ICP MEDICATION MOA Flashcards
WHAT IS THE MECHANISM OF ACTION FOR ADRENALINE?
Stimulation of Alpha and Beta Receptors to cause flight or fight response by the SNS.
A1 - vasoconstriction of peripheral blood vessels, ↑ perfusion pressure of vital organs. ↓ capillary permeability, ↓ mucosal oedema, pupil dilation.
A2 - ↓insulin release, ↓ presynaptic inhibition of noradrenaline release.
B1 - ↑ HR (chronotropic), ↑ contractility (inotropic)
FOC and HR increase due to ↑ cAMP (cyclic adenosine monophosphate).
= ↑ Ca2 and ↑ Na => ↓ K+ = ↑ ROR (Rate of rise) in phase 4. Shortens the time between action potentials (AP)
(Pacemaker potential)
B2 - ↑ bronchodilation (↑ cAMP = ↓ Ca channels = smooth muscle relaxation), ↓ inflammatory mediator release from mast cells and basophils.
WHAT IS THE MECHANISM OF ACTION OF ATROPINE?
Anticholinergic and vagolytic (blocks vagal action of heart). Increases sympathetic drive and prevents actions of PNS.
Competitively binds to Acetylcholine and M2 Muscarinic receptors located on the SA and AV node, increasing rapid firing of SA/AV node. This results in ↑ NA, CA+ ∴ ↓ in K+.
Decreased conduction time at AV node, ↑ HR.
This ↑ ROR of phase 4 = shorter duration of APs
= ↑ HR (pacemaker potential)
↑ rate at SA node and ↑ conduction at AV junction
WHAT IS THE MECHANISM OF ACTION OF AMIODARONE?
Class III antiarrhythmic:
- Blocks K+ channels causing a prolonged phase 3 (repolarisation), ↑ refractory period and causing prolonged QT. (cardiac action potential on myocytes and pacemaker cells).
- Blocks inactivated Na+ channels
- ↓ peripheral vascular resistance (afterload) by inhibiting B1 adrenoceptors.
- Acts as a Beta Blocker to slow HR
WHAT IS THE MECHANISM OF ACTION OF LIGNOCAINE 2%?
Class 1b antiarrhythmic that ↓ ventricular excitability
Blocks inactivated voltage gated Na+ channels.
This ↓ slope in phase 4 = ↓ ROR = longer to depolarise.
Phase 0 & 4 delayed ∴ slowing force of contraction.
(Cardiac action potential)
WHAT IS THE MECHANISM OF ACTION OF CALCIUM GLUCONATE?
Electrolyte that ↓ excitability of cardiomyocytes by ↑ membrane threshold potential. (hyperkalemia = shortens gap to TP)
↑ distance between resting membrane potential and TP = ↓ myocardial excitability
↑ Ca+ = Inhibits Na+ channels opening = ↓ myocardial excitability
↑ Ca+ = P2 stabilises cell membrane and ↑ FOC
WHAT IS THE MECHANISM OF ACTION OF SODIUM BICARBONATE?
Hyperkalaemia:
NaHC03 dissociates in solution to give us Na+ and HC03. The high Na+ load causes Na/H pump to shift Na+ IC and H+ EC.
HC03 binds with H+ = H2C03 = ↓ EC H+ = ↓ acidosis
↑ Na+ IC causes Na/K pump to bring K+ into the cell
↑ Na/K pump function (pump fails when acidotic)
Sodium Bic moves equation left.
Tricyclic OD:
↑ Na+ uncouples TCA from Na+ channels ∴ ↑ Na/K pump function and overcoming Na+ channel blockade
WHAT IS THE MECHANISM OF ACTION OF FRUSEMIDE?
Frusemide is a potent loop diuretic that acts on the thick ascending limb of the loop of Henle in the nephron. It inhibits the Na⁺/K⁺/2Cl⁻ symporter by binding to the Cl⁻ site, preventing the reabsorption of sodium, potassium, and chloride ions.
This disruption leads to reduced sodium transport from the tubular lumen into the interstitial space, creating a hypertonic lumen and diminishing the osmotic gradient required for water reabsorption. Consequently, more water remains in the filtrate and is excreted as urine.
Since approximately 25% of sodium reabsorption occurs at the thick ascending limb, frusemide’s action at this site makes it a highly effective diuretic.
What is the mechanism of action of Morphine?
Opioid analgesic. Morphine has an affinity for delta, kappa and mu-opioid receptors.
Morphine produces most analgesic effects by binding to the mu-opioid receptor within CNS and PNS.
Activation of descending inhibitory pathways of the CNS. Inhibition of the nociceptive afferent neurons of PNS = reduction of nociceptive transmission = reduced pain transmission.
What is the mechanism of action of Ketamine?
Dissociative anaesthetic with analgesic effects
• NMDA receptor antagonist resulting in dissociative anaesthesia (profound analgesia with superficial sleep) by inhibiting the somato-sensory input to the thalamo-cortical pathways in the CNS. This occurs due to its inhibitive effects on the excitatory neurotransmitters glutamate and glycine which decreases influx of Na+ and Cl- and decreases the efflux of K+ of neurons making it more difficult for an action potential to trigger.
• interacts with opioid receptors – mu, delta and kappa
• muscarinic receptors – partial antagonist effect (bronchodilation, sympathomimetic, delirium)
• Na+ channel – mild Local Anaesthetic like properties
- provides some SNS stimulation.
What is the mechanism of action of MIDAZOLAM?
Benzodiazepine agonist – coupled to the GABA receptor. Stimulation of GABA increases frequency of opening of GABA CL- channels ∴ hyperpolarise of membrane. (Influx of chloride into the cell). When hyperpolarized, this moves the neurons resting membrane potential further away from its threshold potential making it less likely the neuron will fire an action potential. This neural inhibition is the basis for benzodiazepines.
GABA is a neurotransmitter in the brain.
Theraputic effects:
o hypnosis
o sedation
o anterograde anaesthesia
o anxiolysis
o anticonvulsant
o muscle relaxation
