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Pharmacology for Amjad > EXAM #3: REVIEW > Flashcards

EXAM #3: REVIEW Flashcards

1
Q

What sedative drug classes are “selective” CNS depressants?

A

1) Barbiturates
2) Benzodiazepines
3) Ethanol

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2
Q

Outline the progression of dose-dependent effects seen with the sedative hypnotics.

A

1) Sedation
2) Sleepiness
3) Anesthesia
4) Coma
5) Respiratory depression/ death

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3
Q

List the six clinical indications for the sedative hypnotics.

A

1) Anxiety
2) Insomnia
3) Amnesia-induction
4) Seizures
5) Ethanol withdrawal
6) Muscle relaxation

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4
Q

What are the two suffixes associated with the Benzodiazepines?

A
  • “zepam”

- “zolam”

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5
Q

What are the two benzodiazepines that undergo metabolism to weakly active, short lived metabolites with intermediate duration of action?

A
  • Alprazolam

- Triazolam

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6
Q

What effects are associated with Alpha-1 GABA receptor agnoism?

A

1) Sedation
2) Anticonvulsant
3) Anterograde amnesia

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7
Q

What effect is associated with Alpha 2,3, and 5 GABA receptor agonism?

A

Anxiolysis

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8
Q

What are the five adverse effects associated with benzodiazepines?

A

1) Respiratory depression
2) Anterograde amnesia
3) Tolerance
4) Dependence
5) Withdrawal

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9
Q

What drug classes will cause additive CNS depression when combined with benzodiazepines?

A

1) Ethanol
2) Opoids
3) Anticonvulsants
4) Phenothiazine
5) Antihistamines
6) TCAs

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10
Q

List the four indications for Barbiturates.

A

1) Anticonvulsant
2) Sedative-hypnotic
3) Anesthesia
4) Medically induced coma

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11
Q

List the three common side effects of the MAOIs.

A
  • Orthostatic hypotension
  • Weight gain
  • Sexual dysfunction
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12
Q

What are TCAs first line therapeutic agents for?

A

Chronic pain

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13
Q

What are TCAs second line therapeutic agents for?

A

Major depression

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14
Q

What TCA is used to treat neuropathic pain?

A

Desipramine

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15
Q

What TCA has the most sedative effects?

A

Amitriptytline

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16
Q

What is the MAJOR side effect to remember as being associated with the TCAs?

A

Cardiac toxicity i.e. induction of lethal cardiac arrhythmias

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17
Q

What are all of the side effects of the TCAs?

A

1) Cardiac toxicity
2) Orthostatic hypotension
3) Delirium in the elderly
4) Sexual dysfunction

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18
Q

What is important to remember about the safety of SSRIs compared to other antidepressants?

A

SSRIs are much safer than MAOIs or TCAs

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19
Q

What symptoms compose the triad of Serotonin Syndrome?

A

1) AMS
2) Autonomic hyperactivity
3) Neuromuscular abnormalities

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20
Q

What is the MOA of Venlafaxine?

A

SNRI

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21
Q

What receptor does Venlafaxine have its major effect on? Minor?

A 
Major= SERT 
Minor= NET
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22
Q

What is the clinical indication for Venlafaxine?

A

Severe Depression

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23
Q

What is the MOA of Duloxetine?

A

SNRI with balance SERT and NET inhibition

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24
Q

What is the primary clinical indication for Duloxetine?

A

Chronic pain (increasingly prescribed over the TCAs i.e. Desipramine)

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25
Q

What is the MOA of Trazadone?

A

Antihistamine (H1 antagonist)

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26
Q

What is the primary clinical indication for Trazadone?

A

Depression + insomnia (unlabeled)

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27
Q

What is the MOA of Buproprion?

A

1) NE/ DA reuptake inhibitors

2) Increases catecholamine release

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28
Q

What are the clinical indications for Bupropion?

A

1) Major depression

2) Smoking cessation

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29
Q

What drug class does Mirtazapine fall under?

A

TCA

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30
Q

What is the MOA of Mirtazapine?

A

1) TCA (SERT and NET inhibitor)
2) Alpha-2 antagonist
3) Antihistamine (H1)
4) 5-HT2/3 antagonist

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31
Q

List the three antidepressants that are potent CYP2D6 inhibitors.

A
  • Paroxetine
  • Fluoxetine
  • Fluvoxamine
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32
Q

What two anticonvulsants are prescribed for Bipolar Disorder?

A

1) Valproate

2) Carbamazepine

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33
Q

What is the MOA of Lithium?

A

Decreases the post-synaptic response to NE and 5-HT by:

  • Decreasing cAMP
  • Decreasing IP3
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34
Q

What are the four major side effects associated with Lithium?

A

1) Tremors
2) Hypothyroid
3) Nephrogenic Diabetes Insipidus
4) Skin reactions

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35
Q

What is the most common type of partial seizures?

