Final!! #1 Flashcards by Yuko Porter

The perfect drug?

T: treat the pt condition
R: rapid
M: mouth
A: No ADRs

I:inexpensive
I:infrequently take
N:No med interaction
E:elminated from the body quickly

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Medication errors

Wrong drug 22%
Overdosage 17%
Wrong route 8%

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Pure food and drug act of 1906

Protect public from mis labelled drugs
Drug company lists 1 of 11 dangerous things

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Sherly amendment (1912)

no fraudulent claims

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Food, drug and cosmetic act (1938)

Must test for harmful objects and drugs labels complete

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Durham humphrey amendment (1952)

how drugs can be ordered and dispensed

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Kefauver-Harris amendment (1962)

Safety and efficacy, permitted generic versions

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FDA drug approval

Preclinical: 6.5 years
Phase I: 1.5 years - small set of volunteers
Phase II: 2 years - patients with disease, tests for effectiveness and side effects
Phase III: 3.5 years - tests for safe dosage
FDA review - 1.5 years

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Drug price competition and patent term restoration act of 1984

5 years of market exclusivity before making generics

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Generic approve criteria
pharmaceutical equivalence
Same active?
May have different?

ingredients, dosage form, strength, route
shape, scoring, and excipients

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Generic approve criteria
bioequivalence
AUC?:
Cmax?
Tmax?

Must line within 80 to 125%
(-20%, +20%)
AUC: area under curve, level of drug in blood over 24 hrs
C: max concentration
T:how much time it takes to make

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Schedule I drugs

high abuse potential
no accepted medical use
severe dependence

Heroin, marijuana, LSD, ecstasy

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Schedule II drugs

accepted medical use
prescription pad ONLY, no refills

Opioids, cocaine, barbiturates

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Schedule III drugs

low physical dependence
high psychological dependence
6 months of refills

Norco, nalbuphine, steroids, ketamine

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Schedule IV drugs

limited dependence
6 months of refills

Phenobarbital, diazepam

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Schedule V drugs

may or not require a prescription

codeine

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Pharmaceutics

science of drug administration
Dosage forms

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Pharmacokinetics

what the body does to the drug
absorption
distribution
metabolisum
elimination

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Pharmacodynamics

what the drug does to the body

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Antagonism

prevents a response to an agonist
can be irreversible or reversible

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Enteral administration
Small intestine

high surface area,
rich blood supply,
basic pH (BEST PLACE)

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Parenteral administration
Advantages

used for drugs that are poorly absorbed immediate onset
long lasting
specific location
predictable, titratable

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Parenteral administration
Disadvantages

pain, irreversible
phlebitis, no self admin
infection

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Parenteral location

Intravenous, intramuscular, subcutaneous, epidural
intrathecal
intra-articular
intra-arterial

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intra-articular, where?

Joint

Intrathecal, where?

subarachnoid space spinal cord

Topical admin local or systemic? Skin: Eyes: Ears: Intranasal: Inhalation Vaginal

S: local and systemic Eyes: local ONLY Ears: local ONLY Nasal: local and systemic Inhalation: local and systemic V: local and systemic

Oral dosage forms In order to fastest to slowest suspensions powders sustained-release enteric coated capsules dissolved liquids(elixir, syrup) tablets coated tablets

D: dissolved liquids (elixir, syrup) FASTEST S: suspensions P: powders C: capsules T: tablets C: coated tablets E: enteric coated S: sustained-release SLOWEST

onset action duration of action therapeutic range Toxic range

Drag interaction Pharmacokinetic

One drug causes change in the plasma of another drug

Drag interaction Pharmacodynamic

changes pts response without changing drugs kinetics

Drag interaction Pharmaceuticals

physical and chemical incompatibilities

Characteristics of object drugs

Narrow range Steep dose response Metabolized by hepatic enzymes Typically used chronically

Mechanisms of altered absorption

Complexation: chemical complexes change rate of absorption Changes in pH Changes in GI mobility

