lab general

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. Sodium2. Potassium3. Calcium4. Magnesiu

m5. Phosphate6. Chloride7. Creatinine8. Urea

9. Amylase10.T. Proteins (= albumin +

globulin)

11. ALT12. AST13. ALP14. T.

Bilirubin15. gGT

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 systems1. volume control2. osmoregulation

– Sometimes, both systems activated (SIADH)

High LowVolume / pressure (factors:

circ. vol. & resistance)

ANP released–increases GFR and Na filtration–deactivates RAA system

1. Baroreceptors activate

catecholamines.

2. JGA activates RAA cascade

Osmoregulation

Osmolality sensed by

osmoreceptors– thirst–vasopressin

Dec. vasopressin =

dec. water reabsorption =

dilute urine

Na – clinical scenario examples

Volume/pressure regulators

Water / osmoregulation

Scenario RAA ANP V.pressin

Thirst Result

Admin. isotonic saline

-

↑- - Excretion of Na

load in appropriate amount of iso-osmotic urine

Ingestion of salty nuts (!)

↓ ↑ ↑ ↑ Excretion of

concentrated urine (both systems activated)

SIADH

↓ ↑ ↑ ↓ Excretion of

concentrated urine in presence of relative hyponatraemia

Na – signs and symptoms

Fatigue, weakness, headache, nausea

When it’s serious: confusion, coma, convulsions, death

Fatigue, weakness, headache, nausea

When it’s serious: confusion, coma, convulsions, death+ muscle twitching

High Low

Causes of hypernatraemia

High intake / producti

on

Administration of hypertonic solutions or drugs (e.g. saline)

Reduced excretio

n

Primary aldosteronism 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 hyponatraemiaIs the patient dehydrated?

Is the urinary Na >20mmol/L?

NoYes

Is the patient oedematous

Yes (i.e. kidney

loss)

•Addisons

•Diuretics

•Osmotic diuresis

No (i.e. extrarenal

loss)

•D&V

•Burns

•Obstruction

•Trauma – post -op

•Heat

•CF

No

•Water overload

•Glucocorticoid insufficiency

•Severe hypothyroidism

No

Is urine osmolality >500 mmol/kg?

Yes

•SIADH

Yes

•Nephrotic syndrome

•Cardiac failure

•Cirrhosis

•Renal failure

TreatmentHypernatraemia – • 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

Cardiac excitability arrhythmias, decreased cardiac contractility

Muscle function hypotonia, lethargy, muscle weakness, cramps

Cardiac excitability rapid HR, VF, arrhythmias, ECG changes

High Low

Causes of hyperkalaemia

High intake / producti

on

Blood transfusions LoSalt

Reduced excretio

n

Renal failure 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 / producti

on

Hypokalaemic IV therapy Ileus Intestinal obstruction Anorexia

Increased excretio

n

Drugs – diuretics, purgatives Aldosterone 2o to CCF, liver

failure Endocrine problems: Cushings,

Conns D&V

Redistribution

Hormones – insulin, cortisol B adrenergic stimulation – B2

agonist nebs Metabolic alkalosis

TreatmentHyperkalaemia – • 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

Neuromuscular excitability – Tetany (Chvosek’s)– Muscle

cramps/spasms (Trousseau’s)

– AsphyxiationExcitation-

contraction – ECG changes

Bone/teeth integrity– Short stature– Short metacarpals

Neuromuscular excitability

– NM depression– Arrythmias

Excitation-contraction– High BP– Cardiac arrest

Other– Bones, stones, abdo

groans, and psychic moans

– Polyuria / polydipsia

High Low

Ca - regulation

• Inverse relationship with P activates regulatory mechanisms

• To increase Ca1. PTH – bones, kidneys2. Calcitriol (activated vitamin D) – GI tract,

bones

• To decrease Ca1. Calcitonin

Low plasma Ca

Parathyroid glands

Increased PTH

Intestine

Kidneys

Increased activation of vitamin D

Increased Ca absorption

Increased plasma Ca

Increased Ca reabsorption

Increased Ca resorbed from bone

Increases responsiveness of bone to PTH

Bone

Note: low vitamin D also stimulates PTH release

Causes of hypercalcaemia

High intake / producti

on

10 HyperPTH Malignancy

Reduced excretio

n

Sarcoidosis / granulomatous diseases

Familial hypocalciuric hypercalcaemia

Other Paget’s disease Addison’s Drugs – lithium, antacids

Hypercalcaemia

Albumin normal/lowAlbumin raised

Urea raised

•Dehydration

Urea normal

•Cuffed specimen

ALP high

•Bone mets

•Sarcoid

•Hyperthyroid

P low/norm

Urea normal

•10/tertiary hyperPTH

P high/norm

ALP normal

•Myeloma

•Vit D excess

•Sarcoid

Causes of hypocalcaemia

Low intake / producti

on

HypoPTH / pseudo / pseudopseudo

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-)

