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MRCP Part 1 > Nephro > Flashcards

Nephro Flashcards

1
Q

Causes of Acute interstitial nephritis

A
  1. drugs: the most common cause, particularly antibiotics

penicillin

rifampicin

NSAIDs

allopurinol

furosemide

  1. systemic disease: SLE, sarcoidosis, and Sjögren’s syndrome
  2. infection: Hanta virus , staphylococci
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2
Q

Features of Acute interstitial nephritis

A

fever, rash, arthralgia

eosinophilia

mild renal impairment

hypertension

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3
Q

Investigations of acute interstitial nephritis

A

sterile pyuria

white cell casts

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4
Q

Tubulointerstitial nephritis with uveitis(TINU) usually occurs in ……?

A

young females.

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5
Q

Criteria to diagnose AkI

A
  1. rise in serum creatinine of >= 26 micromol/litre within 48 hours
  2. 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
  3. urine output < 0.5 ml/kg/hourfor > 6 hours in adults and more than
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6
Q

Stage 1 of AKI

A
  1. urine output to<0.5mL/kg/hour for≥ 6 hours

Or
2. Increase in creatinine to1.5-1.9times baseline

Or

  1. Increase in creatinine by ≥26.5 µmol/L
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7
Q

Stage 2 of AKI

A
  1. urine output to<0.5mL/kg/hour for≥12 hours

Or

  1. Increase in creatinine to2.0 to 2.9times baseline
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8
Q

Stage 3 of AKi

A
  1. urine output <0.3mL/kg/hour for≥24 hours

Or

  1. Increase in creatinine to≥ 3.0times baseline

Or

  1. Increase in creatinine to ≥353.6 µmol/L
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9
Q

ADPKD type 1 vs ADPKD type 2

Which Chromosome ….?

A

Type 1 : Chromosome 16

Type 2: Chromosome 4

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10
Q

Ultrasound diagnostic criteria of ADPKD (in patients with positive family history)

A
  1. Age < 30 years ; 2 cysts uni/ bilateral
  2. Age 30 - 59 years ; 2 cysts in each kidneys
  3. Age > 60 ; 4 cysts in each kidneys
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11
Q

Management of ADPKD

A

tolvaptan(vasopressin receptor 2 antagonist) may be an option. For select patients

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12
Q

Extra-renal manifestations of ADPKD

A
  1. Liver cysts may cause hepatomegaly
  2. berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
  3. cardiovascular system:mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
  4. cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
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13
Q

Causes of a raised anion gap metabolic acidosis

A

lactate: shock, hypoxia

ketones: diabetic ketoacidosis, alcohol

urate: renal failure

acid poisoning: salicylates, methanol

5-oxoproline: chronic paracetamol use

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14
Q

Causes of a normal anion gap or hyperchloraemic metabolic acidosis

A

gastrointestinal bicarbonate loss:diarrhoea, ureterosigmoidostomy, fistula

renal tubular acidosis

drugs: e.g. acetazolamide

ammonium chloride injection

Addison’s disease

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15
Q

ARPKD is due to a defect in a gene located on chromosome ….. which encodes ………

A

Chromosome 6

encodes fibrocystin

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16
Q

Autosomal recessive polycystic kidney disease (ARPKD) on biopsy

A

Renal biopsy typically shows multiple cylindrical lesions at right angles to the cortical surface.

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17
Q

The time taken for an arteriovenous fistula to develop is …….?

A

6 to 8 weeks.

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18
Q

Calciphylaxis presents with ……?

A

painful necrotic skin lesions.

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19
Q

The risk of developing calciphylaxis is linked with

A

hypercalcaemia,

hyperphophataemia and

hyperparathyroidism.

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20
Q

Treatment of calciphylaxis

A

reducing calcium and phosphate levels, controlling hyperparathyroidism and avoiding contributing drugs such as warfarin and calcium containing compounds.

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21
Q

What is the most common presenting feature of Retroperitoneal fibrosis?

A

Lower back/flank pain

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22
Q

Retroperitoneal fibrosis is associated with (4)

A

Riedel’s thyroiditis

previous radiotherapy

sarcoidosis

inflammatory abdominal aortic aneurysm

drugs: methysergide

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23
Q

Indications for plasma exchange

A

Guillain-Barre syndrome

myasthenia gravis

Goodpasture’s syndrome

ANCA positive vasculitis if rapidly progressive renal failure or pulmonary haemorrhage

TTP/HUS

cryoglobulinaemia

hyperviscosity syndrome e.g. secondary to myeloma

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24
Q

Complications of plasma exchange

A

hypocalcaemia: due to the presence of citrate used as an anticoagulant for the extracorporeal system

metabolic alkalosis

removal of systemic medications

coagulation factor depletion

immunoglobulin depletion

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25
Q

Contrast media nephrotoxicity may be defined as a …….%….. increase in creatinine occurring……..days after administration.

