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Toxicology > Test #2 > Flashcards

Test #2 Flashcards

1
Q

What the body does to the drug

A

Pharmacokinetics

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2
Q

What the drug does to the body

A

Pharmacodynamics

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3
Q

Area of pharmacology concerned w/ unusual response to drugs caused by genetic differences b/w individuals

A

Pharmacogenetics

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4
Q

Repetitive sequence of experimentation & characterization involving biologic assays ranging from the molecular to organism level

A

Drug screening

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5
Q

What is the end result of drug screening process called?

A

Lead compound (a patentable entity)

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6
Q

What is the goal of preclinical studies?

A

Identifying potential human toxicities & designing mechanism to monitor for these toxicities in clinical trials

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7
Q

What are the 3 types of toxic doses?

A
  1. No effect: max dose showing no toxicity
  2. Min. lethal dose: min. dose that kills a subject
  3. Median lethal dose: kills 1/2 of test subjects
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8
Q

What are some limitations of preclinical testing?

A
  1. toxicity testing is time consuming & expensive
  2. Large numbers of animal subjects needed
  3. Extrapolation of animal data to humans may not be accurate
  4. Rare adverse effects are unlikely to be detected
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9
Q

What are 5 confounding factors in clinical trials?

A
  1. Most ds’s have a variable clinical course
  2. Presence of other ds & risk factors
  3. Known & unknown ds/risk factors may influence clinical study results
  4. Subject & observer bias
  5. Study design must account for placebo effect
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10
Q

The administrative body charged w/ oversight of the drug evaluation process.

A

FDA

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11
Q

These trials determine the dose-response relationship of the drug. Subjects are normally healthy volunteers. The main goal is to identify the maximal tolerated dose in the absence of severe toxicity. Pharmacokinetic parameters are determined in these trials

A

Phase I trials

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12
Q

During these trials, the drug is studied in a small group of pts w/ the target ds to detemine efficacy. A single blinded protocol is usually used.

A

Phase II trials

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13
Q

These trials try to establish safety & efficacy. These trials are designed to minimize potential confounding factors. Often involve double-blind crossover protocols.

A

Phase III Trials

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14
Q

These trials involve monitoring drug safety when used by a large number of pts. This relies on the voluntary, timely, & complete reporting of toxicity by prescribers

A

Phase IV trials

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15
Q

This Act provided incentives for the investigation & development of drugs for rare ds’s

A

Orphan Drug Act of 1983

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16
Q

A reaction to a drug that is harmful or an unintended response. Claimed to be the 4th leading cause of death in the US

A

Adverse Drug reactions

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17
Q

A fundamental principle of pharmcodynamics is that drugs only modify what?

A

Normal biochemical & physiologic processes; they don’t endow new capabilities

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18
Q

The pharmacologic effect is mediated through what?

A

Drug/receptor binding

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19
Q

The most biologically important & common receptors are __________ that bind extracellular molecules (ligands) which results in an intracellular change (transduction).

A

Integral membrane proteins

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20
Q

What are the 4 major types of integral membrane proteins?

A
  1. Ligand gated ion channels
  2. G-protein coupled receptors
  3. Enzyme-linked receptors
  4. Intracellular receptors
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21
Q

These channels are responsible for regulation of the flow of ions through the cell membrane. Respond rapidly & have a very short duration of effect. Can open channels or modify the function of ion channels.

A

Ligand gated ion channels

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22
Q

Voltage gated ion channels in peripheral nerves are receptor sites for what type of drugs?

A

Local anesthetics

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23
Q

Ligand binding to the extracellular receptor site of a G-protein couple receptor leads to what?

A

Activation of the alpha-subunit of the G-protein, the release of bound GDP, & binding of a GTP

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24
Q

Stimulation of G-protein coupled receptors results in responses lasting how long?

A

Seconds to minutes

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25
Q

Enzyme-linked receptors elicit responses that last how long?

A

Minutes to hours

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26
Q

What is the M/C enzyme type assoc. w/ enzyme-linked receptors?

A

Tyrosine kinase

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27
Q

These hormones pass directly through the cell membrane binding to an intranuclear receptor

A

Steroid hormones (receptor-steroid complex binds to DNA segment causing altered gene expression)

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28
Q

Intracellular receptors elicit responses that can last for how long?

A

at least 30 minutes but can last for hours to days (b/c it involves new protein synthesis)

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29
Q

Binding of a small number of receptors can dramatically alter total cellular metabolism due to what?

