in CKD

A

=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

31
Q

what type of DI can hereditary haemochromatosis cause

A

CRANIAL DI

32
Q

what happens in urea: creatinine ration in pre renal disease

A

RAISED serum urea: creatinine ratio

33
Q

HSP prognosis

A

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

34
Q

mnemonic for kidney functions x 7

A 
A - WET - BED
Acid-base balance
Water balance
Electrolyte disturbance
Toxin removal
BP control
EPO production
Vitamin D metabolism
35
Q

Mx of CKD - based on ftns x5

A
  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)
36
Q

Cx of AV fistula

A

Pain, infection, bleeding

Thrombosis, stenosis, aneurysm, steal syndrome, high output HF

37
Q

Cx of Tesio line

A

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

6th Year Endo/Haem/Misc MJ (7 decks)

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