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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
Young female, hypertension and asymmetric kidneys
fibromuscular dysplasia
26
drug treatment for polycystic kidney disease
tolvaptan (vasopressin receptor 2 antagonist) --- to slow the progression of cyst development
27
What is Fanconi syndrome
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
three main antigens responsible for graft vs host disease;
HLA-A, HLA-B, and HLA-DR
29
most important HLA antigen to match in renal transplant
HLA-DR
30
which vitamin D supplement in end-stage renal disease
Alfacalcidol is used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys
31
time taken for an arteriovenous fistula to develop is?
6 to 8 weeks
32
which skin cancer is common in renal transplant patients
scc
33
red congo stain
amyloid
33
Alport's syndrome
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
most common cause of peritonitis secondary to peritoneal dialysis
Coagulase-negative Staphylococcus e.g. Staphylococcus epidermidis and Staphylococcus capitis peritonitis
35
how do aminoglycosides (gent/vanc/amik) cause AKI?
acute tubular necrosis
36
ADPKD is associated with which heart defect?
mitral valve prolaspe
37
renal transplant, most likely infection?
CMV
38
what renal disease causes hyperlipidaemia specifically hypercholesterolaemia, as opposed to hypertriglyceridaemia?
nephrotic syndrome This results in low levels of albumin and increased lipoprotein production, leading to hypercholesterolaemia (high cholesterol).
39
most common cause of peritonitis secondary to peritoneal dialysis
Coagulase-negative Staphylococcus eg. Staphylococcus epidermidis
40
what type of glomerulonephritis is caused by HIV?
HIV-associated nephropathy (HIVAN) causes collapsing FSGS and usually presents as nephrotic syndrome
41
what type of glomerulonephritis is caused by malignancy?
Membranous nephropathy is frequently associated with malignancy
42
How can CKD result in neuropathy
Uraemic nephropathy = sensory
43
where is Phosphate reabsorbed?
Phosphate is reabsorbed in the proximal tubule
44
trimethoprim vs the kidneys (creatinine)
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
How does nephrotic syndrome cause clots
increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
46
screening test for adult polycystic kidney disease
Ultrasound is the screening test for adult polycystic kidney disease
47
Medications to prevent renal stones
High calcium = thiazides Oxalate = cholesyramine or pyridoxine Utica stones =allopurinol
48
Acute interstitial nephritis vs acute tubular necrosis
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
On CT imaging, actue vs chronic haematomas
On CT imaging, acute haematomas appear bright (hyperdense) whereas chronic haematomas appear dark (hypodense).
50
Complications of nephrotic syndrome
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
CKD on haemodialysis - most likely cause of death is ?
IHD
52
What is the most useful marker of prognosis in myeloma?
B2-microglobulin
53
what is calciphylaxis
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
link between hepcidin and CKD
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
link between metabolic acidosis and CKD and anaemia
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
ATN vs AIN
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
ATN or prerenal uraemia?
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
lithium desensitizes the kidney's ability to respond to ADH in which part of the nephron?
the collecting ducts
59
Flash pulmonary oedema, U&Es worse on ACE inhibitor, asymmetrical kidneys diagnosis and investigation
renal artery stenosis - do MR angiography
60
Bendroflumethiazide and effect on kidney stones
Bendroflumethiazide may help prevent the formation of calcium based renal stones. theoretically increase the risk of urate based stones
61
drugs that prevent each of the different kidney stone types
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
diuretics mechanism of action
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
how does alcohol impact ADH
suppresses it --> polyuria
64
Urinalysis with 'muddy brown casts' is indicative of
acute tubular necrosis.

MRCP Part 1 (21 decks)

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