The most

commonly ordered
(chemistry)
laboratory
investigations

Deborah Hillman White, 4th year student, PMS

Doctors as Teachers SSU 2007
Day 1
 Course objectives
• To provide participants with the knowledge required to:
– Run the appropriate tests
– Select the correct boxes and blood bottles
– Facilitate diagnosis
– Understand why electrolyte imbalances lead to body s/s
– Know the key s/s associated with derangements
– Understand treatment principles
– Comprehend test limitations
Investigations covered in this course

1. Sodium 9. Amylase
2. Potassium 10. T. Proteins
(= albumin + globulin)
3. Calcium 11. ALT
4. Magnesium12. AST
5. Phosphate 13. ALP
6. Chloride 14. T. Bilirubin
7. Creatinine 15. gGT
8. Urea
 Fun, fun, fun exercise no. 1
It’s your first day of F1 on EMU…and you’ve got the
job assisting the ward monkey. During the morning
round, they request that you “take bloods from bed 3,
fill-out ‘the form’ and send it to the lab in the pod – do
FBC, U&Es and a bone study”.

1. What boxes are you going to tick?

2. Exactly what electrolytes are you testing when you test for
U&Es?
3. What tests are conducted as part of a ‘bone study’?
4. (Additionally) What is tested when you mark the box entitled,
‘renal’?
5. What is tested when you mark the box entitled, ‘Liver’
 Punxsutawney Phil says
• Order only when necessary
• Interpret results within context
• Repeat deranged tests if
possible
• COMPLETELY fill it in
• Confine the alphabet to the
boxes
• Use a new form if you make a
mistake
Sodium (Na)
 Na – source, storage, functions
• Source: diet
• Storage: most abundant EC cation
• Functions:
1.Primary determinant of extracellular
volume
2.Key solute influencing the osmotic
pressure of the interstitial fluid
3. Nerve and muscle function
 Na - regulation
• Two mechanisms involved
– ECF volume (& BP) – kidneys (RAA) / ANP
– Plasma osmolality – vasopressin
• Plasma Na not closely correlated to Na
excretion
– Think of two separate systems
1. volume control
2. osmoregulation
– Sometimes, both systems activated (SIADH)
 High Low
Volume / ANP released 1. Baroreceptors
–increases GFR activate
pressure and Na filtration catecholamines.
(factors: circ. vol. –deactivates
2. JGA activates
RAA system
& resistance) RAA cascade

Osmoregulation Osmolality Dec. vasopressin =

sensed by dec. water
osmoreceptors reabsorption =
– thirst dilute urine
–vasopressin
 Na – clinical scenario examples
Volume/pressure Water / osmoregulation
regulators
Scenario RAA ANP V.pressin Thirst Result
Admin. - - -  Excretion of Na load
isotonic
saline
↑ in appropriate
amount of iso-
osmotic urine
Ingestion of  Excretion of
salty
nuts (!)
↓ ↑ ↑ ↑ concentrated urine
(both systems
activated)
SIADH  Excretion of
↓ ↑ ↑ ↓ concentrated urine in
presence of relative
hyponatraemia
 Na – signs and symptoms
High Low
Fatigue, weakness, Fatigue, weakness,
headache, headache, nausea
nausea
When it’s serious:
When it’s serious: confusion,
confusion, coma,
coma, convulsions,
convulsions, death
death+ muscle
twitching
 Causes of hypernatraemia

High intake /  Administration of hypertonic solutions

production or drugs (e.g. saline)

Reduced  Primary aldosteronism

excretion  Renal failure
 Drugs – NSAIDs, mineralcorticoids
Other  Impaired thirst / conscious state
 Diabetes insipid us
 Water loss: burns, vomit, diarrhoea etc.
 Osmotic diuresis – e.g. DKA
 Causes of hyponatraemia
Is the patient dehydrated?

