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Clinical Med (Year 2) > Pharm Quiz 3 (Exam 2) > Flashcards

Pharm Quiz 3 (Exam 2) Flashcards

1
Q

What are the primary goals for sedative - hypnotic and anti anxiety drugs?

A
  • relax patient
  • Promote normal sleep
  • decrease anxiety
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2
Q

What is the primary agent for sedative- hypnotic and anti anxiety drugs?

A
  • Benzodiazepines
  • Many others
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3
Q

What is the mechanism of benzodiazepines?

A
  • Increase effects of GABA
  • Bind to a specific receptor (GABAa receptor) in brain
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4
Q

What is GABA?

A

Inhibitory neurotransmitter that decreases excitation throughout the CNS

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5
Q

Diazepam (Valium) and other benzodiazepines used to treat anxiety and insomnia bind to specific GABA receptors in the CNS, and inhibit neuronal activity by (BLANK) the conductance of (BLANK) ions into the neurons

A
  • Increasing
  • Chloride
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6
Q

What are “Z” drugs?

A
  • Newer sedative hypnotics
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7
Q

What is the mechanism of Z drugs?

A
  • Not benzodiazepines
  • Still bind to GABA receptors in brain (alpha 1 subunit)
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8
Q

What is the mechanism of the new sedative - hypnotic drug, Eszopiclone (Lunesta)?

A
  • Non Benzodiazepines
  • Binds to GABA receptors (alpha 1 subunit)
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9
Q

What is the mechanism of Ramelteon (Rozerem) (newer sedative - hypnotic) ?

A

Melatonin receptor agonist

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10
Q

What is the mechanism of Azapirones (buspirone) (BuSpar)?

A

Stimulate serotonin receptors in CNS

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11
Q

What is a benefit of Azapirones?

A
  • May decrease anxiety with less sedation and less dependence
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12
Q

What is a drawback of Azapirones (Newer antianxiety drugs) ?

A
  • Slow onset
  • Moderate efficacy
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13
Q

What is a benefit of Z drugs?

A

May produce fewer problems when stopped (less rebound insomnia)

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14
Q

What is the benefit of using antidepressants as anxiolytics?

A
  • May have fewer side effects; less chance of addiction
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15
Q

T/F: Antidepressant’s can not have a direct anxiolytic effect

A
  • False (They can)
  • Anxiety often occurs with depression so patients may need both types of drugs
  • Paroxetine (Paxil) & Venlafaxine (Effexors) are examples
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16
Q

What are some adverse effects of sedative hypnotics?

A
  • Residual (hangover) effects
  • Anterograde amnesia
  • Complex behaviors (sleep walking/ driving)
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17
Q

What are some adverse effects of sedative hypnotics and anti anxiety meds?

A
  • Rebound effect (insomnia, increased anxiety)
  • Falls
  • Tolerance & dependence
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18
Q

What are some non- drug strategies that might complement and eventually replace drugs for sleep disorder/ insomnia?

A
  • Regular exercise
  • Decrease caffeines
  • Establish pre bedtime routine
  • Sleeping environment
  • Dark, quiet room
  • No TV, phone
  • Soothing sounds (white noise)
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19
Q

What are some non- drug strategies that might complement and eventually replace drugs for anxiety?

A
  • Regular exercise
  • Try to identify & reduce source of anxiety
  • Counseling, support groups
  • Meditation, relaxation techniques
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20
Q

What are some rehab concerns of sedative hypnotics and anti anxiety drugs?

A
  • Treat sxm not the cause
  • Trade off: benefit vs sedation, risk of falls, possible long term on brain
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21
Q

What is depression?

A
  • Most common mental illness
  • Sadness that is incapacitating
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22
Q

What is the neurophysiology of depression?

A

Theory is it is caused by defect in CNS biogenic amines (Norepinephrine, dopamine, serotonin )

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23
Q

What is the drug strategy for depression?

A

Increase/ prolong effects of amine transmitters

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24
Q

What are the types of antidepressants?

A
  • Selective Serotonin Reuptake inhibitors (SSRI)
  • Serotonin Norepinephrine reuptake inhibitors (SNRI)
  • Tricyclics
  • MAO inhibitors
  • Others
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25
Q

Other type of Antidepressant:
What is the mechanism of Nefazodone (Serzone) & Trazodone (Desyrel)?

