1
Q
What is the vasoconstrictive mechanism of action of methylene blue?
A
Inhibits nitric oxide induced cGMP activity resulting in vasoconstriction.
2
Q
How does vancomycin work?
A
Glycopeptide antibiotic: Inhibit cell wall synthesis by binding to and interfering with the ongoing synthesis of peptidoglycan cell wall.
3
Q
What is carboprost?
A
Prostaglandin F2-alpha analogue used in management of PPH. It can precipitate bronchospasm.
4
Q
What is the mechanism of action of nicorandil?
A
Potassium channel activator
Activation of ATP-sensitive potassium channels within the walls of arterioles causes hyperpolarisation, which reduces intracellular calcium. In turn, this leads to arteriolar vasodilation and subsequent reduced blood pressure.
5
Q
Describe the pKa, protein binding and relative solubility of prilocaine.
A
- pKa: 7.7
- Protein Binding: 55%
- Solubility: 50 times the solubility of procaine
6
Q
Which class of antibiotics exhibits concentration-dependent killing?
A
Aminoglycosides
(the higher the concentration, the greater the bactericidal action)
Beta-lactams are time-dependent.
7
Q
What is the mechanism of action of aminoglycoside antibiotics?
A
Prevent protein synthesis by binding to the 30S ribosomal subunit
8
Q
Which classes of antibiotics work by inhibiting bacterial protein synthesis?
A
50S: macrolides, clindamycin, chloramphenicol
30S: aminoglycosides, tetracycline
9
Q
Which intravenous antiviral agent causes obstructive crystal nephropathy?
A
Aciclovir
10
Q
What is a structural isomer of dobutamine used in anaesthetics?
A
Dihydrocodeine
11
Q
What dose of intralipid should be used in local anaesthetic toxicity?
A
1: Bolus Dose at 1.5 ml/kg over 1 min
2: Infusion at 15 mL/kg/hour
3: Second Bolus + Increase Infusion to 30 mL/kg/hour (if cardiovascular instability not sorted)
12
Q
List the absolute contraindications for parecoxib.
A
- History of ischaemic heart disease
- Active GI bleeding
- Active GI ulceration
- Cerebrovascular disease
- CABG
- IBD
- Heart failure
- Peripheral vascular disease
13
Q
Which antacids are absorbed in the GI tract and which are not absorbed?
A
NOT Absorbed: magnesium and aluminium
Absorbed: sodium bicarbonate and sodium citrate
Aluminium causes constipation whereas magnesium causes diarrhoea.
14
Q
What is the maximum safe dose of bupivacaine?
A
2 mg/kg
Adrenaline does NOT change max safe dose (as bupivacaine is already vasoconstricting).
15
Q
What is the maximum cumulative dose of intralipid that can be given?
A
12 ml/kg over 30-60 mins
I.e. 840 ml for a 70kg adult.
16
Q
Outline the Vaughan-Williams classification of antiarrhythmics.
A
- Class Ia: blocks fast Na⁺ channels, prolongs refractory period (e.g., procainamide, quinidine, disopyramide).
- Class Ib: blocks fast Na⁺ channels, shortens refractory period (e.g., lidocaine, phenytoin, mexiletine).
- Class Ic: blocks fast Na⁺ channels, no effect on refractory period (e.g., flecainide, propafenone).
- Class II: β-adrenoreceptor blockers (e.g., atenolol, propranolol, esmolol).
- Class III: K⁺ channel blockers (e.g., amiodarone, sotalol).
- Class IV: Ca²⁺ channel blockers (e.g., verapamil, diltiazem).
17
Q
What is the mechanism of action of trimetaphan?
A
Centrally acting ganglion blocker that reduces blood pressure by competing with nicotinic acetylcholine receptors in parasympathetic and sympathetic ganglia.
18
Q
List antiarrhythmics based on their effectiveness for supraventricular, ventricular, or both types of tachyarrhythmia.
A
- Supraventricular only: digoxin, verapamil, adenosine.
- Ventricular only: lidocaine, phenytoin.
- Both: amiodarone, beta-blockers, disopyramide, procainamide, flecainide.
19
Q
Which pharmacokinetic features affect a local anaesthetic’s potency, speed of onset, and duration of action?
A
- Potency: lipid solubility (more lipid soluble = more potent)
- Duration of Action: protein binding (higher binding = longer duration)
- Speed of Onset: pKa (lower pKa = faster onset)
20
Q
State the protein-binding, volume of distribution and half-life of amiodarone.
A
- Protein-binding: 95%
- Volume of Distribution: 60 L/kg
- Half-life: 20-100 days
21
Q
Describe the activity of dopamine at different dose ranges.
A
- Low dose (< 5 µg/kg/min): increased renal blood flow through agonism of D1 and D2
- Moderate dose (5-10): beta adrenoceptor agonist with positive inotropy
- High dose (> 15): alpha agonist causing vasoconstriction and bradycardia
22
Q
Which local anaesthetic can cause methaemoglobinaemia?
A
Prilocaine
23
Q
Which uterotonic agent is contraindicated in pre-eclampsia and why?
A
Ergometrine can cause coronary vasospasm and hypertension and therefore is contraindicated in pre-eclampsia.
24
Q
Which alpha blocker is an irreversible alpha antagonist and, hence, has a long duration of action?
A
Phenoxybenzamine
Non-selective irreversible alpha antagonist (new receptors must be synthesised to overcome the effect).
25
Which anticoagulants can be reversed with **andexanet alfa**?
Apixaban, rivaroxaban and edoxaban
26
What is a consequence associated with long-term use of **hydralazine**?
SLE
27
By what mechanism does **erythromycin** act as a prokinetic?
Mimics the effect of **motilin** by acting as an agonist at motilin receptors at the gastric antrum and proximal duodenum.
28
What is the mechanism of action of **labetalol**?
**Non-cardioselective beta-blocker**. It blocks both α1 and β receptors.
## Footnote
The ratio of α to β blockade is dependent upon the route of administration. When given orally the ratio is 1:3 (α to β) and 1:7 when given intravenously.
29
What is the mechanism of action of **dopexamine**?
Synthetic beta-2 and dopamine receptor agonist
30
What is the mechanism of action of **milrinone and enoximone**?
Selective phosphodiesterase III inhibitors
Primarily found in the heart - results in positive inotropic effect
31
What is the mechanism of action of **aliskiren**?
**Direct renin inhibitor**, prevents conversion of angiotensinogen to angiotensin I.
32
Why are **ACE** inhibitors contraindicated in pregnancy?
