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Neurology > Neuro3 - Drugs > Flashcards

Neuro3 - Drugs Flashcards

1
Q

Amytriptyline and Imipramine ; MOA - these are serotonin reuptake inhibitors with some norepinephrine reuptake inhibition ; USE - these are primarily used for treatment of DEPRESSION, but also have membrane stabilizing effect and thus are usefull in DIABETIC NEUROPATHY (non-responsive to opiods) ; ADRs - CARDIAC effects (prolonged conduction), high level blockade of histamine, high level anticholinergic (may precipitate glaucoma, and is contraindicated in elderly bc of decreased cognitive function), high level alpha1-adrenoreceptor blocking activity, posibility of manic excitement (from flooding the nervous system with neurotransmitters), weight gain with older agents, interferance with sexual performance, sweating (parydoxical), AGRANULOCYTOSIS

A

Terciary TCAs

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2
Q

Desipramine ; USE - these are primarily used to treat depression in ELDERLY, also may be used to treat OCD ; MOA - blocks norepinephrine uptake strongly and weakly blocks serotonin uptake ; ADRs - compred to terciary TCAs these have no effect on the CV system and have less anticholinergic effects ;

A

Secondary TCAs

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3
Q

terciary TCA ; USE - treatment of DEPRESSION, reduction of narcotics necessary for surgery, and sometimes OCD once SSRIs and Desipramine have been tried ; MOA - blocks serotonin uptake more than norepinephrine uptake, and has active metabolites which loose methyl group and degrade to nortriptyline (a secondary TCA) ; ADRs - CARDIAC effects (prolonged conduction), high level blockade of histamine, high level anticholinergic (may precipitate glaucoma, and is contraindicated in elderly bc of decreased cognitive function), high level alpha1-adrenoreceptor blocking activity, posibility of manic excitement (from flooding the nervous system with neurotransmitters), weight gain with older agents, interferance with sexual performance, sweating (parydoxical)

A

Amitriptyline

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4
Q

terciary TCA ; USE - treatment of depression, and ENURESIS (although anticholinergic would work better) ; MOA - blocks serotonin uptake more than norepinephrine uptake, and has active metabolites which loose methyl group and degrade to desipramine (a secondary TCA) ; ADRs - CARDIAC effects (prolonged conduction), high level blockade of histamine, high level anticholinergic (may precipitate glaucoma, and is contraindicated in elderly bc of decreased cognitive function), high level alpha1-adrenoreceptor blocking activity, posibility of manic excitement (from flooding the nervous system with neurotransmitters), weight gain with older agents, interferance with sexual performance, sweating (parydoxical)

A

Imipramine

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5
Q

Secondary TCA ; USE - treatment of depression in ELDERLY, OCD ; MOA - highest ability to block reuptake of NE with minimal potency to serotonin uptake ; ADRs - compred to terciary TCAs these have no effect on the CV system and have less anticholinergic effects ;

A

Desipramine

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6
Q

FLUOXETINE, Paroxetine, Sertraline ; MOA - primary effect is to block serotonin reptake with very little blockage of norepinephrine reuptake ; USE - depression and OCD ; ADRs - ANOREXIA with weight loss, AKATHISIA, N/V, increased bone loss in older women, SEROTONIN SYNDROME, and compred to TCAs - less anticholinergic activity, less hyptoension, less sedation, no effect on CV

A

SSRIs

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7
Q

prototypical SSRI ; USE - depression and OCD ; MOA - primary effect is to block serotonin reptake with very little blockage of norepinephrine reuptake, long half life with metabolites lasting even longer (thus if there is a problem with the medication, it takes time to get out of the system) ; ADRs - STRONG INHIBITORS OF cP450 (may increase actions of other drugs by decreased clearance), increased bleeding if pt is on warfarin, CAUTION IN LIVER DZ, ANOREXIA with weight loss, AKATHISIA, N/V, increased bone loss in older women, SEROTONIN SYNDROME, and compred to TCAs - less anticholinergic activity, less hyptoension, less sedation, no effect on CV ; NOTE - increased risk of SUICIDE

A

Fluoxetine

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8
Q

possibly due to hyperstimulation of serotoning system ; sx - diaphoresis, restlessness, confusion & delirium, shivering-> tremor -> myoclonus, DIC, hyperthermia, tachycardia, acute renal failure, rhabomyolysis ; several drug interactions cause this: tryptophan + MAO inhibitors, tryptophan + floxetine, MAOIs + fluoxetine, MOAIs + meperidine, SSRIs & antimigrane meds ; tx - cyproheptadine, methysergide

A

Serotonin Syndrome

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9
Q

Duloxetine, Venlafaxine ; USE - a class of antidepressant drugs used in the treatment of major depression and other mood disorders, anxiety disorders, obsessive-compulsive disorder (OCD), attention deficit hyperactivity disorder (ADHD), chronic neuropathic pain, fibromyalgia syndrome (FMS), and for the relief of menopausal symptoms ; MOA - work by inhibiting the reuptake of the neurotransmitters serotonin and norepinephrine -> results in an increase in the extracellular concentrations of serotonin and norepinephrine and, therefore, an increase in neurotransmission (more effective than TCAs) ; ADRs - similar to SSRIs ; Contraindications - should never be taken within 14 days of any other antidepressant, especially with monoamine oxidase inhibitors (MAOIs), as combinations of SNRIs with MAOIs can cause hyperthermia, rigidity, myoclonus, autonomic instability with fluctuating vital signs, and mental status changes that include extreme agitation progressing to delirium and coma ; ALSO contraindicated with St. Johns Wort

