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MRCP Part 1 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Contrast-induced nephropathy
- definition
- common interventions
- prevention
- drug to hold to avoid

A

25% increase in creatinine occurring 2 -5 days after administration.

Common interventions: CT, angiography, PCI

Prevention
the evidence base currently supports the use of intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure. There is also evidence to support the use of isotonic sodium bicarbonate

high-risk for contrast-induced nephropathy should have metformin withheld for a minimum of 48 hours and until the renal function has been shown to be normal

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2
Q

acute interstitial nephritis
- causes
- common drugs causing
- symptoms and signs
- diagnosis
- management

A

Acute interstitial nephritis (AIN) typically arises following drug therapy in the majority of cases (~75%), with infections and systemic vasculitides (SLE, sarcoidosis) forming the rest

Common drugs - NSAIDs, penicillins, allopurinol, PPIs, ciprofloxacin

Signs - Sterile pyuria and white cell casts in the setting of rash and fever and joint pain

Diagnosis - renal biopsy

Management - stop drug, steroids, dialysis

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3
Q

Common nephrotoxic drugs

A

NSAIDs, aminoglycosides (amikacin, gentamicin) ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics

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4
Q

Definition of AKI

A

a rise in serum creatinine of 26 micromol/litre or greater within 48 hours

a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days

a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than

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5
Q

Drugs that may have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)

A

Metformin
Digoxin
Lithium

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6
Q

Should be stopped in AKI as may worsen renal function

A

NSAIDs

High dose aspirin 300mg (the cardio protective 75mg dose is safe to continue)

Aminoglycosides (amik, gent)
• ACE inhibitors
• Angiotensin II receptor antagonists
• Diuretics

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7
Q

Indications for dialysis

A

Acidosis
Excess - hyperkalaemia
O- pulmonary oedema
Ureaemia (e.g. pericarditis, encephalopathy)

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8
Q

prevent the formation of ascites in patients with chronic liver disease

A
  1. Aldosterone antagonists such as spironolactone
  2. Loop diuretics
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9
Q

Prostate cancer management

A

T1/2
- watchful wait
- radical prostatectomy (side effect - erectile dysfunction)
- external beam radiotherapy/ brachytherapy (risk of proctitis, increased risk bladder colon cancer)

T3/t4 metastic prostate cancer
- we need to reduce androgen levels
- given GnRH agonists (eg. Zoladex Goserelin) paradoxically decrease LH levels overtime by causing increase overstimulation that disrupts the negative feedback mechanism
- to counteract the initial increase in LH which results in crease in testosterone and tumour flare (pain) we give anti-androgen eg. bicalutamide, cyproterone acetate
Or androgen synthesis inhibitor eg. abiraterone

  • severe cases may benefit from bilateral orchidectomy
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10
Q

Renal transplant HLA matching - which is most important

A

DR is the most important

relative importance of the HLA antigens are as follows DR > B > A

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11
Q

Post kidney transplant problems

A

ATN of graft
vascular thrombosis
urine leakage
UTI

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12
Q

Renal transplantation rejection types

A

Hyperacute rejection (minutes to hours)
- due to pre-existing antibodies against ABO or HLA antigens
- a type II hypersensitivity reaction
- leads to widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
- no treatment is possible and the graft must be removed

Acute graft failure (< 6 months)
- due to mismatched HLA —> Cell-mediated (cytotoxic T cells)
- asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
- other causes include cytomegalovirus infection
- may be reversible with steroids and immunosuppressants

Causes of chronic graft failure (> 6 months)
- both antibody and cell-mediated mechanisms —> fibrosis to the transplanted kidney (chronic allograft nephropathy)
- recurrence of original renal disease (MCGN > IgA > FSGS)

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13
Q

Henoch-Schonlein purpura (HSP)
- causes
- symptoms / signs
- treatment
- prognosis

A

IgA mediated vasculitis

Children - triggered by infection

Symptoms: palpable purpuric rash over buttocks, backs of limbs, localised oedema, haematuria, arthralgia

Treatment: supportive

Prognosis- one third get relapse, majority return to normal renal function

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14
Q

Diabetes insipidus

A

Inability to produce (cranial) or respond (nephrogenic) to anti diuretic hormone (vasopressin)

Cranial DI causes
- idiopathic
- pituitary gland surgery
- infiltration: sarcoidosis, haemochromarosis
- tumour
- head injury

Nephrogenic causes
- lithium
- genetic mutations in the ADH receptor
- tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
- hypercalcaemia, hypokalaemia

Features - polyuria, polydipsia

Investigation - water deprivation test, plasma:urine osmolality (high urine osmolality automatically excludes)

Management
nephrogenic diabetes insipidus
- thiazides
- low salt/protein diet

central diabetes insipidus can be treated with desmopressin (Vasopressin receptor 2 agonist)