Yes No

Is the urinary Na Is the patient oedematous

>20mmol/L?
No Yes
Yes No •Nephrotic
Is urine osmolality
(i.e. kidney (i.e. extrarenal syndrome
loss) loss) >500 mmol/kg?
•Cardiac
•Addisons •D&V failure
Yes No
•Diuretics •Burns •Cirrhosis
•SIADH •Water
•Osmotic •Obstruction overload •Renal
diuresis failure
•Trauma – •Glucocortic
post -op oid
•Heat insufficiency

•CF •Severe
hypothyroidi
sm
 Treatment
Hypernatraemia –
• Tx underlying disease
• H2O, dextrose 5% IVI
• Sometimes 0.9% recommended, as hypotonic in a hypernatraemic
patient (less marked fluid shifts)
• Also vasopressin analogues sometime given.

Hyponatraemia –
• Tx underlying disease (Don’t use plasma Na as guide)
• In hypervolaemic hyponatraemia emergencies - saline +/- a diuretic
(e.g. furosemide). Treat SLOWLY (1-2 mmol/L/hour). Caution:
central pontine myelinolysis.
• Patients with vomiting / severe volume depletion - intravenous
normal saline with K supplements
• SIADH - fluid restrict
Na – summary points
Potassium (K)
 K – source, storage, functions
• Source: diet
• Storage: most intracellular cation
• Functions:
– Key determinant of cell membrane potential
• Fundamental for normal nerve and muscle function
• Important role in kidney function
• Essential for protein and nucleic acid synthesis
• Converts glucose into glycogen (muscle fuel)
• Needed to maintain acid/alkali balance
 K - regulation
• Aldosterone – affects two sites involved in
K homeostasis:
– Kidney
– GI tract
• Affected by acid base balance,
catecholamines and insulin
 K – signs and symptoms
High Low
Cardiac excitability Cardiac
rapid HR, VF, excitability
arrhythmias, arrhythmias,
ECG changes decreased cardiac
contractility
Muscle function
hypotonia,
lethargy, muscle
weakness,
cramps
 Causes of hyperkalaemia

High intake /  Blood transfusions

production  LoSalt

Reduced  Renal failure

excretion  Drugs – diuretics, ACEi
 Aldosterone deficiency / Addisons
Redistribution  Hormones
 Acidosis
 Cell death – burns, chemotherapy
Other  Artefact - venepuncture technique
 Physiological – pregnancy, standing,
AM
 Causes of hypokalaemia
Low intake /  Hypokalaemic IV therapy
production  Ileus
 Intestinal obstruction
 Anorexia
Increased  Drugs – diuretics, purgatives
excretion  Aldosterone 2 o
to CCF, liver failure
 Endocrine problems: Cushings, Conns
 D&V
Redistribution  Hormones – insulin, cortisol
 B adrenergic stimulation – B2 agonist
nebs
 Metabolic alkalosis
 Treatment
Hyperkalaemia –
• Emergency treatment (ECG changes present)
1. Protect myocardium
– 10ml calcium gluconate 10%
2. Drive K into cells
– 10 –20 units insulin + 50mls 50% dextrose IV (repeat as necessary)
– Nebulised salbutamol 2.5mg
3. (If appropriate) correct acidosis (ph <6.9)
– Sodium bicarbonate
4. Deplete body K (After emergency treatment)
– Polystyrene sulphonate resin 15g orally 3/day with laxatives or 30g
rectally followed after 3-6 hours with an enema5.
5. Renal replacement therapy if required

Hypokalaemia –
• Treat underlying disease
• If mild, increase dietary intake (fruit, vegetables) or oral K supplements
• If severe, give IV K cautiously
K – summary points
 Fun, fun, fun exercise no. 2
It’s now 10 minutes into the first day of
F1 on EMU…and the SHO has been
bleeped just as they were finishing-off
writing out a pathology request form.
They ask you to take “take bloods from
side room 5 for the requests that are on
the form”. You see the following boxes
have been marked: renal, liver, coag
screen, glucose.

