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AA Y4 Finals cards NE > Renal > Flashcards

Renal Flashcards

1
Q

what is the main pre renal cause of AKI?

A

lack of blood flow

eg- hypovolemia 2ndary to diarrhoea/vomiting or renal artery stenosis

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2
Q

name 4 causes of intra renal AKI?

A
  • glomerulonephritis
  • ATN
  • rhabdomyolysis
  • tumour lysis syndrome
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3
Q

name 3 causes of post renal AKI?

A

usually due to obstruction

kidney stone in ureter or bladder

BPH

external compression of the ureter

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4
Q

name 5 classes of drugs with nephrotoxic potential?

A
  1. ACEi
  2. ARBs
  3. aminoglycocides
  4. NSAIDs
  5. diuretics
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5
Q

why may arrhythmias be seen in an AKI?

A

arrhythmias may be seen secondary to changes in the K+ and acid base balance

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6
Q

a urine output below what level is suggestive of an AKI?

A

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

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7
Q

which fluid therapy should not be used in patients with hyperkalaemia?

A

hartmaans

it contains potassium itself

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8
Q

what are the recommended levels for maintenance fluids?

A

water- 25/30ml/kg/day

potassium- 1mmol/kg/day

glucose - 50-100g/day

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9
Q

compare the Na levels in the urine in pre renal AKI and acute tubular necrosis?

A

in pre renal AKI, the body holds onto Na to maintain volume

in ATN, the body does not - therefore, there will be a high urine sodium in ATN and low in pre renal AKI

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10
Q

describe the triad seen in HUS?

A
  • AKI
  • microangiopathic haemolytic anaemia
  • thrombocytopenia
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11
Q

how is HUS managed?

A

supportive - fluids

there is no place for antibiotic therapy

plasma exchange is reserved for severe cases of HUS

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12
Q

what is the most common cause of HUS in children?

A

shigella toxin producing E.Coli

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13
Q

what is the role of calcium gluonate in hyperkalemia?

A

stabilises the cardiac membrane so is protective

it doesnt lower serum K+ levels

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14
Q

what is the role of insulin/dextrose infusions in hyperkalemia?

A

they cause a short term shift of K+ intracellularly

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15
Q

in hyperkalaemia, what can be given to remove K+ from the body?

A

calcium resonium

enemas are more effective than oral

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16
Q

how does lithium cause nephrogenic DI?

A

it reduces the kidney’s capacity to respond to ADH in the collecting ducts

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17
Q

compare the Mx of central DI with nephrogenic DI?

A

central: desmopressin (synthetic ADH)
nephrogenic: thiazides, low salt diet

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18
Q

what is the criteria for >45y/os with haematuria being referred urgently via the cancer pathway?

A
  • unexplained visible haematuria without UTI

- visible haematuria that persists or recurs after successful treatment of UTI

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19
Q

why may a patient with CKD develop anaemia?

A

due to reduced erythropoietin levels

this is a normochromic, Normocytic anaemia and becomes apparent when eGFR < 35ml/min

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20
Q

how does minimal change disease most commonly present?

A

most commonly presents as a nephrotic syndrome

very selective proteinuria occurs - only intermediate sized proteins such as albumin and transferrin leak through

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21
Q

how are the majority of minimal change disease’s treated?

A

majority are steroid responsive

if steroids dont work, can give cyclophosphamide

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22
Q

describe the triad seen in nephrotic syndrome?

A
  • hyperproteinuria
  • hypoalbuminemia
  • oedema
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23
Q

which condition causes marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules?

A

acute interstitial nephritis

accounts for 25% of drug induced AKI

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24
Q

what is the commonest extra-renal manifestation of ADPKD?

A

liver cysts

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25
Q

what vascular complication can be seen in ADPKD?

what can this predispose to?

A

berry aneurysms

this can predispose to subarachnoid haemorrhage

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26
Q

name 6 features of ADPKD?

A 
hypertension
recurrent UTIs
renal stones 
haematuria 
CKD 
abdominal pain
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27
Q

what antibody causes goodpasture’s syndrome?

what can be seen on renal biopsy?

