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MU-MCQs-Internal-medicine (2022)

Renal stones: imaging

The table below summarises the appearance of different types of renal stone on x-ray





Type

Frequency

Radiograph appearance

Calcium oxalate

40%

Opaque

Mixed calcium oxalate/phosphate stones

25%

Opaque

Triple phosphate stones

10%

Opaque

Calcium phosphate

10%

Opaque

Urate stones

5-10%

Radio-lucent

Cystine stones

1%

Semi-opaque, 'ground- glass' appearance

Xanthine stones

<1%

Radio-lucent




    1. 61-year-old man with a history of hypertension presents with central chest pain. Acute coronary syndrome is diagnosed and conventional management is given. A few days later a diagnostic coronary angiogram is performed. The following week a deteriorating of renal function is noted associated with a purpuric rash on his legs. What is the most likely diagnosis?







A.

Aspirin-induced interstitial nephritis




B.

Heparin-induced thrombocytopaenia




C.

Renal artery stenosis





D.

Cholesterol embolisation





E.

Antiphospholipid syndrome




Cholesterol embolisation is a well-documented complication of coronary angiography




Cholesterol embolisation

Overview




      • cholesterol emboli may break off causing renal disease

      • seen more commonly in arteriopaths, abdominal aortic aneurysms

Features



      • eosinophilia

      • purpura

      • renal failure

      • livedo reticularis



5 2-Which one of the following statements is true regarding autosomal recessive polycystic kidney disease?





A.

Onset is typically in the third decade


B.

Liver involvement is rare


C.

Is due to a defect on chromosome 16



D.

More common than autosomal dominant polycystic kidney disease


E.

May be diagnosed on prenatal ultrasound



ARPKD

Autosomal recessive polycystic kidney disease (ARPKD) is much less common than autosomal dominant disease (ADPKD). It is due to a defect in a gene located on chromosome 6


Diagnosis may be made on prenatal ultrasound or in early infancy with abdominal masses and renal failure. End-stage renal failure develops in childhood. Patients also typically have liver involvement, for example portal and interlobular fibrosis




5 3-Alport's syndrome is associated with each one of the following, except:





A.

Chronic renal failure


B.

Presentation in childhood


C.

Microscopic haematuria


D.

Lenticonus


E.

Anosmia



Alport's syndrome

Alport's syndrome is a hereditary condition, usually X-linked dominant but may be autosomal recessive or dominant. It is due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM). The disease is more severe in males with females rarely developing renal failure


A favourite question in the MRCP is an Alport's patient with a failing renal transplant. This may be caused by the presence of anti-GBM antibodies leading to a Goodpasture's syndrome like picture


Alport's syndrome usually presents in childhood. The following features may be seen:





      • microscopic haematuria

      • progressive renal failure

      • bilateral sensorineural deafness

      • retinitis pigmentosa

      • lenticonus: protrusion of the lens surface into the anterior chamber



5 4-Each one of the following is a recognised complication of nephrotic syndrome, except:






A.

Hyperlipidaemia



B.

Acute renal failure


C.

Increased risk of infection


D.

Hypercalcaemia


E.

Increased risk of thromboembolism

5 5-You are asked to review a 75-year-old female on the surgical wards due to hyperkalaemia. Results are as follows:






Plasma

Urine

Na+ (mmol/l)

129

5

K+ (mmol/l)

6.8




Urea (mmol/l)

26

350

Creatinine (µmol/l)

262




Osmolality (mosmol/kg)

296

470

What is the most likely diagnosis?




A.

Acute tubular necrosis


B.

Hyperosmolar non-ketotic coma


C.

Hydronephrosis


D.

Prerenal uraemia


E.

Pyelonephritis

ATN or prerenal uraemia? In prerenal uraemia think of the kidneys holding on to sodium to preserve volume
The low urine sodium points towards prerenal uraemia, as does the urine:plasma osmolality and urea ratio
ARF: ATN vs. prerenal uraemia

Prerenal uraemia - kidneys hold on to sodium to preserve volume








Pre-renal uraemia

Acute tubular necrosis

Urine sodium

< 20 mmol/L

> 30 mmol/L

Fractional sodium excretion*





< 1%

> 1%


Fractional urea excretion**

< 35%

>35%

Urine:plasma osmolality



> 1.5




< 1.1

Urine:plasma urea

> 10:1

< 8:1

Specific gravity



> 1020




< 1010

Urine


'bland' sediment



brown granular casts



Response to fluid
challenge

Yes

No




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

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




5 6-A patient with type 1 diabetes mellitus is reviewed in the nephrology outpatient clinic. He is known to have stage 3 diabetic nephropathy. Which of the following best describes his degree of renal involvement?






A.

Overt nephropathy


B.

Microalbuminuria


C.

Latent phase



D.

End-stage renal failure



E.

Hyperfiltration



Diabetic nephropathy: stages
Diabetic nephropathy may be classified as occurring in five stages*: Stage 1

      • hyperfiltration: increase in GFR

      • may be reversible

Stage 2 (silent or latent phase)



      • most patients do not develop microalbuminuria for 10 years

      • GFR remains elevated

Stage 3 (incipient nephropathy)

      • microalbuminuria (albumin excretion of 30 - 300 mg/day, dipstick negative)

Stage 4 (overt nephropathy)



      • persistent proteinuria (albumin excretion > 300 mg/day, dipstick positive)

      • hypertension is present in most patients

      • histology shows diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)

Stage 5



      • end-stage renal disease, GFR typically < 10ml/min

      • renal replacement therapy needed

The timeline given here is for type 1 diabetics. Patients with type 2 diabetes mellitus (T2DM) progress through similar stages but in a different timescale - some T2DM patients may progress quickly to the later stages


5 7-A two-year old boy presents with an abdominal mass. Which of the following is associated with Wilm's tumour (nephroblastoma)?






A.

Deletion on short arm of chromosome 12




B.

Tuberose sclerosis




C.

Beckwith-Wiedemann syndrome




D.

Autosomal dominant polycystic kidney disease




E.

Autosomal recessive polycystic kidney disease

Beckwith-Wiedemann syndrome is a inherited condition associated with organomegaly, macroglossia, abdominal wall defects, Wilm's tumour and neonatal hypoglycemia.


Wilm's tumour
Wilm's nephroblastoma



      • occurs mostly < 3 years (80% < 5 years); 20% of all childhood malignancies

Features



      • abdo mass in otherwise well child

      • also: painless haematuria, abdo pain, anorexia, BP, fever

Associations



      • Beckwith-Wiedemann syndrome

      • AGR triad of Aniridia, Genitourinary, Retardation

      • deletion on short arm of chromosome 11

Management



      • USS --> nephrectomy, chemo

      • prognosis: good, 80% cure rate



5 8-A 45-year-old presents to A&E with chest pain. An ECG shows anterior ST elevation and he is thrombolysed with alteplase. His chest pain settles and he is started on aspirin, atorvastatin, bisoprolol and ramipril. Three days later his blood results are as
follows:

Urea

16 mmol/l

Creatinine

277 µmol/l

What is the most likely cause for the deterioration in renal function?





A.

Renal artery stenosis


B.

NSAID related nephropathy



C.

Statin nephropathy


D.

Dressler's syndrome


E.

Haemorrhage into renal cyst

Flash pulmonary oedema, U&Es worse on ACE inhibitor, asymmetrical kidneys --> renal artery stenosis - do MR angiography

There is likely underlying renal artery stenosis revealed by the addition of an ACE inhibitor

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