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FINALS > RENAL > Flashcards

RENAL Flashcards

1
Q

What is HUS?

A

Haemolytic uraemia syndrome

Thrombosis in small blood vessels

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2
Q

What is the triad of HUS?

A

• Haemolytic anaemia
• AKI
Thrombocytopenia

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3
Q

How does HUS present?

A 
Reduced urine output
Haematuria
Abdominal pain
Lethargy
Hypertension
Bruising
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4
Q

Who is most commonly affected by HUS?

A

Children

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5
Q

What is typical HUS?

A

Secondary to E.coli infection

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6
Q

What is primary HUS?

A

Caused by complement dysregulation

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7
Q

What is STEC?

A

Shiga toxic-producing E.Coli

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8
Q

What is the most common cause of HUS? Name three other causes.

A

E.coli (Shiga toxin) - 90% of cases in children

HIV
Pneumococcal infection
Rare: SLE, drugs, cancer

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9
Q

Which two medications increase the risk of HUS?

A

Antibiotics

Anti-motility drugs (Loperamide)

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10
Q

Which investigations should be done in HUS?

A

FBC - anaemia, thrombocytopenia
U&E - AKI
Stool culture - STEC infection, PCR for Shiga toxins

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11
Q

What is the mortality rate of HUS?

A

10% - medical emergency

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12
Q

How is HUS managed?

A

Supportive - self-limiting

Anti-hypertensives
Blood transfusions
Dialysis

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13
Q

What percentage of patients will fully recover from HUS?

A

80%

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14
Q

What is an AKI?

A

Acute kidney injury (AKI) is defined as an acute drop in kidney function. It is diagnosed by measuring the serum creatinine.

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15
Q

What are the NICE criteria for AKI?

A
  • Rise in creatinine of ≥ 25 micromol/L in 48 hours
  • Rise in creatinine of ≥ 50% in 7 days
  • Urine output of < 0.5ml/kg/hour for > 6 hours
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16
Q

What are the three stages of AKI according to creatinine?

A

Stage 1 = ^1.5-1.9x baseline
Stage 2 = ^2-2.9x baseline
Stage 3 = >3x baseline

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17
Q

What are the three stages of AKI according to urine production?

A

Stage 1 = <0.5ml/kg/hour >6 hours

Stage 2 = <0.5ml/kg/hour >12 hours

Stage 3 = <0.3ml/kg/hour >24 hours OR anuric for 12 hours

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18
Q

What are the risk factors for AKI?

A 
• Chronic kidney disease
• Heart failure
• Diabetes
• Liver disease
• Older age (above 65 years)
• Cognitive impairment
• Nephrotoxic medications such as NSAIDS and ACE inhibitors
Use of a contrast medium such as during CT scans
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19
Q

What are the three types of AKI?

A
  1. Pre-renal - reducing renal perfusion (hypovolaemia/hypoperfusion)
  2. Intra-renal - damage to the kidney (ischaemia, sepsis, inflammation)
  3. Post-renal - outflow obstruction
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20
Q

What is the most common cause of AKI?

A

Pre-renal

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21
Q

What are the causes of pre-renal AKI?

A
  1. Dehydration
  2. Hypotension/shock (sepsis)
  3. Heart failure
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22
Q

What are the causes of intra-renal AKI?

A
  1. Glomerulonephritis
  2. Interstitial nephritis
  3. Acute tubular necrosis
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23
Q

What are the causes of post-renal AKI?

A
  1. Kidney stones
  2. Masses such as cancer in the abdomen or pelvis
  3. Ureter or urethral strictures
  4. Enlarged prostate or prostate cancer
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24
Q

Name some drugs that will cause AKI.

A

Aminoglycosides

Amphotericin

Cytotoxic chemotherapy

Diuretics

Immunosuppressants

Lithium salts

NSAIDs/COX inhibitors

Radiocontrast media

Other

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25
Q

Name some pathological states that are nephrotoxic.

A

Hypoperfusion

Sepsis

Rhabdomyolysis

Hepatorenal syndrome

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26
Q

What is the best measure of renal function?

