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Pharm > Central Nervous System Drugs > Flashcards

Central Nervous System Drugs Flashcards

1
Q

Cerebrum

A

Thinking portion: Perception, Speech, Conscious motor movement, Skeletal muscle movement, memory, smell
Higher brain functioning

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2
Q

Thalamus

A

All nerve endings come here
Relay center: Sounds, sights, pain, touch, temperature.
Sends out motor response - needs to go back to the had to tell it to take it off the burning iron
Controls mood and motivation
- Associated with bipolar, anxiety, panic disorder, OCD

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3
Q

Hypothalamus

A

Ventral to Thalamus
Controls homeostasis
Major visceral control center: Hunger, thirst, water balance, body temp
Part of limbic (emotional balance)
Connection with brainstem (HR, RR, BP, Pupil size)
Plays a big part in the autonomic system

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4
Q

Cerebellum

A

Little brain at base of brain
Controls: Muscle movement, balance, posture, tone
Recieves info on vision, position, equilibrium, touch, and calculates strength
Injury results in uncontrolled jerkiness
A lot of Parkinson drugs work here

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5
Q

Brain Stem

A

Connects spinal cord to brain
Medulla oblongata (A lot of vital signs are regulated here), pons and midbrain here
Major relay center
Major reflex and control center: Breathing, Heart rate, swallowing, coughing, vomiting, vision

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6
Q

Spinal cord

A

Transmits to and from brain
Disruption: Paralysis, Paresthesia
Afferent nerves - to the brain
Efferent nerves - away from brain

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7
Q

Limbic system

A

Group or series of brain pathways
Responsible for emotion and mood
Some pain meds designed to effect Limbic system due to the emotional factor or pain

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8
Q

Reticular Activating System

A

Responsible for heightened alertness
Sleep meds designed to slow down RAS
Some motor units involved

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9
Q

Basal Ganglia

A

Responsible for Posture and movement

Cognitive function.

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10
Q

Blood brain barrier

A

Protects brain from pathogens and toxins
Supplies Oxygen, glucose, and nutrients
CNS drugs must penetrate

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11
Q

Neuron parts

A

Dendrites come before cell body
Carry message to the cell body
Cell body interprets message and pushes info down the axon.
Transfers to another nerve through the synapse

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12
Q

Monoamines

A

Dopamine. Epinephrine, Norepinephrine, Serotonin.

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13
Q

Amino Acids

A

Asperate, Aminobutyric acid (GABA), Glutamate, Glycine.

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14
Q

Gamma Aminobutyric acid (GABA)

A

Inhibits over excitation of brain
Slows things down
Used for seizure medication and sleep disorders

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15
Q

Opiod peptides

A

Dynorphins, Endorphins, Enkephalins

They are endogenous; therefore the body makes it’s own opium.

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16
Q

Nonopioid peptides

A

Neurotensin, Oxytocin, Somatostatin, Substance P, Vasopressin

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17
Q

Substance P

A

Pain control
Acts as a neurotransmitter
Has a role in interpreting pain
Has a role in regulating self produced endogenous analgesic response.
Big reason why we have different pain tolerance levels.

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18
Q

Actions of drugs

A

Blocking the reuptake of neurotransmitters
Blocking the enzymes that break down the neurotransmitters
Stimulating specific receptor sites when neurotransmitter is unavailable
Stimulating presynaptic nerve to release greater amounts of neurotransmitter

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19
Q

Pain definition

A

Whatever the experiencing person says it is and wherever he says it does.
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

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20
Q

Four phases of pain

A

Transduction
Transmission
Perception
Modulation

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21
Q

Transduction

A

Stimulation of first nerve; at the site of injury
Injured tissue release chemicals that propagate pain messages such as prostoglandins or kinnins or histamines (become neurotransmitters)
Neurotransmitters stimulate or sit on nociceptors (nerve ending) located on skin, connective tissue, muscle, circlulatory system, thoracic, abdominal, and pelvic areas.
Stimulated by trauma, injury or chemical mediators.
Stimulates first nerve

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22
Q

Transmission

A

Nerve 1 to the spinal cord then to the brain
Pain stimuli enters spinal cord in the dorsal horn
Substance P is released in response to pain (a peptide in the dorsal horn) (Acts as neurotransmitter)
Glutamate and ATP also act as neurotransmitters
Differences here may be why we have different pain tolerances.

