Phar 100 Flashcards

(168 cards)

1
Q

What are the three major historical influences on modern pharmacology?

A

Ancient civilizations, poisons, and relgion.

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2
Q

What two important drugs come from opium?

A

Morphine (10%) and Codeine (0.5%).

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3
Q

What drug was isolated from the Chinese medicinal plant Ma Huang?

A

Ephedrine

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4
Q

What was curare historically used for?

A

As a poison on arrows causing muscle paralysis and death by respiratory failure.

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5
Q

What is curare used for medically today?

A

As a muscle relaxant in surgery (using safer derivatives).

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6
Q

What two drug compounds come from ergot?

A

Ergotamine (treats migraines) and Ergonovine (used after childbirth to stop bleeding).

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7
Q

What hallucinogen is found in the peyote cactus?

A

Mescaline

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8
Q

What breakthrough antibiotic did Alexander Fleming discover?

A

Penicillin.

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9
Q

What are the 5 stages of drug development?

A
  1. Basic research and discovery.
  2. Preclinical studies.
  3. Clinical trials (Phases 1-3).
  4. Health Canada review and manufacturing.
  5. Post-market surveillance (Phase 4).
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10
Q

What is the main purpose of preclinical studies?

A

To assess safety and potential efficacy in animals (pharmacology and toxicology).

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11
Q

What happens in Phase 1 clinical trials?

A

safety, absorption, distribution, elimination, and tolerability in healthy volunteers (20-80).

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12
Q

What happens in Phase 2 clinical trials?

A

Testing drug effectiveness and safety in patients with the disease (100-500).

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13
Q

What happens in Phase 3 clinical trials?

A

Large-scale testing (1000+) comparing a new drug vs a placebo or gold standard. Determines safety and efficacy.

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14
Q

What makes Phase 3 trials “double blind”?

A

Neither the investigators nor the participants know who receives the drug or placebo.

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15
Q

What is a placebo?

A

An inactive substance identical in appearance to the real drug.

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16
Q

What is a gold standard drug?

A

The best current available treatment that new drugs must be tested against.

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17
Q

What is informed consent in a clinical trial?

A

A document ensuring a participant understands purpose, procedure, risks, and can withdraw anytime.

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18
Q

What is bioequivalence?

A

When a generic drug produces the same blood levels as the bran-name drug.

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19
Q

What is a receptor?

A

A molecule inside or on a cell that a drug binds to in order to produce a response.

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20
Q

What is an agonist?

A

A drug that binds to a receptor and activates it.

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21
Q

What is an antagonist?

A

A drug that binds to a receptor but blocks it from being activated.

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22
Q

What is a dose-response relationship?

A

As drug dose increases, the body’s response increases until a maximum effect is reached.

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23
Q

What is the ED50?

A

The dose that produces 50% of the drug’s maximal effect or is effective in 50% of people.

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24
Q

Define efficacy.

A

The maximum effect a drug can produce. (e.g., morphine > acetaminophen).