A

eGFR

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27
Q

When should creatinine clearance be used instead of eGFR to estimate renal function?

A 
Elderly
Toxic drugs
Extremes of muscle mass
Drugs with narrow therapeutic window
DOACs
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28
Q

What will be seen on urinalysis in AKI?

A
  • Leucocytes and nitrites suggest infection
  • Protein and blood suggest acute nephritis (but can be positive in infection)
  • Glucose suggests diabetes
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29
Q

What imaging might be needed in AKI?

A

US - particularly good for obstruction.

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30
Q

What is the approach to management of an AKI?

A

Prevent the injury and correct the underlying cause: avoid nephrotoxic medications.

  • Fluid rehydration with IV fluids in pre-renal AKI
  • Stop nephrotoxic medications such as NSAIDS and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors)
  • Relieve obstruction in a post-renal AKI, for example insert a catheter for a patient in retention from an enlarged prostate
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31
Q

Which fluid should be prescribed in a patient with and AKI, hypovolaemia and metabolic acidosis?

A

Sodium bicarbonate 1.26%

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32
Q

Name 4 complications of AKI.

A
  1. Hyperkalaemia - kidneys cannot filter excess potassium
  2. Fluid overload - pulmonary oedema, heart failure
  3. Metabolic acidosis - kidneys cannot produce bicarbonate
  4. Uraemia - encephalopathy (confusion), pericarditis
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33
Q

How is pulmonary oedema treated in AKI?

A

Haemodialysis

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34
Q

What is acute tubular necrosis?

A

Damage and death of renal tubular epithelial cells

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35
Q

How does damage to the cells occur in ATN?

A

Secondary to ischaemia

Directly due to toxins

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36
Q

How long does it take for renal tubular cells to recover?

A

7-21 days

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37
Q

Name 3 ischaemic causes of ATN.

A

Shock
Dehydration
Sepsis

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38
Q

Name 3 toxic causes of ATN.

A 
NSAIDs
Contrast dyes
Aminoglycosides
Lithium
Heroin
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39
Q

What is seen on urinalysis in ATN?

A

Muddy brown casts - pathognomonic (only seen in ATN)

Renal tubular epithelial cells

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40
Q

What is the management of ATN?

A

Supportive:

  • Fluids
  • Stop nephrotoxic medications
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41
Q

What are the causes of CKD?

A 
Diabetes
HTN
Age-related decline
Glomerulonephritis
PKD
Drugs - NSAIDs, PPIs, lithium
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42
Q

Which drugs cause CKD?

A

NSAIDs
PPIs
Lithium

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43
Q

What are the risk factors for CKD?

A

Older age
HTN
Diabetes
Smoking

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44
Q

Which two parameters are used to classify CKD?

A

eGFR

Albumin: creatinine ratio

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45
Q

How does CKD normally present?

A

Asymptomatic

Pruritis
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
HTN
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46
Q

What investigations are done in CKD?

A

U&E
Urine dipstick
Renal US

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47
Q

How do you diagnose CKD?

A

2 x eGFR tests

3 months apart

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48
Q

What is the ACR? What result is significant?

A

Urine albumin: creatinine ratio

>3mg/mmol

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49
Q

What is the G score?

A

Based on the eGFR (measure of glomerular filtration rate)

• G1 = eGFR >90
• G2 = eGFR 60-89
• G3a = eGFR 45-59
• G3b = eGFR 30-44
• G4 = eGFR 15-29
G5 = eGFR <15 (known as “end-stage renal failure”)
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50
Q

What is the A score in CKD?

A

The A score is based on the albumin:creatinine ratio:

A1 = < 3mg/mmol
A2 = 3 – 30mg/mmol
A3 = > 30mg/mmol
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51
Q

What are the complications of CKD?

A 
• Anaemia
• Renal bone disease
• Cardiovascular disease
• Peripheral neuropathy
Dialysis related problems
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52
Q

When should you refer a patient to a renal specialist in CKD?

A

• eGFR < 30
• ACR ≥ 70 mg/mmol
• Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15 ml/min in 1 year
Uncontrolled hypertension despite ≥ 4 antihypertensives

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53
Q

What are the aims of management in CKD?

