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HLTH 2511 > Module D > Flashcards

Module D Flashcards

1
Q

Signalling in the CNS is ________ (electrical / chemical / both)

A

Both

neurotransmitters and neuromodulators act at synapses, but there is also direct voltage signalling at electrotonic gap junctions

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2
Q

Most neurotransmitters are ________ (inhibitory / excitatory / either) with the exception of ______, which is only inhibitory

A

either, GABA

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3
Q

The only purely inhibitory CNS neurotransmitter is ________

A

GABA

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4
Q

Excitatory effects promote:

A

release of NTs from the neruronal terminal

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5
Q

inhibitory effects cause _________ and inhibit release of _________

A

hyperpolarization, neurotransmitters

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6
Q

Fast NTs act on what kind of receptors?

A

ligand-gated ion channels

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7
Q

Slow NTs act on which kinds of receptors

A

GPCRs

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8
Q

GABA is a _____ (fast / slow) NT

A

Fast

it acts on ligand-gated ion chanels

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9
Q

CNS agents act in the following 4 ways:

A
  1. Altering synthesis, storage, or release of an NT
  2. Inhibiting reuptake of an NT
  3. Inhibiting degredation of an NT
  4. Activating or blocking the receptor
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10
Q

receptors respond to long-term drug treatments by which two processes?

A
  • sensitization (up-regulation)
  • desentization/tolerance (down-regulation)
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11
Q

Delirium is a disorder of ________, as seen in _________

A

cognitive processing, schizophrenia

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12
Q

Dementia is a disorder of _________, as seen in __________ and ________

A

memory, alzheimers and parkinson

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13
Q

emotional disorders arise from the ________ system

A

limbic

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14
Q

Three classes of drugs used in the management of delirium are:

A
  • antipsychotics
  • CNS stimulants
  • Sedative-hypnotics
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15
Q

Sedative-hypnotic drugs tend to have dose-dependent effects, first causing ________ and then ________

A

sedation/anxiolysis first, and then hypnosis (drowsiness, then sleep)

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16
Q

contrast the common anxiety disorders and their common pharmacological treatments

A
  • Acute Anxiety: self-limiting acute arousal, may be treated with benzodiazepines
  • Panic Disorder: recurrent, acute periods of anxiety with marked psychological and physiological manifestations. May be treated acutely with benzodiazepines and chronically with an SSRI
  • Phobic Disorders: panic diorder with specific triggers. managment is similar to panic disorder, but performance anxiety may be managed with a beta-blocker like propranolol
  • OCD: marked by compulsions, best treated with an antidepressant
  • Generalized anxiety disorder: chronic worry and apprehension, best managed acutely with benzodiazepines and chronically with an SSRI
  • PTSD: similar treatment to panic disorder, GAD, etc.
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17
Q

Generally, treatment for anxiety disorder involves:

A

treatment of acute episodes with a benzodiazepine and chronic managment with an SSRI antidepressent.

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18
Q

There are ___ stages of sleep which tend to occur in ___ minute cycles in healthy individuals. The REM stage is stage ___ and is critical for stable emotional status

A

5, 90, 5

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19
Q

The clinical term for difficulty falling asleep is

A

sleep latency

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20
Q

Benzodiazepines and antidepressants may decrease sleep latency, but have the adverse effect of:

A

changing sleep architecture, reducing REM sleep, and causing emotional disturbance

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21
Q

The advantage of modern sleep agents like sublinox (zolpidem) is:

A

they have a minimal effect on sleep architecture

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22
Q

A disadvantage of all sleep agents is that they may cause:

A

tolerance and dependence

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23
Q

Compare and contrast physical and psychological dependence

A

both manifest as continued seeking of exposure to a drug. Physical dependence is continued use to avoid unpleasant physical withdrawal symptoms. Psychological dependence is continued use to receive the pleasurable effects of the drug or escape reality

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24
Q

Sedative drugs are also called:

A

anxiolytics

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25
Q

The main advantage of benzodiazepines over other sedative-hypnotics is

A

very broad therapeutic index

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26
Q

Explain why some patients taking benzodiazepines may experience increased sedation after a high-fat meal

A

this is due to enterohepatic cycling (active metabolites are reabsorbed from the gut after biliary excretion)

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27
Q

Describe the MOA of benzodiazepine drugs

A
  • bind to an allosteric site on the GABA-gated chloride channel receptor, increasing GABA activity
  • this increases duration and frequency of opening of the chloride channel
  • cause post-synaptic hyper-polarization (puts on the brakes)
  • also inhibit neuronal reuptake of adenosine
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28
Q

Benzodiazepines _____ (can / can not) produce sedation sufficient for general anesthesia

A

can not!