A

Complex partial

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36
Q

What is an absence of Petit Mal seizure?

A

A seizure that is characterized by:

  • Brief LOC
  • Some motor signs/ automatisms

*More common in children

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37
Q

What are the three molecular events underlying EPSPs?

A

1) Na+ influx
2) Ca++ influx
3) Paroxysmal Depolarization

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38
Q

What drugs are best for treating absence/ petite mal seziures?

A

Ethosiximide

Valproate

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39
Q

What drugs are best for treating myoclonic seizures?

A

Clonazepam

Valproate

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40
Q

What drugs are best for treating Status Epilepticus?

A

Diazepam
Lorazepam
Phenytoin
Fos-phenytoin

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41
Q

List the adverse effects associated with anticonvulsant agents.

A

1) Sedation
2) Diplopia
3) Nystagmus
4) Ataxia
5) GI disturbances

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42
Q

What two things do you need to remember about anticonvulsant therapy in women?

A

1) Anticonvulsants decrease the efficacy of oral contraceptives
2) Anticonvulsants are teratogenic

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43
Q

What are the three elements of the Phenytoin MOA?

A

1) Na+ channel blocker
2) Enhanced GABA release
3) Decreased Glutamate release

Generally prevents seizure propagation

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44
Q

What are the clinical indications for Phenytoin?

A

1) Gran mal seizures
2) Partial seizures
3) Status epilepticus

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45
Q

What is the MOA of Carbamazepine in regards to its anticonvulsant effects? What drug class does Carbamazepine fall into?

A

Carbamazepine is TCA that also:

- Blocks Na+ channels –anticonvulsant

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46
Q

What is Oxcarbazepine?

A

Carbamazepine analog that has fewer side effects

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47
Q

List the clinical indications for Carbamazepine.

A

1) General (tonic-clonic) seizures
2) Partial seizures
3) Manic phase of bipolar phase (acute)

AND

4) TRIGEMINAL NEURALGIA

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48
Q

What unique side effect is associated with Carbamazepine?

A

SIADH

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49
Q

What are the clinical indications for phenobarital?

A

1) Neonatal seizures
2) Seizures in pregnancy
3) Status epilepticus

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50
Q

What is the unique side effect associated with Valproate?

A

Hepatotoxicicty

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51
Q

What is the MOA of Lamotrigine?

A

Na+ and Ca++ channel antagonist

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52
Q

What is the MOA of Felbamate?

A

Na+ and Glutamate receptor antagnoist

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53
Q

What are the adverse effects associated with Felbamate?

A

1) Aplastic anemia

2) Liver failure

54
Q

What is the MOA of Tiagabine?

A

Inhibits GABA uptake

55
Q

What is the difference between GABA-A and GABA-B receptors?

A

GABA-A= Cl- ion channel

GABA-B= GPCR that increases K+ conductance on stimulation

56
Q

What are the six characteristics of an ideal anesthetic?

A

1) Unconsciousness
2) Amnesia
3) Analgesia
4) Skeletal muscle relaxation
5) Areflexia
6) Good minute-to-minute control

57
Q

What are the four phases of anesthesia?

A

1) Induction
2) Maintenance
3) Emergence
4) Recovery

58
Q

What are the stages of anesthesia?

A

1) Analgesia
2) Excitement
3) Surgical anesthesia
4) Medullary depression

59
Q

What are the three general mechanisms of action of general anesthetics?

A

1) Increased GABA-A activity
2) Activation of K+ channels
3) Inhibition of NMDA receptors

60
Q

What clinical scenario will cause a decreased MAC value?

A

Presence of CNS depressants

61
Q

What are the three major drawbacks to NO?

A

1) Lack of potency (110% MAC value)
2) Diffusion hypoxia
3) Increased risk of spontaneous abortion

62
Q

List the halogenated anesthetic agents.

A

1) Halothane
2) Enflurane
3) Isoflurane
4) Desflurane

63
Q

What major adverse effect is associated with Halothane?

A

Hepatitis

64
Q

What major side effect is associated with Enflurane?

A

CNS stimulant effects

65
Q

What drug class does Thiopental fall into?

A

Barbiturate (used for anesthesia induction)

66
Q

What is the MOA of Ketamine?

A

NMDA antagonist

67
Q

What type of local anesthetic, protonated (LAH) or non protonated (LA) is more lipophilic? Which binds the internal portion of Na+ channels with higher affinity?

A 
LA= more lipophilic 
LAH+= binds Na+ channels with higher affinity (internally)
68
Q

Which type of LA has a longer half-life, amides or ester?

A

Amides have a longer half-life

69
Q

Which type of LA is metabolized in the liver? Blood?

A
  • AmIdes– with 2x i’s–are metabolized in the lIver

- Esters– with 1x i– are metabolized in the blood

70
Q

What is the Cm?

