Pharmacology U5 SG

Describe PQRST waves, what is happening with the heart, and where

- P wave: depolarization at the SA node which causes systole

- QRS wave: depolarization at the ventricles which causes systole (Ca and Na enter)

- T wave: repolarization which causes diastole. refractory period where heart does not respond to stimuli (K exits)

Define and describe arrhythmias, abnormal impulse generation (such as altered normal activity, abnormal automaticity, and triggered activity), as well as abnormalities of impulse conduction

- arrhythmia: abnormal heart beats caused by disturbances of generation or conduction of action potentials.

- altered normal activity: tachycardia, bradycardia. occurs at SA node

- abnormal automaticity: ectopic (other) pacemaker

- triggered activity: early/ delayed after depolarization

- abnormalities of impulse conduction include conduction block and reentry where circuit impulse continues

Describe Class I (sodium channel blockers). What is the main drug, MOA, use, and concerns

- flecainide

- MOA: blocks open cardiac Na+ channels and slows impulse conduction by widening the QRS complex

- use: life threatening ventricular arrhythmias (tachycardia, fibrillation) and paroxysmal supra ventricular tachycardia

- concerns: cardiotoxitcity in AV node blockers and highly effective in suppressing ventricular arrhythmias but may not reduce mortality

Describe Procainamide. What is the class and use

- class I sodium channel blocker

- used for ventricular tachycardia during CPR. Also used for conversion to and/or maintenance of sinus rhythm in patients with supraventricular (atrial) arrhythmias including tachycardia, fibrillation, flutter etc.

Describe Class II (beta blockers). What is a drug, MOA, and use

- propranolol

- MOA: block beta adrenergic receptors and the related Ca++ inflow resulting in decreases automaticity of SA node, decreased heart rate, decreased AV node conduction, and prolonged PR interval

- use: arrhythmias caused by excessive sympathetic stimulation, supraventricular tachycardia

Describe Class III (potassium channel blockers). What is a drug, MOA, use, adverse effects, and half life

- amiodarone

- MOA: blocks K+ channels in the heart, which delays repolarization. may block some Na+ and Ca+ channels. results in reduced conduction velocity, reduced automaticity of SA node, and reduced contractility.

- prolongs PR and QT intervals

- use: antiarrhythmic for both atrial and ventricular arrhythmias

- AE: pulmonary fibrosis, cardiotoxicity (bradycardia, AV node block, HF), corneal micro-deposits which effect vision, thyroid disfunction, and photosensitivity (grey/blue skin deposits)

- half life: days to weeks which complicates uses.

Describe Class IV (calcium channel blockers). What is a drug, MOA, and use

- diltiazem

- MOA: blocks Ca+ influx reduces SA nodal automaticity (rate), delays AV nodal conduction, impaired SA and AV node function since they rely on Ca+ for influx

- use: tx supraventricular tachycardia, slows ventricular rate in atrial fibrillation or flutter, IV for rapid rate control

Describe Adenosine (other). What is the MOA, use, adverse effects, and half life

- MOA: activates adenosine receptors, increases K+ efflux and hyperpolarizes cardiac cells. This results in decreases automaticity in SA node, slowed conduction in AV node, prolonged PR interval

- use: very effective IV bolus for rapid termination of paroxysmal supra-ventricular tachycardia. SHORT DURATION

- AE: sinus bradycardia, dyspnea, hypotension, facial flushing

Describe the pathophysiology behind angina pectoris and arteriosclerosis

- angina pectoris: chest pain/pressure, is the principle symptom of ischemic heart disease.

- associated with coronary atherosclerosis which together constitutes coronary artery disease.

- the ischemic condition results from an imbalance between myocardial oxygen demand and myocardial oxygen supply.

Describe the components of cardiac output, preload, and afterload

- output: heart rate x stroke volume

- preload: the volume of blood that fills the heart. venous return to the heart. inc preload inc o2 demand

- after load: the pressure against which the heart has to pump to eject blood. systemic arterial blood pressure. inc after load inc o2 demand

Describe nitrates. What is the drug, MOA, uses, route of administration, and adverse effects.