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29
Q

Most BZ drugs are metabolized by the liver to produce _________ and are therefore classified as _________

A

active metabolites, prodrugs

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30
Q

Benzodiazepines have a ________ (fast / slow / etc.) onset

A

fast or very fast

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31
Q

A benefit of BZs like midazolam is that they prodruce __________, limiting unpleasant memories of procedures

A

anterograde amnesia

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32
Q

Five pharmacological effects of BZ drugs are:

A
  • anxiolyis (sedation)
  • amnesia (anterograde)
  • hypnosis
  • skeletal muscle relaxation
  • anticonvulsant
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33
Q

Whereas _________ sedative-hypnotics have a strong ceiling effect, ____________ do not

A

benzodiazepine, barbiturates

this is due to the dependence of BZs on already-existing GABA for their MOA

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34
Q

List advantages and disadvantages of BZ drugs

A

Advantages: Little respiratory/cardiac depression, large therapeutic index, very dose-dependent response (can produce sedation without hypnosis)

Disadvantages: Cause physical and cognitive impairment, rebound effect if discontinued suddenly, physical dependence which may result in delirium

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35
Q

Valium (Diazepam)

A
  • Benzodiazepine, sedative-hypnotic
  • Lipid-soluble GABA agonist, causes CNS depression due to potentiation of GABA receptors and post-synaptic hyperpolarization
  • Fast onset with long duration of action
  • Dose dependent effects with ceiling effect: at low doses sedation only, at higher doses hypnosis and anterograde amnesia
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36
Q

Ativan (Lorazepam)

A
  • Benzodiazepine, sedative-hypnotic
  • Lipid-soluble GABA agonist, causes CNS depression due to potentiation of GABA receptors and post-synaptic hyperpolarization
  • Fast onset with medium duration of action and no active metabolites
  • Dose dependent effects with ceiling effect: at low doses sedation only, at higher doses hypnosis and anterograde amnesia
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37
Q

Versed (Midazolam)

A
  • Benzodiazepine, sedative-hypnotic
  • Lipid-soluble GABA agonist, causes CNS depression due to potentiation of GABA receptors and post-synaptic hyperpolarization
  • Fast onset with short duration of action, generally only given IV (or IM)
  • Dose dependent effects with ceiling effect: at low doses sedation only, at higher doses hypnosis and anterograde amnesia
  • used in acute settings for induction of anaesthesia, termination of seizures, and delirium
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38
Q

Barbiturates are recognized by their names ending in ____

A

-tal

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39
Q

Anexate (Flumazenil)

A
  • Benzodiazepine antagonist, reversal agent
  • Competitive BZ receptor antagonist
  • used to reverse BZ overdose and BZ sedation
  • short half-life (7-15 minutes) with unpredictable effects that may potentiate seizures. Rarely indicated due to low mortality with benzo overdose
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40
Q

Briefly describe the MOA of barbiturates and explain why they do not demonstrate a ceiling effect

A
  • Bind to an allosteric site on the GABA-gated chloride gate (different from BZ site) which increases GABA affinity
  • unlike BZs, also increases chloride gate activity in absence of GABA, explaining the lack of a ceiling effect
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41
Q

Explain some disadvantages of barbiturates

A
  • high risk of physical dependency (unpleasant withdrawal)
  • low therapeutic index
  • less dose-dependent, cause simultaneous sedation, anxiolysis, and hypnosis
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42
Q

describe benefits of modern sedative-hypnotics used for non-acute insomnia (zopiclone, zaleplon, eszoplicone) vs BZs