A

25% increase in creatinine occurring2 -5 days after administration.

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26
Q

5 Risk factors of Contrast media nephrotoxicity

A

known renal impairment (especially diabetic nephropathy)

age > 70 years

dehydration

cardiac failure

the use of nephrotoxic drugs such as NSAIDs

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27
Q

Prevention of Contrast media nephrotoxicity

A

Iv 0.9% sodium chlorideat a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure

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28
Q

Patients who are high-risk for contrast-induced nephropathy should have metformin withheld for …………..

A

metformin withheld for a minimum of 48 hours and until the renal function has been shown to be normal.

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29
Q

Spironolactone is analdosterone antagonist which acts in ……

A

the cortical collecting duct.

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30
Q

Causes of lactic acidosis type A

A

sepsis, shock, hypoxia, burns

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31
Q

Causes of lactic acidosis type B

A

metformin

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32
Q

the Modification of Diet in Renal Disease (MDRD) equation, which uses thefollowing 4 variables:

A

serum creatinine

age

gender

ethnicity

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33
Q

3 Factors which may affect s. Creat

A

pregnancy

muscle mass (e.g. amputees, body-builders)

eating red meat12 hours prior to the sample being taken

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34
Q

Amyloidosis: types

A
  1. AL AMYLOIDOSIS
  2. AA AMYLOIDOSIS
  3. Beta 2 microglobulin AMYLOIDOSIS
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35
Q

Causes of AL amyloidosis

A

myeloma, Waldenstrom’s, MGUS

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36
Q

Causes of AA amyloid

A

chronic infection/inflammation

e.g. TB, bronchiectasis, rheumatoid arthritis

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37
Q

Beta-2 microglobulin amyloidosis is associated with

A

patients on renal dialysis

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38
Q

4 Risk factors for urothelial (transitional cell) carcinoma of the bladder include:

A
  1. Smoking
  2. Exposure to aniline dyes
  3. Rubber manufacture
  4. Cyclophosphamide
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39
Q

2 Risk factors for squamous cell carcinoma of the bladder include:

A

Schistosomiasis

Smoking

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40
Q

What is the investigation of choice of Renal vascular disease?

A

MR angiography

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41
Q

Management of Wilms’ nephroblastoma

A

nephrectomy

chemotherapy

radiotherapy if advanced disease

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42
Q

Renal cell cancer is associated with (3)

A

von Hippel-Lindau syndrome

tuberous sclerosis

autosomal dominant polycystic kidney disease

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43
Q

Features of which condition?

haematuria

loin pain

abdominal mass

paraneoplastic hepatic dysfunction syndrome

Stauffer syndrome typically presents ascholestasis/hepatosplenomegaly

A

Renal cell cancer

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44
Q

Which type of renal stones is radio lucent

A

Urate stones

Xanthine stones

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45
Q

stag-horn calculi are composed of…

A

struvite (ammonium magnesium phosphate, triple phosphate).

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46
Q

Renal stones: risk factors

A

dehydration

hypercalciuria, hyperparathyroidism, hypercalcaemia

cystinuria

high dietary oxalate

renal tubular acidosis

medullary sponge kidney, polycystic kidney disease

beryllium or cadmium exposure

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47
Q

2 Risk factors for urate stones

A

gout

ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid

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48
Q

4 drugs that promote calcium stones

A

loop diuretics,

steroids,

acetazolamide,

theophylline

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49
Q

alpha blockers recommend in renal stones

A

for distal ureteric stones < 10 mm in size

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50
Q

ultrasound should be used in renal stones for ……

A

pregnant women and children

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51
Q

Which drugs can be used to prevent Oxalate stones?

