Title: Lab tests

Q: How do the kidneys reabsorb bicarbonate in acidaemia?
A: Carbonic anyhydrate dependent reabsorption with secretion and entrapment of H+ in tubule by phosphate and ammonia

Q: Why does respiratory compensation for metabolic acidosis not reach normal pH?
A: Each time the plasma pH nears 7.4, ventilation reduces again with subsequent fall in pH due to driving metabolic process

Q: Physiological effects of acidaemia
A: Raises K 0.5 for every 0.1
Increases off-loading of O2 to tissues (right-shift)
Depresses myocardial contractility
Reduces peripheral vasopressor response
Reduced clotting
Pulmonary vasoconstriction
Increased Na-channel blocker toxicity

Q: Effects of alkalosis
A: Reduces ventilatory drive
Left-shift
Reduced serum K
Increased ammonium to CNS

Q: Effects of hypocapnoea
A: Cerebral vasoconstriction
Lowers seizure threshold
Vasoconstriction
Reduced myocardial O2 delivery
Inhibits hypoxic pulmonary vasoconstriction

Q: What are the unmeasured anions that make up the anion gap?
A: Plasma proteins
Phosphate
Sulfate
Lactate
Uraemic
Conjugate bases of ketoacids

Q: What can cause an increased anion gap?
A: Increased unmeasured anions e.g. KULT
Decreased unmeasured cations e.g. hypocalcaemia, hypomagnesaemia

Q: Chance of metabolic acidosis if AG 20-30?
A: 66%

Q: Chance of metabolic acidosis if AG >30?
A: 100%

Q: What causes a reduced anion gap?
A: Increased unmeasured cations e.g. hypercalcaemia/hypermagnesaemia/lithium
Unmeasured positively charged proteins e.g. myeloma
Reduced unmeasured anions e.g. hypoalbuminaemia

Q: Albumin correction for AG
A: AG + 0.25 x (30-serum albumin)

Q: Causes of ketoacidosis?
A: Diabetic
Alcoholic
Starvation

Q: Predominant ketoacid in DKA
A: Beta-hydroxybutyrate

Q: Predominant ketoacid in alcoholic ketoacidosis?
A: Beta-hydroxybutyrate

Q: Toxins that cause HAGMA
A: Methanol
Ethanol
Ethylene glycol
Salicylate
Isoniazid
Metformin
Pyroglutamic acid
Paraldehyde

Q: Causes of pyroglutamic acidosis?
A: Paracetamol
Flucloxacillin
Vagabatrin

Q: Delta gap =
A: Anion gap / Bicarb gap

Q: Delta < 0.4
A: Lone NAGMA

Q: Delta 0.4-0.8
A: HAGMA + NAGMA

Q: Delta 0.8-2
A: HAGMA alone

Q: Delta >2
A: HAGMA + Metabolic alkalosis or compensation for respiratory acidosis

Q: Osmolar gap =
A: Measured - Calculated

Q: Calculated osmolarity =
A: 2Na + Glucose + Urea

Q: Causes of raised osmolar gap
A: Exogenous alcohols e.g. ethanol, ethylene glycol, methanol, isopropyl alcohol
Lactate
Acetone
Glycerol/sorbitol
Glycine
Mannitol
Propylene glycol

Q: Non-toxicological causes of raised osmolar gap
A: Ketoacidosis of any cause
Lactic acidosis
Hyperlipidaemia
Hyperproteinaemia
Shock

Q: Does a normal osmolar gap rule out toxic alcohols?
A: No. Even small amounts can cause significant toxicity and late in course may already be metabolised to non-osmotically active compounds

Q: What is the utility of PvCO2?
A: If <45, rules out hypercarbia. If elevated then poorly correlates

Q: What is the utility of venous lactate?
A: Rules out if <2 but if elevated may be significantly higher than arterial lactate

Q: Why does etCO2 not correlate well in COPD patients?
A: Gas trapping means air involved in gas exchange may not escape

