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Year 6 > Nephro and uro > Flashcards

Nephro and uro Flashcards

1
Q

Methods of removing potassium from the body? [3]

A

calcium resonium (orally or enema)

loop diuretics

dialysis

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2
Q

which method of potassium removal is most effective?

A

calcium resonium enemas are more effective than oral as potassium is secreted by the rectum

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3
Q

what is the serum creatinine increase in stage 1 AKI?

A

Increase 1.5-1.9x baseline

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4
Q

what is the serum creatinine increase in stage 2 AKI?

A

Increase 2.0-2.9x baseline

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5
Q

what is the serum creatinine increase in stage 3 AKI? [2]

A

Increase > 3x baseline or >354 µmol/L

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6
Q

what is the urine production in stage 1 AKI?

A

< 0.5ml/kg/h for >6 consecutive hours

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7
Q

what is the urine production in stage 2 AKI?

A

< 0.5ml/kg/h for >12 consecutive hours

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8
Q

what is the urine production in stage 3 AKI?

A

< 0.3ml/kg/h for > 24h or anuric for 12h

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9
Q

which condition presents with a triad of fever, arthralgia and rash

A

acute interstitial nephritis

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10
Q

drug causes of acute interstitial nephritis [5]

A

penicillin
rifampicin
NSAIDs
allopurinol
furosemide

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11
Q

how much water is replaced in maintenance fluids? adults

A

25-30 ml/kg/day of water

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12
Q

how much potassium, sodium and chloride is replaced in maintenance fluids?

A

approximately 1 mmol/kg/day of potassium, sodium and chloride

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13
Q

how much glucose is replaced in maintenance fluids?

A

approximately 50-100 g/day of glucose to limit starvation ketosis

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14
Q

in which patients should Hartmann’s not be used?

A

Hyperkalaemic patients

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15
Q

time frame for hyper acute graft rejection

how is this managed?

A

minutes to hours

removal of the graft

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16
Q

key investigation in acute interstitial nephritis

A

urinary white cell casts/eosinophils

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17
Q

how is maintenance fluid calculated for a child?

A

over 24 hours:
100ml/kg for first 10
50ml/kg for next 10
20ml/kg for every kg after

or 4/2/1 rule in ml/kg/hour

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18
Q

main investigation for APKD

A

USS

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19
Q

first line bloods in AKI caused by rhabdomyolysis

A

plasma creatine kinase

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20
Q

electrolyte abnormalities in rhabdomyolysis

A

high phosphate
low calcium
high potassium

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21
Q

what is the first line treatment of rhabdomyolysis

A

IV normal saline

not Hartmann’s as they are hyperkalaemic

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22
Q

which drug may be beneficial for a select patients of ADPCKD to slow down CKD disease progression?

A

Tolvaptan

V2 receptor antagonist

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23
Q

most sensitivity investigation for myasthenia gravis

A

single fibre electromyography

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24
Q

what is the tensilon test?

A

IV edrophonium reduces muscle weakness temporarily

  • not commonly used any more due to the risk of cardiac arrhythmia
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25
Q

first line treatment for myasthenia gravis

A

pyridostigmine

(Acetylcholinesterase inhibitor)

eventually immunosuppression: prednisolone, azathioprine, cyclosporin

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26
Q

how high is CK compared to the upper limit in rhabdomyolysis

A

> 5 times i.e. significant elevation

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27
Q

Creatinine increase to diagnose AKI

A

> 26 in 48 hours

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28
Q

Creatinine increase in 7 days to diagnosis AKI

A

> 50%

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29
Q

describe the myoglobinuria

A

tea coloured, dark or reddish-brown

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30
Q

drugs to stop in AKI

A

Diuretics
Aminoglycosides, ACEi, ARBs
Metformin
NSAIDs

aspirin that is not a cardio protective dose i.e. 75mg

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31
Q

what is the urgent referral criteria for haematuria

A

Aged >= 45 years AND:
unexplained visible haematuria without urinary tract infection, or
visible haematuria that persists or recurs after successful treatment of urinary tract infection

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test

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32
Q

which blood test is used to find the cause of post streptococcal glomerulonephritis? [2]