- nitroglycerin

- MOA: causes venous and arterial dilation which decreases preload (v) and slightly after load (a), dilates arteries to increase coronary blood flow (inc o2)

- uses: sublingual for immediate tx of angina pectoris, can be rx orally to prevent anginal attacks in men

- route: huge first pass effect so mostly sublingal admin

- AE: nitrate tolerance (reduced effectiveness with longterm use), excessive vasodilation leading to severe headache, facial flushing, hypotension, dizziness, orthostatic hypotension, and reflex tachycardia

- VIAGRA + NITRATES = SEVERE HYPOTENSION

What is the dosing for nitroglycerin in an attack of angina pectoris

1 tablet every 5 minutes for a max of 3 times

Describe b-adrenergic receptor blockers. What is the drug, MOA, uses, adverse effects, and route of administration.

- propranolol

- MOA: block b adrenergic receptors and reduce responses caused by the activation of the sympathetic nervous system (antagonize nor/e), thereby inhibiting cardiac work and oxygen demand (dec HR and contractility, reduce angiotensin II which dec BP and afterload)

- route: oral

- use: prevent angina, tx hypertension, arrythmias, HF. nonselective to B1 and B2

- AE: respiratory (wheezing, bronchoconstriction) CV (bradycardia, AV block), CNS (insomnia, depression, bizarre dreams)

- abrupt withdrawal can worsen angina

Describe calcium channel blockers. What are the two drugs, MOA, uses, and adverse effects.

- verapamil (cardiac and vascular effects) and amlodipine (vascular)

- MOA: amlodipine blocks L type calcium channels in vascular smooth muscle. verapamil blocks L type calcium channels in vascular smooth muscle and in the heart

- use: prevent angina, decreases cardiac work and demand (v)

- AE: excessive hypotension (facial flushing, headache, dizziness, peripheral edema). verapamil can cause cardiac depression, bradycardia

Describe Ranolazine. What is the MOA, uses, and adverse effects.

- decreases cardiac muscle sodium entry during ischemia which reduces Ca2+ overload & o2 demand

- use: prevent angina, newer drug

- AE: arrhythmias (prolonged QT interval), constipation, nausea, vomiting, dizziness, headache.

What is the sequence of drug treatment for antianginal drugs?

- nitroglycerin sublingually as needed for acute attacks.

- β blocker most common. calcium channel blocker, ranolazine, or long acting nitrate (less used) to prevent angina.

- if drug does not prevent/reduce angina use a combination of drugs

Describe the stages of hypertension and criteria for hypertensive therapy

- normo: <120/ <80

- elevated: 120-129/ < 80

- stage I: 130-139/ 80-89

- stage II: >140/ >90

- crisis: above 180/120

- first must do lifestyle changes, then if not at goal BP drug choices go mono therapy with TD, ACEI, ARB, or CCB. then combination with same drugs.

Describe thiazide diuretics. What is the drug, MOA, uses, and AE

- hydrochlorothiazide

- MOA: block the Na+/Cl- transporter in the distal convoluted tubule of the kidney, decrease Na+ reabsorption

- use: used for monotherapy for mild/moderate HTN with a reduced risk of developing CV disease

- AE: long term hypokalemia which increases mortality

Describe angiotensin converting enzyme (ACE) inhibitors. What is the drug, MOA, uses, and AE

- enalapril

- MOA: inhibits ACE, which decreases angiotensin II, which decreases vascular resistance, aldosterone secretion, Na retention, and CV tissue remodeling

- use: potential inital monotherapy choice mild to moderate HTN

- AE: hypotension (1st dose), cough, angioedema, hyperkalemia (d/t reduced aldosterone mediated K+ excretion), fetal harm (category D)

Describe angiotensin receptor blockers (ARBs). What is the drug, MOA, uses, and AE

- losartan

- MOA: antagonists at angiotensin II receptors (having the same effect as ACEI)

- use: as a substitute for ACEIs- mild to moderate HTN

- AE: little cough and angioedema, first dose HTN, hyperkalemia, fetal risk (category D)

Describe calcium channel blockers. What are the drugs, MOA (2), uses, and AE

- (1) amlodipine, nifedipine. (2) diltiazem, verapamil

- MOA: (1) dipines block L type calcium channels in vascular smooth muscle (2) block L type calcium channels in vascular smooth muscle and in the heart

- use: potential inital monotherapy choice mild to moderate HTN. amlodipine is the most commonly used CCB for HTN

- AE: excessive hypotension (facial flushing, headache, dizziness, peripheral edema). verapamil and diltiazem can cause cardiac depression, bradycardia

Describe beta blockers. What are the drugs and selectivity, MOA, uses, and AE

- propranolol (non selective B1B2), metoprolol (cardioselective B1), carvedilol (mixed B1B2A1)

- MOA: decrease CO by decreasing HR and contractility (heart) and decreases renin release causing less angiotensin and decreases peripheral vascular resistance (kidney)

- use: used in hypertension but not first-line drugs. used in angina pectoris, heart failure etc.