1. How many blood bottles do you need?

2. What colour are they?
Calcium (Ca)
 Ca – source, storage, functions
• Source: diet
• Storage: Skeleton, teeth (99%), intracellular, ECF
• Transport: Bound to plasma proteins and PO. Free
portion regulated.
• Functions:
– Neuromuscular excitability
– Excitation-contraction coupling- cardiac / smooth muscle
– Stimulus-secretion coupling
– Maintenance of tight cell junctions
– Blood clotting
– Structural / functional integrity of bones, teeth etc.
 Ca – signs and symptoms
High Low
Neuromuscular Neuromuscular
excitability excitability
– Tetany (Chvosek’s)
– NM depression – Muscle cramps/spasms
– Arrythmias (Trousseau’s)
– Asphyxiation
Excitation-contraction
– High BP Excitation-contraction
– ECG changes
– Cardiac arrest
Bone/teeth integrity
Other – Short stature
– Bones, stones, abdo – Short metacarpals
groans, and psychic
moans
– Polyuria / polydipsia
 Ca - regulation
• Inverse relationship with P activates
regulatory mechanisms
• To increase Ca
1. PTH – bones, kidneys
2. Calcitriol (activated vitamin D) – GI tract, bones
• To decrease Ca
1. Calcitonin
 Low plasma Ca

Note: low vitamin D also

Parathyroid glands stimulates PTH release

Increased PTH

Bone
Kidneys

Increased activation of
vitamin D Increases responsiveness of
bone to PTH

Intestine
Increased Ca resorbed
Increased Ca absorption from bone
Increased Ca
reabsorption

Increased
plasma Ca
 Causes of hypercalcaemia

High intake /  10 HyperPTH

production  Malignancy

Reduced  Sarcoidosis / granulomatous diseases

excretion  Familial hypocalciuric hypercalcaemia

Other  Paget’s disease

 Addison’s
 Drugs – lithium, antacids
 Hypercalcaemia

Albumin raised Albumin normal/low

P low/norm P high/norm
Urea Urea
raised normal
Urea normal
•Dehydration •Cuffed
specimen •10/tertiary hyperPTH

ALP high ALP normal

•Bone mets •Myeloma
•Sarcoid •Vit D excess
•Hyperthyroid •Sarcoid
 Causes of hypocalcaemia
Low intake /  HypoPTH / pseudo / pseudopseudo
production  Vitamin D deficiency
 Hypomagnaesia
Redistribution  Osteomalacia
 Pancreatitis
 Hypoalbuminaemia
Other  Chronic kidney disease
 Thyroid surgery
 Respiratory alkalosis
 Drugs, frusemide, bisphosphonates
 Treatment
Hypercalcaemia –
• Treat underlying disease
• Rehydration – saline
• Diuretics
• Bisphosphonate - pamidronate

Hypocalcaemia –
• Treat underlying disease
• Calcium +/- phosphate binders
• Others = vitamin D
Ca – summary points
Phosphate (PO43-)
 PO source, storage, functions
4
3-

• Source: diet: meat and milk!

• Storage: Bone, intracellular (10%), extracellular
(1%)
• Transport: Bound to plasma proteins
• Functions:
– In bone, cell membranes, nucleic acids, 2,3-DPG, ATP
– (Involved in) excretion of H in the kidney
– High energy intracellular enzymatic functions
– Main intracellular buffer – buffers CO2
– In coagulation / immune systems cascades
 PO regulation
4
3-

• Inverse relationship with Ca

activates regulatory mechanisms
– PO increased via
• Calcitriol action in GI tract
– PO decreased by
• PTH release
 Low plasma P

Increased plasma Ca Kidneys

Calcitriol

Decreased PTH

Increased P
reab. From Decreased C
kidneys reab. From
kidneys
Increased intestinal Ca
Increased absorption
urinary Ca loss
Decreased
urinary P loss No change in plasma Ca Increased intestinal P
absorption