May cause **oligohydramnios** and **poor renal development**.
33
How does **gabapentin** reduce seizure activity?
Two mechanisms:
* Blockage of the α2δ subunit of L type voltage gated calcium channels leads to reduced release of excitatory transmitters (e.g. glutamate)
* Modulating GAD (glutamic acid decarboxylase) - leading to increased levels of GABA
34
What is the mechanism of action of **fluoroquinolones**?
Inhibit DNA synthesis by inhibiting **DNA gyrase** and **topoisomerase**.
35
What is the mechanism of action of **macrolide antibiotics**?
Inhibit protein synthesis by binding to the **50S** ribosomal subunit
36
What product of the breakdown of **ester local anaesthetics** can cause hypersensitivity reactions?
P-Amino Benzoic Acid
| (PABA)
37
What are the main categories of **antiepileptic** drugs?
* Sodium channel blockers
* Calcium current inhibitors
* GABA enhancers
* Glutamate blockers
* Carbonic anhydrase inhibitors
* Calcium channel blockers
38
Give some examples of **antiepileptic** drugs that are **sodium channel blockers**.
* Phenytoin
* Carbamazepine
* Lamotrigine
39
Give an example of an **antiepileptic** drug that works by inhibiting **calcium currents**.
Ethosuximide
## Footnote
Blocks T-type calcium channels
Used for focal aware seizures
40
Give examples of **antiepileptic** drugs that enhance the activity of **GABA**.
* **GABA-A agonists**: benzodiazepines, barbiturates
* **GABA reuptake inhibitor**: tiagabine
* **GABA transaminase inhibitor**: vigabatrin
* **GAD modulators**: gabapentin, valproate
41
Give examples of **antiepileptic** drugs that work by inhibiting **glutamate**.
* **NMDA blocker**: felbamate
* **AMPA/kainate blocker**: topiramate
42
What is the mechanism of action of **gabapentin** and **pregabalin**?
**They do NOT act on GABA receptors.**
Bind to the α2δ subunit of voltage-gated calcium channels, reducing calcium influx into presynaptic neurons.
This inhibits the release of excitatory neurotransmitters like glutamate, norepinephrine, and substance P, decreasing neuronal excitability to help control seizures and reduce neuropathic pain.
43
What is the mechanism of action of **levetiracetam**?
Modulates neurotransmitter release by binding to **synaptic vesicle protein (SV2A)** in the brain. This reduces excessive neuronal excitability
44
What is the protein binding of **lidocaine**?
70%
45
What is the protein binding of **bupivacaine**?
95%
46
List some drug causes of **erythema nodosum**.
COCP
Sulfonamides
Salicylates
Penicillins
Iodides
Tetracyclines
47
Describe the mechanism of action of **azole antifungals**.
Inhibit formation of ergosterol from lanosterol via inhibition of **lanosterol 14 α-demethylase** e.g. fluconazole, voriconazole, itraconazole.
48
Describe the mechanism of action of **polyene antifungals**.
Amphotericin bind to ergosterol and **create pores in the fungal cell membrane** resulting in a disrupted electrochemical gradient and cell death.
## Footnote
They are nephrotoxic e.g. amphotericin B, nystatin.
49
Describe the mechanism of action of **echinocandin antifungals**.
**Inhibit β1-3 glucan synthase**. They are used to treat invasive candidiasis e.g. caspofungin, anidulafungin, micafungin.
## Footnote
Beta-D glucan is essential in the maintenance of a fungal cell wall.
50
List some of the main side-effects of **sodium valproate**.
* Vomiting
* Alopecia
* Liver toxicity
* Pancreatitis/pancytopenia
* Retention of fat
* Oedema
* Appetite increase
* Tremor
* Enzyme inhibition
51
What is the mechanism of action of **amiodarone**?
**Class III antiarrhythmic** that blocks K⁺ channels, slowing repolarization and increasing action potential duration.
## Footnote
Also exhibits class I, II, and III properties.
52
What is the **dosing** of **amiodarone**?
**IV**: Loading dose 300 mg in 5% dextrose over 1 hour, then 900 mg over 24 hours.
**ORAL**: 200 mg TDS for 1 week, then 200 mg twice daily for another week, followed by maintenance dose, usually 200 mg daily or the minimum needed to control arrhythmia.
53
List some side-effects of **amiodarone**.
* Prolonged QT
* Pneumonitis
* Peripheral neuropathy
* Corneal microdeposits (not anterior uveitis)
* Cirrhosis
* Photosensitive slate-grey skin
* Hypo or hyperthyroidism
54
Are **local anaesthetics** weak acids or weak bases?
Weak bases
55
How does **cangrelor** work?
* Reversible ADP receptor (P2Y12) inhibitor
* Administered IV with rapid onset
* Plasma half-life of 3-5 mins
* Does NOT require activation by the liver
56
What is the **pKa** of lidocaine?
7.9
57
What is the **pKa** of prilocaine?
7.7
58
What is the **pKa** of bupivacaine?
8.1
59
What is the **protein-binding** of prilocaine?
55%
60
What is the mechanism of action of **carbimazole**?
Prodrug that inhibits thyroid peroxidase, interfering with T3 and T4 synthesis.
61
List **specific** alpha-2 blockers.
Yohimbine
Trazodone
62
List **non-specific** alpha blockers.
Phentolamine
Labetalol
Phenoxybenzamine
## Footnote
α1 > α2
63
Outline the **classes** of ACE inhibitors.
* **Class 1**: captopril – active drug with active metabolites.
* **Class 2**: enalapril and ramipril – prodrugs activated by hepatic metabolism.
* **Class 3**: lisinopril – active drug excreted unchanged.
64
Why do local anaesthetics preferentially block **sensory nerves**?
Local anaesthetics bind more readily to **inactivated** or **open** sodium channels, affecting nerves with a **higher firing rate** (i.e., sensory nerves) compared to those with a lower firing rate (i.e., motor nerves).
65
Describe the pharmacological activity of **tricyclic antidepressants** like **amitriptyline**.
Primarily **block serotonin** and **noradrenaline** transporters on the pre-synaptic membrane.
## Footnote
Other effects:
* Cardiac sodium and calcium channel blockers
* 5HT antagonist
* Alpha-1 antagonist
* NMDA antagonist
* H1 and H2 antagonist
* Muscarinic antagonist
66
List examples of **ester** local anaesthetics.
