Drugs Flashcards
What is the mechanism of orlistat?
Reacts with serine residues at the active sites of gastric and pancreatic lipase, irreversibly inhibiting the enzyme and preventing breakdown of fat.
What is the mechanism of hexamethonium?
Selective antagonist (at ganglia) for the neuronal subtype of nicotinic receptor, not competitive, blocks all effects of autonomic stimulation.
What are the effects of parasympathomimetics?
Cardiovascular- decreased heart rate and cardiac output, smooth muscle contracts, vascular muscle dilates via endothelium, exocrine glands secrete.
Give examples of muscarinic agonists
ACh, carbachol, methacholine, bethanecol, muscarine, pilocarpine, oxytremorine
What are the effects pf muscarine poisoning and how are they treated?
-bradycardia, vasodilation (secondary to NO), leading to falling BP
– increased gut motility (colicky pain), bronchoconstriction, pupillary constriction (miosis).
– Salivation, lacrimation, airway secretions
Treated with muscarinic antagonist, atropine
What is the use, administration and action of pilocarpine?
Treats glaucome, topical to the eye. Acts on M3 receptors on ciliary muscle, improving aqueous humour drainage, dropping intraocular pressure.
Give examples of an M1, M2 and M3 antagonists.
M1- Pirenzepine, stomach and salivary glands
M2- Gallamine, cardiac
M3- glycopirellate, smooth muscle
What are the clinical uses of antimuscarinic drugs?
-Asthma- ipratropium- dilates bronchi
-To treat bradycardia- atropine
-To decrease gut motility; decrease secretions
(pirenzapine)
- During operations: decrease secretions, decrease
AChEI side-effects (atropine)
-To dilate pupils (tropicamide)
-Urinary incontinence (oxybutynin)
- Motion sickness (hyoscine)
What are the effects of sympathetic stimulation?
- Tachycardia
- Decreased salivary production
- Vasoconstriction and vasodilation
- Decreased gut motility
- Ejaculation
- Sweating
- Bronchodilation
- Tremor
What are the 5 main types of adrenoceptors?
a1- contract smooth muscle, vasoconstriction
a2- vasoconstriction and presynaptic
b1- increase heart rate and contractility
b2- relax smooth muscle, bronchodilation and vasodilation
b3- relax smooth muscle in the bladder and stimulate lipolysis
What are the signal transduction mechanisms for autonomic receptors?
a1- Gq- PLC, increases IP3 and DAG
a2- Gi- decreases adenylyl cyclase and decreases cAMP
b(all)- Gs- increases adenylyl cyclase and increases cAMP
M1, M3- Gq- PLC, increases IP3 and DAG
M2- Gi- decreases adenylyl cyclase and decreases cAMP
What are the uses of beta receptor agonists?
Cardiogenic shock- b1- adrenaline and dobutamine
Anaphylactic shock- (alpha or beta)- adrenaline
Asthma- b2- salbutamol
ALL delay early labour
What are the main alpha antagonist uses?
Hypertension- a1- doxazosin
Benign prostatic hyperplasia- a1- tamsulosin
What are the main uses of beta antagonists?
Propanolol (b1/2), Metroprolol (b1).
Angina, cardiac arrhythmias, hypertension, anxiety, chronic heart failure, glaucoma (timolol)
What are NET inhibitors?
They enhance the effect of NA as it is not reuptaken. eg.. cocaine and desipramine- antidepressants, tachycardia, euphoria
What are MAO inhibitors?
Most block MAO irreversibly
Used clinically as antidepressants
Increase levels of noradrenaline, dopamine and 5-HT in the brain and peripheral tissues
Adverse effects include postural hypotension, weight gain, restlessness, insomnia, cheese reaction
(hypertensive episode following ingestion of tyramine- containing food, e.g. cheese; flushing)
Examples - phenelzine, tranylcypromine, iproniazid
- moclobemide (reversible, competitive inhibitor)
What are indirectly acting sympathetic amines?
They displace NA from vesicles and cause it to leak into the cleft via NET, this causes increased stimulation at the synapse. Cause bronchodilation and vasoconstriction. Amphetamine, ephedrine and tyramine.
How does lipid transport occur?
Lipoproteins, non polar core and cholesterol esters or triglycerides with a polar coat. Apoproteins for receptor binding. Can be transported via the endogenous or exogenous pathways.
What is the exogenous lipid pathway?
Lipid is emuslified by bile in the GIT and absorbed as chylomicrons. TGs are hydrolysed by lipoprotein lipase and chylomicron remnants go to the liver.
What is the endogenous lipid pathway?
In the liver, synthesis of cholesterol and triglycerides from the exo pathway. VLDL secreted. TG removed to produce CE, LDL. Extra hepatic reverse cholesterol transport, cholesterol from cell turnover produces HDL. CE–LDL–Liver–HDL and promotes LDL removal.
What are the primary types of hyperlipidaemia?
Type IIa- Increased LDL
Type IIb- Increased LDL and VLDL
Increased risk of atherosclerosis, LDL contains apoprotein similar to plasminogen leading to competition and a decrease in plasmin and increased thrombosis.
What are the secondary types of hyperlipidaemia?
Metabolic, diabetes, hypothyroid, renal disease and alcoholism
How do HMG CoA reductase inhibitors, statins, work?
They decrease cholesterol synthesis. Competitive HMG CoA reductase inhibitors. Decrease cholesterol synthesis, increase LDL receptors, reduce plasma LDL.
How do fibrates work?
Activate nuclear receptors and increase transcription of lipoprotein lipase. Decrease VLDL, TG. Increase liver uptake of LDL by increasing receptors for apoproteins. Increase HDL.
How do bile acid binding resins work?
Reduce the reabsorption of bile acid resins, lose cholesterol and bile. This leads to the use of liver cholesterol in synthesis of new bile. Increase LDL receptors, decrease LDL, but increase TG.
How does ezetimibe work?
Inhibits intestinal absorption of cholesterol and blocks receptor uptake.
How does nicotinic acid work?
Decreases the synth of TGs, decreases VLDL, LDL, increases HDL
How does fish oil work?
Decreases TGs
What are the 3 categories of eicosanoids?
Prostaglandins, thromboxanes and leukotrienes
