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Pharmo for medic school > Learning outcome 1 > Flashcards

Learning outcome 1 Flashcards

1
Q

Thalidomide

A

Sedative that caused phocomelia (birth defect - gross malformation or absence of limbs)

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2
Q

Randomized controlled trials (RCT) three distinguishing features

A

Use of controls, randomization, blinding

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3
Q

Use of controls in RCTs

A

Pts are given new drug, others are given a placebo or an already standard treatment. (Standard or placebo pts are controls)

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4
Q

Randomization in RCT

A

Subjects randomly assigned to treatment or control group.

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5
Q

Blinded in RCT

A

Single blind means only subjects don’t know who’s getting what, double blind means they both don’t know

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6
Q

Preclinical testing

A

Done in animals. Take 1 to 5 years. If approved for clinical testing by FDA, drug is awarded investigational

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7
Q

Phase I

A

Done in healthy patients unless the drug has severe sides like cancer drugs

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8
Q

Phase I three goals

A

Evaluating drug metabolism, pharmacokinetics, biologic effects

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9
Q

Phase II and III

A

Testing patients. Object is to determine therapeutic effects, dosage range, safefty, and effectiveness

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10
Q

Phase IV

A

If approved, it gets released for general use permitting observation in a large population.

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11
Q

Failure to detect in clinical trials

A

Relatively small number use the drug, patients are carefully selected and don’t fully represent the population, pts take drug for limited time

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12
Q

Effects which show up after clinical trial

A

Infrequent effects, long term effects, effects in certain populations only (1/2 drugs have serious adverse effects not found until after release)

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13
Q

Chemical name of drug

A

A description of the drug using chemistry nomenclature

N-acetyl-para-aminophenol

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14
Q

Generic name

A

Or nonproprietary. A name assigned, each drug has only one.
Acetaminophen
The final syllables may indicate a class

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15
Q

Cillin suffix means

A

Belongs to the penicillin class

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16
Q

Statin suffix

A

HMG-CoA reductase inhibitor.

Lowers cholesterol

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17
Q

Trade name

A

Proprietary or brand name.. Must be approved. Tylenol

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18
Q

olol

A

Beta-adrenergic blocker htn and angina

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19
Q

barbital

A

barbiturate

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20
Q

pril

A

ACE inhibitor

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21
Q

sartan

A

Angiotensin II receptor blocker

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22
Q

dipine

A

Didropyridine calcium channel blocker

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23
Q

triptan

A

Serontonin 1B/1D receptor agonist

Migraine

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24
Q

parin

A

low-molecular wait heparin

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25
Q

afil

A

PDE-5 inhibitor

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26
Q

glitazone

A

Thiazlidinedione for NIDDM

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27
Q

Prazole

A

Proton pump inhibitor

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28
Q

dronate

A

Bisphosphonate for osteoporosis

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29
Q

floxacin

A

Fluoroquinolone antibiotic

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30
Q

Non equivalent trade names

A

Pts taking dilantin got switched to generic phenytoin and had seizures

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31
Q

Pharmacokinetics

A

Study of drugs moving throughout the body. It includes drug metabolism and excretion.

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32
Q

4 basic pharmacokinetic properties

A

Absorption, distribution, metabolism, excretion

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33
Q

Absorption

A

Movement of a drug from its site of administration into the blood

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34
Q

Distribution

A

Drug movement from blood to interstitial space of tissues, and from there into the cells

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35
Q

Metabolism

A

Enzymatically mediated alteration of a drug

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36
Q

Excretion

A

Movement of drugs and metabolites out of the body

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37
Q

Metabolism plus excretion is called

A

elimination

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38
Q

3 ways drugs pass membranes

A

Passage through channels or pores, passage with aid of transport system, through the membrane itself

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39
Q

Channels and pores

A

Not many drugs go through as they are took big, usually for things under 200 daltons like Na+ and K+

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40
Q

Transport system

A

May or may not use energy

Are selective

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41
Q

P-glycoprotein

A

Aka multidrug transporter protein. Transports many drugs OUT of cells.
Present liver, kidney, placenta, intestine, capillaries in brain.

