Nephrology & Urology Flashcards

1
Q

Indications for IV fluids?

A

Resuscitation
Maintenance
Replacement

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2
Q

Management of fluid resuscitation?

A

500mL 0.9% NaCl or Hartmann’s STAT
→ 250mL if at risk of fluid overload
250-500mL boluses up to 2000mL if needed

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3
Q

Daily water vs Na/K/Cl vs glucose requirement?

A

Water = 25-30mL/kg/day
Na/K/Cl = 1mmol/kg/day
Glucose = 50-100g/day

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4
Q

A 1L bag of IV fluid e.g. 0.9% NaCl contains how much water?

A

1L (you dumbass)

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5
Q

Caution with 0.9% NaCl vs Hartmann’s vs dextrose 5%?

A

0.9% NaCl = risk of hypernatraemia and hyperchloraemic metabolic acidosis
Hartmann’s = risk of hyperkalaemia
Dextrose 5% = do not use for fluid resuscitation

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6
Q

Maximum rate of K infusion?

A

No more than 10mmol/kg/hour

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7
Q

Features and most common cause of nephrotic vs nephritic syndrome?

A

Nephrotic = oedema, proteinuria (“frothy urine”), hypoalbuminaemia, hypercholesterolaemia,
→ minimal change disease (kids), FSGS (adults)
Nephritic = haematuria, hypertension, mild proteinuria, oliguria
→ IgA nephropathy

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8
Q

What causes hypercoagulability in nephrotic syndrome?

A

Antithrombin III loss via urine

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9
Q

Definition of AKI?

A

Rapid onset reduction in renal function causing oliguria and elevated serum urea + creatinine

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10
Q

Cause of pre-renal vs intrinsic vs post-renal causes AKI?

A

Pre-renal (most common) = ischaemia
Intrinsic = kidney damage
Post-renal = obstruction

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11
Q

Urine osmolality and urine sodium in pre-renal vs intrinsic AKI and explain?

A

Pre-renal = urine osmolality high, urine sodium low
→ kidneys concentrate urine and retain sodium to increase blood pressure
Intrinsic = urine osmolality low, urine sodium high
→ damaged kidneys fail to concentrate urine or retain sodium

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12
Q

Investigations for AKI?

A

U&Es
Urinalysis
Renal tract USS (if no cause found)

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13
Q

Biochemical features of AKI?

A

Hyperkalaemia
Hyperphosphataemia
Hyperuricaemia
High creatinine
Metabolic acidosis

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14
Q

Staging of AKI?

A

I = 1.5x creatinine baseline or reduction in urine output to < 0.5mL/kg/hour for ≥ 6 hours
II = 2.5x creatinine baseline or reduction in urine output to < 0.5mL/kg/hour for ≥ 12 hours
III = ≥ 3 x creatinine baseline or reduction in urine output to < 0.3mL/kg/hour for ≥ 24 hours

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15
Q

Management of AKI?

A

Stop nephrotoxic drugs!
Treat hyperkalaemia (if present)
Pre-renal = IV fluid challenge
Intrinsic = treat underlying cause, nephrology referral
Post-renal = catheterise, urology referral

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16
Q

Drugs which should be stopped in AKI?

A

NSAIDs (except aspirin at cardioprotective dose)
Aminoglycosides
ACEi/ARBs
Diuretics

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17
Q

Drugs which may become toxic in AKI?

A

Metformin
Digoxin
Lithium
Opioids

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18
Q

Management of hyperkalaemia?

A

< 6mmol/L = supportive, adjust medication
> 6mmol/L = ECG then treat if abnormal
≥ 6.5mmol/L = urgent treatment
→ IV calcium gluconate + IV insulin/dextrose or + nebulised salbutamol

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19
Q

Most common intrinsic AKI and causes?

A

Acute tubular necrosis
→ ischaemia or nephrotoxins

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20
Q

Urinalysis features of acute tubular necrosis?

A

Muddy brown casts
Renal epithelial cell casts

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21
Q

Most common cause of acute interstitial nephritis?

A

Drugs (especially antibiotics)

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22
Q

Features of acute interstitial nephritis?

A

AKI
Hypertension
Rash, fever
Eosinophilia

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23
Q

Most common type of glomerulonephritis?

A

IgA nephropathy

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24
Q

Outline management of glomerulonephritis?