* Procaine
* Cocaine
* Benzocaine
* Tetracaine
* Chloroprocaine
## Footnote
Broken down by pseudocholinesterase EXCEPT cocaine which is metabolised in the liver.
67
List examples of **amide** local anaesthetics.
* Ropivacaine
* Prilocaine
* Lidocaine
* Bupivacaine
## Footnote
Broken down by hepatic amidases.
68
What effect do **class Ia antiarrhythmics** have on the cardiac action potential?
* Decrease slope of phase 0
* Increase effective refractory period
* Increase action potential duration
## Footnote
Examples: procainamide, quinidine, disopyramide
69
What effect do **class Ib antiarrhythmics** have on the cardiac action potential?
* Decrease slope of phase 0
* Decrease effective refractory period
* Decrease action potential duration
## Footnote
Example: lidocaine, phenytoin, mexiletine
70
What effect do **class Ic antiarrhythmics** have on the cardiac action potential?
* Decrease slope of phase 0
* Normal effective refractory period
* Normal action potential duration
## Footnote
Examples: flecainide, propafenone
71
What effect do **class II antiarrhythmics** have on the cardiac action potential?
* Decrease slope of phase 4 of pacemaker potential
* Decrease slope of phase 0 of pacemaker potential
## Footnote
Examples: beta-blockers like metoprolol and atenolol.
72
What effect do **class III antiarrhythmics** have on the cardiac action potential?
* Prolongs repolarization
* Prolongs effective refractory period
* Prolongs action potential duration
## Footnote
Examples: amiodarone, sotalol.
73
What effect do **class IV antiarrhythmics** have on the cardiac action potential?
* Slows depolarization of pacemaker cells
* Increases PR interval
* Increases effective refractory period
74
By what mechanism do **NSAIDs** cause nephrotoxicity?
NSAIDs inhibit cyclo-oxygenases, reducing **prostacyclin** production, a potent dilator of the afferent renal arteriole. This **decreases glomerular blood flow** and can lower the glomerular filtration rate, leading to kidney injury.
75
What precautions are needed for **GTN** and **sodium nitroprusside** infusions?
* **GTN**: Use glass bottles or polyethylene syringes; it absorbs into PVC bags and giving sets.
* **Sodium nitroprusside**: Avoid sunlight exposure; use opaque giving sets or wrap in foil.
* Administer oxygen to reduce shunt from impaired hypoxic pulmonary vasoconstriction.
76
Which anaesthetic agent raises **intra-ocular pressure**?
Ketamine
77
By what mechanism does **protamine reverse heparin**?
Neutralisation
## Footnote
It is positively charged, and therefore binds and neutralises heparin into an inactive complex that is subsequently excreted.
78
How is **TPN** content determined?
* **Water**: 30-40 ml/kg/day.
* **Energy**: medical patients 30 kCal/kg/day, post operative 30-45 kCal/kg/day, hypercatabolic 45-60 kCal/kg/day.
* **Protein**: medical patients 1 g/kg/day, post operative 2 g/kg/day, hypercatabolic 3 g/kg/day.
79
How does **botulinum toxin** work?
Bind to extracellular glycoproteins on cholinergic nerve terminals and **block presynaptic acetylcholine release**.
80
What is the standard dose of **ondansetron**?
**0.1 mg/kg** but a maximum of **4 mg** as a single dose.
81
What effect do **class I antiarrhythmic** drugs have on an ECG?
Usually **prolongs the QRS** duration.
82
What is the mechanism of action of **metronidazole**?
Metronidazole is a prodrug that **enters microbial cells**, reducing to free radicals that bind to DNA, disrupting its structure and inhibiting nucleic acid synthesis, leading to cell death.
83
What is **ecothiopate**?
Irreversible **acetylcholinesterase** inhibitor, it also binds plasma cholinesterase.
84
What is the mechanism of action of **phentolamine**?
**Alpha-1** and **Alpha-2** blocker.
## Footnote
Causes reflex tachycardia.
85
What is **dabigatran**?
* Reversible **non-peptide thrombin** inhibitor.
* Decreases **fibrin formation** and **reduces platelet aggregation** by inhibiting free and fibrin-bound thrombin.
86
What are the equivalent doses of the following drugs to match **5 mg prednisolone**?
* Dexamethasone
* Hydrocortisone
* Methylprednisolone
* Dexamethasone 750 mcg
* Hydrocortisone 20 mg
* Methylprednisolone 4 mg
87
What is the mechanism of action of **lamotrigine**?
Sodium channel blocker
## Footnote
Stabilises neuronal membranes and inhibits repetitive neuronal firing.
88
Describe how **amiodarone** should be administered in **ventricular fibrillation**.
Initially 300 mg IV after 3rd shock.
## Footnote
Additional 150 mg IV if arrhythmia persists after 5 shocks.
89
What is **vericiguat**?
Novel orally acting **soluble guanylate cyclase** (sGC) stimulator
90
What is **atipamezole**?
Alpha-2 adrenergic antagonist - can be used to **reverse the effects of alpha-2 agonists**.
91
How does adding **adrenaline** to **bupivacaine** affect its pharmacokinetics?
Adrenaline **lowers the pH of bupivacaine** to 3.3-5.5, compared to 5-7 for plain bupivacaine, slightly reducing the unionized fraction.
92
What is the mechanism of action of **chlorhexidine**?
Coagulates the cytoplasm of bacteria (effective against a few viruses but ineffective against spores).
93
Name two **short-acting** local anaesthetics.
* Procaine
* Chloroprocaine
## Footnote
NOTE: lasts 20-30 mins.
94
Which **inotropes** improve splanchnic and renal blood flow?
Those with **dopaminergic** (DA1 agonist) properties.
## Footnote
Examples: dopexamine, dopamine
95
What is the maximum safe dose of **lidocaine**?
**Without**: 3 mg/kg
**With**: 6 mg/kg
96
List lidocaine, bupivacaine and prilocaine in order of **decreasing lipid solubility**.
* Bupivacaine (most lipid soluble)
* Lidocaine
* Prilocaine
97
How do **edrophonium**, **pyridostigmine**, and **neostigmine** differ in acetylcholinesterase inhibition?
* **Pyridostigmine** and **neostigmine**: bind to both sites of AChE
* **Edrophonium**: binds only to the anionic site.
98
Give examples of **non-selective phosphodiesterase** inhibitors.
Aminophylline
Theophylline
99
What are the **effects** of non-selective phosphodiesterase inhibition?
* Vasodilation
* Inhibition of platelet aggregation
* Positive inotropy
100
Which drugs should you avoid with **MAO inhibitors** and why?
