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60 Cards in this Set

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4 Factors that determine intensity of drug responses
1. Administration
2. Pharmacokinetics
3. Pharmacodynamics
4. Sources of individual variation
4 major pharmacokinetic processes
1. Drug absorbtion
2. Drug distribution
3. Drug metabolism
4. Drug excretion
Individual variation: 4 main sources
1. Physiologic variables
2. Pathologic variables
3. Genetic variables
4. Drug interactions
3 ways for drugs to cross the cell membrane
1. Channels and pores
2. Transport system
3. Direct penetration of the membrane
4 factors affecting drug absorption
1. Rate of dissolution
2. Surface area
3. Blood flow
4. Lipid soluability
5. pH partitioning
4 most common routes of drug administration
1. Intravenous
2. Intramuscular
3. Subcutaneous
4. Oral
Drug excretion: 2 main routes
1. Renal routes
a. glomerular filtration
b. passive tubular reabsorption
c. active tubular secretion

2. Non-renal routes
4 primary receptor families
1. cell membrane-embedded enzymes
a. span the entire cell membrane

2. ligand-gated ion channels
a. each channel is specific to one enzyme

3. g protein-coupled receptor systems
a. receptor activates g-protein which activates effector

4. transcription factors
a. found inside the cell
b. response is delayed
Agonists and Antagonists: distinguish between these
1. Agonists: drugs that mimic the body's own regulatory molecules, or the effects of a naturally-occurring compound
a. these are molecules that activate receptors

2. Antagonists: drugs that block the actions of endogenous regulators
a. no effect of their own on receptor function, they work by preventing receptor activation
Non-competitive and competitive agonists: define difference
1. Non-competitive agonists bind irreversibly to receptors, which reduces the number of receptors available to agonists.

2. Competitive antagonists bind reversibly to receptors. They compete with agonists for receptor binding, whichever is present at highest concentration wins the receptor
Therapeutic Index
Measure of a drug's safety

TI = LD/ED

LD: average lethal dose
ED: dose needed to achieve therapeutic response

Low TI: not much room between these two doses

High TI: plenty of room between the doses
3 types of drug-drug ineractions
1. intensification of effects
2. reduction of effects
3. creation of unique response
Basic mechanisms of drug-drug interactions
1. Direct chemical or physical interaction (medicine with herbs, vitamins, etc)

2. Pharmacokinetic interactions (altered ADME)
Absorbtion, Distribution, Metabolism, Excretion
FDA Category A drugs
Controlled studies in women fail to demonstrate a risk to the fetus in the first trimester (and there is no evidence of a risk in later trimesters), and the possibility of fetal harm appears remote.
FDA Category B drugs
Either animal-reproduction studies have not demonstrated a fetal risk but there are no controlled studies in pregnant women, or animal-reproduction studies have shown an adverse effect (other than a decrease in fertility) that was not confirmed in controlled studies in women in the first trimester (and there is no evidence of a risk in later trimesters).
FDA category C drugs
Either studies in animals have revealed adverse effects on the fetus (teratogenic or embryocidal or other) and there are no controlled studies in women, or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the fetus.
FDA category D drugs
There is positive evidence of human fetal risk, but the benefits from use in pregnant women may be acceptable despite the risk (e.g., if the drug is needed in a life-threatening situation or for a serious disease for which safer drugs cannot be used or are ineffective).
FDA category X drugs
Studies in animals or human beings have demonstrated fetal abnormalities, or there is evidence of fetal risk based on human experience or both, and the risk of the use of the drug in pregnant women clearly outweighs any possible benefit. The drug is contraindicated in women who are or may become pregnant.
3 ways the renal system regulates blood pressure
1. Filtration
2. Reabsorption
3. Active tubular secretion
Name the 4 drug classes
1. Sodium Channel Blockers
2. Beta Blockers
3. Potassium Channel Blockers
4. Calcium Channel Blockers
Diuretics: What do they do, and what 3 kinds are there?
These block sodium & chloride reabsorbtion at the renal tubules.

