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Nephrology Flashcards

1
Q

What are the two causes of diffuse proliferative glomerulonephritis?

A
  • Post strep (children)

- SLE

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2
Q

What is nephrotic syndrome?

A

Glomeruli leak protein into urine (>3g/24h)

  • Hypoalbuminia
  • Hyperlipidaemia
  • Albuminuria
  • Oedema - typically legs, feet or ankles. Less commonly, face.
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3
Q

What is the most common cause of nephrotic syndrome in adults?
Children?

A

Adults: Focal segmental glomerulonephritis
Children: Minimal change glomerulonephritis

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4
Q

What is the difference between nephrogenic and cranial diabetes insipidus?
Treatment?

A

Cranial: Body produces insufficient ADH (vasopressin) - Treat with synthetic, i.e. Desmopressin

Nephrogenic: Kidneys unable to respond to ADH. Treat with thiazide diuretics

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5
Q

How do you calculate volume of maintenance fluids for children?

A

First 10kg: 100mL/kg per 24 hours

Next 10kg: 50mL/Kg

Anything over 20kg: 20mL/kg

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6
Q

What are the adult requirements for maintenance fluids?

A

25-30ml/kg/day fluid
Approx 1mmol/kg/day of potassium, sodium and chloride
50-100g/day glucose to limit starvation ketosis.

So typically:
25-30ml/kg/day NaCL 0.18% in 4% glucose (cont 30ml/L each and 40g glucose/L) with 27 mol/L K on day 1.

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7
Q

What would renal failure, sensorineural hearing loss and ocular abnormalities in a child make you think of?

A

Alport syndrome (esp male: x-linked dominant)

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8
Q

What is the screening test for adult polycystic kidney disease?

A

US abdo

Diagnostic criteria: (with +ve family hx)

  • 2 cysts if <30
  • 2 cysts in both kidneys if 30-59
  • 4 cysts in both kidneys if >60
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9
Q

Why does nephrotic syndrome predispose to venous thromboembolism?

A

Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis.

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10
Q

Why do you do a CK following a fall and a long lie?

A

Rhabdomyolysis - death of muscle fibres -> renal failure (myoglobinuria -> tubular cell necrosis)

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11
Q

In terms of mx of hyperkalaemia, which drug(s):

  • Stabilise the cardiac membrane?
  • Shift K into the intracellular compartment?
  • Remove K from body?
A
  • Stabilise the cardiac membrane: IV calcium gluconate
  • Shift K into the intracellular compartment: Combined insulin/dextrose infusion; nebulised salbutamol
  • Remove K from body:
    Calcium resonium
    Loop diuretics
    Dialysis
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12
Q

What would you expect on a blood gas in sepsis?

A

Often have raised lactate -> metabolic acidosis with raised anion gap

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13
Q

What are the causes of high anion gap metabolic acidosis?

Mneumonic

A 
M ethanol
U raemia
D KA
P ropylene glycol
I soniazid/iron
L actate (shock, hypoxia, burns, metformin)
E thylene glycol
S alicylates
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14
Q

What are the causes of metabolic acidosis with a normal anion gap?

A

= hyperchloraemic metabolic acidosis

  • GI HCO3 loss (diarrhoea, ureterosigmoidostomy, fistula)
  • Renal tubular acidosis
  • Acetazolamide
  • Ammonium chloride injection
  • Addison’s
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15
Q

What are the pre-renal causes of AKI?

A

Kidney function is normal, but reduced perfusion. Patients with CKD have impaired compensation so can develop acute-on-chronic failure easily.

  • Blood loss
  • Low arterial blood pressure - HF/sepsis
  • ACE-i, ARBs and NSAIDs
  • Dehydration (vomiting, diarrhoea)
  • Severe burns
  • Pancreatitis, liver disease -> fluid shift
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16
Q

What are the intrinsic causes of AKI?

A
  • Acute tubular necrosis = most common in hospital. (nephrotoxic meds, hypotension, trauma, contrast agents, rhabdomyolysis)
  • Glomerular (SLE, systemic sclerosis, Goodpasture, Wegners, arthritis, hep C, HIV)
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17
Q

What are the post-renal causes of AKI?

A

Prostatic hypertrophy
Kidney stones
Ca: prostate, cervix, colon

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18
Q

What is the triad of haemolytic uraemic syndrome?

A
  • AKI
  • Microangiopathic haemolytic anaemia
  • Thrombocytopenia
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19
Q

Causes of haemolytic uraemic syndrome?