* **Serotonin Syndrome**: SSRI, SNRI, TCA, pethidine, tramadol, methadone
* **Hypertensive Crisis**: tyramine-containing foods, phenylephrine, ephedrine
101
How does **ropivacaine** compare to **bupivacaine**?
* Similar pKa and protein binding
* Less lipid soluble
* Less cardiotoxic
## Footnote
It is a racemic mixture.
102
What is the mechanism of action of **ivabradine**?
Selectively inhibits **funny sodium channels** in the sinoatrial node, slowing heart rate without affecting contractility.
Used for heart failure and angina.
103
Which drugs compete with **warfarin** for protein binding?
* NSAIDs
* Sulphonamides
* Gliclazide
* Amiodarone
104
Describe the mechanism of action of **doxapram**.
Dose-dependent respiratory stimulant acting on **peripheral carotid body and aortic chemoreceptors** at low doses, and the **primary respiratory center** in the medulla at higher doses.
## Footnote
Leads to increased tidal volume.
105
What is the **prednisolone to dexamethasone** conversion?
1 mg PO prednisolone = 0.15 mg PO dexamethasone
106
What is the dose conversion of **prednisolone to methylprednisolone**?
5 mg prednisolone = 4 mg methylprednisolone
107
By what mechanism does terbutaline act as a **tocolytic**?
Beta-2 agonism
## Footnote
Leads to relaxation of uterine smooth muscle.
108
What is **scopolamine**?
Non-selective **muscarinic receptor antagonist** used to treat motion sickness.
## Footnote
Aka hyoscine - crosses the BBB and can cause delirium.
109
Which classes of antibiotics are **bacteriostatic**?
* Macrolides
* Tetracyclines
* Chloramphenicol
* Clindamycin
* Linezolid
* Sulphonamides
* Trimethoprim
110
What is the maximum dose of **levobupivacaine** that can be used?
2 mg/kg
111
What type of reaction occurs between **neostigmine**, **pyridostigmine**, or **physostigmine** and the active site of **acetylcholinesterase**?
Carbamylation
## Footnote
The carbamylated enzyme reacts with water more slowly, reducing ACh breakdown and allowing its accumulation in the cleft.
112
What is the mechanism of action of **dipyridamole**?
Phosphodiesterase 5 inhibitor
## Footnote
Inhibits the breakdown of cAMP
In the platelet, cAMP reduces aggregation
113
What does **sodium nitroprusside** look like?
**Red/brown powder** which is reconstituted in 5% dextrose used for infusions.
114
Why does **glycopyrrolate** not cause much **sedation**?
It is a **synthetic quaternary amine** that does not readily cross the BBB.
115
What are the three main types of **antifungal agent**?
* **Azoles** inhibit formation of ergosterol from lanosterol via inhibition of lanosterol 14 α-demethylase e.g. fluconazole, voriconazole, itraconazole.
* **Polyenes** bind to ergosterol and create pores in the fungal cell membrane resulting in a disrupted electrochemical gradient and cell death. They are nephrotoxic e.g. amphotericin B, nystatin.
* **Echinocandins** inhibit β1-3 glucan synthase. They are used to treat invasive candidiasis e.g. caspofungin, anidulafungin, micafungin.
116
Which classes of **antimicrobials** inhibit **bacterial cell wall synthesis**?
* Penicillins (e.g., tazocin)
* Cephalosporins
* Carbapenems (e.g., imipenem)
* Monobactams (e.g., aztreonam)
* Glycopeptides (e.g., vancomycin)
117
What is the **rapid sequence dose** of **rocuronium** used?
1.2 mg/kg
118
Which **antibiotics** exacerbate weakness in **myasthenia gravis**?
* Aminoglycosides
* Fluoroquinolones
* Macrolides
119
How can **linezolid** cause serotonin syndrome?
It's a weak, non-selective monoamine oxidase A and B inhibitor that may **interact with SSRIs**, leading to serotonin syndrome.
120
How is S-warfarin **different** from R-warfarin?
S-warfarin is **more protein bound** than R-warfarin.
121
What is a main **difference** between L-bupivacaine and D-bupivacaine?
L-bupivacaine is **less cardiotoxic** than D-bupivacaine.
122
What are some of the concerning **side-effects of chlorpromazine**?
* Extrapyramidal symptoms
* Sedation
* Temperature regulation disorders,
* Blood dyscrasias (agranulocytosis, leucopenia, haemolytic anaemia)
123
What is the mechanism of action of **chlorpromazine**?
Antagonises D2, muscarinic, α1, α2, H1 and 5-HT receptors
124
How does **adenosine** terminate **SVTs**?
Binds to A1 receptors in cardiac tissue (Gi-protein coupled), leading to K⁺ channel opening and hyperpolarization. cAMP levels decrease, blocking L-type calcium channels.
125
For which **antibiotics** can you use the **normal dose** in patients having **CVVHDF**?
## Footnote
I.e. the dose for a patient with presumed normal renal function
* Amikacin
* Azithromycin
* Clindamycin
* Ciprofloxacin
* Ceftriaxone
* Doxycycline
* Linezolid
126
Why is **lactate** present in **Hartmann's solution**?
Sodium lactate is a salt of a weak acid (**lactic acid**). It doesn't release H⁺ directly; instead, it's metabolized by the liver to bicarbonate, which buffers excess hydrogen ions.
127
What are the main directly **acting vasodilators**?
Hydralazine
Sodium nitroprusside
128
What is the mechanism of action of **hydralazine**?
* Inhibits IP3-induced calcium release from the sarcoplasmic reticulum.
* Reduced cytosolic calcium decreases smooth muscle contraction.
* Directly-acting.
129
What is the **protein binding** of cocaine?
95%
130
What **initial changes** take place upon administration of a **bolus of mannitol**?
* **Increase** in circulating volume (preload)
* **Decrease** in serum sodium due to dilution
131
Describe the effect of **acetazolamine** on **urinary pH**.
* It inhibits **carbonic anhydrase** leading to impaired excretion of acid in the urine.
* Induced a **metabolic acidosis** and urinary pH will.
132
How is **cyclizine** metabolised?
* Metabolised in the liver by **dealkylation** to inactive metabolites.
* Duration: 4-6 hours.
133
Describe the mechanism of action of **methyldopa**.
Metabolised in the **CNS to alpha-methyl-norepinephrine** which is an alpha-2 blocker.
134
What's the **boiling point** of ethanol?
