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Pharmacology 1 > CNS depressant > Flashcards

CNS depressant Flashcards

1
Q

Criteria for Neurotransmitters:

A
  • The suspected neurotransmitter substnce must be present in the nerve terminals (its presence is justifiable by chemical, physiological, and pharmacological methods)
  • The substance must be released on nerve stimulation (its concentration increases in the perfusate of the organ)
  • Exogenous application of the substance must mimic nerve stimulation
  • it is synthesized and stored in neurons
  • it is inactivated and/or eliminated quickly
  • drugs with known effect on enzymes and receptors for the proposed transmitter must affect the nerve-stimulated response in a predictable manner.
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2
Q

Transmitter goups in CNS

A
  • Excitatory amino acids
  • inhibitory amino acids
  • choline esters
  • monoamines
  • neuopeptides
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3
Q

Excitatory amino acids:

  • Transmitter and effect
A
  • Transmitter: Glutamate, aspartate
  • Effect: depolarisation
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4
Q

Inhibitory amino acids

    • Transmitter and effect
A

Transmitter: Glycine, GABA

effect: Hyperpolarisation

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5
Q

Choline Esters:

  • Transmitter and effect
A
  • Transmitter: Ach
  • Effect: (hyper)- or depolarisation
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6
Q

Monoamines:

  • Transmitter and effect
A
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7
Q

Neuopeptides

  • Transmitter and effect
A
  • Transmitter: Enkephalins, endorphins, substance-P, neurokinins
  • Effect: Analgesia, respiratory and circulatory depression, euphoria, dysphoria
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8
Q

Name the Small-Molecule (rapidly acting) NTs:

A
  • Acethylcholine (Ach, Gq)
  • Norepinephrine (NA)
  • Dopamine receptors D1, D5, (Gs), D2, D3, D4 (Gi)
  • 5-Hydroxytryptamine (5-HT) Serotonin
  • Histamine receptors H1 (Gq), H2 (Gs), H3, H4 (Gi)

Excitatory amino acids:

  • Glutamate and aspartate

Inhibitory amino acids:

  • Gamma-aminobutiric acid (GABA)
  • Glycine
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9
Q

Function of Acethylcholine (Ach) (Gq):

A
  • Widely distributed throughout the CNS
  • Effect: binding to M1 receptors closes the K+-, Ca2+-, Cl- -ionchannels.
  • depending on the cell type it leades either to depolarization or hyperpolarization.
  • inactivates via hydrolysis (Ach-esterase)
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10
Q

Function of Norepinephrine:

A
  • distribution in CNS uneven (locus coeruleus, reticular formation)
  • receptors a (a1 - Gq, a2 - Gi) and B (Gs)
  • a2 presynaptic, important in control of sleep and wakefulness, modd and emotional behaviour, temperature.
  • in elimination both metabolism and reuptake are important
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11
Q

Function of Dopamine

A
  • Receptors D1, D6 (Gs), D2, D3, D4 (Gi)
  • Major NT, precursor of NA. Has primarily an inhibitory effect
  • Largest concentrations are in the basal ganglia and the limbic system.
  • is linked to the fine control of movement, to disturbances of behaviour, to the hypothalic-pituitary functions.
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12
Q

Function of 5-Hydroxytryptamine (5-HT) Serotonin

A
  • serotonin has 7 receptor subtypes
  • it has a strong inhibitory effect, hyperpolarization by increase in K+ and Na+ conductance (5-HT3 ligand gated receptor)
  • it inhibits pain pathways in the spinal cord, helps in control of behavioural mood
  • proposed regulatory functions are: sleep and wakefulness, mood and emotion, temperature, appetite, enuroendocrine control.
  • it inhibits the release of the other NT
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13
Q

Function of Histamine:

A
  • Receptors H1 (Gq), H2 (Gs), H3, H4 (Gi)
  • mainly in posterior Hypothalamus. receptors are H1, H2, H3
  • Involved in the regulation of arousal, temperature and vascular dinamics
  • decreases ACh, 5-HT, NA release (H3)
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14
Q

Function of Glutamate and Aspartate:

A

(Excitatory amino acids)

  • occur in uniquely high concentration in brain
  • they are principal excitatory transmitters, acting by mainly permission of ion (eg Ca2+, NMDA-r) transport
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15
Q

Function of Gamma-aminobutiric acid (GABA):

A

(inhibitory amino acids)

