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Pharmacology > Pharmacology Exam 3 > Flashcards

Pharmacology Exam 3 Flashcards

1
Q

Consists of the brain and spinal cord

A

Central Nervous System

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2
Q

Made up of the autonomic and the somatic.

A

The Peripheral Nervous System

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3
Q

Also called visceral system; acts on smooth muscles and glands.

A

Autonomic nervous system

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4
Q

Functions to control and regulate the heart, respiratory system, gastrointestinal tract, bladder, eyes, and glands.

A

Automatic Nervous System

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5
Q

Voluntary system that innervates skeletal muscles

A

Somatic nervous system

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6
Q

Parasympathetic and Sympathetic are apart of what?

A

Autonomic nervous system

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7
Q

The sympathetic nervous system is also called what?

A

Adrenergic system

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8
Q

Sympathetic nervous system receptors

A

Alpha 1
Alpha 2
Beta 1
Beta 2

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9
Q

Parasympathetic Nervous System Receptor Cells

A

Muscarinic

Nicotinic

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10
Q

Sympathetic Stimulants are called

A

Sympathomimetics, adrenergics, adrenergic agonists

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11
Q

Sympathetic Depressants are called

A

Sympatholytics, adrenergic blockers, adrenergic antagonists

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12
Q

Parasympathetic stimulants are called

A

Direct acting: parasympathomimetic, cholinergic a, cholinergic agonists

Indirect acting: cholinesterase inhibitors

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13
Q

Parasympathetic Depressants are called

A

Parasympatholytics, anticholinergics, cholinergic antagonists, antispasmodics

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14
Q

Alpha receptors are located in

A

Blood vessels, eyes, bladder, and prostate

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15
Q

Alpha 1 Receptors do what when effected?

A
  • Increases cardiac contractility, vasoconstriction
  • Dilates pupils, decreases salivary gland secretion
  • Increases bladder and prostate contraction
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16
Q

Alpha 2 receptors do what when effected?

A
  • Inhibits norepinephrine release
  • Promotes vasodilation and decreased BP
  • Decreases GI motility and tone
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17
Q

Beta 1 Receptors do what when affected?

A
  • Increases cardiac contractility, HR.

* Increases renin secretion and increases BP

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18
Q

Beta 2 receptors do what when affected?

A
  • Decreases GI tone and motility
  • Bronchodilation
  • Increases blood flow in skeletal muscles
  • Relaxes smooth muscles of uterus
  • Activates liver glycogenolysis and increases blood glucose
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19
Q

Domaminergic receptors are located in

A
  • The renal, mesenteric, coronary, cerebral arteries

* When stimulated vasodilation occurs and increasesd blood flow

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20
Q

Neurotransmitter Inactivation by:

A
  • Reuptake of transmitter back into neuron
  • Enzymatic transformation or degradation
    • MAO inside neuron
    • COMT outside neuron
  • Diffusion away from the receptor
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21
Q

Drugs halt termination of neurotransmitter by inhibiting what?

A
  • Norepinephrine reuptake

* Norepinephrine degradation

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22
Q

Classification of adrenergic agonists

A
  • Direct acting
  • Indirect acting
  • Mixed acting
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23
Q

Direct acting adrenergic agonists

A
  • Epinephrine and norepinephrine

* Directly stimulates adrenergic receptor

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24
Q

Indirect-acting adrenergic agonists

A
  • Amphetamine

* Stimulates release of norepinephrine from terminal nerve endings

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25
Q

Mixed-acting adrenergic agonists

A
  • Ephedrine

* Stimulates adrenergic receptor sites and stimulates release of norepinephrine from terminal nerve endings

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26
Q

Catecholamines do what?

A
  • produce a Sympathetic response
  • Endogenous: Epinephrine, norepinephrine, dopamine.
  • Synthetic: Isoproterenol, dobutamine
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27
Q

Noncatecholamines do what?