A

cholestyramine reduces urinary oxalate secretion

pyridoxine reduces urinary oxalate secretion

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52
Q

In Pre renal uremia

  1. Urine sodium
  2. Urine osmolality
  3. Fractional Na excretion
  4. Fractional Urea excretion
  5. Serum Urea: creatinine ratio
  6. Urine:plasma urea
  7. Urine:plasma osmolality
  8. Specific gravity
A
  1. Urine sodium : < 20
  2. Urine osmolality >500
  3. Fractional Na excretion < 1 %
  4. Fractional Urea excretion < 35%
  5. Serum Urea: creatinine ratio : raised
  6. Urine:plasma urea > 10:1
  7. Urine:plasma osmolality > 1.5
  8. Specific gravity > 1020
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53
Q

In ATN

  1. Urine sodium :
  2. Urine osmolality
  3. Fractional Na excretion
  4. Fractional Urea excretion
  5. Serum Urea: creatinine ratio
  6. Urine:plasma urea
  7. Urine:plasma osmolality
  8. Specific gravity
A
  1. Urine sodium : > 40
  2. Urine osmolality < 350
  3. Fractional Na excretion > 1 %
  4. Fractional Urea excretion > 35 %
  5. Serum Urea: creatinine ratio : normal
  6. Urine:plasma urea < 8:1
  7. Urine:plasma osmolality < 1.1
  8. Specific gravity < 1010
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54
Q

fractional sodium excretion =

A

*fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100

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55
Q

fractional urea excretion =

A

fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100

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56
Q

corticomedullary scarring with atrophy of tubules

Seen in …?

A

Chronic pyelonephritis is

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57
Q

Risk factors of Chronic pyelonephritis

A

vesicoureteral reflux in children

obstruction e.g.recurrent renal stones

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58
Q

Red cell casts present in: 4 conditions

A
  1. Acute glomerulonephritis
  2. Renal vasculitis
  3. Accelerated hypertension and
  4. Interstitial nephritis.
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59
Q

Alport’S SYNDROME is due to a defect in the gene which codes for ……

A

type IV (4) collagen resulting in an abnormal glomerular-basement membrane

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60
Q

Alport’S SYNDROME is more severe in …….

A

Males

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61
Q

In Alport’S SYNDROME, deafness occurs……

A

Before the onset of renal failure

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62
Q

90% of Alport’s syndrome develop renal failure by the age of….

A

40 years

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63
Q

Alport’s patient with a failing renal transplant. This may be caused by the presence of …..

A

anti-GBM antibodies leading to a Goodpasture’s syndrome like picture.

64
Q

5 features of Alport’S SYNDROME

A
  1. Microscopic haematuria.

2) Progressive renal failure.

3) Bilateral sensorineural deafness.

  1. Ocular abnormalities: Lenticonus, corneal ulceration, cataract, retinitis pigmentosa
  2. Renal biopsy: splitting of lamina densa seen on electron microscopy, light microscopy may be unremarkable.
65
Q

A definitive diagnosis of Acute interstitial nephritis is established by

A

Renal biopsy which usually shows interstial oedema with a heavy infiltrate of inflammatory cells and variable tubular necrosis

66
Q

Mechanism of acute interstitial nephritis

A

delayed T-cell hypersensitivity or cytotoxic T-cell reaction.

67
Q

5 Causes of Papillary necrosis

A
  1. Chronic analgesia use
  2. Sickle cell disease
  3. TB
  4. Acute pyelonephritis
  5. DM
68
Q

Retroperitoneal fibrosis is associated with ( 5)

A
  1. Riedel’s thyroiditis
  2. Previous radiotherapy
  3. Sarcoidosis
  4. Inflammatory abdominal aortic aneurysm
  5. Drugs: methysergide
69
Q

In plasma exchange most conditions 5% albumin is the plasma substitute of choice, except for …………….. we should use FFP.

A

TTP

70
Q

10 Causes of Sterile pyuria

A
  1. Partially treated UTI
  2. STD
  3. Acute GN
  4. Tubular interstitial diseases
  5. Renal stones
  6. Cancer
  7. Adult polycystic kidney disease
  8. Analgesic nephropathy
  9. Appendicitis
  10. Renal TB
71
Q

1) Renal failure 2) Eosinophilia 3) Purpura 4) Livedo reticularis 5) Low C3. 6) ↑ESR. 7) Urine proteinuria.

Features of which condition?

A

Cholesterol embolisation

72
Q

PD fluid WCC of greater than…… is diagnostic of PD peritonitis

A

100/mm3

73
Q

In PD peritonitis, which is the most common organism?

A

coagulase negative Staphylococcus (CoNS)

Staphylococcus epidermidisis the most common cause.

