Mid 2 Flashcards
Beta blockers suffix
Olol
Beta blockers function
Block Beta 1 receptors:
Heart- increase HR, increase contractility
Kidney- release of renin
Some will be non selective and target both, some will be cardio selective
-In ACS patients, it reduces myocardial oxygen demand
Why do you not wanna stop beta blockers abruptly
Can cause cardiac rebound excitation; tachycardia, angina, MI
Ace inhibitors suffix
Pril
Ace inhibitors function
Block conversion of angiotensin 1 to angiotensin 2
Gives vasodilation, decreased blood volume, decreased cardiac remodelling, potassium retention, can cause fetal injury
What are considerations of ace inhibitors
Cause cough and hyperkalemia so if patient cannot tolerate then switch to ARBs
First dose hypotension
Monitor for angioedema
Angiotensin 2 receptor blockers suffix
Sartan
ARBs function
Blocks angiotensin 2 receptor access on adrenal glands to block release of aldosterone
Blocks receptors on BVs causing vasodilation
Diuretics suffix
Ide or one
Types of diuretics
Thiazide
Loop
Potassium sparing
Thiazide function
Blocks reabsorption of Na and Cl in early segment of DCT
-adverse effect hypokalemia
Ex- hydrochlorothiazide
Loop diuretic function
Blocks Na and Cl at ascending loop of Henle
-works earlier in the nephron and can thus act more effectively and blocking more water
-adverse effects are greater because of more blocking happening: hypokalemia, hyperglycemia, hyperuricemia
Ex Furosemide
Potassium sparing function
Disrupts Na and K exchange at distal nephron- not as much diuresis happening
-conserves K loss
Ex spirinolactone
Calcium channel blockers suffix
Ipine
Exception verapamil
Calcium channel blockers function
Blocks calcium entry into cells
Calcium causes constriction so blocking is going to dilate
-decreases HR and strain on the heart reducing myocardial contractility
Types of calcium channel blockers
Dihydropyridines
Non-dihydropyridines
Difference between the two calcium channel blockers
Dihydropyridines are mainly vasodilation but minimal effect on HR
-ipine
Non…. Heart and blood vessels: used in arrhythmias
-azem and amil
What should you avoid if using calcium channel blockers
Grapefruit juice- it takes away the enzymes that break down the drug so you end up with too high a dose
Nitrates function
Nitrate uptake enduring nitric oxide and vasodilation: more dilation in veins than arteries
Ex nitroglycerin
-treating angina
Don’t wanna use continuously
Ranolazine
Reduction in Na and Ca accumulation in myocardial cells- improved energy efficiency
-treats angina pain
-usually used with other drugs but has many drug interactions
-prolongs QT interval
Angiotensin receptor neprilsyn inhibitor function
Combined sacubitril and valsartan
Sacubitril is a neprilsyn inhibitor- neprilsyn is blocked and cannot break down natriuretic peptides (ANP and BNP)- causing increased Na secretion and vasodilation
Superior to ACEi and ARBs
Adverse effects of ARNI
Sacubitril/valsartan
Risk for hyperkalemia, hypotension
Cannot be used for severe kidney disease and pregnancy
SGLT2i function
Increased natriuresis and thus reduces BP. Blocks reabsorption of glucose
Contraindicated in type 1 diabetes due to diabetic ketoacidosis
Adverse effects for UTIs and fungal infections
SGLT2i suffix
Flozin
Digoxin function
Irotropic agent- Increases contractility of heart, increasing SV, reduces HR
Why is digoxin a second line agent
Many drug interactions and food interactions (black licorice)
Narrow therapeutic range
Hypokalemia and dysrythmias
What are the 3 types of anti platelet agents
Aspirin
P2Y12 inhibitors
Glycoprotein IIb/IIa inhibitors
Fibrinolytic function
Anti-thrombolitic
Dissolves a thrombus by binding to plasminogen and converting more to plasmin
More plasmin is going to cause fibrin lysis
Anteplase- ends in plase
Aspirin function
Antiplatelet drug
Irreversibly inhibits cyclo-oxygenase which is the enzyme platelets use to create thromboxane for platelet aggregation
Clopidogrel function
A P2Y12 inhibitor and antiplatelet drug
Inhibits the P2Y12 receptors on platelets and prevents aggregation
-often used as combo with aspirin
-effects non reversible for 7-10 days so need to stop early if having an operation
Glycoprotein IIb/IIIa receptor inhibitor function
Most effective antiplatelet drug
Reversibly blocks receptors for IIb/IIIa making it so the receptors and platelets cannot bind to fibrinogen and connect to other platelets
Used short term because of ability to reverse
-administered IV
HMG-CoA reductase inhibitors
Most effective statin for treating dyslipidemia
HMG-CoA works in the liver to create cholesterol so inhibiting reduces the amount made and makes clearing LDLs more effective
Cholesterol absorption inhibitor function
Inhibits absorption of cholesterol in SI allowing more to be excreted
Ezitimibe
PCSK9 inhibitors
PCSK9 binds to LDL receptors preventing it from being cleared in the liver
Inhibiting allows more LDL to be cleared
Evolocumab- ends in cumab
difference between unfractioned and low molecular weight heparin
Unfractioned- prevents conversion of fibrinogen to fibrin and prothrombin to thrombin
-more emergent situations like pulmonary embolism
Low molecular weight- prevents conversion of prothrombin to thrombin
-first line therapy in prevention of DVT
Warfarin (Coumadin) function
Vitamin K antagonist- prevents vitamin K from being activated- VT-K activates clotting factors VII, IX, X and prothrombin
Takes longer to take effect (42-72hrs) and thus is not used for emergencies but long term prophylaxis and preventing of DVT
PO
Thrombin inhibitors function
Anti-thrombolytic
Prevents conversion of fibrinogen to fibrin, prevents activation of clotting factor XIII
Ex Dabigatran
Advantage over warfarin: rapid onset and same dose for all patients
Treatment for DVT and because faster acting can be for PE also
Factor Xa inhibitors function
Anti-thrombolytic
Inhibits clotting factor Xa- thus inhibiting thrombin
Advantage over warfarin- rapid onset so can be used to treat PR and DVT
Ex Rivarozaban