Q: What are the 4 phases of the etCO2 trace?
A: I - Inspiratory baseline
II - Expiratory upstroke (Anatomical dead space)
III - Expiratory plateau (alveolar)
0 - Inspiratory downstroke

Q: What does a flat etCO2 trace suggest?
A: Cardiac arrest
No ventilation
ET obstruction/displacement
Disconnection
Capnograph obstruction

Q: etCO2 capnograph in oesophageal intubation
A: <6 waveforms of decreasing height

Q: Expected CO2 in metabolic acidosis
A: 1.5xHCo3 + 8

Q: Expected CO2 in metabolic alkalosis
A: 0.8xBicarb + 20

Q: Max CO2 in metabolic alkalosis compensation
A: 55mmHg

Q: Acute compensation for respiratory acidosis
A: HCO3 up 1 for 10

Q: Chronic compensation for respiratory acidosis
A: 4 for 10

Q: Acute compensation for respiratory alkalosis
A: 2 for 10

Q: Chronic compensation for respiratory alkalosis
A: Bicarb down 5 for 10

Q: Lower limit of CO2 in metabolic acidosis compensation
A: 10mmHg (lower in children)

Q: What should the CO2 be in metabolic acidosis or alkalosis?
A: Last 2 digits of pH

Q: Mortality of Lactate >10
A: 83%

Q: Type A lactic acidosis
A: Impaired tissue oxygenation

Q: Type B lactic acidosis
A: Impaired lactate metabolism

Q: Type B1 lactic acidosis
A: Impaired lactate metabolism due to underlying disease e.g. sepsis, liver failure, thiamine deficiency, malignancy, phaeo, diabetes

Q: Type B2 lactic acidosis
A: Drug or toxin induced e.g. metformin, adrenaline, salbutamol, ethanol, methanol, paracetamol, salicylates, ethylene, propylene glycol, cyanide, isoniazid

Q: Type B3 lactic acidosis
A: Inborn error of metabolism e.g. G6PD deficiency

Q: Causes of Type A lactic acidosis
A: Shock, hypoxaemia, CO poisoning, severe anaemia

Q: Causes of NAGMA
A: Renal loss of bicarb e.g. RTA, diuretics
GIT loss of bicarb e.g. severe diarrhoea, biliary/pancreatic fistulas, chronic laxative abuse, NG drainage, ureterocolonic fistulas
Addition of acid e.g. HCl/NaCl

Q: Causes of hyperkalaemic NAGMA
A: RTA type IV
Hypoaldosteronism
K-sparing diuretics

Q: Causes of hypokalaemic NAGMA
A: RTA I and II
Acetazolamide
Loop diuretics
Acute diarrhoea
Ureterosigmoidostomy
Ileal conduit
Dilution acidosis (NaCl)

Q: What is the urinary anion gap useful for?
A: Differentiating renal or GI NAGMA.
Negative urinary anion gap = GI loss of bicarb
Normal urinary anion gap (0-20) = RTA II
Positive urinary anion gap = RTA I or IV

Q: Describe Type I RTA
A: Distal failure to acidify urine
Urine pH >5.5, elevated urinary anion gap
Stones

Q: Describe RTA II
A: Proximal failure to reabsorb bicarb
Normal urinary anion gap
Urinary bicarb elevated

Q: Describe RTA IV
A: Hyperkalaemic
Elevated urinary anion gap

Q: What acid-base disturbances do diuretics cause?
A: Loop diuretics - Contraction alkalosis
K-sparing diuretics - Contraction alkalosis + NAGMA + hypokalaemia

Q: Indications for bicarbonate therapy
A: Hypobicarbonataemia - If very low, unable to buffer acidosis
Acidaemia <7.1 (or higher if haemodynamic instability)
Severe NAGMA
Hyperkalaemia
Na-channel toxicity i.e. TCA, propranolol
Rhabdo/crush injury
Salicylate toxicity

