• Allergy; rash; pruritis
• Nausea, abdominal pain, diarrhoea
• GI irritation / ulcers
• Bleeding secondary to inhibition of platelet aggregation
• Nephrotoxicity
• Peripheral oedema; fluid retention
• Headache

Pass Criteria:

• 3 bold to pass

• Salicylism – vomiting, tinnitus, hearing loss and vertigo
• Exacerbation of asthma
• Histamine induced flushing
• Irreversible platelet inhibition
• Raised LFTs

Pass Criteria:

• Any 2 to pass

• Morphine is a full agonist in the mu receptor -> analgesia, sedation, decreased respirations, decreased GIT transit, modulation of hormone and neurotransmitter release
• Also affects delta -> analgesia, modulation of hormone and neurotransmitter release and kappa -> analgesia, psychomimetic effects, decreased GIT transit

Pass: Agonist mu receptor + 1 receptor

• CNS: Analgesia, euphoria, sedation, respiratory depression; miosis, hyperthermia
  • Stimulates release of ADH, prolactin and somatotrophin
  • Truncal rigidity,
• Resp: depression, Cough suppression,
• CVS: bradycardia
• GIT: constipation, contracting biliary smooth muscle, N&V,
• Renal: Depressed renal function
• Gynae: Decreases uterine tone
• Skin: Pruritis, urticaria

Pass: CNS + resp + 2 others

• Blockade of voltage-gated Na channels

• CNS: sleepy, light-headed, circumoral numbness, seizures
• Cardiovascular: direct and indirect, depress pacemaker, excitability and conduction
• Haematology: Methemoglobinaemia ( accumulation of 0 –toluidine)
• Neurotoxicity
• Allergy

Pass: At least 2

• Amide link hydrolysed by P 450 in liver and then renal excretion

• Aspirin Steroidal anti-inflammatory drugs via COX 2
• NSAIDS: Non selective COX-1 and COX –2 inhibitors
• COX 2 selective agents: Celecoxib & Rofecoxib

• Alteration and inhibition in the biosynthesis of prostaglandins but also may: inhibit IL-1
• Inhibit chemotaxis
• Decrease production of free radicals
• Interference with calcium mediated intracellular events

• Antipyretic [PGE1 and PGE 2]
• Anti-inflammatory [complex:COX-2 inhibition more important]
• Analgesic [peripherally via effects on inflammation]
• Reversible anti-platelet effect[TXA₂]
• Inhibtion of gastric cytoprotection[PGE₁ and E group]
• Renal impairment[PGE₁ and PGE₂ and PGI₂ increase GFR through vasodilation
• Effects on smooth muscle: inhibit vasodilation, bronchodilation[PGE₂]
• Closure of PDA[PGE₁ & PGE₂]
• All NSAIDS are roughly equally efficacious –there is no best NSAID for all patients

Common or Common to group

• Allergy
• Anaphylaxis
• Angioedema
• Asthma exacerbation [ Nasal polyps association]
• Gastritis
• Peptic ulceration
• GI bleeding
• Increase bleeding tendency
• Renal impairment especially if dehydration, elderly or pre-existing renal disease is also present
• Nausea and vomiting
• Peripheral oedema
• Pregnancy –fetal PDA closure

Some NSAID’s

• Hepatic impairment
• Agranulocytosis
• Aplastic anaemia
• Thrombocytopaenia
• Neurlogical –various
• Headaches
• Diarrhoea
• Pancreatitis
• Pseudoporphyria

• Blockade of voltage-gated Na channels in neurones
• Increasing doses lead to higher excitation threshold, slower impulse conduction, lower AP
• Blocks conduction if 2-3 nodes of Ranvier in a myelinated nerve affected

Pass: Blockage of Na channels and blocked conduction.