A

anti streptolysin O titre

alongside a low C3

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33
Q

mechanism behind hyperacute graft rejection

A

due to pre-existing antibodies against ABO or HLA antigens

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34
Q

mechanism behind acute graft failure (<6m)

A

usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)

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35
Q

mechanism behind chronic graft rejection

A

both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)

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36
Q

most common and important viral infection in solid organ transplant recipients

A

cytomegalovirus

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37
Q

reasons for failing to respond to EPO replacement

A

iron deficiency
inadequate dose
concurrent infection/inflammation
hyperparathyroid bone disease
aluminium toxicity

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38
Q

first line treatment of minimal change disease

A

prednisolone

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39
Q

causes of normal anion gap metabolic acidosis

A

Hyperalimentation
Addisons
RTA
Diarrhoea
Acetozolamide
Spironolactone
Saline

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40
Q

causes of raised anion gap metabolic acidosis

A

Methanol
Uraemia
DKA
Propylene glycol
Isoniazid
Lactic acidosis (sepsis, tissue isch.)
Ethylene glycol
Salicyclates

or KULT

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41
Q

Causes of transient or spurious non-visible haematuria [4]

A

exercise
sex
UTI
menstruation

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42
Q

leading cause of death in CKD patients

A

IHD

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43
Q

investigations for urethral stricture [2]

A

uroflowmetry
ultrasound postvoid residual (PVR) measurement

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44
Q

treatment for urethral stricture [2]

A

dilation
endoscopic urethrotomy

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45
Q

key feature in history of a young man with urethral stricture

A

STI e.g. gonorrhoea

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46
Q

features of urethral stricture [4]

A

weak stream
dribbling/incomplete emptying
dysuria
spraying

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47
Q

first line medications for overactive bladder [3]

A

oxybutynin (immediate release), tolterodine (immediate release), or darifenacin (once daily preparation)

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48
Q

second line med for overactive bladder

A

mirabegron

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49
Q

LUTS: voiding symptoms [5]

A

hesistancy
Poor or intermittent stream
Straining
Incomplete emptying
Terminal dribbling

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50
Q

LUTS: storage symptoms [4]

A

Urgency
Frequency
Nocturia
Urinary incontinence

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51
Q

treatment for moderate to severe voiding symptoms

A

alpha blocker e.g. tamsulosin

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52
Q

treatment for enlarged prostate with voiding symptoms

A

alpha blocker and alpha reductase inhibitor

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53
Q

treatment for renal stones < 5mm

A

watch and wait

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54
Q

treatment for renal stones 5-10mm

A

shockwave lithotripsy

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55
Q

treatment for renal stones 10-20 mm

A

shockwave lithotripsy OR ureteroscopy

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56
Q

treatment for renal stones >20mm

A

percutaneous nephrolithotomy

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57
Q

how are bladder voiding symptoms of an overactive bladder best investigated?

A

urodynamic studies

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58
Q

infection of stag horn calculi is most commonly by

A

proteus mirabilis

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59
Q

how should a patient with mixed symptoms of voiding and storage be treated?

A

alpha blocker with anti muscarinic

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60
Q

IPSS score grades

A

Score 20–35: severely symptomatic
Score 8–19: moderately symptomatic
Score 0–7: mildly symptomatic

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61
Q

which two stones are radiolucent

A

urate and xanthine

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62
Q

what are staghorn calculi made of?

A

struvite (ammonium magnesium phosphate, triple phosphate

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63
Q

main investigation for kidney stones

A

CT KUB

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64
Q

main investigation for kidney stones in the pregnant and children

A

USS

65
Q

how are renal stones removed in the pregnant

A

ureteroscopy

as lithotripsy is contraindicated

66
Q

what are 4 medical indications for circumcision

A

phimosis
recurrent balanitis
balanitis xerotica obliterans
paraphimosis

67
Q

what GUM anatomy tends to be affected in pelvis fracture due to trauma [2]

A

urethra or bladder

68
Q

how do you investigate urethral injury

A

ascending urethrogram

69
Q

how do you investigate bladder injury

A

IV urogram or cystogram

70
Q

what are communicating hydroceles

A

caused by patency of the processus vaginalis allowing peritoneal fluid to drain down into the scrotum. Communicating hydroceles are common in newborn males (clinically apparent in 5-10%) and usually resolve within the first few months of life

