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Pharm Block 3 > Block 3 Drugs > Flashcards

Block 3 Drugs Flashcards

1
Q

parenterally administered anesthetic barbiturate quick action, short duration, long half-life

A

sodium thiopental activates GABA A receptors

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2
Q

barbiturate side effects

A

CNS depression (can be good) cardiovascular (vasodilation, venodilation) respiratory depression (must intubate)

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3
Q

parenteral general anesthetic used to induce & maintain anesthesia antiemetic 3.5 hr half life

A

propoforl GABA A mechanism

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4
Q

propofol side effects

A

pain on injection (inject w/ lidocaine into larger vein) initial excitation on induction CV: severe BP reduction AND decr myocardial contractility respiratory depression (more than thiopental)

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5
Q

used to induce anesthesia in patients at risk for hypotension

A

etomidate

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6
Q

etomidate side effects

A

lots of pain w/ injection, myoclonus nausea & vomiting suppression of adrenocortical response to stress only used w/ patients w/ hemodynamic problems CNS same as thiopental CV FAR less than thiopental Respiratory less than thiopental

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7
Q

produces dissociative anesthesia analgesia, amnesia doesn’t affect respiration, bronchodilator

A

ketamine NMDA receptor antagonist

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8
Q

ketamine side effects

A

nystagmus, salivation, lacrimation, spontaneous movement/increased muscle tone increase cerebral blood flow → increased intracranial pressure emergence delirium (less in kids) hypertension

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9
Q

ketamine’s usefulness

A

patients with bronchospasm kids for short, painful procedures

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10
Q

short-acting benzodiazepine GABA A activator use alone for conscious sedation, short procedures induction agent (less so), decreases anxiety

A

midazolam

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11
Q

midazolam pharmacokinetics

A

slower induction time, longer duration than thiopental metabolized to active metabolite

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12
Q

midazolam side effects

A

resp depression/arrest (esp IV) use w/ caution in patients w/ neuromuscular disease, parkinsons’, bipolar CV similar to thiopental

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13
Q

commonalities of inhalation general anesthetics

A

low therapeutic indices gaseous or volatile

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14
Q

factors that affect induction with a gaseous anesthetic

A

anesthetic concentration in inspired air pulmonary ventilation pulmonary blood flow arteriovenous concentration gradient

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15
Q

anesthesia achieved when?

A

when brain partial pressure is equal to MAC

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16
Q

moderate blood:gas PC, not quick recovery excreted unchanged into expired air uses: inhaled induces and especially maintains anesthesia, used with NO

A

isoflurane

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17
Q

isoflurane side effects

A

respiratory: airway irritant, coughing, decreases tidal vol, increase resp rate, depresses respiration, increases PaCO2 cardio: myocardial depression, decreased BP, arrhythmias, cerebral vessel vasodilation → increased intracranial pressure

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18
Q

volatile and RT; low solubility in blood, rapid induction and recovery; excreted unchanged used in outpatient surgeries, maintenance not induction, causes skeletal relaxation

A

desflurane

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19
Q

desflurane side effects

A

CV same as isoflurane resp: worse as irritant, bronchospasm

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20
Q

low blood:gas PC; 5% metabolized to fluoride ion in liver; degraded to compound A by absorbants inpatient and outpatient; induce and maintain; kids and adults; not resp irritant

A

sevoflurane

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21
Q

sevoflurane side effects

A

similar to isoflurane, not as much respiratory depression

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22
Q

rapid equilibration; used to enhance induction; weak anesthetic, don’t get MAC sedation, analgesia; use with others to reduce dose

A

nitrous oxide when emerging, use 100% O2

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23
Q

nitrous oxide side effects

A

CI w/ pneumothorax; negative inotrope (decr HR); sympathomimetic (helps increase HR); minimal resp effects besides O2 dilution; abuse liability

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24
Q

injection of local anesthetic around individual nerves/nerve plexuses

A

nerve block anesthesia

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25
Q

local anesthesia mechanism of action

A

act directly on nerve cells to block ability to conduct impulses bind directly to voltage-dependent sodium channel higher affinity for inactive channel than unopened channel

