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Intro to Pathopharm > Week 1- Intro to Pharmacology + Intro to Pathophysiology + Pharm Principles > Flashcards

Week 1- Intro to Pharmacology + Intro to Pathophysiology + Pharm Principles Flashcards

1
Q

dPharmacology (Def)

A

The study of the biological effect of drugs (chemicals) that are introduced into the body to cause some sort of change

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2
Q

Pharmacokinetics (Def)

A

What happens to drugs in the body

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3
Q

Pharmacodynamics (Def)

A
  • Mechanism of action
  • Effects on the body
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4
Q

Chemical name

A

(N-acetyl-para-aminophenol)
- long and complex
- used in research
-often when it is getting created

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5
Q

Generic name

A

(acetaminophen)
- This is the name you really need
- Official name of drug
- Only 1 generic name, usually more complicated, lower case letter.

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6
Q

Trade name

A

(Tylenol)
- Brand name, given by pharmaceutical company
- Easier to remember and pronounce
-Upper case

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7
Q

Prototype

A
  • One drug, typically the first, that represents a group or class of medication.
  • New drugs in the class are compared to the prototype (effectiveness/ side effects). Other manufactures of ibuprofen get compared to the prototype
  • Ex: ibuprofen/ Advil- represents class NSAIDS
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8
Q

Therapeutic effect (Def)

A

Intended effect of the drug and what we want to happen

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9
Q

Side effect (Def)

A

Unintended effect, often unaviodable

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10
Q

Adverse effects (Def)

A

Unexpected reaction, dangerous reaction

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11
Q

Toxicities (Def)

A

Harmful effects

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12
Q

Allergic reaction

A

Unexpected, may be dangerous, involves an immune response to the drug

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13
Q

What do you need to know about each drug?

A

1) Name: trade and generic –> only generic on test
2) Classification (drug class): given to describe a group of medications that usually work similarly
3) Mechanism of action: how the drug works in the body
4) Indications: Why are we giving the med? What is it used to treat?
5) Common/Serious Adverse Effects: most common ones
6) Contraindications
7) Nursing indications: what to worry about when giving the med? Prior assessments? CYP?

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14
Q

New drugs are approved though:

A

FDA- chemical identified, strict testing (5 in 100,000 will be marketed)

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15
Q

Preclinical Trials

A

Tested on animals for therapeutic adverse effects

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16
Q

Phase I studies

A

Human volunteers are used to test

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17
Q

Phase II studies

A

Drug is tested on patients who have the disease that drug is designed to treat

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18
Q

Phase III studies

A

Vast clinical market. Prescribers informed of adverse effects and monitor patients closely. Can still be withdrawn from market

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19
Q

Phase IV studies

A

Continued evaluation by FDA

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20
Q

Schedule 1 drugs

A

Not approved for medical use, no reason to prescribe (Heroin, LSD)

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21
Q

Schedule 2 drugs

A

Used medically, but HIGH potential for abuse. NO refills allowed. Narcotics. (Hydromorphine, oxycodone)

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22
Q

Schedule 3 drugs

A

Less potential for abuse but still some (Non barbiturate sedatives, non-amphetamines, stimulants (Lortab, Vicodin)

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23
Q

Schedule 4 drugs

A

Some potential for abuse. Primarily sedatives, anti-anxiety (Xanax, valium)

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24
Q

Schedule 5 drugs

A

Low potential for abuse. Medications containing small amounts of certain narcotics or stimulants usually antitussives (cough suppressants with codeine, ephedrine containing meds)

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25
Q

Over the Counter Meds

A

Criteria: consumers must be able to dx. own condition and monitor effectiveness EASILY
- Over 80 classes of OTC
-Prescription strength OTC- same drug available OTC but with higher dose. Abuse potential available behind the pharmacy counter

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26
Q

Dietary and Herbal Supp.