Staphylococcus aureusis another common cause

74
Q

Treatment of PD peritonitis i

A
  1. vancomycin (or teicoplanin) + ceftazidime added to dialysis fluidOR
  2. vancomycin added to dialysis fluid + ciprofloxacin by mouth
  • aminoglycosides are sometimes used to cover the Gram negative organisms instead of ceftazidime
75
Q

basket-weave’ appearance in biopsy
Can be seen in ?

A

Alport’s syndrome

76
Q

7 Side-effects of erythropoietin

A
  1. accelerated hypertension potentially leading to encephalopathy and seizures
  2. bone aches
  3. flu-like symptoms
  4. skin rashes, urticaria
  5. pure red cell aplasia* (due to antibodies against erythropoietin)
  6. raised PCV increases risk of thrombosis (e.g. Fistula)
  7. iron deficiency 2nd to increased erythropoiesis
77
Q

5 reasons why patients may fail to respond to erythropoietin therapy:

A

iron deficiency

inadequate dose

concurrent infection/inflammation

hyperparathyroid bone disease

aluminium toxicity

78
Q

3 Features of Renal papillary necrosis

A

visible haematuria

loin pain

proteinuria

79
Q

Primary HUS (‘atypical’) is due to

A

complement dysregulation

80
Q

Typical HUS secondary to ( 6 )

A
  1. classically Shiga toxin-producing Escherichia coli (STEC) 0157:H7
  2. Pneumococcal infection
  3. HIV
  4. SLE
  5. Drugs
  6. Cancer
81
Q

indications for plasma exchange in HUS

A

severe cases of HUS not associated with diarrhoea

82
Q

eculizumab has evidence of greater efficiency than plasma exchange alone in the treatment of …..??

A

adult atypical HUS

83
Q

eculizumab is …..

A

C5 inhibitor monoclonal antibody

84
Q

Causes of Fanconi syndrome

A

cystinosis (most common cause in children)

Sjogren’s syndrome

multiple myeloma

nephrotic syndrome

Wilson’s disease

85
Q

6 Features of Fanconi syndrome

A
  1. Type 2 RTA
  2. Polyuria
  3. Glycosuria
  4. Aminoaciduria
  5. Phosphaturia
  6. Osteomalacia
86
Q

Fanconi syndrome describes a

A

generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule

87
Q

Thin basement membrane disease is An inherited disorder of type …. collagen

A

type IV collagen

88
Q

Vesicoureteric reflux (VUR) is normally diagnosed by …….

A

a micturating cystourethrogram

89
Q

Cystinuria is due to a defect in the membrane transport of …..?

A

cystine, ornithine, lysine, arginine (mnemonic = COLA)

90
Q

chromosome 2: SLC3A1 gene, chromosome 19: SLC7A9

A

Cystinuria

91
Q

Diagnosis of cystinuria

A

cyanide-nitroprusside test

92
Q

Management of cystinuria

A

hydration

D-penicillamine

urinary alkalinization

93
Q

8 Causes of cranial DI

A
  1. idiopathic
  2. post head injury
  3. pituitary surgery
  4. craniopharyngiomas
  5. DIDMOAD
  6. histiocytosis X
  7. sarcoidosis
  8. haemochromatosis
94
Q

6 Causes of nephrogenic DI

A
  1. genetic, mutation in the gene that encodes the aquaporin 2 channel
  2. hypercalcaemia
  3. hypokalaemia
  4. lithium
  5. demeclocycline
  6. tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
95
Q

Investigations of DI

A

high plasma osmolality,

low urine osmolality

a urine osmolality of >700 mOsm/kg excludes diabetes insipidus

water deprivation test

96
Q

Management of DI

A
  1. nephrogenic diabetes insipidus
  • thiazides
  • low salt/protein diet
  1. central diabetes insipidus can be treated with desmopressin
97
Q

Risk factors of Benign prostatic hyperplasia

A
  1. Age
    - around 50% of 50-year-old men will have evidence of BPH and 30% will have symptoms
  • around 80% of 80-year-old men have evidence of BPH
  1. ethnicity: black > white > Asian
98
Q

Causes of minimal changes disease

A

drugs: NSAIDs, rifampicin

Hodgkin’s lymphoma, thymoma

infectious mononucleosis

99
Q

Management of Minimal changes disease

A

oral corticosteroids: majority of cases (80%) are steroid-responsive

cyclophosphamide is the next step for steroid-resistant cases

100
Q

What is the third most common cause of end-stage renal failure (ESRF).

