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MRCP Part 1 > Renal Clinical > Flashcards

Renal Clinical Flashcards

1
Q

What is the most sensitive imagine for ureteric stones?

A

CT KUB

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2
Q

What are the criteria for emergency dialysis?

A
  1. Refactory hyperkalaemia
  2. Metabolic acidosis
  3. Complications of uraemia eg pericarditis or encephalopathy
  4. Severe pulmonary oedema
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3
Q

What is the criteria for diagnosing an AKI?

A

Rise in creatinine of 26µmol/L or more in 48 hours OR
>= 50% rise in creatinine over 7 days OR
Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) OR
>= 25% fall in eGFR in children / young adults in 7 days.

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4
Q

What is IgA nephropathy?

A

Macroscopic haematuria in young people following an upper respiratory tract infection

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5
Q

What is the pathophysiology of IgA nephropathy?

A

Mesangial deposition of IgA immune complexes

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6
Q

How do you differentiate between IgA nephropathy and post streptococcal glomerolonephritis?

A
  1. Post streptococcal glomerulonephritis is associated with low complement levels
  2. The main symptoms in post streptococcal glomerulonephritis is proteinuria where as in IgA nephropathy its haematuria
  3. In post streptococcal there is an interval of around a week where as IgA is a few days
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7
Q

What are the causes of nephrogenic diabetes insipidus?

A

Genetic - affecting the ADH receptor of the aquaporin 2 channel
Lithium - desensitises the kidneys ability of respond to ADH in the collecting ducts
Demeclycycline

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8
Q

What is the investigation for diabetes insipidus?

A

Water deprivation test

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9
Q

What is the treatment for nephrogenic diabetes insipidus?

A

Thiazides

Low salt/protein diet

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10
Q

What is nephrogenic diabetes insipidus?

A

The collecting ducts of the kidneys do not respond to ADH and therefore the urine lose the ability to concentrate the urine.

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11
Q

How do you diagnose renal amyloidosis?

A

Kidney biopsy which stains positively for congo red which combined with polarised light appears apple green

Serum amyloid precursos scan

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12
Q

What medication is given in autosomal dominant polycystic kidney disease to slow progression of cysts development and renal insufficiency?

A

Tolvaptain (Vasopressin receptor 2 antagonist)

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13
Q

What are the main complications of plasma exchange?

A 
Hypocalcaemia 
Metabolic alkalosis
Removal of systemic medications 
Coagulation factor depletion 
Immunoglobulin depletaion
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14
Q

What do you see on electron microscopy of alports syndrome?

A

Longitudinal splitting of the lamina densa of the glomerular basement membrane resulting in a basket weave appearance.

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15
Q

What are the causes of rapidly progressive glomerulonephritis?

A

Anti GBM (Goodpastures)
ANCA glomerulonephritis
Immune complex glomerulonephrits

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16
Q

What are the distinctive features of rapidly progressive glomerulonephritis?

A

Loss of GFR by over 50%

Extensive glomerular crescents (seen on microscopy)

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17
Q

What antibodies are present in goodpastures disease?

A

Anti Glomerular basement membrane antibodies against type 4 collagen

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18
Q

What is the treatment for goodpastures?

A

Plasmophoresis

Steroids

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19
Q

What accounts for the majority of rapidly progressive glomerulonephritis?

A

ANCA associated glomerulonephritis

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20
Q

What do you NOT see on immunoflorescence of ANA associated glomerulonephritis?

A

Immune deposits

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21
Q

What are the main types of immune complex glomerulonephritis?

A

IgA Nephropathy
Post streptocccal GN
Lupus nephritis

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22
Q

What is the most common types of glomerulonephritis in adults?

A

Membranous glomerulonephritis

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23
Q

What do you see on a renal biopsy/electron microscopy of membranous glomerulonephritis?

A

Thickened basement membrane with subepithelial electron dense deposits. This creates a spike and dome appearance.