78 degrees
135
What are the three components of the **structure** of a local anaesthetic?
* Aromatic group
* Intermediate chain
* Amine group
136
What are the two functional groups that can form the **intermediate chain** in local anaesthetic agents?
Ester and Amide
137
Which **enantiomer** of local anaesthetics is most useful?
* Increased vasoconstriction for prolonged action and reduced systemic absorption
* Reduced cardiotoxicity
* Reduced motor blockade
## Footnote
Applies to bupivacaine, prilocaine, ropivacaine, and mepivacaine.
138
How is **methylene blue** useful in **vasodilatory shock**?
Blocks soluble guanylate cyclase, preventing NO-induced cGMP increase that leads to vasodilation.
139
List examples of **medium** and **long-acting** **acetylcholinesterase** inhibitors.
**Medium-acting:**
* Neostigmine
* Pyridostigmine (for myasthenia gravis)
* Physostigmine (for glaucoma)
**Long-acting:**
* Ecothiopate (lasts weeks; includes sarin and VX nerve gases)
140
Describe the mechanism of action of **carbonic anhydrase** inhibitors.
They inhibit **carbonic anhydrase** in the proximal convoluted tubules, affecting sodium-H⁺ exchange, leading to urine alkalinization and metabolic acidosis.
141
Give an example of a **selective COX inhibitor**.
Parecoxib - COX-2
142
List some **non-selective** MAO inhibitors.
Phenelzine
Hydralazine
143
List some **selective** MAO-A inhibitors.
Moclobemide
Pirlindole
144
List some **selective** MAO-B inhibitors.
Selegiline
Rasagiline
145
What are some **risks** associated with **MAO inhibitors**?
Hypertensive crises (due to raised catecholamines)
Serotonin syndrome
146
List some **reversible** inhibitors of **monoamine oxidase**.
* Methylene blue
* Moclobemide
* Brofaromine
147
Describe the mechanism of action of **pralidoxime**.
Used within 36-48 hours of onset. Displaces phosphate from the esteratic site. Administer oximes to help enzyme recovery.
## Footnote
Without treatment, recovery relies on new AChE synthesis.
148
Which antibiotic is a reversible **MAO inhibitor**?
**Linezolid** - reversible MAO inhibitor
149
Describe the mechanism of action of **streptokinase**, **alteplase**, and **urokinase**.
Induces conversion of **plasminogen** to **plasmin**, promoting clot breakdown.
150
Which **enantiomer** of warfarin is most potent?
S-warfarin
151
What is the maximum safe dose of **prilocaine**?
6 mg/kg
152
What is the intravenous dose of **adrenaline** in intra-operative anaphylaxis?
50 µg (0.5 mL of 1:10,000)
## Footnote
Paediatrics: 1 µg/kg IV (0.1 mL/kg of 1:100,000)
153
What is the **pKa** of ropivacaine?
8.1
154
What is the **pKa** of cocaine?
8.6
155
What is the **maximum dose of ropivacaine** that can be used?
3 mg/kg
156
What is the **maximum dose of lidocaine** that can be used?
3 mg/kg
7 mg/kg with adrenaline
157
What **bolus dose of glycopyrronium** should be used in bradycardia?
200-400 µg (5 µg/kg)
158
What **bolus dose of atropine** should be used in mild bradycardia?
300-600 µg (5 µg/kg)
## Footnote
If CRITICAL bradycardia, give 20 µg/kg (0.5-1 mg).
159
What **dose of dantrolene** should be used for malignant **hyperthermia**?
2-3 mg/kg immediate IV bolus (approximately 200 mg)
## Footnote
Repeat 1 mg/kg every 5 mins until ETCO2 < 6 kPa and temp < 38.5 and repeat as required to maintain parameters.
160
What **bolus dose of phenylephrine** should be used in hypotension?
100 µg (5 µg/kg)
161
What **bolus dose of labetalol** can be used as a temporising measure in hypertension?
25-50 mg (0.5 mg/kg)
## Footnote
Esmolol dose is the same
162
What **dose of hydralazine** can be used as a temporising measure in hypertension?
5-10 mg (0.1 mg/kg)
163
What rate of **GTN** infusion is used for intraoperative hypertension?
0.5-5 µg/kg/min
## Footnote
This equals 2-20 mL/hr of 1 mg/mL solution.
164
What **dose of ephedrine** should be used in bradycardia?
3-12 mg (100 µg/kg)
165
What **dose of calcium** should be used in massive intraoperative haemorrhage?
**Adult**: 10 ml of 10% calcium chloride
**Adult**: 20 ml of 10% calcium gluconate
**Child**: 0.2 ml/kg of 10% calcium chloride
**Child**: 0.5 ml/kg of 10% calcium gluconate
166
What dose of **tranexamic acid** is used in intraoperative massive haemorrhage?
**Adult**: 1 g bolus, then:
* Obstetric: repeat 30 mins later
* Non-obstetric: 1 g infusion over 8 hrs
**Child**: 15 mg/kg bolus, then 2 mg/kg/hr until bleeding stops.
167
What is the intravenous dose of **salbutamol** for intraoperative bronchospasm?
**Bolus**
* Adult: 250 µg
* Child (2-17 yrs): 15 µg/kg (max 250 µg)
* Child (<2 yrs): 5 µg/kg
**Infusion**
* Adult: 5-20 µg/min
* Child: 0.5-1 µg/kg/min (max 20 µg/min)
168
What is the dose of **adrenaline** for treating intraoperative bronchospasm (nebulised, IM, IV)?
**Nebulised**
* Child: 0.5 mL of 1:1000
* Adult: 5 mL of 1:1000
**IM**
* < 6 months: 50 µg
* < 6 yrs: 120 µg
* < 12 yrs: 250 µg
* Adult: 500 µg
**IV Bolus**
* 0.1-1 µg/kg (Adult: 10-100 µg)
169
What **dose of ketamine** should be used to treat intraoperative bronchospasm?
* **Adult**: 20 mg
* **Infusion**: 1-3 mg/kg/hr
170
What dose of **aminophylline** is used for intraoperative bronchospasm?
5 mg/kg over 20 mins.
## Footnote
Infusion:
* <9 yrs: 1 mg/kg/hr
* <16 yrs: 0.8 mg/kg/hr
* Adult: 0.5 mg/kg/hr
171
What **dose of IV hydrocortisone** should be given to treat intraoperative bronchospasm?
4 mg/kg (Adult: 200 mg)
172
What are the drug doses for treating **laryngospasm**?
