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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
define elimination in pharmacology
removal of drug or metabolite from body without further chemical change
26
how are most drugs eliminated
through the kidney and urine other ways include: bile, sweat, spit, breast milk, exhalation
27
what is clearance (CI) in pharmacology
volume of blood that is cleared of a drug per unit time it is a rate
28
how many half-lives for a drug to be removed from the body
4-5 half-lives 1 half life - 50% 2 - 75% 3 - 87.5% 4 - 93.75% 5 - 96.86%
29
how do agonist vs. antagonist drugs interact with receptors in order to work?
agonist drugs = activate receptors and enhance it's effects antagonist drugs = block receptors and inhibiting their effects
30
what do B1 receptors control?
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)
31
B1 and B2 receptors connect where?
B1 = heart B2 = lungs
32
What are the differences between threshold dose and ceiling effect?
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.
33
Explain down-regulation and up-regulation
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
34
Therapeutic Index
measure of drug's safety - ratio between toxic dose and effective dose. **BELOW <0.25 IS TOXIC STOP THE DRUG
35
Characteristics of a High TI?
safer bc larger gap between effective and toxic dose, no high risk of toxicity
36
Characteristics of a Low TI?
requires careful monitoring as the therapeutic dose is close to the toxic dose.
37
ADRs vs. ADEs vs. Side Effects?
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
38
Drug Toxicity
medical emergency - go to hospital to treat and reduce toxicity
39
Drug Tolerance
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
40
Risk Factors for / What Leads to ADEs
Drug itself, poly-pharmacy, genetic polymorphisms, drug-disease, age, prescriber factors, non-adherence, medication errors, drug-drug interactions, drug allergies
41
Type I Drug Allergy Reaction Symptoms
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
42
Type II Drug Allergy Reaction Symptoms
IgG/IgM Cytotoxic - delayed by several days/weeks hemolytic anemia, thrombocytopenia, leukopenia Life threatening discontinue drug - self resolves
43
Type III Drug Allergy Reaction Symptoms
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
Type IV Drug Allergy Reaction Symptoms
cell mediated hypersensitivity symptoms: contact dermatitis - rash discontinue offending agent and can use steroids
45
Urticarial rashes occurs with what Types?
Types I and III
46
Non-urticarial rashes occurs with what Types?
Types I, II, IV
47
What drug allergy types are possibly life threatening?
Types I and II
48
Polypharmacy
use of multiple medications in someone with comorbidities.
49
Polymorphisms
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
Nonadherence
pt who failed to meet treatment targets described being prescribed appropriate therapy bc they dont take their meds
51
Changes with age and drugs?
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
Drug-Drug interactions
Combination of 2 drugs causing synergistic or diminished effects
53
Food-Drug interactions
Combination of drug and food leads to synergistic or diminished effect of drug
54
What is the classification of ADRs?
ABCDEF Augumented Pharmacologic Effects Bizarre Effects Chronic Effect Delayed effects End of treatment effects Failure of Therapy
55
Augumented Pharmacologic Effects
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
Bizarre Effects
type of reaction: non-dose related features: occurs unpredictably, serious, high mortality, uncommon management: Discontinue immediately and avoid drug class.
57
Chronic Effects
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
Delayed Effects
time related reaction uncommon, usually dose related, effects occur AFTER treatment ended often intractable - treat symptomatically -- avoid known teratogens in pregnant women
59
End-of-Treatment Effects
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
Failure of Therapy
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
What are Pharmacy Databases?
Clinical Pharmacology, Micromedex, LexiDrug/Comp
62
What are Dietary/Herbal Databases?
Natural Medicine / Nat Med Pro
63
What are Open Access Resources?
Physician's Desk Reference
64
What is the database for Medical AI?
Open Evidence
65
What Databases are not Recommended?
Epocrates, Google, ChatGPT, etc.
66
key characteristics of sympathetic nervous system?
- 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
key characteristics of parasympathetic nervous system?
