FINAL Capstone Pharmacology Review PDF

2 AT 30 CEL 50 for the ABX that target proteins Know the importance of folate in DNA synthesis 3 Local anesthetics are bases Articaine has an ester group. 4 Note: the LA needs to cross membrane in unionized form...

2 AT 30 CEL 50 for the ABX that target proteins Know the importance of folate in DNA synthesis 3 Local anesthetics are bases Articaine has an ester group. 4 Note: the LA needs to cross membrane in unionized form, gets re-ionized inside the cell, and then binds to the Na+ channel in its ionized form. In order to be in the un-ionized form, you want the local anesthetic to have a pKa lower than the surrounding pH or near the value of the pH. 6 ACE Inhibitors have the suffix –pril Can cause dry cough bc ACE is an enzyme that breaks down bradykinins and without this, bradykinins build up cough RAAS overview Renin is made by the kidneys, and it converts Angiotensinogen made by the liver to Angiotensin 1 Angiotensin 1 gets converted to Angiotensin 2 by ACE enzyme Angiotensin 2 stimulates aldosterone release, leading to more re- absorption of water = increase in BP 7 Verapamil affects cardiac muscle cells and can be used for arrythmias because it reduces contraction force and slows heart rate it is a non-dihydropyridine 8 Cardiac muscle cells differ from skeletal muscle AP’s in the sense that they have a plateau phase where Ca2+ channels open to allow for the positive state of the cell to be maintained with the influx of calcium 9 Certain arrythmia medications target each specific part of the action potential 10 Class 1: Sodium channel blockers ex: quinidine Class 2 : beta blockers ex: metoprolol Class 3 : potassium channel blockers ex: sotalol Class 4 : NON-dihydropyridines ex: verapamil 11 Ionotropy = increase the heart’s contractions positive ionotropic effect Chronotropy = increases heart rate, this medication has a negative chronotropic effect bc it enhances vagal tone --> parasympathetic system 12 Biguianides act on the liver and sulfonylureas act on the pancreas DPP4 inhibitors have the suffix –gliptin and they are going to affect DPP4 the enzyme that breaks down incretin hormones. Incretin hormones are essential for the release of insulin 13 14 16 19 Intrinsic Pathway: Triggered by blood vessel damage, involving factors XII, XI, IX, and VIII. Extrinsic Pathway: Triggered by external trauma, involving tissue factor and factor VII. The extrinsic pathway of blood coagulation is a faster, shorter pathway that's triggered when tissue is damaged and the bloodstream comes into contact with tissue factor: 1.Tissue factor exposure: When a vessel is damaged, endothelial cells release tissue factor, a glycoprotein found on the surface of subendothelial tissues. Tissue factor is especially abundant in the brain, lungs, and placenta. 2.Factor VII activation: Tissue factor binds with calcium and factor VII to activate factor VIIa. Factor VII is present in the blood and needs vitamin K to be activated. 3.Factor X activation: Factor VIIa activates factor X into factor Xa. 4.Prothrombin activation: Factor X activates prothrombin into thrombin, which requires factor V. 5.Fibrinogen conversion: Thrombin converts fibrinogen into fibrin, forming a clot. Primary hemostasis and secondary hemostasis are two stages of hemostasis, or blood clotting, that occur simultaneously: Primary hemostasis Also known as platelet clotting, this stage involves the formation of a temporary platelet plug to seal an injury. Platelets stick to damaged tissue and activate, and the process is also characterized by vasoconstriction, or vascular spasm, which can stop blood flow. Secondary hemostasis 20  Also known as the coagulation cascade, this stage involves stabilizing the platelet plug into a clot using a fibrin network. This process is dependent on interactions between clotting actors, such as coagulation factors, to form a fibrin clot. 21  Difference between High Molecular Weight vs Low Molecular Weight Heparin: HMW: will bind to anti-thrombin and will cause antithrombin to bind to factor Xa -> inhibiting the production of fibrin clot BUT it can also cause anti-thrombin to bind to thrombin = bad -> forms complexes that can clump together in vessels leading to complications like heparin induced thrombocytopenia Heparin can cause HIT -> heparin binds to PF4 -> complex leads to platelet activation and aggregation hence thrombosis -> macrophages destroy these cells resulting in low PLT count LMW: will bind to antithrombin ONLY and will promote binding of factor 10a, therefore, fibrin clot cannot be produced Warfarin Drug Drug Interactions: o Metronidazole interacts with warfarin by inhibiting the CYP450 enzyme o Drugs that block CYP450 enzyme from breaking down warfarin: cimetidine, omeprazole, metronidazole, trimethoprim/sulfa, amiodarone Fibrinolytic: Alteplase 23 *these are going to break down the fibrin* Anti-platelet: Clodiprogel 25 Always give a combination of folic acid + vitamin B12 Furosemide can cause hypocalcemia, increase Ca2+ excretion Hydrochlorothiazide can cause hypercalcemia, decrease Ca2+ excretion 32 Benzos increase the frequency of the Cl- channel opening Barbs increase the duration of the Cl- channel opening * Barbs are stronger and act longer * hence, increase duration 35 Barbiturates increase duration of Cl- channel being open, therefore, more potent. 36 Carbidopa is the protector of levadopa in the periphery 37 Nitrogen containing are inhibiting osteoclasts from attaching to bone Non-nitrogen are killing energy metabolism of the osteoclasts 38 Low yield → “mab” = monoclonal antibodies