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23
Q

Afferent Neurons

A

Carry signals TO CNS

Pain begins in nociceptors in afferent neurons and gets carried to CNS

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24
Q

Perception of pain

A

Pain impulse reaches brain
Brain now has a conscious awareness of pain sensation
LIMBIC SYSTEM ACCOUNTS FOR EMOTIONAL RESPONSE
Higher cortical structures will identify as “pain”

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25
Q

Modulation

A

Brain interprets and decides what to do with the information
Pain message is inhibited through this phase
Descending from brain to spinal cord, we produce another set of neurotransmitters that will impeded pain impulse
Neurotransmitters include serotonin, norepinephrine, neurotensin, GABA, our own endogenous opioids

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26
Q

Modulation of pain

A

Within spinal cord are opioid receptors called kappa and mu.
Endogenous opioids can block kappa and mu
Exogenous opioids or opioid medications kick off the endogenous opioids because they are stronger and block kappa and mu
If kappa and mu are not blocked then move to thalamus in brain

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27
Q

Opioid Receptors

A

Mu and Kappa
(And Delta… red headed step child no one cares about)
Mu most important from a pharmacological stand point

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28
Q

Responses of an activated Mu receptor

A

Analgesic, Respiratory depression, sedation, euphoria, Physical dependence, Decreased GI motility

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29
Q

Responses of and activated Kappa receptor

A

Analgesic, Sedation, Decreased GI motility, Miosis

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30
Q

Miosis

A

Pinpoint pupils

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31
Q

Endorphins

A

endogenous opioids, enkephalins, and dynorphins are made in own body
Released in synapse and bind with opioid receptors on (mu and kappa recepters) dorsal horn to prevent further transmission of painful stimuli.

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32
Q

Nociceptive pain

A

Pain caused by damage to the body.

Somatic and Visceral

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33
Q

Somatic Pain

A

Pain to skin, muscle. More superficial. Injury to tissues.

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34
Q

Visceral pain

A

Dull, throbbing, poorly localized. Deep tissue; organs.

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35
Q

Neuropathic pain

A

Pain in the nerve pathway. Hardest to treat. Tingling, burning, stabbing, radiates. Usually long term.

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36
Q

Vascular pain

A

Caused by spasms which cause inflammation which causes pain. Migraines an example

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37
Q

Psychogenic pain

A

No cause; in patients head

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38
Q

Phantom Pain

A

Nerve endings still raw from amputation. Brain is interpreting the pain wrong. (Egg.. I mean Leg pain when there is no leg). Will go away within 6 mo-1 year.

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39
Q

Acute pain

A

Organic cause: Common
Environmental contributions and family involvement: small
Insomnia: Unusual
Treatment goal: Cure
Usually has a physical cause that can be treated

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40
Q

Chronic pain:

A

Harder to treat than acute. Can be life changing.
Dependence and tolerance to medication is common.
Psychological component: Often a major problem
Organic cause: Often not present
Environmental contributions and family involvement: Significant
Insomnia: Common
Treatment goal: Functionality
Pain lasting longer than 3 mo or longer than medically expected.