A

SNERI

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10
Q

SNRI ; USE - DEPRESSION and pain related to diabetic PERIPHERAL NEUROPATHY ; MOA - blocks 5HT and NE more effectively than TCAs, also weak inhibition of DA reptake ; LOW affinity for histamine and cholinergic receptors

A

Duloxetine

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11
Q

SNRI ; USE - used primarily for the treatment of DEPRESSION, general ANXIETY disorder, social PHOBIA, PANIC disorder, and vasomotor symptoms ; MOA - Blocks reuptake of both 5HT and NE -> biotransformed by cytochrome p450 to active metabolite ; t1/2 is 5hrs but t1/2 of active metabolite is 11hrs (half life increases in liver and renal impairment) ; NO significant activity at muscarinic, histaminic or alpha-1 receptors, does NOT inhibit MAO ; ADRs - susteined HYPERTENSION (dose-dependent), anorexia, N/V, dizziness, anxiety ; Interactions - Cimetidine (increases hlaf life), MAOIs (possibly fatal hyperthermia)

A

Venlafaxine

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12
Q

USE - SMOKING CESATION, depression, anxiety ; Mechanism is unknown - does not inhibit MAO - weak blockade of dopamine, serotonin and norepinephrine reuptake ; ADRs - GRAN MAL SEIZURES that subside when medication is D/C therefore contraindicated in pts with seizure disorders

A

Bupropion

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13
Q

alpha-2 antagonist -> leads to increased norepinephrine and 5HT transmission ; antagonist at 5HT2 and 5HT3 receptors ; weak anticholinergic and antihistamine ; USE - primary use is the treatment of major DEPRESSIVE disorder and other mood disorders ; effective, safe and well tolerated ; NOTE - may see SEROTONIN SYNDROME

A

Mirtazapine

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14
Q

MOA - decrease reuptake of 5-HT but less than SSRIs, also ANTAGONIST (maybe at the autoreceptor??) at 5-HT2a, 5-HT2c, alpha-1 adrenergic and H-1 receptors ; sedative effects may result from srtong blockade of 5-HT2a and alpha-1 sites and moderate blockade of H-1 receptors ; ADRs - PRIAPISM (although not common, surgical intervention is required in 1/3 of cases and may lead to permanent impotence)

A

Trazodone

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15
Q

Analog of trazadone, weaker blockade of 5HT-2, significant inhibition of pre-synaptice uptake of 5HT, weaker blockade of alpha-1 ; ADRs - less sedation, dry mouth and nausea

A

Nefazodone

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16
Q

Phenelzine (hydrazine - irreversible) and tranylcypromine (non-hydrazine - reversible) ; much greater toxicity compared to other psychiatric drugs reserved for pts not responding to other therapies ; USE - DEPRESSION, NARCOLEPSY, phobic-anxiety ; ADRs - anticholinergic effects, cardiovascular (hypertensive crisis, orthostatic hypotension), central nervous system (agitation, dizziness, fatigue, hallucinations, headache, vertigo), constipation, hepatotox, hyperreflexia, hyperpyrexia, interference with ejaculation, skin rash ; NOTE - in patients with hypertension Tranylcypromine is not recommended

A

MAOIs

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17
Q

NON-selective MAOI

A

Isocarboxazid

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18
Q

MAO-A inhibitor which is reversible

A

Tranycycloprine

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19
Q

MAO-A inhibitor which is IRreversible

A

Phenezine

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20
Q

anchovies, avocados, bananas, beans, beer, caffeine, caviar, chocolate, CHEESE, cream, figs, herring, liqueurs, liver, meat, raisins, sherry, snails, soy sauce, sour crea, wine, YEAST PRODUCTS

A

Dietary restrictions for people on MAOIs

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21
Q

increased risk of hypertension - amphetamine, cocaine, sympathomimetics, BUSPIRONE, L-dopa ; increased risk of hyperpyrexia - meperidine and related narcotics ; increased risk of psychosis - dextromethorphan ; increases peak and duration of effect (by reducing biotransformation) of: alcohol, anticholinergics (atropine), antihistamine

A

Drug restrictions for people on MAOIs

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22
Q

enkephalins, beta-endorphin, and dynorphin are metabolized by enkephalinase, and angiotensin converting enzyme and have a very short half-life ; bind to mu, delta and kappa receptors (in the CNS) ; will also bind to receptors in the peripheral tissues ; MOSTLY inhibitory but can be disinhibitory to hyppocampus and spinal cord gabba neurons ;

A

Endogenous opiod peptides

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23
Q

found mostly in the limbic areas, periaquaductal gray mater, rostroventral medualla, spinal cord dorsal horn (laminae I and II) ; binds weakly to mu receptors but STRONGLY to delta receptors, also binds very weakly to kappa receptors

A

Enkephalin

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24
Q

found mostly in the hypothalamus ; binds VERY STRONGLY to mu receptors and STRONGLY to delta receptors, also binds somewhat weakly to kappa receptors