A
  • Can only claim effect on body STRUCTURE or FUNCTION (no medical conditions). Can’t say the treat anything, no MOA, or how it works.
  • Not FDA approved
  • Ex: St. John’s Wort - affects emotional balance (not treat depression)
  • !! Some herbals can increase the toxicity of rx. meds and cause decreased therapeutic effects !!
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27
Q

Example of adverse interaction b/w drugs and herbals

A

Ginko biloba suppresses platelet aggregation (therefore can increase risk of bleeding)

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28
Q

Teratogens

A

Can cause congenital malformations in developing fetus (alcohol, marijuana, nicotine)

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29
Q

Teratogens: Category A

A

Safe for fetus

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30
Q

Teratogens: Category B

A

Lack of studies to show benefit v. risk

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31
Q

Teratogens: Category C

A

No studies, animals studies possible risk, talk to OB

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32
Q

Teratogens: Category D

A

Drugs that have possible risk to the fetus. Discussion with OB about risk to fetus

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33
Q

Teratogen: Category X

A

Drugs that have KNOWN RISK that CAN’T be outweighed by possible benefit (Thalidomide, chemo agents, isotretinoin/ retin A)

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34
Q

Pharmacogenomics

A

Study how genes affect a person’s response to the drug. Combines pharmacology and genomics to develop effective, safe meds and doses that will be tailored to person’s genetic makeup

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35
Q

Three disruptions of homeostasis

A
  • physical, mental, and social
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36
Q

Cause of disease

A
  • Intrinsic: autoiminne disorder
  • Extrinsic: bacteria/ virus
  • For disease to occur: pathogen, conducive environment, susceptible host
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37
Q

Intrinsic factors

A

Genes, immunity, age (very old/ very young), gender

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38
Q

Extrinsic factors

A

Bacteria, viruses, injury, behaviors, stressors, fungi

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39
Q

Process of Disease

A
  • Identification - signs/symptoms
  • Occurrence - how often/ when
  • Diagnosis - identify
  • Etiology - cause
  • Prognosis - likelihood of recovery
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40
Q

Stages of disease

A
  • Exposure
  • Onset
  • Remission
  • Covalescence
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41
Q

Types of Onset

A
  • Sudden
  • Insidious- slow and gradual, chronic disease process (GI bleed)
  • Latent- not active but can be (Chickenpox)
  • Prodromal- pre sickness
  • Manifestations- true signs/ symptoms
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42
Q

Types of disease: Idiopathic

A

We don’t know what cause it. Unknown, we might have ideas or theories

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43
Q

Types of disease: Iatrogenic

A

Caused by some treatment. A ‘medical’ cause. Ex: getting a colonoscopy and intestinal lining cut

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44
Q

Types of disease: exacerbation

A

Worsening of a disease, acute decline in a person’s chronic disease

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45
Q

Hypo___

A

under

46
Q

Hyper___

A

above, over

47
Q

____penia

A

lack of, deficiency

48
Q

____cytosis

A

refers to cells, increase

49
Q

____osis

A

process or condition, production or increase, invasion or infection

50
Q

____itis

A

inflammation

51
Q

____pathy

A

disease or suffering

52
Q

Three phases of drug action

A

1) Pharmaceutic
2) Pharmacokinetic
3) Pharmacodynamic

53
Q

Pharmaceutic Phase

A

The dissolution phase occurs

54
Q

In the pharmaceutical phase all oral drugs must go through ____ in order to be absorbed.

A

dissolution

Tablet –> granules –> smaller particles –> solution in GI tract –> drug absorbed

55
Q

Four processes of pharmacokinetic phase

A

1) Absorption (small intestines)
2) Distribution (in blood)
3) Metabolism/ Biotransformation (think about liver)
4) Excretion (kidneys, a little excreted in liver)

56
Q

What phase of the pharmacokinetic phase do IV medications start at?

