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Biochemical DDx Flashcards

1
Q

normal level of urea

A

2.5–6.6 mmol/L

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2
Q

INCREASED BUN

A 
• Renal failure (acute and chronic)
• Dehydration
• Shock
• Congestive cardiac failure
• Gastrointestinal haemorrhage (digested blood increases
blood urea)
• Excessive protein intake
• Excessive protein catabolism
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3
Q

DECREASED BUN

A
  • Malnutrition
  • Liver failure
  • Overhydration, e.g. prolonged i.v. fluids
  • Pregnancy (increased plasma volume)
  • Impaired protein absorption
  • SIADH
  • Anabolic steroid use
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4
Q

BUN Sx

A

Signs of uraemia, e.g. oliguria, anuria, fatigue, confusion, thirst,
bronze colour of skin, oedema (peripheral and pulmonary), uraemic
frost (rare).
Signs of dehydration, e.g. dry skin, loss of skin turgor.
Signs of congestive cardiac failure, e.g. oedema, JVP . GI
haemorrhage, e.g. tachycardia, hypotension, haematemesis and
melaena. Decreased intake, e.g. oedema, ascites.
Signs of liver failure. SIADH, e.g. head injury, small cell lung
cancer.

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5
Q

BUN Dx

A 
INVESTIGATIONS
■■ UEs
■■ Creatinine
■■ FBC
■■ LFTs
■■ MSU
■■ CXR
■■ Urine electrolytes
■■ Urine osmolality
■■ US
■■ MAG 3 scan
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6
Q

A grossly raised BUN in association with metabolic
acidosis, hyperkalaemia, fluid overload and clinical
symptoms, e.g. coma, pericarditis, is an indication for

A

urgent haemodialysis

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7
Q

Hypercalcaemia is above

A

2.62 mmol/L

Sx @ 3.5

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8
Q

Hypercalcaemia CAUSES

A

• Malignancy
• Solid tumour with lytic bony metastases, e.g. Ca breast,
bronchus
• Solid tumours with humoral mediation, e.g. inappropriate
PTH secretion with carcinoma of the bronchus, carcinoma
of the kidney
• Multiple myeloma
• Hyperparathyroidism (primary, secondary, tertiary)
• Sarcoidosis
• Drugs, e.g. thiazide diuretics, lithium
• Excess intake of vitamin A, vitamin D or calcium
• Prolonged immobilisation
• Milk-alkali syndrome (excess calcium intake)
• Hyperthyroidism
• Addison’s disease
• Paget’s disease of bone
• Familial hypocalciuric hypercalcaemia

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9
Q

hypercalcaemia Sx

A

nausea and vomiting, fatigue,
depression, confusion, psychosis; abdominal pain, constipation,
acute pancreatitis, peptic ulceration, polyuria/nocturia, haematuria,
renal colic, renal failure, bone pain, hypertension and arrhythmias.

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10
Q

hypercalcaemia +

hyperparathyroidism Sx

A

stones, bones, abdominal groans and

psychiatric overtones

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11
Q

hypercalcaemia Dx

A 
■■ Fasting calcium and phosphate
Ca increased PO4 decreased.
■■ U&Es
I creatinine I urea. Renal failure
■■ PTH levels
I hyperparathyroidism.
■■ Protein electrophoresis and Bence Jones protein
Multiple myeloma.
■■ ECG
Short QT interval. Widened T waves.
■■ Serum amylase
I in acute pancreatitis associated with hyperparathyroidism.
■■ AXR
Stones. Nephrocalcinosis.
■■ US
Renal stones. Carcinoma of the kidney (inappropriate PTH
secretion). Parathyroid lesions.
■■ Skull X-ray
Myeloma. Abnormal sella turcica in MEN associated pituitary
tumour. Paget’s disease of bone.
■■ Sestamibi scan
Hyperparathyroidism.
■■ 24-hour urinary calcium excretion
 calcium excretion in hyperparathyroidism (calcium-restricted
diets).
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12
Q 
with depression or psychosis
OR
presenting with polyuria, if diabetes has
been excluded 
always
check the
A

serum calcium. Hyperparathyroidism may

be a cause.