A

Beta-endorphin

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25
Q

found mostly in the limbic areas, periaquaductal gray mater, rostroventral medualla, spinal cord dorsal horn (laminae I and II) ; binds VERY STRONGLY to kappy receptors, moderately to mu receptors, and very weakly to delta receptors

A

Dynorphin

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26
Q

analgesia, hyPOthermia, cardiovascular (baroreceptor reflex inhibition, bradycardia), prolactin release, respiratory depression

A

Mu Receptor activation concequences

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27
Q

analgesia, hyPERthermia, cardiovascular (edotoxemic hypotension), growth hormone release, inhibition of LH and testosteron, respiratory depression

A

Delta receptor activation concequences

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28
Q

VISCERAL analgesia, appetite supression, endotoxemic hypotension, inhibit ADH secretion, may increase secondary spinal cord injury due to reduced blood flow

A

Kappa receptor activation concequences

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29
Q

occurs naturally in the environment - produced by living organisms which can be toxic to the nervous system ;

A

Neurotoxin

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30
Q

man made compunds that are toxic to the nervous system ;

A

Xenobiotic agents

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31
Q

Stabilization -> ABCs, IV dextrose, thiamine, naloxone, oxygen ; History (medical, occupational, environmental), examination (physical and mental) ; remove the source (hose the patient down if exposure is on skin), enduce emesis, gastric lavage ; antidote (deferoxamine, ethanol, naloxone, D-penicillamine, pralidoxime, antivenim ; increase excretion - activated charcoal, foreced saline diuresis, alkaline diuresis, hemodialysis, hemoperfusion ; supportive tx - manage cardiac arrhythmias, seizures, ionic and pH balance

A

Management of poisoned patient

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32
Q

xenobiotic agent ; prolonged coma -> degeneration of neurons ;

A

Barbituate overdose

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33
Q

acute reaction - degeneration of CNS gray mater ; secondary reaction - degeneration of white mater

A

Carbon monoxide poisoning

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34
Q

degeneration of gray mater ; CNS stimulation, hypoxic convulsions ; ANTIDOTE - amyl nitrite, cobalt EDTA, hydroxocobalamin

A

Cyanide poisoning

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35
Q

peripheral neuritis

A

Isoniazid overdose

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36
Q

adults - segmental myelin degeneration ; children - encephalopathy, central demyelination, cerebral edema ; competitively inhibits Ca++ -> decrease in neurotransmitter release -> decrease in the muscle endplate potential ; ANTIDOTE - D-penicillamine, EDTA

A

Lead poisoning

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37
Q

profile like combined systems disease -> marked by increased difficulty in walking, spasticity in lower extremities, a feeling of vibration in the legs, and a loss of sense of position ; NOTE - this is usually seen as a disorder of the nervous system caused by a deficiency of vitamin B12 that results in pernicious anemia and degeneration of the spinal cord and peripheral nerves ; Epidemiology - dentist & dental staff @ greatest risk - preferred drug of abuse for dentists

A

Nitrous oxide poisoning

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38
Q

axonal degeneration of distal segments of motor neuron axons

A

Alcohol poisoning

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39
Q

three-fold syndrome - polyneuritis (weakness, paresthesia), tremor (secondary Parkinsonism), psychosis (severe depression -> suicide) ;

A

Carbon disulfide poisoning

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40
Q

peripheral axon degeneration, weakness, ataxia ; these are acetocholinesterase inhibitors that cause ataxia, parestheis, insomnia, slurred speech, tinnitus, amblyopia, nystagmus, abnormal pupil reactions, nervousness, irritability, depression, anxiety, psychosies, memory disorders ; ANTIDOTE - pralidoxime, atropine

A

organophosphate poisoning

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41
Q

myelin degeneration -> SPASTICITY (unique because usually you see flacidity)

A

Trethyltin poisoning

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42
Q

axonal degeneration, motor polyneuropathy, neurogenic muscular atrophy

A

n-Hexane poisoning

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43
Q

damage to cells of dorsal root ganglion and CNS -> visual disturbance, ataxia, paresthesia, neurasthenia, hearing loss, dysarthria, mental deterioration, muscle tremor, movement disorders, paralysis, decreased DTR ; seen in gardeners, farmers, etc - also used in pesticides

A

Organomercury poisoning

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44
Q

damage to cell cytoplasm and severe motor nerve atrophy ;

A

Vinca alkaloid poisoning

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45
Q

binds to presynaptic terminal -> reduces the release of acetylcholine (response is equal to axonotomy) ; clinically used to reduces spasticity & wrinkles -> may result in facial paralysis

A

Botulinum toxin poisoning

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46
Q

blocks Na+ channels in excitable membranse (blocks all nerve transmission) ; puffer fish must be prepared by a government certified chef - highest concentration of toxin in puffer fish gonads

A

Tetrodotoxin poisoning

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47
Q

increases Na+ permeability -> membranse remain depolarized state ; extremely potent cardiotoxic and neurotoxic steroidal alkaloids found in certain species of frogs (poison dart frog), melyrid beetles, and birds

A

Batrachotoxin poisoning

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48
Q

maintains Na+ channels OPEN for long periods -> impulses generated rapidly -> tremors and convulsions ; Epidemiology - people working in environmental protection agencies - DDT is still in the environment