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25
Define potency.
The amount of drug needed to produce a given effect (usually the ED50).
26
Which is more clinically important: efficacy or potency?
Efficacy - it determines the maximal therapeutic effect.
27
Which ancient drug originates from rye?
Ergot.
28
What would be the target population for a phase 3 clinical trial about some specific severe form of a disease.
Patients between the ages of like 20 and 70 with the specific severe form of the disease.
29
Something about explaining to a friend why a generic and brand name drug are identical in efficacy.
Both drugs were ensured to be bioequivalent.
30
Something about what are phase 4 clinical trials also known as.
Post-market surveillance.
31
What structures do drugs/neurotransmitters bind to.
Receptors.
32
Something about how a point on the dose-response curve where you finally see effects.
The receptor threshold.
33
Something about the therapeutic range of a drug is between 15 mg/ml and 40 mg/ml but you find that the blood concentration of the drug in a patient is like 50 mg/ml what do you do.
Not 100% sure, I put decrease dose but could also be stop using the drug immediately and switch to a less efficacious one.
34
Drug A has a therapeutic range of 2 and Drug B has a therapeutic range of 20 which is safer.
Drug B because of higher TI.
35
A question about different methods of administration.
I put that IV administration has a drawback since it can only be used with small volumes of drug (from google) but it could also be something with a topical thing as the answer.
36
How did ancient civilizations influence modern pharmacology?
Ancient societies experimented with natural substances (plants, minerals, poisons) and documented their effects. These early discoveries (like opium, Ma Huang, curare, ergot, peyote) became the foundation for modern drugs and helped scientists understand receptors, toxicity, pain relief, and nervous system effects.
37
Why do people respond differently to the same drug?
Drug variability occurs because of genetics, age, sex, weight, disease, diet, drug interactions, environment, and differences in drug metabolism.
38
What is the path a drug takes through the body (ADME)?
Absorption – enters bloodstream Distribution – travels to tissues Metabolism – broken down (mainly in liver) Excretion – removed (mainly by kidneys)
39
What causes adverse drug reactions?
Binding to unintended receptors Dose too high Genetics or age Underlying health conditions Drug–drug interactions Individual metabolic differences
40
What are drug–drug interactions, and why do they occur?
When one drug changes the effect of another by: Changing metabolism (speeding/slowing breakdown) Competing for receptors Having additive or opposing effects Altering absorption or excretion
41
How do nerve impulses travel through the body?
Electrical signal travels along the neuron (action potential). At the synapse, neurotransmitters are released. Neurotransmitters bind receptors on the next cell, continuing the signal. Neurotransmitters are then broken down or reabsorbed.
42
How do drugs modify or restore normal nervous system function?
Increase neurotransmission (e.g., SSRIs) Decrease neurotransmission (e.g., benzodiazepines) Mimic neurotransmitters (e.g., nicotine, opioids) Block receptors (e.g., antipsychotics) Prevent neurotransmitter breakdown Stabilize electrical activity (e.g., anti-seizure drugs)
43
What is Substance Use Disorder (SUD)?
A medically diagnosed disease based on clinical criteria that indicate impaired control, risky use, social impairment, and physiological dependence.
44
What factors influence the development of SUD?
Genetics Early life experiences Environment Mental health Pharmacology of the drug (how quickly/effectively it activates reward pathways)
45
What is the dopamine hypothesis of addiction?
Addictive drugs strongly increase dopamine in the brain’s reward pathways, reinforcing drug-taking behavior.
46
What is drug tolerance?
When repeated drug use leads to reduced effects, requiring higher doses to achieve the same effect.
47
What is drug withdrawal?
Physical symptoms that occur when drug use stops, caused by the body adapting to the drug’s presence.
48
What is harm reduction?
A philosophy emphasizing safer use, reduced stigma, and practical strategies to minimize harm associated with drug use.
49
What properties of a drug increase misuse potential?
Fast onset of action High potency Strong dopamine release Short duration (leading to repeated use)
50
What is the mechanism of action of amphetamines?
They stimulate the CNS by increasing release of dopamine and norepinephrine.
51
What are therapeutic uses of amphetamines?
ADHD Narcolepsy (Always under controlled medical supervision.)
52
What are the main effects/toxicities of amphetamines?
Increased alertness and energy Elevated heart rate and blood pressure Risk of psychosis High misuse potential due to dopamine release
53
What is the mechanism of action of cocaine?
Cocaine blocks the reuptake of dopamine, norepinephrine, and serotonin, increasing their levels in the synapse.