A

• Slow the progression of the disease
• Reduce the risk of cardiovascular disease
• Reduce the risk of complications
Treating complications

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54
Q

How can you slow the progression of CKD?

A

• Optimise diabetic control
• Optimise hypertensive control
Treat glomerulonephritis

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55
Q

How do you reduce the risk of complications in CKD?

A

• Exercise, maintain a healthy weight and stop smoking
• Special dietary advice about phosphate, sodium, potassium and water intake
Offer atorvastatin 20mg for primary prevention of cardiovascular disease

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56
Q

How do you treat anaemia caused by CKD?

A

Iron

EPO

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57
Q

How do you treat HTN in CKD?

A

ACEi’s offered to all patients:
• Diabetes plus ACR > 3mg/mmol
• Hypertension plus ACR > 30mg/mmol
All patients with ACR > 70mg/mmol

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58
Q

How do you manage end stage renal failure?

A
  • Dialysis in end stage renal failure

- Renal transplant in end stage renal failure

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59
Q

What is allosensitisation?

A

Blood transfusions should be limited as they can sensitise the immune system (“allosensitisation”) so that transplanted organs are more likely to be rejected.

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60
Q

What is CKD-MBD?

A
  1. Osteomalacia (softening of bones)
  2. Osteoporosis (brittle bones)
  3. Osteosclerosis (hardening of bones)
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61
Q

What is seen on an XR of the spine in CKD-MBD?

A

“rugger jersey” spine

sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white)

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62
Q

How does CKD-MBD result in a secondary hyperparathyroidism?

A

parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone.

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63
Q

How is CKD-MBD managed?

A
  • Active forms of vitamin D (alfacalcidol and calcitriol)
  • Low phosphate diet
  • Bisphosphonates can be used to treat osteoporosis
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64
Q

What is interstitial nephritis?

A

Inflammation of the cells surrounding the tubules within the kidney.

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65
Q

What are the two types of interstitial nephritis?

A

Acute interstitial nephritis

Chronic tubulointerstitial nephritis

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66
Q

How does acute interstitial nephritis present?

A

AKI
HTN

(rash, fever or eosinophilia is hypersensitivity reaction)

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67
Q

Give three causes of acute interstitial nephritis.

A

Toxins
Infection
Hypersensitivity reaction

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68
Q

How do you treat acute interstitial nephritis?

A

treat underlying cause

steroids

69
Q

How does chronic tubulointerstitial nephritis present?

70
Q

Give four causes of chronic tubulointerstitial nephritis

A

Autoimmune
Infectious
Iatrogenic
Granulomatous disease

71
Q

What is the management of chronic tubulointerstitial nephritis?

A

treat underlying cause

Steroids (under specialist supervision)

72
Q

What is renal tubular acidosis (RTA)?

A

Metabolic acidosis due to pathology in the tubules of the kidney.

73
Q

What is the normal function of the proximal and distal renal tubules?

A

Proximal - reabsorb bicarbonate back into the blood

Distal - excrete H+ ions

74
Q

How many types of RTA are there?

75
Q

Which are the two most clinically relevant types of RTA?

76
Q

What is the treatment for steroid resistant minimal change disease?

A

cyclophosphamide

77
Q

What is the prognosis of minimal change disease?

A

1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood

78
Q

What is the first-line management of minimal change disease?

A 
PO prednisolone (80% of cases will respond)
Urgent outpatient review
79
Q

What is the definition of hyperkalaemia? What is classified as severe?

A

> 5.3mmol/L

>6.5mmol/L

80
Q

Give 6 causes of hyperkalaemia.

A 
• Acute kidney injury
• Chronic kidney disease
• Rhabdomyolysis
• Adrenal insufficiency
• Tumour lysis syndrome
Drugs
81
Q

Name 5 drugs that commonly cause hyperkalaemia?

A 
• Aldosterone antagonists (spironolactone and eplerenone) 
• ACE inhibitors
• Angiotensin II receptor blockers
• NSAIDs
Potassium supplements
82
Q

What can cause a falsely elevated potassium level?

