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Pharmacology Exam 1 > Exam 1 Topics > Flashcards

Exam 1 Topics Flashcards

1
Q

Define Pharmacotherapeutics

A

the use of drugs to treat, cure, prevent disease

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2
Q

define pharmacokinetics

A

the journey of the drug through the body / what the body does to the drug

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3
Q

define pharmacodynamics

A

what the drug does to the body

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4
Q

what is the absorption of a drug?

A

absorption is the movement of drug from site of administration to systemic circulation (blood flow)

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5
Q

what is the bioavailability of a drug (definition)

A

bioavailability (F) is the proportion of a drug dose that you administer that reaches systemic circulation

how much of it actually gets into the blood stream

example: if you swallow a 100mg pill and 70mg is eliminated from the body, only 30mg reaches systemic circulation meaning that F = 30%

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6
Q

what type of drug administration are always 100% bioavailable?

A

intravenous drugs

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7
Q

what factors can influence bioavailability from peripheral tissues?

A
  • regional blood flow
  • type of tissue (fat, muscle, bone, etc.)
  • drug’s chemical properties
  • limitation of physiologic transport processes
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8
Q

what is lipophilic?

A

a fat soluble drug

crosses cell membranes easily
* same for molecules w/ neutral electric charge (nonpolar / non-ionized)

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9
Q

what is hydrophilic?

A

water soluble drug

does not cross cell membranes easily
* same for molecules w/ pos or neg charge (polar, ionized)

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10
Q

what is the first pass effect?

A

when the drug is absorbed in the stomach and enters the blood stream via the portal vein but goes straight to the liver to get metabolized. whatever the liver lets through is what gets into our systemic circulation and starts helping us.

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11
Q

how does acidity (pH) affect drug absorption

A

drugs are either weak acids or weak bases

best absorbed in their non-ionized state

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12
Q

what is the definition of distribution

A

movement of drug from systemic circulation to peripheral tissues

the drug is in the blood stream now!

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13
Q

what is volume distribution (Vd) of a drug

A

the relative extent to which a drug moves to other body compartments

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14
Q

what is a small Vd

A

≤ 0.25L/kg

drug remains mostly in blood stream

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15
Q

what is a mid-range Vd

A

0.25 - 0.7 L/kg

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16
Q

what is a large Vd

A

> 0.7 L/kg

drug distributes extensively to cells/tissues (peripheral compartment)

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17
Q

what type of Vd do fat and water soluble drugs have

A

water soluble drugs have a small Vd

fat soluble drugs have a large Vd

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18
Q

what type of drugs cross the BBB easier?

A

Fat-soluble drugs cross the BBB more easily because the barrier’s tightly packed cells are more permeable to lipids, allowing easier diffusion. Water-soluble drugs require specific transport, making entry harder

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19
Q

Factors that increase Volume of Distribution (Vd)

A
  • Higher Lipid Solubility: Fat-soluble drugs easily cross cell membranes.
  • Lower Plasma Protein Binding: Less binding allows more drug to enter tissues.
  • Greater Peripheral Tissue Binding: Strong affinity for tissues increases distribution.
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20
Q

define metabolism in pharmacology

A

biochemical transformation of a drug to form a metabolite that is usually less active and/or more water soluble than the parent drug

(easier for body to eliminate)

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21
Q

What occurs in Phase I of drug metabolism?

A

Types: Oxidation, reduction, hydrolysis

Function: Adds functional groups (-OH, -COOH, -SH, -O, -NH2) to drugs

Outcome: Prepares drugs for Phase II, often decreasing potency or inactivating the drug.

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22
Q

What occurs in Phase II of drug metabolism?

A

Types: Conjugation reactions

Function: Attaches large polar molecules (e.g., glucuronic acid, sulfate)

Outcome: Increases water solubility for easier excretion; less susceptible to liver dysfunction.

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23
Q

what enzyme is phase 1 metabolism mediated by?

A

Cytochrome-P (CYP)-450

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24
Q

What are the effects of substrates, inducers, and inhibitors on CYP450 enzyme activity?

A

Substrates: Molecules metabolized by CYP450 enzymes.

Inducers: Increase CYP450 activity, enhancing metabolism and clearance of substrates, potentially reducing drug effectiveness.

Inhibitors: Decrease CYP450 activity, slowing metabolism of substrates, leading to greater drug exposure and increased risk of side effects or toxicity.