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26
Q

co-administration of local anesthetic with vasoconstrictors (eg epinephrine)

A

decrease rate of absorption into circulation, increasing duration of anesthesia less potential for systemic toxicity

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27
Q

order of CNS toxicity for local anesthetics

A

CNS stimulation first then CNS depression at higher doses death due to respiratory depression

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28
Q

cardiovascular toxicity of local anesthetics

A

general depression of CV after CNS effects: decreased contractility, decreased BP, decreased rate of conduction (arrhthmias), arteriolar vasodilation cardiac arrest

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29
Q

how are ester local anesthetics inactivated?

A

by plasma esterases

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30
Q

how are amide local anesthetics metabolized?

A

by the liver

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31
Q

local anesthetic; blocks pre-synaptic NE uptake potent vasoconstrictor topical anesthesis of upper respiratory tract

A

cocaine

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32
Q

short acting, synthetic local anesthetic low potency, slow onset, short duration

A

procaine

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33
Q

long acting, more potent, longer duration ester anesthetic spinal anesthesia, topical and opthalmic preparations

A

tetracaine

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34
Q

low water solubility so low toxicity applied to wounds and ulcerated surfaces

A

benzocaine

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35
Q

amide, intermediate duration of action; faster, longer lasting and more extensive anesthesia often used with vasoconstrictors

A

lidocaine

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36
Q

long acting amide, prolonged anesthesia, more sensory than motor block, more cardiotoxic

A

bupivicaine

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37
Q

long acting amide, S-enantiomer, less cardiotoxicity, motor sparing epidural and regional anesthesia

A

ropivacaine

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38
Q

amides

A

metabolized by liver not associated with allergic reactions

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39
Q

esters

A

metabolized by plasma cholinesterases rare allergic reactions

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40
Q

neuropsych drugs pt 1

A

amitriptyline clomipramine fluoxetine sertraline buproprion mirtazapine duloxetine phenelzine chlorpromazine clozapine thioridazine fluphenazine haloperidol olanzapine risperidone quetiapine aripiprazole

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41
Q

Which drugs are used in the treatment of depressive disorders?

A

SSRIs, SNRIs, Atypical drugs, Tricyclic antidepressants, MAOIs

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42
Q

5-HT uptake inhibitors

A

SSRIs- fluoxetine, sertraline

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43
Q

SSRI side effects

A

nausea, insomnia, and sexual dysfunction no food rxns, but dangerous “serotonin reaction” (hyperthermia, muscle rigidity, CV collapse) can occur if given with MAOIs

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44
Q

Do SSRIs have fewer or more adverse effects than TCAs and MAOIs?

A

less, so overdose risk is reduced

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45
Q

Symptoms of SSRI withdrawal

A

-dizziness, light-headedness, vertigo or feeling faint, shock-like sensation, paresthesia, anxiety, diarrhea, fatigue, gait instability, headache, insomnia, irritability, nausea or vomiting, tremor, visual disturbances -symptoms begin within 1-7 days after stopping an SSRI

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46
Q

SSRI approved uses

A

Major Depression OCD Panic disorder Social Anxiety Disorder PTSD Generalized Anxiety disorder PMS (now PDD) Hot flashes associated with menopause

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47
Q

effects on drug metabolism, long half-life active metabolite (7 days or more). now available as a sustained release product. used to treat PMS

A

fluoxetine

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48
Q

used to treat OCD, PTSD, Panic attacks; less effects on metabolism than fluoxetine, shorter half life.

A

sertraline

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49
Q

block both 5-HT and NE reuptake, side effect profile is more SSRI-like than TCA-like

A

SNRI drugs

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50
Q

12-18 hr half-life. also approved for neuropathic pain syndromes, fibromyalgia, back pain, and osteoarthritis pain. What is the drug and which patients to do you have to use caution with?