A

DDT poisoning

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49
Q

maintains Na+ channels OPEN (toxicity is quite rare because of rapid biotransformation - not in children because their livers are not as good) - found in cacaroche poison trap ;

A

Pyrethrins poisoning

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50
Q

ganglionic stimulation, headache, disturbed hearing and vision, confusion, muscular weakness, clonic convulsions, cessation of respiration ; 2-5 mg cause sign of nicotine tox in adults and only 1.5-2mg in children

A

Nicotine overdose

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51
Q

increase in the size of astrocytes in the basal ganglia and cerebellum ; formely used in dry cleaning but is now prohibited ; used in certain manufacturing processes

A

Carbon tetrachloride poisoning

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52
Q

increase in intracellular Ca++ and Na+ -> seizures -> excitotoxicity of neurons (NMDA receptor)

A

Glutamate poisoning

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53
Q

atrophy and cell depletion particularly in the granular layer of cerebellum ;

A

Organic mercury (methyl mercury) poisoning

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54
Q

decrease in synthesis of dopamine -> signs and sx of parkinsonism

A

Manganese poisoning

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55
Q

degrades to MPDP+ -> MPP+ = kills catecholaminergic neurons (particularly dopaminergic neurons)

A

MPTP poisoning

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56
Q

resembles drunken behaviour - incoordination, restlessness/excitement, confusion, ataxia ; teenagers might abuse these ;

A

Gasoline or Kerosine poisoning

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57
Q

euphoria, hallucinations, seizures, coma, optic neuropathy, ataxia, quadriparesis ;

A

Toluene poisoning

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58
Q

blindness, extrapyramidal motor signs ; ANTIDOTE - ethanol

A

Methanol poisoning

59
Q

confusion, hallucinations, hypotonia, hyperreflexia, tremors, tetany, seizures, coma ; ANTIDOTE - ethanol

A

Ethylene Glycol

60
Q

decreased conciousness, muscle twitching, hypertonia, areflexia, ataxia, paralysis, coma ; these are found in gardening supply chemicals (herbicides) ; NOTE - 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) is often a contaminant in these compunds causing psychiatric disturbances

A

Chlorophenoxy compounds

61
Q

CNS excitation, tetanus-like rigidity, convulsions (opisthotonos) ;

A

Strychnine

62
Q

headache, malaise, somnolence, loss of consciousness, clonic seizures, optic nerve lesion

A

Castor beans

63
Q

Group I most deadly - acetaldehyde dehydrogenase inhibition activity (antibuse-like), CNS toxicity 3-6 days later ; Group II - hallucinations, anticholinergic symptoms (ANTIDOTE - physostigmine) ; Group III - dizziness, vertigo, delirium, seizure, coma, ataxia, weaknes, muscular cramps, hyperreflexia (ANTIDOTE - pyridoxine) ; Group IV - parasympathetic stimulation (cholinergic poisoning), blurred vision (ANTIDOTE - atropine) ; Group VI - hallucinations, impaired judgement, impared motor, compulsive movements, vertigo, ataxia, weakness, drowsiness, hyperreflexia ;

A

Mushrooms

64
Q

blood/gas partition coefficient (B/G PC) is relative index of solubility of the gas in the blood ; high B/G PC is more “soluble” in blood which means it less readily moves out of the blood into tissue -> induction takes longer (20-30 mins) ; Low B/G PC indicates that the gas has limited solubility in the blood and thus it will leave the blood rapidly and enter the tissues -> induction time is shorter (only a few minutes) ; solubility is affected by size, charge, and concentration

A

Solubility of general anesthetics

65
Q

recovery will be slower than induction because gas gradually released from tissue storage ; Expired air is the major route for elimination, note that those general anesthetics with high B/G PC will take longer to be exhaled -> longer recovery time ; Biotransformation is a contributory factor but minimal

A

Elimination of general anesthetics

66
Q

used only for inhalational general anesthetics ; 1 MAC = conc. of general anesthetic in alveolar (lung) space at which 50% of pts do not feel initial incision with the assumption that partial pressure of the anesthetic in the lung air is related to general anesthetic concentration in the brain ; it has a very steep dose-response curve where 95% of all pts do not feel the initial surgical incision at 1.1 MAC

A

Minimum alvelolar concentration

67
Q

Phase I - ANALGESIA which is characterized by administration of anesthetic, depression of transmission signals in RAS (general sensory) and dorsal horn cells (pain) ; Phase II - DELIRIUM which is characterized by loss of consiousness, depression of cortex which results in less inhibition of subcortical ares -> disinhibition (hyperreflexia, irregular respiration, vomiting) ; Phase III - SURGICAL ANESTHESIA which begins with muscualr relaxation and return to a regular but lower respiratory rate and blood pressure AND a greater depression of RAS and spinal cord ; Phase IV - MEDULLARY PARALYSIS which begins with cessation of spontaneous respiration and depresion of pons and medulla -> ends in circulatory failure ;

A

Anesthesia general

68
Q

Anxiety relief (benzodiazepine) ; decrease salivary secretions (scopolamine) ; counteract bradycardia (atropine) ; elevate gastric pH (Cimetidine)

