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Zero to Finals: Medicine > Renal > Flashcards

Renal Flashcards

1
Q

what is an acute kidney injury (AKI)? how is it measured?

A
  • an acute drop in kidney function

- serum creatinine

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2
Q

NICE criteria to diagnose an AKI?

A
  • rise in creatinine of 20 micromol/L or more in 2 days (48 hours)
  • rise in creatinine of 50% or more in 7 days
  • urine output of less than 0.5ml/kg/h for over 6 hours
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3
Q

what is normal urine output?

A

0.5ml per kg per hour

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4
Q

risk factors for developing an AKI?

A
  • chronic disease: CKD, HF, DM, liver disease
  • old age (>65)
  • cognitive impairment
  • drugs (NSAIDs, ACE-i)
  • contrast used in CT scans
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5
Q

how can the causes of AKI be classified? which is most common?

A
  • pre-renal (most common)
  • renal
  • post-renal
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6
Q

examples of pre-renal causes of AKI?

A
  • dehydration
  • hypotension (shock)
  • HF
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7
Q

describe the pathophysiology of pre-renal AKI

A
  • pathology causing reduced blood flow to the kidneys

- less blood gets filtered through them

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8
Q

describe the pathophysiology of renal AKI

A
  • intrinsic disease of the kidney

- makes it less able to filter blood

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9
Q

examples of renal causes of AKI?

A
  • glomerulonephritis
  • interstitial nephritis
  • acute tubular necrosis
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10
Q

describe the pathophysiology of post-renal AKI

A

an obstruction to outflow causes urine to build up in the kidney and reduce kidney function

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11
Q

examples of post-renal causes of AKI?

A
  • kidney stones
  • Ca of abdomen / pelvis
  • ureter / urethral strictures
  • enlarged prostate (BPE)
  • Ca of prostate
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12
Q

investigations in AKI?

A
  • urinalysis

- USS of urinary tract (?obstruction)

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13
Q

what might urinalysis show in AKI?

A

depends on underlying cause:

  • leukocytes and nitrites (infection)
  • protein and blood (acute tubular necrosis, infection)
  • glucose (diabetes)
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14
Q

how can AKI be prevented?

A
  • avoid nephrotoxic meds where possible

- ensure adequate fluids are given

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15
Q

management of AKI?

A

treat underlying cause:

  • fluid rehydration (IV)
  • stop NSAIDs / antihypertensives
  • relieve obstruction (e.g. catheter to get past an enlarged prostate)

if severe without clear cause, refer to renal

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16
Q

complications of AKI?

A
  • hyperkalaemia
  • fluid overload, HF, pulmonary oedema
  • metabolic acidosis
  • uraemia
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17
Q

which 2 complications could uraemia (secondary to AKI) cause?

A
  • pericarditis

- encephalopathy

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18
Q

what is CKD?

A

permanent and progressive reduction in kidney function

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19
Q

causes / risk factors of CKD?

A
  • DM
  • HTN
  • age-related decline
  • glomerulonephritis
  • polycystic kidney disease
  • drugs
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20
Q

drug causes of CKD?

A
  • NSAIDs
  • PPIs
  • lithium
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21
Q

presentation of CKD?

A
  • may be asymptomatic
  • pruritus
  • reduced appetite, nausea
  • oedema
  • muscle cramps
  • peripheral neuropathy
  • pallor
  • HTN
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22
Q

investigations for CKD?

A
  • eGFR
  • urine albumin : creatinine ratio (ACR)
  • urine dipstick
  • renal USS
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23
Q

how must eGFR be done in order to diagnose CKD?

A

2 tests done 3m apart

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24
Q

what is a significant urine ACR reading in CKD? what does this mean?

A
  • 3mg/mmol or more

- indicates proteinuria

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25
Q

what might urine dipstick show in CKD? why is this important?

A
  • haematuria

- could be bladder Ca, investigate!!!!

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26
Q

which CKD patients should be offered renal USS?

A
  • accelerated disease
  • haematuria
  • FHx of polycystic kidney disease
  • evidence of obstruction
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27
Q

how is CKD staged?