A
  • Post-dysentery (E.coli) = most common
  • Tumours
  • Pregnancy
  • Ciclosporin
  • COCP
  • SLE
  • HIV

Most common in children.

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20
Q

What is seen on FBC in haemolytic uraemic syndrome?

A

Anaemia
Thrombocytopaenia
Fragmented RBC

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21
Q

Which type of cancers are renal transplant patients are risk of?

A

SSC particularly

Also lymphoma and cervical.

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22
Q

What are the 4 main symptoms of nephritic syndrome?

A
  • Haematuria
  • Proteinuria
  • HTN (mild)
  • Low urine volume
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23
Q

What are the 3 primary and 5 secondary causes of nephrotic syndrome?

A

1:

  • Minimal change glomerulonephritis
  • Focal segmental glomerulonephritis
  • Membranous glomerulonephritis

2:

  • SLE
  • Hep B and C
  • HIV
  • DM
  • Malignancy
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24
Q

What are the 5 causes of nephritic syndrome?

A
  • Post-strep glomerulonephritis
  • IgA nephropathy
  • Rapidly progressive glomerulonephritis (Goodpastures or vasculitic)
  • Membranoproliferative glomerulonephritis (SLE, Hep B/C)
  • Henoch-Schonlein purpura
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25
Q

What is the main cause of death in patients on haemodialysis?

A

IHD

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26
Q

What are urine eosinophilic casts indicative of?

A

Tubulointerstitial nephritis (often due to drug reactions)

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27
Q

What 3 drugs would you stop in AKI due to increased risk of toxicity?

A
  • Metformin (risk of lactic acidosis)
  • Lithium
  • Digoxin
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28
Q

What 5 classes of drugs would you discontinue in AKI as they may worsen renal function?

A
  • NSAIDs (except aspirin at cardioprotective dose - 75mg)
  • Nephrotoxic abx, especially gent and nitro.
  • ACE-i
  • Angio II R antag
  • Diuretics
29
Q

What would you expect in terms of urine and plasma osmolality in diabetes insidious?

A

High plasma osmolality (hence why patient feels thirsty)

Low urine osmolality

30
Q

How do you confirm a diagnosis of diabetes insidious?

A

Water deprivation test.
Normal patients would produce small quantity of conc urine to maintain normal plasma osmolarity.

In DI there is a rise in plasma osmolarity with the production of low osmolarity (dilute) urine. If you then give ADH, Cranial will produce conc urine, nephrogenic will have no response.

31
Q

What would be the differential for HTN with low K?

How would you tell them apart?

A

Conn’s, Cushing’s, renal artery stenosis, Liddle’s.

Do renin and angiotensin levels:

  • Cushing’s and Conn’s = high aldosterone, low renin
  • Renal A stenosis: high both
  • Liddle’s: low both
32
Q

What would you switch a patient to if they developed gynaecomastia with spironolactone?

A

Eplerenone

33
Q

Which antibiotics are most likely to cause an intrinsic AKI?

A 
Penicillins
Cephalosporins
Aminoglycosides - Gent
Vancomycin
Quinolones
34
Q

What is the gold standard for bladder cancer diagnosis?

A

Cystoscopy

35
Q

What are the features of Henock-Scholein purpora?

A

IgA mediated vasculitis, usually seen in children following an infection.

  • Palpable purpuric rash (+localised oedema) over buttocks and extensor surfaces of arms and legs
  • Abdo pain
  • Polyarthritis
  • Features of IgA nephropathy (haematuria, renal failure)
36
Q

What is the most common causative organism in peritonitis as a complication of peritoneal dialysis?

A

Staph epidermis

Staph aureus is also common

37
Q

What is the most common viral infection in solid organ transplant recipients?
Mx?

A

CMV

Ganciclovir

38
Q

How does muscle mass affect eGFR?

A

Can be inappropriately low in body builders.

39
Q

What type of diuretic would you use to prevent re-accumulation of ascites following drainage?

A

Spironolactone (aldosterone antagonist - acts in collecting duct). Add a loop if no response.

40
Q

What are the variables used in Modification of Diet in Renal Disease (MDRD) estimation of eGFR?

A 
CAGE:
Creatinine
Age
Gender
Ethnicity
41
Q

What is the maximum infusion rate in potassium replacement therapy?
Why do you dilute it in high volumes of saline?

A

20mmol/hr

High concentrations can be phlebitic

42
Q

What drugs can cause nephrogenic DI?