A

antiglomerular basement membrane antibodies

they work against type IV collagen

renal biopsy: linear IgG deposits along the basement membrane

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28
Q

name the 2 main features in Goodpasture’s syndrome?

A
  • pulmonary haemorrhage

- rapidly progressive glomerulonephritis, resulting in a rapid AKI- this results in proteinuria and haematuria

29
Q

how is goodpasture’s syndrome managed?

A
  • plasma exchange
  • steroids
  • cyclophosphamide
30
Q

describe 2 key roles of the kidney that are impaired in CKD and have subsequent effects on bone mineral density?

A
  1. kidneys activate vitamin D - CKD leads to low vit D

2. kidneys excrete phosphate - CKD leads to high phosphate

31
Q

what metabolic disturbance does the low vit D and high phosphate cause in CKD?

A

low calcium levels - caused by low vit D and high phosphate

the high phosphate ‘drags’ calcium from the bones

this low calcium results in secondary hyperparathyroidism

32
Q

what is the aim in bone mineral management in CKD?

how is this done?

A
  • reduce phosphate levels
  • reduce parathyroid hormone levels

1st line: reduce dietary phosphate intake
2nd line: phosphate binders, vit D supplements
3rd line: parathyroidectomy

33
Q

what is the commonest cause of glomerulonephritis worldwide?

A

IgA nephropathy

34
Q

what is the classic presentation of an IgA nephropathy?

A

macroscopic haematuria in a young person following an URTI

35
Q

compare what is found on renal biopsy in goodpasture’s syndrome and IgA nephropathy?

A

goodpastures: linear IgG

IgA nephropathy: IgA deposition in glomerulus

36
Q

in IgA nephropathy and post strep glomerulonephritis, there is onset of renal symptoms following an URTI.

how can they be differentiated?

A
  1. complement levels - they are low in post strep glomerulonephritis but high in IgA nephropathy
  2. post strep glomerulonephritis is more associated with proteinuria rather than haematuria. IgA nephroapthy causes macroscopic haematuria
  3. there is usually a delay in onset between the URTI and renal symptoms in post strep glomerulonephritis (occurs 1-2 weeks after URTI but in IgA nephropathy, it is 1-2 days)
37
Q

how is IgA nephropathy managed?

A

if isolated haematuria, no or minimal proteinuria and normal eGFR: no tx- just follow up to check renal function

if persist proteinuria and a normal/slightly reduced eGFR: Tx with ACEi

if there is active disease (a falling GFR) - immunosuppression with corticosteroids

38
Q

what blood test can help differentiate post strep glomerulonephirits from IgA nephropathy?

A

post strep glomerulonephritis causes low C3

39
Q

compare the timeframes in post strep glomerulonephritis and IgA nephropathy?

A

IgA nephropathy: renal symtoms occur immediately after URTI

post strep glomerulonephritis: renal symptoms occur 1-2 weeks after URTI

40
Q

describe the features of rhabdomyolysis?

A

AKI with disproportionately raised creatinine

elevated CK

myoglobinuria - causes a hypocalcemia

41
Q

in which classes of heart failure is spironolactone indicated?

A

NYHA III and IV - in patients already taking an ACEi

low dose spirinolactone has been found to reduce all cause mortality

42
Q

how is proteinuria in CKD managed 1st line?

A

ACEi or ARBs

they should be used 1st line in patients with co-existent hypertension and CKD

43
Q

what are the 2 best ways to differentiate AKI from CKD?

A
  1. renal U/S - most patients with CKD have bilateral small kidneys
  2. hypocalcemia- if it is present, most likely due to CKD (due to lack of vit D)
44
Q

what is the most common cause of glomerulonephritis in adults?

how does this condition present on a renal biopsy?

A

membrenous glomerulonephritis

presents with thickened basement membrane with sub epithelial electron dense deposits - creates a “spike and dome” appearance

45
Q

name the main complication of nephrotic syndrome?

how does this occur?