- slows down function of organs - once on, usually specific organ system -**ganglia usually found in organ/tissue -**1:1 preganglionic:postganglionic -**ACh
68
Parasympathetic Ganglion
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
Sympathetic Ganglion
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
Define Direct Agonist
the drug does something that you want it to do - binds directly with the receptor
71
define indirect agonist
does what you want it to but doesn't bind directly with that receptor
72
define antagonists
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
what do direct cholinergic agonists do
mimics acetylcholine and binds directly to muscarinic receptor
74
what do indirect cholinergic agonists do
meds that stop/inhibit cholinesterase enzyme that increases Ach at post-synaptic cholinergic receptor goes thru enzyme first
75
what are common cholinergic stimulant side effects (ADRs)?
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
what are common anti-cholinergic stimulant ADRs
- 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
how do anticholinergics work?
blocks acetylcholine from stimulating / going to the muscarinic receptor
78
in what cases/diagnoses would an anticholinergic be prescribed?
- IBD - cardiology: bradycardia - motion sickness - overactive bladder - asthma/COPD
79
most common anticholinergic for motion sickness?
scopolamine (skin patch)
80
most common anticholinergic for overactive bladder?
oxybutynin
81
what do a1 agonists usually work on and how?
arteries, BP most likely causes vasoconstriction which can increase BP (dangerous!)
82
when are a1 agonists used?
- primarily used in shock states as a last resort **phenylephrine
83
what are adverse drug reactions for a1 agonists?
- 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
what do a2 agonists usually work on and how?
works on muscle spasticity complete opposite of a1 agonist -- it is a vasodilator and lowers BP
85
when are a2 agonists used?
primarily used to treat HTN or muscle spasticity
86
what specific a2 agonist agents used for HTN and ADHD?
HTN and ADHD - Clonidine
87
when are a1 antagonists used and how do they work?
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
when are B1 agonists used?
shock states and acute heart failure (dobutamine - increases CO)
89
where do B2 agonists work on?
in the lungs, bronchioles to dilate
90
what do mixed a1/b1 agonists work on and what do they do?
arteries (a1) and heart (b1) and increases HR and BP. Increases norepinephrine + epinephrine. Also helps ADHD
91
when are B antagonists used?
most common autonomic nervous system medication used in: - CVD/post-MI - tachy-arrythmias - HTN - HF
92
what is selective vs non-selective?
selective - primarily B1 selectivity non-selective - effects mostly B1 but some B2. could cause bronchoconstriction
93
what changes affect PK and PD
- age - renal function - liver dysfunction - overweight - low weight/malnourished
94
Diuretic PT Considerations
muscle weakness/cramping (hypokal/mag), hyperreflexia/numbess (hyperkal), orthostatic hypotension, dehydration
95
Beta-Blocker PT Considerations
During exercise HR and CO may be depressed enough to reduce exercise capacity Masks symptoms of hypoglycemia
96
Direct Vasodilator PT Considerations
vasodilation/edema may antagonize cryotherapy effects increased by thermotherapy
97
ACE Inhibitor/ARB PT Considerations
hypotension hyperkalemia
98
CCB Dihydropyridine PT Considerations
hypotension, dizziness, headache, peripheral edema
99
CCB Non-Dihydropyridine PT Considerations
hypotension, bradycardia, headache, fatigue, dizziness
100
Nitrates PT Considerations
sublingual 5-10min before activity thermotherapy can cause vasodilation may lead to syncope orthostatic hypotension dizziness
101
Antiarrhythmic Agent PT Considerations
may reduce exercise tolerance may precipitate arrhythmias in some patients faintness/dizziness
102
Thiazide Diuretics job
primary BP lowering
103
Loop Diuretics
very potent, may lower BP but not used to manage. seen in getting peripheral edema out in HF.
104
Potassium Sparing Diuretic
very gentle diuretic and sometimes used to raise someone's potassium and can use in HF
105
What PT interventions are contraindicated for patients on anti-coagulants
debridement, deep tissue massage, upper cervical manipulation
106
Statin PT considerations
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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