A

Lithium

Demeclocycline

43
Q

What is the treatment for urinary retention due to clots?

A

Continuous bladder irrigation via a 3-way urethral catheter

44
Q

How would you differentiate ATN and pre renal AKI?

A

Pre-renal: Kidneys hold on to Na to preserve volume, so urine sodium <20. Would also respond to fluid challenge.

45
Q

What is the normal outcome following minimal change nephropathy?

A

Full recovery, but likely (2/3) recurrent episodes.

46
Q

What is the main concern with painless visible haematuria?

A

Bladder ca - Refer urgently

47
Q

What drugs can commonly cause haematuria?

A 
NSAIDs 
Captopril
Cephalosporins
Cipro
Furosemide
48
Q

What are the risk factors for renal tract ca?

A

Smoking
Chronic analgesic use
Toxin exposure

49
Q

What is the empirical treatment of UTI in adult, non-pregnant women?

A

Trimethoprim or Nitrofurantroin or Amox.

E. Coli

50
Q

What are the 3 criteria for diagnosing AKI?

A
  • Rise in creatinine >26 in 48hrs
  • Rise in creatinine >1.5x baseline (use best figure in last 3/12)
  • Urine output <0.5ml/kg/h for 6 consecutive hours
51
Q

How might you avoid AKI in a patient going for a contrast scan?

A

1L Normal saline over 12 hours pre- and post-procedure

52
Q

How do you define chronic kidney disease?

A

Impaired renal function for >3 months based on abnormal structure or function

or

GFR <60ml.min for >3 months

53
Q

What are the 5 main/groups of causes of CKD?

A
  • Diabetes (2>1)
  • Glomerulonephritis: commonly IgA
  • Unknown, up to 20% present with no obvious cause and shrunken kidneys you wouldn’t biopsy
  • HTN or renovascular disease
  • Pyelonephritis and reflux nephropathy
54
Q

What is the commonest cause of inherited CKD?

A

Adult polycystic kidney disease

55
Q

Who would you screen for CKD?

A
  • Diabetics
  • HTN
  • IHD, PVD, CVD
  • Structural renal disease, known stone or BPH
  • Recurrent UTIs or childhood history of vesicouteric reflux
  • SLE
  • FHx end-stage disease
56
Q

What is the target BP in CKD?

A

<130/80
or
<125/75 if diabetic

57
Q

What is the mx of diabetic kidney disease?

A

ACE-i or ARB even if BP normal

58
Q

What would you suspect if iron/B12/folate and subsequent erythropoietin therapy failed to resolve anaemia?

A

Red cell aplasia - refer to haem.

59
Q

How do you mx oedema in CKD?

A

Loop diuretics e.g. furosemide.

Fluid and sodium intake restriction.

60
Q

How might you treat acidosis in CKD?

A

Consider sodium bicarb supplements - improves symptoms and may also slow progression. Caution as sodium load may increase BP.

61
Q

How do you treat restless legs/cramps in CKD?

A

Check ferritin (low levels -> worse symptoms)

  • Clonazepam
  • Gabapentin
62
Q

When might you use haemofiltration rather than haemodialysis?
What is the difference?

A

In critically ill patients - less haemodynamic instability as the filtrate is replaced with equal amount of fluid. Not used routinely as takes much longer.

63
Q

What is the annual mortality in dialysis? Why?

A

Around 20%
MI and CVA
Also high mortality if sepsis develops.

64
Q

What is the difference between nephrotic and nephritic syndrome in terms of:
BP
Urine
GFR

A

NephOtic:

  • BP: Normal, mild inc
  • Urine: PrOtein
  • GFR: Normal, mild dec

Nephritic:

  • BP Mod-severe inc
  • Urine: Haematuria
  • GFR: Mod-severe dec
65
Q

What would be a typical patient with IgA nephropathy?

A
  • Young man
  • Episodic haemautria
  • NephrItic syndrome
  • Rapid recovery between attacks
66
Q

What would you see on renal biopsy in IgA and Henoch-Schonlein purpura?

A

Mesangial proliferation
IgA and C3 deposits

(HSP is a systemic variant of IgA - can also see deposition in skin)

67
Q

What is Goodpasture’s disease/Anti-glomerular basement membrane disease due to?

A

Caused by auto-antibodies to type IV collagen.

T4 collagen also found in lung so pulmonary haemorrhage can occur, especially in smokers

68
Q

Is Goodpasture’s nephritic or nephrotic?

A

Nephritic, but also haematuria.

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