71
Q

what are non communicating hydroceles

A

caused by excessive fluid production within the tunica vaginalis

72
Q

when do infantile hydroceles resolve by

A

1-2 years

73
Q

contraindication for circumcision

A

hypospadias

74
Q

complications of vasectomy [5]

A

bruising
haematoma
infection
sperm granuloma
chronic testicular pain (affects between 5-30% men)

75
Q

what a proportionally larger increase urea compared to creatinine indicate

A

a pre renal cause to AKI

76
Q

how is acute clot retention causing bladder retention initially treated

A

bladder irrigation via 3 way catheter

77
Q

what does electron microscopy show in minimal change disease renal biopsy

A

fusion of podocytes and effacement of foot processes

78
Q

how is steroid resistant minimal change disease treated

A

cyclophosphamide

79
Q

what is the triad in Haemolytic uraemic syndrome

A

haemolytic anaemia
thrombocytopenia
AKI

80
Q

most common cause of HUS

A

e.coli O157:H7

81
Q

treatment of HUS

A

supportive

82
Q

when is plasma exchange used in HUS treatment

A

in severe cases of HUS with no associated diarrhoea

83
Q

which 3 conditions cause nephrotic syndrome

A

Minimal change disease
focal segmental glomerulosclerosis membranous glomerulonephritis

84
Q

Post-streptococcal glomerulonephritis is caused by which organism usually

A

group A beta-haemolytic Streptococcus infection (usually Streptococcus pyogenes)

85
Q

which cancer are renal transplant patients at risk of

A

squamous cell carcinoma of the skin due to the immunosuppression

86
Q

what three things do patients on immunosuppression post renal transplant need to be monitored for

which immunosuppressive medication are the main causes

A

cardiovascular disease
renal failure
malignancy

tacrolimus and ciclosporin- Tacrolimus and ciclosporin can cause hypertension and hyperglycaemia. Tacrolimus can also cause hyperlipidaemia.

87
Q

signs in someone over filled [4]

A

Ascites
Crackles
Tachypnoea
Elevated JVP

88
Q

signs in someone underfilled [4]

A

Tachycardia
Hypotension
Oliguria
Sunken eyes and reduced skin turgor

89
Q

fluid balance and values for underfilled and over filled

A

input-output

too +ve –> overfilled
too -ve –> under filled

90
Q

what is the earliest, clinically detectable manifestation of classic diabetic kidney disease

A

microalbuminuria

91
Q

how is diabetic nephropathy tested for

A

measure albumin:creatinine ratio (ACR) on a first pass urine sample

if a first pass sample is not available, repeat the test on a first pass sample the next day

92
Q

management of diabetic nephropathy

A
  • dietary protein restriction
  • tight glycaemic control
  • BP control: aim for < 130/80 mmHg
    ACE inhibitor or angiotensin-II receptor antagonist
  • control dyslipidaemia e.g. Statins
93
Q

what drugs are used in the control of BP in diabetic nephropathy

A

ACEi or ARB

never together

94
Q

what albumin:creatinine ratio defines microalbuminuria

A

> 2.5

95
Q

high lactate post triple AAA repair cause

A

mesenteric ischaemia

96
Q

first line management of phosphataemia

A

reduce dietary phosphate

97
Q

which abx causes an isolated increase in creatinine

A

trimethoprim

98
Q

treatment of choice for UTI in renal dysfunction

A

trimethoprim

nitrofurantoin not given to those with a eGFR <45

99
Q

side effects of EPO [3]

A

bone aches
flu like sx
skin rash

100
Q

prevention of calcium stones

A

high fluid intake
add lemon juice to drinking water
avoid carbonated drinks
limit salt intake
potassium citrate may be beneficial NICE
thiazides diuretics (increase distal tubular calcium resorption)

101
Q

GOLD STANDARD investigation for bladder cancer

A

cystoscopy

102
Q

In a patient with suspected anaemia of chronic disease secondary to CKD, what must be checked before starting EPO