A

Block serotonin receptors and serotonin reuptake

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26
Q

Other Type of antidepressant:
What is the mechanism of Bupropion (Wellbutrin)?

A

Norepinephrine- dopamine reuptake inhibitor

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27
Q

In general what is the mechanism of antidepressant drugs; SSRIs, SNRIs, tricyclics; others?

A

Inhibit reuptake of one or more amine neurotransmitters

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28
Q

In general what is the mechanism of antidepressant drugs MAO inhibitors?

A

Decrease neurotransmitter breakdown

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29
Q

Upon reaching the brain, most antidepressant drugs (BLANK) the effects of (BLANK)

A
  • Prolong
  • Amine neurotransmitter such as norepinephrine, serotonin & dopamine
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30
Q

What is the latest theory as to why prolonged amine neurotransmitter, decrease depression?

A
  • Drugs increase activity of amine neurotransmitters
  • Increase transmitter activity increases brain- derived neurotrophic factor (BDNF)
  • BDNF stimulates growth (neurogenesis) in hippocampus
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31
Q

What is the adverse effect of tricyclics?

A
  • Sedation
  • Anticholinergic effects
  • Cardiovascular issues (ortho hypo, arrhyth’s)
  • Seizures
  • Increase risk of fatal OD
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32
Q

What is the adverse effect of MAO inhibitors?

A
  • CNS excitation
  • Increase BP (especially with other drugs/ foods that catecholamine release)
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33
Q

What is the adverse effects of SSRI & SNRI?

A
  • Generally better tolerated
  • May increase seizures
  • Some GI problems
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34
Q

What medication is serotonin syndrome possible with and when does this occur?

A
  • Possible with all antidepressants
  • Occurs when CNS serotonin receptors are overstimulated
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35
Q

What are some symptoms of serotonin syndrome?

A
  • Increase HR/BP
  • Confusion
  • Hallucinations
  • Agitation
  • Sweating
  • Shivering
  • Dystonias
  • Dyskinesias
  • Muscle pain
  • GI problems
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36
Q

In antidepressants when do they take effect and when you see max effects?

A
  • Often 1-2 wks before taking effect
  • May take 6-8 wks for max effect
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37
Q

There is a time lag before beneficial effects from antidepressants what may this cause?

A
  • Increase depression during initial treatment (especially in teenagers & children)
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38
Q

What is ketamine usually used for?

A

Used to initiate and maintain anesthesia in certain situations (dissociative effect)

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39
Q

What is the mechanism of ketamine?

A

Blocks NMDA receptors which decrease effects of excitatory amino acids

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40
Q

When would ketamine be used as an antidepressant?

A
  • Sub anesthetic doses may cause decrease in depression in severe, resistant cases that have no respond to other treatments
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41
Q

How long does it take for ketamine to take effect?

A
  • Rapidly
  • Benefits sometimes seen within hours of 1st dose
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42
Q

How can ketamine be administered?

A
  • Single slow IV infusions (repeated as needed)
  • Nasal Spray (1-2 times per week)
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43
Q

What are the potential problems with ketamine use?

A
  • High abuse potential & side effects limit widespread use
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44
Q

What are some common syndromes that antidepressants may be used for chronic pain?

A
  • Fibromyalgia
  • Neuropathic pain
  • Headache
  • Low back pain
  • Raynaud’s phenomenon
  • Other chronic pain syndrome
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45
Q

What is the classic treatment of bipolar syndrome?

A

Lithium
- Prevents manic episodes

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46
Q

What is the big problem with lithium and how does it occur?

A
  • Lithium Toxicity
  • Lithium is an element not degraded in body and eliminated intact by kidneys
  • If problems with kidney lithium can accumulate rapidly and cause lithium toxicity
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47
Q

Range of serum levels of lithium effects for:
Maintenance Phase
Acute manic episode
Toxicity Begins
Toxicity require treatment

A

Maintenance: 0.6-1.2
Acute manic episode: 1.0-1.5
Toxicity begins: about 1.5
Require treatment: >2.0

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48
Q

What is the symptoms of mild lithium toxicity in the CNS?

A
  • Fine hand tremor
  • Fatigue
  • Weakness
  • Dizziness
  • Blurred vision
  • Slurred speech
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49
Q

What are the symptoms of moderate- severe lithium toxicity in the CNS?