  • major inhibitory NT
  • widely distributed in CNS. Highest concentration in basal ganglia, hippocampus, cerebellum, spinal cord
  • GABAa (is a ligand gated Cl-ion channel) and GABAb receptor types, they facilitate Cl - or K+ -ion transport
  • GABAb Gi-type receptor
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16
Q

Function of Glycine

A

(inhibitory amino acids)

  • inhibits transmission between spinal interneurons and motor neurons.
  • action is restricted to the spinal cord
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17
Q

The major purposes of the applications of drugs acting on CNS:

A
  • increasing the well-being of animals
  • alteration of behaviour
  • improvement of animal-human interaction
  • induction sleep
  • induction anaesthesia
  • induction arousal
  • prevention seizures
  • identification the site and mechanism of action of different compounds
  • CNS-action as unwanted side-effects (eg. seizures caused by local anaesthetics)
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18
Q

Classification of CNS stimulatons based on their site of action:

A
  • Cortical: Xanthines (coffeine, teophylline, theobromine), cocaine, ephedrine, amphetamines, psychotomimetics (eg. LSD)
  • Medullar: Xanthines (coffeine, teophylline, theobromine), pentetrazole, doapram, picrotoxin
  • Spinal: strychnine
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19
Q

Convulsants and respiratory stimulants (analeptics):

  • example, mode of action, clinical significance
A
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20
Q

Psychotomimetic drugs (hallucinogens):

  • Examples, mode of action, clinical significance
A
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21
Q

Psychomotor stimulants:

  • Examples, mode of action, clinical significance
A
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22
Q

The different identifiable actions of Caffeine in vitro:

A

In ascending order of dose response (from most sensitive to least sensitive)

  1. Adenosine receptor blockade
  2. Phosphodiesterase inhibition:
    - this enzyme is resposible for the breakdown of cAMP and therefore this action of the methylxanthines leads to increased xAMP 2nd messenger functions
  3. Action of Ca2+ channels to increase entry of Ca2+ into cells, and to decrease sarcolemma sequestration of Ca2+.
    - this may be related to the weak positive inotropic effect at high dose rates (together with increased cAMP)
  4. Binding to GABA receptors at the benzodiazepine site (query clinical relevance because of high KD)
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23
Q

Caffeine action on Adenosine receptors:

A
  • Caffeine potentially has pharmacological actions other than blockage of adenosine receptors, but it requires 20 times as much caffeine to inhibit phosphodiesterase, 40 times as much caffeine to block GABAA receptors and 100 times as much caffeine to mobilize intracellular calcium as is required to block adenosine receptors.
  • caffeine acts primarily by the deirect action of blocking adenosine receptors and by the indirect action upon the receptors for neurotransmitters.
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24
Q

Caffeine vs. Adenosine:

A
  • Adenosine stimulates and caffeine blocks all classes of adenosine receptors nonselectively (antagonist)
  • the general effect of adenosine in the brain is to inhibit neural activity, whereas the general effect og caffeine is to increase neural activity
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25
Q

Functions of Caffeine:

A
  • Caffeine´s antagonism of adenosine (action on A2a receptors in the globus pallidus) decreases release of the inhibitory neurotransmitter GABA
  • Caffeine can neutralize the effects of benzodiazepine tranquilizers. Benzodiazepines act by enhancing the effect og GABA and GABAa receptors, whereas caffeine has an opposite effect bu inhibiting GABA release
  • Like other methylxanthines, caffeine at high dosage may be associated with positive ionotropic and chronotropic effects of the heart
  • caffeine may also produce an increase in systemic vascular resistance, resulting in elevation of blood pressure
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26
Q

Adenosine A2a receptors are prominet in?

A
  • the endothelial cells, resulting in the vasodilation effect og adenosine (and the vasoconstrictive effect og caffeine on cerebral blood vessels)
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27
Q

Therapy with products containin caffeine (methylxanthines):

A
  • should be administered cautiously in patients with severe cardiac disease, hypertension, hyperthyroidism, or acute myocardial injury.
  • recommended to avoid caffeine in patients with symptomatic cardiac arrhytmias
  • methylxanthines are known to stimulate peptic acid secretion. And therefore should be used with caution in patients with active peptic ulcer disease.
28
Q

Methylxanthines:

A
29
Q

Analeptics classification:

A
  1. Central analeptics:
    - Methylcanthins, pentetrazole Ø, picrotoxin (ivermectin, barbiturate antidote), strychnine O.
  2. Peripheral analeptics:
    - Cropropramide:crotetamide = prethcamid, lobelin
  3. Mixed analeptics:
    - doxapram, nicetamid, carbon-dioxide, camphor
30
Q