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42
Q

P-glycoprotein in organs

A

Transports drugs for bile elimination.
In kidneys it pumps drugs out for excretion
Placenta transports back to maternal blood
Intestine transports to intestinal lumen (and can reduce absorption into blood because of this)

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43
Q

Direct penetration of the membrane

A

Most drugs depend on this because they are too big for channels or pores, often lack transport system to help them cross all of the membranes that separate them from their sites of action, metabolism and excretion

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44
Q

Likes disolve

A

likes

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45
Q

NOT lipid soluble are

A

Polar and ion

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46
Q

Polar molecules

A

E.g gentamicin because of hydorxyl groups.

Polar molecules have no net charge.

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47
Q

Ions

A

Net positive or negative charge. Can’t cross membrane unless tiny

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48
Q

Quaternary Ammonium Compounds

A

At least one atom of nitrogen, and carry a positive charge all the time.

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49
Q

pH-dependent Ionization

A

Weak acids and bases can contain or not contain a charge.
If an acid is in an acid it is less likely to give up its H+ (therefore gaining a negative charge) and can still cross the membrane

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50
Q

Ion trapping

A

Or pH partitioning. Acids stay on acidic side, bases stay on basic bitch side

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51
Q

Factors affecting absorption

A

Rate of dissolution
Surface area - small intestine has more surface area (microvilli) so oral drugs normally absorbed here not stomach
Blood flow - large gradient maintained by rapid blood flow
Lipid solubility - lipid soluble = more rapid (as a rule)
pH Partioning

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52
Q

Enteral

A

Via the GI tract

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53
Q

IV advantages

A 
No absorption barrier
Instantaneous absorption pattern
Rapid onset
Precise control
Permits large fluid volumes
Permits use of irritant drugs
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54
Q

IV disadvantages

A

Irreversible, expensive, inconvenient, difficult to do, risk of fluid overload, infection risk, emoblism

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55
Q

IM/SUB absorb/ advtanges

A 
Cap wall barrier to absorption 
Rapid with water soluble drugs
Slow with poorly soluble drugs
Permits use of poorly soluble drugs
Depot preparations
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56
Q

IM/ Sub Q disadvantages

A

Discomfort, inconvenient, injury potential

57
Q

Oral barriers to absorption and absorption pattern

A

Epithelial lining of GI tract, cap wall

Slow and variable absorption

58
Q

Advantages PO

A

Easy, convenient, cheap, potentially reversible

59
Q

Disadvantages of PO

A

Variability
GI inactivation
N/V
Pt needs to be conscious and cooperative

60
Q

Slow IVP

A

CNS toxicity occurs after 15 seconds with IV therefore only 25% has gone in if you’re pushing over 1 minute

61
Q

IV embolism

A

Hypotonic and hypertonic kill RBCs, which can cause emoblism. Also obviously the trauma to the vessel wall.
Also drugs not fully disolved (don’t give cloudy drugs or ones with visible particles)

62
Q

IM absorption

A

Big spaces in cells that make cap wall, so not much of a barrier to get through
Water soluble drugs absorb much more rapidly.
Good for drugs which dissolve poorly

63
Q

Chemical equivalence

A

Contain the same amount of the identical chemical compound

64
Q

Equal in bioavailability

A

Same drug is absorbed at the same rate

Not possible to for drugs to be chemically equivalent but differ in bioavailability

65
Q

Tablets

A

Drug plus binders and fillers compressed together.

66
Q

Enteric coated

A

Drugs covered with a material designed to be digested by the intestine but not stomach
Protect drug from stomach and stomach from drug.
Absorption is even more variable due to delays in gastric emptying or not desolving

67
Q

Materials used for enteric coating

A

Fatty acids, waxes, shellac.

68
Q

Sustained release preparations

A

Capsule contains spheres with active drug inside, spheres dissolve at different rates
Potential for variable absorption and expensive

69
Q

Distribution defined as

A

Movement of drugs throughout the body

70
Q

Three major factors of drug distribution

A

Blood flow, ability of drug to exit the vascular system, and ability of drug to enter cells

71
Q

Two pathologic conditions effecting blood flow

A

Abscesses - no blood flow so antiobiotics can’t reach, must be drained first
Tumors - Limited blood supply, blood flow becomes less as you can inward in a tumor. Limited blood flow is a major reason tumors are resistant to drugs

72
Q

Typical capillary beds

A

Drugs move between cap cells rather than through them, therefore leaving is easy

73
Q

BBB

A

Unique caps in CNS, as they have tight junctions between, so dougs need to pass through cap membrane and therefore need to be lipid soluble or have a transport system.
CNS also has P-glycoprotein to pump back out any drugs that get in
Can impede antiobiotics

74
Q

Newborns and BBB

A

BBB not fully evolved, vulnerable to CNS toxicity

75
Q

Placental drug transfer

A

Drugs which are highly polar, ionized, or protein bound cannot pass. Same with substrates for P-glycoprotein

76
Q

Protein bonds

A

Albumin most abundant. 69,000 daltons so stays in blood.