A

Pre-anesthetic medication

69
Q

general anesthetic - NMDA antagonist - inhaled analgesic ; 20% provides analgesia = morphine with a decrease in beta-endorphin levels ; 50% used in dental procedures, nosignificant respiratory depression ; 65% highest concentration without causing hypoxia ; Advantages - safe compound, B/G PC = not very soluble in the blood -> rapid induction and recovery ; Disadvantages - not potent (cant produce surgical anesthesia), inadequate muscle relaxation, dreams of sexual assault ; Substance of abuse ; chronic exposure may lead to peripheral neuropathy - loss of balance, leg weakness, impotence

A

Nitrous oxide inhaled anesthetic

70
Q

general anesthetic - rarely used ; Advantages - non-explosive, nonflammable, smooth-rapid induction, bronchodilator, low incidence of toxicity, highly potent with MAC = 0.75 and a concentration required for surgery of 1.2-1.8% ; Disadvantages - volatile liquid - evaporates easily, poor analgesia, poor muscle relaxation, cardiac arrhytmias - due to halogenated hydrocarbons -> decreased interactions of Ca2+ with contractile proteins of cardiac muscle, hepatitis (possibly due to an allergic reaction), hypotension - due to decreased myocardial contractility and decrease in compensatory tachycardia - may be severe

A

Halothane inhaled anesthetic

71
Q

general anesthetic - rarely used due to flouride-induced renal toxicity ; used in small doses during labor ; Most potent - 1MAC = 0.16% ; slow induction because B/G PC = 12 ; hihg level of biotransformation (50-70%) can result in toxic levels of flouride ion -> renal dysfunction -> flouride diabetes insipidus

A

Methoxyflurane inhaled anesthetic

72
Q

general anesthetic - potent, biotransforms into flouride ion but much less nephrotoxic than methoxyflurane

A

Enflurane, Isoflurane, Desflurane, SEVOFLURANE inhaled anesthetics

73
Q

barbituate used for iduction of general anesthesia - target is RAS ; rapid induction due to quick redistribution from brain to other tissues, and easy admin by syringe rather than by gas ; stron CNS depressant, no analgesia (may cause HYPERanalgesia), contraindicated in pts with porphyria, powerful respiratory depressant

A

Thiopental IV anesthetic

74
Q

also refered to as extrathalamic control modulatory system, is a set of connected nuclei in the brains of vertebrates that is responsible for regulating arousal and sleep-wake transitions ; it is a major target of anesthetics

A

RAS (reticular activating system)

75
Q

used for induction of general anesthesia ; NOT an analgesic, possible muscle movements after injection ; non-barbituate ; NOTE - a modulator at GABA-A receptors

A

Etomidate (non-barbituate) IV anesthetic

76
Q

commonly used (colonoscopies, endoscopies) ; Advantages - rapid onset, can be used continously, biotransformed into INACTIVE molecules -> no buildup ; Disadvantages - minor analgesia, pain at injection site, potential seizures, caustion in pts with increased ICP, hihger clearance rate in burn pts ; NOTE - has been proposed to have several mechanisms of action, both through potentiation of GABA-A receptor activity, thereby slowing the channel-closing time, and also acting as a sodium channel blocker

A

Propofol (non-barbituate) IV anesthetic

77
Q

initially developed for burn pts as an alternative to morphine ; DISSOCIATIVE anesthesia ; Advantages - strong analgesia, slight increase or no effect on RR & BP ; Disadvantages - severe psychological reaction (hallucinations) upon emergence, a drug of abuse ; NOTE - common features of this drug are excessive salivation and minor motor tremors

A

Phencyclidine (PCP) IV anesthetic (dissociative agent)

78
Q

USE - changing of burn dressings, diagnostic procedures in children, emergency surgery, outpatient procedures ; MOA - NDMA antagonist thus will cause increased glutamate release after effects have waned ; NOTE - Chemically related to PCP - DISSOCIATIVE anesthesia ; Advantages - rapid onset, strong analgesia, no significant respiratory depression (compared to morphine), reduced psychological reactions (compred to PCP), support of the CV system (increased HR and BP) ; Disadvantages - flashbacks (occur up to 1yr after admin), adverse spychological reactions upon emergence - more frequent in pts over 30 - may be prevented by pre-medicating with diazepam

A

Ketamine IV anesthetic (dissociative agent)

79
Q

these are the natural (morphine, codeine) and semi-synthetic opiates (hydromorphone, buprenorphine, heroin) ; MOA - target periaqueductal gray in supraspinal area and spinal cord - stimulate Mu, Kappa, and Delta receptors -> analgesia, respiratory depression, ephoria

A

Phenanthrene narcotics

80
Q

Fentanyl, Meperidine ; MOA - target periaqueductal gray in supraspinal area and spinal cord - stimulate one, two or all of the follwoing receptors: Mu, Kappa, and Delta receptors -> analgesia, respiratory depression, ephoria

A

Phenylpiperidine narcotics

81
Q

Methadone, Propoxyphene ; MOA - target periaqueductal gray in supraspinal area and spinal cord - stimulate one, two or all of the following receptors ; Mu, Kappa, and Delta receptors -> analgesia, respiratory depression, ephoria

A

Phenylheptane narcotics

82
Q

Naloxone (short acting), Naltrexone (longer lasting) ; these are antagonists to opiod receptors and are used to treat narcotic overdose and to treat physical addiction ; short acting antagonists are typically used to treat overdose, and long lasting antagonists are used to treat addiction ; these may also be added to agonist to prevent injection of crushed opiod pills -> seen in addicts -> will have no effect due to blocking agent (Naloxone)