Q: Why does metabolic alkalosis present with tetany?
A: Reduced H+ leads to plasma protein binding of other cations e.g. Calcium

Q: Why is metabolic alkalosis of significant concern in COPD patients?
A: Compensation okay but if second primary process leads to:
 - Impaired ventilatory drive
 - Left-shift of O2 dissocation curve with impaired O2 delivery to tissues

Q: How do you classify metabolic alkaloses?
A: Chloride responsive (Ur Cl <10) vs. chloride resistant (Ur Cl >20)

Q: Causes of chloride responsive metabolic alkalosis?
A: GI or renal loss of Cl e.g. diarrhoea, vomiting, diuretic therapy

Q: Causes of chloride-resistant metabolic alkalosis?
A: Ur Cl >20
Driven by hypokalaemia so must fix this
Hypertensive: Renal artery stenosis, hyperaldosteronism (Conn's), renin tumors, Cushing's, licorice, fludrocortisone
Hypotensive: Bartter's, Gitelman's syndromes

Q: Treatment of metabolic alkalosis
A: Remove cause if able
NaCl if chloride responsive/hypovolaemic
Replace K if hypokalaemic
Consider HCl if severe (Bicarb >45)

Q: What proportion of COPD patients have hypoxic respiratory drive?
A: 5-10%

Q: pH drop for acute respiratory acidosis
A: 0.8 for 10

Q: pH rise for chronic respiratory acidosis
A: 0.03 for 10

Q: pH rise for acute respiratory alkalosis
A: 0.08 for 10

Q: pH rise for chronic respiratory alkalosis
A: 0.03 for 10

Q: What does the rise in CK correlate with in rhabdo?
A: Severity of illness
NOT renal failure or mortality

Q: What is the diagnostic threshold of CK rise in rhabdo?
A: 5x ULN

Q: When does CK peak in rhabdo?
A: 24-72 hours

Q: Rate of decline of CK
A: 39% of previous days value

Q: When should one suspect myoglobinuria?
A: Red urine, positive dipstick for blood but negative microscopy

Q: What proportion of the population do not secrete CRP as a part of acute inflammatory response?
A: 20%

Q: Antibodies in Graves
A: Anti-thyroid peroxidase
Anti-thyroglobulin

Q: Diagnostic threshold of HbA1c for DM?
A: >6.5%

Q: DDx of microcytic anaemia
A: TICS
 - Thalassaemia
 - Iron deficiency
 - Chronic disease
 - Sideroblastic

Q: DDx of normocytic anaemia
A: RACH
 - Renal disease
 - Aplastic
 - Chronic disease
 - Haemoglobinopathies

Q: DDx of macrocytic anaemia
A: B12
Liver disease
Folate
Ethanol
Drugs

Q: How do you differentiate iron deficiency from thalassaemia?
A: Iron deficiency - Red cell distribution width high and low serum ferritin
Thalassaemia - RCDW normal with normal or high red cell count

Q: How do you differentiate B12-folate deficiency from other causes of macrocytic anaemia?
A: Red cell distribution width is high in B12 and folate deficiency vs. normal in others

Q: How do you test for B12 and folate deficiency?
A: Serum B12, red cell folate

Q: What does the Direct Coomb's test for?
A: Antibodies on RBC's
Positive in autoimmune haemolytic anaemias, transfusion reactions and some drug-induced haemolytic anaemias

Q: What is anisocytosis?
A: Unequal red cell size. Seen in macrocytic anaemia

Q: What is poikilocytosis?
A: Irregular red cell shape seen in dyserythropoiesis

Q: What are target cells?
A: Red cells with central loss of staining. Seen in iron deficiency, liver disease, sickle cell disease, thalassaemia, post-splenectomy

Q: What are burr cells?
A: Mature red cells with spikes. Seen in uraemia and red cell trauma