A

Distribution

57
Q

What do meds go through between distribution and absorption

A

Phospholipid layer

58
Q

What types of medications go through the first Pass Effect

A

Anything orally/ PO

59
Q

First Pass Effect

A

Alters the amount of drug that becomes absorbed. This is occurring in the absorption phase in the liver during the pharmacokinetic process.

60
Q

_______is the amount of drug left after the first pass

A

bioavailability

61
Q

How much of a drug is bioavailable after going in an IV

A

100- does not go through liver

62
Q

Three Routes of absorption

A

1) Enteral
2) Parenteral - cath
3) Topical

63
Q

Enteral absorption

A

By way of GI tract (oral/gastric mucosa, small intestine, rectum)
- EC (enteric coated) intended to break down in small intestine NOT stomach. Still goes through first pass effect

-PO break down starts in stomach, absorbed in small intestine, first pass effect

  • SL, buccal, rectal all highly vascularized tissue. NO first pass effect, by-pass liver
64
Q

Parenteral absorption

A
  • SQ, IM, IV, intrathecal (into spinal canal), epidural. IV is the fastest, no barriers to absorption. No first pass effect
65
Q

Topical (transdermal)

A

Application of meds to body surface. Eyes, skin, ears, nose, lungs

66
Q

What effects distribution?

A

Blood flow
Blood brain barrier
Protein- Binding effect

67
Q

Pharmacokinetic: distribution

A

Process by which the drug molecules leave the blood stream and arrive at site of action.

Depends a lot of adequacy of blood circulation.

Decreased blood flow, decreased distribution

68
Q

Blood brain barrier

A

Cells in the capillary wall in the brain with very tight junctions that prevent drug passage

Only drugs that have a transport system or aare

69
Q

What drugs can cross the BBB? & what two substances

A

Alcohol + Glucose

  • Have the specific transport system OR are lipid-soluble that can cross BBB

It is a protective mechanism

70
Q

Protein-Binding Effect

A

Temporary storage of drug molecule that allows drug to be available for a longer period of time

-Drug ratio of bound to unbound molecules varies
- Binding is reversible (a rapid process)

71
Q

Goal of protein-binding effect

A

Maintain a steady free drug concentration (Steady State)

72
Q

What do protein-binding drugs bind to in our blood?

A

Albumin

73
Q

Pharmacokinetic phase: Metabolism

A

When the drug is no longer in action and becomes broken down (inactivated). New structure is called a metabolite

Also called biotransformation

74
Q

Where is the major place that metabolism takes places

A

Liver. Converts lipid-soluble drugs into water soluble metabolites. Uses Cytochrome P-450 enzymes

75
Q

What is Cytochrome P450?

A

A group of isoenzymes that metabolize drugs .

About 1/2 drugs are metabolized by this.

Be aware of drug-drug interactions

76
Q

Three ways drugs work through CYP450

A

1) Substrate
2) Inducer
3) Inhibitor

77
Q

Substrate CYP450

A

If a drug uses the CYP450 system for metabolism. Pro-drug is a substrate that uses the CYP450 system to convert to an active form.

78
Q

Inducer CYP450

A

Speeds up metabolism of the CYP450 system. Reduces the amount in the body, reduces therapeutic effect

79
Q

Inhibitor CYP450

A

Slows down metabolism of CYP450. Increases the amount of drug in body, increases toxicity

80
Q

Pharmacokinetic: excretion

A

Elimination of drug from the body, generally only hydrophilic drugs can be excreted effectively

81
Q

Three ways the kidney excretes

A

1) Glomerular filtration
2) Tubular secretion
3) Tubular reabsorption

81
Q

What to assess regarding kidney function and excretion

A

Renal labs (blood urea nitrogen (BUN), creatinine

GFR (glomerular filtration rate). Best measure of kidney function, calculated from the creatinine level, age, body size and gender.