Convulsants and respiratory stimulants:

A

This is a diverse gropu of drugs that have little clinical use, although several are useful as experimental tools

  • certain short-acting respiratory stimulants (eg. doxapram) can be used in acute respiratory failure
  • Strychnine is a convulsant poison that acts ainly on the spinal cord by blocking receptors for the inhibitory transmitter glycine
  • Picrotoxin actsa as GABAa antagonist, picrotoxin appears to block the ion channel.
31
Q

CNS depressants, general considerations:

A
  1. the nature of effects (stimulation, inhibition)
    - CNS stimulants: stimulation –> inhibition
    - CNS depressants: analgesia <– increase of pain (doses)
    - CNS depressants: inhibition - excitation ay occur
  2. the site of action
    - general anaesthetics <–> central muscle relaxants
  3. the selectivity of effect
    - non-selective depressants (general anaesthetics)
    - selective depressants (tranquilliser, anticonvulsive drugs, but selectivity is relative!)
  4. the mode of action
    - GABA, glycin <–> aspartate, glutamate
32
Q

types of CNS depressants:

A
  • tranquilliser sedatives (neuroleptics)
  • hypnosedatives (classical sedatives, anxiolytics)
  • analgesics (Major: narcotic analgesics. Minor: NSAIDS analgesics)
  • general anaesthetics: inhalation, injectable, dissociative
  • (neurolaptanalgesic)
  • anticonvulsants (antipileptics)
  • central muscle relaxants (myorelaxantia centralia)
33
Q

Tranquillisers:

A
  1. Phenothiazine derivatives:
    - propiopromazine (Combelen)
    - Acepromazine (vetranquil, atrovet)
    - chloropromazine (hibernal)
    - prometazine (pipolphen)
  2. Butyrophenones:
    - azaperone (stresnil)
    - (haloperidol, droperidol, fluanisone)
  3. (Rauwolfia alkaloids - reserpine)
34
Q

Hypnosedatives:

A
  1. Alpha A2- agonist:
    - Xylazine (rompun, rometar, xylavet)
    - medetomidine, dexmedetomidine (domitor, dexdomitor)
    - romifidne (sedivet) detomidine (domosedan)
    - anxiolytics (minor tranquillisers)
  2. Benzodiazepines:
    - diazepam (seduxen)
    - chlorodiazepoxide (elenium)
  3. Propandiol - derivatives
    - meprobamate
  4. other compounds:
    - barbiturates (long acting)
    - alcohols, aldehydes, Br- - and Mg2+ salts
35
Q

Psychotherapeutic drugs, psychotropic drugs:

A

Those compounds that influence behaviour, mood and emotional reactions.

  • Anxiolytic drugs, sedative-hypnotic drugs
  • antipsychotic drugs (neuroleptics)
  • antidepressant drugs
36
Q

Tranquillisers: Phenothiazine derivatives receptoral effects:

A
  1. Dopaminergic receptor - (D2)- antagonistic:
    - antipsychotic effect, antiemetic effect, increased prolactin
    - parkinson-syndrome
  2. a-adrenoceptor - antagonistic:
    - hypotension, sedation (?)
  3. muscarinic receptor - antagonistic:
    - mainly side effects
  4. H1-receptor - antagonistic:
    - sedation, antiemetic effects etc.
  5. 5HT-receptor- antagonistic
    - enhancement of several effects.
37
Q

Tranquillisers - Phenothiazine derivatives pharmacological effects:

A
  • potentiation (sedatives, hypnotics, analgesics)
  • vegeative tone decreased, with increased relative parasympathetic tone
  • circulation
  • central antiemetic effect
  • regulation of body temperature
38
Q

Tranquillisers: uses of Phenothiazines

A
  • Calming, sedation (vicious, aggressive animals), to alleviate handling during veterinary investigations.
  • muscle relaxation (no analgesia)
  • premedication before general anaesthesia (neuroleptanalgesia)
  • important: all drugs in this group have similar efficacy, they cary in potency and side effects.
  • PK: slow onset (even after IV.)
  • Poor oral absorption (F=0.2) (plasma protein binding approx. 95%)
  • metabolism in liver, excretion via urine.
  • slow elimination from the body (long withdrawal period)
39
Q