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13
Q

Hyperglycaemia

A

plasma glucose >7.0 mmol/L

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14
Q

Hyperglycaemia causes

A 
ENDOCRINE
• Diabetes mellitus (types 1 and 2)
SYSTEMIC DISEASE
• Cushing’s syndrome
SEVERE STRESS
• Stroke
• Myocardial infarction
PSYCHOGENIC
• Bulimia nervosa
PHYSIOLOGICAL
• Infection
• Inflammation
OTHER
• Pregnancy
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15
Q

DRUGS causing Hyperglycaemia

A
  • Corticosteroids
  • Beta blockers
  • Thiazide diuretics
  • Niacin
  • Pentamidine
  • Protease inhibitors
  • l-asparaginase
  • Antipsychotic agents
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16
Q

Hyperglycaemia Sx

A

polydipsia, polyuria,
polyphagia, fatigue, weight loss and blurred vision

Acute DKA
hyperventilation, stupor or coma
Recurrent infections

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17
Q

Hyperglycaemia

INVESTIGATIONS

A 
■■ BM stix
■■ Blood glucose
■■ Urinalysis
■■ Oral glucose tolerance test
■■ U&Es
■■ FBC
■■ bHCG
■■ HbA1c
■■ ABGs
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18
Q

Hyperkalaemia is above

A

5.0 mmol/L

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19
Q

Hyperkalaemia CAUSES

A

• Excess administration of potassium, especially rapidly
• Renal failure
• Haemolysis
• Massive blood transfusion
• Crush injuries (rhabdomyolysis)
• Tissue necrosis, e.g. burns, ischaemia
• Metabolic acidosis
• Adrenal insufficiency (Addison’s disease)
• Drugs interfering with urinary excretion: ACE inhibitors
and angiotensin receptor blockers, potassium-sparing
diuretics (spironolactone and amiloride), NSAIDs (ibuprofen,
naproxen), calcineurin inhibitors for immunosuppression
(ciclosporin and tacrolimus), trimethoprim, pentamidine

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20
Q

Hyperkalaemia Sx

A

Cardiac arrest
Mild breathlessness (hyperkalaemia associated with
metabolic acidosis). Paraesthesiae, areflexia. Weakness.
Palpitations.
Abdominal pain. Hypoglycaemia. Hyperpigmentation associated with Addison’s disease.

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21
Q

Hyperkalaemia Dx

A 
U+Es
FBC
ABGs
Blood Glucose
ECG
Cr
Plasma cortisol
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22
Q

Hypokalaemia =

A

3.5 mmol/L

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23
Q

Hypokalaemia two big causes

A

INADEQUATE INTAKE
• Potassium-free i.v. fluids
• Reduced oral intake, e.g. coma, dysphagia

EXCESSIVE LOSS
Renal
• Diuretics
• Renal tubular disorders
Gastrointestinal
• Diarrhoea
• Vomiting
• Fistulas
• Laxatives
• Villous adenoma
Endocrine
• Cushing’s syndrome
• Steroid therapy
• Hyperaldosteronism
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24
Q

Hypokalaemia Sx

A

Muscle weakness. Myalgia. Constipation. Paralytic ileus. Cardiac arrhythmia (ranging from ectopics to serious arrhythmias with
sudden death at very low levels of potassium)

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25
Q

Hypokalaemia Dx

A 
U+Es
ABG
ECG 
Flattened T waves. ST depression. U waves. Prolonged QT
intervals.
Serum Mg
Plasma aldosterone, renin, cortisol
urinary free cortisol
ACTH levels
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26
Q

• In a patient with prolonged ileus post-operatively
or
In a patient presenting with unexplained lethargy,
fatigue and muscle weakness

A

serum potassium

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27
Q

normal serum sodium level

Hypernatraemia

A

135–145 mmol/L

> 145 mmol/L.