* **Propofol**: 0.25-0.5 mg/kg IV
* **Rocuronium**: 0.25-0.5 mg/kg IV
* **Atracurium**: 0.25-0.5 mg/kg IV
* **Suxamethonium**: 4 mg/kg IM
173
What is the **pKa** of amethocaine?
8.5
174
What is the **pKa** of procaine?
8.9
175
How does **ethyl chloride** spray work?
* **Ethyl chloride** is a colorless gas with a boiling point of 12°C.
* Stored as a liquid under pressure, it is applied to the skin as a fine jet.
* Heat from the skin causes it to vaporize (**latent heat of vaporization**), rapidly cooling the skin and impairing sensory nerves.
## Footnote
Used to test blocks in neuraxial anaesthesia.
176
What are the two ways of classifying **antiarrhythmic** drugs?
Vaughan-Williams classification
Functional (SVT, VT and both)
177
How can **positive inotropy** be achieved?
* Beta-agonists (increase cAMP)
* Non-adrenergic agents (e.g. glucagon) which increase cAMP
* Phosphodiesterase inhibitors (inhibit breakdown of cAMP)
178
What are the clinical features of **local anaesthetic toxicity**?
**CNS (early)**:
* Tingling tongue/lips
* Light-headedness
* Tinnitus
* Slurred speech
* Loss of consciousness (LOC)
**CVS (later)**:
* Myocardial depression
* Arrhythmias (e.g., VF)
179
What is **Ametop** and how does it work?
4% **tetracaine** in a white gel. Apply for 30-45 mins; lasts 4-6 hours. Causes venous **dilation**.
180
What are the doses for a **lidocaine** infusion for analgesia?
* **Bolus**: 1.5 mg/kg over 2-4 mins
* **Infusion**: 1 mg/kg/hr
## Footnote
Use lean body mass.
181
What is **EMLA** and how does it work?
**Eutectic mixture** of local anaesthetics: **2.5% lidocaine** and **2.5% prilocaine** in a white oil-water emulsion.
Apply 1 hour before cannulation; lasts 2 hours.
Causes venous **constriction**.
182
How can **adrenaline** be administered?
* **Bolus**: cardiac arrest, anaphylaxis
* **Infusion**: ICU
* **Nebuliser**: upper airway obstruction
* **Local Anaesthetic**: local vasoconstriction
* **Ophthalmic**: open-angle glaucoma
183
What is the onset of action and duration of action of **phentolamine**?
**Onset**: 2 mins
**Duration**: 20 mins
## Footnote
Alpha-1 and alpha-2 blocker.
184
How long do the effects of **phenoxybenzamine** last?
3 days
185
Describe the presentation of intravenous **amiodarone**.
**150 mg** in solution, diluted with **5% dextrose**, administered via wide **bore cannula** or central line.
186
What is the mechanism of action of **glyceryl trinitrate**?
* Act via production of NO.
* NO causes an **increase in cGMP** in vascular smooth muscle.
* This increases Ca uptake into the sarcoplasmic reticulum resulting in **vasodilation**.
187
What are the three classes of **calcium channel blockers**?
* **Class 1**: e.g. **verapamil** (L-type channels in SA/AV node, primarily antiarrhythmic)
* **Class 2**: e.g. **nifedipine** (L-type channels in periphery, reduces SVR, increases coronary blood flow)
* **Class 3**: e.g. **diltiazem** (L-type channels peripheral and nodal, increases coronary blood flow, decreases SVR and AV conduction)
188
Which **beta-blockers** can be given intravenously?
* **Atenolol**: 2.5 mg IV bolus
* **Esmolol**: 10 mg IV bolus
* **Landiolol**: S enantiomer of esmolol
* **Labetalol**: 20 mg IV bolus
* **Metoprolol**: 5 mg IV bolus
* **Propranolol**: 0.5 mg IV bolus
* **Sotalol**: 50-100 mg IV bolus
189
What are the uses of **beta-blockers**?
* Angina
* Hypertension
* Myocardial Infarction (MI)
* Atrial Fibrillation (AF) Rate Control
* Migraine Prophylaxis
* Essential Tremor
* Anxiety
* Hyperthyroidism
190
How do **phosphodiesterase 3 inhibitors** cause vasodilation?
1. Increased cAMP
2. More PKA activity
3. Reduced calcium influx
4. Relaxation
## Footnote
cAMP increases intracellular Ca in cardiomyocytes, leading to positive inotropy.
191
Describe the **presentation** and **dosing** of **noradrenaline**.
Dilute to **protocol concentration** (e.g., 4 mg in 50 mL). Start at **0.1** µg/kg/min.
192
Why are **amide** local anaesthetics preferred over **ester** local anaesthetics?
* Lower allergic reaction rates
* Longer duration of action
* Greater chemical stability for storage
193
Which classes of antibiotics inhibit **nucleic acid synthesis**?
* Sulphonamides and Trimethoprim (folate synthesis)
* Quinolones (inhibit DNA gyrase)
* Imidazoles
* Rifampicin (RNA polymerase inhibitor)
194
Which classes of antibiotics interfere with **cell wall synthesis**?
* **Beta-lactams**: prevent cross-linking of peptidoglycan
* **Glycopeptides** (e.g., vancomycin, teicoplanin): inhibit peptidoglycan formation
195
Which classes of antibiotics inhibit **protein synthesis**?
* **Aminoglycosides** (30S ribosome)
* **Tetracyclines** (30S ribosome)
* **Macrolides** (50S ribosome)
* **Chloramphenicol** (50S ribosome - inhibits peptidyl transferase)
196
What is the mechanism of action of **Dabigatran**?
Direct thrombin inhibitor
## Footnote
Twice daily dosing and used to treat non-valvular AF and VTE prophylaxis
197
Describe the metabolism and excretion of **apixaban** and **rivaroxaban**.
**Apixaban**: hepatic metabolism, 75% biliary excretion, 25% renal excretion.
**Rivaroxaban**: hepatic metabolism, 70% renal excretion, 30% biliary excretion.
198
What is the protein binding of **warfarin**?
99%
199
Describe the mechanism of action of **unfractionated heparin**.
* Naturally occurring **glycosaminoglycan** found in mast cells and basophils.
* Binds to **antithrombin III**, enhancing its activity by 1000 times.
* Primarily **inactivates thrombin** and factor Xa.
200
What is the **offset time** of unfractionated heparin infusions?
4 hours
201
What are the **advantages** and **disadvantages** of **LMWH** compared to **UFH**?