A

Membranous glomerulonephritis

101
Q

electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance

A

Membranous glomerulonephritis

102
Q

Management of membranous GN

A
  1. ACEi/ ARBs
  2. immunosuppression
    combination of corticosteroid + another agent such as cyclophosphamide is often used

many patients spontaneously improve only patient with severe or progressive disease require immunosuppression

103
Q

3 Good prognostic features of Membranous glomerulonephritis

A
  1. female sex,
  2. young age at presentation and
  3. asymptomatic proteinuria of a modest degree at the time of presentation.
104
Q

Causes of FSGS

A

idiopathic

secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy

HIV

heroin

Alport’s syndrome

sickle-cell

105
Q

Focal segmental glomerulosclerosis & renal transplants

A

Focal segmental glomerulosclerosis is noted for having a high recurrence rate in renal transplants.

106
Q

renal biopsy

focal and segmental sclerosis and hyalinosis on light microscopy

effacement of foot processes on electron microscopy

A

FSGS

107
Q

Treatment of FSGS

A

steroids +/- immunosuppressants

108
Q

Types of organ rejection

A
  1. Hyperacute: This occurs immediately through presence of pre formed antibody (such as ABO incompatibility).
  2. Acute: Occurs during the first 6 months and is usually T cell mediated. Usually tissue infiltrates and vascular lesions
  3. Chronic: Occurs after the first 6 months. Vascular changes predominate.
109
Q

In Nephrotic syndrome, increased risk of thromboembolism related to loss of

A

antithrombin III and plasminogen in the urine

110
Q

What’s the most common cause of Epididymo-orchitis
1. in sexually active younger adults ?

  1. In adults with a low-risk sexual history ?
A
  1. Chlamydia trachomatis and Neisseria gonorrhoeae
  2. E. Coli
111
Q

Membranoproliferative glomerulonephritis
Causes of Type 1
Causes of Type 2
Type 3

A

type 1: cryoglobulinaemia, hepatitis C

type 2: partial lipodystrophy

Type 3: hepatitis B & C

112
Q

4 Disorders associated with glomerulonephritis and low serum complement levels

A
  1. post-streptococcal glomerulonephritis
  2. subacute bacterial endocarditis
  3. systemic lupus erythematosus
  4. mesangiocapillary glomerulonephritis
113
Q

Post-streptococcal glomerulonephritis typically occurs…………. daysfollowing a …………………..infection

A

Post-streptococcal glomerulonephritis typically occurs7-14 daysfollowing a group A beta-haemolyticStreptococcusinfection

114
Q

Post-streptococcal glomerulonephritis is caused by

A

immune complex (IgG, IgM and C3) deposition in the glomeruli

115
Q

electron microscopy:subepithelial ‘humps’ caused by lumpy immune complex deposits

immunofluorescence:granular or ‘starry sky’ appearance

A

post-streptococcal glomerulonephritis

116
Q

renal biopsy

electron microscopy: subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance

A

Type 1 MPGN

117
Q

renal biopsy

electron microscopy: intramembranous immune complex deposits with ‘dense deposits’

A

Type 2 MPGN

118
Q

Treatment of MPGN

A

Steroids

119
Q

IgA nephropathy is associated with (3)

A

alcoholic cirrhosis

coeliac disease/dermatitis herpetiformis

Henoch-Schonlein purpura

120
Q

mesangial hypercellularity, positive immunofluorescence for IgA & C3

A

IgA nephropathy

121
Q

Treatment of Ig A nephropathy

A

if there is active disease (e.g. falling GFR) or failure to respond to ACE inhibitors

immunosuppression with corticosteroids

122
Q

1 marker of good prognosis of Ig A nephropathy

A

frank haematuria

123
Q

6 markers of poor prognosis of IgA nephropathy

A
  1. male gender,
  2. proteinuria (especially > 2 g/day),
  3. hypertension,
  4. smoking,
  5. hyperlipidaemia,
  6. ACE genotype DD
124
Q

4 Causes of transient or spurious non-visible haematuria

A
  1. UTI
  2. Menstruation
  3. Vigorous e exercise
  4. Sexual intercourse
125
Q

6 Causes of persistent non-visible haematuria

A
  1. cancer (bladder, renal, prostate)
  2. stones
  3. benign prostatic hyperplasia
  4. prostatitis
  5. urethritis e.g.Chlamydia
  6. renal causes: IgA nephropathy, thin basement membrane disease
126
Q