- AE: bronchoconstriction, bradycardia, bizzare dreams

Describe alpha 1 blockers. What is the drug, MOA, uses, and AE

- terazosin

- MOA: blocks vascular a1-receptors that cause vasoconstriction

- use: not first line drugs for hypertension

- AE: first dose phenomenon (orthostatic hypotension, dizziness, fainting), tachycardia (beta blockers will prevent this), fatigue

Describe sympathetic nerve blockers. What is the drug, MOA, uses, and AE

- clonidine

- MOA: A2 AGONIST. stimulate sympathetic a2 to cause a centrally mediated vasodilatation and reduction in heart rate, lowering blood pressure.

- use: secondary drugs used for mild-moderate hypertension. use with methyldopa in pregnancy.

- AE: sedation, dry mouth, withdrawal syndrome (hypertension, tachycardia, nervousness)

Describe direct vasodilators. What are the drugs, MOA, uses, and AE

- hydralazine, nitroprusside

- MOA: directly causes vasodilatation. decrease Ca2+ in vascular smooth muscle cells and/or release the vasodilator nitric oxide (NO).

- use: nitroprusside is used IV to treat hypertensive emergency which rapidly lowers BP

- AE: not used as monotherapy for hypertension due to tachycardia, sodium and water retention, dizziness etc

Describe loop diuretics. What is the MOA, uses, and AE

- furosemide

- MOA: blocks the Na+/ K+/ Cl- transporter in the loop of henle and decreases Na+ absorption

- use: tx edema and heart failure

- AE: hypokalemia

Describe K+ sparing diuretics. What is the MOA and uses

- spironolactone

- blocks aldosterone receptors in the kidney. causes a small decrease in Na+ reabsorption and increases plasma K+

- use: maintains normal plasma K+ when combined with thiazides in HTN and HF

Describe the impact/ causes/ pathophysiology, and s/s for heart failure

- inability of the heart to supply enough blood to maintain adequate tissue perfusion

- causes: chronic hypertension, myocardial infarction, heart valve problems, coronary artery disease

- CHF can lead to ventricular remodeling, which causes reduced CO, leading to insufficient tissue perfusion, fluid retention, and volume overload

- s/s: fatigue, exercise intolerance (inadequate tissue perfusion) venous distention, peripheral/ pulmonary edema (volume overload)

Describe compensatory mechanisms caused by remodeling and a decrease of cardiac output during heart failure

- increase in sympathetic discharge: norepinephrine (NE)

- activation of renin-angiotensin-aldosterone system (AII)

- increase in blood pressure (afterload)

- increase fluid retention

Describe ACE inhibitors. What is a drug, the MOA, use, and AE.

- enalapril

- MOA: inhibition of angiotensin II formation, increase bradykinin. this leads to less vasoconstriction (dec BP and afterload), less aldosterone and Na/H2O retention (dec venous return and preload)

- use: heart failure, results in less cell proliferation and less cardiac remodeling

- AE: intractable cough and angioedema from bradykinen, hypotension (1st dose), hyperkalemia (d/t reduced aldosterone mediated K+ excretion), fetal harm (category D)

Describe angiotensin II receptor blockers (ARBS). What is a drug, the MOA, use, and AE

- losartan

- MOA: block angiotensin II receptors, which decreases preload, afterload, fluid retention, cell proliferation and cardiac remodeling

- use: increases survival in HF patients and is a replacement for ACEI if they cannot be tolerated

- AE: same as ACE but less bradykinen (so less cough and angioedema)

Describe beta adrenergic receptor blockers. What is a drug, the MOA, use, AE, and drug to drug interactions

- carvedilol

- MOA: prevent down-regulation of the β1 adrenergic receptors in the heart as a result of excessive sympathetic stimulation during heart failure

- heart responsive to sympathetic drive and reduces heart muscle remodeling

- use: increase survival in heart failure patients.