A
  • Ataxia
  • Fasciciulations
  • Nystagmus
  • Confusion
  • Stupor
  • Seizures
  • Coma
50
Q

What are the symptoms of mild lithium toxicity in the GI?

A
  • Nausea
  • Loss of appetite
  • Dry mouth
  • Abdominal pain
51
Q

What are the symptoms of moderate- severe lithium toxicity in the GI?

A
  • Vomiting
  • Diarrhea
52
Q

What are the symptoms of mild lithium toxicity in the cardiovascular system?

A
  • ECG changes
53
Q

What are the symptoms of moderate- severe lithium toxicity in the cardiovascular system?

A
  • Syncope
  • Bradycardia
  • A - V block
  • Other atrial & ventricular arrhythmias
54
Q

What are the symptoms of mild lithium toxicity in the renal system?

A
  • Polyuria
  • Polydipsia
55
Q

What are the symptoms of moderate to severe lithium toxicity in the renal system?

A
  • Renal insufficiency
  • Possible permanent kidney damage
  • Decrease glomerular filtration
56
Q

What is psychosis?

A

More severe forms of mental illness

57
Q

What is the cause of psychosis?

A

Increased dopamine activity in specific CNS pathway

58
Q

In general what is the mechanism of antipsychotics?

A

Block CNS dopamine receptors (especially D2 receptors in mesolimbic pathway)

59
Q

Describe the mechanism of atypical antipsychotics

A
  • Weak blockers of dopamine type 2 (D2) receptors
  • Strong blockers of specific serotonin receptors
60
Q

What are the adverse effects of traditional agents antipsychotics?

A
  • Orthostatic hypotension
  • Sedation
  • Anticholinergic effects
61
Q

What are some adverse effects of atypical agent antipsychotics?

A
  • Weight gain
  • Disturbed lipid/glucose metabolism
62
Q

What is the primary concern for all antipsychotics?

A

Extrapyramidal side effects
- Tardive dyskinesia (extensive movement around face and jaw)
- Pseudoparkinsonism
- Akathisia (severe restlessness)
- Other dystopias, dyskinesias

63
Q

What is the risk factors for Tardive dyskinesia?

A
  • Advanced age
  • Genetic predisposition
  • Affective mood disorders
  • DM
  • Hx of alcohol abuse
  • > 6 months continuous use
64
Q

What is the best treatment for Tardive dyskinesia?

A
  • Early recognition
  • Change in type or dose of drug
65
Q

How do drugs for Tardive dyskinesia work?

A
  • Block vesicular transporters in pre synaptic terminals
  • Prevent storage of monoamine (DA, NE, 5HT) in pre synaptic terminals
  • Deplete neurotransmitters from these terminals
66
Q

Antipsychotic drugs can cause abnormal movement patterns because these drugs block the effect of (BLANK) in the brain

A

Dopamine

67
Q

With what drugs can Neuroleptic malignant syndrome occur? What are the symptoms?

A
  • Occur with all antipsychotics
  • Symptoms: Catatonia, rigidity, tremors & fever
68
Q

When does neuroleptic malignant syndrome have an increase risk?

A
  • High dose
  • Agitated patient
  • impaired mental functions
69
Q

T/F: Neuroleptic Malignant Syndrome can be fatal

A

True- need to be detected early so drug can be discontinued

70
Q

What are the rehabilitation concerns for antipsychotics?

A
  • Trade off: benefits vs sedation
  • Be alert for orthostatic hypotension
  • Recognize extrapyramidal side effects
71
Q

Alzheimer Disease is (BLANK) dementia with (BLANK) change in neuronal structures & function.

A
  • Irreversible
  • Degenerative
72
Q

What are the goals of drug therapy in dementia?

A
  • Improve cognitive & intellectual function
  • Improve/ modify behavior
73
Q

How can cholinergic stimulants improve cognitive function in those with dementia?

A
  • Neuronal changes lead to decreased acetylcholine activity in brain
  • Cholinergic stimulants increase ACH activity either directly or indirectly
74
Q

What is the mechanism of indirect cholinergic stimulants in dementia?

A
  • Drug inhibits cholinesterase enzyme
  • ACh breakdown is inhibited
  • Ash activity/effects are prolonged
75
Q

What are the indications and efficacy for cholinergic stimulants?