77
Q

Ablumin

A

Warfarin binds 99%, gentamicin 10%.
Bound drugs are restricted because Albumin is so big. Also drugs won’t be metabolized while bound.
Also two drugs competing for albumin increases the free concentration of the one getting bumped

78
Q

Entering cells

A

Some drugs must enter cells to reach site of action (some bind to external receptors)
All drugs must enter cells to undergo metabolism

79
Q

CYP 450

A

12 CYP families, first three metabolize drugs, other 9 metabolize endogenous compounds like steroids and fatty acids

80
Q

6 possible consequences of drug metabolism

A 
Accelerated renal excretion
Drug inactivation
Increased therapeutic action
Activation of prodrugs
Increased toxicity
Decreased toxicity
81
Q

Accelerated renal drug excretion

A

Most important consequence of metabolism.

Kidneys are unable to excrete highly lipid soluble drugs, and most convert to hydrophilic.

82
Q

Two main conversions to increase renal drug excretion

A

Adding a hydroxyl group, or glucuronidation (add glucuronic acid) (may enter enterohepatic recirc)

83
Q

Age and drug metabolism

A

Up till 1 year liver is not developed and so infants are very sensitive to drugs
Old people lose ability to metabolize and dosages need to be reduced to prevent toxicity

84
Q

Malnourishment

A

May mean lack of co factors in liver for metabolism

85
Q

Competition for metabolism

A

If two drugs are metabolized by one limited resource drugs may accumulate

86
Q

Enterohepatic reciruclation

A

Liver to duodenum (via bile duct) and back to liver (via portal blood)
Only glucorinidated drugs.
Beta-glucuronidase breaks the glucorinated acid from the drug, where it is again lipid soluble so it absorbs across intestinal wall, goes back to liver, and starts again
*Not all glucuronidated drugs do this

87
Q

Renal drug excretion

A

Most important for removing drugs, therefore with renal failure excretion is all badness
1) Glomerular filtration, 2) passive tubular reabsoprtion, 3)active tubular secretion

88
Q

Glomerular filtration

A

Only drugs small enough to enter can be excreted (not ones bound to proteins like albumin)

89
Q

Passive tubular reasoprtion

A

Fat soluble drugs re enter at distal tubule

90
Q

Active tubular secretion

A

P-glycoproteins can pump drugs from blood into urine, as can two transport systems, one for organic acids and one for organic bases

91
Q

pH dependent ionization

A

Drugs ionized at pH of tubular urine will remain in tubule and be excreted. Therefore manipulating urinary pH is a way to clear drugs out.
Giving a drug to make urine more basic is a way to clear ASA out of children (acids ionize in bases, and therefore less is reabsorbed)

92
Q

Competition for active tubular transport

A

Probenecid uses the same pumps penicillin does and can be used to prolong the time penicillin stays in the body, as it is normally rapidly excreted
Used when penicillin was very expensive

93
Q

Age and kidneys

A

Newborns underdeveloped kidneys have a hard time excreting drugs, as to old people.

94
Q

Breast milk excretion

A

Lipid soluble drugs have ready access to baby boobie juice

95
Q

Minimum Effective Concentration

A

Below which, therapeutic effects will not occur

96
Q

Therapeutic Range

A

Between MEC and toxic

97
Q

Time to plateau

A

Four half lives

98
Q

Three techniques to reduce fluctuations

A

Administer via continuous infusion
Administer a depot preparation
Reduce size and interval of each dose

99
Q

Decline from Plateau

A

94% will be eliminated in four half lives

100
Q

Pharmacodynamics

A

Study of biochemical and physiologic effects of drugs, or what drugs do to the body and how

101
Q

Dose responses are

A

Graded, as the dosage increases, the response becomes progressively larger

102
Q

Phase I II III dose response

A

I is before an effect occurs (flat line)
II Is the upward curve, increased dose = increased response
III threshold response has been hit, more drug does not illicit more response

103
Q

Potency

A

The amount of drug needed to illicit a response. It is rarely important (you can just give less in terms of units)
*has nothing to do with max efficiancy

104
Q

Receptor definition

A

Any functional macromolecule in a cell to which a drug binds to produce its effects.
Receptors are on or off.