A

Haemolysis (lab may request another sample)

83
Q

How does hyperkalaemia present?

A 
Nausea
Muscle weakness
ECG changes
Ventricular fibrillation
Cardiac arrest
84
Q

What are the ECG changes in hyperkalaemia?

A

• Tall peaked T waves
• Flattening or absence of P waves
Broad QRS complexes

85
Q

What are the three aims of treatment in Hyperkalaemia?

A

Protect the heart
Lower serum potassium concentration
Remove excess potassium

86
Q

What drug us used for cardio protection?

A

10ml calcium gluconate 10% solution, slow IV injection over 3-5 minutes
Titrate and adjust according to ECG

(mix with glucose 5% over 20 mins if taking digoxin)

87
Q

How should you treat patients with a potassium of <6 mmol/L and otherwise stable renal function?

A

Diet

Adjust medications

88
Q

When do patients require urgent treatment for hyperkalaemia?

A

ECG changes

>6.5mmol/L

89
Q

What is first-line treatment for hyperkalaemia?

A

Insulin and dextrose

Calcium gluconate

90
Q

Which medication can be used to lower serum potassium?

A

Oral calcium resonium

91
Q

What management might be needed in severe hyperkalaemia?

92
Q

What is the definition of hypokalaemia?

A

<3.5mmol/L

93
Q

Name some causes of hypokalaemia.

A

Internal distribution:

  • Alkalosis
  • ^insulin
  • B-agonists

Excretion:

  • Vomitting, diarrhoea
  • RTA
  • Diuretics, steroids
  • Cushing’s, Conn’s syndrome

Inadequate intake:
- Inappropriate fluid management

94
Q

Which drugs commonly cause hypokalaemia?

A 
Laxatives
Glucocorticoid therapy
Insulin
Loop diuretics
Salbutamol
Antibacterial
Thiazide diuretics
Theophylline
95
Q

What are the ECG changes in hypokalaemia?

A 
• Flattened/inverted T waves
• Prominent U waves
• ST depression
• Long PR interval
Long QT interval
96
Q

How does hypokalaemia present?

A

Often asymptomatic

Muscle weakness
Cramps
Fatigue
Constipation
Palpitations
97
Q

How should low potassium be corrected?

A

1L IV sodium chloride 0.9% with 40 mmol KCl over 4 hours

potassium chloride 0.3% (1L is 40mmol of K)
IV potassium chloride 0.15% (1L is 20mmol of K)

98
Q

What is the max dose of potassium that can be given IV in 1 hour?

99
Q

Which other electrolyte should be checked in hypokalaemia?

A

Mg - must be corrected for K to return to normal

100
Q

What is glomerulonephritis?

A

an umbrella term applied to conditions that cause inflammation of or around the glomerulus and nephron.

101
Q

What are the two syndromes caused by glomerulonephritis?

A

Nephritic syndrome

Nephrotic syndrome

102
Q

What is glomerulosclerosis?

A

A pathological process of scarring of the tissue in the glomerulus.
Caused by any type of glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a specific disease called focal segmental glomerulosclerosis.

103
Q

What is the most common cause of primary glomerulonephritis?

A

IgA nephropathy (AKA Berger’s disease)

104
Q

What is Goodpasture’s syndrome?

A

Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes.

This causes glomerulonephritis and pulmonary haemorrhage.

105
Q

How might a patient present with Goodpasture’s syndrome?

A

Acute renal failure

Haemoptysis

106
Q

Which differential diagnoses should be considered in a patient presenting with acute renal failure and haemoptysis?

A

Goodpasture’s syndrome

Wegener’s granulomatosis (granulomatosis with polyangiitis)

107
Q

What investigations should be done in glomerulonephritis?

A 
Urine dipstick
Light microscopy
Electron microscopy
Immunofluorescence
Bloods - Strep Ab's
108
Q

What might be seen on a urine dipstick in glomerulonephritis?

A

Proteinuria
Haematuria
WBCs

109
Q

What can be seen on light microscopy in glomerulonephritis?

A

Glomerular inflammation

Sclerosis

110
Q

What can be seen on electron microscopy in glomerulonephritis?

