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high yield- year 2 > renal investigations + findings > Flashcards

renal investigations + findings Flashcards

1
Q

Nodular glomerulosclerosis (Kimmelstein- Wilson lesions)

A

Diabetic nephropathy

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2
Q

management of diabetic nephropathy?

A
  • tight glycemic control
  • ACEI/ ARB (aim for BP <130/80)
  • statins
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3
Q

investigations chronic pyelonephritis?

A
  • micturating cystography
  • renal USS
  • CT urogram

may all be useful

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4
Q

most common cause of chronic pyelonephritis?

A
  • reflux nephropathy
  • vesico ureteric reflex (genetic disposition) usually presenting in childhood with recurrent infection but often asymptomatic
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5
Q

investigations renal artery stenosis?

A

1st= MR angiography or CT angiography

Duplex USS (difficult in obese patients)

-renin: aldosterone (both high)

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6
Q

renal artery stenosis treatment

A
  • ACEI (contraindicated in bilateral disease)
  • statin
  • antiplatelets

surgical angioplasty +/- stent in severe cases

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7
Q

string bean appearance on angiography

A

fibromuscular dysplasia

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8
Q

string bean appearance on angiography

-what treatment?

A

-this is fibromuscular dysplasia (rare cause of renal artery stenosis)

treatment= surgical stenting

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9
Q

diabetic nephropathy on USS

A

bilaterally enlarged kidneys

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10
Q

what type of glomerulonephritis causes haematuria

A

nephritic syndrome

-mesangial cell damage/ endothelial (vasculitis) is proliferative leading to haematuria

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11
Q

what type of glomerulonephritis causes proteinuria?

A
  • nephrotic syndrome

- prodocyte damage (non priliferative atrophy) causes proteinuria

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12
Q

nephrotic syndrome presentation?

A
  • proteinuria (>3g/day)
  • hypo albuminaemia (<30g/l)
  • eodema
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13
Q

nephritic syndrome presentation?

A
  • oliguria
  • haematura (red cell casts in urine)
  • hypertension
  • some proteinuria/ fluid retention
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14
Q

light microscopy shows mesengial cell proliferation + immunofluorescence shows IgA and C3 deposits

A

IgA nephropathy

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15
Q

podocyte fusion and foot process effacement?

A

minimal change

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16
Q

minimal change treatment

A

1st- steroids

cyclophophamide= if steroid resistant

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17
Q

IgA nephropathy treatment?

A

ACEI/ ARB

18
Q

minimal change- nephritic or nephrotic?

A

nephrotic

19
Q

FSGS- nephritic or nephrotic

A

nephrotic

20
Q

light microscopy= focal/ segmental sclerosis + hyalinosis

electron microscopy= effacement of foot processes

immunofluorescence= minimal Ig/ complement deposition

A

focal segmental glomerulosclerosis

21
Q

focal segmental glomerulosclerosis treatment

A

steroids +/- immunosuppression

22
Q

membranous nephropathy- nephritic or nephrotic

A

nephrotic

23
Q

electron microscopy= thick BM with sub epithelial electron complex depositions (spike and dome appearance)

A

-membranous nephropathy

24
Q

treatment- membranous nephropathy

A
  • ACEI/ ARBs
  • immunosuppression (steroids + cyclophosphamide +/- B cell monoclonal antibodies)

1/3rd spontaneously resolve, 1/3rd respond to immunosuppression, 1/3 rd end stage renal failure

25
Q

patient just started amoxicillin, presents with fever, rash, arthralgia, elevated creatinine

urine test:

  • raised eosinophils
  • white cell casts
  • sterile pyuria
A

acute interstitial nephritis

26
Q

urinary ACR >30mg/mmol + hypertension

treatment?

A

ACIE (ramipril)

27
Q

what formula is used to help estimate GFR?

A

Modification of Diet in Renal Disease Equation (MDRD):

  • serum creatinine
  • age
  • gender
  • ethnicity

used as serum creatinine may not provide an accurate estimate of renal function due to differences in muscle mass

28
Q
  • nephritic

- rapid decline in renal function + glomerular epitherlial crescent formation on biopsy

A

-rapidly progressive glomerulonephritis

29
Q

treatment- radpidly progressive glomerulonephritis

A

-immunosuppression (steroids + cyclophosphamide + azathioprine) +/- plasma + temporary RRT

30
Q

congo red staining

-apple green birefringence under polarised light

A

amyloidosis

31
Q

longitudinal splitting of lamina densa seen on electron microscopy (characterised by basket weave appearance)

  • microscopic haematuria
  • progressive renal failure
  • bilateral sensorineural deafness
  • ocular manifestations
  • proteinuria
A

Alport’s syndrome (X linked dominant defect in type IV collagen)

32
Q

indications for dyalisis?

A

AEIOU

  • Acidosis (PH <7.15)
  • Electrolyte abnormalities (K > 7 or resistant to treatment)
  • Intoxication (overdose of certain meds)
  • Oedema (severe and unresponsive pulmonary oedema)
  • Uraemia > 40 (seizures, loss of conscioussness)
33
Q

causes of interstitial nephritis?

A 
Drugs: (Not All Pills Fuck Renals)
NSAIDS
Allopurinol
Penicillin
Furesomide
Rifampicin

Infection:
-TB

Systemic:
-sarcoidosis

34
Q

causes of tubular injury?

A
  • iscaemia (prolonged renal hypoperfusion)
  • drugs (gentamycin)
  • contrast
  • rhabdomyolysis
35
Q

treatment- hyperkalaemia?

A
  • ECG + IV access
  • 10 ml 10% calcium gluconate (protect myocardium)
  • insulin actrapid 10 units + 50ml 50% dextrose or nebuliser salbutamol (short term shift)
36
Q

hyperkalaemia- ECG findings

A
  • tall tented T waves
  • small p waves
  • wide QRS
37
Q

hypokalaemia- ECG findings

A
  • U waves
  • small or absent T waves
  • prolonged PR interval
  • ST depression
38
Q

findings of acute tubular necrosis

A
  • AKI
  • muddy brown casts in urine
  • high urine sodium + low urine sodium (with poor response to fluid challenge)
39
Q

findings in rhabdomyolysis?

A
  • AKI
  • disproportionall raised creatinine
  • raised CK
  • metabolic acidosis
  • hyperkalaemia
  • high phosphate
  • low calcium
  • myoglobinuria

Patient often has had a fall or been immobile for hours + is associated with statins

40
Q

rhabdomyolysis treatment?

A

IV fluids +/- urinary alkalinisation

41
Q

Drugs that should be stopped/avoided in AKI

A
  • ARB
  • Diuretics
  • Trimethoprin (co trimoxazole)
  • Contrast
  • Gentamycin
  • NSAIDs
  • ACEI

Avoid Drugs That Can Give Nasty AKIs

42
Q

ascites treatment

A

spironolactone

high yield- year 2 (20 decks)

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