PO43- source, storage,

functions • 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

PO43- regulation

• 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

Calcitriol

Increased intestinal P absorption

Increased P reab. From

kidneys

No change in plasma Ca

Increased plasma P

Decreased PTH

Increased intestinal Ca absorption

Kidneys

Decreased C reab. From

kidneys

Decreased urinary P loss

Increased urinary Ca loss

PO43- signs and

symptoms

Symptoms of low Ca

Component bone, cells, 2,3-DPG etc.– High BP– Bone pain

High Low

Symptoms of high Ca

Component bone, cells, 2,3-DPG etc.– Encephalopathy– Hallucinations– Arrhythmias– Muscle weakness– Bone pain

Causes of hyperphosphataemia

High intake / producti

on

Enemas / laxatives TPN Vitamin D excess

Reduced excretio

n

CKD HypoPTH Hypomagnaesia Drugs - bisphosphonates

Redistribution

Cellular insult – trauma, burns, exercise, chemotherapy

Acidosis

Other Acromegaly Thyrotoxicosis

Causes of hypophosphataemia

Low intake / producti

on

Poor diet Malabsorption - Crohns

Increased excretio

n

10 HyperPTH 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 cause2.Oral or in some circumstances, IV P3.+/- vitamin

P – summary points

Magnesium (Mg2+)

Mg2+ source, storage, functions

• 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

Cardiovascular excitability– Bradycardia (BP)– Heart block– Arrest

Neuromuscular depression– Hyporeflexia– Facial paraesthesia

CNS function– Coma– Respiratory

depression and apnoea

Coagulation– Increased coagulation

time

High Low

Cardiovascular excitability– Arhythmias– Cardiac arrest

Neuromuscular depression– Tetany– Paraesthesia

CNS function– Fits

Coagulation– Increased coagulation

time

Mg2+ regulation

• Mg2+ derangements uncommon• Relationship between Mg2+,

Ca2+ and K • Mg levels determined by:

1. Kidneys2. PTH – kidney, intestine, bone3. Insulin

Causes of hypermagnaesia

High intake / producti

on

Iatrogenic Drugs (esp. antacids) haemodialysis

Reduced excretio

n

Renal failure Drugs (lithium) Familial hypocalciuric

hypercalcaemia

Other Hypothyroidism Addisons Disease Depression

Causes of hypomagnaesia

Low intake / producti

on

Reduced dietary intake (TPN) Intestinal malabsorption Alcohol

Increased excretio

n

Diarrhoea 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 cause2.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 / producti

on

Excessive ingestion of high salt diets (CCF patients)

Reduced excretio

n

Kidney failure

Causes of hypochloraemia

Low intake / producti

on

(Infants) chloride deficient 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

• 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

High (uraemia)

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 / producti

on

• High protein diet• GI bleeding, catabolism, sepsis,

surgery = a high protein ‘meal’• Drugs- steroids

Reduced excretio

n

• Dehydration• Kidney failure (all causes) • Drugs – tetracyclines,

nephrotoxics

Causes of low urea

Low intake / producti

on

• Liver disease• 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 CrHigh intake / producti

on

• Diet• Race (Afro Caribbean• Body-builders• Drugs – steroids• Muscle injury

Reduced excretio

n

• Renal failure• Drugs:

– trimethoprim, sulphamethoxazole etc.

Other • Drugs – interfere with assay for Cr

• Rheumatoid arthritis

Causes of low Cr

Low intake / producti

on

• increasing age - age-related 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 liverRole:• Screen, confirm diagnosis, construct differential

diagnoses• Indicate prognoses• Monitor progress and response to therapyProblems:• 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 functionUptake, conjugation & excretion of anionic compounds

Serum total bilirubinBile acidsUrinary bilirubin (also urobilinogin)

Synthetic functionSerum albumin Serum proteinsINR / APTT

Hepatocellular damageASTALTSerum ferritinB12ALPGGT

ALT/AST source, transport & functionSource:

• 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 pancreasTransport:• Released into blood when hepatocytes damagedFunction:• 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 &

functionTest: • Total protein = albumin + globulinSource:• 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 / producti

on

• Raised immunoglobulins– 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 / producti

on

Liver disease (cirrhosis) Malabsorption syndromes –

coeliac, post bowel resection

Increased excretio

n

Kidney disorders – diabetes, 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

Bilirubin

Bile released

Conjugated bilirubin

glucoronysl transferase

Bilirubin + glucoronic acid

Iron/globin removed from haem

Biliverdin

Stercobilin or urobilinogen

Reticuloendothelial system

Albumin

Hyperbilirubinaemia - causes

UNconjugated ConjugatedExcessive production Hepatocellular

abnormalities (unconjugated sometimes)

Ineffective haemopoesis Haemolytic disorders

• Primary hepatocyte disease: cirrhosis, hepatitis, malignancies, drug reactions, iron overload Pregnancy Postoperative jaundice

Abnormal bilirubin metabolism (congenital)

Obstructive

Enzyme system immaturity: newborn jaundice Inherited defects: Gilbert’s Crigler-Najjar syndrome, drugs

• Calculi• Neoplasms• Strictures• Atresia

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

HyperamylasaemiaGI 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