Final!! #1 Flashcards

1
Q

The perfect drug?

A

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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2
Q

Medication errors

A

Wrong drug 22%
Overdosage 17%
Wrong route 8%

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3
Q

Pure food and drug act of 1906

A

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

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4
Q

Sherly amendment (1912)

A

no fraudulent claims

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5
Q

Food, drug and cosmetic act (1938)

A

Must test for harmful objects and drugs labels complete

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6
Q

Durham humphrey amendment (1952)

A

how drugs can be ordered and dispensed

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7
Q

Kefauver-Harris amendment (1962)

A

Safety and efficacy, permitted generic versions

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8
Q

FDA drug approval

A

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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9
Q

Drug price competition and patent term restoration act of 1984

A

5 years of market exclusivity before making generics

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10
Q

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

A

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

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11
Q

Generic approve criteria
bioequivalence
AUC?:
Cmax?
Tmax?

A

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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12
Q

Schedule I drugs

A

high abuse potential
no accepted medical use
severe dependence

Heroin, marijuana, LSD, ecstasy

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13
Q

Schedule II drugs

A

accepted medical use
prescription pad ONLY, no refills

Opioids, cocaine, barbiturates

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14
Q

Schedule III drugs

A

low physical dependence
high psychological dependence
6 months of refills

Norco, nalbuphine, steroids, ketamine

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15
Q

Schedule IV drugs

A

limited dependence
6 months of refills

Phenobarbital, diazepam

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16
Q

Schedule V drugs

A

may or not require a prescription

codeine

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17
Q

Pharmaceutics

A

science of drug administration
Dosage forms

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18
Q

Pharmacokinetics

A

what the body does to the drug
absorption
distribution
metabolisum
elimination

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19
Q

Pharmacodynamics

A

what the drug does to the body

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20
Q

Antagonism

A

prevents a response to an agonist
can be irreversible or reversible

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21
Q

Enteral administration
Small intestine

A

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

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22
Q

Parenteral administration
Advantages

A

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

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23
Q

Parenteral administration
Disadvantages

A

pain, irreversible
phlebitis, no self admin
infection

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24
Q

Parenteral location

A

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

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25
Q

intra-articular, where?

A

Joint

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26
Q

Intrathecal, where?

A

subarachnoid space
spinal cord

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27
Q

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

A

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

28
Q

Oral dosage forms
In order to fastest to slowest

suspensions
powders
sustained-release
enteric coated
capsules
dissolved liquids(elixir, syrup)
tablets
coated tablets

A

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

28
Q

onset action
duration of action
therapeutic range
Toxic range

A
29
Q

Drag interaction
Pharmacokinetic

A

One drug causes change in the plasma of another drug

30
Q

Drag interaction
Pharmacodynamic

A

changes pts response without changing drugs kinetics

31
Q

Drag interaction
Pharmaceuticals

A

physical and chemical incompatibilities

31
Q

Characteristics of object drugs

A

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

32
Q

Mechanisms of altered absorption

A

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

33
Q

Cytochrome P-450

A

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

34
Q

Enzyme induction

A

Increasing metabolic enzymes

35
Q

Enzyme inhibition:

A

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

36
Q

Pharmacodynamic interactions
Antagonistic

A

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

37
Q

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

A

bleeding
bleeding
CNS depression
bleeding
no MAOIs or SSRIs

38
Q

Thiazide diuretics
Agents

A

Hydrochlorothiazide - most
Metolazone
Chlorothiazide
Indapamide
Chlorothalidone

39
Q

Loop diuretics
Agents

A

Furosemide - most used
Bumetanide
Torsemide

40
Q

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

A

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%

41
Q

Loop and Thiazide ADRs

A

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

42
Q

Potassium sparing diuretics
Agents

A

Amiloride
Triamterene
in combo with thiazide
weak diuretics
Hyperkalemia is ADRs

43
Q

Aldosterone antagonists
Agents

A

hormon effect
Spironolactone
Eplerenone
Spironolactone + HCTZ: aldactazide

44
Q

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

A

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

45
Q

Osmotic diuretics
Agents

A

Mannitol
Urea
Glycerin

46
Q

Carbonic anhydrase inhibitors
a) Agents
b) Uses

A

a) acetazolamide
b) glaucoma

47
Q

Bile Acid Resins
agent

A

Cholestyramine
Colestipol
Colesevelam

Cole: all drugs start with “cole”

48
Q

Bile Acid Resins
a) MOA:
b) ADRs

A

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

49
Q

Bile Acid Resins
form

A

Powder
Tablet
Chewable Bars

50
Q

Niacin
a) MOA
b) ADR

A

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

51
Q

HMG CoA reductase inhibitors
Agent end of??

A

Atorvastatin
*Fluvastatin
*Lovastatin
*Pitavastatin
“Statins”

52
Q

HMG CoA reductase inhibitors
MOA
ADR

A

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

53
Q

What is the statin magic?

A

reduce cardiovascular morbidity mortality

54
Q

PCSK9 inhibitors:
Agent end of??

A

Alirocumab
Evolocumab
“cumab”

55
Q

PCSK9 inhibitors
MOA
ADR

A

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

56
Q

Ezetimibe
MOA
ADR

A

decreases cholesterol absorption
No ADRs

57
Q

Fibric acids
Agents:

A

Gemfibrozil
Fenofibrate

58
Q

Fibric acids
MOA
ADR

A

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

59
Q

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

A

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

60
Q

Omega-3 fatty acids:
Agents:

A

Lovaza
Vascepa
Epanova

61
Q

Omega-3 fatty acids:
MOA
ADR

A

reduces TG
allergy, fish burps, dyspepsia

62
Q

Aldosterone

A

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

63
Q

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

A

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

64
Q

What bile acid made of?

A

Cholesterol
97% are reused