A
  • Stimulate adrenergic receptors
  • Most have longer duration of action than endogenous and synthetic
  • Phenylephrine, metaproterenol, albuterol
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28
Q

Inotropic means:

A

Strengthen myocardial contraction

ex: Epinephrine

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29
Q

Epinephrine is used for:

A
  • Anaphylaxis
  • Anaphylactic shock
  • Bronchospasms
  • Status asthmaticus Cardiogenic shock
  • Cardiac arrest
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30
Q

Epinephrine Side effects

A

•Cardiac dysrhythmias, palpitations, tachycardia, hypertension, dizziness, headaches, sweating, insomnia, restlessness, tremors, hyperglycemia, renal vasoconstriction

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31
Q

Epinephrine drug interactions

A

Beta blockers
•Decrease epinephrine action Digoxin
•Causes cardiac dysrhythmias TCAs and MAOIs intensify and prolong effects

Digoxin
•Can cause dysrhythmias

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32
Q

Epinephrine is:

A

Nonselective

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33
Q

Epinephrine activates what receptors and what do they do?

A

Alpha 1: increases BP
Beta 1: increases HR
Beta 2: prompts bronchodilation

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34
Q

Epinephrine contraindications and cautions

A
  • Cardiac dysrhythmias
  • Hypertension
  • Hyoerthyroidism
  • Diabetes mellitus
  • Pregnancy
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35
Q

Epinephrine contraindications and cautions

A
  • Cardiac dysrhythmias
  • Hypertension
  • Hyoerthyroidism
  • Diabetes mellitus
  • Pregnancy
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35
Q

Epinephrine contraindications and cautions

A
  • Cardiac dysrhythmias
  • Hypertension
  • Hyoerthyroidism
  • Diabetes mellitus
  • Pregnancy
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36
Q

Epinephrine contraindications and cautions

A
  • Cardiac dysrhythmias
  • Hypertension
  • Hyoerthyroidism
  • Diabetes mellitus
  • Pregnancy
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37
Q

Epinephrine contraindications and cautions

A
  • Cardiac dysrhythmias
  • Hypertension
  • Hyoerthyroidism
  • Diabetes mellitus
  • Pregnancy
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38
Q

Epinephrine actions are:

A
  • Inotropic
  • Vasoconstrictor
  • Bronchodilator
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39
Q

Albuterol is

A

Selective

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40
Q

Albuterol acts on what receptor and it does what?

A

Acts on beta 2 adrenergic receptors and promotes bronchodilation

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41
Q

Albuterol uses

A
  • Treats bronchospasms
  • Treats asthma
  • Treats bronchitis
  • Treats COPD
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42
Q

Albuterol Cautions

A

•Severe cardiac disease Hypertension, hyperthyroidism, Diabetes mellitus, pregnancy, renal dysfunction

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43
Q

Albuterol Side effects/adverse reactions

A
  • Tremors
  • Nervousness
  • Restlessness
  • Dizziness
  • Tachycardia
  • Palpitations
  • Cardiac dysrhythmias
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44
Q

Nursing Interventions for Adrenergic Agonists

A
  • Monitor IV site frequently when administering norepinephrine or dopamine because extravasation of these drugs causes tissue damage and necrosis within 12 hours.
  • Moniyor ECG for dysrhythmias when adrenergic agonists are given IV
  • Explain the continuous use of nasal sprays or drops that contain an adrenergic agonists may result in rebound nasal congestion
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45
Q

IV Epinephrine extravasation antidote

A

Phentolamine mesylate

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46
Q

Blocks alpha receptors relaxing vascular smooth muscle and increasing blood flow to area

A

Phentolamine mesylate

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47
Q
  • Selective alpha 2 adrenergic agonists
  • Used primarily to treat hypertension
  • Can cause orthostatic hypotension
A

Clondine (Central-acting alpha agonist)

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48
Q
  • Alpha adrenergic agonists that acts with the CNS

* Alpha 2 activation leads to vasodilation and decreased BP

A

Methyldopa (Central Acting Alpha Agonist)

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49
Q

Methyldopa (Central Acting Alpha Agonist) Side effects

A
  • Drowsiness
  • Headache
  • Nasal Congestion
  • Nightmares
  • Edema
  • Constipation
  • Ejaculation dysfunction
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50
Q
  • Blocks effects of adrenergic neurotransmitters
  • Indirectly by inhibiting release of neurotransmitters epinephrine and norepinephrine
  • Directly by occupying receptors
A

