block 1 Flashcards
Atropine
antimuscarinic agent
MECHANISM: Atropine binds to and inhibits the muscarinic acetylcholine receptor.
USES: bradycardia, asystole produced by injection of choline esters, and cardiac arrest, lessen the degree of partial heart block when vagal activity is an etiologic factor.
Betamethasone
A glucocorticoid receptor agonist
MECHANISM: Binding of Betamethasone to the glucocorticoid receptor, forms a complex, which moves to the nucleus, binds DNA causing alteration in gene transcription. This alter gene transcription causes the production of lipocortins, which inhibits phospholipase A2, and therefore reduces the biosynthesis of prostaglandins and leukotrienes.
USES:drives the anti-inflammatory, immunosuppressive and anti-mitogenic effects of steroids
Digoxin
A cardiac glycoside
MECHANISM; . Its mode of action is via inhibition of the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium. This causes in turn the sodium calcium exchanger (NCX) to extrude the sodium and pump in more calcium. This alteration in calcium concentration is thought to promote activation of contractile proteins (e.g., actin, myosin). Digoxin also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.
USES:congestive heart failure, and supraventricular arrhythmias
(Still used in Atrial Fibrillation, but now very much third line treatment option. Rarely used in heart failure as much better drugs available.
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Edrophonium
cholinesterase Inhibitor
MECHANISM: Edrophonium is a rapid-onset, short-acting cholinesterase inhibitor
USES: cardiac arrhythmias and in the diagnosis of myasthenia gravis
Ethanol
MECHANISM: Binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors. The sedative effects of ethanol are mediated through binding to GABA receptors and glycine receptors (alpha 1 and alpha 2 subunits). It also inhibits NMDA receptor functioning.
Has an anti-infective role as it acts as a dehydrating agent that disrupts the osmotic balance across cell membranes.
Rarely used therapeutically, and fomepizole has replaced it as the first line treatment for methanol/ethylene glycol poisoning
Ethinylestradiol
MECHANISM: Ethinylestradiol interacts with the estrogen receptor (Erα or Erβ) present on female organs, breasts, hypothalamus and pituitary gland. Upon ligand binding, the estrogen receptor enters the nucleus, and regulates gene transcription. This leads to an increase in the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppresses follicle-stimulating hormone (FSH) from the anterior pituitary. During menstruation, increased oestradiol levels cause the maturation and release of the egg; as well as the thickening of the uterus lining to allow a fertilized egg to implant. The hormone is made primarily in the ovaries, so levels reduce as women age and decrease significantly during menopause.
Oestrogen nuclear hormone receptor agonist
A synthetic derivative of the natural estrogen estradiol
USES:A synthetic derivative of the natural estrogen estradio
Ketaconazole
broad spectrum anti-fungal agent
MECHANISM: Ketoconazole inhibits 14-α demethylase, a cytochrome P-450 enzyme which converts lanosterol to ergosterol. This inhibition of ergosterol causes increased fungal cellular permeability
Morphine
analgesic
The precise mechanism of the analgesic action of morphine is unknown.
Naloxone
opiate antagonist
MECHANISM: Its mechanism of action is not clear but it is though to be able to antagonise all three opioid receptors (Mu, Kappa, and Gamma), although it has the strongest binding to the Mu receptor.
USES: depression, sedation and hypotensio
Rifampicin
broad spectrum bactericidal
MECHANISM: Its mode of action is via the inhibition of DNA-dependent RNA polymerase, leading to a suppression of RNA synthesis and cell death.
Suxamethonium
depolarising skeletal muscle relaxant.
MECHANISM: Suxamethonium mode of action is to mimic acetylcholine at the neuromuscular junction. However Suxamethonium is hydrolysed much slower than acetylcholine, causing prolonged depolarisation and therefore desensitisation, and muscle relaxation. Unlike the non-depolarising neuromuscular blocking drugs, Suxamethonium cannot be reversed and recovery is spontaneous.
USES: Suxamethonium is given after a general anaethetic as muscle relaxation can be preceded by painful muscle fasciculations.
Tamoxifen
selective estrogen receptor modulator (SERM)
MECHANISM: The mode of action of Tamoxifen is via binding to the estrogen receptor (ER), leading to a conformational change in the receptor and therefore altering the expression of estrogen dependent genes. Prolonged binding of Tamoxifen to the nuclear chromatin reduces DNA polymerase activity, impairs thymidine utilization, blocks estradiol uptake, and decreases estrogen response. Tamoxifen can bind either the ER-a or Erb receptors, and most likely will interact with multiple co-repressors, or co-activators leading to its ability to have either estrogenic or antiestrogenic effects
Tubocurarine
neuromuscular blocker
MECHANISM: Tubocurarine binds stereo-selectively to nicotinic-cholinergic receptors at the autonomic ganglia, the adrenal medulla, neuromuscular junctions, and in the brain. Tubocurarine has two main effects, stimulation and reward.
USES: Tubocurarine has been superceded by Suxamethonium as the clinically used depolarising neuromuscular blocker
Paracetamol
analgesic and Antipyretic compound
MECHANISM: There are three possible mechanisms
It indirectly inhibits COX, which is ineffective in the presence of peroxides. This could explain why it does not work well within platelets.
It inhibits COX-3. This enzyme is not well understood.
Its antipyretic effects are due to effects on the hypothalamus, resulting in peripheral vasodilation and sweating.
USES: Paracetamol is used when NSAIDs cnnot be.
Pyridostigmine
cholinesterase inhibitor
MECHANISM: reversible inhibition of acetylcholinesterase in the synaptic cleft by competing with acetylcholine for attachment to acetylcholinesterase. This inhibition leads to a reduction in the hydrolysis of acetylcholine, prolonging its effects. Furthermore this reduction in hydrolysis increases efficiency of cholinergic transmission in the neuromuscular junction.
USES: myasthenia gravis and to reverse the actions of muscle relaxant