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24
Q

What are the causes of membranous glomerulonephritis?

A

Idiopathic - due to anti - phospholipase A2 antibodies
Infections - hepatitis B, malaria, syphillis
Malignancy
Drugs (gold, penicillamine, NSAIDS)
Autoimmine (SLE, thyroiditis, rheumatoid

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25
Q

What is the management for membranous glomerulonephritis?

A
  1. ACEi/ARB
  2. Immunsuppression
  3. Steroids+ Cyclophosphamide
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26
Q

What is the prognosis of membranous glomerulonephritis?

A

One third - remission
One third - proteinuria
One third - End stage renal failure

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27
Q

What are the causes of focal segmental glomerulosclerosis?

A 
Idiopathic 
IgA nephrpathy 
Reflux nephropathy 
HIV
Heroin 
Alports syndrome 
Sickle cell disease
28
Q

How long does an AV fistula, put in for dialysis, take to be fully functioning?

A

6 - 8 weeks

29
Q

What do you see on the renal biopsy on goodpastures disease?

A

Linear IgG deposits

30
Q

What are the extra renal manifestations of autosomal dominant polycystic kidney disease?

A

Liver cysts
Berry aneurysmss
Mitral valve prolapse , Aortic root dilatation and aortic dissection.
Cysts in other organs such as the pancreas and spleen

31
Q

What is henoch schonlein pupura?

A

An IgA vasculitis that presents with a purpuric rash on the buttocks and legs of children.

32
Q

What is the classic tetrad of nephrotic syndrome?

A

High cholesterol
Low albumin
Peripheral oedema
Proteinuria

33
Q

What are the main primary nephrotic syndromes?

A
  1. Minimal change disease
  2. Membranous glomerulonephritis
  3. Focal segmental glomerulosclerosis
34
Q

What are the main secondary nephrotic syndromes?

A

Diabetic nephropathy
SLE
Amyloidosis
Hepatitis B/Hepatitis C and HIV

35
Q

What does electron microscopy on membranous glomerulonephritis show?

A

Basement membrane thickening and subepithelial depositis (causes by complements and IgG ) - this looks like spikes ! It is the immune deposits that damage the podocytes and allow the protein to filter through

36
Q

What does light/electron microscopy show in focal segmental golmerulosclerosis

A

Sclerosis on specific areas, thickening of the basement membrane

37
Q

What drugs can cause a nephrotic syndrome?

A

Peniclliamine

Gold

38
Q

What is the cause of atypical haemolytic uraemic syndrome?

A

Complement dysregulation

39
Q

What drug can be used in atypical haemolytic uraemic syndrome?

A

eculizumab 9a C5 inhibitor monoclonal antibody

40
Q

What is a normal anion gap?

A

8 - 14

41
Q

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

A

GI loss (eg diarrhoea, fistula)
Renal tubular acidosis
Drugs eg acetazolamide
Addisons

42
Q

What are the causes of a raised anion gap metabolic acidosis?

A

Lactate
ketones
Urate
Acid poisoning

43
Q

What are the causes of acute interstitial nephritis?

A

Drugs (NSAIDs, penicillin, sulphur based medications, PPI, ciprofloxacin and allupurinol) Infections
Vasculitis

44
Q

What type of renal stones do proteus UTI’s increase the risk of?

A

Struviate (magnesium ammonium phosphate)

45
Q

What are the types of organ rejection?

A

Hyperacute - occurs immediately through the presence of pre formed antibodies (eg ABO incompatibility)
Acute - occurs during the first 6 months and is usually T cell mediated.
Chronic - Occurs after the first 6 months and is dominated by vascular changes

46
Q

What HLA is goodpastures syndrome associated with?

A

HLA DR2

47
Q

What are the types of lupus nephritis?