Q: What are Howell-Jolly bodies?
A: Post-splenectomy remnants of nuclear material

Q: What are schistocytes?
A: Red cell fragmentation by shearing forces seen in DIC, TTP, prosthetic heart valve and post-splenectomy

Q: What are spherocytes?
A: Seen in haemolytic anaemia of all types and hereditary spherocytosis

Q: When are tear drop cells seen?
A: Extramedullary haematopoiesis e.g. myelofibrosis

Q: What are Heinz bodies?
A: Denatured Hb seen in drug-related haemolytic anaemias

Q: What is toxic granulation?
A: Lysosomal granules in neutrophils. More specific for bacterial infection than neutrophilia

Q: What do metamyelocytes or myelocytes suggest?
A: Leukaemia or sepsis with premature release from bone marrow

Q: Causes of neutrophilia
A: Bacterial infection
Steroids
Leukaemia
Vasculitis

Q: Causes of neutropaenia
A: Viral infection
Chemotherapy
Clozapine
Sulphonamides
Beta-lactams

Q: Causes of lymphocytosis
A: Viral infection
TB
Toxoplasmosis
Syphilis
Thyrotoxicosis
Leukaemia/lymphoma

Q: Causes of lymphocytopaenia
A: Stress response
Prior steroid use
Autoimmune disease e.g. SLE
Viral infection
Severe sepsis
TB
HIV
Cytotoxic drugs
Irradiation
Malnutrition

Q: Causes of monocytosis
A: Leukaemia
Lymphoma
Myelodysplasia
Chronic inflammation
Stress response
Granulomatous disease e.g. TB, sarcoid

Q: Causes of eosinophilia
A: Parasitic infection
Allergy
Addison's
DRESS
Sarcoidosis
Polyarteritis nodosa
Leukaemia/lymphoma
Irradiation

Q: Causes of pancytopaenia
A: Malignant marrow replacement
Idiosyncratic drug reaction e.g. sulphonamides, phenytoin, carbamazepine
Megaloblastic haematopoiesis (B12 deficiency)
SLE
Myelofibrosis/myelodysplasia
Cytotoxics
Overwhelming infection

Q: Causes of thrombocytopaenia
A: Pernicious anaemia/marrow failure
Sepsis
HITTS
HUS/TTP
ITP
Intravascular device
Drug-induced e.g. antibiotics, thiazides, antihistamines
Antiphospholipid syndrome
DIC
HELLP
Haemolysis

Q: Plasma osmolality and ADH release?
A: Osm <280 = impaired ADH release
>295 - Maximal ADH release

Q: Causes of hyperosmolar hyponatraemia
A: Mannitol, glucose, glycerol

Q: What causes an iso-osmolar hyponatraemia?
A: Pseudohyponatraemia from hyperprotein/lipid/glycine (TURP)

Q: What is TURP syndrome?
A: Iso-osmolar hyponatraemia presenting within 24 hours of TURP/endometrial ablation
 - CV instability, ALOC, seizures, transient visual disturbance (glycine)

Q: Treatment of TURP syndrome
A: Haemodialysis indicated if hypotensive, bradycardic or unresolving neurological symptoms
Hypertonic saline if Posm <260 and severe non-visual neurological disturbance

Q: Causes of hypervolaemic hypo-osmolar hyponatraemia
A: CCF, nephrotic syndrome, cirrhosis, CKD

Q: Causes of euvolaemic hypo-osmolar hyponatraemia
A: SIADH, cerebral salt wasting, psychogenic polydipsia, Addison's, hypokalaemia, thiazides, beer potomania

Q: How do you differentiate psychogenic polydipsia from other causes of euvolaemic hypo-osmolar hyponatraemia?
A: Urinary Na <10 (vs. all other types U Na >20)

Q: DDx of hypovolaemic hypo-osmolar hyponatraemia
A: Renal loss - Diuretics, Addison's, post-obstructive diuresis, hypokalaemia (U Na >20, U osm >100
GI loss - Vomiting (metabolic alkalosis), diarrhoea (metabolic acidosis), excessive sweating (U Na <20, Uosm >100)