A

duloxetine -use caution in patients with liver disease

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51
Q

neuropsych drugs pt 1

A

amitriptyline clompiramine fluoxetine sertraline buproprion mirtazapine duloxetine phenelzine chlorpromazine clozapine thioridazine fluphenazine haloperidol olanzapine risperidone quetiapine aripiprazole

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52
Q

drugs without typical TCA structure of SSRI or SNRI action. May or may not block catecholamine uptake

A

Atypical antidepressants

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53
Q

weakly blocks NE and dopamine uptake. No weight gain or sexual dysfunction. what is the drug and what is it also approved for?

A

bupropion -also approved for nicotine withdrawal and seasonal affective disorder

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54
Q

blocks presynaptic alpha2 receptors in the brain. increases appetite

A

mirtazapine -good for AIDS patients with AIDS wasting syndrome

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55
Q

blocks NE and 5-HT reuptake; first highly effective drugs for the treatment of depression; now used secondarily to SSRIs and other newer compounds

A

tricyclic antidepressants

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56
Q

pharmacokinetics of TCAs

A

rapidly absorbed after parenteral or oral administration; relatively high concentrations are found in the brain and heart.

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57
Q

demethylated to active metabolites which are used as drugs themselves; long plasma half-life (8-100 hrs)

A

amitriptyline

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58
Q

side effects of TCAs

A

sedation cardiac abnormalities (due to anticholinergic effects and increased NE concentrations–>palpitations, tachycardia, and arrhythmias) overdoses: acute toxicity (symptoms include hyperpyrexia, hyper- or hypotension, seizures, coma, and cardiac conduction defects)

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59
Q

side effects of TCAs

A

sedation cardiac abnormalities (due to anticholinergic effects and increased NE concentrations–>palpitations, tachycardia, and arrhythmias) overdoses: acute toxicity (symptoms include hyperpyrexia, hyper- or hypotension, seizures, coma, and cardiac conduction

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60
Q

contraindications for TCAs?

A

recent MIs

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61
Q

TCAs and drug interactions?

A

TCAs effect absorption and metabolism of other drugs TCAs block guanethidine uptake sympathomimetic drugs; particularly indirect acting agents

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62
Q

therapeutic uses of TCAs

A

major depressive disorder (3rd choice) enuresis in childhood- imipramine chronic pain (neuropathic pain that opiates do not handle as well)- amitriptyline OCD- clomipramine and SSRIs

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63
Q

non-selective MAOI

A

phenelzine

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64
Q

produces mood elevation in depressed patients; may progress to hypomania particularly in bipolar disease; corrects sleep disorders in depressed patients; may produce stimulation in normals; antidepressant action takes about 2 weeks

A

MAOIs

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65
Q

symptoms of actue toxicity of MAOIs

A

agitation, hallucinations, hyperpyrexia, convulsions, and changes in bp

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66
Q

what do you have to restrict in patients on MAOIs?

A

dietary intake of tyramine

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67
Q

therapeutic uses of MAOIs

A

major depression (not first drug of choice, however) narcolepsy

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68
Q

other treatments for depression

A

electroconvulsive shock therapy (ECT) transcranial magnetic stimulation (TMS) cortical and subcortical electrical stimulation (still experimental)

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69
Q

nonspecific blockers of NE and 5-HT reuptake

A

amitriptyline

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70
Q

selective serotonin reuptake inhibitors (SSRIs)

A

fluoxetine, sertraline

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71
Q

serotonin-norepinephrine reuptake inhibitors (SNRIs)

A

duloxetine

72
Q

monamine oxidase inhibitors (MAOI)

A

phenelzine

73
Q

drugs with other monamine mechanisms

A

bupropion, mirtazapine

74
Q

SSRI-like; used to treat OCD

A

clomipramine

75
Q

actions of antipsychotic drugs

A

(treatments are not curative) decrease in psychotic behavior (negative symptoms of schizophrenia are not well treated by older typical agents) sedation

76
Q

actions of antipsychotic drugs

A

decrease in psychotic behavior (negative symptoms of schizophrenia are not well treated by older typical agents) sedation extrapyramidal effects (biggest concern; dystonias, parkinsonism, akathisia, tar dive dyskinesia)

77
Q

side effects of antipsychotic drugs. How can the long-term side effects be prevented?