Increased
plasma P
 PO43- signs and symptoms
High Low

Symptoms of low Symptoms of high

Ca Ca
Component bone, Component bone,
cells, 2,3-DPG etc. cells, 2,3-DPG etc.
– High BP – Encephalopathy
– Bone pain – Hallucinations
– Arrhythmias
– Muscle weakness
– Bone pain
 Causes of hyperphosphataemia
High intake /  Enemas / laxatives
production  TPN
 Vitamin D excess
Reduced  CKD
excretion  HypoPTH
 Hypomagnaesia
 Drugs - bisphosphonates
Redistribution  Cellular insult – trauma, burns,
exercise, chemotherapy
 Acidosis
Other  Acromegaly
 Thyrotoxicosis
 Causes of hypophosphataemia
Low intake /  Poor diet
production  Malabsorption - Crohns

Increased  10 HyperPTH
excretion  Antacids

Redistribution  Alkalosis
 Refeeding syndrome
 Catecholamines
 Insulin
Other  Steroids
 Alcoholism
 Treatment
Hyperphosphataemia –
• Dietary restriction
• Phosphate binders – e.g. Ca carbonate
• Enhance excretion via dehydration with saline
and diuresis with diuretic, e.g. furosomide
• If necessary, control, hyperparathyroidism –
vitamin D metabolites

Hypophosphataemia –
1. Treat underlying cause
2. Oral or in some circumstances, IV P
3. +/- vitamin
P – summary points
Magnesium (Mg2+)
 Mg source, storage, functions
2+

• Source: diet
• Storage: 2/3 bone, 1/3 intracellular, <1% plasma
• Transport: ionised, plasma proteins, anion complexes
• Functions:
– Numerous – Muscle / nerve activity, vasomotor
tone, cardiac excitability, catecholamine depressant
– Neuromuscular depression - CNS function
– K regulation - PTH release
– Coagulation
 Mg2+ signs and symptoms
High Low
Cardiovascular excitability Cardiovascular excitability
– Bradycardia (BP) – Arhythmias
– Heart block – Cardiac arrest
– Arrest Neuromuscular depression
Neuromuscular depression – Tetany
– Hyporeflexia – Paraesthesia
– Facial paraesthesia CNS function
CNS function – Fits
– Coma Coagulation
– Respiratory depression – Increased coagulation
and apnoea time
Coagulation
– Increased coagulation
time
 Mg regulation
2+

• Mg2+ derangements uncommon

• Relationship between Mg2+, Ca2+
and K
• Mg levels determined by:
1. Kidneys
2. PTH – kidney, intestine, bone
3. Insulin
 Causes of hypermagnaesia
High intake /  Iatrogenic
production  Drugs (esp. antacids)
 haemodialysis
Reduced  Renal failure
excretion  Drugs (lithium)
 Familial hypocalciuric hypercalcaemia
Other  Hypothyroidism
 Addisons Disease
 Depression
 Causes of hypomagnaesia
Low intake /  Reduced dietary intake (TPN)
production  Intestinal malabsorption
 Alcohol
Increased  Diarrhoea
excretion  Drugs (diuretics)

Redistribution  (Keto)acidosis
 Alkalosis
 Severe illness
Other  Endocrine disorders (hyperthyroidism,
Conn’s)
 Pancreatitis
 Alcoholism
 Treatment
Hypermagnaesia –
• Treat underlying cause
• Calcium gluconate
• Insulin

Hypomagnaesia –
1.Treat underlying cause
2.Magnesium salts PO or IV
Mg – summary points
Chloride
 Cl source, storage, functions
-

• Source: diet
• Storage: primarily extracellular
• Functions:
– Maintenance of serum osmolality (together with cations, Na and K)
and ECF volume
– Nerve conduction
– Key constituent of HCl (thus helps activate intrinsic factor)
– Regulation of carbon dioxide transport in erythrocytes and thus Ph
– Control of acid-base balance - Cl acts as buffer
• No specific symptoms associated with Cl derangements
(alkalosis = exception)
• Cl regulation is achieved by the kidneys
 Causes of hyperchloraemia