GFR is related to free drug concentration in plasma

82
Q

Elimination: Half life

A

Serum half life is time required for the serum concentration of a drug to decrease by 50%

83
Q

Takes ____half-lives for ____% of the drug to be eliminated

A

5 half-lives for 97%

84
Q

Elimination goal

A

Get to steady state. Takes about 4-5 half lives.

Steady state occurs when intake of drug equals amount metabolized/ excreted

85
Q

Around the Clock Dosing

A

Goal to maintain 50% concentration in body. Used to treat chronic pain

86
Q

Onset of drug

A

time it takes for drug to elicit therapeutic response (latent period)

87
Q

Peak of drug

A

Time it takes to reach its maximum therapeutic effect

88
Q

Duration of drug

A

Drug concentration is sufficient to elicit a therapeutic response

89
Q

What is phase 3 of drug action and what does it do?

A

Pharmacodynamic phase- it is what the drug does to the body

90
Q

Pharmacodynamic Phase

A

-Drugs may increase/decrease/replace/inhibit/destroy/protect or irritate to create a response

-Drugs exert multiple rather than single effects on the body (desired or not)

91
Q

Pharmacodynamics: receptors

A
  • receptors are protein located on cell surfaces
    -chemicals in the body interact with drugs to produce effects (Hormones and neurotransmitters)
    -these chemicals bind with the drug = drug receptor complex
92
Q

Receptor Theory of Drug action: Agonist

A

Drug that has the ability to INITIATE a desired therapeutic effect by BINDING to a receptor. Typically what we want

93
Q

Receptor Theory of Drug action: Antagonist

A

A drug that produces its action NOT by stimulating receptors but PREVENTING or BLOCKING or INHIBITING other natural substances from binding and causing a response

94
Q

What is it called when drugs act through simple physical or chemical interactions with small molecules

A

Receptor-less activation

95
Q

Narrow therapeutic Index (NTI)

A

-The measure of relative safety of drug
-NTI have a ratio of lowest concentration at which clinical toxicity commonly occurs

96
Q

Black Box Warning

A

Required by the FDA for drugs that are especially dangerous. Strongest safety warning a drug can carry and still be on market

97
Q

Where does the black box warning need to be?

A
  • package insert
    -product label
    -magazine or advertising
98
Q

Who created high alert medication standards and when?

A

1995 Institue for Safe Medication Practices (ISMP)

99
Q

High alert drugs

A
  • insulin
    -heparin
    -opioids
    -injectable potassium chloride
    -neuromuscular blocking agents
    -chemotherapy drugs
100
Q

Drug-drug interactions

A
  • may be intended/unintended
    -increased risk with polypharmacy
  • narrow therapeutic index drugs
    -drug-food
    -drug-herb
    -drug-disease
101
Q

What are the four drug interactions that INCREASE therapeutic effects

A

1) additive
2) synergism/potentiation
3) activation
4) displacement

102
Q

Additive effect

A

2 drugs taken with similar MOA

103
Q

Synergism/potentiation

A

2 drugs with DIFFERENT MOA but result in a combined drug effect greater than that of either drug alone

104
Q

Activation

A

of drug- metabolizing enzymes in the liver –> decreases metabolism rate of the drug (CYP450)

105
Q

Displacement

A

Displacement of one drug from plasma protein- binding sites by a second drug –> increases effect of displaced drug

106
Q

Three drug interactions that DECREASE therapeutic effect

A

1) Antidote
2) Decreased intestinal absorption
3) Activation

107
Q

Antidote

A

Drug given to ANTAGONIZE the toxic effects of another drug

108
Q

Decreased intestinal absoption

A

Applied to PO meds

109
Q

Activation

A

of drug-metabolizing enzymes in the liver –> enzyme inducers
— increase metabolism rate of the drug (quicker out of the system)
— CYP450 system

110
Q

Older adults and pharmacokinetic consequnces

A

1) Hepatic changes
2) Cardiac and circulatory changes
3) GI changes
4) Renal changes

Intro to Pathopharm (4 decks)

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