Biochemistry

Question 1

VBG flow chart

Answer 1

Question 2

How do you work out the anion gap?
Interpret

Answer 2

Anion Gap = Na – (Cl + HCO3)

4-12 normal

Question 3

What are the cause of a HAGMA

Answer 3

Causes (CATMUDPILES)

• CO, CN
• Alcoholic ketoacidosis and starvation ketoacidosis
• Toluene
• Metformin, Methanol
• Uremia
• DKA
• Paracetamol,
• Iron, Isoniazid
• Lactic acidosis
• Ethylene glycol
• Salicylates

Question 4

What are the causes of a NAGMA

Answer 4

Causes (CAGE)

• Chloride excess
• Acetazolamide/Addisons
• GI causes – diarrhea/vomiting, fistulae (pancreatic, ureters, billary, small bowel, ileostomy)
• Extra – RTA

Question 5

What are the main causes of acute respiratory acidosis

Answer 5

things that cause hypoventilation:
* CNS depression - injury, stroke, drugs
* respiratory depression - myopathy, drugs, spinal injury
* mechanical hypoventilation - pain, chest wall injury, raised intra abdominal pressure
* Resp failure - pneumonia, pneumothorax, oedema, bronchial obstruction

Question 6

what are the causes of chronic resp acidosis

Answer 6

COPD
restrictive lung disease

Question 7

How do you work out if the resp acidosis is acute or chronic?

What does it mean if the expected value is not met?

Answer 7

Acute - bicarb to increase by 1mmol/l for every 10mmhg of co2 above 40
use 24 as baseline fot bicarb
Chronic- increases by 4

if expected is below measured then concurrent metabolic acidosis

Question 8

What are the causes of respiratory alkalosis

Answer 8

CHAMPS

• CNS disease - stroke, haemorrhage
• Hypoxia - PE, asthma
• Anxiety and pain
• Mechanical or excessive ventilation
• Progesterone and pregnancy
• Salicylates and sepsis

Question 9

What are the causes of metbolic alkalosis?

Answer 9

CLEVER PD

• Contraction - volume contraction
• Liquorice abuse
• Endocrine - cons, Cushings
• Vomiting
• Excess alkali - Antacids
• Renal - Bartlers
• Post hypercapnia
• Diuretics

Question 10

How do you work out if the resp alkalosis is acute or chronic?

Answer 10

Acute -Bicarb should reduce by 2mmol/l for every 10mmhg under 40
Chronic - reduce by 5

Question 11

When do you use Winters formula?

Answer 11

Has the metabolic acidosis been compensated for or is there also a respiratory acidosis?

Expected Pc02 = (1.5 x bicarb) + 8 (+/-2)
if expected is correct then its compensation

Question 12

How do you calculate the delta gap?
When do you use the delta ratio?

Answer 12

(AG -12) / (24-bicarb)
to work out the metabolic acidosis component

<0.4 pure NAGMA
0.4-0.8 mixed
0.8 - 2 Pure Hagma
Over - Hagma plus metabolic alkalosis or resp acidosis

Question 13

What is the metabolic acid base status. Show working and differentials

Answer 13

HAGMA - 137 – (98 + 18) = 21
Delta ratio (AG -12) / (24-bicarb) =9/6 = 1.5 therefore pure HAGMA

Causes (CATMUDPILES)

Question 14

list major abnormalities and differentials

Answer 14

High anion gap metabolic acidosis
‐ Ketones – DKA, alcoholic
‐ Lactate (type A or B with liver failure)
Inadequate respiratory compensation (expect CO2 to be lower)
‐ Decreased consciousness eg alcohol, head injury, other drugs

Delta ratio (42‐12)/(22‐11) = v. high almost (1 mark)
No differential acceptable

Lactate high
‐ Type A hypoperfusion
‐ Type B – liver failure
Hyperglycaemia
‐ DKA

Question 15

What is the difference between Type A and B lactic acidosis?

Causes?

Answer 15

product of anaerobic glycolysis which reflects:

type A oxygen delivery
type B altered metabolism with no evidence of inadequate tissue delivery

Type A causes:
anaerobic muscular activity
hypoperfusion eg shock or cardiac arrest
hypoxaemia eg anaemia

Type B causes:
pancreatitis
diabetes
leukemia
drugs - panadol, salicylates, methanol

Question 16

What are the clinical features of severe hypocalcaemia and how do you manage?

Answer 16

Features:
* Tetany
* carpopedal spasm
* decreased cardiac output
* seizures
* Prolonged QT
Chovestek sign

Management
* make sure to treat low mg with IV mg
* IV 10% calcium gluconate and then calcium infusion

Question 17

What are the signs of hyperkalaemia on ECG?

Answer 17

• Peaked T
• Wide QRS/bundle branch blocks
• P wave widening or flattening
• Bradyarrhytmias

Question 18

What are the signs of hypokalaemia ECG

Answer 18

ST depression
T wave flattening
prominent U waves
prolonged PR

Question 19

given ECG findings of hyperkalaemia how do you treat?