A

G score for each eGFR:

  • G1 = >90
  • G2 = 60-89
  • G3a = 45-59
  • G3b = 30-44
  • G4 = 15-29
  • G5 = <15 (end-stage renal failure)
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28
Q

what is A score in CKD?

A

score based on the albumin : creatinine ratio

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29
Q

how is CKD diagnosed?

A

at LEAST eGFR <60, OR proteinuria

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30
Q

complications of CKD?

A
  • anaemia
  • bone disease
  • CVD
  • peripheral neuropathy
  • dialysis-related problems
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31
Q

when does a CKD patient need a renal referral?

A
  • eGFR <30
  • ACR 70mg/mmol or more
  • accelerated disease
  • uncontrolled HTN despite 4 or more any-hypertensives
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32
Q

in CKD, what is classed as “accelerated disease”?

A 
one of the following:
- eGFR drops by 15
- eGFR drops by 20%
- eGFR drops by 15ml/min
all within 1 year
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33
Q

how can the progression of CKD be slowed?

A
  • optimise DM and HTN control

- treat glomerulonephritis

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34
Q

how can complications be reduced in CKD?

A
  • exercise to maintain healthy weight
  • stop smoking
  • special dietary advice on phosphate, sodium, potassium and water intake
  • atorvastatin 20mg for CVD prevention
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35
Q

how are complications in CKD treated?

A
  • PO sodium bicarbonate (metabolic acidosis)
  • iron and erythropoietin (anaemia)
  • vit D (bone disease)
  • dialysis / transplant for ESRF
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36
Q

first line drug for HTN in CKD? target BP?

A
  • ACE-i

- <140/90

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37
Q

which electrolyte needs to be monitored closely in someone with CKD and on an ACE-i?

A
  • serum K+

- hyperkalaemia can result from both of these

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38
Q

how does CKD cause anaemia?

A

healthy kidney cells should produce erythropoietin but they don’t in CKD

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39
Q

How should the iron deficiency in CKD be treated?

A
  • erythropoietin

- IV iron used in dialysis patients

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40
Q

which bone diseases can arise from CKD?

A
  • osteomalacia (softening)
  • osteoporosis (brittle)
  • ostesclerosis (hardening)
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41
Q

X-ray changes seen in CKD bone disease?

A
  • “rugger jersey”
  • sclerosis on both ends of vertebra
  • osteomalacia in the middle
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42
Q

how does CKD cause secondary hyperparathyroidism?

A

the parathyroid glands respond to the low Ca by secreting more PTH

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43
Q

management of renal bone disease in CKD?

A
  • active forms of vit D (alfacalcidol, calcitriol)
  • low phosphate diet
  • bisphosphates if osteoporotic
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44
Q

AEIOU: indications for acute dialysis in AKI patients

A
  • Acidosis (severe, refractory)
  • Electrolytes (severe hyperkalaemia)
  • Intoxication (drug OD)
  • Oedema (severe, pulmonary)
  • Uraemic symptoms
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45
Q

features of uraemia indicating dialysis?

A
  • seizures

- reduced consciousness

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46
Q

2 indications for long-term dialysis?

A
  • ESRF (CKD stage 5)

- any acute indications continuing long-term

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47
Q

what are the 3 main types of dialysis?

A
  • continuous ambulatory peritoneal dialysis
  • automated peritoneal dialysis
  • haemodialysis
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48
Q

which factors are taken into account when choosing a method for dialysis?

A
  • patient preference
  • comorbidities
  • individual risks of each type
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49
Q

which factors are taken into account when choosing a method for dialysis?

A
  • patient preference
  • comorbidities
  • individual risks of each type
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50
Q

complications of peritoneal dialysis?

A
  • bacterial peritonitis
  • peritoneal sclerosis
  • ultrafiltration failure
  • weight gain
  • psychosocial effects
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51
Q

which 2 methods are there to access blood flow in order to carry out haemodialysis?

A
  • tunnelled cuff catheter

- AV fistula

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52
Q

complications of an AV fistula?

A
  • aneurysm
  • infection
  • thrombosis
  • stenosis
  • STEAL syndrome
  • high output heart failure
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53
Q

what is STEAL syndrome?