A

iron studies

103
Q

level of serum haptoglobin in HUS

A

low

104
Q

3 things that can alter eGFR reading

A

pregnancy –> increased
muscle mass (e.g. amputees, body-builders) –> decreased
eating red meat 12 hours prior to the sample being taken –> decreased

105
Q

anion gap calculation

A

(Na+ + K+) – (Cl- + HCO3-) = Anion Gap

106
Q

what type of metabolic acidosis does renal tubular acidosis cause

A

hyperchloraemic normal anion gap metabolic acidosis

107
Q

which nephrotic syndrome shows:
basement membrane thickening on light microscopy
subepithelial spikes on silverr stain
positive immunohistochemistry for PLA2

A

membranous glomerulonephritis

108
Q

which nephrotic syndrome has a spike and dome appearance on electron microscopy

A

membranous glomerulonephritis

109
Q

management of membranous glomerulonephritis

A

all patients should receive an ACE inhibitor or an angiotensin II receptor blocker (ARB):

immunosuppression: A combination of corticosteroid + another agent such as cyclophosphamide is often used

consider anticoagulation for high-risk patients

110
Q

indications of haemdialysis

A

Acidosis
Electrolyte imbalance
Intoxication (overdose)
Oedema
Uraemia (confusion, pericarditis, encephalopathy, seizures, decreased consciousness).

111
Q

management of proteinuria in CKD [2 lines]

A

1st line: ACEi/ARB
2nd: SGLT-2 inhibitor

112
Q

prognosis of minimal change disease

A

1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood

113
Q

contraindications to fluid challenge in patient with AKI [2]

A

signs of fluid overload
haemorrhage

114
Q

key finding in rapidly progressive glomerulonephritis on microscopy

which vasculitis can lead to this

A

epithelial crescents

Wegener’s

115
Q

microscopy finding in the kidney in diabetic nephropathy

A

Kimmelstiel-Wilson nodules

116
Q

patients with non-visible haematuria and taking warfarin. Who do they need to be referred to

A

<40 –>nephrology

> 40/older –> urology for cystoscopy

117
Q

how is acute graft failure picked up in renal transplant

A

picked up by a rising creatinine, pyuria and proteinuria

118
Q

Which post op complication is responsible for around 90% acute renal failure episodes in the first few weeks after a renal transplant.

A

acute tubular necrosis of graft

esp cadaver donor

119
Q

1st line investigation of hydronephrosis

A

USS

120
Q

metabolic change in diarrhoea vs vomiting

A

diarrhoea- acidosis
vomiting -alkalosis

121
Q

treatment of metastatic prostate cancer

A

hormonal e.g. GnRH agonists like goserelin

122
Q

which electrolyte abnormality may prolonged diarrhoea cause

A

hypokalaemia

123
Q

extra renal manifestation of ADPKD

A
  • liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly
  • berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
  • cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
  • cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
124
Q

how does TURP syndrome present

what causes it

A

TURP syndrome typically presents with CNS, respiratory and systemic symptoms

It is caused by irrigation with large volumes of glycine during TURP, which is hypo-osmolar and is systemically absorbed when prostatic venous sinuses are opened up during prostate resection. This results in hyponatremia, and when glycine is broken down by the liver into ammonia, hyper-ammonia and visual disturbances.

treat with fluid restriction

125
Q

treatment of nephrogenic DI

A

thiazides and low salt diett

126
Q

treatment of central DI

A

desmopressin

127
Q

what are patients at increased risk of post radiotherapy for prostate cancer

A

Patients are at increased risk of bladder, colon, and rectal cancer following radiotherapy for prostate cancer

128
Q

cause of epididymo-orchitis in:
- young sexually active
- older, low risk

A
  • young sexually active: chlamydia and gonorrhoea
  • older, low risk: E.coli
129
Q

when are hyaline casts seen in the urine [4]