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25
Q

define elimination in pharmacology

A

removal of drug or metabolite from body without further chemical change

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26
Q

how are most drugs eliminated

A

through the kidney and urine

other ways include: bile, sweat, spit, breast milk, exhalation

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27
Q

what is clearance (CI) in pharmacology

A

volume of blood that is cleared of a drug per unit time

it is a rate

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28
Q

how many half-lives for a drug to be removed from the body

A

4-5 half-lives

1 half life - 50%
2 - 75%
3 - 87.5%
4 - 93.75%
5 - 96.86%

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29
Q

how do agonist vs. antagonist drugs interact with receptors in order to work?

A

agonist drugs = activate receptors and enhance it’s effects
antagonist drugs = block receptors and inhibiting their effects

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30
Q

what do B1 receptors control?

A

heart rate

norepinephrine (NE) is an endogenous B1 agonist (binds to/activates receptor and increases HR)

metoprolol is a B1 antagonist (binds to receptor but doesn’t activate and prevents NE from binding = decreases HR)

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31
Q

B1 and B2 receptors connect where?

A

B1 = heart
B2 = lungs

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32
Q

What are the differences between threshold dose and ceiling effect?

A

Threshold Dose: Minimum dose required to produce a measurable effect; below this dose, the drug has no significant effect.

Ceiling Effect: Maximum effect a drug can produce; after this point, increasing the dose does not enhance the therapeutic effect and may increase side effects.

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33
Q

Explain down-regulation and up-regulation

A

down-regulation: constantly exposed to a drug so the body stops sending receptors to not have as much of a reaction
up-regulation: not exposed as often to the drug so the body sends more receptors in order to have a reaction

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34
Q

Therapeutic Index

A

measure of drug’s safety - ratio between toxic dose and effective dose. **BELOW <0.25 IS TOXIC STOP THE DRUG

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35
Q

Characteristics of a High TI?

A

safer bc larger gap between effective and toxic dose, no high risk of toxicity

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36
Q

Characteristics of a Low TI?

A

requires careful monitoring as the therapeutic dose is close to the toxic dose.

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37
Q

ADRs vs. ADEs vs. Side Effects?

A

ADRs: unintended, undesirable response to a drug that doesn’t include human error or non-adherence
ADEs: ADRs + errors (prescribing, dosing, administration)
Side Effects: minor well-known ADR of a drug, doesn’t change management

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38
Q

Drug Toxicity

A

medical emergency - go to hospital to treat and reduce toxicity

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39
Q

Drug Tolerance

A

how well someone tolerates the drug/if it works the way it should
slowly increasing the dose based on how the person responds and if they were on like 5mg then doesn’t work so they go up to 10mg

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40
Q

Risk Factors for / What Leads to ADEs

A

Drug itself, poly-pharmacy, genetic polymorphisms, drug-disease, age, prescriber factors, non-adherence, medication errors, drug-drug interactions, drug allergies

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41
Q

Type I Drug Allergy Reaction Symptoms

A

Anaphylaxis - IgE mediated - Immediate
Pulmonary: dyspnea, cyanosis, bronchospasm, edema, cough, respiratory arrest
Cardiac: tachycardia, hypotension, arrythmia
Skin: erythema, puritis, urticarial
GI: N/V/D
can be life threatening
discontinue immediately and seek emergency services - epi-pen

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42
Q

Type II Drug Allergy Reaction Symptoms

A

IgG/IgM Cytotoxic - delayed by several days/weeks
hemolytic anemia, thrombocytopenia, leukopenia
Life threatening
discontinue drug - self resolves

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43
Q

Type III Drug Allergy Reaction Symptoms

A

autoimmune - inflammatory cascade - 1-3 weeks

serum sickness, drug induced systemic lupus erythematosus
arthritis/arthalgia
fever/malar rash

discontinue drug: prognosis is excellent and self-resolves

44
Q

Type IV Drug Allergy Reaction Symptoms

A

cell mediated hypersensitivity
symptoms: contact dermatitis - rash
discontinue offending agent and can use steroids

45
Q

Urticarial rashes occurs with what Types?

A

Types I and III

46
Q

Non-urticarial rashes occurs with what Types?

A

Types I, II, IV

47
Q

What drug allergy types are possibly life threatening?

A

Types I and II

48
Q

Polypharmacy

A

use of multiple medications in someone with comorbidities.

49
Q

Polymorphisms

A

genetic variations in the DNA sequence - variations that affect how individuals metabolize and respond to drugs.
often influences drug efficacy, safety, and likelihood of ADRs.