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41
Q

Signs of acute pain

A

Hypoxia
Hypercapnia (Hanging on to CO2 from holding breath)
Hypertension
Tachycardia
Emotional difficulties
If left untreated can lead to chronic pain

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42
Q

Chronic pain - 4 subtypes

A
  1. Pain that persists past the normal healing time for an acute injury
  2. Pain related to chronic disease (arthritis)
  3. Pain without identifiable organic cause
  4. Pain that involves both the chronic and acute pain associated with cancer (not worried about them about becoming addicted. We treat differently)
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43
Q

Consequences of unrelieved pain

A
  1. Stress hormone response
  2. Impaired muscle movement
  3. Quality of life changes (Decreased social relationships, decreased sleep, depression, anger, hopelessness)
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44
Q

Barriers to pain management: The professional

A
  1. Lack of knowledge about pain medication
  2. Misconceptions
  3. Inadequate assessment
  4. Concerns about opioids (addiction, respiratory depression, side effects)
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45
Q

Barriers to pain pain management: The patient and family

A

Stoicism (Lack of reporting pain, pain is weakness)
(Supposedly men complain of pain less then women… apparently they needed to include our husbands in this study)
Concerns about medication (Addiction, just say no, side effects)
Medication administration (confusion about dose, times, etc)

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46
Q

True or false: Pain is a natural consequence of getting old.

A

False

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47
Q

True or false: Older patients don’t feel pain as acutely as younger

A

False: Transmission of pain may be altered by chronic disease, but they will still feel it.

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48
Q

True or false: Older patients can’t reliably report pain

A

False: Make sure hearing aids are in and glasses on if using a pain scale.

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49
Q

What is the first step in pain management??

A

Assessment!

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50
Q

What do we need to know about the patient’s pain?

A 
Location
Severity
Type
Duration
Effect of daily life
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51
Q

What are some non-pharmacological treatments?

A

Heat for muscle, Cold for acute injury, Accupuncture, Massage, Biofeedback, Guided imagery, Relaxation, Exercise, Trancutaneous Electrical Nerve Stimulation (TENS)

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52
Q

Opioid agonist

A

Occurs when opioid “Turns on” the opioid receptors. They kick our endogenous opioids off and are able sit on the receptors longer, thus causing better and longer pain relief.

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53
Q

Opioid Agonist Effects

A

Analgesia, sedation, mental clouding, Euphoria, Respiratory depression, Miosis, Decreased GI movement, Depression of cough reflex, Orthostatic hypotension, Stimulate vomiting reflex.

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54
Q

Opioid Kinetics

A

Absorption: Good oral (Thats what she said) and Large first pass effect
Metabolism: Hepatic
Elimination: Renal, Feces (With morphine when given PO)
Onset: 15-30 minutes
Duration: 3-7 hours

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55
Q

Opioid Cautions

A

Contraindicated for patients with a TBI, respiratory depression, pts receiving other CNS depressants, head injury.
Dose reduction may be necessary in elderly due to altered pharmacokinetic properties.
Drug addicts assess case my case. Monitor how much. May give a lower dose.

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56
Q

Opioid Adverse effects

A

CNS: mood changes, lethargy, delerium, euphoria, pupillary constriction
Respiratory: Decreased RR, Resp Arrest, apnea
Cardiovascular: Hypotension, bradycardia, Cardiac arrest, shock, coma
GI: N/V, constipation
GU: Urinary retention (Watch with elderly men with BPH)
Histamine release: Pruritis and uticaria (May need to give benedryl)

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57
Q

Why would we give someone having a Heart Attack opioids?

A

Opioids cause bradycardia and lower BP

58
Q

Opioid drug interactions

A

Possible with any other hepatically cleared drug (Will increase opioid level or other drug level)
Potentiation of sedation and respiratory depression
Caution with other CNS depressant drugs including alcohol

59
Q

Opioid Patient Education

A

Correct any fears or misconceptions about pain meds
Reassure that you will listen and act on their reports of pain
If patient is going home with a prescription, avoid operating heavy machinery, driving, alcohol or other CNS depressants, Storage of drugs (away from children)
Educate on High Fiber diet

60
Q

Treatment of an opioid overdose??