**Advantages:**
* Predictable pharmacokinetics (no monitoring required)
**Disadvantages:**
* Accumulates in renal failure
* Risk of underdosing in obese patients
202
What is the time to offset of **LMWH**?
**Prophylactic Dose**: 12 hours
**Therapeutic Dose**: 24 hours
203
List the main classes of **antiemetics** with examples.
* Antihistamines (e.g. cyclizine)
* 5HT3 Antagonists (e.g. ondansetron)
* Anticholinergics (e.g. hyoscine)
* Dopamine Antagonists (e.g. metoclopramide, domperidone)
* Phenothiazines (e.g. chlorpromazine)
* Neurokinin 1 Antagonist (e.g. aprepitant)
204
What is the mechanism of action of **phenothiazine antiemetics**?
* **Dopamine (D2)** antagonist (main mechanism)
* Muscarinic antagonist
* Histamine (H1) antagonist
## Footnote
Examples: prochlorperazine, promethazine
205
Which classes of **antifungals** target the fungal cell wall?
* **Polyenes** (e.g., amphotericin, nystatin)
* **Azoles** (e.g., imidazoles like ketoconazole, triazoles like fluconazole)
* **Allylamines** (e.g., terbinafine)
## Footnote
These interfere with ergosterol synthesis.
206
Which **antifungals** target the fungal cell nucleus?
**Flucytosine**: inhibits DNA and RNA synthesis
**Griseofulvin**: inhibits mitosis
207
What are some side-effects of **amphotericin**?
* Nephrotoxicity
* Electrolyte disturbance
* Bone marrow suppression
* Anaphylactoid reactions
208
What are some side-effects of **azole antifungals**?
* Hepatic dysfunction
* Prolonged QT interval
* Can inhibit P450 system
209
What are the main classes of **antiplatelet agents**?
* **COX Inhibitors** (e.g., aspirin)
* **ADP Antagonists** (e.g., clopidogrel, prasugrel, ticagrelor)
* **PDE3 Inhibitors** (e.g., dipyridamole)
* **Glycoprotein IIb/IIIa Inhibitors** (e.g., abciximab, tirofiban, eptifibatide)
## Footnote
Glycoprotein IIb/IIIa inhibitors are intravenous only.
210
What is the onset of action, peak effect and duration of **short-acting insulins**?
* **Onset**: 10-15 mins
* **Peak Effect**: 1 hour
* **Duration**: 4 hours
*
*
## Footnote
Examples: Novorapid (aspart), Humalog (lispro)
211
What is the onset and duration of **intermediate** and **long-acting insulins**?
* **Intermediate** (e.g., Insulatard): 90-120 mins onset, 8-10 hours duration
* **Long-acting** (e.g., Lantus): 18-36 hours duration, 2-3 days to reach steady state
212
How does **MDMA** work?
* Stimulates release of endogenous monoamines like dopamine and serotonin, causing **euphoria and excitation**.
* It **reverses monoamine transporter** function and inhibits **reuptake**.
213
What is the mechanism of action of **LSD**?
* 5HT-2 receptor agonist
* Hallucinogen
214
Which **hormones** or stimuli cause **uterine contraction** and **relaxation**?
**Contract**
* Alpha stimulation
* Prostaglandin EP3 activation
* Oxytocin receptors
**Relax**
* Beta-2 adrenoceptors
215
Describe the clinical effect of **syntocinon**.
* **Dosage**: 5 units bolus, 10 units/hr infusion
* **Uterus**: increased contraction frequency and amplitude
* **Mammary**: contraction
* **CVS**: vasodilation, hypotension, tachycardia
* **Renal**: ADH effect (similar structure)
216
Describe the clinical effects of **ergometrine**.
* **Dosage**: 0.5 mg IM
* **Uterus**: contraction (alpha, serotonin, and D2 agonism)
* **CVS**: hypertension, vomiting
217
Describe the clinical effects of **misoprostol**.
* **Dosage**: 800 µg PR (prostaglandin E1 analogue)
* **Uterus**: cervical relaxation, uterine contraction
* **CVS**: may cause diarrhoea, pyrexia, shivering
218
Describe the clinical effects of **carboprost**.
* **Dosage**: 0.25 mg IM (prostaglandin F2-alpha analogue)
* **Uterus**: contraction
* **Side effects**: hypertension, bronchospasm
219
List commonly used drugs that cause **uterine relaxation**.
* **Atosiban**: oxytocin receptor antagonist
* **Beta-2 agonists**: e.g. terbutaline 5 µg/min IV
* **Calcium channel blockers**: e.g. nifedipine 20 mg PO
* **GTN**
* **Inhalational anaesthetics**: except nitrous oxide
220
Which antiemetics target the two parts of the **vomiting centre**?
**Chemoreceptor Trigger Zone**
* Dopamine antagonists (e.g. metoclopramide, droperidol)
* 5HT3 antagonists (e.g. ondansetron)
**Nucleus Tractus Solitarius**
* Antimuscarinics (e.g. hyoscine)
* Antihistamines (e.g. cyclizine)
221
What **dose of IV adrenaline** is used in intraoperative anaphylaxis?
50 µg
222
Which drug classes improve **coronary blood flow**?
* Nitrates
* Beta-blockers (increase diastolic time)
* Calcium channel blockers (CCBs)
* Potassium channel openers
223
Which antiemetics are contraindicated in **Parkinson's disease**?
* Prochlorperazine (phenothiazine)
* Droperidol (butyrophenones)
* Metoclopramide (benzamides)
224
What classes of drugs reduce **stomach acid** secretion?
* **H2 Receptor Antagonists** (e.g., ranitidine)
* **Proton Pump Inhibitors** (e.g., omeprazole)
* **5-HT3 Antagonists** (minor role)
225
Which drugs can be used to **protect the gastric mucosa** without altering the pH?
* Sucralfate
* Misoprostol
226
What is the mechanism of action of **metformin**?
Activates AMP-activated protein kinase which **reduces hepatic gluconeogenesis** and enhances peripheral glucose uptake.
227
What is the mechanism of action of **sulfonylureas**?
Close ATP-sensitive K channels in pancreatic beta cells, causing depolarization. This opens **voltage-gated Ca channels**, leading to insulin release.
## Footnote
Meglitinides act similarly but are faster.
228
What is the mechanism of action of **cyclizine**?
* H1 antagonist (in vestibular system and vomiting centre)
* Anticholinergic (muscarinic) adds to antiemetic effect
229
What are the main **differences** between first and second generation antihistamines?