A

seen in normal urine, after exercise, during fever or with loop diuretics

130
Q

In which condition are red cell casts seen in the urine

A

nephritic syndrome

131
Q

in which condition are brown granular casts seen in the urine

A

acute tubular necrosis

132
Q

in which condition are ‘bland’ urinary sediment seen in the urine

A

pre renal uraemia

133
Q

swelling you can’t get over o/e

which ones can you get over

A

inguinal hernia

can get over hydrocele

134
Q

which carcinoma can a varicocele be a presentation of

A

renal cell carcinoma

135
Q

swelling separate from the testes and behind it

A

epididymal cyst

136
Q

normal post void residual volume in someone < 65

A

< 50ml

137
Q

normal post void residual volume in someone > 65

A

< 100 ml

138
Q

how much urine in the bladder after voiding defines chronic urinary retention

A

> 500ml

139
Q

Post-catheterisation urine volume of >_______ suggests acute-on-chronic urinary retention.

A

Post-catheterisation urine volume of >800 ml suggests acute-on-chronic urinary retention.

140
Q

how much urine in the bladder after voiding defines acute urinary retention

A

> 300ml

141
Q

Investigations for suspected epididymo-orchitis are guided by age:
- sexually active younger adults (<35)
- older adults with a low-risk sexual history (>35)

A

sexually active younger adults: NAAT for STIs
older adults with a low-risk sexual history: MSSU

142
Q

treatment of epididymo-orchitis in:
- young sexually active (<35)
- older, low risk (>35)

A
  • mx: send for NAAT and ceftriaxone 500mg intramuscularly single dose, plus doxycycline 100mg by mouth twice daily for 10-14 days
  • mx: send an MSU and treating empirically with an oral quinolone for 2 weeks (e.g. ofloxacin)
143
Q

on which side do varicoceles typically occur on

A

left side due to direct drainage to renal vein

144
Q

in which conditions is Prehns sign positive

A

epididymis orchitis

pain relieved by lifting the testis

145
Q

which renal stones are associated with an inherited metabolic condition

A

cystine

146
Q

which stones form in alkaline urine

A

struvite

and sometimes calcium phosphate

147
Q

difference in presentation between testicular torsion and epididymo-orchitis

A

Testicular torsion would typically cause more acute symptoms and more severe pain.
EO is gradual pain and swelling

148
Q

what is the importance of cyproterone acetate (anti-androgen) in the hormonal treatment of prostate cancer

A

prevent ‘tumour flare’ when taking GnRH agonist like goserlin initially which increases symptoms

Initially, treatment of prostate cancer with GnRH agonists can cause a paradoxical increase in symptoms such as bone pain, bladder obstruction and other symptoms, this is referred to as a ‘tumour flare’.
This occurs because GnRH temporarily causes the pituitary to increase luteinizing hormone (LH) secretion before it begins to inhibit LH release. The increase in LH causes increased stimulation of Leydig cells in the testicles which in turn produce more testosterone. Testosterone stimulates the survival and growth of prostate cancer.
Therefore the initial increase in production of testosterone caused by GnRH agonists can cause paradoxical survival, growth and resultant symptoms of prostate cancer.
Anti-androgens act by blocking androgen receptors which prevent androgens such as testosterone from binding their receptors and suppressing luteinizing hormone, which in turn reduces testosterone levels.

149
Q

chemotherapy used in prostate cancer

A

docetaxel

150
Q

which hormones are non-seminoma germ cell testicular tumours associated with

A

AFP and b-hCG

151
Q

hormone in seminomas

A

20% have elevated hCG, mostly normal

152
Q

1st line investigation of testicular cancer

treatment

A

USS

orchidectomy, chemo, radio

153
Q

types of testicular cancers

A

germ cell (95%)

within those are seminomas and non-seminomas

non seminomas include embryonal, yolk sac, teratoma and choriocarcinoma

154
Q

3 features of testicular cancer

A

a painless lump is the most common presenting symptom (pain may also be present in a minority of men)
hydrocele
gynaecomastia

155
Q

complications of TURP: TURP

A

T urp syndrome
U rethral stricture/UTI
R etrograde ejaculation
P erforation of the prostate

156
Q

which testicular tumours have normal AFP and HCG

A

seminomas

157
Q

treatment of prostatitis

A

14 days of quinolones e.g. cipro

158
Q

how do you calculate serum osmolarity

A

2Na + glucose + urea

159
Q
A

Year 6 (19 decks)

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