A

Effacement

111
Q

How is glomerulonephritis generally treated?

A
  • Immunosuppression (e.g. steroids)
  • Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)
112
Q

Name a complication of glomerulonephritis?

A

Infection (due to loss of Ig in urine)

113
Q

Which types of glomerular disease are likely to cause nephritic syndrome?

A
  • IgA nephropathy (AKA mesangioproliferative glomerulonephritis or Berger’s disease)
  • Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
  • Rapidly progressive glomerulonephritis
114
Q

What are the features of nephritic syndrome?

A 
• Abrupt onset
• Oedema +
• BP raised
• Proteinuria <3.5g/day
• Haematuria ++++
RBC casts
115
Q

What is another name for IgA nephropathy?

A

Berger’s disease

116
Q

What is the peak age at presentation for IgA nephropathy?

117
Q

What is seen on histology in IgA nephropathy?

A

IgA deposits and glomerular mesangial proliferation

118
Q

When do patients present with post-streptococcal glomerulonephritis?

A

1-3 weeks after infection

<30 years

119
Q

What type of hypersensitivity reaction causes post-streptococcal glomerulonephritis?

120
Q

What is seen on histology in rapidly progressive glomerulonephritis?

A

Crescentic glomerulonephritis

121
Q

What are the features of nephrotic syndrome?

A 
• Insiduous onset
• Oedema ++++
• Normal BP
• Proteinuria >3.5g/day
• Hyperlipidaemia
Low albumin
122
Q

Which types of glomerular disease are likely to cause nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis

123
Q

What is the most common cause of nephrotic syndrome in children? And adults?

A 
Children = minimal change disease
Adults = focal segmental glomerulosclerosis
124
Q

Which disease is associated with minimal change disease?

A

Hodgkin’s lymphoma

125
Q

What are the causes of focal segmental glomerulosclerosis?

A

Idiopathic

Sickle-cell disease
HIV
Heroin
HTN

126
Q

What is seen on histology (immunofluorescence) in membranous glomerulonephritis?

A

IgG complement deposits on the basement membrane

127
Q

What are the two types of PKD? Which is more common? Which is more severe?

A

autosomal dominant - common

autosomal recessive - severe

128
Q

Which two genes are responsible for autosomal dominant PKD?

A

PKD-1: chromosome 16 (85% of cases)

PKD-2: chromosome 4 (15% of cases)

129
Q

Which gene are responsible for autosomal recessive PKD?

A

a gene on chromosome 6

130
Q

When does autosomal dominant PKD present?

A

30-40 years

131
Q

When does autosomal recessive PKD present?

A

In pregnancy with oligohydramnios (foetus does not produce enough urine)
Patients may require dialysis in the first few days of life
Usually have end-stage renal failure by adulthood

132
Q

Name 5 extra-renal manifestations of autosomal PKD.

A
  • Cerebral aneurysms
  • Hepatic, splenic, pancreatic, ovarian and prostatic cysts
  • Cardiac valve disease (mitral regurgitation)
  • Colonic diverticula
  • Aortic root dilatation
133
Q

What is the screening investigation for ADPKD? Who should be screened?

A

Abdominal US

Relatives of someone with ADPKD

134
Q

What are the US criteria for patients with a positive family history of PKD?

A
  • 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
135
Q

What is shown in renal biopsy in ARPKD?

A

multiple cylindrical lesions at right angles to the cortical surface

136
Q

What drug can be used to slow the development of cysts in autosomal dominant PKD?

A

Tolvaptan (vasopressin receptor antagonist)

137
Q

What advice should be given to patients with PKD?

A
  • Genetic counselling
  • Avoid contact sports due to the risk of cyst rupture
  • Avoid anti-inflammatory medications and anticoagulants
138
Q

What monitoring is required in PKD?

A

• Kidney US
• Regular bloods to monitor renal function
• Regular blood pressure to monitor for hypertension
- MR angiogram can be used to diagnose intracranial aneurysms in symptomatic patients or those with a family history

139
Q

How can the complications of PKD be managed?