• Lignocaine – oral spray for procedures, viscous for pharynx, with prilocaine in EMLA, other mixtures for wound and ENT care, eye drops
• EMLA (Eutectic Mixture of Local Anaesthetics – mixture of lignocaine and prilocaine) – skin anaesthesia for cannula insertion, etc.
• Cocaine – ENT procedures (combines vasoconstriction)
• Eye Drops: Proxymetacaine, amethocaine, oxybuprocaine
• Benzalkonium – oral gels

Pass Criteria:

• 2 agent

Peak 30- 60 min, slightly prot bind
[symple_toggle title=”How is paracetamol eliminated from the body?
Liver metabolised via microsomal enzymes, (sulphate and glucuronide) 5% hydroxylated and conjugation with glutathione/cysteine via P450 (< 5% excreted unchanged),
Describe the mechanism of liver damage caused by paracetamol toxicity.
N ac benzoiminoquinone reacts with sulphhydryl groups on proteins. (Prevention using N ac cysteine)

Converts to polar metabolites in form of glucuronides in liver.

Primarily conjugated to morphine-3-glucuronide (M3G) -> 5neuro-excitatory properties. 10% of morphine conjugated to morphine-6-glucuronide (M6G) -> analgesic effect
What opioid receptor sites does it act on?
Full agonist at mu receptor. But also acts on delta and kappa receptor sites.

Close voltage-gated Ca channels -> decreased 4. 1 Ca influx on presynaptic nerve terminals and decreased transmitter release
Hyperpolarise postsynaptic neurones by increased K conductance -> inhibitory postsynaptic potential

• Sodium channel blacker
• Voltage gated

NOTES: Interfere with propagation of AP by blocking the increase in sodium permeability during depolarization. Provide pain relief by blocking nociceptive fibers. Other fibers are affected as well.

Sensitivity depends on: fiber diameter, fiber type, degree of myelination. Sensory modalities are affected in the following order: pain, cold, warmth, touch, and pressure. Most local anesthetics are weak bases, pKa 7.5-9M

 
How are local anaesthetics classified? Give an example of each group?”] Esters and Amides: Esters are hydrolyzed by plasma and liver esterases. Amides are metabolized in the liver.

Patients with severe hepatic damage or advanced congestive

heart failure may be unusually sensitive to these drugs. Some amides are partially excreted unchanged in the urine Esters: cocaine, procaine, amethocaine and chloroprocaine, amides lignocaine, prilocaine, mepivacaine and

bupivacaine.

Pass: 1 example of each

NOTES: Allergic reactions are rare, especially with 2mide local anesthetics.

 

Ease of application (Not messy; No dressing; Well tolerated by kids; Not painful)

Rapid Onset of action

Low (nil) systemic toxicity eg MetHb with EMLA in neonates

High analgesic efficacy

Reasonable duration of action

Not allergenic

May be applied to the skin, the eye, the ear, the nose and the mouth as well as other mucous membranes.

EMLA cream a eutectic mixture of LAs provides surface anaesthesia of the skin (partic paeds). A mixture of base forms of lignocaine & prilocaine in equal proportions in an

emulsion. Cutaneous contact (usually under an occlusive dressing) should be maintained for at least 60 min prior to venipuncture

Other LA agents may be abs in significant amounts

particularly after topical application to the more vascular

areas, fatalities have occurred after application of these agents to mucosal surfaces.

NOTES:

Allergic reactions are rare, especially with 2mide local anesthetics.

Absorption of LAs

through intact skin is usually slow and unreliable and high concentrations (e.g.20% benzocaine or 40% lignocaine) are required. In general, cocaine, amethocaine, lignocaine and prilocaine are the most useful and effective local anaesthetics for this purpose. When used to produce topical anaesthesia, they usually have a rapid onset of action (5-10mins) and a moderate duration of action (30-60 mins).

 

•             Renal toxicity

•             GIT but fewer than non selective NSAIDs

•             Possible increased CVS thrombotic events.

Pass: 2 of 3

Aspirin

Non steroidals

Amides and esters

Increased ionisation