A

Cascade effect

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30
Q

Repeated or continous administration of an agonist (or antagonist) may lead to changes in receptor population & thereby responsiveness leading to what?

A

Receptor desensitization (to protect cell from damage)

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31
Q

Normal cytosolic proteins that recognize agonist-activated, phosphorylated receptors & bind them.

A

Arrestins (binding makes receptor inaccessible for G-proteins)

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32
Q

The magnitude of a drugs effect depends on what?

A

Concentration at the receptor site which is determined by the dose of the drug & the drugs particular pharmacokinetics

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33
Q

As the drug’s concentration increases the magnitude of the pharmacologic effect increases. This is called what?

A

Graded dose response

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34
Q

A plateau in the drug’s effect is reached when what happens?

A
  1. All receptors are occupied

2. For receptors w/ a large “spare” population maximal cellular response is attained

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35
Q

This is the amount of drug necessary to produce an effect 50% of an agent’s max. effect.

A

Potency

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36
Q

A significant contributing factor to potency is what?

A

Affinity of a drug for the receptor

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37
Q

The ability of an agent to produce an effect of a given magnitude, the max. biologic response to a drug.

A

Efficacy

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38
Q

If a drug binds to a receptor & produces a biologic effect that mimics the response of the endogenous ligand it is called what?

A

Agonist (ex: phenylephrine –> epinephrine; meth –> MAO enzymes)

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39
Q

These are drugs which decrease the response of another drug or endogenous ligand.

A

Antagoinsts

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40
Q

What are 4 mechanisms by which antagonists work?

A
  1. Bind to same receptor site as agonists (blocking)
  2. Non competitive (allosteric inhibition); bind to different site causing a conformational change
  3. Irreversible binds a receptors (ex: ASA –> COX-1)
  4. Chemical antagonists; bind w/ another drug making it inactive (ex: Protamine sulfate –> heparin)
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41
Q

These drugs have some intrinsic activity by it’s less than a full agonist.

A

Partial antagonists (partial agonists) (Ex: Pentazocine –> morphine; methadone)

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42
Q

When a drug binds to a separate receptor but the response opposes the response to an agonist

A

Functional (Physiologic) antagonism (Ex: epinephrine –> histamine)

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43
Q

Type of agonist that inhibits receptors that are active in the absence of an agonist

A

Inverse agonist (seen in benzodiazepine & cannabinoid receptors)

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44
Q

These are used to determine the ability of a drug to produce a response of a predetermined magnitude in a pt population. Useful in determining toxic dose in populations

A

Quantal Dose-Responses

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45
Q

The ratio of the dose that produces toxicity to the dose that produces the desired response

A

Therapeutic Index

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46
Q

A large Therapeutic Index indicates what?

A

Toxicity requires a much larger dose than required for the desired effect.(penicillin)

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47
Q

What does a small Therapeutic Index indicate?

A

The dose for the therapeutic effect approaches the toxic dose, these drugs are potentially dangerous.(warfarin)

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48
Q

Attempts to explain an unexpected drug response via a genetic mechanism. Goal is to understand the role that genetic make-up in responses to drugs, both therapeutic & toxic responses

A

Pharmacogenetics

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49
Q

Identifies genetic differences w/i a population to try to explain observed responses or susceptibilities to drugs or ds processes

A

Pharmacogenomics

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50
Q

What are some characteristics of all anti-anxiety agents?

A
  • Have sedative properties (hypnotics)
  • Many possess anticonvulsant properties
  • Able to induce anterograde amnesia
  • Most potentiate GABA activity
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51
Q

What is the target of Benzodiazepines?

A

GABA receptors

52
Q

How do benzos work?

A

Reduce anxiety through the promotion of GABAnergic transmission which results in inhibiting neuronal circuits in the limbic system

53
Q

Sedative/hypnotic/anterograde amnesia/anticonvulsant effects of benzos occur because of what?

A

Larger doses that involve interaction of alpha-1 GABA receptors

54
Q

Muscle relaxant effects of benzos occur because of what?

A

Large doses that work by increasing pre-synaptic inhibition in the spinal cord via alpha-2 GABA receptors

55
Q

Benzos are most frequently used for what?

A

Generalized anxiety disorders

56
Q

What type of muscle disorders respond to diazepam (Benzos)?

A

Muscular disorders resulting spasm particularly spasticity assoc. w/ degenerative disorders of spinal cord dysfunction

57
Q

What is the goal of short acting benzos?

A

Amnesia (used prior to invasive or unpleasant procedures)

58
Q

How can benzos affect sleep/be used to tx sleep disorders?