54
What are the short-term effects of cocaine?
Euphoria Increased energy Increased confidence Elevated heart rate and blood pressure
55
Why is cocaine highly addictive?
Rapid dopamine increase and extremely fast onset (especially when smoked or injected).
56
Why is cocaine withdrawal not typically life-threatening?
It produces mainly psychological, not physical, withdrawal symptoms.
57
What is nicotine’s mechanism of action?
Nicotine stimulates nicotinic acetylcholine receptors → increases dopamine and other neurotransmitters.
58
Why is nicotine highly addictive?
Very fast absorption to the brain (seconds) and strong dopamine reinforcement.
59
What are short-term effects of nicotine?
Increased alertness Increased heart rate Relaxation (in dependent users)
60
What are long-term effects of nicotine?
Cardiovascular disease Cancer risk (due to smoking exposure) Chronic respiratory conditions
61
What is caffeine’s mechanism of action?
Blocks adenosine receptors → increases alertness and decreases fatigue.
62
What are toxicities of caffeine at high doses?
Anxiety Tremors Insomnia Heart palpitations
63
Why are many performance-enhancing drugs banned in sports?
They provide unfair advantage and pose significant health risks.
64
What are the five major classes of performance-enhancing drugs covered in Module 02?
Amphetamines Anabolic steroids Benzodiazepines Blood doping & erythropoietin Diuretics
65
What do amphetamines do in sports performance?
Mask pain and fatigue, increase endurance and alertness.
66
What are anabolic steroids used for?
Increasing muscle mass (anabolic effect) and promoting male characteristics (androgenic effect).
67
What risks do anabolic steroids pose?
Liver damage Heart attack/stroke (thrombotic events) Hormonal disturbances Aggression
68
What are benzodiazepines used for in sports?
Reducing anxiety and tremors (but illegal for competition due to sedation).
69
What is blood doping?
Increasing red blood cell count to boost oxygen delivery and endurance.
70
What risks are associated with blood doping?
Stroke Heart attack Blood clots
71
Why are diuretics used as performance-enhancing drugs?
Rapid weight loss Masking other drugs in urine tests
72
What are the two major divisions of the nervous system?
Central nervous system (CNS): brain & spinal cord Peripheral nervous system (PNS): nerves outside the brain/spinal cord
73
What are the main functions of the CNS?
Receives and processes information Initiates appropriate responses Controls behavior, thought, and movement
74
What are the two divisions of the PNS?
Somatic nervous system: voluntary control of muscles Autonomic nervous system: involuntary control of organs
75
What neurotransmitter is used in the somatic nervous system?
Acetylcholine (ACh).
76
What are the two branches of the autonomic nervous system (ANS)?
Sympathetic: “fight or flight” Parasympathetic: “rest and digest”
77
What neurotransmitters mediate the sympathetic nervous system?
Norepinephrine & epinephrine.
78
What neurotransmitter mediates the parasympathetic nervous system?
Acetylcholine.
79
What is a neuron?
A specialized cell that generates and transmits electrical and chemical signals.
80
What are the three functional regions of a neuron?
Dendrites: receive signals Cell body: processes signals Axon: sends signals
81
What is a synapse?
The junction where a neuron communicates with another neuron or target cell using neurotransmitters.
82
What are the steps of synaptic transmission?
Nerve impulse reaches axon terminal Neurotransmitter released Neurotransmitter binds to receptors Signal is generated or modified Neurotransmitter is removed (breakdown or reuptake)
83
What are the two main types of neurotransmitter receptors?
Ionotropic: fast, directly open ion channels Metabotropic: slow, use second messenger systems
84
What are the three ways neurotransmitters are removed from the synapse?
Reuptake Enzymatic breakdown Diffusion away from synapse
85
What are the major excitatory and inhibitory neurotransmitters?
Excitatory: Glutamate Inhibitory: GABA
86
What neurotransmitter is associated with reward and addiction?
Dopamine.
87
What neurotransmitters regulate mood?
Serotonin and norepinephrine.
88
Which neurotransmitter is essential for learning and memory?
Glutamate.
89
How can drugs modify neurotransmission?
Increase release Decrease release Block receptors Activate receptors Block reuptake Inhibit metabolism of neurotransmitters
90
Give an example of a drug that blocks neurotransmitter reuptake.
SSRIs (block serotonin reuptake).
91
Give an example of a drug that inhibits neurotransmitter breakdown.
MAO inhibitors.
92
What do parasympathomimetic drugs do?
Stimulate the parasympathetic system by acting like acetylcholine.
93
What do parasympatholytic drugs do?
Block parasympathetic activity (e.g., atropine).
94
What are common effects of parasympathomimetics?
Decreased heart rate Increased digestion Increased gland secretion Pupil constriction
95
What are common effects of parasympatholytics?
