renal Flashcards

1
Q

haemolytic uraemic syndrome causative organism

A

e. coli 0157:H7

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2
Q

HUS triad

A

AKI
microangiopathic haemolytic anaemia
thrombocytopenia

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3
Q

rhabdomyolysis blood results: (5)

A

raised CK (at least x5 upper limit of normal)
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia
metabolic acidosis

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4
Q

how to differentiate AKI vs CKD (2)

A

USS - CKD have small kidneys*
hypocalcaemia (due to low vit D)

  • exceptions:
  • PCKD
  • early diabetic nephropathy
  • amyloidosis
  • HIV associated nephropathy
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5
Q

most common cause of death for CKD pts on haemodialysis

A

IHD

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6
Q

stage 1 AKI
i. creatinine
ii. urine production

A

i. Increase 1.5-1.9x baseline
ii. < 0.5ml/kg/h for >6 consecutive hours

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7
Q

stage 2 AKI
i. creatinine
ii. urine production

A

i. Increase 2.0-2.9x baseline
ii.< 0.5ml/kg/h for >12 consecutive hours

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8
Q

stage 3 AKI
i. creatinine
ii. urine production

A

3 Increase > 3x baseline or >354 µmol/L < 0.3ml/kg/h for > 24h or anuric for 12h

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9
Q

most common cause of glomerulonephritis worldwide:

A

IgA

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10
Q

IgA nephropathy associated conditions:

A

alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

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11
Q

IgA nephropathy gold standard ix

A

renal biopsy

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12
Q

IgA vs post streptococcal glomerulonephritis

A

IgA nephropathy
- 1-2 days post URTI
- usually young males
- macroscopic haematuria

post strp:
- 1-2 weeks post URTI
- proetinuria
- low complement

(but both have hx recent URTI and haematuria)

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13
Q

IgA nephropathy mgt

A
  1. conservative
  2. ACEi (if persisitent proteinuria or drop in renal function
  3. corticosteroids (if no response from ACEi or active disease i.e. falling eGFR)
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14
Q

post-strep glomerulopnephritis
features:

A

recent URTI 1-2 weeks ago
general: headache, malaise
visible haematuria
proteinuria + oedema
hypertension
oliguria

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15
Q

post-strep glomerulonephritis bloods:

A

raised anti-streptolysin O titre
low C3

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16
Q

how to calculate anion gap

A

(Na+ + K+) - (Cl- + HCO-3)

17
Q

normal anion gap

A

10-18

18
Q

metabolic acidosis with normal anion gap
(hypercholeraemic metabolic acidosis)

A

gastrointestinal bicarbonate loss:
prolonged diarrhoea: may also result in hypokalaemia
ureterosigmoidostomy
fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease

19
Q

metabolic acidosis with raised anion gap:

A

lactate:
- shock
-sepsis
- hypoxia
ketones:
- diabetic ketoacidosis
- alcohol
urate: renal failure
acid poisoning: salicylates, methanol

20
Q

eGFR adjusted dependent on:
MDRD (modification of diet in renal disease)

A

CAGE

creatinine
age
gender
ethnicity

21
Q

CKD classification based on eGFR

A

1
Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2
60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a
45-59 ml/min, a moderate reduction in kidney function
3b
30-44 ml/min, a moderate reduction in kidney function
4
15-29 ml/min, a severe reduction in kidney function
5
Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

22
Q

most common cause of glomerulonephritis in children

A

minimal change disease

23
Q

causes of minimal change disease

A

IDIOPATHIC
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
mono

24
Q

minimal change disease mgt:

A

PO corticosteroids

25
Q

diabetes insipidus
what is it?

A

condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).

26
Q

cranial DI causes

A

idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis

27
Q

nephrogenic DI causes

A

genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes
hypercalcaemia
hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

28
Q

diabetes insipidus ix:

A

high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test

29
Q

diabetes insipidus mgt:

A

nephrogenic diabetes insipidus:
-thiazides
-low salt/protein diet
central diabetes insipidus can be treated with desmopressin

30
Q

acute interstitial nephritis causes:

A

drugs: the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci

31
Q

acute interstitial nephritis features:

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

ix:
sterile pyuria
white cell casts

32
Q

iv fluids maintenance requirements:

A

25-30 ml/kg/day of water
1 mmol/kg/day of potassium, sodium and chloride
50-100 g/day of glucose to limit starvation ketosis

33
Q

renal a. stenosis
most common cause in:
i. <50
ii. >50

A

i. fibromuscular dysplasia
ii. atherosclerosis