Adrenergic Antagonists

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51
Q

Adrenergic Antagonists Types

A

Alpha-adrenergic antagonists

Beta-adrenergic antagonists

52
Q

Effects of Adrenergic Antagonists at Receptors Alpha 1

A
  • Vasodilation, dizziness
  • Orthostatic hypotension, reflex tachycardia
  • Pupil constriction
  • Suppresses ejaculation
  • Reduces contraction of smooth muscles in bladder neck and prostate
53
Q

Effects of Adrenergic Antagonists at Receptors Beta 1

A

Reduces cardiac contractility and decrease pulse

54
Q

Effects of Adrenergic Antagonists at Receptors Beta 2

A
  • Bronchoconstriction
  • Contracts uterus
  • Inhibits glycogenolysis which leads to hypoglycemia
55
Q

Drugs that inhibit a response at alpha-adrenergic receptor site

A

Alpha Adrenergic Antagonists

56
Q

Alpha Adrenergic Antagonists Drugs

A

Selective- blocks alpha 1
Nonselective- block alpha 1 and alpha 2

Action: is to promote vasodilation
Use: decrease symptoms of BPH, PVD

57
Q

Alpha Adrenergic Antagonists Drugs

A

Selective- blocks alpha 1
Nonselective- block alpha 1 and alpha 2

Action: is to promote vasodilation
Use: decrease symptoms of BPH, PVD

58
Q

Beta Blocker Action (Beta Adrenergic Antagonists)

A

Decrease BP and pulse

59
Q

Nonselective Beta Blockers

A

Blocks beta 1: decreases BP and pulse

Blocks beta 2: bronchoconstriction; use with caution in patients w/ COPD or asthma

Propranolol HCl: used for angina, cardiac dysrhythmias, hypertension, HF

60
Q

Selective Beta Blockers

A
  • Metoprolol

* Atenolol

61
Q
  • Blocks Beta 1 Only
  • Decreases BP and HR
  • Fewer Side Effects
A

Selective Beta Blockers

62
Q

Selective Beta Blockers Side Effects/Adverse Reactions

A
  • Bradycardia
  • Hypotension
  • Dysrhythmias
  • Headaches
  • Dizziness
  • Fainting
  • Fatigue
  • Drowsieness
  • Depression
  • Nausea
  • Vomiting
  • Diarrhea
  • HF
  • Tell patient to monitor their HR and BP
  • Can mask signs and symptoms of hypoglycemia so monitor closely of they are a diabetic
63
Q

Beta Adrenergic Drug Interactions

A
  • Decreased side effects w/ NSAIDs
  • Increased effects w/ Atropine & other anticholinergics
  • Increasef risk of hypoglycemia w/ insulin, sulfonylureas
64
Q

•Block release of norepinephrine.
•User to decrease BP
•Example Reserpine:
Reduces the serotonin and catecholamine transmitters. Depletion of these neurotransmitters may lead to severe mental depression

*Ask about st. John’s wort

A

Adrenergic Neuron Antagonists

65
Q

Adrenergic Neuron Antagonists Assessment

A
  • Obtain a Health History.

* Determine what drugs the patient currently takes.

66
Q

Adrenergic Neuron Antagonists Nursing Diagnosis

A
  • CO
  • Decreased related to hypotension and bradycardia
  • Fatigue related to medication adverse effects
67
Q

Adrenergic Neuron Antagonists Planning

A

BP lowered

68
Q

Adrenergic Neuron Antagonists Nursing Interventions

A
  • Monitor vitals and report significant changes especially low BP.
  • Assist patient with ambulation due to orthostatic hypotension (FALLS!!!!)
  • Therapeutic effects might not occur for 2-3 weeks after initiation of therapy
69
Q

Cholinergic receptors

A

Muscarinic receptors

Nicotinic receptors

70
Q

Affects smooth muscles, slow heart rate

A

Muscarinic receptors

71
Q

Affects skeletal muscles

A

Nicotinic receptors

72
Q

Types of cholinergic agonists

A

Direct acting: acts on receptors to activate tissue response

Indirect acting: Inhibits action of enzyme cholinesterase

73
Q

Effects of Cholinergic Agonists Cardiovascular

A

Decrease HR, BP, vasodilation, slow conduction of AV node

74
Q

Effects of Cholinergic Agonists Cardiovascular

A

Decrease HR, BP, vasodilation, slow conduction of AV node

75
Q

Effects of Cholinergic Agonists GI

A

Increase tone, motility, peristalsis, and relax spincter muscles, stimulate urination

76
Q

Direct-acting cholinergic agonists

A

Primarily selective to muscarinic receptors

77
Q

Muscarinic receptors are located:

A

In smooth muscles.