Q: Causes of SIADH
A: Neuropsych - Meningitis, encephalitis, thrombosis, haemorrhage, malignancy, TBI, delirium tremens
Lung - Pneumonia, TB, abscess
Ectopic vasopressin release
Drugs - Carbamazepine, haloperidol, SSRI, SNRI, narcotics, amiodarone, desmopressin

Q: Diagnostic criteria for SIADH
A: UNa >20
Uosm >100 (>200 usually)
Euvolaemic hypo-osmolar hyponatraemia
Normal adrenal, liver, cardiac, renal, thyroid fx

Q: Sodium deficit =
A: 140-serum Na x TBW [0.6 x weight]

Q: Expected change in Na =
A: (Infusion Na - serum Na) / (TBW + 1)

Q: Indications for hypertonic saline
A: Raised ICP
Na <120 with severe symptoms
 - Aim to increase 4-6mmol/L or until resolution of severe symptoms

Q: Target rise in Na in chronic hyponatraemia?
A: 6mmol/L/24 hours (12 if low risk)

Q: Risk factors for osmotic demyelination syndrome?
A: Na <120
Elderly
CCF
Chronic hyponatraemia
Alcoholism
Cirrhosis
Hypokalaemia
Malnutrition

Q: Treatment of suspected osmotic demyelination syndrome
A: Supportive cares
5% dextrose 3mL/kg/hr
Desmopressin

Q: How does pontine demyelination present?
A: Dysarthria
Dysphagia
Quadriparesis

Q: How does extra-pontine demyelination present?
A: Tremor
Ataxia
Mutism
Parkinsonism
Dystonia
Catatonia

Q: Free water deficit =
A: TBW x (Posm - 285)/Posm

Q: DDx of hypervolaemic hypernatraemia
A: Cushings
Primary hyperaldosteronism (Conns)
Salt water intake
Iatrogenic

Q: DDx of euvolaemic hypernatraemia
A: Central DI (Uosm <300)
Nephrogenic DI
Hypodipsia
Extrarenal water loss (U osm >800)

Q: DDx of hypovolaemic hypernatraemia
A: Renal (UNa >20, Uosm >100)
 - Osmotic diuretics, loop diuretics, post-obstructive diuresis
GI (UNa <10, Uosm >800)
 - Vomiting, diarrhoea, fistulas, burns, DI

Q: Management of hypernatraemia
A: N/S resus if required
0.45% saline maintenance
Treat underlying cause
If onset <48 hours: Correct Na at 1mmol/L/hr
If onset >48 hours: Correct Na at 0.5mmol/L/hr

Q: Causes of nephrogenic DI
A: Renal: Amyloidosis, medullary sponge kidney, PCKD, pyelonephritis
Drugs: Ethanol, lithium, phenytoin
Severe hypokalaemia or hypercalcaemia

Q: How do you differentiate renal from GI potassium losses in hypokalaemia?
A: Renal: Spot urine K >20
GI: Spot urine K <20

Q: Causes of renal hypokalaemia?
A: Primary hyperaldosteronism (hypertension, metabolic alkalosis, hypokalaemia, hypernatraemia
Secondary hyperaldosteronism (CCF, cirrhosis, renal artery stenosis, licorice)
Diuretics
RTA type 1
Hypomagnesaemia

Q: Maximum K replacement per hour via any means?
A: 20mmol/hr

Q: Threshold for acute kidney injury to cause hyperkalaemia?
A: eGFR <20; <10% renal function, Creatinine >800