50
Q

Nonadherence

A

pt who failed to meet treatment targets described being prescribed appropriate therapy bc they dont take their meds

51
Q

Changes with age and drugs?

A

balance/gait - ability to compensate for ADE
changes in body comp - fat soluble drugs
CNS - ADE vs. age?
GI - decreased motility / absorption/sensitivity
***Hepatic/Renal Function - decreased clearance of meds
skin - thinning / absorption changes of topical meds

52
Q

Drug-Drug interactions

A

Combination of 2 drugs causing synergistic or diminished effects

53
Q

Food-Drug interactions

A

Combination of drug and food leads to synergistic or diminished effect of drug

54
Q

What is the classification of ADRs?

A

ABCDEF
Augumented Pharmacologic Effects
Bizarre Effects
Chronic Effect
Delayed effects
End of treatment effects
Failure of Therapy

55
Q

Augumented Pharmacologic Effects

A

overreactive response to what the drug does - reduce the dose if this happens.

Type of reaction: dose-related response
features: related to pharnacologic action, predictable, common, low mortality
Management: reduce to lowest tolerated dose

56
Q

Bizarre Effects

A

type of reaction: non-dose related
features: occurs unpredictably, serious, high mortality, uncommon
management: Discontinue immediately and avoid drug class.

57
Q

Chronic Effects

A

type of reaction: dose/time related
features: only occurs with chronic use, not after 1 dose.
management: limit length of treatment - discontinue and may need to taper down dose

58
Q

Delayed Effects

A

time related reaction
uncommon, usually dose related, effects occur AFTER treatment ended
often intractable - treat symptomatically – avoid known teratogens in pregnant women

59
Q

End-of-Treatment Effects

A

type of reaction: withdrawal
features: uncommon, effects occur immediately after discontinuation, effects may be what drug was treating
management: stress important of adherence to pts and taper drug when discontinuation is desired

60
Q

Failure of Therapy

A

Type of reaction: dose-related
Features: common, no response despite appropriate dose, may be caused by drug interactions or genetic difference
Management: increase dosage, switch to different drug

61
Q

What are Pharmacy Databases?

A

Clinical Pharmacology, Micromedex, LexiDrug/Comp

62
Q

What are Dietary/Herbal Databases?

A

Natural Medicine / Nat Med Pro

63
Q

What are Open Access Resources?

A

Physician’s Desk Reference

64
Q

What is the database for Medical AI?

A

Open Evidence

65
Q

What Databases are not Recommended?

A

Epocrates, Google, ChatGPT, etc.

66
Q

key characteristics of sympathetic nervous system?

A
  • increases function of organs
  • once on, usually results in more massive/diffuse response thru multi-organ systems

-ganglia usually found near spinal cord or target area
-1:15 preganglionic:postganglionic
-**NE + EPI

67
Q

key characteristics of parasympathetic nervous system?

A
  • slows down function of organs
  • once on, usually specific organ system

-ganglia usually found in organ/tissue
-1:1 preganglionic:postganglionic
-**ACh

68
Q

Parasympathetic Ganglion

A

Pre/Post-Ganglionic Neurotransmitter: ACh
Ganglionic Receptor: Nicotinic
Effector Cell Receptor: Muscarinic
Functions: slows HR, bronchocontrict, increases digestion, stimulates urination, constricts pupils, increases salivation+tears

69
Q

Sympathetic Ganglion

A

Pre/Post-Ganglionic Neurotransmitter: NE + EPI
Ganglionic Receptor: Nicotinic
Effector Cell Receptor: Alphas, Betas adrenergic receptors
Functions: incr. HR, bronchodilate, decreases digestion, inhibits urination, dilates pupils, incr. glucose release

70
Q

Define Direct Agonist

A

the drug does something that you want it to do - binds directly with the receptor

71
Q

define indirect agonist

A

does what you want it to but doesn’t bind directly with that receptor

72
Q

define antagonists

A

whatever you want the drug to do, it does the opposite

e.g. you have bad stomachache so you take prilosec – body stops producing acid

73
Q

what do direct cholinergic agonists do

A

mimics acetylcholine and binds directly to muscarinic receptor

74
Q

what do indirect cholinergic agonists do

A

meds that stop/inhibit cholinesterase enzyme that increases Ach at post-synaptic cholinergic receptor

goes thru enzyme first

75
Q

what are common cholinergic stimulant side effects (ADRs)?