A

1st line = supportive management
2nd line = ACEi/ARB
3rd line = steroid

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25
Q

Features of IgA nephropathy?

A

12-72 hours post-URTI
Nephritic syndrome (haematuria dominant)

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26
Q

Features of post-streptococcal glomerulonephritis?

A

7-14 days post-URTI
Nephritic syndrome (proteinuria dominant)

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27
Q

Investigation for IgA nephropathy vs post-streptococcal glomerulonephritis?

A

IgA nephropathy = renal biopsy
Post-strep = anti-streptolysin O titre

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28
Q

Biopsy features of membranous glomerulonephritis?

A

Thickened basement membrane
IgG and complement deposits
“Spike and dome” appearance

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29
Q

Biopsy feature of minimal change disease?

A

Fusion of podocytes

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30
Q

Biopsy feature of rapidly progressive glomerulonephritis?

A

Epithelial crescents

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31
Q

Biopsy features of FSGS?

A

Focal and segmental sclerosis

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32
Q

Features of Henoch-Schönlein purpura (HSP)?

A

Post-URTI
Vasculitis → purpuric rash
Abdominal pain
Arthralgia/Arthritis
IgA nephropathy

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33
Q

Monitoring of Henoch-Schönlein purpura (HSP)?

A

BP and urinalysis for 6-12 months

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34
Q

Features of rhabdomyolysis?

A

AKI
PMH trauma e.g. long lie
Muscle pain and swelling
Red/brown “tea coloured” urine

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35
Q

Biochemical features of rhabdomyolysis?

A

Severely raised CK
Raised LDH
Hypocalcaemia (Ca absorbed by muscle)
Hyperkalaemia/phosphataemia/uricaemia

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36
Q

Features of haemolytic uraemic syndrome (HUS)?

A

Triad of:
→ AKI
→ microangiopathic haemolytic anaemia
→ thrombocytopaenia

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37
Q

Blood film features of HUS?

A

Reticulocytes
Schistocytes

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38
Q

Most common causes of CKD?

A

Diabetes
Hypertension
Chronic glomerulonephritis
Polycystic kidney disease

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39
Q

Staging of CKD?

A

I = GFR > 90ml/min with evidence of kidney damage
II = GFR 60-90ml/min with evidence of kidney damage
III = GFR 30-59ml/min
IV = GFR 15-29ml/min
V = GFR < 15ml/min
N.B. patients are usually asymptomatic until IV or V

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40
Q

eGFR variables?

A

CAGE:
Creatinine
Age
Gender
Ethnicity

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41
Q

Investigation and management of CKD proteinuria?

A

Albumin:creatinine ratio
Management = ACEi/ARB

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42
Q

Complications of CKD?

A

Fluid overload → hypertension, oedema
Hyperkalaemia → arrhythmias
Hyperuricaemia → itch, pericarditis, encephalopathy
Low EPO → anaemia → LVH
Low vitamin D → hypocalcaemia/hyperphosphataemia → bone disease, secondary/tertiary hypoparathyroidism

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43
Q

Management of CKD anaemia?

A

1st line = correct iron deficiency (oral or IV)
2nd line = EPO injections

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44
Q

Management of CKD bone disease?

A

1st line = low phosphate diet
2nd line = phosphate-binders (sevelamer) + vitamin D analogue (alfacalcidol)
Total parathyroidectomy for tertiary hyperpathyroidism

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45
Q

Renal USS feature of CKD and exception?

A

Bilateral small kidneys
Enlarged in early diabetic nephropathy

46
Q

Renal failure definition?

A

eGFR < 15mL/min (stage V CKD)

47
Q

Management of renal failure and options?

A

Renal replacement therapy (RRT)
→ haemodialysis
→ peritoneal dialysis
→ renal transplant

48
Q

Indications for dialysis?

A

AEIOU:
Acidosis (pH <7.2)
Electrolyte (hyperkalaemia >7)
Intoxication (poisoning)
Oedema (pulmonary)
Uraemia (uraemic pericarditis, encephalopathy)

49
Q

Surgery required prior to haemodialysis and timescale?

A

Creation of arteriovenous fistula
At least 8 weeks before

50
Q

Most common cause of peritoneal dialysis peritonitis?

A

Staphylococcus epidermidis

51
Q

Management of hyperacute (minutes) vs acute (<6 months) renal transplant rejection?