Q: How long does calcium take to work in hyperkalaemia?
A: 1-3 minutes

Q: How long does effect of calcium last in hyperkalaemia?
A: 30-60 minutes

Q: Dose of salbutamol in hyperkalaemia
A: 10-20mg over 10 minutes

Q: How long does insulin therapy take to work in hyperkalaemia?
A: 30 minutes

Q: How long does salbutamol take to work in hyperkalaemia?
A: 15-30 min

Q: Management of hypermagnesaemia
A: 10-20mL of 10% calcium gluconate

Q: Causes of hypocalcaemia
A: Reduced absorption - Vit D deficiency, malnutrition, malabsorptive
Increased excretion
 - Alcoholism (hypoMg inhibits PTH release)
 - Hypoparathyroidism
 - Hypomagnesaemia
 - Phosphates
 - Loop diuretics
 - Glucocorticoids
 - Bisphosphonates
 - Calcitonin
 - Sepsis
 - Acute pancreatitis
 - Citrate toxicity
 - Rhabdomyolysis

Q: Hypocalcaemia with low PTH
A: Post-operative
Autoimmune hypoPTH
Parathyroid gland infiltration
Radiation-induced hypoPTH
Hungry bone syndrome
HIV infection

Q: Hypocalcaemia with high PTH
A: Vitamin D deficiency
PTH resistance
Renal disease
Hyperphosphataemia
Tumor lysis syndrome
Acute pancreatitis
Osteoblastic metastases
Sepsis
Acute respiratory alkalosis

Q: Hypocalcaemia with metabolic acidosis
A: Acute renal failure
Tumor lysis syndrome
Sepsis
Rhabdomyolysis
Pancreatitis
Ethylene glycol
Hydrofluoric acid

Q: ECG changes of hypocalcaemia?
A: Prolonged ST (QT)

Q: How does hypercalcaemia present?
A: Bone osteolysis, renal stones, constipation, pancreatitis, peptic ulcer disease, neuropsychiatric issues, loss of renal concentrating ability + osmotic diuresis

Q: Proportion of hypercalcaemia in ED due to malignancy?
A: 50%

Q: Malignant causes of hypercalcaemia?
A: PTHrp
Osteolytic
Vitamin D-mediated (lymphoma)
Ectopic parathyroid hormone
Most commonly multiple myeloma, leukaemia, lung cancer and breast cancer

Q: Non-malignant causes of hypercalcaemia
A: Primary hyperPTH (25% of ED cases)
Hyperthyroidism
Vitamin D toxicity
Milk-alkali syndrome
Sarcoidosis (Vitamin D toxicity)
Paget's
Vitamin A toxicity
Lithium
Chronic thiazide use
Familial hypocalciuric hypercalcaemia
Late rhabdo

Q: Which diuretic causes hypercalcaemia?
A: Chronic thiazide use

Q: How sensitive/specific is serum ACE for sarcoidosis?
A: 70%

Q: Treatment of hypercalcaemia
A: Severe/symptomatic
 - N/S 500-1000mL/hr for 2-4 hours
 - Frusemide targeting UO 200-400mL/hr
 - Steroids if Addison's, sarcoidosis or haematological malignancy/breast Ca
 - Haemodialysis if critical
 - IV bisphos if hypercalcaemia of malignancy
 - Calcitonin third-line

Q: Dose of IV bisphosphonate for hypercalcaemia?
A: Zoledronic acid 4mg IV over 15 minutes

Q: Dose of calcitonin in hypercalcaemia
A: 4U/kg SC or IM

Q: Causes of primary hyperPTH
A: 80% due to single parathyroid adenoma
<1% carcinoma

Q: DDx of hypophosphataemia
A: Refeeding
Malnutrition
Malabsorption
Vitamin D deficiency
Chronic antacid use
Hyperparathyroidism
RTA
Diuretics
Bisphosphonate
Corticosteroids

Q: What proportion of DKA patients suffer hypophosphataemia?
A: 90%

Q: Effects of hypophosphataemia?
A: Reduced platelet/white cell fx and lifespan
Weakness, tremor, paraesthesia, confusion
Impaired myocardial fx
Lower threshold for arrhythmia
Insulin resistance