A

Minimum anesthetic concentration for standard block in 50% of the population

71
Q

List the amide type LAs.

A

Lidocaine
Bupivicaine
Ropivacaine
Articaine

72
Q

List the ester type LAs.

A 
Cocaine 
Procaine 
Tetracaine 
Benzocaine
Chloroprocaine
73
Q

What is the clinical utility of Benzocaine?

A

This is an ester-LA that has enhanced lipid solubility–it can be used topically

74
Q

What is the clinical utility of Chloroprocaine?

A

This is an ester-LA that is used as an epidural agent in labor b/c:

  • Low risk of systemic toxicity
  • Low risk of fetal exposure
75
Q

What is Exparel-Liposome? What is it used for?

A
  • Encased Bupivacaine (amide LA) w/ extended half-life

- Provides up to 72 hours of post-op pain relief

76
Q

What are the four clinical indications for antipsychotic medications?

A

1) Schizophrenia
2) Psychotic behavior
3) Severe mania
4) Antiemetic

77
Q

List the typical antipsychotics.

A

Chlorpromazine
Thioridazine
Fluphenazine
Haloperiodol

78
Q

List the atypical antipsychotics.

A 
Clozapine
Olanzapine
Risperiodone 
Aripiprazole 
Quetiapine 
Zisprasidone
79
Q

What is the difference between the metabolism of the typical and atypical antipsychotics?

A

Typical= metabolism into an INACTIVE metabolite

Atypical= metabolism into an ACTIVE metabolite

80
Q

What receptor/s is primarily antagonized by typical antipsychotics? Atypical?

A

Typical= D2

Atypical D2 + 5-HT2A

81
Q

What antipsychotic is associated with high 5-HT2A affinity?

A

Clozapine

82
Q

List the subtypes of extrapyramidal symptoms.

A

1) PD-like Syndrome
2) Akathesia
3) Dystonia
4) Tardive Dyskinesia

83
Q

List the four most common reasons that patients will stop taking antipsychotics.

A

1) Lack of efficacy
2) Cannot tolerate side effects in general
3) Weight gain
4) Sexual dysfunction

84
Q

List the five hallmark cognitive symptoms of AD.

A

1) Loss of short-term memory
2) Disorientation
3) The A’s
- Aphasia
- Apraxia
- Agnosia

85
Q

Describe the pathologic changes that underly the development of the AD phenotype specifically in regards to Beta-amyloid.

A

1) ABPP or Amyloid Precursor Protein is cleaved into Beta-Amyloid
2) There is an IMBALANCE between Beta-Amyloid production and clearance
3) Beta-amyloid accumulates and is TOXIC to neurons

86
Q

What is the function of “Presenilin?”

A

Presenilin cleaves Amyloid Precursor Protein

87
Q

What are the consequences of neurofibrillary tangles in AD?

A

1) Microtubular disintegration and instability
2) Collapse of the neuronal transport system
3) Altered neurotransmitter release
4) Cell death

88
Q

List the four drugs that are used as first line agents in AD. What drug class do they belong to?

A

Cholinesterase inhibitors:

1) Tacrine
2) Donepezil
3) Rivastigmine
4) Galantamine

89
Q

What adverse effect of Tacrine limits its clinical use today?

A

Hepatotoxicity

*Also has a v. short half-life and had to be dosed 4x per day

90
Q

Which first line agent for AD can be given as a transdermal patch? What are the clinical implications?

A

Rivastigmine can be given transdermally

- Limits the adverse GI disturbances

91
Q

What is the MOA of Memantine?

A

Non-competitive NMDA antagonist

92
Q

What class of antidepressants are contraindicated in the treatment of depression in AD patients?

A

TCAs–alpha-1 effects have an increased risk for orthostatic hypotension and falls

93
Q

What are the four cardinal symptoms of PD?

A

1) Bradykinesia
2) Muscular rigidity
3) Resting tremor
4) Postural instability

94
Q

What are the adverse effects associated with L-DOPA administration in PD?

A

1) Dyskinesia
2) Response fluctuations
3) Postural hypotension/tachycardia
4) Behavioral disturbance
5) GI disturbances

95
Q

What is the drug interaction between L-DOPA and the antipsychotics?

A
  • L-DOPA is aiming to increase DA concentrations
  • Antipsychotics are D2 ANTAGONISTS

Thus, the drugs counteract each other.

96
Q

List three DA receptors agonists that are used to treat PD.

A

Pramipexole
Ropinirole
Apomorphine

97
Q

List the two MAO-B receptor antagonists used to treat PD.

A

Rasagiline

Selegiline

98
Q

List the two COMT inhibitors used to treat PD.

A

Entacapone

Tolcapone

99
Q

What is the MOA of Amantadine to treat PD?

