C&R Drugs Flashcards
Beta blockers
Propanol (non-selective)
Atenolol (selective b1)
Compete with NA for binding on beta 1 receptors in heart reducing sympathetic tone and thus cardiac output.
ACE inhibitor
Captopril, Enalapril, Lisinopril, Ramipril.
Inhibits angiotensin converting enzyme ACE which converts angiotensin I into angiotensin II. Decreased vasodilation, decreased aldosterone secretion (decreased Na/Water retention and decreased sympathetic activity)
Angiotensin II Receptor Blockers
Losartan and Candesartan
Blocks Angiotensin II receptor which mediates the vasoconstrictor and aldosterone releasing actions of Angiotensin II.
Alpha-adrenoceptor blockers
Phentolamine (non selective), Prazosin and Doxazosin (alpha1)
Competitive reversible antagonist of alpha-1-adrenoceptors in vascular smooth muscle of blood vessels. Causes decrease in total peripheral resistance and thus a decrease in blood pressure. Also acts on kidneys to prevent sympathetically mediated renin release.
Calcium channel blockers
Verapamil and Diltiazem (cork in bottle - blocks Ca pore - act on heart)
Amlodipine and Nifedipine (bind to receptor causing conformational change, these mainly act on smooth muscle causing vasodilation).
Block L-type voltage operated calcium channels.
Diuretics
Bendroflumethiazide
Thiazide diuretic that inhibits Na resorption at beginning of DCT.
Furosemide
Loop diuretic that decreases sodium transport out of thick ascending limb of loop of henle.
Diuretics increase urine volume thus decrease blood plasma volume.
Organic Nitrates
GTN (Glyceryl l Trinitrate)
These drugs relax smooth muscle by producing Nitrous Oxide (NO) which increases levels of cGMP and thus causes vasodilation.
Dilation of venous capacitance vessels causes:
• Reduced preload in heart thus reduce CO and reduced cardiac demand
• Decreased arterial blood pressure so reduced systemic peripheral resistance
Dilation of coronary arteries causes:
• Increases myocardial perfusion.
Administered sublingually (spray or tablet) not digested due to first pass effect (i.e. concentration is reduced by the time it reaches circulation).
Statins
Simvastatin, Pravastatin.
Statins inhibit endogenous cholesterol production by competitive inhibition of HMG-CoA reductase (HMGCR), the enzyme that catalyses conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol synthesis. Also increase expression of LDL receptors on hepatocytes meaning more cholesterol is taken from blood stream into liver to be metabolised.
Antiplatelet therapy
Aspirin
Inhibit COX enzyme therefore inhibit biosynthesis of prostaglandins/ thromboxane’s/ prostacyclin’s
COX has two isoforms - COX1 and COX2. COX 1 is present in most tissues all the time and COX2 is typically only present in inflammation response.
COX1 (TXA2). Tissue homeostasis. Produces prostaglandins responsible for gastric cytoprotecting, platelet aggregation, renal blood flow regulation and the initiation of child birth (parturition).
COX2 (PGE2/PGI2). Production of prostanoid mediators of inflammation. Note prostanoids include prostaglandins, thromboxane’s and prostacyclin’s.
B2 adrenoreceptor agonists
Salbutamol, Terbutaline - Short acting
Salmeterol, Formoterol - Long acting LABA
Dilate bronchi - main action. Also stabilise mast cells, monocytes, cilia.
Anticholinergic agents
Ipratropium - Short acting
Tiotropium - Long acting: LAMA (long-acting muscarinic antagonist)
Bronchodilator and are antisecretory. Block parasympathetic action of restricting airways.
Leukotriene antagonists
Montelukast, Zafirlukast
Block action of leukotrienes (allergic inflammatory response). Mild bronchodilators. Potentially weak anti -inflammatory agents.
Xanthine’s
Theophylline, Aminophylline
Bronchodilator and weak anti-inflammatory
Corticosteroids
Beclomethasone, Budesonide, Fluticasone
Prednisolone, Hydrocortisone
Mimic Glucocorticoids
• Metabolic, anti-inflammatory, immunosuppressant
Also mimic mineralocorticoids
• Peripheral action on salt/water metabolism
• Overall Increase expression of anti-inflammatory mediators (Annexin 1 for example) and decreased expression of inflammatory mediators.