A

extrapyramidal effects (biggest concern; dystonias, parkinsonism, akathisia, tardive dyskinesia); tardive dyskinesia can be prevented by “drug holidays” anticholinergic (dry mouth, blurred vision, urinary retention) orthostatic hypotension neuroendocrine effects (result of dopamine receptor blockade; prolactin effects and gynocomastia) allergic and idiosyncratic effects (liver, blood, and cutaneous) cardiac effects (thioridazine) decreased seizure threshold (particularly phenothiazines) weight gain (diabetes related events are more common with atypicals, particularly olanzapine, risperidone, clozapine, and quetiapine)

78
Q

what is the potentially lethal side effect of antipsychotic drugs and what does it involve? How do you treat this?

A

neuroleptic malignant syndrome; potentially lethal hypodopaminergic side effect) hyperthermia, parkinson-like symptoms (muscular rigidity and tremor), mutism, and possible death treatment: cooling and hydration, bromocriptine and dantrolene (muscle relaxants, most common when used with SSRIs or SRNIs

79
Q

original antipsychotics, currently less commonly used

A

phenohiazines

80
Q

phenothiazine; aliphatic side chain; low to medium potency, sedative, pronounced anticholinergic actions

A

chlorpromazine

81
Q

phenothiazine; piperidine side chain; low potency, sedative, less exrapyramidal actions, anticholinergic

A

thioridazine

82
Q

phenothiazine; piperazine side chain; high potency, less sedative, more exrapyramidal reactions, less cholinergic

A

fluphenazine

83
Q

why are atypical antipsychotics used over older typical antipsychotics?

A

need for better antipsychotic drugs, more acceptable side-effect profile, more efficacious in treating negative symptoms of schizophrenia in general, atypical antipsychotics have lower incidence of extrapyramidal symptoms (better compliance), possible lower incidence of tardive dyskinesia, improve negative symptoms, improve positive symptoms in many antipsychotic-resistant or refractory patients, less impact on cognitive functioning (??), more cost effective (???)

84
Q

why are atypical antipsychotics used over older typical antipsychotics?

A

need for better antipsychotic drugs, more acceptable side-effect profile, more efficacious in treating negative symptoms of schizophrenia

85
Q

atypical antipsychotic agents (5)

A

clozapine, olanzapine, risperidone, quetiapine, aripiprazone

86
Q

blocks D4 and 5-HT2 receptors, little effect of D2, muscarinic antagonist, improves positive symptoms even in patients not helped by other drugs, improves negative symptoms

A

clozapine

87
Q

side effects of clozapine

A

lowers seizure thresholds more than other antipsychotics (5-10% incidence) can cause fatal agranulocytosis, which requires monitoring!!

88
Q

potent 5-HT2 antagonist, D1 and D2 antagonist, some D4, few extrapyramidal symptoms (5-HT>D)

A

olanzapine

89
Q

side effects of olanzapine

A

weight gain and diabetes related adverse events reports of olanzapine abuse no agranulocytosis less seizure incidence than clozapine

90
Q

combined D2 and 5-HT2 antagonist, greater reduction in negative symptoms and less extrapyramidal symptoms than traditional antipsychotics; paliperidone is the active metabolite, both are available as intramuscular depot preparations

A

risperidone

91
Q

side effects of risperidone worse or better than clozapine?

A

less seizure activity and less antimuscarinic than clozapine

92
Q

structurally related to clozapine, similar to risperidone and olanzapine in effects on schizophrenia symptoms and side effects; shorter half-life; approved for augmentation in depression. any abuse?