High intake /  Excessive ingestion of high salt diets

production (CCF patients)

Reduced  Kidney failure

excretion
 Causes of hypochloraemia

Low intake /  (Infants) chloride deficient

production formulas
Other • Water overload
• Wasting conditions
• Extensive body burns
• Systemic acidosis
 Case study 1
• XX man post operation. Received X ml/Ls
5% dextrose post operatively
• You are the SHO bleeped because he’s
collapsed in trying to get out of the bed to
go to the toilet. He’s nauseous, has a
headache and seems a little groggy
– What may be the problem?
– What may have caused it?
– How may it be avoided?
 Case study 2
• XX year old woman found on the floor by her
husband. She is confused, weak and reports that
she’s nauseous. In trawling through her notes,
you see she’s well known to the hospital given
her extensive psychiatric Hx, noting that four
months ago, she was diagnosed with lung
cancer.
• Her chemistry results show that she’s
hyponatraemic.
• What could be the cause?
• What test would you like to do next?
 Case study 2 continued
• Her test results show:
• Urine >500mosmol/kg (high)
• So what has she got?
 Case study 3
• You are asked to see a patient whom has been admitted on
the ward via GP referral after a series of very high Cr
results (>800mmol/L). He is known to the hospital and has
a long history gout.
• What may his condition be?
• What sort of imbalances would you expect in a patient with
this condition? (High or Low)
– Na -K
– Ca - Phosphate
– PTH - Hb
– Ph
Day 2
 Renal function tests
(Na, K, creatinine + urea for
completeness)
 Urea source, storage, functions
• Source: amino acids (AA)
– AAs catabolised to ammonium and then into urea in the
liver via the ornithine cycle
– Urea = major mechanism to eliminate ammonia
(extremely toxic)
– Urea is transported to the kidneys for excretion
• Function:
– Mechanism to eliminate ammonia
– Contributes to the renal countercurrent mechanism
– Used as a marker of GFR
 Urea signs and symptoms
High (uraemia)
• General: nausea, vomiting, fatigue,
anorexia, weight loss, muscle cramps,
thirst, uraemic fetor
• Neurological: encephalopathy, visual
disturbances
• Dermatological: pruritus, uraemic frost,
sallowness
• Cardiovascular: uraemic pericarditis
• +other renal failure signs/symptoms
• Uraemia can progress to death
 Urea regulation
• Urea level = amount of protein
catabolism – excretion by kidneys
• Uraemia = clinical syndrome resulting
from severe kidney dysfunction
 Causes of high urea

High intake / • High protein diet

production • GI bleeding, catabolism, sepsis,
surgery = a high protein ‘meal’
• Drugs- steroids
Reduced • Dehydration
excretion • Kidney failure (all causes)
• Drugs – tetracyclines, nephrotoxics
 Causes of low urea
Low intake / • Liver disease
production • Malnutrition / decreased protein
intake / prolonged IV
• Pregnancy
 Treatment
High urea –
• Treat underlying cause
• Example in metabolic disorders:
– 1.Dietary protein limitation
– 2.Increased ammonia secretion (levulose /
antibiotics)
– 3. Replacing missing urea cycle constituents
 Cr source, functions
• Source: by-product of muscle metabolism
• Function: marker of kidney function (GFR)
• Regulation:
– Kidney – freely filtered at glomerulus, only slightly re-
absorbed. Limited secretion.
– Steadily excreted compared to urea
• Decreased GFR = increased secretion
• ‘No muscle’ patients = ‘false’ low Cr reading despite low GFR
• No known symptoms associated with high Cr
 Causes of high Cr
High intake / • Diet
production • Race (Afro Caribbean
• Body-builders
• Drugs – steroids
• Muscle injury
Reduced • Renal failure
excretion • Drugs:
– trimethoprim, sulphamethoxazole etc.
Other • Drugs – interfere with assay for Cr
• Rheumatoid arthritis
 Causes of low Cr
Low intake / • increasing age - age-related
production decline in muscle mass
• females - reduced muscle mass
• malnutrition/ muscle wasting/
amputation - reduced muscle
mass ± reduced protein intake
• vegetarian diet - decrease in
creatinine generation
RFTs – summary points
Liver function tests (ALT, ALP,
bilirubin and albumin)