A

inadequate blood flow to limb distal to AV fistula (it literally STEALS the blood rip)

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54
Q

describe the scar left by a renal transplant

A

hockey stick scar over ipsilateral iliac fossa

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55
Q

describe the scar left by a renal transplant

A

hockey stick scar over ipsilateral iliac fossa

56
Q

what is the immunosuppressant regime used after a kidney transplant? hint: there are 3

A
  • tacrolimus
  • mycophenolate
  • prednisolone
57
Q

how long is the immunosuppressant regime continued for after a renal transplant?

A

lifelong

58
Q

complications of a renal transplant?

A
  • transplant rejection
  • transplant failure
  • electrolyte imbalances
  • any complications relating to immunosuppressant therapy
59
Q

features of nephritic syndrome?

A
  • haematuria
  • oliguria
  • proteinuria
  • fluid retention
60
Q

features of nephrotic syndrome?

A
  • peripheral oedema
  • proteinuria (>3g/day)
  • frothy urine
  • low serum albumin
  • hypercholesterolaemia
61
Q

define glomerulonephritis

A

an umbrella term used to describe any condition which causes inflammation of the glomerulus

62
Q

define interstitial nephritis. what are the 2 main diagnoses?

A
  • inflammation between the cells and tubules of the nephron
  • acute interstitial nephritis
  • chronic tubulointerstitial nephritis
63
Q

define glomerulosclerosis

A
  • scarring of the glomerulus tissue
64
Q

list 3 causes of glomerulosclerosis

A
  • glomerulonephritis
  • obstructive uropathy
  • focal segmental glomerulosclerosis
65
Q

management of glomerulonephritis?

A
  • steroids

- ACE-i / ARB

66
Q

complications of untreated nephrotic syndrome?

A
  • thrombosis
  • HTN
  • high cholesterol
67
Q

most common cause of nephrotic syndrome in children?

A

minimal change disease

68
Q

most common cause of nephrotic syndrome in adults?

A

focal segmental glomerulosclerosis

69
Q

what is IgA nephropathy?

A
  • Berger’s disease

- most common cause of primary glomerulonephritis

70
Q

when does IgA nephropathy typically present?

A

in 20s

71
Q

what is seen on histology in IgA nephropathy?

A
  • IgA deposits

- glomerular mesangial proliferation

72
Q

what is the most common type of glomerulonephritis overall?

A

membranous glomerulonephritis

73
Q

how does post-strep GN present?

A
  • patient <30 years old
  • weeks after a strep infection
  • nephritic syndrome presentation
  • full recovery
74
Q

which streptococcal infections could be followed by post-strep GN?

A
  • tonsillitis

- impetigo

75
Q

key feature of diabetic nephropathy?

A

proteinuria

76
Q

how is diabetic nephropathy prevented?

A

it is screened for using albumin:creatinine ratio (ACR) and UEs

77
Q

management of diabetic nephropathy?

A
  • optimise BMs and BP
  • ACE-i is antihypertensive of choice
  • start even if they have a normal BP
78
Q

how does acute interstitial nephritis present?

A

delayed onset, 2-40 days after drug trigger:

  • AKI
  • HTN
  • rash
  • fever
  • eosinophilia
  • transient arthralgia in some
79
Q

causes of acute interstitial nephritis?

A

infection but mostly drugs:

  • ABx
  • NSAIDs
  • diuretics
  • rifampicin
  • allopurinol
  • PPIs
80
Q

management of acute interstitial nephritis?

A
  • remove underlying cause

- steroids

81
Q

pathophysiology of acute tubular necrosis?

A

ischaemia / toxins causing death of epithelial cells of the renal tubules

82
Q

causes of acute tubular necrosis? (hint: split into ischaemic and nephrotoxic)

A

ischaemic:

  • shock
  • sepsis
  • dehydration

nephrotoxic:

  • radiology contrast dye
  • gentamicin
  • NSAIDs
  • lithium
  • statins
  • ACE-i, ARBs
  • heroin
83
Q

investigation and findings in acute tubular necrosis?