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15
Q

Autosomal dominant polystic kidney disease

A

ADPKD type 1 ADPKD type 2
85% of cases 15% of cases
Chromosome 16 Chromosome 4
renal failure earlier

Diagnostics: ultrasound
two cysts, unilateral or bilateral, if aged < 30 years
two cysts in both kidneys if aged 30-59 years
four cysts in both kidneys if aged > 60 years

Management: if already developed CKD - tolvaptan (vasopressin receptor 2 antagonist) which also slows cyst development

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16
Q

Most common cause of nephrotic syndrome in children

A

Minimal change >80%

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17
Q

Minimal change disease
- causes
- signs
- pathophysiology
- diagnosis by microscopy
- treatment
- prognosis

A

Causes nephrotic syndrome

Signs: peripheral oedema, hypoalbuminaemia, proteinuria

Causes: idiopathic (80-90%)
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

Pathophysiology - T cell and cytokine mediated —> effacement of foot processes and podocyte loss —> permeability of glomerular basement membrane

renal biopsy
normal glomeruli on light microscopy
electron microscopy shows fusion of podocytes and effacement of foot processes

Treatment
1. Oral steroids
2. Cyclophosphamide

Prognosis: thirds
1/3 have one episode
1/3 have infrequent episodes
1/3 have frequent relapses which cease by adulthood

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18
Q

Causes of nephrogenic Diabetes insipidus

A

Genetic - mutation to ADH receptor
Electrolytes - hypoK, hyperCa
Lithium demeclocycline
Tubulo-interstitial disease - obstruction, sickle cell, pyelonephritis

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19
Q

most common histological pattern seen in lupus nephritis

A

diffuse proliferative glomerulonephritis

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20
Q

which chromosome is implicated in ADPKD

A

type 1 - chr 16
type 2 - chr 4

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21
Q

what clotting factor is lost in nephrotic/nephritic syndrome resulting in clot formation?

A

antithrombin III and plasminogen

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22
Q

normal anion gap

A

8-14

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23
Q

antibody for
Idiopathic membranous glomerulonephritis

A

anti-phospholipase A2 antibodies

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24
Q

stones produced by Proteus mirabilis bacteria in UTI

A

magnesium ammonium phosphate stones

staghorn calculi

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25
Q

Young female, hypertension and asymmetric kidneys

A

fibromuscular dysplasia

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26
Q

drug treatment for polycystic kidney disease

A

tolvaptan (vasopressin receptor 2 antagonist)

— to slow the progression of cyst development

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27
Q

What is Fanconi syndrome

A

disorder of PCT in tubules

loss of potassium, glucose, bicarbonate, amino acids

–> bone demineralisation (osteomalacia in adults, or rickets in children) due to phosphate wasting

–> polyuria, polydipsia and dehydration, growth failure, acidosis, hypokalaemia and hyperchloraemia

caused by congenital (inborn errors of metabolism) or acquired with other autoimmune disease

28
Q

three main antigens responsible for graft vs host disease;

A

HLA-A, HLA-B, and HLA-DR

29
Q

most important HLA antigen to match in renal transplant

A

HLA-DR

30
Q

which vitamin D supplement in end-stage renal disease

A

Alfacalcidol is used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys

31
Q

time taken for an arteriovenous fistula to develop is?

A

6 to 8 weeks

32
Q

which skin cancer is common in renal transplant patients

A

scc

33
Q

red congo stain

A

amyloid

33
Q

Alport’s syndrome

A
  1. haemorrhagic nephritis renal failure - glomerular basement membrane problem
    renal biopsy: splitting of lamina densa seen on electron microscopy
  2. sensorineural deafness
  3. visual problems

x linked dominant - inherited defect in type IV collagen

34
Q

most common cause of peritonitis secondary to peritoneal dialysis

A

Coagulase-negative Staphylococcus
e.g. Staphylococcus epidermidis and Staphylococcus capitis peritonitis

35
Q

how do aminoglycosides (gent/vanc/amik) cause AKI?

A

acute tubular necrosis

36
Q

ADPKD is associated with which heart defect?

A

mitral valve prolaspe

37
Q

renal transplant, most likely infection?

A

CMV

38
Q

what renal disease causes hyperlipidaemia specifically hypercholesterolaemia, as opposed to hypertriglyceridaemia?

A

nephrotic syndrome

This results in low levels of albumin and increased lipoprotein production, leading to hypercholesterolaemia (high cholesterol).

39
Q

most common cause of peritonitis secondary to peritoneal dialysis

A

Coagulase-negative Staphylococcus
eg. Staphylococcus epidermidis

40
Q

what type of glomerulonephritis is caused by HIV?

A

HIV-associated nephropathy (HIVAN) causes collapsing FSGS and usually presents as nephrotic syndrome

41
Q

what type of glomerulonephritis is caused by malignancy?

A

Membranous nephropathy is frequently associated with malignancy

42
Q

How can CKD result in neuropathy

A

Uraemic nephropathy = sensory

43
Q

where is Phosphate reabsorbed?