1. Thiazide Diuretics
2. Loop Diuretics
3. Potassium-Sparing Diuretics
Thiazide (give example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
Hydrochlorothiazide
1. Acts at early distal convoluted tubule
2. B
3. Hypokalemia, Hyponatremia, Hyperglacemia
4. None mentioned
Loop Diuretics (give example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
Forosemide
1. Acts at ascending loop of henle to block reabsorbtion
2. B
3. Hypokalemia, Hyponatremia, Hyperglacemia
4. Digoxin, Potas-sparing, Lithium
Potassium-Sparing Diuretics (give example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
Spironolactone
1. Blocks sodium/pot exchange in distal nephron
2. B
3. Hyperkalemia, tumors, irregular menses, deeper voice
4. ACE inhibitors, Pot supp.
Drugs acting on RAAS:
4 categories
1. Renin Inhibitors
2. ACE Inhibitors
3. Angiotensin II Receiver Blockers
4. Aldosterone Antagonists
Renin Inhibitors (example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
Aliskiren
1. Inhibits renin directly-interferes with conversion of angiotensinogen
2. C/D
3. Angioedema, Hyperkalemia, Hypotension, GI issues, increased BUN/Cr values
4. Interferes with substrate 3A4 which inhibits metabolism of the drug--does not break down well
ACE Inhibitors (example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
Captopril, Ramipril
1. Inhibits ACE enzyme
2. C/D
3. 1st dose hypotension, cough, hyperkalemia, renal failure, neutropenia, fetal harm
4. Lithium
Angiotensin II receptor blockers (example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
Losartan, Valsartan
1. prevent angio-mediated vasoconstriction and aldosterone mediated volume expansion
2. C/D/D
3. Angioedema, fetal harm, renal failure
4. Reacts with diuretics, anti-hypertanseive agents, ant-inflamataries, potassium raising drugs
Aldosterone antagonists:

Give two main types, mechanism of action, adverse effects
1. Spironolactone
2. Eplereone

Block aldosterone receptors and promote excretion of Na + H20.

Adverse: hyperkalemia
Spironolactone
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
1. Blocks aldosterone in distal nephron, retention of K+, increases Na excretion, binds with steroid receptors
2. D
3. Hyperkalemia, tumors,
4. Interacts with thiazides, agents that increase K+ levels
Eplereone
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
1. selective blockade of aldosterone receptors
2. B
3. Hyperkalemia
4. Interacts with inhibiotrs of CYP3A4, drugs that increase K+levels, lithium
Calcium-Channel Blockers
Give 2 main types