A

Narcan

61
Q

Nursing interventions

A 
Assess pain prior to and during therapy
Use pain assessment tool
Assess vital signs, esp resp
Keep pulse ox on pt
Administer stool softeners/laxatives prn
Assist patient when getting out of bed
62
Q

Strong Narcotic Agonists are ordered when pain level is a ___________ out of 10 and higher

A

7

63
Q

Morphine is ordered in ______

A

mg

Morphine is prototype

64
Q

fentanyl is ordered in __________

A

mcg

65
Q

Fenanyl is ______ times more potent than morphine

A

100

66
Q

Meperidine (Demerol)

A

Synthetic; less resp depression than morphine. Less likely to have constipation.

67
Q

Methadone

A

Half life 36 hours so we can help patients with withdrawls

68
Q

Oxycodone (Percodan, Percocet (Oxycodon + Tylenol))

A

Prescribed for moderate to strong pain
Often mixed with tylenol
Oycodone has more of an effect on the brain
Tylenol effects more peripheral
Wont need as much of narcotic if mixed with tylenol

69
Q

Morphine mechanism of action

A
  1. Occupies mu and kappa in brain and dorsal horn or spinal cord which…
  2. Reduces the release of neurotransmitters in the presynaptic space which…
  3. Produces hyperpolarization of postsynaptic dorsal horn neurons
  4. These actions prevent transmission of nociceptor pain
  5. Decreases release of substance P which modulates pain perception.
    Morphine has high first pass effect.
70
Q

Hydrocodone (Vicodin)

A

Considered a Mild Narcotic Agonist
Codeine
#1 drug abused
Schedule 2 drug

71
Q

Codeine is ____________ the potency of morphine

A

1/6

72
Q

Codeine mechanism of action

A

Similar to morphine
Acts on opioid receptors in the CNS to produce analgesia (less than morphine), euphoria, and sedation
Acts on medullary cough relfex center to depress the cough reflex.
Has drying effect on mucous membranes

73
Q

Codeine adverse effects as cough suppressant

A

Dry mouth, drowsiness, sedation.
When dosed as an analgesic similar adverse effects as morphine
Less physical dependence than with morphine
Less sedation, euphoria

74
Q

Caution use of codeine with…

A

need their cough reflex. Patients with a chest tube, Patients who have had abdominal surgery, Stroke patients, patients with an aspiration risk.

75
Q

Opioid Agonist-Antagonist

A

Have mixed opioid effects
Agonist as some receptor and antagonist at other receptor
Blocks opioid effect on one receptor while producing opioid effects on a second receptor.
May be good with addicts

76
Q

Narcotic Agonist-Antagonist

A 
pentazocine (Talwin)
buprenophine (Buprenex)
butorphanol (Stadol)
nalbuphine (Nubain)
Dont have to worry about resp depression. 
Prescribed for mild to moderate pain
Often ordered for addicts
77
Q

Drugs that end in -erase

A

break down neurotransmitters are destroy

78
Q

Opioid Antagonist

A

High affinity for opioid receptor but cause no effect

Opioid antedote: Narcan

79
Q

Tolerance

A

Body has become accustomed to the effects of the substance and that the patient must use more of it to achieve the desired effect
Develops to analgesia, resp effects, and euphoria

80
Q

Dependence

A

Body physically dependent on drug.
Characterized by withdrawal symptoms when drug is discontinued
Physiological effects… not psychological
May need to taper medication when possible

81
Q

Addiction

A

Psychological syndrome
Compulsive use of drug for secondary gain, not for pain control
Genetic, psychosocial and environmental factors influence the development of addiction.
Addiction to opioids rare for med reasons

82
Q

Opioid Withdrawl symptoms

A

Sweating, runny nose, irritability, Increased BP, tremor, anorexia, N/V, diarrhea, cramps, muscle spasms, pupils dialated, seizure risk

83
Q

Narcan (naloxone)

A

Adverse effects: hypotention/HTN
Given IV
Only stays in the system one hour
Have to monitor closely