+ AST, gGT, total protein for

completeness
 LFT overview
• LFTs = more than the liver
Role:
• Screen, confirm diagnosis, construct differential diagnoses
• Indicate prognoses
• Monitor progress and response to therapy
Problems:
• Single liver tests not clinically useful
– Serious liver diseases can have normal levels
– ‘Benign’ situations can cause transitory derangements
– Many diseases similar LFT profile
 LFT parameters
• LFTs assess various aspects of the biliary
tract structure and function
Uptake, conjugation & Hepatocellular damage
excretion of anionic AST
compounds ALT
Serum total bilirubin Serum ferritin
Bile acids B12
Urinary bilirubin (also ALP
urobilinogin) GGT

Synthetic function
Serum albumin
Serum proteins
INR / APTT
 ALT/AST source, transport & function
Source:
• ALT
– cytosolic enzyme
– most specific to liver (also in kidneys, muscle, heart)
• AST
– mitochondrial enzyme (think high energy)
– in liver, heart, kidneys, muscle, brain, red cells and
pancreas
Transport:
• Released into blood when hepatocytes damaged
Function:
• ALT: role in processing of proteins
• AST: role in metabolism
 ALT/AST derangements
• ALT: levels may be misleading
– Normal/low levels in compensated
cirrhosis
– Raised by heavy drinking
• Generally:
– hepatocellular injury = very high
– Obstructive jaundice = mildly high
• ALT/AST ratio unreliable guide to
diagnosis
 Causes of ALT/AST derangements
• Liver - acute hepatitis, cirrhosis, neoplasia,
haemochromatosis, alcoholic liver disease
• Biliary duct pathologies – cholestasis
• Heart damage - MI, acute HF, myocarditis
• Myopathies – Duchenne muscular dystrophy,
polymyositis
• Kidney damage
• Shock
• Drugs – carbamazapine, paracetamol, heparin
etc.
 LFTs principles of management
• Additional lab tests if Hx and exam don’t
explain derangements
– (ALP / bilirubin should be part of the
initial lab evaluation)
– ferritin, hepatitis A, B, and C serology etc.
– Prothrombin time (PT) / albumin
– FBC
• Then treat underlying pathology
 ALP source and derangements
Source:
• Cannicular and sinusoidal membranes of the liver
• Tissue specific isoenzymes also found in bone, intestine,
placenta
High:
• Liver / biliary tract diseases - obstruction, malignancies
• Bone - Paget’s, bone metastases, endocrine abnormalities
• Intestine – Crohns, UC
• Placenta - pregnancy
• Other – Normal, drugs, Hodgkins, polymylagia rheumatica
 ALP principles of management
• Of limited value to differentiate liver
diseases; helpful to assess bone-related
• ALT hepatic or bony origin? (e.g. met
breast Ca)
– Other tests: GGT, bone scan, Liver USS
 gGT source, transport & function
Source:
• Microsomal enzyme in many tissues: liver, kidneys,
pancreas, intestine and prostate. In liver, found in
hepatocytes and biliary epithelial cells
Causes of derangements:
• GGT = unreliable marker
• Interpret gGT alongside other LFTs:
– Mild liver disease = ALT:AST >1 – anticipate raised gGT
– Extensive liver disease tends = ALT:AST <1 – gGT compatible
with alcohol damage
• If AST/ALT normal, gGT indicates alcohol intake
 gGT derangements
• Liver disease – cholestasis, hepatitis
• Alcohol
• Drugs – phenytoin, phenobarbitol and
other enzyme inducing drugs
• Pancreatitis
• Miscellaneous - MI, diabetes mellitus,
anorexia, Guillain Barre Syndrome,
hyprthyroidism, neurological disease
 Total plasma proteins source,
transport & function
Test:
• Total protein = albumin + globulin
Source:
• Mostly liver. Also production outside liver