1. Give mechanism of action
2. Pregnancy Category
Dihydropyridines and Non-dihydropyridines

1. Relaction of vascular smooth muscle causes vasodilation by preventing Ca from entering cells. Reduces arterial pressure and increases coronary perfusion--acts primarily on arterioles
2. C
Dihydropyridines (example)
1. Adverse effects
2. Other drug interactions
Nifedipine, Amidopine
1. Flushing, dizziness, headache, peripheral edema, reflex tachycardia (greater risk than non-dihydropyridines)
2. Interacts with beta-blockers
Non-Dihydropyridines
1. Mechanism of action
2. Adverse effects
3. Name the 4 sub-categories
Phenylalkylamine, Benzothiazipine
1. suppression of SNS influence on heart and blood vessels
2. Constipation, dizziness, flushing, headache
3. Beta blockers, Alpha blockers, Alpha/Beta blockers, Andrenogeric Neuron blockers
Beta Blockers (example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
proranolol, metoprolol
1. blockagde of cardiac and juxtaglomerular beta 1 receptors, suppress reflex tachycardia caused by vasodilators
2. varries
3. brachycardia (decreased AV conduction as well) decreased atrioventricular conduction, reduced contractility, bronchoconstriction, asthma excaberator
4. other hypotensives, CCBs, Digoxin, hypoglycemic agents
Alpha Blockers (example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
doxazosin, tarazosin
1. prevents stimulation of alpha receptors on arterioles and veins
2. C
3. orthostatic hypotension (largest effect--also worst with first dose), reflex tachycardia, inhibition of ejaculation, nasal congestion
4. PDE-5 inhibitors (viagra, cialis, etc) and other hypotensives
Alpha/Beta Blockers (example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
Carvidalol, labetalol
1. promotes dilation of areterioles & veins, reduces heart rate and contractility, suppresses release of renin
2. C
3 &4: Combine effects and drug interactions of Apha and Beta-blockers
Centrally-acting Alpha 2 antagonists:
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
Clonidine, methyldopa
1. Acts in brainstem to suppress sympathetic outflow to heart and blood vessels
2. C/D, B
3. dry mouth, sedation, hepatoxicity (liver disorders) **can cause hypotension if removed abruptly--works at brainstem
Adrenergic Neuron Blockers (example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
Reserpine
1. Decrease BP through acting in terminals of post-ganglionic symptomatic neurons
2. C
3. depression, nasal congstion, bradycardia, orthostatic hypotension, GI issues, erection killer
4. Digoxin, levodopa, other hypotensive agents
Direct-acting vasodilators (example)
1. Give mechanism of action
2. Pregnancy Category
3. Adverse effects
4. Other drug interactions
Hydralazine, minoxidil
1. promotes dilation of arterioles
2. C
3. reflex tachycardia, expansion of blood volume, Na/H20 retention, cardiac tamponade, hypertrichosis (excessive hair growth). Minoxidil = 1 more issue: pericardial effusion (fluid buildup)
4. Interacts with other hypotensives
Cardiac Glycosides (example)
1. Give mechanism of action
2. Adverse Events
Digoxin is the only drug of this class approved in US
1. Increases miocardial contractility, increasing cardiac output
2. Mechanism of action can also cause severe dysrhytmias, therefore these are 2nd-line agents. K+ and digoxin are antagonistic competitors for same binding sites--K+ high=reduced therapeutic benefit, K+low=hypokalemia

*this drug is distributed widely and crosses placenta, ultimately eleminated by renal system. Half-life of 1.5 days
Heart Failure Management:

Four drugs to try

Three drugs to avoid
GIVE: 1. ACE Inhibitors, ARMS 2. Aldosterone Antagonists 3. Beta Blockers 4. Digoxin

AVOID: 1. Antidysrhythmic agents 2. Calcium-channel blockers 3. NSAIDS
4 Stages of Heart Failure
A: Asymptomatic, but high risk (diabetes, hypertension, family) MGT: reduce risk

B: Asymptomatic, but structural issues. MGT: prevent symptomatic HF

C: Symptoms with structural heart disease. MGT: releave symptoms, improve funct capacity, slow card remodeling, prolong life. Give diuretics, ACE, B-block, Digoxin

D: Advanced structural issues. Repeated hospitalization necessary. MGT: New Heart!
Angina Pectoris: Define

1. Give 2 goals of drug therapy

2. Give 3 types
02 supply not enough to meet heart demand

1. Prevent MI, prevent M ischemia & pain

2. Variant, Stable, Unstable
3 families of anti-anginal agents and their mechanism of action
1. Organic Nitrates
decrease 02 demand by dilating veins, decreasing preload

2. Beta Blockers
decrease 02 demand by decreasing heart rate and contractility

3. Calcium-channel blockers
decrease 02 demand by dilating arterioles, decreasing afterload
Antiarrythmics: name two types and two fundamental causes
1. Tachydysrhythmias: HR increase, this one is most common and responds best to drug therapy.

2. Bradydysrhythmias

2 causes:
1. Disturbance in automaticity
2. Disturbance in conduction
Vaughan Williams classification of antidysrhythmic drugs: Name all four
1. Sodium: slow contraction in atria, ventricles

2. B-blockers: lower automasticity (SA) conduction (AV) contractility (A&V)

3. K-ch blockers: lower repolarization

4. C-ch blockers: lower automasticity (SA) conduction (AV) contraction (A&V)
Class IA antiarrythmics:
1. Give Example
2. Give Method of Action
3. Adverse effects
4. Drug interactions
1. Quinidine

2. Blocks Na channels, slows impulse conduction, delays repolarization, blocks vagral input to heart, widens QRS, prolongs QT, used against supraventricular and ventricular dysrythmias