A
  • less effect on sleep archtecture (protection of REM sleep)
  • lower risk of dependence/tolerance
  • shorter duration of action for less daytime effects
43
Q

Imovane (Zopiclone)

A
  • non-BZ sedative-hypnotic
  • used in management of sleep disorders
  • increases GABA activity in CNS
  • less tolerance and dependence forming than the BZ drugs
  • preserves sleep architecture
44
Q

Sublinox (Zolpidem)

A
  • non-BZ sedative-hypnotic
  • used in management of sleep disorders
  • increases GABA activity in CNS
  • less tolerance and dependence forming than the BZ drugs
  • preserves sleep architecture, less effect on next-day cognitive performance and coordination
45
Q

Sotacor (Zaleplon)

A
  • non-BZ sedative-hypnotic
  • used in management of sleep disorders
  • increases GABA activity in CNS
  • less tolerance and dependence forming than the BZ drugs
  • preserves sleep architecture
46
Q

Noctec (Chloral hydrate)

A
  • Non-BZ sedative hypnotic
  • given as a prodrug
  • generally only given as preanesthetic sedation in pediatric patients
47
Q

Precidex (Dexmetetomidine)

A
  • alpha-2 agonist
  • used in treatment of hypertension and for sedation in anaesthetized/intubated patients in an ICU setting
  • used due to lack of respiratory depression
48
Q

contrast analgesia and anaesthesia

A

analgesia is the blockage or reduction of only pain sensation. Anaesthesia is the blockage of all sensation

49
Q

The two major classes of local anaesthetics and the prototype drugs of each are:

A

Ester-type (procaine/cocaine) and Amide-type (lidocaine)

50
Q

Describe the MOA of local anaesthetics

A

they bind to sodium channels and prolong the inactivated state, reducing excitability.

51
Q

Describe the methods of administration of local anaesthetics

A

Topical: may reduce pruritis or pain of IV placement. May be given as a eutectic mixture of agents

Infiltration: most common, injected into SC tissue. Duration depends on local blood flow (slow flow prolongs duration) so sometimes given with epinephrine (but never at terminal arterioles in digits)

Iontophoreis: delivery using small electric current, mainly in dentistry

Nerve block and field block

Intrathecal and epidural

52
Q

Describe the effects of size-dependent and use-dependent blockade in local anaesthetics

A

Local anaesthetics have greatest effect on small, unmyelinated fibres (size-dependent) and on fibres that are actively firing frequently (use-dependent).

53
Q

Xylocaine (Lidocaine)

A
  • Amide-type local anaesthetic
  • sodium channel blocker that produces use-dpendent and size-dependent blockade
  • may be given with epi to induce vasoconstriction and prolong duration of action
  • relatively strong local anaesthetic effect
54
Q

Cocaine

A
  • Ester-type local anaesthetic
  • Sodium channel blocker
  • causes local vasoconstriction, prolonging duration of action
  • relatively weak anaesthetic effect and high risk of abuse, so rarely used
55
Q

Adverse effects of local aneasthetics include:

A
  • CNS effects (stimulation, then inhibition)
  • Cardiovascular effects (hypotension and arrhythmogenesis)
  • NMBA potentiation
  • Allergic reactions (especially ester-type)
56
Q

The 4 stages of general anaesthesia are:

A
  1. Analgesia and conscious sedation
  2. Paradoxical excitation (not commonly seen with modern, balanced anaesthesia)
  3. Surgical anaesthesia (desired state)
  4. Vasomotor and respiratory depression with cardiovascular collapse (not desired!)
57
Q

Factors that effect the rate of induction when using inhalational anaesthetics are: (list 4)

A
  1. Solubility of the gas
  2. Alveolar partial pressure of the anaesthetic
  3. Pulmonary ventilation
  4. Pulmonary blood flow
58
Q

Inhalational anaesthetics with _______ (high / low) blood:gas partition coefficient will have a rapid onset

A

Low

gasses with a high BG partition require high concentrations to achieve saturation of blood proteins and exist as free gas at tissue beds