A

Antagonist narcotics

83
Q

Pentazocine, Butophanol, Dezocine ; these compounds were developed to prevent opiod addiction ; additionally they are prescribed to patients who display addictive behaviour (crushing pills to inject - nullifying the effect due to antagonist)

A

Agonist+antagonist narcotic

84
Q

MOA - decrease adenylate cyclase -> decreased intracellular cAMP -> INCREASED K+ Efflux -> hyperpolarization -> decreased C2+ influx -> reduced availability of Ca2+ -> reduction in relsease of pain NTs (substance P) , because of this Ca2+ channel blockers can be used to aid in analgesia to prevent the ADR of seizures with higer doses of opiods ; Function - supraspinal analgesia, euphoria, spinal analgesia, respiratory depression, constipation ; Agonists - morphine, buprenorphine (partial agonist) ; Antagonists - Pentazocine, Naloxone, Naltrexone ; NOTE - increased prolactin secretion

A

Mu receptor - function, agonists, and antagonists

85
Q

MOA - reduced availability of Ca2+ -> reduction in relsease of pain NTs (substance P) , because of this Ca2+ channel blockers can be used to aid in analgesia to prevent the ADR of seizures with higer doses of opiods ; Function - spinal analgesia, and some but LESS respiratory depression ; Agonist - morphine, pentazocine, ; Antagonist - naloxone, naltrexone ; NOTE - decreased ADH secretion

A

Kappa receptor - function, agonists, and antagonists

86
Q

MOA - decrease adenylate cyclase -> decreased intracellular cAMP -> INCREASED K+ Efflux -> hyperpolarization ; Function - supraspinal analgesia, spinal analgesia ; NOTE - increased growth hormone secretion and decreased LH/Testosterone

A

Delta receptor - function, agonists, and antagonists

87
Q

opiods cause - analgesia, sedation, emesis, depression of cough reflex, respiratory depression because of effect at periaqueductal gray in supraspinal area and spinal cord Mu, Kappa and Delta receptors

A

Narcotic CNS Effects

88
Q

opiods cause - direct hypotension via depression of the vasomotor center ; INDIRECT hypotension via release of histamine -> peripheral vasodilation -> may cause redness of skin that may falsely give the appearance of allergic reaction

A

Narcotic Cardiovascular Effects

89
Q

opiods cause - hypomobility of GI -> constipation, decreased peristalsis, delated gastic emptying

A

Narcotic GI Effects

90
Q

opiods cause - miosis ; OD will see pinpoint pupills

A

Narcotic Eye Effects

91
Q

opiods cause - smooth muscle increased tone especially in non-vascular smooth muscle therefore CONTRAINDICATED in pain due to gall bladder attack

A

Narcotic Smooth muscle Effects

92
Q

opiods cause - iimmunosuppressant effects, Delta receptor causes stimulation of GH, and inhibiton of LH/testosterone, Mu receptor causes prolactin release, Kappa receptor inhibits ADH

A

Narcotic Endocrine Effects

93
Q

pts with seizures/epilepsy , pts with increased ICP, pts with undiagnosed acute abdominal conditions ; all of these are contraindications to this class of drugs

A

Contraindications of narcotics

94
Q

in pts with substance tolerance ADRs include: nausea, sedation, euphoria and dysphoria, analgesia, vomiting, respiratory depression, cough suppression ; in pts with NO tolerance ADRs include: headache, dizziness, seizures (treat with Ca2+ channel blockers), miosis, GI hypomobility, dry mouth, anorexia, biliary tract spasm, urinary retention, interfere with sexua desire

A

ADRs of narcotics

95
Q

most wide spread narcotic ; USE - relief of dyspnea and improvement of respiration in pts on ventilators, pain control, terminal pt pain control ; MOA - biotransformed to 2 metabolites M6G (analgesic activity at Mu receptor -> increased K+ efflux -> Ca2+ decrease -> hyperpolarization) and M3G (causes seizure at high doses) ; ADRs - may cause seizures (M3G), histamine release, N/V, miosis, increased tone of billiary tract, sedation ; NOTE - PO concentration is 6:1 vs IM concentration ;

A

Morphine (narcotic agonist)

96
Q

USE - most potent narcotic available for doctors to prescribe in USA ; MOA - sustained-releases form of morphine - designed to resist gastric breakdown ; ADRs - do not take with alcohol bc the solven can dissolve the sustained release pill -> 6x greater amoun of drug released -> OD

A

Hydromorphone (narcotic agonist)

97
Q

USE - often used in the emergency department, also found as the transdermal patch with XR, oral lozenge and lollipop (abs through oral mucosa, no PO route of admin ; MOA - highly lipid soluble, NO active metabolites, Short-acting, extremely potent 100x morphine ; ADRs - the patch is contraindicated post-op bc it takes hours to work, heat at location of transdermal patch -> vasodilation -> increased systemic abs

A

Fentanyl (narcotic agonist)

98
Q

USE - acute pain, not used much today ; MOA - short acting thus not extensively used today ; ADRs - chronic admin -> accumulation of metabolite -> twitches -> seizures (not readily reversed with Naloxone)

A

Meperidine (narcotic agonist)