Increased heart rate Decreased secretions Pupil dilation Relaxed smooth muscle
96
What do sympathomimetic drugs do?
Stimulate the sympathetic nervous system (e.g., epinephrine).
97
What do sympatholytic drugs do?
Block the sympathetic nervous system (e.g., beta-blockers).
98
What are common effects of sympathomimetics?
Increased heart rate Bronchodilation Increased blood pressure Pupil dilation
99
What are common effects of sympatholytics?
Decreased heart rate Lower blood pressure Reduced fight-or-flight responses
100
What is the blood–brain barrier (BBB)?
A protective barrier that prevents many substances from entering the brain.
101
Why is the BBB important for drug therapy?
Only drugs that can cross the BBB can affect the CNS; this limits which medications are effective for brain disorders.
102
What class of drugs treats anxiety?
Benzodiazepines.
103
What class of drugs treats depression?
Antidepressants (SSRIs, SNRIs, MAOIs, TCAs).
104
What class of drugs treats psychosis?
Antipsychotics (e.g., dopamine receptor antagonists).
105
What class of drugs treats epilepsy?
Anticonvulsants (stabilize neuronal firing).
106
What drugs treat Parkinson’s disease?
Drugs that increase dopamine or mimic dopamine (e.g., levodopa).
107
What drugs treat Alzheimer’s disease?
Drugs that prevent breakdown of acetylcholine (cholinesterase inhibitors).
108
What are the main functions of the kidney?
Remove waste Regulate water balance Regulate electrolytes (Na+, K+, Cl-) Regulate acid-base balance Regulate blood pressure Activate vitamin D Produce erythropoietin
109
What is the functional unit of the kidney?
The nephron
110
What are the 5 major parts of the nephron?
Glomerulus Proximal convoluted tubule (PCT) Loop of Henle Distal convoluted tubule (DCT) Collecting duct
111
What is glomerular filtration?
The process by which blood is filtered into the nephron to form urine.
112
What substances normally do not pass through the glomerulus?
Proteins and blood cells.
113
What hormone regulates water reabsorption in the kidney?
ADH (antidiuretic hormone).
114
What hormone regulates sodium and potassium balance?
Aldosterone.
115
What happens when ADH levels increase?
Water reabsorption increases which then in turn makes urine become more concentrated.
116
What happens when aldosterone increases?
Sodium is reabsorbed, potassium isa excreted which increses blood volume and BP.
117
How does the kidney regulate acid-base balance?
Excretes hydrogen ions (acid). Reabsorbs or generates bicarbonate (base).
118
Where do loop diuretics act and what do they do?
Block Na+, K+, 2Cl- reabsorption, strongest diuresis. Toxicities: include dehydration, hypokalemia, low sodium, hearing damage (high does).
119
Where do thiazide diuretics act and what are their risks?
Block Na+, Cl- reabsorption, moderate diuresis. Toxicities: include hypokalemia, dehydration, increased glucose, increased uric acid (gout risk). First-line for hypertension.
120
What is the mechanism and main risk of potassium-sparing diuretics?
Block aldosterone (spironolactone) or block Na+ channels (amiloride). Main toxicity: hyperkalemia, which can cause fatal arrhythmias.
121
What is mannitol and when is it used?
Osmotic diuretic acting in the proximal tubule + loop of Henle. Uses: reduce intracranial pressure, reduce intraocular pressure, support kidneys in acute failure.
122
What conditions are treated with diuretics?
Hypertension (thiazides), edema (heart/kidney/liver failure), glaucoma, cerebral edema (mannitol), acute kidney injury.
123
What are the major electrolyte risks with diuretics?
Hypokalemia: loop & thiazide diuretics Hyperkalemia: potassium-sparing diuretics Both can cause dangerous arrhythmias.
124
What is the difference between AKI and CKD?
Acute kidney injury (AKI): sudden loss of kidney function. Chronic kidney disease (CKD): gradual, long-term loss of function.
125
What medications are used to treat complications of CKD?
Phosphate binders Vitamin D supplements Erythropoiesis-stimulating agents (treat anemia) Bicarbonate (correct acidosis)
126
When is dialysis needed?
When kidneys cannot maintain fluid balance, remove waste, or correct electrolytes/acid–base disturbances.
127
Which drugs interact with diuretics and why?
NSAIDs: reduce kidney blood flow, weaken diuretic effect. ACE inhibitors: increase hyperkalemia risk Digoxin: risk of toxicity increase when potassium is low. Lithium: levels increase with diuretics, toxicity.
128
What hormones regulate sodium, potassium, and water?
ADH: increases water reabsorption. Aldosterone: increases sodium reabsorption and potassium excretion, increase BP.
129
When is it appropriate to use OTC drugs?
Only for mild, self-diagnosable symptoms. Stop if adverse effects occur; don’t self-medicate for more than 2 weeks; consult a pharmacist if unsure.
130
What factors make an OTC drug the “best choice”?
Proven efficacy, known toxicity, simple formulations (single ingredient), effective dose, and generic equivalence.
131
How does ASA work and what is it used for?
Inhibits prostaglandin synthesis → decreases pain, fever, inflammation; low doses prevent stroke/MI via platelet inhibition.
