Pharmacology Flashcards
1
Q
Class and mechanism of enalapril, lisinopril, ramipril and captopril
A
- Competitive inhibitor of ACE
- Inhibition of ATII
- Inhibits the deactivation of bradykinin (>levels). Increased bradykinin causes vasodilation and decreased blood pressure
2
Q
True or false: angiotensin 2 induces thirst?
A
True
3
Q
Class and mechanism of amiloride
A
- Antikaliuretic-diuretic agent
- Antihypertensive, potassium sparing diuretic used in conjunction with thiazide or loop diuretics
- Hyperkalaemia usually observed
- Inhibits sodium reabsorption predominantly in the collecting ducts. Promotes loss of sodium and water whilst retaining potassium and hydrogen: resulting in hyperkalaemic metabolic acidosis
4
Q
Class and mechanism of furosemide
A
- Loop diuretic
- Inhibits the sodium-potassium-chloride cotransporter, via competitive inhibition of the Chloride binding site, in the thick ascending limb of the loop of Henle.
- This inhibition prevents sodium transport from the lumen of the loop of Henle into the basolateral interstitium. Therefore, as the lumen becomes more hypertonic, this alters the osmotic gradient, causing the retention of water within the lumen.
- As the thick ascending limb is responsible for 25% of sodium reabsorption, furosemide is a very potent diuretic.
5
Q
Class and mechanism of bendroflumethiazide
A
- Thiazide diuretic
- 2 mechanisms of action:
1. It inhibits the Na-Cl co-transporter, blocking active chloride reabsorption in the early distal tubule, keeping sodium in the tubule which will bring water with it. This results in an increase in the excretion of sodium, chloride, and water in the urine.
- It inhibits sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism
6
Q
Class and mechanism of doxazosin
- Indications
A
- Alpha-adrenergic blocking agent
- Inhibitor of alpha 1 adrenergic receptors, so blocking the effects of A/NA which are vasoconstricting effect on smooth muscle
- used to treat hypertension and BPH
7
Q
Class and mechanism of spironolactone
A
- Mineralocorticoid receptor antagonist
- Potassium sparing diuretic
- Spironolactone inhibits the effect of aldosterone by competitively competing for intracellular aldosterone receptor in the distal convoluted tubule cells.
- Aldosterone interacts with a cytoplasmic mineralocorticoid receptor to enhance the expression of the Na+, K+-ATPase and the Na+ channel involved in a Na+ K+ transport in the distal tubule.
- More sodium going out = diuretic effect
- More potassium staying in = avoid hypokalaemia
- Spironolactone binds to this mineralcorticoid receptor, blocking the actions of aldosterone on gene expression.
- Furthermore spironolactone increases the secretion of water and sodium, while decreasing the excretion of potassium.
8
Q
Class and mechanism of acetazolamide
A
- Carbonic anhydrase inhibitor
- Leads to the reduction in the availability of H+ ions for active transport in the renal tubule lumen
- Leads to alkaline urine and increase in excretion of bicarbonate, sodium, potassium and water.
9
Q
Class, mechanism and indications of methotrexate
A
- Antineoplastic anti-metabolite
- Methotrexate inhibits folic acid reductase which converts folic acid to tetrahydrofolic acid. Tetrahydrofolic acid is required for both purines and pyrimidine biosynthesis, Thus, DNA synthesis cannot proceed due to a lack of purine and pyramidines. Given this effect on DNA, Methotrexate affects the most rapidly dividing cells.
- Used at low dose in management of severe, active, classical, or definite rheumatoid arthritis
10
Q
What are anti-metabolites?
A
Anti-metabolites are synthetic versions of purine or pyrimidines, which are the building blocks of DNA. They prevent purine or pyrimidines becoming incorporated in to DNA during the “S” phase (of the cell cycle), stopping normal development and cell division
11
Q
Class and mechanism of pethidine
A
- Synthetic opiate antagonist
- Opiate receptors are coupled with G-protein receptors, which activate adenylate cyclase and the production of cAMP. Opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of the nociceptive neurotransmitters substance P, GABA, dopamine, acetylcholine and noradrenaline and the hormones vasopressin, somatostatin, insulin and glucagon is inhibited
12
Q
Class and mechanism of mannitol
A
- Osmotic diuretic
- Mannitol elevates blood plasma osmolality!! Resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma.
- Mannitol induces diuresis as it is not reabsorbed in the renal tubule, and therefore increases the osmolality of the glomerular filtrate. This aids water excretion.
- Its excretion rate may serve as a measurement of GFR
13
Q
Class, mechanism and indication/contraindication of warfarin
A
- Anti-coagulant
- Warfarin inhibits vitamin K reductase, reducing levels of the reduced form of vitamin K. As vitamin K is required for the production of coagulation factors II, VII, IX, and X and anticoagulant proteins C and S, these levels also drop.
- Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decreased prothrombin levels, decreased thrombin generation and reduced ability to form a clot.
- IND: Warfarin is used in the prevention and treatment of thromboembolic disease including venous thrombosis, thromboembolism, and pulmonary embolism as well as for the prevention of ischemic stroke in patients with atrial fibrillation (AF).
- CONTRAIND: Warfarin can cross the placental barrier during pregnancy resulting in foetal bleeding, spontaneous abortion, and neonatal death.
14
Q
Where does acetazolamide act? (brief mechanism)
A
Proximal tubule
- Carbonic anhydrase inhibitor
- Increases NaHCO3 excretion
15
Q
Where does mannitol act? (brief mechanism)
A
- Descending loop of Henle and the beginning of the thick ascending
- Osmotic diuretic –> >H2O excretion