99
Q

USE - treatment of heroin adiction ; MOA - Mu-receptor partial agonist ; hart to revers OD in pts bc of strong affinity -> takes almost 4 ampules of Naloxone to reverse effects

A

Buprenorphrine (narcotic agonist)

100
Q

USE - tx for narcotic addiction - used as a baseline drug to keep pt stable, prevent death from OD (must pass Naloxone test), also used for Cancer Pain (baseline drug + addition of immediate-release drug for breakthrough pain) ; MOA - LONG-acting, cross-tolerance with heroin & morphine thus used to stabilize pts by mitigating opiod withdrawal syndrome ; NOTE - higher doses of this druge can block euphoric effect of heroin, morphine and similar drugs -> wein patiens off drugs ; ADRs - duration of respiratory depression > duration of analgesia

A

Methadone (narcotic agonist)

101
Q

old drug used for tx of narcotic addiction ; has ben replaced by sub-oxone, and subutex

A

Levomethadyl (narcotic agonist)

102
Q

analgesic via 2 routes - 1) central acting compound block 5HT uptake -> serotonin activation, 2) activate Mu receptor

A

Tramadol (narcotic agonist)

103
Q

for acute use ; MOA - increase dosages w/out worrying about respiratory depression (there is a maximum levle of respiratory depression) -> this is because of interaction with Kappa riceptors in the cord and less interaction with Mu receptors in the hypothalamus ; ADrs - severe withdrawal reactions if the patient has been on opiods such as morhpine as some of these drugs act as Mu antagonists -> precipitate withdrawal

A

General characteristics of Narcotic Agonist+Antagonist

104
Q

partial antagonist to Mu and agonist to Kappa ; similar to Sub-oxone - the amount of Naloxone will not interfere with analgesia when taken PO but if the pt decides to inject it, Naloxone will block the effect of the opiod ;

A

Pentazocine + Naloxone (agonist+antagonist narcotic)

105
Q

nasal spray - useful in terminally ill pts ; narcotic agonist/antagonist

A

Butophanol (agonist+antagonist narcotic)

106
Q

narcotic agonist/antagonist ; Caution - correlation between analgesic dose and degresse of respiratory depression (like morphine)

A

Dezocine (agonist+antagonist narcotic)

107
Q

rapid reversal of narcotic OD -> on crash carts ; MOA - considerable affinity for narcotic receptors -> rapid reversal of OD ; ADRs - precipitated withdrawal with drug addicts ; if you hive this drug to an addic that is currently OD/unsconcious -> conscious -> CNS excitation -> withdrawal within se/mins ; NOTE - can use this drug to test if a person is a drug addict -> will precipitate a minor drug withdrawal reaction (precipitated withdrawal)

A

Naloxone (narcotic antagonist)

108
Q

long-term dependence control of narcotic addiction, may also be used to treat alcohol dependence ; MOA - very stron opiod receptor antagonist -> if a pt decides to inject heroin, no “high” feeling ; ADRs - contraindicated if failed Naloxone challenge, acute hepatitis or liver failure

A

Naltrexone (narcotic antagonist)

109
Q

shorter lasting because esterases throughout the body will metabolize them ; dissociation constant (pKa) is crucial to know how fast the drug will work ; ADRs - antihistaminic, anticholinergic and antiarrhythmic effects, harder to reverse with long acting anesthetics, these develope mostly when inadvertent injection into vessel, in the CNS - tremors, convulsions, CNS depression, headache ; Interactions - increase effects of neuromuscular blocking agents, quinidine, propranolol, phenytoin ; NOTE - if pt is taking a cholinesterase inhibitor the local anesthesia is increased

A

Ester-type local anesthetics

110
Q

longerlasting because they must be metabolized by the liver ; dissociation constant (pKa) is crucial to know how fast the drug will work ; ADRs - antihistaminic, anticholinergic and antiarrhythmic effects, harder to reverse with long acting anesthetics, these develope mostly when inadvertent injection into vessel, in the CNS - tremors, convulsions, CNS depression, headache ; Interactions - increase effects of neuromuscular blocking agents, quinidine, propranolol, phenytoin

A

Amide-type local anesthetics

111
Q

is applied to local anesthetics - load cell membrane and disrupt membrane integrity ; theory that adsorption of anesthetics into membranes alters the membrane function to produce anesthesia.

A

Membrane expansion theory

112
Q

charged form of anesthetic binds in or near the Na+ channel ; theory explains the mechanism of action of almost all local anesthetics. Local anesthetic agents block nerve conduction by inhibiting the voltage-gated sodium channels of the neuronal membrane. On the other hand, the membrane expansion theory explains the action of benzocaine, a local anesthetic that doesn’t have ann amino acid terminus and, therefore, cannot be protonated (i.e., cannot bind electrostatically to the negatively charged group in the sodium channel.