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28
Q

Hypernatraemia CAUSES

A

DECREASED WATER INTAKE
NON-RENAL WATER LOSSES
RENAL WATER LOSSES
SODIUM EXCESS

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29
Q

Hypernatraemia CAUSES

DECREASED WATER INTAKE

A
  • Confusion

* Coma

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30
Q

Hypernatraemia CAUSES

NON-RENAL WATER LOSSES

A
  • Gastrointestinal losses (e.g. vomiting, diarrhoea)
  • Pyrexia
  • Burns
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31
Q

Hypernatraemia CAUSES

RENAL WATER LOSSES

A
  • Osmotic diuresis
  • Hyperglycaemia
  • Nephrogenic diabetes insipidus
  • Drugs (e.g. lithium)
  • Bence Jones proteins
  • Post-relief of obstructive uropathy
  • Recovering acute tubular necrosis
  • Congenital diabetes insipidus
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32
Q

Hypernatraemia CAUSES

SODIUM EXCESS

A
  • Excessive intravenous sodium therapy
  • Chronic congestive cardiac failure
  • Cirrhosis of the liver
  • Steroid therapy
  • Cushing’s syndrome
  • Primary hyperaldosteronism (Conn’s syndrome)
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33
Q

Hypernatraemia Sx

A

Thirst 3–4 mmol/L
above upper limit of normal

coma, seizures, muscular tremor and rigidity above
158 mmol/L.

34
Q

Hypernatraemia Dx

A

■■ U&Es
Na+ 150–170 mEq/L usually indicates dehydration. Na+ >170 mEq/L
usually indicates diabetes insipidus. Na+ >190 mEq/L usually
indicates long-term salt ingestion.
■■ Urine osmolality
Central versus nephrogenic diabetes insipidus.
■■ CT head
Central diabetes insipidus, e.g. cerebral tumour/trauma.

35
Q

BEWARE in Hypernatraemia

A

Rapid correction of hypernatraemia can lead to
cerebral oedema.

Lack of thirst is associated with CNS disease.

36
Q

normal serum sodium level

Hyponatraemia

Severe hyponatremia

A

135–145 mmol/L

less than 135 mmol/L

less than 120 mmol/L

37
Q

Hyponatraemia 3 types of causes

A

hypovolemic
euvolemic
oedematous

38
Q

Hyponatraemia hypovolemic causes

A 
Gastrointestinal losses
• Diarrhoea
• Vomiting
• Fistula
• Small bowel obstruction
• Paralytic ileus

Renal sodium losses
• Diuretics
• Osmotic diuresis (e.g. hyperglycaemia)
• Renal failure

Other sodium losses
• Burns
• Ascites
• Crush injuries
• Peritonitis
39
Q

Hyponatraemia euvolemic causes

A

Endocrine
• Severe hypothyroidism
• Addison’s disease

Water load
• Intravenous infusions
• Water drinking
• TURP (transurethral resection of prostate) syndrome

SIADH
• Pulmonary disease (e.g. pneumonia, lung cancer)
• Drugs (e.g. carbamazepine)
• Intracranial disease (e.g. tumour, head injuries)

40
Q

Hyponatraemia oedematous causes

A
  • Cardiac failure

* Nephrotic syndrome

41
Q

Hyponatraemia Sx

A 
asymptomatic 
mild nausea
vomiting
headache
malaise 
diminished reflexes
seizures
stupor 
coma
42
Q

Hyponatraemia Dx

A

U+Es
Paired serum and urine osmolality
Paired serum and urinary sodium

43
Q

SIADH is suggested by

A

inappropriately concentrated urine (>100 mOsm/kg)

serum hypo-osmolality (<270 mOsm/kg).

inappropriately concentrated urinary sodium (>20 mmol/L).