59
Q

Decribe the MOA of inhalational anaesthetics

A

the free gas form of these drugs binds to GABA receptors and increases chloride influx, leading to cell hyperpolarization

60
Q

inhalational anaesthetics with a _________ (high / low) oil:gas partition coefficient have the highest efficacy

A

high

61
Q

give examples of halogenated and non-halogenated inhalational anaesthetics

A

halogenated: Halothane, desflurane, isoflurane, sevoflurane

non-halogenated: nitrous oxide

62
Q

describe why sevoflurane is considered a near-ideal inhalational anaesthetic

A
  • it has a relatively low blood:gas partition coefficient and high oil:gas partition coefficient leading to rapid induction and high efficacy
  • it provides smooth induction and emergence
  • it has very little CV or other toxicity
63
Q

A rare but important adverse effect of inhaled halogenated anaesthetics is:

A

malignant hyperthermia

64
Q

explain why inhalational anaesthetics should be used with caution in patients with low cardiac output

A

these patients may have pulmonary arterial hypertension which will increase pulmonary bloodflow and potentiate the rate and depth of induction

65
Q

the value used to measure the potency of inhalational anaesthetics is the:

A

minimum alveolar concentration

this is the partial pressure in the lungs required to produce desired anaesthesia in 50% of patients

66
Q

The inhalational anaesthetic which provides the most potent analgesia is:

A

nitrous oxide

67
Q

All halogenated anaesthetics cause _______ (CP effects)

A

cardiovascular and respiratory depression (decreased cardiac ouput, decreased resp rate and tidal volume)

68
Q

What are three advantages of parenteral (IV) anaesthetics over inhalational ones?

A
  • they have a rapid onset
  • they do not require specialized equipment
  • they have fast recovery/emergence rates

Fast on, fast off, and easy

69
Q

Outline popular parenteral anaesthetic agents

A

Benzodiazepines: especially midazolam, used as a sedative-hypnotic for premedication and during surgical procedures. Amnesic properties useful

Opioids: especially Fentanyl, for analgesia and combined with sedatives to provide general anaesthesia without CV depression

Propofol: Rapid on, rapid off sedation and amnesia which reduces ICP and BP. Ideal for head injury, caution in hypotension.

Etomidate: Rapid induction with minimal CV effects, but causes long term inhibition of steroid synthesis so only useful in acute setting (RSI)

Ketamine: Rapid induction, strong analgesia, minimal CV effects, but unpleasant emergence. Useful in children since emergence effects are less pronounced

70
Q

Diprivan (Propofol)

A
  • Parenteral, non-opioid anaesthetic
  • Cause GABA potentiation (similar to BZs) to produce sedation and anaesthesia
  • generally used to induce anaesthesia which is maintained by an inhalational anaesthetic, except in short, minor procedures. (20s onset, 5-10 min duration)
  • Reduces ICP and BP, so near ideal for head injury management
  • prolonged use potentiates cardiovascular depression
71
Q

Amidate (Etomidate)

A
  • Parenteral anaesthetic
  • Acts on GABA receptors to produce anaesthesia/sedation
  • Rapid onset and very few cardiovascular side effects, so ideal for hyperacute situations
  • used in RSI and conscious sedation
  • Prolonged use inhibits steroid synthesis
72
Q

Ketamar (Ketamine)

A
  • Non-opioid parenteral anaesthetic, sedative, dissociative
  • Blocks excitatory NTs at NMDA receptors. Produces dissociative anaesthesia
  • Anaesthesia characterized by analgesia, reduced sensory perception, incomplete loss of consciousness, immobility, and amnesia
  • Causes increased BP and no respiratory depression (great for trauma)
  • produces unpleasent emergence including hallucinations and delirium; less common in pediatric patients!
73
Q

Typical and atypical antipsychotics are also known as _________ and are differentiated based on _________

A

first and second generation anipsychotics; differentiated based on D2 to 5-HT2 receptor specificity (second-generation have greater 5-HT2 specificity)

74
Q

Common drug name endings for atypical (2nd gen) antipsychotics are:

A
  • -Pine (Clozapine, Olanzapine, Quetiapine)
  • -Idone (Respiridone, Paliperidone)
  • Apripirazole (gets its own darn name!)