A

urinalysis shows “muddy brown casts”

84
Q

management of acute tubular necrosis? hint: same as other AKIs

A
  • supportive
  • IV fluid resus
  • stop / remove any nephrotoxins
  • haemofiltration / haemodialysis if severe
85
Q

pathophysiology of type 1 renal tubular acidosis?

A
  • pathology of distal tubule making it unable to excrete hydrogen ions
  • results in acidosis
86
Q

causes of type 1 renal tubular acidosis?

A
  • genetic
  • SLE
  • sjogren’s syndrome
  • PBC
  • hyperthyroidism
  • sickle cell anaemia
  • marfan syndrome
87
Q

how does type 1 renal tubular acidosis present?

A
  • FTT in children
  • hyperventilation (compensatory)
  • CKD
  • osteomalacia
88
Q

investigation findings in renal tubular acidosis (type 1 and type 2)?

A
  • low K+
  • metabolic acidosis
  • urinary pH >6 (high)
89
Q

management of renal tubular acidosis (types 1 and 2)?

A

PO bicarbonate

90
Q

pathophysiology of type 2 renal tubular acidosis?

A

pathology of proximal tubule making it unable to reabsorb bicarbonate

91
Q

main cause of type 2 renal tubular acidosis?

A

fanconi syndrome

92
Q

which group of people is fanconi syndrome most associated with?

A

Ashkenazi Jews

93
Q

features of fanconi syndrome?

A
  • cafe au lait spots
  • triangular face
  • microcephaly
  • absent radii bones
94
Q

what causes type 4 renal tubular acidosis?

A

low aldosterone

95
Q

investigation findings in type 4 renal tubular acidosis?

A
  • high K+
  • high Cl-
  • metabolic acidosis
  • low urinary pH (due to low ammonia production)
96
Q

most common type of renal tubular acidosis?

A

type 4

97
Q

causes of type 4 renal tubular acidosis? hint: these all lower aldosterone levels

A
  • adrenal insufficiency
  • ACE-i
  • spironolactone
  • SLE
  • DM
  • HIV
98
Q

what is haemolytic uraemic syndrome (HUS)? what causes this?

A
  • thrombosis in all the small vessels throughout the body

- caused by shiga toxin

98
Q

management of type 4 renal tubular acidosis?

A
  • fludrocortisone (mineralocorticoid, so mimics aldosterone)
  • sodium bicarbonate
  • treat hyperkalaemia (IV insulin w/ glucose + calcium gluconate)
99
Q

what is haemolytic uraemic syndrome (HUS)? what causes this?

A
  • thrombosis in all the small vessels around the body

- caused by shiga toxin

100
Q

features of HUS? hint: classic triad

A
  • haemolytic anaemia
  • AKI
  • thrombocytopenia
101
Q

where does the shiga toxin come from?

A

either E. coli or shigella infection

102
Q

presentation of HUS?

A
  • E. coli gastroenteritis (bloody diarrhoea)
  • reduced UO
  • haematuria (dark brown)
  • abdo pain
  • lethargy, irritability
  • confusion
  • HTN
  • bruising
103
Q

management of HUS?

A
  • medical emergency!
  • anti-hypertensives
  • blood transfusions
  • dialysis
104
Q

prognosis of HUS?

A
  • 10% mortality rate

- approx 75% make a full recovery

105
Q

what do muscle cells release when they die? (features of rhabdomyolysis)

A
  • myoglobin (myoglobinurea)
  • potassium
  • phosphate
  • creatinine kinase (raised CK)
106
Q

complication of potassium release from rhabdomylosis?

A
  • high K+
  • increased risk of arrhythmias
  • cardiac arrest
107
Q

causes of rhabdomyolysis?

A
  • prolonged immobility
  • extremely rigorous exercise
  • crush injuries
  • seizures
108
Q

presentation of rhabdomyolysis?

A
  • muscle aches / pains
  • oedema
  • fatigue
  • confusion (esp in elderly)
  • red-brown urine
109
Q

investigations and findings in rhabdomyolysis?

A
  • CK (raised, remains high for 1-3 days)
  • urine dipstick (positive for blood due to myoglobin)
  • UEs (AKI, hyperkalaemia)
  • ECG (hyperkalemia changes)
110
Q

management of rhabdomyolysis?