A
  • Decrease sleep latency
  • Increase stage 2 non-REM sleep
  • Decrease both slow wave & REM sleep
59
Q

How are benzos absorbed & distributed?

A

Benzos are lipophilic & rapidly absorbed/distributed after oral administration

60
Q

How are benzos metabolized?

A

By hepatic microsomal enzyme systems. Excreted in the urine as glucuronides or oxidized metabolites

61
Q

Abrupt discontinuation of benzos results in what withdrawal symptoms?

A
  • Insomnia
  • Anxiety
  • Agitation
  • Muscle tension
62
Q

What type of benzos are more assoc. w/ withdrawal syndromes?

A

Short-acting agents

63
Q

What are adverse effects of benzos?

A
  • Drowsiness & confusion (M/C)
  • Ataxia
  • CNS depression when taken w/ other CNS depressants
  • Overdose is seldom lethal unless w/ other CNS depressants
64
Q

What are some types of non-benzo anxiolytic & hypnotic agents?

A
  • Zolpidem (Ambien-lacks anticonvulsant & muscle relaxant properties)
  • Zaleplon (Sonata-used for sleep initiation but not maintenance, less side effects than zolpidem)
  • Eszopiclone (Lunesta-sedative for insomnia for 6 months)
65
Q

This drug is a GABA receptor antagonist that rapidly reverses the effects of benzos when overdose is suspected

A

Flumazenil (reverses all effects of benzos & can begin a withdrawal syndrome)

66
Q

Type of agents that used to be used as sedatives but were replaced by benzos b/c they were safer

A

Barbiturates

67
Q

What are some of the negative effects of barbiturates?

A
  • Induce tolerance, drug-metabolizing enzymes
  • Induce physical dependence
  • Have severe withdrawal syndrome
68
Q

What is the mechanism of barbiturates?

A

Enhance GABAnergic transmission through binding to a different site on the GABA receptor

69
Q

Larger doses of barbiturates can cause what to happen?

A

Impair function of Na+ channels leading to general anesthesia

70
Q

What are actions of barbiturates?

A
  • CNS depression (low dose=sedative/anticonvulsant, high dose=anesthesia)
  • Respiratory depression
  • Enzyme induction
71
Q

What is the only common therapeutic indication for barbiturates?

A

Generalized seizures which are resistant to less sedating anticonvulsants (1st-line drug for pediatric seizure disorders)

72
Q

How are barbiturates absorbed/distributed?

A

Well absorbed across the GI tract & rapidly distributed. Highly bound to plasma proteins & compete w/ other plasma protein bound drugs

73
Q

What are adverse effects of barbiturates?

A
  • Physical dependence
  • Rapid withdrawal causes a withdrawal syndrome
  • Overdose is a common cause of death
74
Q

What 2 categories are CNS stimulants divided into?

A 
Psychomotor stimulants (cause excitement, euphoria, relieve fatigue, & increase motor activity
Psychomimetic drugs (hallucinogens; produced profound changes in thought patterns & mood)
75
Q

What are examples of psychomotor stimulants?

A 
Methylxanthines
Nicotine
Cocaine
Amphetamines
Methylphenidate (Ritalin)
76
Q

Theophylline, Theobromine, & Caffeine are examples of what type of psychomotor stimulant?

A

Methylxanthines

77
Q

What are the proposed mechanisms of Methylxanthines?

A
  1. Translocation of extracellular calcium
  2. Increase in cAMP & cGMP d/t phosphodiesterase inhibition
  3. Blockade of adenosine receptors (most likely the main effect at common plasma levels)
78
Q

What actions does caffeine have on the body?

A

CNS: decrease fatigue & increased alertness. Can produce anxiety & tremors
CV: may cause symptoms of cardiac ischemia/arrhythmias
Renal: mild diuretic
Gastric mucosa: it stimulates secretion HCl

79
Q

How is caffeine absorbed & distributed?

A

Absorbed orally & rapidly distributed throughout the body including the brain

80
Q

What are adverse effects of caffeine?

A

Moderate doses cause insomnia, anxiety, & agitation.
Higher doses can cause emesis & convulsions.
Lethal dose is 10g (100 cups of coffee) d/t arrhythmias

81
Q

Bruprpion (Zyban) is an antagonist to what drug?

82
Q

How does nicotine work (mechanism)?

A

Low does causes ganglionic stimulation by depolarization

High doses it causes ganglionic blockade

83
Q

What actions does nicotine have on the body?