3. diarrhea, cardiotoxicity, arterial embolism

4. Digoxin
Class IB antiarrythmics:
1. Give Example
2. Give Method of Action
3. Adverse effects
1. Lidocane

2. blocks cardiac sodium channels, slows conduction in atria, ventricles, HIS purkinje system, minimal EKG changes. Give to help ventricular dysrhythmias

3. CNS efects, drowsiness, confusion
Class IC antiarrythmics:
1. Give Example
2. Give Method of Action
3. Adverse effects
1. Flecainide or Propafenone
2. block Na channels and delay ventricular repolarization
3. Same as IA/IB
Class II Antiarrythmics
1. Give Example
2. Give Method of Action
3. Adverse effects
1. Propranadol, Acebutolol, Esneolol, Sotalol
2. Decreases automatacity of SA node, decreases myocardial contractility, slows ventricular rate
3. heart block, heart failure, AV block, hypotension, sinus arrest, bronchospasm
Class III antiarrythmics:
1. Give Example
2. Give Method of Action
3. Adverse effects
1. Bretylium
2. Delays repolarization of fast potentials, prolongs QT interval, used for V-fib and V-tach
3. Hypotension
Aminodarane:
1. Class
2. Mechanism of action
3. Adverse Effects
4. Metabolization
1. Class III antiarythmic
2. lowers contractility, conduction velocity.
3. Optic neuropathy, pulmonary toxicity, cardiotoxicity
4. Highly lipid soluble, metabolized in liver (CYP34A)
Class IV Antiarythmics:
1. Give Example
2. Give Method of Action
3. Adverse effects
4. Drug interactions
1. Verapamil, diltiazem
2. delay AV node conduction, lower myocardial toxicity, prolong PR interval, slows ventricle rate
3. Bradycardia, hypotension, AV block, HG, peripheral edema, constipation
4. Digoxin, b-blockers
Anti-hyperlipidemics

Name 4
1. HMG-CoA reductase inhibitors
2. Bile-acid sequestrants
3. Nicotinic acid (niacin)
4. Fibrates
HMG-CoA reductase inhibitors

1. Give Example
2. Give Method of Action
3. Adverse effects
4. Contraindications
1. STATINS!
2. treatment of hypercholesterolemia--reduces proceedures like CABG/PTCA. This is an inhibitor of HMG-CoA reductase, thereby reducing cholesterol synthesis, and increases LDL receptors on hepatocytes increasing removal of LDL from blood. Also promotes plaque stability and reduces inflamation at plaque site

3. Myopathy, increased liver enzymes. ** Must do liver and renal workup before giving this drug, as it is metabolized rapidly in the liver and secreted in bile. Significant amounts found in urine.

4. Pregnancy (X), liver disease
Nicotinic Acid (Niacin)

1. Give Example
2. Give Method of Action
3. Adverse effects
4. Contraindications
1. Niacin

2. Reduces major coronary events and total mortality. Can be given immediate, sustained, and extended release.

3. Flushing of skin, GI, hyperglycemia, hyperuremia

(PREG: C)

4. Liver disease or gout, perhaps diabetes
Bile Acid Sequestriants

1. Give Example
2. Give Method of Action
3. Adverse effects
4. Contraindications
1.

2. Reduce coronary events and CHD mortality

3. Decreases absorbtion of digoxin, warafin, antibiotics

(PREG: B)

4. Bowel obstructions, TG level >400
Fibric Acid Derivatives

1. Give Example
2. Give Method of Action
3. Adverse effects
4. Contraindications
1. Fibrates

2. Decreases plasma TG content, lowers VLDL levels, raises HDL levels

3. Rashes, GI, glalstones, myopathy, liver injury

(PREG: C)

4. Severe renal or hepatic disease, also reacts with warfarin, statins
EXETIMIBE:

1. Give Example
2. Give Method of Action
3. Adverse effects
4. Contraindications
1. Tradename: Zetia

2. Inhibits cholesterol absorption, lowers LDL, raises HDL, lowers TG

3. Myopathy, hepatitis, pancreatitis, thrombocytopenia

(PREG: C)

4. Statins, fibrates, warfarin, bile-acid sequestriants