78
Q

Direct-Acting Cholinergic Agonists Medications

A
  • Metoclopramide
  • Pilocarpine
  • Bethanechol chloride
79
Q

Metoclopramide is used for:

A
  • Increasing gastric emptying

* Treats gastroparesis, nausea, GERD

80
Q

Pilocarpine is used for:

A

Constricting pupils

81
Q

Bathanechol chloride is used for:

A

Increasing urination by contracting the bladder

82
Q

Bethanechol Side effects/adverse reactions

A
  • Blurred vision, miosis
  • Hypotension bradycardia, sweating
  • Increased salivation and gastric acid, nausea, vomiting, diarrhea, abdominal cramps
  • Bronchocomstriction
  • Cardiac dysrhythmias
83
Q

Bethanechol Contraindications

A
  • Bradycardia
  • Hypotension
  • COPD
  • Peptic ulcer
  • Parkinsonism
  • Hyperthyroidism
84
Q

Bethanechol Nursing Assessment

A
  • Assess baseline vital signs for future comparisons
  • Assess urine output (should be >1500 mL/day)
  • Obtain patient history of health problems such as peptic ulcer, urinary obstruction, or asthma
85
Q

Bethanechol Nurse Planning

A

Patient will void more frequently

86
Q

Bethanechol Nursing Interventions

A
  • Monitor BP and HR
  • Teach patient to rise slowing to avoid dizziness and orthostatic hypotension
  • Auscultate breath sounds for rales, crackling from fluid congestion in the lungs.
  • Monitor the patient for possible cholinergic crisis (overdose), including symptoms of muscular weakness and increases salivation
87
Q

Indirect-Acting Cholinergic Agonists Functions

A
  • Inhibit cholinesterase enzyme

* Allow ACh to activate muscarinic and nicotinic cholinergic receptors

88
Q

Indirect Acting Cholinergic Agonists Effects

A
  • Skeletal muscle contraction
  • Increased tone
  • Greater GI motility
  • Bradycardia
  • Miosis
  • Bronchial constriction
  • Promote urination
89
Q

Indirect acting Cholinergic Agonists Contraindications

A

Intestinal and urinary obstruction

90
Q

Reversible Cholinesterase Inhibitors Uses

A
  • Produce pupil constriction in glaucoma

* Increases muscle strength in myasthenia gravis

91
Q

Reversible Cholinesterase Inhibitors Examples

A
  • Neostigmine
  • Pyridostigmine
  • Ambenonium chloride
  • Edrophonium
92
Q

Reversible Cholinesterase Inhibitors Side Effects

A
  • Muscle cramps
  • Bradycardia
  • Hypotension
  • Blurred vision
  • Hypersalivation
  • Seizures
93
Q

Cholinesterase Inhibitor used to treat patient with Alzheimer’s because these patients have decreased acetocholine.

A

Donepezil

94
Q

Irreversible Cholinesterase Inhibitor

A
  • Potent agents due to long-lasting effects
  • Used to produce pupillary constriction (treatment for glaucoma
  • Effects can last from days to weeks because there body has to regenerate cholinesterase
95
Q

Anticholinergics

A

Inhibit action of ACh by occupying ACh receptors

96
Q

Cholinergic Antagonists effects of Heart, Lungs, GI

A

Heart: large doses increase HR; small doses decrease HR

Lungs: Bronchodilation, decrease secretions

GI: Relax smooth muscle tone, decrease motility and peristalsis, decrease secretions

97
Q

Cholinergic Antagonists GU, Eye, Glands, CNS

A

GU: Relax detrusor muscle, increase sphincter constriction

Eye: Dilate pupils, decrease accommodation

Glands: Decrease salivation and perspiration

CNS: Decrease tremors and rigidity of muscles

98
Q

Atropine (Anticholinergics) Action

A
  • Increase HR

* Decrease GI motility, spasms, peristalsis, salivary and gastric secretions

99
Q

Atropine Side Effects/adverse reactions

A
  • Tachycardia, photophobia, headache, blurred vision
  • Abdominal distention, nausea, constipation
  • Dry mouth and skin, decreased sweating
  • Urinary retention, impotence
  • Palpitations, dysrhythmias
100
Q

What is contraindicated in glaucoma?