A

Phosphate is reabsorbed in the proximal tubule

44
Q

trimethoprim vs the kidneys (creatinine)

A

moderate risk in creatinine
- trimethoprim competitively inhibits the tubular secretion of creatinine
- reversible when drug stops

Interstitial nephritis secondary to trimethoprim
- more dramatic rise in creatinine
-haematuria, proteinuria or eosinophiluria and systemic symptoms like rash or fever

45
Q

How does nephrotic syndrome cause clots

A

increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine

46
Q

screening test for adult polycystic kidney disease

A

Ultrasound is the screening test for adult polycystic kidney disease

47
Q

Medications to prevent renal stones

A

High calcium = thiazides
Oxalate = cholesyramine or pyridoxine
Utica stones =allopurinol

48
Q

Acute interstitial nephritis vs acute tubular necrosis

A

Acute interstitial nephritis is an inflammatory process so there is a higher white cell content in the urine, while acute tubular necrosis is not so the urine has no cellular component.

49
Q

On CT imaging, actue vs chronic haematomas

A

On CT imaging, acute haematomas appear bright (hyperdense) whereas chronic haematomas appear dark (hypodense).

50
Q

Complications of nephrotic syndrome

A

increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
deep vein thrombosis, pulmonary embolism
renal vein thrombosis, resulting in a sudden deterioration in renal function

hyperlipidaemia
increasing risk of acute coronary syndrome, stroke etc

chronic kidney disease

increased risk of infection due to urinary immunoglobulin loss

hypocalcaemia (vitamin D and binding protein lost in urine)

51
Q

CKD on haemodialysis - most likely cause of death is ?

A

IHD

52
Q

What is the most useful marker of prognosis in myeloma?

A

B2-microglobulin

53
Q

what is calciphylaxis

A

rare complication of end-stage renal failure.

linked with hypercalcaemia, hyperphophataemia and hyperparathyroidism.

results in deposition of calcium within arterioles causing microvascular occlusion and necrosis of the supplied tissue. It most commonly affects the skin and presents with painful necrotic skin lesions.

warfarin increases risk.

54
Q

link between hepcidin and CKD

A

hepcidin is an acute phase protein, so increased in CKD

furthermore there is reduced hepcidin clearance in CKD

elevated hepcidin levels lead to decreased iron absorption from the gut

55
Q

link between metabolic acidosis and CKD and anaemia

A

metabolic acidosis, a common condition in CKD, can inhibit the conversion of ferric iron (Fe³º) to its absorbable form, ferrous iron (Fe²º), in the duodenum → reduced iron absorption.

56
Q

ATN vs AIN

A

Acute tubular necrosis is associated with granular, muddy-brown urinary casts

acute interstitial nephritis - triad of rash, fever and eosinophilia are all not present
The urine sediment, if present, is more likely to be white cell (and/or red cell) casts/pyuria.

57
Q

ATN or prerenal uraemia?

A

In prerenal uraemia think of the kidneys holding on to sodium to preserve volume

a FENa (fractional sodium excretion) greater than 1% suggests ATN rather than pre-renal uraemia

58
Q

lithium desensitizes the kidney’s ability to respond to ADH in which part of the nephron?

A

the collecting ducts

59
Q

Flash pulmonary oedema, U&Es worse on ACE inhibitor, asymmetrical kidneys

diagnosis and investigation

A

renal artery stenosis - do MR angiography

60
Q

Bendroflumethiazide and effect on kidney stones

A

Bendroflumethiazide may help prevent the formation of calcium based renal stones.

theoretically increase the risk of urate based stones

61
Q

drugs that prevent each of the different kidney stone types

A

Calcium stones: may be due to hypercalciuria, which is found in up to 5-10% of the general population.
high fluid intake
add lemon juice to drinking water
avoid carbonated drinks
limit salt intake
potassium citrate
thiazides diuretics (increase distal tubular calcium resorption)

Oxalate stones:
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion

Uric acid stones:
allopurinol
urinary alkalinization e.g. oral bicarbonate

62
Q

diuretics mechanism of action

A

Amiloride inhibits the epithelial sodium transporter in the distal convoluted tubules.

Carbonic anhydrase inhibitors include dorzolamide and act in the proximal tubules.

Loop diuretics such as furosemide act to block the sodium/potassium/chloride transporter in the loop of Henle.

Thiazide diuretics such as bendroflumethiazide block the sodium/chloride transporter in the distal convoluted tubules.

Spironolactone is an aldosterone antagonist, therefore, acts to inhibit the mineralocorticoid receptor in the cortical collecting ducts.

63
Q

how does alcohol impact ADH

A

suppresses it –> polyuria

64
Q

Urinalysis with ‘muddy brown casts’ is indicative of

A

acute tubular necrosis.

MRCP Part 1 (21 decks)

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