Cytochrome P-450

Enzyme that metabolizes drugs Some people have more than others, more means higher doses needed

Enzyme induction

Increasing metabolic enzymes

Enzyme inhibition:

Most common interaction between two drugs Less enzymes leads to toxicity Onset max effect and offset all within 24 hrs

Pharmacodynamic interactions Antagonistic

meds work against each other produce opposite effects (EFFECT ANTAGONIST)

Herbs and drug interactions ADRs Ginkgo biloba: Ginseng: Kava: Garlic: St. John's wort:

bleeding bleeding CNS depression bleeding no MAOIs or SSRIs

Thiazide diuretics Agents

**Hydrochlorothiazide - most** Metolazone Chlorothiazide Indapamide Chlorothalidone

Loop diuretics Agents

**Furosemide - most used** Bumetanide Torsemide

a) used for? b) act on where? c) Inhibit what?

a) moderate/severe edema HTN from volume overload b) ascending Loop of Henle c) Sodium reabsorption **Special things** high ceiling, most effective drug class 20-25%

Loop and Thiazide ADRs

Hypokalemia - cardiac arrhythmias **More pee=more lose K** **Ototoxicity (=ear) - loop only** Dehydration Hypovolemia Calcium wasting Glucose intolerance

Potassium sparing diuretics Agents

Amiloride Triamterene in combo with thiazide weak diuretics **Hyperkalemia is ADRs**

Aldosterone antagonists Agents

hormon effect **Spironolactone** Eplerenone Spironolactone + HCTZ: aldactazide

Aldosterone antagonists a)MDR b) Main use c) ADR

a) distal tubule and collecting duct Blocking the action of aldosterone b) pts w/ high aldosterone c) hyperkalemia, hormonal effects (**spironolactone** only)

Osmotic diuretics Agents

Mannitol Urea Glycerin

Carbonic anhydrase inhibitors a) Agents b) Uses

a) acetazolamide b) glaucoma

Bile Acid Resins agent

Cholestyramine Colestipol Colesevelam Cole: all drugs start with “cole”

Bile Acid Resins a) MOA: b) ADRs

a) bind to bile acids to stop reuse, lower LDL b) constipation, bloating, nausea Drug interactions: take 4 hr before BAR

Bile Acid Resins form

Powder Tablet Chewable Bars

Niacin a) MOA b) ADR

a) lower LDL, raise HDL **Best for HDL!!** b) “not nice on skin” flushing, itching, hives, rash DO NOT administration with hot fluids and alcohol

HMG CoA reductase inhibitors Agent end of??

Atorvastatin *Fluvastatin *Lovastatin *Pitavastatin **“Statins”**

HMG CoA reductase inhibitors MOA ADR

lower LDLs a fuck ton **best for Lower LDLs!!** headache, myopathy, flu like, hepatotoxicity

What is the statin magic?

reduce cardiovascular morbidity mortality

PCSK9 inhibitors: Agent end of??

Alirocumab Evolocumab “cumab”

PCSK9 inhibitors MOA ADR

prevent LDL receptors from getting destroyed allergic reaction, muscle aches, injection site stuff

Ezetimibe MOA ADR

decreases cholesterol absorption No ADRs

Fibric acids Agents:

Gemfibrozil Fenofibrate

Fibric acids MOA ADR

lowers TG dyspepsia, abdominal pain, myopathy (avoid w/ statins)

a) Low Density Lipoproteins (LDL) b) triglyceride (TG)

a) bad Risk for heart disease and stroke. b) increase risk of heart disease

Omega-3 fatty acids: Agents:

Lovaza Vascepa Epanova

Omega-3 fatty acids: MOA ADR

reduces TG allergy, fish burps, dyspepsia

Aldosterone

helps control the balance of water and salts in the kidney by keeping sodium in and releasing potassium from the body

a) Bile is what? b) Made by where? c) Store in where? d) Bile help with what?

a) digestive juice b) liver c) gallbladder d) small intestine help to absorb fat

What bile acid made of?

Cholesterol 97% are reused