- AE: CV (bradycardia, AV block), fatigue, cold hands/feet, CNS (insomnia, bizarre dreams)

What is a contraindication of B adrenergic receptor blockers

those who have pre-existing conduction disturbances

Describe combination vasodilators. What is a drug, the MOA, use, AE, and drug to drug interactions

- isosorbide dinitrate+hydralazine (Bidil)

- MOA: ID dilates veins and decreases preload, H dilates arteries and decreases Ca+ and afterload

- use: moderate to severe heart failure, usually a combo. reduced morbidity and mortality

- AE: orthostatic hypotension, reflex tachycardia. hydralazine can cause lupus erythematosus like syndrome

Describe digitalis. What is a drug, the MOA, use, AE, and drug to drug interactions

- digoxin: cardiac glycoside heart failure drug

- MOA: inhibits the enzyme Na+K+ ATPase in the heart, alters cell Na+ and increases Ca+, which increases the force of ventricular contraction (a cardiotonic drug)

- use: reduces symptoms

- AE: bradycardia and arrhythmias, anorexia, N/V, fatigue, blurry vision, halos, yellow/green tinge

Describe the 3 hemodynamic effects of Digoxin and the signs/symptoms and treatment of cardiac glycoside toxicity/ ineffectiveness.

1. decreased sympathetic tone

2. decreased renin release

3. increased urine production which reduces edema

- too little K+ means too much digoxin block = toxicity

- too much K+ means too little digoxin block = ineffective

- treatment for toxicity: digifab or activated charcoal

Describe the physiology of the kidney and the use of diuretics in therapy for edema and hypertension

1. work by blocking sodium reabsorption from renal tubule urine to blood

2. sodium in the renal tubule creates osmotic pressure that prevents water from being reabsorbed

3. water that is not reabsorbed is excreted

4. sodium that is not reabsorbed is also excreted

5. diuretics thus reduce blood volume and extracellular fluid volume: reduce edema

Describe loop diuretics. What is a drug, the MOA, site of action, use, and AE

- furosemide

- MOA: blocks the Na+/K+/Cl- transporter in the loop of henle and decreases Na+ reabsorption. causes a large reduction in plasma volume.

- use: treat edema and in heart failure to tx symptoms caused by edema

- AE: ototoxicity, hypokalemia, dehydration, hypotension, thrombosis, caution in pregnancy

Describe thizades diuretics. What is a drug, the MOA, site of action, use, and AE

- hydrochlorothiazide

- MOA: block the Na+/Cl- transporter in the distal convoluted tubule of the kidney, decrease Na+ reabsorption, mild diuresis. reduce plasma volume, reduce total body Na+

- use: treats mild edema in heart failure and other conditions, as well as mild-moderate hypertension

- AE: hypokalemia, dehydration, hypotension,

thrombosis

Describe potassium-sparing diuretics. What is a drug, the MOA, site of action, use, and AE

- spironolactone

- MOA: blocks aldosterone receptors in the collecting duct, increasing plasma K, decreasing Na+ and blood volume

- use: limited diuresis, hypertension (reduced thiazide by retaining K+), heart failure (reduces remodeling), and decreases mortality

- AE: hyperkalemia, gynecomastia, menstrual irregularities, hirsutism. NO PREGNANCY

Describe osmotic diuretics. What is a drug, the MOA, site of action, use, and AE

- mannitol

- MOA: promotes diuresis by creating an osmotic force. draws in and holds water in the lumen of the

- use: prevents renal failure by maintaining urine output, reduction in ICP and edema by drawing fluid out of the brain into blood vessels

- AE: headache, N/V, F/E imbalance

What are some nursing implications for diuretics including dietary requirements and time of dosing

- dose early in the day and not at bedtime

- a potassium supplement may be prescribed for the patient: except in spironolactone

- there may need to be a restriction of Na+ and fluids intake.

Define and describe hyperlipidemia

- abnormally high levels of lipids/ lipoproteins

- this is a modifiable risk factor for cardiovascular disease. hyperlipidemia, elevated LDL-cholesterol, is associated with atherosclerosis.

Differentiate between VLDL, LDL, and HDL and how they contribute to coronary artery disease

- VLDL: delivers TAGs to non hepatic tissue. may contribute to atherosclerosis, is a major risk for pancreatitis.