A

quetiapine; some reports of abuse

93
Q

partial D2 agonist and 5-HT2 antagonist; also approved as an adjunct in depression (augmentation)

A

aripiprazole

94
Q

uses of antipsychotic drugs

A

acute psychotic episodes (no matter what the cause) chronic schizophrenia manic episodes, bipolar disorder (aripiprazole, olanzapine, quetiapine, risperidone) schizoaffective disorder (paliperidone) augmentation in depression (aripiprazole, olanzapine, quetiapine) Tourette’s syndrome (haloperidol, pimpozide) antiemesis (not thioridazine)

95
Q

monovalent cation, blocks manic behavior, no behavioral effects in “normals” inhibits phosphatase that converts IP2 to IP1 unbound to plasma proteins, 95% of dose eliminated in urine narrow therapeutic window

A

lithium levels raised by diuretics, ACE inhibitors, Ang II receptor blockers

96
Q

lithium side effects

A

fatigue, tremor, GI symptoms, ataxia higher levels cause hyperactive deep reflexes, rigidity, coma

97
Q

CI of lithium

A

pregnancy

98
Q

clinical uses of lithium

A

mania, prevent recurrences of bipolar disease, cluster headaches

99
Q

alternatives to lithium

A

carbamazepine, valproic acid for initial control of manic symptoms: haloperidol

100
Q

blocks sodium channels, no interaction with GABA unpredictable absorption, hepatic enzyme induction used for partial seizures

A

carbamazepine

101
Q

blocks repetitive neuronal firing, can reduce some Ca currents, increases GABA concentrations bound to plasma protein, in extracellular fluid used as first line drug in bipolar disease, sedating

A

valproic acid inhibits metabolism of drugs including carbamazepine

102
Q

treatment of depressive episodes associated with bipolar disease (drug combination)

A

olanzapine and fluoxetine

103
Q

carbamazepine side effects

A

CNS side effects such as sedation, confusion and ataxia, diplopia

104
Q

valproic acid side effects

A

GI upset, weight gain, hair loss not dose related: hepatotoxicity and teratogenic (spinal bifida)

105
Q

somatic correlates of anxiety

A

ANS arousal, voluntary muscle activation (jitteriness, tremor) complications: substance abuse

106
Q

treatment of anxiety and insomnia

A

benzodiazepines, SSRIs, buspirone, classical antihistamines, EtOH, cannabis, opiates, barbiturates

107
Q

benzodiazepine receptor agonists

A

diazepam, zolpidem

108
Q

benzodiazepine receptor antagonists

A

flumazenil

109
Q

partial agonist for 5-HT 1A, also binds to dopamine receptors delayed onset, little sedation, no dependence or cross-tolerance used for GAS

A

buspirone

110
Q

benzodiazepines used to treat anxiety

A

diazepam, alprazolam, lorazepam

111
Q

rapid onset of action, long duration used as hypnotic

A

flurazepam

112
Q

fast onset of action, high lipid solubility, rapid redistribution muscle relaxant due to actions in spinal cord

A

diazepam

113
Q

less lipophilic, slower absorption and onset of action, longer duration of action after single dose used as hypnotic

A

lorazepam

114
Q

CNS effects of benzodiazepines

A

decreased anxiety, sedation, hypnosis, muscle relaxation, anterograde amnesia, anticonvulsant action, minimal CV/resp actions alone

115
Q

benzodiazepine drug interactions

A

produce additive CNS depression with other depressants, can affect hepatic metabolism of drugs like cimetidine

116
Q

clinical uses of benzodiazepines

A

anxiety states, sleep disorders, seizure treatment, IV sedation and anesthesia some used for alcohol withdrawal, acute manic episodes

117
Q

benzo used for alcohol withdrawl

A

chlordiazepoxide

118
Q

benzo used for acute manic episodes

A

clonazepam

119
Q

symptoms of benzo withdrawal

A

anxiety, insomnia, irritability, headache, hyperacusis, hallucinations, seizures

120
Q

other treatments for anxiety

A

SSRIs & SNRIs, beta-blockers, other sedatives (rarely)

121
Q

hypnotic that binds to BDZ receptor on GABA complex weak anxiolytic, muscle relaxant and anticonvulsant preserves stage 3 and 4 sleep, duration 5-6hr

A

zolpidem

122
Q

adverse effects of hypnotic effects

A

daytime sedation, ataxia, rebound insomnia, tolerance and dependence, occasional idiosyncratic excitement and stimulation

123
Q

act at GABA A, rapidly absorbed and distributed, highly lipid soluble, renal excretion, additive with other CNS depressants used as anticonvulsant