A
  • CNS: Rapidly crosses the BBB, low doses produce aroused relaxation, improves attention, learning, problem solving, & reaction time. High doses produce medullary paralysis causing respiratory/CV failure
  • Peripheral: stim. sympathetic system results in increased BP/HR. Stim parasym. increases intestinal motility. High doses result in hypotension/GI paralysis
84
Q

What are the pharmokinetics of nicotine?

A

Highly lipid soluble so absorption occurs across any mucosa. 90% of inhaled nicotine is absorbed across the alveolar membrane. Clearance involves metabolism in the lung/liver ending w/ urinary excretion. Tolerance to toxic effects develops rapidly.

85
Q

What are the adverse effects of nicotine?

A

CNS: irritability & tremors

Intestinal cramps, diarrhea, HTN, tachycardia.

86
Q

What are withdrawal symptoms of nicotine?

A

Physical dependence develops rapidly. Withdrawal is charac. by irritability, anxiety, restlessness, difficulty, concentrating, HAs, & insomnia

87
Q

What is the mechanism of action of cocaine?

A

Central & peripheral action is the blockade of reuptake of monoamines (NE, 5-HT & DA) into presynaptic terminals which causes them to be more potent especially DA. This leads to intense sublime euphoria.

88
Q

What are the actions of cocaine?

A
  • CNS: produces an acute increase in awareness & euphoria, higher doses cause hallucinations, delusions & paranoia; tremors, convulsions followed by respiratory & vasomotor depression
  • Symp. nervous system: increases action of norepi. producing fight or flight syndrome
  • Hyperthermia: impairs thermoregulation
89
Q

What is a therapeutic use of cocaine?

A

Topical anesthetic

90
Q

Explain the pharmacokinetics of cocaine

A
  • Nasal administration results in peak levels at 15-20 mins.
  • IV or inhalation (smoking) peaks w/i seconds but wears off faster
  • Rapidly de-esterfied & de-methylated to be exreted in urine
91
Q

What are the adverse effects of cocaine?

A
  • Anxiety: includes HTN, tachycardia, sweating, paranoia
  • Depression: major component of withdrawal
  • Cerebrovascular ds: fatal arrhythmias, MI, seizures, stroke, intracranial hemorrhage
92
Q

What is the mechanism of action of Amphetamines?

A

Effects on CNS & PNS involving elevated levels of neurotransmitters in the synaptic space by promoting release of intracellular stores of catecholamines & inhibition of monoamine oxidase

93
Q

The major behavioral effects of amphetamines are d/t the release of what?

94
Q

What are the effects of amphetamines?

A

Stimulates the entire neuraxis resulting in increased alertness, insomnia, decreased appetite, & decreased fatigue. In symp. nervous system, it prolongs action of NE in adrenergic system

95
Q

What are therapeutic uses of amphetamines?

A

ADHD tx: Dextroamphetamine/methylphenenidate (Ritalin), Atomoxetine (strattera)
Narcolepsy

96
Q

Explain the pharmacokinetics of amphetamines?

A

Completely absorbed from the GI tract, metabolized in the liver & excreted in the urine. Duration of action is 4-6 hours

97
Q

What are adverse effects of amphetamines?

A
  • Causes addiction & drug seeking behavior
  • CNS: insomnia, irritability, weakness, tremor, confusion, delirium, panic states, suicidal tendencies, acute schizo episode
  • CV: palpitations, tachyarrthymias, HTN, acute coronary ischemia, CV collapse
  • GI: Nausea, vomiting, ab cramps, diarrhea
98
Q

What is the mechanism of action of Methylphenidate (Ritalin)?

A

Potent dopamine elevator (better than cocaine) but enters brain slower than cocaine so produces less of a high

99
Q

What are the therapeutic uses of Methylphenidate (Ritalin)?

A

ADHD

Nacrolepsy

100
Q

Explain the phamacokinetics of Methylphenidate (Ritalin)

A

Rapidly absorbed after oral administration & is concentrated in the brain. Excreted in the urine

101
Q

What are adverse reactions of Methylphenidate (Ritalin)?

A

Ab pain, nausea, anorexia are M/C

Insomnia, irritability, may increase seizure freq. in pts w/ seizure disorders

102
Q

What is the mechanism of antidepressants?

A

Increase the cnetral actions of NE &/or serotonin (5-HT)

103
Q

SSRIs specifically inhibit what?

A

5-HT (serotonin) reuptake at the presynaptic terminal

104
Q

What are the therapeutic uses of SSRIs?