A

Hyperacute = removal of graft
Acute = steroids/immunosuppressants

52
Q

Post-surgical infection vs malignancy linked to renal transplant?

A

Infection = CMV
Malignancy = SCC

53
Q

Features of ADPKD?

A

Renal failure
Haematuria
Flank pain
Hypertension
Palpable kidneys

54
Q

Extra-renal manifestations of ADPKD?

A

Liver cysts (most common)
Berry aneurysms
Heart valve disease

55
Q

Investigation and management of ADPKD?

A

Investigation = renal USS
Management = anti-hypertensives, tolvaptan (slows cyst formation)

56
Q

Most common renal malignancy?

A

Renal cell carcinoma (clear cell)

57
Q

Features and management of renal cell carcinoma?

A

Frank haematuria
Flank/loin pain
Palpable abdominal mass
Left-sided varicocele
Management = partial or total nephrectomy

58
Q

Paraneoplastic features of renal cell carcinoma?

A

Polycythaemia
Hypertension
Hypercalcaemia
Stauffer syndrome (deranged LFTs)

59
Q

Renal malignancy seen in children?

A

Nephroblastoma (Wilm’s tumour)

60
Q

Features and investigation of renal colic?

A

Loin to groin pain
Haematuria
N&V
Investigation = non-contrast CT KUB

61
Q

Most common composition of renal stone?

A

Calcium oxalate

62
Q

Investigation and management of renal stone?

A

Investigation = non-contrast CT KUB
Management = NSAID (e.g. diclofenac), < 5mm should pass on their own, medical management (e.g. tamsulosin) or shockwave lithotripsy/nephrolithotomy

63
Q

Invasive management of choice for renal stone in pregnancy?

A

Ureteroscopy

64
Q

Management of ureteric obstruction?

A

Urgent surgical decompression e.g. stent

65
Q

Most common causes of UTI?

A

E.Coli (most common)
Klebsiella
Enterococcus
Pseudomonas
Staphylococcus saprophyticus

66
Q

Features of a UTI?

A

Dysuria
Smelly urine
Urinary frequency/urgency/hesitancy
Suprabubic/back pain or discomfort

67
Q

Urine dipstick features of UTI?

A

Leukocytes
Nitrites
Haematuria

68
Q

Who needs a urinalysis to confirm UTI?

A

Children
Pregnant
Men
Catheterised

69
Q

Management of UTI in women?

A

Non-pregnant = nitrofurantoin or trimethoprim 3 days
Pregnant = nitrofurantoin (1st line), amoxicillin or cefalexin (2nd line)

70
Q

Management of UTI in men?

A

Nitrofurantoin or trimethoprim 7 days

71
Q

Management of UTI in catheterised patients?

A

Only treat if symptomatic
Remove or change the catheter

72
Q

Features, investigation and management of pyelonephritis?

A

Fever
N&V
Flank/loin/back pain
UTI symptoms e.g. dysuria
Investigation = MSU
Management = broad-spectrum antibiotics

73
Q

Investigation and management of hydronephrosis?

A

Investigation = renal tract USS
Management = nephrostomy tube

74
Q

Most common bladder cancer?

A

Transitional cell carcinoma

75
Q

Risk factors for transitional cell carcinoma?

A

Smoking
Aniline dye exposure
Cyclophosphamide

76
Q

Investigation and management of bladder cancer?

A

Investigation = cystoscopy
Low grade = TURBT +/- chemotherapy
High grade = surgery e.g. cystectomy

77
Q

Features of acute vs chronic urinary retention?

A

Acute = anuria, suprapubic pain, confusion
Chronic = typically painless

78
Q

Investigation and management of acute urinary retention?

A

Investigation = bladder USS
Management = treat underlying cause, catheterise

79
Q

Complication after relieving urinary retention?

A

Post-obstruction diuresis

80
Q

Voiding vs storage symptoms?

A

Voiding = hestitancy, straining, spraying, weak or intermittent flow, terminal dribbling, incomplete emptying
Storage = frequency, urgency, nocturia, incontinence

81
Q

Investigation for lower urinary tracy symptoms (LUTS) in men?

A

Urodynamic studies

82
Q

Drug options for overactive bladder?

A

1st line = antimuscarinic e.g. oxybutynin, tolterodine
2nd line = mirabegron

83
Q

Features of BPH?