A

Anticholinergics

101
Q

Atropine Nursing Interventions

A
  • Monitor vital signs, urine output, bowel sounds
  • Monitor safety, bedside rails, driving motor vehicles
  • Provide mouth care
  • Avoid hot environments
  • Wear sunglasses in bright light
102
Q

Antiparkinsonism Anticholinergics

A

Benztropine

103
Q

Benztropine Side Effects

A
  • Tachycardia, headache
  • Blurred vision, ocular hypertension
  • Dry mouth/skin constipation
  • Urinary retention
104
Q

Benztropine uses

A
  • Parkinson’s disease

* Pseudoparkinsonism

105
Q

Anticholinergics for motion sickness

A
  • Antihistamine
  • Scopolamine:treats motion sickness, nausea, vomiting
  • Transdermal patch delivers dose over 3 days
106
Q

Anticholinergics for motion sickness Side Effects

A
  • Tachycardoa, hypotension
  • Dry mouth, constipation
  • Blurred vision, flushing
  • Muscle weakness, drowsiness
  • Urinary retention
107
Q

Insomnia treatments

A

Sedative-hypnotics

108
Q

Sleep stages and length

A

REM (hard to wake someone up & most dreams)
NREM
Cycles last around 90 minutes

109
Q

How many stages are in the NREM

A

4

110
Q

Children have long of what sleep stage?

A

Stage 3 and 4 of NREM sleep and older adults have a decreased of this stage.

111
Q

Sedatives do what?

A

Calm or slow brain activity

112
Q

Hypnotics do what?

A

Cause sleep
•Short acting (help you get to sleep)
•Intermediate acting (help to stay asleep) can cause “hangover”

113
Q

What is the mildest form of CNS depression?

A

Sedation

114
Q

OTC sleep aids examples

A
  • Antihistamines (diphenhydramine)

* Tylenol PM

115
Q

Barbiturates classifications are:

A

Long acting
Intermediate acting
Short acting

116
Q

Barbiturate long acting group includes

A

Phenobarbital which is used to control seizures in epilepsy

117
Q

Intermediate acting barbiturates include

A

Butabarbital which is used as sleep sustainers for maintaining long periods of sleep. They usually take 1 hour for onset

118
Q

Short acting Barbiturates

A

Can be used for procedure sedation and vital signs should be monitored closely

119
Q

Barbiturates are classified as a

A

Controlled Substance
Schedule II for short acting
Schedule III for intermediate acting
Schedule IV for long acting

120
Q

Sedative Hypnotic General Side Effects

A 
•Residual drowsiness (hangover) 
•Vivid dreams, nightmares
•Drug dependence 
•Drug tolerance
•Excessive Depression
Respiratory depression
•Hypersenitivity
121
Q

Barbiturates should be restricted to use for how long?

A

2 weeks

122
Q

Barbiturate Interactions

A
  • Alcohol, opioids, other sedative-hypnotics

* Decrease effects of oral anticoagulants, glucocorticoids, tricyclic antidepressants, quinidine

123
Q

Secobarbital sodium is used for

A

Surgery also.

124
Q

Pentobarbital can increase

A

Hepatic enzymes which increases metabolism of other drugs like:
•Oral anticoagulants, glucocorticoids, tricyclic antidepressants, and quinidine

125
Q

Benzodiazepines used as hypnotics are

A
  • Flurazepam
  • Alprazolam
  • Temazepam
  • Triazolam
  • Estazolam
  • Quazepam
126
Q

Benzodiazepines are classified as

A

Controlled substances Schedule IV

127
Q

Benzodiazepines are what at low does?

A

Anxiolytics

Pharmacology (2 decks)

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