Function:
• Proteins = building blocks of cells and tissues
• (Alb) Maintenance of blood colloid oncotic pressure:
therefore volume and distribution of ECF 
• (Alb) Transportation of thyroid, adrenocortical and
gonadal hormones
• (Globs) Antibodies, enzymes + other misc. proteins
• Anions – provide 15% of buffering capacity of blood
 Total protein derangements
High intake / • Raised immunoglobulins
production – Autoimmune conditions – RA,
SLE
– Genetic conditions
– Cancer – myeloma
• Drugs – anabolic steroids,
androgens, GH, insulin,
progesterone
Other  Dehydration
 Tourniquet left on
 Total protein derangements
Low intake /  Liver disease (cirrhosis)
production  Malabsorption syndromes – coeliac,
post bowel resection

Increased  Kidney disorders – diabetes,

excretion hypertension, glomerulonephridites
 GI Tract loss
 Burns / exudative skin disease
 Inflammatory states
 Diuretics
Other  Dilutional - Fluid retention, SIADH, IV
fluids
 Increased catabolism – injury, post op.
 Bilirubin – source, transport
• Source – pigment resulting from blood
breakdown
• Transport
– Unconjugated, insoluble bilirubin bound to
albumin
– Conjugated bilirubin ‘free’ – if raised, more
joins to albumin
Mature red cells
Iron/globin removed from haem

Reticuloendothelial system

Biliverdin
Bilirubin + glucoronic glucoronysl
transferase
acid
Bilirubin

Conjugated bilirubin

Albumin

Bile released

Stercobilin or
urobilinogen
 Hyperbilirubinaemia - causes
UNconjugated Conjugated
Excessive production Hepatocellular abnormalities
(unconjugated sometimes)
 Ineffective haemopoesis • Primary hepatocyte disease:
 Haemolytic disorders cirrhosis, hepatitis, malignancies,
drug reactions, iron overload
 Pregnancy
 Postoperative jaundice
Abnormal bilirubin Obstructive
metabolism (congenital)
 Enzyme system • Calculi
immaturity: newborn • Neoplasms
jaundice • Strictures
 Inherited defects: Gilbert’s • Atresia
Crigler-Najjar syndrome,
 Hyperbilirubinaemia – symptoms
• Jaundice
• Tiredness
• Abdominal pain
• Weight loss
• Vomiting
• Fever
• Itchy
• Dark urine
• Pale stools
 Amylase - source
• Source: pancreas (as distinct from salivary amylase)
• Functions:
– Carbohydrate digestion
– Differentiates acute pancreatitis from other causes of the
acute abdomen (unreliable)
>400 U/L
• Acute pancreatitis: rises quickly, returns to normal in ~ 4
days
<400 U/L
• Acute peritonitis: elevates amylase. Usually not above
400 U/L.
• Chronic pancreatitis does not raise amylase. Acute on
chronic exacerbation may
 Hyperamylasaemia
GI  Acute pancreatitis – also pancreatic pseudocysts,
abscesses,pancreatic trauma
 Peritonitis
 AAA
 Acute mesenteric infarctions
 Perforated duodenal ulcers
 Intestinal obstructions
 Acute appendicitis
 Liver metastases, also biliary tract diseases
Other  Malignancies - Ovarian / Prostatic, Lung
 Renal failure
 CCF
 Alcohol
 DKA
 Drugs – optiates, azathioprine etc.
 Septicaemia
LFTs – summary points
 Great resources
• World Anaesthesia online – great stuff on
physiology,
http://www.nda.ox.ac.uk/wfsa/index.htm
• Ye olde OHCM ‘clinical chemistry’ section