A
  • Indications: Improve cognition, behavioral function
  • Efficacy: Help patient retain more cognitive/intellectual function in early stage of AD
76
Q

What is the mechanism of Memantine (used for dementia)?

A
  • Blocks NMDA-glutamate receptors in brain
    (Glutamate: excitatory amino acid, important in memory & learning)
  • Glutamate activity disrupted in AD (drug therapy normalizes glutamate influence)
  • Provides another strategy to slow AD progression (sustain memory & intellect)
77
Q

T/F: Can a cholinergic stimulant be combined with a drug that normalizes glutamate

A

True
- Namzaric

78
Q

What is the mechanism of the newest anti- AD drug, Aducanumab (Aduhelm)?

A

Antibody binds to amyloid beta protein fragments
- Decreasing their ability to accumulate into plaques in brain neurons

79
Q

How is Aducanumab (Aduhelm) administered?

A

Monthly IV injections (very costly)

80
Q

The government regulated the use of antipsychotics in Alzheimer’s Disease. What did this put more an emphasis on?

A
  • Using symptom specific medications
  • Consider nonpharmacologic interventions
81
Q

What do diuretics do?

A
  • Act on kidneys
  • Increase sodium and water excretion
  • Decrease fluid in vascular system
82
Q

What are the indications for diuretics?

A
  • Hypertension
  • Congestive heart failure
83
Q

What is the adverse effect and rehab concerns of diuretics?

A
  • possible fluid depletion (electrolyte imbalance)
  • Watch for:
    Orthostatic hypotension
    Weakness, fatigue
    Confusion, mood changes
84
Q

How do sympatholytic: beta blockers work?

A
  • Bind to heart, block effects of epinephrine & norepinephrine
  • Decrease HR & contraction force
  • Can also produce a more general decrease in sympathetic responses
85
Q

What are cardiovascular indications for beta blockers?

A
  • Hypertension
  • Angina
  • Arrhythmias
  • Heart failure
  • Recovery from MI
86
Q

What is the common beta blockers suffix of beta blockers?

A
  • olol
87
Q

what are some adverse effects and rehab concerns of beta blockers?

A
  • bronchoconstriction
  • Orthostatic hypotension
  • Psychotropic effects (depression, lethargy, decrease libido)
  • Decreased maximal exercise capacity
88
Q

What do vasodilators do and what are the indications?

A
  • Act directly on vascular smooth muscle, inhibit contraction
  • Indications: Hypertension, heart failure
89
Q

What are some adverse effects of vasodilators?

A
  • reflex tachycardia
  • Orthostatic hypotension
  • Dizziness, headaches
  • Edema, fluid retention
  • Avoid systemic heat
90
Q

What is the Renin-angiotensin system (RAS)?

A

Neuroendocrine response that helps control BP & other physiological reactions in various tissues

91
Q

What is the mechanism of Angiotensin converting enzyme (ACE) inhibitors?

A
  • Inhibit ACE
  • Decrease formation of angiotensin II
92
Q

What does ACE inhibitors prevent and what are the indications for use?

A
  • Prevent acute vasoconstriction from Ang II (decrease BP)
  • Prevent vascular hypertrophy from Ang II (decrease long term detrimental effects on heart, vasculature)
  • Indications: Hypertension, heart failure
93
Q

What does Ang - II receptors blockers do and prevent?

A
  • Block angiotensin II receptors
  • Prevent detrimental effects of Ang II on heart, vasculature
94
Q

What is the mechanism of direct renin inhibitors?

A
  • Aliskiren (Tekturna): inhibits renin’s ability to convert angiotensinogen to Ang 1
  • Prevents production of precursor to Ang II
95
Q

What are some adverse effects and rehab concerns for RAS drugs?

A
  • Generally well tolerated some nausea, dizziness
  • possible allergic reaction
  • ACE inhibitors; dry cough
96
Q

How does calcium channel blockers work?

A
  • Limit calcium entry into vascular smooth muscle & cardiac muscles
  • Promotes vasodilation, stabilize HR
97
Q

What are the indications for Calcium channel blockers?

A
  • Hypertension
  • Angina pectoris
  • Arrhythmisas
98
Q

What are some adverse effects and concerns of calcium channel blockers?

A
  • Swelling in feet, ankles
  • Orthostatic hypotension
  • Altered heart rate
  • Avoid systemic heat
99
Q

How are anti-anginals: Organic nitrates administered? What is the primary indication?