A

Voiding symptoms
Storage symptoms
Complications e.g. UTI

84
Q

Investigations of BPH?

A

PSA
Urinary dipstick
Urine frequency-volume chart
International prostate symptom score (IPSS)

85
Q

Management of BPH?

A

1st line = alpha-agonist (e.g. tamsulosin)
2nd line = 5-alpha-reductase inhibitor (e.g. finasteride)
3rd line = combination therapy of above
4th line = surgery e.g. TURP

86
Q

Alpha-agonist example, mechanism of action and side effects?

A

Example = tamsulosin
Mechanism of action = reduces smooth muscle tone of the bladder and prostate
Side effects = postural hypotension

87
Q

5-alpha-reductase inhibitor example, mechanism of action and side effects?

A

Example = finasteride
Mechanism of action = decreases prostate size by inhibiting conversion of testosterone to dihydrotestosterone
Side effects = erectile dysfunction, gynaecomastia

88
Q

Advice on starting finasteride?

A

Can take up to 6 months for improvement

89
Q

Counselling on PSA test?

A
  • PSA is a protein made by prostate cells
  • High levels may indicate prostate cancer
  • Disadvantages: raised PSA does not mean cancer, low PSA does not exclude cancer
  • If elevated, may indicate need for biopsy +/- treatment which may not be necessary
90
Q

Factors which can elevate PSA?

A

Acute urinary retention
Benign Prosthetic Hypertrophy
Recent ejaculation
PR examination
Urethral instrumentation
Urinary tract infection
Prostatitis
Prostate cancer

91
Q

Investigations for prostate cancer?

A

Multiparametric MRI
Prostate biopsy

92
Q

Management of prostate cancer?

A

Low grade = watch and wait
High grade = radiotherapy, prostatectomy, hormonal therapy

93
Q

Posterior scrotal lump separate to the body of the testicle?

A

Epididymal cyst

94
Q

Soft, non tender swelling of the hemi-scrotum which transilluminates?

A

Hydrocele

95
Q

Patient with fertility issues with scrotum that feels like a bag of worms?

A

Varcicocele

96
Q

Investigation for scrotal/testicular lumps?

A

USS or USS + doppler (varicocele)

97
Q

Red, swollen testicle that has retracted upwards?

A

Testicular torsion

98
Q

Management of testicular torsion?

A

Bilateral orchidopexy

99
Q

Swollen testicle with dysuria and urethral discharge?

A

Epididymo-orchitis

100
Q

Most common causes of epididymo-orchitis?

A

Young = STIs e.g. chlamydia
Older = E.Coli

101
Q

Investigation and managament of epididymi-orchitis?

A

Investigation = NAAT for STIs, MSU
Management = treat underlying cause

102
Q

Features to differenciate testicular torsion vs epididymo-orchitis?

A

Pain will ease on elevation of testis in epididymo-orchitis, not in testicular torsion
Cremasteric reflex is lost in testiclar torsion

103
Q

Features and management of acute bacterial prostatitis?

A

Generally unwell e.g. fever
Penis/perineum/rectum/back pain
Voiding symptoms
Management = quinolone for 14 days

104
Q

Management of balantitis?

A

Saline wash
Topical steroid/antifungal/antibiotic
Circumcision if recurrent

105
Q

Phimosis vs paraphimosis?

A

Phimosis = tight foreskin can’t be retracted
Paraphimosis = foreskin stuck behind glans penis, medical emergency!!

106
Q

What needs to be ruled out before circumcision?

A

Hypospadias

107
Q

Investigations and management of erectile dysfunction?

A

Free testosterone (between 9am-11am)
If low, repeat with FSH, LH and PRL
Management = sildenafil

108
Q

Prevention of contrast-induced nephropathy?

A

IV 0.9% NaCl infusion

109
Q

Anion gap calculation and causes of normal vs raised?

A

(Na + K) - (Cl + HCO3)
Normal = HCO3 loss e.g. diarrhoea, renal tubular acidosis, Addison’s disease
Raised = high lactate, high ketones, high urate, acid poisoning e.g. salicylate

110
Q

Cause of type 1 vs type 2 RTA and biochemical complication?

A

Type 1 = poor H+ excretion
Type 2 (Fanconi) = poor HCO3- reabsorption
Hyperchloraemic metbaolic acidosis