44
Q

Hyponatraemia BEWARE

A

Falsely low sodium values can occur with high
circulating levels of lipids, proteins and in severe
hyperglycaemia.

Most patients with hyponatraemia do not require
treatment with intravenous sodium chloride, but,
if this is required, the rate of correction of serum
sodium levels must be carried out with great care to
minimise the risk of central pontine demyelination.

45
Q

Hypoglycaemia plasma glucose

A

<2.5 mmol/L

46
Q

Hypoglycaemia CAUSES

A 
DRUGS
• Insulin
• Sulfonylurea
• Alcohol
• Aminoglutethimide
• Quinolones
• Pentamidine
• Quinine

ENDOCRINE
• Pituitary insufficiency
• Addison’s disease

NEOPLASTIC
• Pancreatic islet cell tumours; insulinoma
• Non-pancreatic tumours; retroperitoneal fibrosarcoma,
haemangiopericytoma

LIVER DISEASE
• Inherited glycogen storage disorders
• Cirrhosis
• Acute liver failure
• Alcohol

OTHER
• Post-prandial dumping syndrome (post-gastrectomy, postvagotomy
and drainage)
• Immune mediated (e.g. anti-insulin receptor antibodies in
Hodgkin’s disease)

47
Q

Hypoglycaemia Sx

A 
sweatiness
palpitations
weakness
hunger
drowsiness
restlessness
tremor
seizures 
coma
personality changes
48
Q

Diagnosis of insulinoma

A 
Whipple’s triad: 
(1) attacks precipitated by fasting
(2) blood sugar is low during the attack
(3) symptoms are relieved
by administration of glucose
49
Q

Hypoglycaemia

A 
BM stix
BG
LFTs
Tox screen
U+Es
Insulin + C peptide levels
Pituitary hormone levels
Prolonged oral glucose tolerance test
IV Insulin suppression test
Arterial stimulation with venous sampling
CT MRI
50
Q

Hypocalcaemia =

A

serum calcium of <2.0 mmol/L ionised fraction <0.8 mmol/L.

51
Q

Hypocalcaemia CAUSES

A 
ASSOCIATED WITH HIGH SERUM PHOSPHATE
• Renal failure
• Hypoparathyroidism
• Rhabdomyolysis
• Phosphate therapy

ASSOCIATED WITH LOW OR NORMAL SERUM PHOSPHATE
• Hypomagnesaemia
• Acute pancreatitis
• Critical illness including sepsis, burns
• Osteomalacia
• Overhydration

MASSIVE BLOOD TRANSFUSION DUE TO CITRATE-BINDING

HYPERVENTILATION WITH RESPIRATORY ALKALOSIS AND
REDUCTION IN IONISED PLASMA CALCIUM

DRUGS
• Bisphosphonates
• Calcitonin

52
Q

Hypocalcaemia Sx

A

Circumoral paraesthesia
peripheral tingling and paraesthesia
cramp
tetany (carpo-pedal spasm) hypotension
hyperactive
tendon reflexes
Chvostek’s sign (tapping over the facial nerve causes facial spasm)
Trousseau’s sign (inflating blood pressure cuff
to above systolic pressure causes carpal spasm), laryngospasm (lifethreatening),
cardiac arrhythmias
dystonia and psychosis

53
Q

Hypocalcaemia Dx

A 
Serum Ca P
U+E
ABG
Serum amylase
Serum Mg
PTH
Serum Vit D
ECG
54
Q

The first symptom of hypocalcaemia is

A

circumoral paraesthesia

If this occurs after thyroid or
parathyroid surgery, it is an indication for an
urgent check of the serum calcium and appropriate
treatment.

