Nephrology Flashcards

1
Q

Give causes of minimal change disease

A

drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

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2
Q

What is the pathophysiology of minimal change disease

A

T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
increased glomerular permeability to serum albumin

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3
Q

What does renal biopsy show in minimal change disease?

A

Normal glomeruli on light microscopy
electron microscopy shows fusion of podocytes and effacement of foot processes

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4
Q

What is the management of minimal change disease?

A

Management
oral corticosteroids: majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases

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5
Q

How do we manage ascites in liver cirrhosis?

A

Spironolactone is a potassium-sparing diuretic that is the recommended first-line therapy for managing ascites in patients with liver cirrhosis.

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6
Q

How does transitional cell carcinoma of the bladder present?

A

Painless haematuria

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7
Q

Would you expect hypo or hypercalcaemia in CKD?

A

Hypo

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8
Q

How does HSP present?

A

Henoch-Schonlein purpura classically presents with abdominal pain, arthritis, haematuria and a palpable purpuric rash over the buttocks and extensor surfaces of arms and legs

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9
Q

What is spironolactone?

A

Aldosterone antagonist

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10
Q

How does HUS present?

A

Haemolytic uraemic syndrome is generally seen in young children and produces a triad of:
acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia

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11
Q

How do we manage HUS?

A

treatment is supportive e.g. Fluids, blood transfusion and dialysis if required
there is no role for antibiotics, despite the preceding diarrhoeal illness in many patients

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12
Q

What normally causes HUS?@

A

Haemolytic uraemic syndrome - classically caused by E coli 0157:H7

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13
Q

How does Post-streptococcal glomerulonephritis present?

A

A 21-year-old woman presents to the emergency department with visible haematuria. On further questioning, she states that 10 days ago she had ‘tonsillitis’ which has resolved but she continues to feel very tired.

Her blood pressure is 182/72mmHg. Other observations are normal. Urine dip is positive for blood and protein.

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14
Q

What do we use to confirm recent streptococcal infection in post-streptococcal glomerulonephritis?

A

raised anti-streptolysin O titres are used to confirm the diagnosis of a recent streptococcal infection

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15
Q

How do we determine if kidney disease is chronic or acute?

A

Hypocalcaemia is an indication that kidney disease is chronic and not acute

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16
Q

How does minimal change disease present?

A

Minimal change disease is the most likely diagnosis. This child has clinical signs of nephrotic syndrome: oedema with proteinuria. The bi-basal lung crackles are suggestive of pulmonary oedema. The most common cause of glomerulonephritis in children is minimal change disease, making this the best answer

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17
Q

How does renal cell carcinoma present?

A

Features of renal cell carcinoma:
classical triad: haematuria, loin pain, abdominal mass
pyrexia of unknown origin
left varicocele (due to occlusion of left testicular vein)
endocrine effects: may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH
25% have metastases at presentation

18
Q

What is Berger’s disease?

A

IgA Nephropathy

19
Q

How does acute tubular necrosis and pre-renal uraemia differ?

A

ATN = AllTheNa = high Na everything else low
Pre renal urine = low Na everything else high

20
Q

Give the most common presentation of HUS in exams

A

Normocytic anaemia, thrombocytopaenia and AKI following diarrhoeal illness - consider HUS

21
Q

What is a common complication of significant NaCl fluid therapy?

A

Use of 0.9% Sodium Chloride for fluid therapy in patients requiring large volumes = risk of hyperchloraemic metabolic acidosis

22
Q

What is the glucose requirement of a person?

A

50-100g - not influenced by weight

23
Q

Which electrolyte abnormality do you see in rhabdomyolysis, and why?

A

Patients with rhabdomyolysis should have a bone profile taken to measure calcium and phosphate. Calcium typically binds to myoglobin released from damaged muscle tissue causing serum hypocalcaemia.

24
Q

How do we diagnose AKI in adults?

A

NICE recognise any of the following criteria to diagnose AKI in adults:
↑ creatinine > 26µmol/L in 48 hours
↑ creatinine > 50% in 7 days
↓ urine output < 0.5ml/kg/hr for more than 6 hours

25
Q

Which acid-base disorder is seen in diarrhoea on ABG?

A

Vomiting = normal anion gap metabolic alkalosis

Diarrhoea= normal anion gap metabolic acidosis

26
Q

What causes hyperacute transplant rejection?

A

Signs of rejection within the immediate (24-48h) post-transplant period should always raise suspicions of hyperacute rejection, the rapidity of which is caused by pre-existing of antibodies against a donor’s ABO/HLA antigens.

27
Q

Where do you see Cell-mediated (cytotoxic T-cell) mediated rejection?

A

Cell-mediated (cytotoxic T-cell) mediated transplant rejection is a cause of acute rejection but usually manifests within the first 6 months as oppose to the first 24h.

28
Q

What can change the eGFR?

A

Creatinine, Age, Gender, Ethnicity

29
Q

What is the most likely cause of death with CKD on haemodialysis?

A

CKD on haemodialysis - most likely cause of death is IHD

30
Q

How do we measure AKI staging with creatinine?

A

Basically if creatinine doubles (2x), its stage 2. If it triples (3x), its stage 3
(copied from another Q)

31
Q

How do we determine AKI staging with urine production?

A
  1. < 0.5ml/kg/h for >6 consecutive hours
    2 < 0.5ml/kg/h for >12 consecutive hours
    3 >354 µmol/L < 0.3ml/kg/h for > 24h or anuric for 12h
32
Q

How do we classify CKD stage?

A

CKD stage GFR range
1 Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a 45-59 ml/min, a moderate reduction in kidney function
3b 30-44 ml/min, a moderate reduction in kidney function
4 15-29 ml/min, a severe reduction in kidney function
5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

*i.e. normal U&Es and no proteinuria

33
Q

What is the most common cause of peritonitis secondary to peritoneal dialysis

A

Staphylococcus epidermidis

34
Q

What causes raised anion gap acidosis?

A

The only listed cause of raised anion gap metabolic acidosis is septic shock, which results in acidosis due to the production of lactic acid due to inadequate tissue perfusion.

35
Q

How do we calculate anion gap?

A

To determine the cause of metabolic acidosis, the anion gap can be calculated. The anion gap is calculated by calculating the difference between positively charged ions (sodium and potassium) and negatively charged ions (bicarbonate and chloride)

36
Q

What is a normal anion gap?

A

A normal anion gap is 8-14 mmol/L

37
Q

How does IgA nephropathy present?

A

IgA nephropathy classically presents as visible haematuria following a recent URTI

38
Q

What is the most common cause of haematuria worldwide?

A

Berger’s disease

IgA nephropathy

39
Q

How do we treat hyperacute transplant rejection?

A

Removal of transplant

40
Q

How does minimal change disease present?

A

Tetrad:
Hypercholesterolaemia
Hypoalbuminaema
Proteinuria
Oedema