Tranquillisers: side effects-contraindication of Phenothiazines

A
  • Hypotension –> collapse
  • tissue irritation, allergy (liver injury), in horses excitation
  • penile proplase (horses) and thir eyelid prolapse (pets)
  • Prolactin increase, FSH, LH decrease, ADH and oxytocin
  • epilepsy, extrapyramidal symptoms (high dose) (tremors, shivering, rigidity)
  • bulldogs, boxers are sensitive
40
Q

Tranquillisers: dosage of Phenothiazines

A
  • IV, IM or PO in a range of 0.05-5 mg/kg
  • do not use before transportation to abattoir (metabolites)
41
Q

Tranquillisers: side effects - contraindications of Phenothiazines derivatives

A
  1. Chlorpromazine:
    - side effects - frequently
    - paradox reaction in horses (cyclic ataxic reaction with excitation - hypotension and tachycardia), tissue irritation, allergy
  2. Propiopromazine:
    - more reliable, less side effects
  3. Acepromazine:
    - more efficacious than chlorpromazine, less side effects
    - good oral bioavailablity
    - halothan hypertheria and arrythmogenicity decrease
  4. Prometazine:
    - less potent tranquillizer, increased antihitaminic and anti-5-HT effect
42
Q

Tranquillisers: Butirophenones

A
  • more potent than Phenothiazines (some analgesic effect)

In CNS:

  • Dopamine inhibition (D2), NA-inhibition, Anticholinergic effect.
  • (with weaker antagonistic effect on a1-, H1-receptors)
  • Droperidol, Haloperidol, Fluanisone, Azaperone (only in swine)
43
Q

Tranquillisers: side effects - contraindications of Butirophenones

A
  • transient salvation or panting
  • hypotension, respiratory stim., boar penile prolapse
  • avoid use in very cold condition

( but can reduse hyperthermia caused by Halothane)

44
Q

The most characteristic effects of Sedative-hypnotics:

A
  • sedative effect
  • anxyolytic effect
  • hypnotic effect (hypnotic effect = drugs induce sleep. Hypnogen drugs = to maintain sleep)
  • muscle relaxation
  • anticonvulsive (exception a2-agonist)
45
Q

Alpha2-agonists:

A
  • clonidine
  • xylazine (rompun, rometar, xylavet)
  • detomidine (domosedan)
  • medetomidie (domitor)
  • dexmedetomidine (dexdomitor)
  • romifidine (sedivet)
46
Q

Alpha2-agonists:

  • Postsynaptic and presynaptic receptors and effects:
A
47
Q

Alpha2-agonists:

  • Pharmacological effects
A
  • Sedative: locus coeruleus
  • Analgesic: spinal cord
  • reduced motor activity: spinal cord
  • further effects: relaxation of GI smooth muscle, mydriasis, bulbar tension decrease, ACTH secretion increase, insulin-, renin-, ADH- decrease, hyperglycaemia, microsomal enzyme decrease.
48
Q

Alpha2-agonists pharmacological effects:

  • Activation of postsynaptic receptors
A

(a2 and a1 due to poor specificity)

  • vasoconstriction
  • transient hypertension
  • activation of baroreceptor
  • vagallymediated bradykardia
49
Q

Alpha2-agonists pharmacological effects:

  • Activation of presynaptic a2-receptors
A

Inhibits the release of NA

  • suppressed vasomotor tone:hypotension
  • analgesia and sedation
  • reduced motor activity -> recumbency
  • vagal bradycardia (direct central action)
50
Q

Alpha2-agonists pharmacological effects:

  • further effects due to activation of a2-receptors
A
  • GI smooth muscle relaxation

mydriasis, intraocular pressure decrease

  • salivation decrease
  • release of insulin-, renin-, ADH- decrease
  • ACTH increase
51
Q

Side effects of Alpha2-adrenoceptor

  • dogs/cats, cattle, horse
A
52
Q

Pharmacokintics of a2-agonist:

A
53
Q

Alpha2-agonist:

  • Xylaxine usage, side effects, dose
A

sedative-analgesic drug with depressed motor activity can be used in all domestic animals.