A

Increased DA release

100
Q

What adverse effect is associated with Amantadine?

A

Livedo Reticularis

101
Q

List the two anticholinergic agents used to treat PD.

A

Benztropine

Trihexyphenidyl

102
Q

Name the three endogenous opioids.

A

Endorphins
Enkephalins
Dynorphins

103
Q

What is the difference between Mu1 and Mu2 receptors?

A 
Mu1= outside the CNS 
Mu2= inside the CNS
104
Q

How does agonism of Mu opioid receptors produce analgeisa?

A

1) Mu opioid receptors are GPRCs coupled to Gi subunits
2) Activation causes decreased adenylyl cyclase
3) Decreased adenylyl cyclase causes decreased cAMP

The final result is LESS intracellular Ca++ and increased K+ conductance i.e. INHIBITION

105
Q

List five clinical indications for opioids.

A

1) Analgesia
2) Anesthesia
3) Anti-tussive
4) Anti-diarrheal
5) Acute pulmonary edema

106
Q

What class of drugs are contraindicated with opioids?

A

MAOIs

107
Q

List the “strong” opioids.

A 
Morphine 
Hydromorphone 
Oxymorphone
Methadone 
Fentanyl 
Sufentanil 
Meperidine 
Heroin
108
Q

List the mixed opioid agonist-antagonists.

A

Bupreneorphine
Butorphanol
Nalbuphine
Pentazocine

109
Q

List the “other” opoid agonists.

A

Dextromethorphan
Diphenoxylate
Loperamide
Tramadol

110
Q

What effects will CNS stimulants produce?

A

1) Alterness
2) Productivity and motivation
3) Arousal
4) Euphoria
5) Nervousness and anxiety

111
Q

What is Methylxanthine?

A
  • CNS/ Respiratory stimulant

- Derivative of xanthine

112
Q

What are the clinical indications for Theophylline?

A
  • COPD
  • Asthma

Note that this drug has bronchodilator properties

113
Q

List the sympathomimetic amide stimulants.

A

1) Amphetamine analogs including:
- Methamphetamine
- Dexamphetamine
- Methylphenidate
2) Cocaine
3) Modafinil
4) Atomoxetine

114
Q

How are the amide psychomotor stimulants metabolized?

A

1) MAO

2) CYP p450

115
Q

What classes of drugs will have adverse interactions with CNS stimulants?

A

MAOIs

SSRIs

116
Q

List the CNS related side effects seen with the psychomotor stimulants.

A 
Euphoria 
Dysphoria 
Insomnia 
Irritability 
Tremor 
Headache 
Anorexia
117
Q

List the stimulant drugs that are used to treat ADHD.

A

Methylphenidate
Amphetamine salts (adderall)
Dextroamphetamine

118
Q

List the non-stimulant drugs that can be prescribed for ADHD.

A

1) Atomoxetine
2) Clonidine
3) Modafininl
4) Antidepressants
- TCAs
- MAOIs
- Bupropion

119
Q

List the psychological manifestations of drug withdrawal.

A
  • Dysphoria
  • Depression
  • Anxiety
  • Craving
  • Psychosis
120
Q

What are the three drugs “targets” of the VTA?

A

1) Gi GPCRs that inhibit GABA
2) Inonotropic DA receptors
3) DA uptake transporter

121
Q

What drugs act on ionotropic DA receptors in the VTA?

A

1) Benzodiazepines
2) Nicotine
3) Alcohol

122
Q

What is the MOA of GHB?

A

Disinhibition of GABA-B receptors in the VTA

123
Q

What are the side effects associated with Methamphetamine use?

A

Methamphetamine is sympathomimetic, thus:

  • Mydriasis
  • Tachycardia
  • Hypertension
124
Q

What is the MOA of MDMA?

A

1) SERT Antagonism

2) Increases the release of 5-HT

125
Q

Wha toxicity is associated with MDMA?

A

Acute hyperthermia and dehydration

126
Q

List the Psychedelcis.

A

1) LSD
2) Psilocybin
3) Ketamine
4) Phecyclidine

127
Q

What is the MOA of LSD and Psilocybin?

A
  • Increase glutamate release

- 5-HT2A agonist

128
Q

What is the MOA of Ketamine and PCP?

A

NMDA antagonists

129
Q

What is the RR of opioid addiction?

A

4

130
Q

List the four most commonly abused opioids.

A

1) Codeine
2) Heroin
3) Morphine
4) Oxycodone

131
Q

What is the MOA of euphoria seen in opioid use?

A

1) Activation of Mu opioid receptors
2) Inhibition of GABAnergic neurons in the VTA

Result in disinhibition of VTA DA neurons

132
Q

What is the MOA of THC?

A

Blocks GABA-A receptors on DA neurons in the VTA

Pharmacology for Amjad (64 decks)

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