A

Specific receptor theory

113
Q

small nerve fibers are more susceptible to blockade than large fibers ; 1) pain, 2) cold, 3) warm touch, 4) deep pressure, 5) proprioception ; large fibers that are heavily myelinated require the anesthetic to dissociated through the myelin in contrast small non-myelinated fibers dont have this problem ; small fibers also have sodium channels closer

A

Differential blockade

114
Q

Chloroflouroalkanes, Ethyl chloride and Combination ; MOA - rapid/deep cooling of skin surface (-20*C) ; route of administration - spray 2-12 inches above skin ; USE - bruises, contusions, minor sprains, dermabrasion, minor surgery, muscle spasms, myofascial pain, restricted motion, sports injuries ; ADRs - hypersensitization of tissue, altered pigmentation, reduced resistance to local infection, slow rate of healing, thawing of tissue is often painful ; NOTE ETHYL CHLORIDE - If inhaled, NEPHROTOXIC, HEPATOTOXIC, narcosis, general anesthesia, coma, respiratory arrest, cardiac arrest ; Contraindicated in pts with known hypersensitivity and vascular impairments of extremities ;

A

Vapocoolant Local Anesthetic

115
Q

used in the treatment of persistent, chroninc - intractable pain - to permanently destroy the pain pathway by destroying axons and dendrites ; must try to block C fibers and to a lesser degree A-delta fibers and B fibers ; TARGET injections to the peripheral nerve, spinal posterior root, sympathetic chain, sympathetic ganglia/plexi ; ADRs - cardiovascular and systemic when absorbed into the bloodstream, local tissue irritation (swelling, cellulitis, abscess, gangrene, sloughing), punctures of other structures (vessels, viscera, dura, pleura)

A

Neurolytic agents

116
Q

repeated or prolonged application -> decreased levels of substance P in spinal cord -> decreased transmission via C-fiver pathway -> decreased pain ; deplete substance P

A

Capsaicin

117
Q

neurolytic ; high concentration injections of - bupivacaine, etidocaine, procaine, chloroprocaine, or mixed with corticosteroieds - may last several months and can keep giving them injections when the pain returns ;

A

High doses of local anesthetics

118
Q

neurolytic ; extraction of cholesterol, phospholipids and cerebrocides - precipitation of lipoproteins, mucoproteins ; kills nerves ; Specific ADRs - neuritis, severe ADHESIONS, if intravascular injection - pleasurable but may thrombose

A

Ethyl alcohol (50-95%) - neurolytic

119
Q

neurolytic ; coagulation of proteins, degeneration of fibers of posterior columns, degeneration of posterior roots, demyelination, wallerian degeneration ; specific ADRs - intravascular injection can cause severe tinnitus and flushing, when absorbed systemically - decreased consciousness, decreased blood pressure, renal damage ; NOTE - it is a CNS stimulant and can cause muscle tremors and convulsions

A

Phenol (1-10%) - neurolytic

120
Q

neurolytic ; intraneural - nerve fibers destroyed ; topical nerve application - localized subperineural damage including inflammatory cells, myelin swelling, axonolysis ; unique treatment for TRIGEMINAL nerve

A

Glycerol (50%) - neurolytic

121
Q

neurolytic ; abolishes C-fiber potentials and produces an acute degenerative neuropathy ;

A

Ammonium salts (10%) - neurolytic

122
Q

tremors, tachycardia, erectile and ejaculatory dysfunction, blockage of the antihypertensive effects of guanethidine and guanadrel, augmentation of pressor effects of sympathomimetic amines

A

What clinical concequences happen when you blockade norepinephrine reuptake at nerve endings?

123
Q

gastrointestinal distrubaces, increases or decrease in anxiety (dose dependent), sexual dysfunction, extrapyramidal side effects, interactions with L-tryptophane, MAOIs, and fenfluramine

A

What clinical concequences happen when you blockade serotonin reuptake at nerve endings?

124
Q

psychomotor activation, antiparkinsonian effect, aggravation of psychosis

A

What clinical concequences happen when you blockade dopamine uptake at nerve endings?

125
Q

potentiation of central depressant drugs, sedation drowsiness, weight gain, hypotension

A

What clinical concequences happen when you blockade H1 receptors?

126
Q

blurred vision, dry mouth, sinus tachycardia, constipation, urinary retention, memory dysfunction,

A

What clinical concequences happen when you blockade muscarinic (cholinergic) receptors?

127
Q

potentiation of the antihypertensive effect of prazosin, terazosin, doxazosin, and labetalol, postural hypotension, dizzines, reflex tachycardia

A

What clinical concequences happen when you blockade alpha-1 adrenergic receptors?

128
Q

extrapyramidal movement disorder, endocrine changes (prolactin increase), sexual dysfunction in males

A

What clinical concequences happen when you blockade D2 receptors?

129
Q

procaine

A

ester-type local anesthetic

130
Q

chloroprocaine

A

ester-type local anesthetic

131
Q

tetracaine

A

ester-type local anesthetic

132
Q

cocaine

A

ester-type local anesthetic

133
Q

benoxinate

A

ester-type local anesthetic

134
Q

benzocaine

A

ester-type local anesthetic

135
Q

butaben

A

ester-type local anesthetic

136
Q

proparacaine

A

ester-type local anesthetic

137
Q

cyclomethycaine

A

ester-type local anesthetic

138
Q

lidocaine

A

amide-type local anesthetic

139
Q

mepivicaine

A

amide-type local anesthetic

140
Q

bupivacaine

A

amide-type local anesthetic

141
Q

etidocaine

A

amide-type local anesthetic

142
Q

prilocaine

A

amide-type local anesthetic

143
Q

dibucaine

A

amide-type local anesthetic

Neurology (6 decks)

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