A

Class 1: Normal kidney
Class 2: Mesangial glomerulonephritis
Class 3: Focal segmental proliferative glomerulonephritis
Class 4 (most common) Diffuse proliferative glomeruloenephritis
Class 5 Diffuse membranous glomerulonephritis
Class 6: Sclerosing glomerulonephritis

48
Q

What do you see on a biopsy on class 4 lupus nephritis (diffuse proliferative glomerulonephritis)

A

Endothelial and mesangial proliferation in the glomeruli (wire loop appearance)
Capillary wall thickening
Subendothelial immune compex deposits (electon microscopy)

49
Q

What is the treatment of lupus nephritis?

A

Steroids

Immunosupression (azathioprine, cyclophosphamide)

50
Q

What are the stages of diabetic nephropathy?

A
  1. Hyperfiltration
  2. Latent phase
  3. Microalbuminuria (albumin excretion of 30 - 300mg/day, dipstick negative)
  4. Persistent proteinuria (albumin excretion over 300mg/day, dipstick positive). Hypertension, Histology shows diffuse glomerulosclerosis and focal glomerulosclerosis (kimmelsteil wilson nodules)
  5. End stage renal disease (GFR less than 10ml/min)
51
Q

Why do you get an increase in GFR in the first stage of diabetic nephropathy?

A

Glycation of the basement membrane due to gluocse causes the efferent arteriole to thicken (hyaline arteriosclerosis) which is an obstruction to blood flow. There is also arteriole dilation of the afferent arteriole which increases the flow. Both of these incrase the pressure in the efferent arteriole and increase the GFR

52
Q

What can be done to prevent calcium renal stones?

A 
High fluid intake 
Low protein, low salt diet 
Thiazide diuretic (increase distal tubular calcium resorption)
53
Q

What can be done to prevent oxalate stones?

A

cholestyramine
pyridoxine

These both reduce urinary oxalate secretion

54
Q

What can be done to prevent uric acid stones?

A 
Allopurinol 
Urinary alkalinization (oral bicarbonate)
55
Q

What is cystinuria?

A

An autosomal recessive disorder characterised by the formation of recurrent renal stones. It is due to a defect in the transport of cystin, ornthine, lysine and arginine. Abnormality is on chromosome 2.

56
Q

How do you diagnose cystinuria?

A

Cyanide nitroprusside test

57
Q

What is the management of cystinuria?

A

Hydration
D penicillamine
Urinary alkalinization

58
Q

How do alpha 1 antagonists eg tamsulosin work?

A

Decrease smooth muscle tone in the prostate and bladder

59
Q

How do 5 alpha reductase inhibitors eg finasteride work?

A

Block the conversion of testosterone to dihydrotestosterone. this causes a reduction in prostate volume and may slow disease progression

60
Q

What do you see on electron microscopy of alports syndrome?

A

Longitudinal splitting of the lamina densa of the GBM - results in a basket weave appearance.

61
Q

What type of renal stones have a semi opaque ground glass appearance on X Ray

A

Cystine stones

62
Q

What are the 5 features of HIV associated nephropathy?

A
  1. Massive proteinuria (nephrotic syndrome)
  2. Normal/large kidneys
  3. Focal segmental glomerulosclerosis
  4. Normotension
  5. Elevated urea and creatanine
63
Q

What is fanconi syndrome?

A

Generalised reabsorptive disorder of renal tubular transport in the proximal convolyted tubule resulting in renal tubular acidosis, polyuria, aminoaciduria, glycosuria, phosphaturia, osteomalacia

64
Q

What are the causes of fanconi syndrome?

A 
Cystinosis 
Sjogrens 
Myeloma
nephrotic syndrome 
Wilsons disease
65
Q

What is calciphylaxis?

A

A rare complication of end stage renal failure . It results in deposition of calcium within arterioles which causes microvascular occlusion and necrosis of the supplied tissue. It affects the skin and presents with painful necrotic skin lesions.

MRCP Part 1 (30 decks)

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