A

barbiturate

124
Q

barbiturate side effects

A

general CNS depression, anticonvulsant, respiratory depression tolerance (not uniform) physical dependence with withdrawal symptoms (seizures)

125
Q

skeletal muscle relaxants

A

used to reduce muscle tone associated with spasticity related to MS injuries/other musculoskeletal disorders

126
Q

GABA-mimetic agent working at GABA B receptors, interferes with release of NT used to reduce spasticity less sedation

A

baclofen

127
Q

alpha2 adrenergic agonist, relieves muscle spasm side effects include drowsiness, hypotension, dry mouth interacts with CYP1A2 inhibitors

A

tizanidine

128
Q

other agents used as muscle relaxants

A

botulinum toxin, dantrolene

129
Q

what is the single “dose” size for alcohol. What is the dosing for beer, wine, and 80 proff liquor?

A

about 14 grams

this is the amount in:

12 ounces of beer

5 ounces of wine

1.5 ounces of 80 proof liquor

130
Q

when a 70 kg person consumes 14 g of alcohol what does their blood alcohol become?

A

30 mg/dl

30mg%

0.03% w/v

This is equal to 7mM concentration

131
Q

pharmacokinetics of alcohol

A

primary route of administration is oral

rapid absorption

primarily from the sall intestine, but can be absorbed through the GI tract

132
Q

what factors effect the absorption of alcohol?

A

increased by gastric emptying

enhanced by carbonated beverages

decreased by the presence of food

133
Q

what is effects the rate of absorption of alcohol

A

ethanol concentration

rate of ethanol consumption

134
Q

distribution of ethanol?

does it cross membranes?

distribution to organs?

A

total body water

thus, Vd is equal to the volume of body water; essentially equal to the body weight

crosses membranes freely (including INTO the alveolae from the lung capillaries=basis for the brethalizer test of expired air)

distribution to individual organs depends on the degree of tissue vascularization and the amount of blood flow

135
Q

what is ethanol metabolized to?

A

90-98% of ethanol that is ingested is metabolized to acetaldehyde by two enzymatic routes (the remainder is eliminated unchanged in the breath, sweat, and saliva)

136
Q

does ethanol undergo a first pass effect?

A

Yes, ethanol has a significant first pass effect by both gastric and liver alcohol dehydrogenases

137
Q

what is the primary, rate-limiting pathway of alcohol metabolism?

what type of kinetics does this enzyme undergo?

A

alcohol dehydrogenase

primarily in liver and GI tract

zero order kinetics (ex. 10g/hr in 70kg person-since one drink is 14g, takes about 1.5 hours to metabolize one drink)

138
Q

what pathway does alcohol get shunted to once the alcohol dehydrogenase pathway becomes overwhelmed?

A

mixed function oxidase system (MFOS) through CYP2E1

139
Q

pharmacokinetics for CYP2E1 pathway of ethanol metabolism?

A

high Km for ethanol (low affinity)

induced in chronic alcoholics

results in important drug interactions

140
Q

what enzyme converts acetaldehyde to acetic acid during ethanol metabolilsm?

A

aldehyde dehyrdogenase

141
Q

what are some properties of aldehyde dehydrogenase?

A

mitochondrial enzyme

inhibited by disulfiram

genetic polymorphisms in the gene that are very prevalent in Asian cultures

142
Q

what are two consequences of alcohol metabolism?

and what do these two things cause/lead to?

A

increased NADH (causes inhibition of the TCA cycle; reduced gluconeogenesis; reduced fatty acid oxidation)

increased acetaldehyde (protein adduct formation; results in inflammation; inhibition of microtubules which can interfere with cellular and liver function; depletion of glutathione)

143
Q

metabolic changes from alcohol metabolism can cause what side effects?

A

fatty liver

hepatic inflammation

induction of CYP2E1 (metabolism of xenobiotics to carcinogenic agents)

–>Bad news for the liver!!

144
Q

what can heavy ethanol loads produce?

A

heavy alcohol load produces transient hypogylcemia (due to insulin secretion)

alcohol-induced ketoacidosis (increased serum ketones along with a mild increase in glucose; when our bodies start to use fat as fuel we get acid-base and metabolic dysfunction)

145
Q

what are the CNS effects of ethanol?