The schizoprenic pt, afraid his penis had disappeared, shouted “help, my ole peen is done!” for -ole, -pine, -idone.

75
Q

The advantages of 2nd generation antipsychotics are:

A

effective in management of positive symptoms (hallucinations, delusions, agitation) with fewer extrapyramidal symptoms (EPSs) and less exacerbation of negative symptoms (social withdrawal, anhedonia)

76
Q

Long term treatment with antiphsychotics may lead to __________, an irreversible disorder of movement that includes involuntary repetitive movements of the perioral and ocular muscles

A

tardive dyskinesia

77
Q

the ________ hypothesis is an attempt to explain the underlying cause of schizophrenia and states:

A

dopamine; schizophrenia is caused by imbalances in dopamine trasnmission in the mesolimbic and mesocortical pathways.

78
Q

Haldol (Haloperidol)

A
  • first generation, typical antipsychotic
  • blocks D2 receptors in the mesocortical, mesolimbic and other pathways
  • high potency, very high risks of extrapyramidal side effects
  • generally only useful in treatment of positive symptoms of schizophrenia.
  • prolonged use may lead to tardive dyskinesia or neuroleptic malignant syndrome
79
Q

Clozaril (Clozapine)

A
  • second generation, atypical antipsychotic
  • blocks 5-HT and D2 receptors in the mesocortical, mesolimbic and other pathways
  • high potency, low risk of EPSs, but many other systemic side effects stemming from alpha blockade and anticholinergic effects
  • useful in treating both positive and negative symptoms of schizophrenia
  • prolonged use may lead to tardive dyskinesia or neuroleptic malignant syndrome
80
Q

The two types of affective disorder are:

A

depressive and bipolar

81
Q

Affective disorders are thought to be rooted in imbalance of _______, _______, and _________ as stated by the ___________ hypothesis

A

norepinephrine, serotonin (5-HT), and dopamine; biogenic amine hypothesis

82
Q

The most commonly used, and first-line anti-depressants are _________ due to _______

A

SSRIs due to good effectiveness and lower risk of adverse effects than other antidepressents

83
Q

TCAs ______ (are / are not) highly effective in treating depression and have many potentially severe side effects, including:

A
  • They are very effective
  • Side effects include; sedation, anticholinergic effects, orthostatic hypotension, and cardiac conduction disturbances
  • prolonged use and overdose may cause serotonin syndrome and wide-QRS tachycardia with seizures, respectively
84
Q

Elavil (amitryptiline)

A
  • tricycylic antidepressent (TCA)
  • inhibits reuptake of serotonin and norepinephrine, increasing synaptic concentration
  • highly effective in treatment of depression, but with many adverse effects
  • onset of 2-4 weeks
  • adverse effects include; sedation, anticholinergic effects, orthostatic hypotension, and cardiac dysrhythmia. OD may cause wide-QRS tachy. Prolonged use may lead to serotonin syndrome
85
Q

serotonin syndrome, which may be caused by TCA, MAOI, SSRI, or SNRI antidepressents as well as other drugs, manifests as:

A
  • flushing
  • tremor and hyperreflexia
  • diaphoresis
  • hyperthermia
  • agitation
  • dilated pupils
  • diarrhea
86
Q

Because many antidepressants are biogenic amine analogues, they end their names in _____

A

-ine

ex: amitryptiline (TCA), fluoxetine (SSRI), sertraline (SSRI), venlafaxine (SNRI), selegiline (MAOI)

87
Q

Prozac (fluoxetine)

A
  • SSRI antidepressent
  • selectively blocks reuptake of serotonin, increasing serotonin concentration in the synaptic cleft
  • highly effective with a low rate of adverse effects (e.g. sedation, anticholinergic effects, ortho hypo, dysrhythmia)
  • most common and first line drug in treatment of depression
88
Q

Compare and contrast TCA and SNRI antidepressants

A
  • both inhibit the reuptake of serotonin and norepinephrine
  • SNRIs are much more selective for these two NTs, whereas TCAs have far more broad systemic effects, and therefore more adverse effects
89
Q