55
Q

normal range of serum magnesium

Hypomagnesaemia
serum level below

A
  1. 7–1.0 mmol/L

0. 7 mmol/L

56
Q

Hypomagnesaemia CAUSES

EXCESSIVE LOSSES
or
INADEQUATE INTAKE

A 
EXCESSIVE LOSSES
• Diuretics
• Severe diarrhoea
• Prolonged vomiting
• Polyuria (poorly controlled diabetes)
• Prolonged and excessive nasogastric aspiration
INADEQUATE INTAKE
• Starvation
• Alcoholism
• Malabsorption syndrome
• Parenteral nutrition
57
Q

Hypomagnesaemia Sx

A 
muscle weakness
lethargy
irritability
confusion
seizures 
arrhythmias
58
Q

Hypomagnesaemia Dx

A

Serum magnesium
U+Es
Serum Ca

59
Q

If symptoms related to hypocalcaemia and
hypokalaemia are resistant to calcium and potassium
supplements, respectively, remember to check

A

serum magnesium level

60
Q

Metabolic acidosis is caused by increased production of hydrogen ions from metabolic causes or from excessive bicarbonate loss (pH decreased, HCO3- decreased)

Compensatory mechanisms are

A
  • decreased pCO2 by hyperventilation

* decreased H+ by kidneys (unless in renal failure)

61
Q

Metabolic acidosis causes

A 
EXCESSIVE PRODUCTION OF H+
• Diabetic ketoacidosis
• Lactic acidosis secondary to hypoxia, e.g. shock, ischaemic gut
• Septicaemia
• Starvation
• Drugs, e.g. ethanol, salicylates

DECREASED H+ EXCRETION
• Renal failure

EXCESSIVE LOSS OF BASE
• Diarrhoea
• Fistula – pancreatic, intestinal or biliary

EXCESSIVE INTAKE OF ACID
• Parenteral nutrition

62
Q

Metabolic acidosis Sx

A 
chest pain
palpitations
headache
nausea
vomiting
abdominal pain
weight loss
Kussmaul respirations DKA
Extreme acidosis 
lethargy
stupor
coma
seizures
arrhythmias
ventricular tachycardia
63
Q

Metabolic acidosis Dx

A 
ABGs
FBC
U+Es
BG
Serum salicylate
64
Q

Anion gap = ( [Na+] + [K+] ) – ( [Cl–] + [HCO–3] )

normally about 8–16 mmol/L.

Increased anion gap >16 mmol/L causes

A 
■■ Lactic acidosis.
■■ Ketoacidosis.
■■ Chronic renal failure.
■■ Intoxication, e.g. salicylate, ethanol, ethylene glycol, metformin.
■■ Massive rhabdomyolysis
65
Q

Rapidly increasing metabolic acidosis over minutes

or hours is not due to renal failure.

A

Severe sepsis
tissue hypoperfusion
tissue necrosis

66
Q

Rapidly increasing metabolic acidosis over minutes

or hours is not due to renal failure.

A

Severe sepsis
tissue hypoperfusion
tissue necrosis

67
Q

Metabolic alkalosis is caused by an increase in HCO–
3 or decrease in
H+ (increased pH, increased HCO–3).

Compensatory mechanisms are:

A

• increased pCO2 by hypoventilation (limited by hypoxia)
• decreased HCO–
3 by kidneys.

68
Q

Metabolic Alkalosis causes

A 
EXCESS LOSS OF H+
• Vomiting
• Nasogastric aspiration
• Gastric fistula
• Diuretic therapy (thiazide or loop)
• Cushing’s syndrome (mineralocorticoid effect)
• Conn’s syndrome (mineralocorticoid excess)
EXCESSIVE INTAKE OF BASE
• Antacids, e.g. milk-alkali syndrome
• Ingestion of HCO–
3 (usually iatrogenic)
69
Q

Metabolic Alkalosis Sx

A

ASx

hypoventilate

70
Q

Metabolic Alkalosis Dx

A

blood gases
U+Es
Plasma cortisol
Plasma aldosterone

71
Q

Metabolic alkalosis will cause a left shift of the

A

oxyhaemoglobin curve, reducing oxygen availability

to the tissues

72
Q 
Respiratory acidosis is caused by CO2 retention due to inadequate
pulmonary ventilation (decreased pH, increased pCo2).