Spurious causes - red/orange urine, where blood is not present on dipstick

A

foods: beetroot, rhubarb

drugs: rifampicin, doxorubicin

127
Q

Urgent cancer referral (i.e. within 2 weeks)

A
  • Age >= 45 years and
  1. unexplained visible haematuria without urinary tract infection, or
  2. 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
128
Q

persistent non-visible haematuria is often defined as

A

blood being present in 2 out of 3 samples tested 2-3 weeks apart

129
Q

Causes of RPGN

A

Goodpasture’s syndrome

Wegener’s granulomatosis

others: SLE, microscopic polyarteritis

130
Q

Anti-glomerular basement membrane (GBM) disease is associated with

A

both pulmonary haemorrhage and RPGN

131
Q

Anti-glomerular basement membrane (GBM) disease is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type ….. collagen

A

IV

132
Q

Anti GBM disease is associated with HLA ……

A

HLA DR2.

133
Q

renal biopsy: linear IgG deposits along the basement membrane

A

Anti GBM disease

134
Q

Treatment of anti GBM disease

A

plasma exchange (plasmapheresis)

steroids

cyclophosphamide

135
Q

One of the main complications of anti GBM disease is pulmonary haemorrhage.
5 Factors that increase the likelihood of this include:

A
  1. Smoking
  2. LRTI
  3. pulmonary oedema
  4. inhalation of hydrocarbons
  5. young males
136
Q

What is the most common type of lupus nephritis

A

Class IV (diffuse proliferative glomerulonephritis)

137
Q

Treatment of lupus nephritis

A
  1. treat hypertension
  2. glucocorticoids with either mycophenolate or cyclophosphamide
138
Q

glomeruli shows endothelial and mesangial proliferation,’wire-loop’ appearance

electron microscopy shows subendothelial immune complex deposits

granular appearance on immunofluorescence

A

Class IV lupus nephritis ( DPGN )

139
Q

Xanthogranulomatous pyelonephritis is a Chronic/subacute infection by organisms such as……………..predispose to ……….

A
  1. Proteus mirabilis
  2. renal stones including staghorn calculi.
140
Q

5 features of HIV-associated nephropathy

A
  1. massive proteinuria resulting innephrotic syndrome

2.normal or large kidneys

  1. FSGS
  2. Elevated urea and creatinine
  3. Normotension
141
Q

PSA levels may also be raised by ( 6 )

A
  1. benign prostatic hyperplasia (BPH)
  2. prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at least 1 month after treatment)
  3. ejaculation (ideally not in the previous 48 hours)
  4. vigorous exercise (ideally not in the previous 48 hours)
  5. urinary retention
  6. instrumentation of the urinary tract
142
Q

HLA is coded on chromosome ….

A

chromosome 6.

143
Q

Post op renal transplant problems

A

ATN of graft

vascular thrombosis

urine leakage

UTI

144
Q

when HLA matching for a renal transplant the relative importance of the HLA antigens are as follows

A

DR> B > A

145
Q

Stones < ……. mm will usually pass spontaneously.

A

Stones < 5 mm

146
Q

percutaneous nephrolithotomy if renal stone > …..

A

> 20 mm

147
Q

Hydroceles may develop secondary to:

A

epididymo-orchitis

testicular torsion

testicular tumours

148
Q

Epididymal cysts associated with

A

polycystic kidney disease

cystic fibrosis

von Hippel-Lindau syndrome

149
Q

seminomas: hCG may be elevated in around …..%

A

20%

150
Q

non-seminomas: AFP and/or beta-hCG are elevated in ……%

A

80-85%

151
Q

IgGdeposits on renal biopsy

anti-GBM antibodies

A

Goodpasture’s syndrome ( anti GBM disease)

152
Q

Patients who have received an organ transplant are at risk of ….. cancer

A

Skin cancer particularly Squamous cell carcinoma

153
Q

Which type of complement is likely to be low in lipodystrophy ?

A

C3

154
Q

Mechanism of DI due to alcohol

A

ADH inhibition

155
Q

Renal biopsy showed basket weave appearance?

A

Alport’s syndrome

156
Q

HTN
High aldosterone & renin
Hypokalemia

Features of….?

A

Bilateral renal artery stenosis

157
Q

Finasteride treatment of BPH may take….. before results are seen

A

6 months

MRCP Part 1 (15 decks)

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