A

several ion channels are sensitive to the presence of ethanol

most important is the GABAAreceptor-ligand gated chloride channel (causes a hyperpolarization)

disturbs the balance between excitatory and inhibitory neurotransmission in the brain; promotes inhibition

146
Q

acute effects of ethanol?

A

dose-dependent; CNS depressant

effects from alcohol:

sedation, “euphoria”, increased reaction time, poor motor function, ataxia, emesis, stupor, coma, and death

147
Q

chronic ethanol effects?

(Liver and GI specific effects)

A

Liver and GI effects:

steatosis (fatty liver)

Hepatitis C (often a co-morbid disease)

cirrhosis (due to liver necrosis and chronic inflammation)

gastritis, pancreatitis, malabsorption of vitamins

chronic diarrhea

cancers, including esophageal, liver, and bladder

148
Q

chronic ethanol effects on the CNS?

A

tolerance occuring due to: adaptive neuronal changes (chronic ethanol–>CNS depression–>up-regulation of excitatory transmission to compensate) and metabolic tolerance (due to up-regulation of CYP2E1)

both psychological (craving) and physical dependence (withdrawal can be dangerous, especially because of seizures if metabolic imbalance occurs)

alcohol addiction

149
Q

how prevalent is alcoholism?

A

alcohol addicition occurs in 5-10% of men and 3-5% of women

150
Q

what are the effects of neurotoxicity of alcoholism?

A

neuralgias and peripheral nerve injury

memory impairment; blackouts

thiamine deficiency associated with chronic use can produce: cerebral/cerebellar atrophy, Wericke’s encephalopathy, Korsakoff’s psychosis

151
Q

what are the teratogenic effects of alcohol?

A

associated with chronic maternal alcohol abuse

traid of symptoms in new born:

retarted body growth

facial abnormalities

CNS dysfunction

Ethanol and/or acetaldehyde affect embryonic cell proliferation

dose-dependent, but minimum dose is not known

152
Q

do alcohol/ drug interactions occur?

A

Yes

CNS depressants are additive (barbituates; benzodiazepines; opiates; neuroleptics)

interactions with drug metabolism (acute, high doses can inhibit CYP-mediated metabolism; chronic ethanol induces CYP2E1, therefore accelerates metabolism of some drugs)

acetaminophen toxicity (is worse in alcoholics of when intoxicated because glutathione is depleted)

153
Q

clinical pharmacology of ethanol-actue toxicity?

how can you treat acute alcohol toxicity?

A

acute intoxication:

generally 400mg/dl is lethal

(12 drinks)

support respiration and prevent aspiration of vomit

correct any metabolic problems (ex. dehydration, hypoglycemia, ketosis, electrolyte imbalance)

154
Q

what are the signs of alcohol withdrawal and how do you treat alcohol withdrawal?

A

signs: alcohol craving, agitation, anxiety, insomnia, seizures, mood swings, sweating, tachycardia
goal: prevent seizures, delirium, arrythmias
therapy: short acting benzodiazepines: diazepam and chlordiazepoxide (subtutes for alcohol, then can taper off gradually; remember that the brain has increased excitatory transmission in response to chronic alcohol; atenolol is used to prevent cardiac arrythmias)

155
Q

pharmacologic treatment of alcholism?

A

naltrexone, acamprosate, disulfiram (antabuse)

156
Q

mu opiate receptor antagonist, can reduce craving, increase self-control in alcoholics, best when used in combo with psychosocial therapy

A

naltrexone

157
Q

GABAA agonist, decreased drinking frequency and relapse, thought to normalize dysregulated neurotransmission (remove ethanol, left with unopposed increase in excitation)

A

acamprosate

158
Q

SE of acamprosate?

A

diarrhea

159
Q

inhibitor of alcohol dehydrogenase, results in the accumulation of acetaldehyde (very uncomfortable for the patient)

used as aversion therapy in alcoholics

A

disulfiram (antabuse)

(not very effective, requires considerable will-power to conform)

160
Q

what is the role of CNS stimulants on CNS neurons?

what is a SE of all CNS stimulants at sufficient doses?