Answer 19

• stabilise myocardium with calcium chloride or calcium carbonate
• move K to intracelluar space with salbutamol and insulin dextrose
• remove K via frusemide or dialysis

Question 20

How do you manage life threatening hypokalemia/

Answer 20

risk of VF/VT so keep cardiac monitored
Check MG as need to replace this
replace 10mm/hr peripherally or quicker centrally
discuss with family in case of deterioration
check Cl
Disposition - HDU v ICU

Question 21

What are the causes of hyponaetremia

Answer 21

Question 22

what are important features of a history when investigating low sodium

Answer 22

• Hx organ failure – heart, renal, liver – causes hypervolemic hypoNa
• Drug history – drugs that cause SIADH, diuretics
• Mental health history – drugs that cause SIADH, water intake for psychogenic polydipsia
• Intercurrent illnesses – eg sepsis, pancreatitis, gastroenteritis– causes of hypovolemic hypoNa
• Malignancy – SIADH

Question 23

What are the risk factors for osmotic demyelination syndrome?

Answer 23

• Sodium level at presentation - most occur if under 105. Unusual over 120
• Duration of hyponaetremia - rare if developed over hours to a day eg ingesting large volumes of water
• Over rapid correction - should be 6-12 mmol/day
• other risk factors associated with ODS with less severe levels - alcoholics, liver disease, malnutrition

Question 24

How do you use hypertonic saline in TBI?What are the targets and end points?

Answer 24

3% 3ml/kg bolus IV repeating every 2-4 hours

Target:
ICP <20mmhg
osmolality 300-320mosm/l
Sodium 145-150

Question 25

What are the advantages and disadvantages of hypertonic saline vs mannitol in TBI?

Answer 25

hypertonic saline BETTER * more effective in lowering ICP * more prolonged effect on ICP * more haemodynamically stable as less change of diuresis and hypotension

Question 26

What are the most common causes of renal failure in young indiginous women

Answer 26

* diabetic nephropathy * post strep glomerulonephritis * Drug side effect

Question 27

Management priorities?

Answer 27

Move to monitored bed. Need for ECG Needs potassium replacement in monitored environment, likely to need central line for IV potassium replacement. Need to contact HDU Need for IVF as likely element of pre-renal failure in view of mild CK rise

Question 28

How do you calculate Corrected sodium

Answer 28

Corrected sodium = Na + (glucose/4)

Question 29

You notice the patient is making some spontaneous respiratory efforts which are triggering the high pressure alarms. Give your strategy for improving this patient’s ventilation, stating your desired endpoints.

Answer 29

1 - Achieve synchrony – sedate further +/‐ drug paralyse patient 2 - Improve Ventilation – increase RR to 16‐20 3 - Improve Oxygenation – 4 - increase PEEP to 10‐15cm H20 5 - Tidal volume to 480‐500mls (6mls/kg)

Question 30

State four (4) important principles regarding your fluid and electrolyte treatment of this patient while in ED, and give a justifying statement (which may include doses) for why it is an important principle.

Answer 30

* rehydrate over 48 hours - 10% dehydrated so want to ensure no fluid shifts * insulin infusion early to shift glucose into cells * closely monitor glucose to watch for rapid falls * monitor K closely as insulin can cause it to move intracellularly

Question 31

What are the management priorities for HHS

Answer 31

1. Fluids- This patient is likely to be severely dehydrated. Aim correction over next 24 hours. Example N/S 500ml/hr for first 2 hours. Then 250ml/hr next 4 hours. 2. Insulin- 0.05-0.1units/kg/hr. No bolus. 3. Electrolytes- Watch K, will need to add extra potassium as pH improves and blood K levels drop. 4. Seek and treat precipitant of current state 5. Anticipate and treat complications eg cerebral oedema. 6. Disposition to ICU as requiring close observation and possibility for deterioration.

Question 32

How do you alter potassium for PH?

Answer 32

Inversely proportional. 0.1 PH = 0.6 k

Question 33

What is the Aa gradient

Answer 33

**PA02 - Pa02** * PA02 = Partial pressure of oxygen in alveoli Pa02 = partial pressure of oxygen in the blood * PA02 worked out from alveolar gas equation Pa02 from Gas The ‘short’ form of the alveolar gas equation is: PAO2 = fi02 (713) – (PaCO2 x 1.25) fi02 of 1 = 713 fi02 of 0.21 = 150 * Pa02 from Gas

Question 34

What is a normal Aa Gradient? What can cause an abnormal gradient?

Answer 34

normal is 5-10mmHg in a non smoker on air. Increaes by 1 with each decade of life Causes 1. Diffusion defect 2. V/Qmismatch 3. right to left shunt - cardiac or pulmonary 4. increased 02 extraction

Question 35

What are the causes of a low anion gap

Answer 35

Decrease in unmeasured anions (albumin, dilution) Increase in unmeasured cations (multimyeloma (cationic IgG paraprotein), hypercalcaemia, hypermagnesaemia, lithium OD, polymixin B) bromide OD (causes falsely elevated chloride measurements)

Question 36

How do you work out expected co2 in metabolic alkalosis

Answer 36

Expected pco2= (0.7 x HCO)+ 20 (+/-5)

Question 37

what are the causes of SIADH

Answer 37

MADCHOP MAjor surgery eg abdo ADH from tumours Drugs - TCA/SSRI CNS - cerebral tumours/SAH Hormone deficiency - hypothyroid Others - GBS/HIV Pulmonary - pneumonia/TB