- LDL: delivers cholesterol to non hepatic tissue. definitely contributes to atherosclerosis via oxidized LDLs

- HDL: transports cholesterol FROM non hepatic tissue BACK TO the liver. protects against atherosclerosis by scavenging cholesterol, interfering with LDL oxidation, and inhibiting platelet activity.

Describe the goals and management of high cholesterol, as well as drug treatment options

- goal: lower LDL, increase HDL

- diet modification: low fat diet should be tried before drug therapy

- drugs: Statins, cholesterol absorption inhibitors, PCSK9 inhibitors, bile acid binding resins, nicotinic acid, and fibric acid derivatives.

Describe HMG-CoA reductase inhibitors (aka statin). What is the drug, MOA, use, contraindications, and AE

- atorvastin

- MOA: inhibits the synthesis of cholesterol in the liver which causes a decrease in hepatic cholesterol → liver increases LDL receptors on hepatocytes → LDL receptors uptake LDL from plasma → lower LDL levels

- use: most commonly used drug for tx of hypercholesterolemia, cardiovascular disease reduction, and plaque stabilization

- AE: minor joint pain, dyspepsia, GI upset. may cause myopathy, liver disfunction, rhabdomyolysis

- contraindicated in pregnancy and breastfeeding

Describe Cholesterol Absorption Inhibitors. What is the drug, MOA, use, and AE

- ezetimibe

- MOA: converetd to glucuronide in SI and liver which inhibits intestinal absorption of cholesterol in SI and decreases hepatic cholesterol → increased LDL receptors causing decreased plasma LDL

- use: effective in hypercholesterolemia as monotherapy in small LDL gaps. with large, combined with statin

- AE: avoid with hepatic dysfunction and pregnancy. can cause myopathy with statins

Describe PCSK9 Inhibitors. What is the drug, MOA, use, AE, and unique factors.

- evolocumab

- MOA: monoclonal antibodies which bind to PCSK9, preventing degradation of LDL receptors → more LDL receptors available to remove LDL from blood

- use: SQ 2x month which drastically lowers LDL

- AE: nasopharyngitis, itching, joint pain, injection site reactions

- unlike the other drugs, this is the only one that DECREASES HDL

Describe bile acid binding resins. What is the drug, MOA, use, AE, and lifespan/ dose considerations

- colesevelam

- MOA: resins bind and form insoluble complex with bile acids in intestine which prevents reabsorption of bile acids and accelerates their excretion → liver needs cholesterol to make more bile acids so it increases uptake of LDLs → decreased LDL levels

- use: hypercholesrolemia and is effective in pregnancy and elderly. dose before meals

- AE: GI upset, may decrease absorption of drugs and fat soluble vitamins (A, D, E, K)

Describe nicotinic acid. What is the drug, MOA, use, dosing, and AE.

- niacin (vitamin b3)

- MOA: inhibits hormone sensitive lipase which reduces free fatty acid release from adipose tissue. less FFA's and triglycerides in liver reduces synthesis of VLDL and ultimately LDL.

- pts usually have high TAGs rather than LDLs

- dose before evening meal

- use: limited in hyperlipidemia, used to lower TAGs in those at risk of pancreatitis.

- AE: facial flushing, pruritus (prevented by asprin), N/V, hepatotoxicity

Describe fibric acid derivatives. What is the drug, MOA, use, AE, and contraindications

- fenfofibrate

- MOA: increases lipoprotein lipase which removes VLDL (lowering) and raises HDL by an active nuclear transcription factor PPAR-a which regulates genes that controls lipid metabolism.

- use: principle use for elevated VLDLs and triglycerides in patients at risk for pancreatitis

- AE: GI upset

- CI: gallstones/ gallbaldder dysfunction, pregnancy, and with statins (risk for myopathy)

Describe nursing considerations regarding dosing of antilipid drugs

for some drugs, they are most effective when taken at night because the liver synthesizes most cholesterol at night.

Describe normal clotting process and how anticoagulants and thrombolytic agents interact with the intrinsic and extrinsic blood clotting pathways.

1. platelet adherence, activation, and secretion with vasodilation

2. aggregation and formation of platelet plug

3. extrinsic (tissue) coagulation pathway

4. intrinsic (blood) coagulation pathway

- both intrinsic and extrinsic act on Xa → allows prothrombin to convert into thrombin → fibrinogen converts into fibrin.