A

increased risk of thromboembolism

due to increased loss of antithrombin III and plasminogen in the urine (proteins are lost in the urine in nephrotic syndrome)

46
Q

what medication is most likely to cause nephrogenic DI in a psychiatric patient?

A

lithium

47
Q

which nephropathy is frequently associated with malignancy?

esp lung, bowel and haematological

A

membranous nephropathy

also the most common cause of nephrotic syndrome in adults

48
Q

what medication should ALL patients with CKD be started on?

why?

A

all patients with CKD should be started on a statin

for prevention of CVD

49
Q

what is the most appropriate screening test for ADPKD?

A

US abdomen

genetic testing is still not routinely recommended

50
Q

what is the Tx for acute clot retention?

A

continuous bladder irrigation

51
Q

how is nephrogenic DI Tx?

how does this Tx work?

A

thiazide diuretics

the thiazide diuretic increases Na excretion in the urine, which reduces blood osmolality which helps break the polyuria-polydipsia cycle

52
Q

what is 1st line Tx of minimal change disease?

A

prednisolone

53
Q

which condition causes podocyte fusion and effecement of the podocyte foot processes on renal biopsy?

A

minimal change disease

causes a nephrocytic picture

54
Q

describe the urea:creatinine ratio in pre renal AKI compared to renal AKI?

A

pre renal: increased urine:creatinine ratio

renal: normal urine: creatinine ratio

55
Q

what renal condition can penicillins cause?

describe the casts that are present?

A

penicillins can cause acute interstitial nephritis

presents with eosinophilic casts

56
Q

compare the most common cause of nephrotic syndrome in children and in adults?

A

in children: minimal change disease

in adults: membranous nephropathy

57
Q

why is nephrotic syndrome associated with a hypercoaguable state?

A

due to loss of antithrombin III and plasminogen via the kidneys

58
Q

what does acute interstitial nephritis most commonly occur as a result of?

how can it be differentiated from acute tubular necrosis?

A

drug toxicity

acute tubular necrosis causes muddy brown casts, acute interstitial nephritis does not

59
Q

what MSK side effects can statins have?

A

statins can cause myalgia and myopathies but can also go on to cause rhabdomyolysis

60
Q

compare the presentation of acute graft failure and ATN of the graft in patients following renal transplants?

A

acute graft failure: more commonly occurs following live graft transplant, asymptomatic and is usually picked up within months

ATN of graft: occurs in the 1st few weeks of renal transplant, more common in cadaver transplant than living donor transplant

61
Q

which symptoms are present in HSP but not meningitis?

A

both cause non blanching, purpuric rash

HSP also causes haematuria, abdominal pain and joint pain

62
Q

how can the urine Na level be used to help distinguish pre renal from renal AKI?

A

in pre renal AKI, urine sodium is LOW - the body is trying to hold on to sodium to preserve volume

this causes high sodium in the blood and low sodium in the urine

63
Q

what is the most common cause of transplant rejection?

A

acute T cell mediated rejection

occurs weeks to months following transplant and is mediated by lymphocytic infiltration of the graft

64
Q

what triad of symptoms is present in Alport’s syndrome?

A

renal failure
SN hearing loss
ocular abnormalities

65
Q

how can the renin levels help differentiate between primary and secondary aldosteronism?

A

if the renin levels are high, then a secondary cause of aldosteronism is more likely

eg- renal artery stenosis

66
Q

how does a salicylate poisoning (aspirin) present?

A

nausea, vomiting, tinnitus, headache

high anion gap metabolic acidosis

Mx of minor ODs is supportive, but significant ones require alkalisation with IV sodium bicarbonate

67
Q

which renal condition causes crescentic glomerulonephritis on renal biopsy?

A

rapidly progressive glomerulonephritis

a term used to describe a rapid loss of renal function associated with the formation of epithelial crescents in majority of glomeruli

68
Q

compare the urinary osmolality and Na content in pre renal and renal kidney injury?

A

pre renal: kidneys act to concentrate urine to retain Na, so high urine osmolality, low urine Na

renal: kidneys lost their function so cannot concentrate urine: urine osmolality low, urine Na content high

AA Y4 Finals cards NE (40 decks)

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