Side-effects:

  • emesis and vomiting in cats and dogs
  • bradykardia, malignant arrhytmias
  • sweating in horses
  • ecbolicaction: in late pregnancy its use is contraindicated

Dose:

  • horse: 2-3 mg/kg IM, 0.5-1.0 mg/kg IV
  • cattle: 0.05-0.2 mg/kg IM
  • dog: 1-2 mg/kg IM
  • cat: 3 mg/kg IM
54
Q

Alpha2-agonist:

  • Detomidine usage, side effects, dose
A

More poteint than xylazine, licensed for equine ise. does not cause loss of consciousness. duration of action is dose dependant

side effects:

  • hypertension, then hypotension
  • bradycardia, respiratory depression, duiresis (microturation)
  • hypothermia, sweating, snoring, tremor

Use:

  • alone or in combination with ketamine, thipentone or opioid drugs
    dosage: 10-80 ug/kg IM or IV. 40 ug/kg PO
55
Q

Alpha2-agonist:

  • Medetomidine and Dexmedetomidine usage, side effects, dose
A
  • effects are similar to those of Xylazine, but it seems to be more reliable and sager.
  • developed for cats and dogs
  • duration of action is dose dependent. (sedation 1-3 hours, DM 2hours. Analgesia 5-15 min, DM 90min)

Dose:

  • M dogs: 10-80 ug/kg alone IM, or IV 10-20 ug/kg combination
  • cats: 50-150 ug/kg IM

DM:

  • dogs and cats 375 ug/m2 IV, 500 IM ug/m2
  • (cats only IM) premedication 123-375 ug/m2
  • Dog 125 ug/m2 PO

Body Surface Area: BSA = KgBW0.67/10^2

  • Km = 10.4 in cats, 10.1 in dogs
56
Q

Alpha2-agonist:

  • Romfidineromifidine usage, side effects, dose
A

Dosage:

  • 40-120 ug/kg IV, IM horse, dog, 200-400 cat

onset:

  • 2-4min IV, 10-20 min IM

Duration:

  • sedation a bit longer and causes less ataxia or recumbency than Xylazine and Detomidien
57
Q

Alpha2-agonist:

  • Antipamezole usage, side effects, dose
A

Antipamezole = antisedan

  • alpha2-adrenoreceptor blocking agent
  • reverse the effect og medetomidine (and other a2-agonists too)

Side effects: (weell tolerated by dogs and cats)

  • tachycardia (high dose) transient hypotension, hypothermia, vomitting, defecation, panting, muscle tremor
  • contraindication: ketamin-medetomidine

Dose:

  • horse 150 ug/kg
  • dogs 5 times, cats 2.5 times the dose of medetomidin
58
Q

Alpha2-agonist:

  • Yohimbine and Telazoline usage
A
  • much less specific a2-adenoreceptor antagonist than atipamezole, and so has significant a1-antagonistic action
  • reverse the effect og xylazine
  • yohimbine is mainly used in conjugation with fampridine which facilitate the relase of neurotransittters from nerve endings.
59
Q

Benzodiazepines:

A
  • Receptoral ation: they facilitate or amplify the inhibitory activity of GABA, possibly by eliciting a structural alteration in the GABA-receptor complex, which results in the opening of chloride ion channels (Postivie Allosteric Modulators)
  • BZD-receptors are located in all levels of CNS (and in muscle)

Effects:

  • sedation and anxiolytic effect
  • anticonvulsive effect, muscle relaxation
  • hypnotic (some at high dose)

Antidote:

  • Flumazenil and Sarmazenil - in case of overdose of certain BDZs,
  • dose 100 ug/yykg IV and 40 ug/ttkg (horses) IV q24h
60
Q

Diazepam:

  • pharmaxokinetics, clinical use
A

pharmacokinetics:

  • oral absorption good, IM delayed
  • signifiant binding to plasma proteins
  • excretion: after demehylation and conjugation via the kidney

Clinical use:

  • premedication and combincation (ketamine)
  • muscle relaxation
  • prevention and control of epilepsy
  • sedation (tamin during grouping of animals)
61
Q

Diazepam:

  • interaction and contraindication, dosage
A

Interaction and contrainication:

  • paradoxical reacion (cat, greyhound)
  • aminoglycosides (inhibition of respiration)
  • before and during delivery
  • liver disease

Dose:

  • sedation: 1-1.5 mg(kg PO
  • pre medication: 0.2 mg/kg IV
  • statis epilepticus: 5-10 mg/kg IV (then 2-5mg /hour IV)
62
Q

Midazolam

A
  • shorter effect, produce less sedation than diazepam

Dosage:

  • horses: 0.05-0.2 mg/kg IV
  • dogs, cats: 0.1-0.5 mg/kg IV, 0.3-1 IM
63
Q

Anxiolytic drugs:

A
64
Q

Comparison of hypno-sedatives (H-S) and Tranquillisers (TR):

A
65
Q
A

Pharmacology 1 (12 decks)

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