* **First generation** (e.g., chlorphenamine, hydroxyzine):
- Crosses BBB (sedating)
- Anticholinergic side effects
* **Second generation** (e.g., loratadine, cetirizine, fexofenadine):
- Does NOT cross BBB
- Fewer anticholinergic side effects
230
Describe the mechanism of action of **dipyridamole**.
* Inhibits PDE3 --> prevents breakdown of cAMP and cGMP
* Leads to inhibition of platelet activation and aggregation
231
What **bolus of naloxone** is given in suspected opioid overdose?
200 µg IV
232
What are some features of **TCA overdose**?
* **Anticholinergic Effects**: dry mouth, dry nose, blurred vision, constipation, urinary retention, sweating, increased body temperature.
* **CNS Effects**: drowsiness, confusion, myoclonus, seizure, coma.
* **CVS Effects**: tachycardia, arrhythmias, hypotension, transient hypertension, VT, VF and prolonged QT interval.
233
What does the **ratio** when describing **adrenaline** mean (e.g. 1 in 1000)?
* 1 gram of adrenaline in 1000 mL (e.g. 1 mg/mL)
* 1 in 10,000 = 100 mcg/mL
* 1 in 100,000 = 10 mcg/mL
234
Give examples of **irreversible enzyme inhibitors**.
* **Aspirin** (non-selective COX)
* **Phenelzine** and **tranylcypromine** (MAO inhibitors)
235
List examples of **enzymes** used as drugs.
* **Fibrinolytics**: streptokinase, urokinase, alteplase
* **Hyaluronidase**: promotes diffusion in the ophthalmic region.
236
Give examples of **MAO inhibitors**.
* **MAO-A**: moclobemide
* **MAO-B**: selegiline, rasagiline
* **Non-Selective**: phenelzine, tranylcypromine
237
Outline the classification of **beta-blockers**.
* **Cardio-selective**: bisoprolol, esmolol, atenolol, metoprolol
* **Non-selective (beta)**: propranolol
* **Alpha- and beta-blockers**: labetalol, carvedilol
238
List classes of drugs that can be used as **tocolytics in obstetrics**.
* Beta-2 agonist (e.g. terbutaline)
* Calcium channel blockers (e.g. nifedipine)
* Oxytocin antagonist (e.g. atosiban)
* Magnesium
* Nitrates
239
What **dose of mannitol** should be administered in raised ICP?
100 mL 20% Mannitol
240
Outline the mechanism of action of **cocaine**.
Blocks monoamine reuptake (dopamine, noradrenaline and serotonin)
241
Outline the mechanism of action of **cannabis**.
* Agonist at CB1 and CB2 cannabinoid receptors (CB1 primarily in CNS, CB2 mainly in immune system).
* CB1 receptor activation → inhibition of adenylate cyclase → reduced cAMP → decreased neurotransmitter release (e.g., GABA and glutamate).
242
Outline the mechanism by which **glucagon** exerts an inotropic effect.
* **Glucagon receptors** (Gs) activate adenylate cyclase, increasing cAMP.
* This **activates PKA**, enhancing calcium availability (via increased Ca influx through L-type channels and sarcoplasmic release).
* Result: ↑ contractility (positive inotropy) and ↑ heart rate (positive chronotropy).
243
What is a key **difference** between hyoscine butylbromide and hyoscine hydrobromide?
Both are **antimuscarinics** but:
* **BUTYLbromide**: does not cross BBB (e.g. buscopan)
* **HYDRObromide**: crosses BBB producing sedation
244
What are clinical uses of **antimuscarinics**?
* **Antiemetic**: e.g. hyoscine
* **Antisialagogue**: e.g. glycopyrronium
* **Bradycardia**: e.g. atropine
* **Bronchodilator**: e.g. ipratropium
* **Antispasmodic**: e.g. hyoscine butylbromide
## Footnote
Hyoscine is also known as scopolamine.
245
What is the **maximum dose of cocaine** local anaesthetic?
3 mg/kg
246
What are the main classes of **dopamine antagonists** used as antiemetics?
* **Phenothiazines**: prochlorperazine
* **Butyrophenones**: haloperidol
* **Benzamides**: metoclopramide, domperidone
247
What is the main **difference** between **aminoglycosides** and **beta-lactams** regarding their effectiveness?
* Aminoglycosides: **concentration-dependent killing**; dosing maximizes peak concentration/MIC.
* Beta-lactams: **time-dependent killing**; dosing maximizes duration above MIC.
248
Outline the mechanisms of **penicillin resistance**.
* Drug inactivation (e.g. beta-lactamase)
* Alterations in penicillin-binding protein
* Alterations in cell wall permeability (drug efflux)
249
How do **thiazides** cause **hypercalcaemia**?
* Thiazides inhibit the Na/Cl cotransporter, **reducing intracellular Na**.
* This triggers increased Na/Ca exchange, leading to more calcium reabsorption and **hypercalcaemia**.
250
What are the main **uterotonic agents** and their mechanisms?
* **Syntocinon**: oxytocin agonist (Gq → increased calcium)
* **Ergometrine**: alpha agonist, 5HT2 agonist
* **Carboprost**: PGF2α analogue (acts on FP receptor)
* **Misoprostol**: PGE1 analogue (acts on EP receptor)
251
What are the pH values of **Plasma-Lyte**, **Hartmann's**, and **0.9% NaCl**?
* **Plasma-Lyte**: 7.4
* **Hartmann’s**: 6.5
* **0.9% NaCl**: 5.5
Primary FRCA
flashcards
Decks in class (17)
# Cards
-
Anatomy for Anaesthesia223
-
Physiology: Respiratory303
-
Physiology: Cardiovascular179
-
Physiology: Renal, Hepatic & GI63
-
Physiology: Neuro, Endo, & Haem237
-
Pharmacokinetics and Pharmacodynamics213
-
Pharmacology: Inhalational & Intravenous Agents232
-
Pharmacology: Analgesics & Muscle Relaxants160
-
Pharmacology: Emergency & Miscellaneous Drugs251
-
Part 1: Physics & Equipment242
-
Part 2: Physics & Equipment227
-
Part 3: Physics & Equipment232
-
Part 4: Physics & Equipment217
-
Statistics & Evidence-Based Practice36
-
Part 1: Applied Clinical Anaesthesia165
-
Part 2: Applied Clinical Anaesthesia169
-
Part 3: Applied Clinical Anaesthesia157