Compensatory mechanisms

A

• increased HCO–
3 by bicarbonate buffer system
• decreased H+ by kidneys (can take several days)

73
Q

Respiratory acidosis CAUSES (any cause of hypoventilation)

A 
CNS Depression
Neuromuscular disease
Skeletal disease
Artificial ventilation (uncontrolled and
unmonitored)
Impaired gaseous exchange
74
Q

Respiratory acidosis CAUSES detailed

A 
CNS Depression
• Head injury
• Drugs, e.g. opiates, anaesthetics
• Coma
• Stroke
• Encephalitis

Neuromuscular disease
• Myasthenia gravis
• Guillain–Barré syndrome

Skeletal disease
• Kyphoscoliosis
• Ankylosing spondylitis
• Flail chest

Artificial ventilation (uncontrolled and
unmonitored)

Impaired gaseous exchange
• Chronic obstructive pulmonary disease
• Alveolar disease, e.g. pneumonia, ARDS (acute respiratory
distress syndrome)
• Thoracic injury, e.g. pulmonary contusions

75
Q

Respiratory acidosis Sx

A 
anxiety 
disorientation
confusion
lethargy 
somnolence
tachycardia 
bounding arterial pulse cyanosis and
hypotension
76
Q

Respiratory acidosis Dx

A 
■■ ABGs
pH <7.35.
pCo2 >5.8 kPa.
 HCO–
3.
■■ CXR
Underlying pulmonary disease.
■■ Pulmonary function tests
COPD which usually manifests as an obstructive defect (FEV1 ,
FVC normal). Skeletal disease (reduced chest movement).
■■ EMG and nerve conduction studies
Myasthenia gravis and Guillain–Barré syndrome.
■■ CT/MRI head
Central (brain stem) lesion.
77
Q

Beware in Respiratory acidosis

A

! • Exercise caution when correcting chronic
hypercapnia. Rapid correction of hypercapnia can
alkalinise the CSF causing seizures.
• Associated hypoxaemia secondary to
hypoventilation is the major threat to life and must
be reversed rapidly.

78
Q

Respiratory alkalosis is a common disorder in critically ill patients.
It occurs when carbon dioxide is lost via excessive pulmonary
ventilation (increased pH, decreased PCO2). Compensatory mechanisms are:

A

• Decreased HCO–
3 by bicarbonate buffer system
• Increased H+ by kidneys (slow process – may take several days).

79
Q

Respiratory alkalosis CAUSES (any cause of hyperventilation)

A 
CENTRAL NERVOUS SYSTEM
• Pyrexia
• Pain
• Anxiety
• Hysteria
• Head injury
• Stroke
• Encephalitis
RESPIRATORY DISORDERS
• Pneumonia
• Pulmonary oedema
• Pulmonary embolus
PHYSIOLOGICAL
• Pregnancy
• High altitude
• Severe anaemia
DRUGS
• Salicylates
OTHER CAUSES
• Sepsis
• Mechanical ventilation
• Metabolic acidosis (overcompensation)
80
Q

Respiratory alkalosis Sx

A

light headedness
circumoral paraesthesia
dizziness and numbness of the hands and feet

Acute development
of low carbon dioxide levels can occasionally cause cerebral
vasoconstriction leading to confusion, syncope, fits.

81
Q

Respiratory alkalosis Dx

A 
■■ ABGs
pH >7.45.
Pco2 <4.4 kPa.
Decreased HCO–
3 (compensatory mechanism due to bicarbonate buffer
system).
■■ Serum calcium
Decreased Ca2+ (due to increased calcium binding to serum albumin).
■■ Serum salicylate level
If overdose is suspected.
■■ CT/MRI head
Intracranial lesion as a cause of hyperventilation.
82
Q

Prolonged artificial ventilation with inadequate

monitoring should be remembered as a cause of

A

respiratory alkalosis.

DDx (3 decks)

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