A 
Endogenous depression (primary use)
OCD
Panic disorder
Generalized anxiety
Premenstrual dysphoric disorder
Bulimia nervosa
105
Q

Explain the pharmacokinetics of SSRIs

A
  • Well absorbed after oral abministration
  • Undergo extensive P450 metabolism & conjugation
  • Excretion is primarily through kidneys
106
Q

What are adverse effects of SSRIs?

A
  • Sleep disturbances
  • Sexual dysfunction
  • Increased suicidal ideation in young people
  • Overdose may cause Serotonin Syndrome
107
Q

What is the Serotonin Syndrome Triad?

A 
Cognitive effects (confusion, hypomania, hallucinations, etc)
Autonomic effects (shivering, sweating, hyperthermia, HTN, etc)
Somatic effects (myoclonus, hyperreflexia, tremor)
108
Q

What drugs are assoc. w/ Serotonin Syndrome?

A 
Antidepressants
Opioids
CNS stimulants
5-HT agonists
Psychedelics
Herbs
109
Q

Type of drug that may be effective in those unresponsive to SSRIs. Have been shown to be effective in treating neuropathic pain (chronic pain) that freq. accompanies depression

A

Serotonin/NE Re-uptake Inhibitors (SNRIs)

110
Q

These were the first drugs to be consistently effective at relieving depression in large numbers of depressed pts. They block NE & 5-HT re-uptake into the pre-synaptic neuron. Useful in pts not responding to SSRIs & SNRIs

A

Tricyclic Antidepressants

111
Q

What are the mechanisms of action of TCAs?

A
  • Potent inhibitors of neuronal reuptake of NE & 5-HT into presynaptic nerve terminals. Don’t block dopamine reuptake.
  • Block serotonergic, alpha-adrenergic, histaminergic, & muscarinic receptors
112
Q

What are the therapeutic uses of TCAs?

A

Tx severe major depression

Can be effective in tx of chronic pain

113
Q

Explain the pharmacokinetics of TCAs.

A

Well absorbed orally & widely distributed d/t their lipophilic nature. Hepatic metabolism involves both the P450 system & glucuronidation w/ urinary excretion of the inactive metabolites

114
Q

What are adverse effects of TCAs?

A
  • Blockade of muscarinic receptors
  • Epilepsy can be exacerbated
  • Alpha receptor blockade can cause orthostatic hypotension & tachycardia
  • Sedation, insomnia
  • Can exacerbate manic behavior in bipolars
  • Can be lethal at only 5-6x avg daily dose
115
Q

Monoamine Oxidase Inhibitors (MAOIs) are in limited use d/t what?

A

Dietary restriction required w/ their use

116
Q

What is the mechanism of action of MAOIs?

A

Form stable complexes w/ the enzyme causing irreversible inactivation resulting in increased stores of monoamines in neurons & diffusion of neurotransmitter into the synaptic cleft

117
Q

What are the therapeutic uses of MAOIs?

A
  • Limited to those not responding to less potentially toxic agents
  • May be useful in phobic disorders & atypical depression
118
Q

Explain the pharmacokinetics of MAOIs

A

Well absorbed orally.

Regeneration of MOA activity requires up to 4 wks after stopping drug use

119
Q

What are adverse effects of MAOIs?

A

Side effects caused by excess tyramine which is also found in foods & is normally metabolized by MOA. Leads to HA, tachycardia, HTN, arrhythmias, stroke

120
Q

MAO-A inihibition reduces breakdown of what?

A

Serotonin
NE
Dopamine

121
Q

MAO-B inhibition reduces breakdown of what?

A

Mainly dopamine & phenethylamine (no dietary restrictions)

122
Q

Lithium salts can be used as a prophylactic tx for what?

A

Manic-depressive pts & tx of manic episodes

123
Q

What is the mechanism of action of lithium?

A

Unknown; inhibits inositol monophosphatase which is thought to interfere w/ the generation/recycling of an intracellular 2nd messenger PIP

124
Q

Explain the pharmacokinetics of lithium

A

Renally excreted, 80% is reabsorbed in the prox. tubule, caution in decreased renal function & fluid shifts.

125
Q

What are adverse effects of lithium?

A
  • May interfere w/ thyroid function
  • Nausea, vomiting, diarrhea, tremor, polydipsia, edema
  • NSAIDs may decrease renal clearance by blocking renal PG synthesis
126
Q

What is the only acutely effective tx for depression?

A

Electroconvulsive therapy

Toxicology (3 decks)

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