Q: Causes of hyperphosphtaemia
A: Renal failure
Hypoparathyroidism
Rhabdomyolysis
Tumor lysis syndrome

Q: How is cerebral salt wasting differentiated from SIADH?
A: Cerebral salt wasting hypovolaemic vs SIADH euvolaemic by definition

Q: DDx of hypertensive hypokalaemia with urinary K >20
A: Normal aldosterone - Cushing's, Ectopic ACTH, licorice, Liddle's syndrome
Raised aldosterone
 - Normal renin: Conn's
 - Elevated renin: Secondary hyperaldosteronism

Q: How does hypokalaemic periodic paralysis present biochemically?
A: Hypokalaemia, Urine K >20, normotensive, normal serum pH, not hypoMg and not thyrotoxic

Q: How can thyrotoxic hypokalaemic periodic paralysis be confirmed?
A: Spot urine Ca/Phosphate ratio > 1.7 + thyrotoxic TFT's

Q: INR and platelet count that CI LP?
A: INR >1.5 or platelets <50

Q: What PCR is available for CSF?
A: N. meningitidis, S. pneumoniae, H. influenzae, L. monocytogenes, M. tuberculosis, all viruses

Q: What size needle should be used for LP?
A: 20G or smaller (less risk of headache)

Q: Which needles should be used for LP?
A: Sprotte > Whitacre > Quinke with respect to postdural headache

Q: Which patients warrant a CT prior to LP?
A: GCS <15, focal neurological deficit, age >60, new seizures, papilloedema, immunocompromised, HIV, malignancy hx, history of focal CNS disease, concern for CNS mass lesino

Q: Which meningitides cause raised ICP?
A: Bacterial and fungal

Q: What proportion of LP in bacterial meningitis are Gram stain positive if no prior Ab's?
A: 60-80%

Q: What proportion of LP in bacterial meningitis are Gram stain positive after antibiotics?
A: 7-41%
Sterile within 2 hours meningococcal/6 hrs pneumococcal

Q: Normal WCC in CSF?
A: <5

Q: Typical WCC in bacterial meningitis?
A: >1000

Q: Typical WCC in viral meningitis?
A: <1000, predominant monocytes

Q: What proportion of viral meningitis have predominant neutrophils?
A: 10%

Q: Typical glucose in bacterial meningitis CSF?
A: <2.2 (CSF:serum < 0.4)

Q: Typical protein in bacterial meningitis?
A: >1g/L

Q: Typical glucose in viral meningitis?
A: Normal

Q: Typical protein in viral meningitis?
A: <1g/L

Q: Typical WCC in fungal meningitis?
A: 100-500

Q: Causes of raised opening pressure on LP?
A: Bacterial meningitis, fungal meningitis, venous sinus thrombosis, pseudotumor cerebri

Q: How long does xanthochromia take to develop?
A: 12 hours

Q: WCC and neutrophil count suggestive of Spontaneous bacterial peritonitis?
A: >1000/mm3 and >250/mm3 respectively

Q: Criteria for exudate effusion?
A: Pleural:Serum protein >0.5
Pleural:Serum LDH >0.6
Pleural LDH > 2/3 upper limit of normal for serum LDH

Q: Tests for exudative pleural fluid
A: Gram stain and culture
Cell count
Glucose
Cytology
pH
Amylase
Mycobacterial and fungal stains as indicated
PCR M. tuberculosis, adenosine deaminase, IFN-gamma (all for TB)

Q: What does neutrophil predominant pleural fluid indicate?
A: Parapneumonic, PE or pancreatitis

Q: What does lymphocyte predominant pleural fluid indicate?
A: TB, cancer, post-cardiac surgery

Q: Which lung cancer is pleural fluid cytology most useful for?
A: Adenocarcinoma

Q: What does parapneumonic effusion pH help with?
A: If <7.2 suggests drainage of benefit