A
  • IV fluids
  • IV sodium bicarbonate
  • IV mannitol (raises GFR)
  • treat hyperkalaemia
111
Q

main complication of hyperkalaemia?

A
  • arrhythmias

- particularly VF

112
Q

causes of hyperkalaemia?

A
  • AKI
  • CKD
  • rhabdomyolysis
  • adrenal insufficiency
  • tumour lysis syndrome
  • drugs
113
Q

drug causes of hyperkalaemia?

A
  • spironolactone
  • ACE-i, ARBs
  • NSAIDs
  • potassium supplements
114
Q

what can cause a falsely raised potassium in a blood test?

A

haemolysis of the sample

115
Q

ECG signs in hyperkalaemia?

A
  • tall tented T waves
  • flat / absent P waves
  • broad QRS complexes
116
Q

management of acute hyperkalaemia?

A
  • close ECG monitoring
  • IV insulin and dextrose infusion
  • IV calcium gluconate
117
Q

management of less urgent hyperkalaemia?

A
  • nebulised salbutamol
  • IV fluids
  • PO calcium resonium
  • IV / PO sodium bicarbonate
  • dialysis
118
Q

at what level of K+ does hyperkalaemia need to be managed urgently?

A
  • > 6mmol/L with ECG changes, OR:

- >6.5 mmol/L regardless of ECG

119
Q

what is polycystic kidney disease (PKD)? what does it cause?

A

genetic condition where the kidneys develop fluid-filled cysts

120
Q

which other organs can have cysts in them in PKD?

A
  • liver
  • spleen
  • pancreas
  • ovaries
  • prostate
121
Q

extrarenal findings in ADPKD?

A
  • cysts in liver, pancreas, spleen
  • cerebral aneurysms
  • mitral regurg (from mitral valve prolapse)
  • colonic diverticula
  • aortic root dilatation
122
Q

what is the mode of inheritance of PKD?

A
  • there are both autosomal dominant and recessive forms

- autosomal dominant (ADPKD) is more common

123
Q

how is PKD diagnosed?

A
  • USS of kidneys

- genetic testing

124
Q

which genes are associated with autosomal dominant PKD?

A
  • PKD-1 (chrom 16), majority

- PKD-2 (chrom 4)

125
Q

complications of PKD?

A
  • chronic loin pain
  • HTN
  • CVD
  • gross haematuria
  • renal stones
  • ESRF aged 50
126
Q

management of PKD?

A
  • tolvaptan
  • manage the complications
  • genetic counselling
  • avoid contact sports
  • regular USS to monitor cysts
128
Q

how does autosomal recessive PKD (ARPKD) present?

A
  • oligohydramnios in pregnancy
  • underdeveloped lungs, resp failure shortly after birth
  • flat nasal bridge
  • low set ears
  • ESRF before reaching adulthood
129
Q

renal features of ADPKD?

A
  • flank pain
  • renal dysfunction
  • HTN
  • haematuria
  • microalbuminuria
130
Q

most common complication of dialysis?

A

dialysis-induced hypotension

131
Q

criteria for stage 1 AKI?

A

either:

  • Cr >1.5x baseline
  • UO <0.5ml/kg/hr for 6h
132
Q

criteria for stage 2 AKI?

A

either:
- Cr >2x baseline
- UO <0.5ml/kg/hr for 12h

133
Q

criteria for stage 3 AKI?

A

any of these:

  • Cr >3x baseline
  • Cr >354
  • UO <0.3ml/kg/hr for 24h
  • anuria for 12h
134
Q

which other conditions are associated with focal segmental glomerular sclerosis?

A
  • IgA nephropathy (berger’s disease)
  • HIV
  • sickle cell disease
135
Q

first line renal replacement therapy in ESRF? why is this preferred?

A
  • peritoneal dialysis
  • does not require AV fistula
  • can be done at home
136
Q

which variables are taken into account to calculate eGFR?

A
  • age
  • sex
  • Cr
  • weight

Zero to Finals: Medicine (11 decks)

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