132
What are the key adverse effects of ASA?
Gastric irritation, tinnitus, Reye’s syndrome in children, allergic reactions.
133
What are acetaminophen’s properties and primary risk?
Analgesic + antipyretic (NOT anti-inflammatory). Major risk: fatal liver toxicity in overdose or long-term high dosing.
134
What are NSAIDs used for and their main adverse effects?
Analgesic, antipyretic, anti-inflammatory. Side effects include gastric irritation (less than ASA), rash, dizziness, fluid retention.
135
How do they differ?
Both block histamine receptors, but 1st gen causes sedation; 2nd gen (cetirizine) is less sedating and preferred.
136
Compare antacids, H₂ antagonists, and PPIs.
Antacids: Neutralize acid. H₂ blockers: Reduce acid secretion via receptor blockade. PPIs: Most effective, permanently block proton pump (90%+ reduction).
137
How do decongestants work?
Constrict nasal blood vessels, reduce fluid leakage. Risks: rebound congestion, BP changes; do not use >3 days.
138
What is the preferred OTC cough suppressant and why?
Dextromethorphan HBr, effective at proper doses (20–30 mg q6h). Codeine carries opioid misuse risk.
139
What are the main laxative categories?
Increase gut motility (bisacodyl). Draw water into stool; preferred; act in 2–3 days. Avoid dehydration.
140
What are the main types?
Adsorbents: Add bulk (Pepto-Bismol). Loperamide: Opioid acting peripherally, decreases motility; drug of choice except in fever/bloody stool.
141
What is OTC hydrocortisone used for?
Topical anti-inflammatory for poison ivy/oak, insect bites, mild skin inflammation. More effective than calamine.
142
What are major problems with herbal products?
Lack of RCTs, poor standardization, adulteration, varying global quality, and drug interactions.
143
What is it used for and what risks exist?
Mild–moderate depression; risks: serotonin syndrome with antidepressants, phototoxicity, drug interactions.
144
What effect does echinacea have?
Possibly shortens common cold slightly; stimulates immune cells; avoid in autoimmune disease.
145
Difference between vitamins, nutritional vs megavitamin approach?
Nutritional: Meets RDA. Megavitamin: Excess of RDA; risks toxicity (fat-soluble A, D, E; B6 nerve damage).
146
Vitamin A what are the functions and dangers?
Required for growth, epithelial cells, night vision. Deficiency: night blindness. Excess: liver enlargement, skin changes.
147
Vitamin D what are the functions and dangers?
Promotes calcium/phosphate absorption; prevents osteoporosis. Excess: high blood calcium, tissue calcification, kidney issues.
148
Vitamin E what are the functions and dangers?
Antioxidant protecting tissues. Excess: inhibits platelet aggregation, increases warfarin effect.
149
What is the difference between acute and chronic toxicity?
Acute = single large exposure; Chronic = repeated small exposures over long time.
150
How does aflatoxin B1 illustrate acute vs chronic toxicity?
Acute = liver failure; Chronic = liver cancer.
151
What are the three major environmental toxicant categories?
Air pollution, tobacco smoke, pesticides.
152
What are the two major categories of air pollutants?
Particulate matter and gaseous pollutants.
153
What human activities produce major air pollutants?
Heating/power (fossil fuels), automobiles, industrial processes.
154
Who is most susceptible to air pollution?
Young children, older adults, and people with cardiorespiratory diseases.
155
What is environmental tobacco smoke?
Combination of mainstream + sidestream smoke; increases lung cancer risk.
156
What are the two major categories of pesticides discussed?
Insecticides (organochlorine, organophosphorus) and herbicides (Agent Orange, paraquat).
157
Mechanism of toxicity of organochlorines like DDT?
Increase neuronal excitation, tremors, convulsions, death.
158
Why are organophosphorus insecticides toxic?
Irreversibly inhibit acetylcholinesterase increase acetylcholine result in respiratory failure.
159
What is the toxic contaminant in Agent Orange, and what does it cause?
TCDD, chloracne, liver/CNS impairment, cancer, birth defects.
160
Why is paraquat deadly?
Causes severe lung damage, fibrosis, respiratory failure. Even 2 teaspoons can be fatal.
161
What systems are affected by chronic lead toxicity?
CNS, PNS, kidneys, and blood.
162
Compare mercuric vs methyl mercury toxicity.
Mercuric is kidney damage. Methyl mercury is CNS toxicity (most dangerous).
163
List major routes by which drugs enter the environment.
Agriculture, pet treatment, improper disposal, aquaculture, human excretion, manufacturing discharge.
163
Why is BPA controversial?
It has estrogen-like activity; potential reproductive and developmental concerns.
164
Name five drug classes commonly detected in the environment.
Neuroactives, steroid hormones, antibiotics, antihypertensives, analgesics.
165
What are the three hallmark features of cancer cells?
Unlimited division, invasion, metastasis.
166
What four environmental areas contribute most to cancer?
Tobacco, diet, occupational exposures, viruses.
167