Cymbalta (duloxetine)

A
  • SNRI antidepressant
  • Inhibits reuptake of Serotonin and Norep with few other NT interactions
  • Used in treatment of affective and anxiety disorders
  • Fewer adverse effects than TCAs
90
Q

The major potential adverse effect of MAOIs is:

A

Hypertensive Crisis

91
Q

Identify three common classifications of pain

A

Somatic, visceral, and neuropathic

92
Q

Identify neurotransmitters that are important to the neurotransmission and modulation of pain

A

Substance P and glutamate are important in the ascending transmission of pain

Serotonin and norep are important in downregulation of the pain cascade

Enkephalins inhibit pain transmission and the release of substance P

93
Q

The three common classifications of opioids based on efficacy are:

A

full agonists, partial agonists, and mixed agonists/antagonists

94
Q

Common pharmacologic effects of opioids include:

A
  • analgesia
  • sedation
  • euphoria/dysphoria
  • miosis
  • nausea/vomiting
  • cough supression
  • Constipation
  • respiratory depression
  • vasodilation and decreased HR
  • pruritis and flushing
95
Q

Describe the general mechanism of action of opioid analgesics

A
  • primarily bind to mu-opioid receptors (along with delta and kappa) in the CNS and descending inhibitory pathways of pain
  • opioid receptors are Gi GPCRs and their activation decreased cAMP and decreases Ca2+ transmission, leading to decreased activation of pain pathways
96
Q

Give examples of common opioid full agonists, partial agonists, and mixed agonists/antagonists

A
  • Full: Morphine, hydromorphone, fentanyl, meperidine, methadone, oxycodone
  • Partial: Codeine, hydrocodone
  • Mixed: Buprenorphine (with naloxone = suboxone)
97
Q

Dilaudid (Hydromorphone)

A
  • Strong, semi-synthetic opioid, full opioid agonist
  • 10x potency relative to morphine with fewer CNS, GI, and CV effects than morphine
  • powerful analgesic for acute and chronic pain
  • adverse effects include sedation, respiratory depression, constipation, miosis, N/V
98
Q

Morphine

A
  • Strong, natural opioid, full opioid agonist
  • considered the prototype opioid
  • powerful analgesic for acute and chronic pain
  • adverse effects include sedation, respiratory depression, constipation, miosis, N/V
  • hydromorphone preferred for chronic pain management due to fewer adverse effects
99
Q

describe benefits of morphine in MI management

A
  • decreased pain and agitation due to analgesic and sedative effects
  • vasodilation and negative chronotropy reduce myocardial workload and oxygen demand
100
Q

Sublimaze (Fentanyl)

A
  • Strong, synthetic opioid, full opioid agonist
  • 100x potency relative to morphine with fewer CV effects, faster onset, and less hangover than morphine
  • powerful analgesic for acute and chronic pain
  • adverse effects include sedation, respiratory depression, constipation, miosis, N/V
101
Q

Sufenta (Sufentanil)

A
  • Strong, synthetic opioid, full opioid agonist
  • 1000x potency relative to morphine with fewer CV effects, faster onset, and less hangover than morphine
  • powerful analgesic for acute and chronic pain
  • adverse effects include sedation, respiratory depression, constipation, miosis, N/V
102
Q

Demerol (Meperidine)

A
  • Strong synthetic full opioid analgesic
  • 0.1X potency relative to Morphine
  • Less smooth muscle effects less pronounced than with other opioids. Fewer GI, biliary, and uterine side effects
  • Safer for pregnant patients, or those with cholecystitis
103
Q

Dolophine (Methadone)

A
  • Long-acting synthetic full opioid agonist
  • Does not tend to produce euphoria or other reinforcing effects
  • Used in management of chronic pain and in opioid addiction treatment
104
Q

The 6 modes of brain function that neuropharmacological agents can act on are:

A
  1. Cognitive Processing
  2. Memory
  3. Emotional Processing
  4. Sensory Processing
  5. Motor Processing
  6. Autonomic Processing

HLTH 2511 (11 decks)

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