A

as dose increases, # and intensity of ADRs can increase

  • increase in SLUD (saliva, lacrimation (tears), urination, defecation)
  • decreased HR
  • increased sweating (sweating because you’re not in the AC!)
76
Q

what are common anti-cholinergic stimulant ADRs

A
  • decreased SLUD (saliva, lacrimation(tears), urination, defecation)
  • increased HR
  • decreased sweating (not sweating bc you’re in AC!)
  • risk of falls in elderly (orthostasis)
77
Q

how do anticholinergics work?

A

blocks acetylcholine from stimulating / going to the muscarinic receptor

78
Q

in what cases/diagnoses would an anticholinergic be prescribed?

A
  • IBD
  • cardiology: bradycardia
  • motion sickness
  • overactive bladder
  • asthma/COPD
79
Q

most common anticholinergic for motion sickness?

A

scopolamine (skin patch)

80
Q

most common anticholinergic for overactive bladder?

A

oxybutynin

81
Q

what do a1 agonists usually work on and how?

A

arteries, BP most likely

causes vasoconstriction which can increase BP (dangerous!)

82
Q

when are a1 agonists used?

A
  • primarily used in shock states as a last resort
    **phenylephrine
83
Q

what are adverse drug reactions for a1 agonists?

A
  • oral agents (sudafed) should not be used in CVD
  • raises BP
  • nasal spray - do not use for more than 3 days due to rebound congestions
84
Q

what do a2 agonists usually work on and how?

A

works on muscle spasticity

complete opposite of a1 agonist – it is a vasodilator and lowers BP

85
Q

when are a2 agonists used?

A

primarily used to treat HTN or muscle spasticity

86
Q

what specific a2 agonist agents used for HTN and ADHD?

A

HTN and ADHD
- Clonidine

87
Q

when are a1 antagonists used and how do they work?

A

they work on the arteries and blocks the receptors

used as a last line of treatment for HTN and first line of treatment for BPH. also migraines.

88
Q

when are B1 agonists used?

A

shock states and acute heart failure (dobutamine - increases CO)

89
Q

where do B2 agonists work on?

A

in the lungs, bronchioles to dilate

90
Q

what do mixed a1/b1 agonists work on and what do they do?

A

arteries (a1) and heart (b1) and increases HR and BP. Increases norepinephrine + epinephrine.

Also helps ADHD

91
Q

when are B antagonists used?

A

most common autonomic nervous system medication

used in:
- CVD/post-MI
- tachy-arrythmias
- HTN
- HF

92
Q

what is selective vs non-selective?

A

selective - primarily B1 selectivity

non-selective - effects mostly B1 but some B2. could cause bronchoconstriction

93
Q

what changes affect PK and PD

A
  • age
  • renal function
  • liver dysfunction
  • overweight
  • low weight/malnourished
94
Q

Diuretic PT Considerations

A

muscle weakness/cramping (hypokal/mag), hyperreflexia/numbess (hyperkal), orthostatic hypotension, dehydration

95
Q

Beta-Blocker PT Considerations

A

During exercise HR and CO may be depressed enough to reduce exercise capacity
Masks symptoms of hypoglycemia

96
Q

Direct Vasodilator PT Considerations

A

vasodilation/edema
may antagonize cryotherapy
effects increased by thermotherapy

97
Q

ACE Inhibitor/ARB PT Considerations

A

hypotension
hyperkalemia

98
Q

CCB Dihydropyridine PT Considerations

A

hypotension, dizziness, headache, peripheral edema

99
Q

CCB Non-Dihydropyridine PT Considerations

A

hypotension, bradycardia, headache, fatigue, dizziness

100
Q

Nitrates PT Considerations

A

sublingual 5-10min before activity
thermotherapy can cause vasodilation may lead to syncope
orthostatic hypotension
dizziness

101
Q

Antiarrhythmic Agent PT Considerations

A

may reduce exercise tolerance
may precipitate arrhythmias in some patients
faintness/dizziness

102
Q

Thiazide Diuretics job

A

primary BP lowering

103
Q

Loop Diuretics

A

very potent, may lower BP but not used to manage. seen in getting peripheral edema out in HF.

104
Q

Potassium Sparing Diuretic

A

very gentle diuretic and sometimes used to raise someone’s potassium and can use in HF

105
Q

What PT interventions are contraindicated for patients on anti-coagulants

A

debridement, deep tissue massage, upper cervical manipulation

106
Q

Statin PT considerations

A

myopathy and muscle aches - be concerned
pts w liver disease may not be able to take statins

Pharmacology Exam 1 (5 decks)

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