A
  • Traditionally sublingual
  • Transdermal through creams & patches
  • Primary indication is angina pectoris
100
Q

What is the primary effects of Nitrates?

A
  • Dilate peripheral vasculature
    Venous dilation causes decreased cardiac preload (blood returning to heart)
    Arterial dilation causes decreased after load (pressure heart pumps against)
  • Results in decrease cardiac workload, decrease O2 demand
101
Q

When is Nitrate tolerance seen?

A

Continuous administration reduces drug effects
- Effectiveness restored quickly when nitrates are discontinues

102
Q

What are the adverse effects and rehab concerns of nitrates?

A
  • Headache, dizziness
  • Orthostatic hypotension
  • Increase vasodilation (exaggerated response to systemic heat)
  • Sublingual doses (check drug viability, have it ready before rehab)
103
Q

What are the 4 drug classes for treating cardiac arrhythmias?

A

I: Sodium channel blockers
II: Beta blockers
III: Drugs that prolong repolarization
IV: Calcium channel blockers

104
Q

How does class II (Beta Blockers) of drugs treating cardiac arrhythmias work?

A

Decrease excessive sympathetic stimulation of heart

105
Q

How does class IV (Calcium channel blockers) of drugs treating cardiac arrhythmias work?

A

Limit Ca excitation of SA, AV nodes

106
Q

How does class I (Sodium channel blockers) work?

A

Inhibit (abnormal) Na channel opening in cardiac cells, stabilize excitability

107
Q

What are the 3 subclasses of Class I drugs (Sodium channel blockers)?

A

1A: Moderate slowing of depolarization & AP conduction prolonging repolarization
IB: Shorten cardiac repolarization
IC: marked slowing of depolarization & AP conduction

108
Q

How do class III, drugs that prolong repolarization work?

A

Lengthen time interval before next AP can be generated

109
Q

What are the primary clinical indications for
Class I
Class II
Class III
Class IV

A

Class I: Various arrhythmias, PVC’s, VTach
Class II: Afib, Vtach
Class III: Afib, Vtach, VFib
Class IV: Afib, supra ventricular tachycardias

110
Q

What are the rehab concerns and problems with anti-arrhythmic drugs?

A
  • Various side effects depending on class
  • Primary concern is change in type of arrhythmia
  • Monitor HR & sxm, especially during exercise
111
Q

What is a seizure?

A

Recurrent, uncontrolled cerebral excitation
- Initiated by certain neurons, activity spreads to adjacent areas of brain

112
Q

What is the cause of seizures in:
Youth?
Adults?

A
  • Youth: often unknown
  • Adult: often secondary to specific event
113
Q

How are seizures classified?

A

According to extent of cerebral involvement, EEG activity, symptoms

114
Q

What are the primary classes of seizures?

A
  • Focal (partial) seizures: Simple, complex
  • Generalized: absence, tonic clonic
  • Unknown
115
Q

What is the goal of antiseziure medications?

A

Selective effect on hyperexcitable neurons

116
Q

What are the benefits of 2nd generation anti seizure drugs?

A
  • Not necessarily more effective but tend to have milder side effects
  • Allow more drug combos
  • Some also used to treat neuropathic pain
117
Q

What are the 4 primary mechanisms of anti seizure medication?

A
  • Decrease Na entry into rapidly firing neurons
  • Decrease Ca entry into thalamic neurons
  • Increase GABA inhibition
  • Decreased release or effects of excitatory amino acids
118
Q

What are some relatively minor side effects of anti seizure meds?

A
  • Sedation
  • Headache
  • Dizziness
  • Incoordination
  • GI problem
119
Q

What are some more serious side effects of anti- seizure meds?

A
  • Liver toxicity
  • Blood dyscrasias (aplastic anemia, agranulocytosis)
  • Increased risk of birth defects
120
Q

Success with discontinuing seizure meds is associated with what?

A
  • Being free of seizures for at least 2 years while on meds
  • Having good seizure control within 1 year after seizures begin
  • Having normal neurologic exam prior to withdrawal
  • Having initial seizure onset in childhood
121
Q

What are some rehabilitation concerns for seizure meds?

A

Document seizure activity

122
Q

What is the suffix of common ACE inhibitors?

A

-pril

Clinical Med (Year 2) (17 decks)

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