105
Q

General equation for drug interactions with their receptors

A

D = drug
R = receptor
D+RD-R Complex –> Response

106
Q

4 primary families of receptors

A

Cell membrane-embedded
Ligand-gated ion
G protein-coupled
Transcription factors

107
Q

Cell Membrane-Embedded Enzymes

A

Span the cell membrane, ligand-binding domain is located on cell surface, enzymes catalytic side is inside.
Response occurs in seconds
E.g insulin

108
Q

Ligand-Gated Ion Channels

A

Also span cell membrane, regulated ions. When an endogenous ligand or agonist binds the channels open. Responses are extremely fast, milliseconds
E.g ACTH, GABA

109
Q

G-Protein-Couple receptors

A

Made of the receptor itself, the G-protein (its GTP) and effector (ion channel or enzyme)
Binding of endogenous ligand or agonist activates receptor, which activates G protein, which activates the effector
Responses happen rapidly
E.g NE, serotonin, histamine, many peptides.
Receptors transverse membrane 7 times

110
Q

Transcription Factors

A

Only one within the cell, delayed response compared to the rest. Must be lipid soluble to activate
E.g thyroid hormone, all steroid hormones

111
Q

Simply occupancy theory

A

The intensity of the response to a drug is proportional to the number of receptors occupied by that drug and a maximal response will occur when all available receptors have been occupied.

112
Q

Modified occupancy theory

A

Affinity refers to strength of attraction between drug and receptor
Intrinsic refers to ability of drug to activate receptor
These are independent properties and explain why drugs can have different potency and maximal effects

113
Q

Affinity

A

Strength of attraction between a drug and its receptor.

Drugs with high affinity are potent

114
Q

Intrinsic activity

A

Ability of drug to activate receptor.

Intrinsic activity is its max efficiency.

115
Q

Agonists/Antagonists

A

Agonist have affinity and high intrinsic

Antagonist have affinity and no intrinsic

116
Q

Noncompetitive antagonists

A

Bind irreversibly. Also called insurmountable.

117
Q

Receptor modulation

A

Receptors can be destroyed or modified to respond less

118
Q

Drugs without receptors

A

React through physical or chemical interactions with other small molecules
Antacids, saline laxatives, chelating agents

119
Q

ED50

A

Dose required to produce a defined therapeutic response in 50% of the population
It can be considered a standard dose

120
Q

LD50/ED50 =

A

TI. For a drug to be truly safe, the highest dose required to produce therapeutic effects must be substantially lower than the lowest dose to produce death

121
Q

First ‘merican law to regulate drugs

A

Federal Pure food and Drug Act in 1906

122
Q

Canada food and drug act

A
  1. To review safety/efficiancy before marketed and decide script or no script.
    Controls labeling
123
Q

Controlled drug act canada

A

1997

124
Q

Schedules 1 examples

A

Opiates

125
Q

Schedule 2

A

Cannabis

126
Q

Sched 3

A

Amphetamines

127
Q

Sched 4

A

Sedative-hypnotics like benzons and barbs

128
Q

Sched 5

A

Propylhexadine

129
Q

Sched 6

A

Precursors for controlled substances

130
Q

Schedule 7 and 8

A

Cannabis resin 3k then 1g for 8

Mary j 3k then 30g

131
Q

Years to create new drug

A

10-15 years, 20% ever get approval.

132
Q

Preclinical testing

A

On animals, 1-5 years

133
Q

Stages of clinical testing (takes 2-10years)

A

1 volunteers for pharmokinetics/dynamics
2 pts 500-5000 for therapuetic dose and effect
3 pts 500-5000 Safety and efficiancy, application is made at conclusion
4 post market surveliance

134
Q

Potentiative

A

One drug intensifies another

135
Q

Unique response

A

Two drugs can make a third unique response (antabuse with booze creates N/V syncope tachycardia SOB headaches circulatory collapse)

136
Q

A g coupled protein receptor is also known as a

A

Metabotropic

137
Q

Jeopardy ligand

A

Any molecule which binds to another (polar molecules, ions etc)

138
Q

3 components of a G protein coupled receptor

A

Receptor on cell surface activated by ligand
G protein, the serpentine structure
An effector, ion channel or enzyme

Pharmo for medic school (26 decks)

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