A
  • Antihypertensives for hypertension.
  • Analgesia for renal colic related to stones or cysts.
  • Antibiotics for infection. Drainage of infected cysts may be required.
  • Dialysis for end-stage renal failure.
  • Renal transplant for end-stage renal failure.
140
Q

What are the complications of autosomal dominant PKD?

A
  • Chronic loin pain
  • Hypertension
  • Cardiovascular disease
  • Gross haematuria can occur with cyst rupture (this usually resolves within a few days
  • Renal stones are more common in patients with PKD
  • End-stage renal failure occurs at a mean age of 50 years
141
Q

What is renal tubular acidosis (RTA)?

A

Metabolic acidosis due to pathology in the tubules of the kidney.

142
Q

What is the normal function of the proximal and distal renal tubules?

A

Proximal - reabsorb bicarbonate back into the blood

Distal - excrete H+ ions

143
Q

How many types of RTA are there?

144
Q

Which are the two most clinically relevant types of RTA?

145
Q

What are the causes of type I RTA?

A 
• Genetic (autosomal dominant/recessive)
• Sjogren's syndrome
• SLE
• Primary biliary cirrhosis 
• Hyperthyroidism
• Sickle-cell anaemia
Marfan's
146
Q

What is found on a blood gas in RTA type I and type IV?

A

Type I:

  • Hypokalaemia
  • Metabolic acidosis
  • High urinary pH

Type IV:

  • Hyperkalaemia
  • Hyperchloraemia
  • Metabolic acidosis
  • Low urinary pH
147
Q

What is the treatment for type I RTA?

A

Bicarbonate PO

148
Q

What is the treatment for RTA type IV?

A

Fludrocortisone
Sodium bicarbonate
Treat hyperkalaemia

149
Q

What causes type IV RTA?

A

Reduced aldosterone:

  • Adrenal insufficiency
  • ACEi’s
  • Spironolactone
150
Q

How many years does a renal transplant add to life expectancy?

151
Q

How are donors matched?

A

HLA matching

152
Q

Which chromosome are HLA types found?

153
Q

How is a donor kidney transplanted into the recipient?

A

Old kidney remains in place
Donor kidney blood vessels are anastomosed with the patient’s pelvic blood vessels
Kidney is anterior in the abdomen (can be palpated in the iliac fossa)

154
Q

Where can a donor kidney be palpated?

A

Iliac fossa

155
Q

Which incision is typically used?

A

Hockey-stick incision

156
Q

What are the indications for renal transplantation?

A

End stage renal failure

157
Q

Which three drugs are used for immunosuppression in renal transplant? Name three other immunosuppressants that can be used.

A
  1. Tacrolimus
  2. Mycophenolate
  3. Prednisolone

Cyclosporine
Sirolimus
Azathioprine

158
Q

What side effects do immunosuppressants cause?

A

Skin changes - seborrheic warts/skin cancers
Tremor - tacrolimus
Gum hypertrophy
Cushing’s syndrome - steroids

159
Q

What are the complications of a renal transplant?

A

Transplant related - rejection, failure, electrolyte imbalances
Immunosuppressant complications - ischaemic heart disease, T2DM, infections, non-Hodgkin lymphoma, skin cancer (particularly SCC)

160
Q

What are the three types of transplant rejection?

A

Hyperacute (minutes to hours)
Acute (<6 months)
Chronic (>6 months)

161
Q

What is the cause of hyperacute rejection? What type of reaction is it?

A

Pre-existing antibodies against ABO or HLA antigens

Type II hypersensitivity reaction

162
Q

How is a hyperacute rejection managed?

A

Removal of kidney

163
Q

What are the causes of an acute rejection?

A

HLA mismatch

CMV infection

164
Q

How does an acute rejection present?

A

Usually asymptomatic

Picked up by rising creatinine, pyuria and proteinuria

165
Q

Why are patients with nephrotic syndrome predisposed to VTE?

A

Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis.

166
Q

What is the most common cause of peritionis secondary to peritoneal dialysis?

A

S.epidermis

167
Q

What are the causes of a raised anion gap?

A

lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use

168
Q

What are the causes of a normal anion gap metabolic acidosis?

A 
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison's disease

FINALS (26 decks)

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