Q: Sensitivity of serum amylase for pancreatitis?
A: 70%

Q: Is serum amylase in addition to lipase helpful?
A: No

Q: What does an ALP >150 suggest in acute pancreatitis?
A: Gallstone pancreatitis with >85% PPV if within 48 hours

Q: What are indicators of hepatic catabolic function?
A: Bilirubin and ammonium

Q: What does raised unconjugated bilirubinaemia suggest?
A: Haemolytic anaemia or liver injury preventing catabolic activity

Q: What does an isolated raised LDH in unconjugated hyperbilirubinaemia suggest?
A: Haemolysis

Q: What does AST  = ALT suggest?
A: Acute process as AST has a much shorter half-life
i.e. if subacute, AST will have gone back to normal, leaving ALT raised alone

Q: What does an AST:ALT ratio >2 suggest?
A: Alcoholic hepatitis

Q: Which is more specific ALT or AST?
A: ALT

Q: Typical pattern of drug-induced cholestasis?
A: Transaminitis with raised ALP

Q: Typical drugs causing cholestasis
A: Allopurinol, augmentin, carbamazepine, erythromycin, flucloxacillin, oestrogens, phenytoin and bactrim

Q: Causes of raised LDH
A: Hepatic disease
Rarely if isolated obstructive cholestasis
Lung disease
APO
MI
Muscle injury
Haemolysis

Q: Which is a better indicator of hepatic synthetic function: Albumin or PT?
A: PT

Q: How is acute hepatitis A diagnosed?
A: Positive IgM anti-hepatitis A

Q: How is acute hepatitis B diagnosed?
A: Positive HBsAg

Q: Adverse effects of CT contrast
A: Allergy
Histamine release
AKI
Myocardial depression
Osmotic load
Coagulopathy
Potential seizure if non-intact BBB

Q: What proportion of patients suffer a moderate allergic reaction to contrast?
A: 1%

Q: What proportion of patients suffer a mild allergic reaction to contrast?
A: 5%

Q: What is the mortality rate of severe allergic contrast reactions?
A: 1/40 000

Q: How can allergic reactions to contrast be prevented?
A: IV hydrocort 200mg 5 hours prior
Promethazine 25mg PO 1 hour prior
Ranitidine 50mg PO 1 hour prior

Q: Define contrast-induced nephropathy?
A: Increase in creatinine by 25% or >44micromol/L from baseline at 48 hours

Q: Risk factors for contrast-induced nephropathy?
A: Arterial scans
GFR <30
Age >70
DM
Nephrotoxic drug use
Metformin
Dehydration
Haemodynamic instability

Q: Risk of AKI with contrast?
A: 5%

Q: Prevention of contrast nephropathy?
A: Saline 100-150mL/hr for 8-10 hours
No evidence for bicarb or NAC

Q: What is a type 1 error?
A: False positive e.g. rejecting null hypothesis incorrectly

Q: What is a type II error?
A: False negative i.e. accepting null hypothesis incorrectly

Q: What is the alpha of a study?
A: Probability of finding a difference when one does not exist
Probability of a type I error
Probability that perceived difference is due to chance
Cut-off = 0.05

Q: What is the beta of a study?
A: Probability of a type II error
Probability that study misses actual difference
Beta = 1-Power
Cut-off 0.2 usually

Q: What is the power of a study?
A: The pre-study probability that the study correctly rejects the null hypothesis

Q: What does the power of a study depend upon?
A: Alpha cut-off
Magnitude of effect
Population variance
Baseline incidence

Q: What is the precision of a study?
A: Measure of accuracy i.e. Coefficient of variation

Q: What is a ROC?
A: Receiver operator curve
Demonstrates graphically the relationship between sensitivity and specificity
AUC = 1 = Perfect test
AUC = 0.9-1 = Excellent

Q: Total body water for men, women, elderly men and elderly women?
A: 0.6, 0.5, 0.5, 0.45