A

increase activity of CNS neurons

(can be produced either through enhancement of excitation or suppression of inhibition)

in sufficient doses all CNS stimulants can produce convulsions

161
Q

what is the clinical usefulness of CNS stimulants?

A

attention-deficity, hyperactive disorder

narcolepsy

162
Q

a methylxanthine, similar structure to purines, competitive antagonist of adenosine receptors.

where is this compound found?

A

caffeine

found in coffee beans, cocoa beans and kola nuts, is also added to OTC stimulants and analgesics (ex. Excedrin)

163
Q

compounds with similar structure to caffeine found in tea

A

theophylline and theobromine

164
Q

mechanism of action of caffeine?

A

primary effect at normal caffeine doses: competitive antagonist of adenosine receptors (postsynaptic adenosine receptors produce IPSPs–>hyperpolarize the membrane; presynaptic adenosine receptors inhibit glutamate release)

=>caffeine inhibits these inhibitory effects (dis-inhibition) resulting in CNS stimulation and excitation

165
Q

what effects does caffeine have at higher doses?

A

at higher doses, caffeine inhibits cAMP phosphodiesterase (results in increased cAMP; responsible for its beneficial effects in the treatment of asthma-not as efficacious as other methylxanthines, however)

at higher doses, it also induces the release of calcuim from intracellular (ER) stores

166
Q

pharmacological actions of caffeine when delivered in caffeine-containing drinks?

A

CNS stimulant

increased alertness, increased attention during sustained tasks

decreased fatigue and drowsiness

can cause nervousness, restlessness, tremors

high doses stimulate medullary respiratory and CV centers; can get tachycardia

167
Q

peripheral effects of caffeine?

A

positive ionotropic and chronotropic effects (direct effects on the myocardium)

dilates coronary and systemic blood vessels; constricts cerebral blood vessels (this may underlie the beneficial effects of caffeine in headache)

produces diuresis

increases gastric secretions

modest bronchodilation

168
Q

therapeutic usefulness of caffeine?

A

primarily used as an aid to stay awake in various OTC preparations

added to some aspirin preparations to treat headache (Excedrin)

169
Q

toxicity and consequences of chronic use of caffeine?

A

“overdose” results in excessive CNS stimulation (nervousness, insomnia, excitement)

consequences of chronic use:

  • tolerance develops to the stimulant effects of caffeine
  • physical dependence develops to caffeine at the dose of two cups of coffee per day
  • withdrawal symptoms include feelings of fatigue and sedation; headaches and nausea; vomiting (rare)
170
Q

what are the three sympathomimetic stimulants that act through enhancement of catecholaminergic neurotransmission?

A

cocaine, amphetamines, methylphenidate

171
Q

extracted from the coca plant, major use is illicit, weak base (unionized in the unprotonated form [B] which predominates at alkaline pH)

A

cocaine

172
Q

two major forms of cocaine

A

hydrochloride salt and free base forms

173
Q

how is free base cocaine formed?

what is the benefit of having a free base form of cocaine for users?

A

free base cocaine (crack cocaine that can be smoked) is made by extracting the hydrochloride salt from an alkaline solution into ether or another organic solvent

free base is absorbed more quickly across membranes; but more importantly it is volatile and can be smoked

174
Q

pharmacokinetics of cocaine?

A

well absorbed through any mucous membrane

time to peak effect and duration of action are dependent upon the route of administration (shortest are i.v. and smoked)

metabolized in plasma and liver

short plasma half-life (50 min); CNS half-life is even shorter (10-30 min)

urine screens detect metabolites

175
Q

mechanism of action of cocaine?

A

potent inhibitor of the reuptake of norepinephrine, dopamine, and serotonin

cocaine binds to the transporter itself and inhibits the bindng of the neurotransmitter (reinforcing effects are due to increased dopamine in the synapse)

increases the activity of tyrosine and tryptophan hydroxylases (due to loss of end-product-monamine- inhibition)

is a loca anesthetic and vasoconstrictor

Pharm Block 3 (15 decks)

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