List the types of indirect thrombin inhibitors and their subcategories

1. antithrombin: endogenous anticoagulant

2. heparins: catalyze antithrombin → (1) high molecular weight heparin, (2) low molecular weight heparin and (3) fondaparinux

Describe Heparins as a whole. What is the MOA, use, and AE

- MOA: indirect acting by binding to antithrombin which inhibits factors Xa, thrombin (IIa)

- use: rapid onset for prevention of DVT/ pulmonary embolism. initial treatment preventing thrombosis

- does not cross placenta so is used for anticoagulation in pregnancy

- AE: bleeding (gums), intracranial/ GI, hypersensitivity, osteoporosis, alopecia, Heparin-Induced Thrombocytopenia (HIT) which is huge decrease in platelets (must stop drug)

Describe LMW Heparins. What is a drug, MOA when combined with antithrombin, and the use

- lovenox

- MOA: in conjunction with antithrombin they inhibit thrombin (factor IIa) and factor Xa

- use: more predictable anticoagulant response so they have a lower incidence of HIT

- fast acting

Describe Fondaparinux. What is it, AE, and half life

- synthetic pentasaccharide binds to antithrombin inhibiting factor Xa but NOT thrombin (IIa)

- AE: bleeding risk. lowers platelets with no HIT

- long half life so 1x day dosing

Describe the drug and mechanism for reversal of heparin action. What Heparin does it work best on

- protamine sulfate: binds to heparin and inactivates it

- incomplete reversal of LMW heparin so it is not as beneficial

Describe oral vitamin K antagonists. What is a drug, MOA, use, and AE

- warfarin

- MOA: competitive inhibition of vitamin K-dependent synthesis of clotting factors II, VII, IX, X, and protein C and S.

- use: widely used for issues causing thromboembolism such as venous thrombi, rheumatic heart valves, embolic disease, prosthetic heart valves, A. Fib, etc.

- AE: bleeding, rash, skin necrosis, alopecia, diarrhea, fetal bone defects (NEVER USE IN PREGNANCY)

Describe the drug and mechanism for reversal of warfarin action.

- stop the drug →

- oral or parenteral phytonadione →

- prothrombin-complex concentrates (CHEST guidelines): vitamin K-dependent factors II, VII, IX, X for rapid reversal of warfarin in bleeding patients

Differentiate between direct factor Xa inhibitors and direct thrombin inhibitors. When are they used.

- oral direct factor Xa inhibitors: highly selective Xa inhibitors with a rapid onset and shorter half-life. no titration and monitoring required (unlike warfarin)

- direct thrombin inhibitors: act by inhibiting thrombin, without interacting with antithrombin. used for stroke prevention and a fib

- use in prophylaxis of DVT for surgery and stroke prophylaxis in pts with afib and pulmonary embolism

Compare direct thrombin & direct Xa inhibitors with warfarin in terms of adverse effects

- similar antithrombotic efficacy

- lower bleeding rates

- rapid therapeutic effect

- no monitoring required

- fewer drug interactions

- not affected by diet

- fixed doses

- noncompliance leads to loss of anticoagulant effect d/t short half life

Describe oral anti-platelet agents such as aspirin. What is the MOA and use

- irreversible acetylation of cyclooxygenase resulting in inhibition of thromboxane A2, platelet aggregation and prolongation of bleeding time

- use: low doses for secondary prevention of vascular events

Describe oral anti-platelet agents such as ticlopidine, clopidogrel, and prasugrel. What is the MOA and use

- MOA: platelet ADP receptor antagonists inhibit platelet aggregation.

- use: thrombosis prevention when placing coronary stent,

stroke and MI prevention

Describe fibrinolytic/ thrombolytic agents. What are some types, MOA, and uses

- "clot busters"

- TPA: tissue plasminogen activator

- streptokinase: MOA binds to proactivator plasminogen catalyzing conversion of plasminogen to plasmin

- use: pulmonary embolism, acute ischemic stroke, acute myocardiac infarction, severe deep venous thrombosis

Describe agents used in bleeding disorders and their MOA

- vitamin K: confers biological activity on prothrombin, factors VII, IX & X. used in warfarin toxicity and deficiency. often given to newborns.

- aminocaproic acid/ tranexamic acid: inhibits activation of plasminogen thus fibrinolysis which increases clot formation. used in hemophilia, bleeding from fibrinolytic therapy & rebleeding prophylaxis from intracranial aneurysms.