84
Q

Principles of pain management with opioids

A

Start with low dose and titrate up

Around the clock is better than PRN

85
Q

Equianalgesia

A

Producing the same degree of analgesia
Equianalgesic dose charts show the dose of an analgesic required to produce the same effect as 10 mg of morphine. (Standard measure of pain relief)
ALWAYS COMPARING TO 10 mg OF MORPHINE

86
Q

Inflammation Signs

A

Heat, Redness, Swelling, Pain, Loss of Function

We treat with corticosteroids

87
Q

Inflammation process

A 
Vascular resoponse (vasoconstriction and vasodilation)
Cellular response (neutrophils)
88
Q

Pathophysiology of inflammation - Vascular response

A

Occurs immediately after injury
Vasocostriction happens in the surrounding tissues first (10-15 min)
Then, vasodilation occurs (increased blood flow to the area)
Capillary permeability increases (Fluid accumulates in tissues so WBC can get into the tissue leaking fluid/swelling. Chemical mediators are released causing pain and impaired function

89
Q

Pathophysiology of inflammation - Cellular response

A

WBC’s prepare for emigration by moving to periphery of blood vessels
WBC’s pass through cappilary walls into tissue spaces
Cellular debris or bacteria become attracted to WBC’s
Neutrophils and monocytes engulf the cellular debris

90
Q

Pathophysiology of inflammation - Chemical response

A

Mast cells rupture and release biochemical mediators such as histamine, prostaglandins, and leukotrines. All which contribute to inflam.

91
Q

Prostaglandins

A

Help regulate some parts of inflammation, body temp, pain transmission, platelet aggregation
Derived from an acid which is released from the cell membrane in response to stimuli
Acid is converted to prostaglandin by cyclooxygenase (COX) enzyme)

92
Q

Prostaglandins effects

A

Increase uterine or other smooth muscle contraction
Decrease BP
Decrease gastric acid secretion and increase mucous production
Increase body temp
Increase platelet aggregation - clotting
Increase renal vasodilation
Increase inflammation and capillary permeability
Effect blood vessels and bronchials

93
Q

COX 1

A

Synthesizes prostaglandins that are involved in regulating normal cells activity
Found in blood vessels, stomach, kidney
Leads to prostaglandin formation that protects gastric mucosa and helps maintain normal renal function and temperature

94
Q

COX 2

A

Produces prostaglandins at sites of inflammation
Found in brain and kidney
Leads to prostaglandin formation that causes inflammation
Do not have any antiplatelet activity

95
Q

Prostaglandins again

A

acid + cyclooxygenase (COX 1 or 2)

96
Q

COX 1 again

A 
Good!
Normal cell activity
Protects GI mucosa - Decrease HCl acid
Blood vessels = Vasodilation = decreased BP
Lungs and Bronchials = dilation
Help renal function
Promote platelet aggreagtion
97
Q

COX 2 again

A 
BAD
Sensitive to pain
Increase fever
Increase inflammation
Increase cap permeability
98
Q

NSAIDS block ___________

A

Prostaglandins

99
Q

NSAIDS are COX ____________

A

Blockers

Some may only inhibit 1 and some only 2

100
Q

COX 1 on NSAIDS

A

Increase HCl acid (Therefore GI Ulcers and GI bleeds)
Increase risk for bleeding
Impaired renal function
Bronchoconstriction (Caution NSAIDS with Asthma and COPD)

101
Q

COX 2 on NSAIDS

A

Decrease risk of colorectal cancer (fun fact)
Cause renal impairement
Decrease vasodilation; therefore increase vasoconstriction therefore risk of MI or Stroke

102
Q

NSAIDS - Mechanism of action

A

Inhibit COX

Decrease production of prostaglandings

103
Q

NSAIDS - Indications

A

Arthritis (both osteo and rheumatoid)
Mild to moderate pain
Fever
Inflammation

104
Q

NSAIDS - Absorption

A

Oral

First pass effect variable between agents

105
Q

NSAID - distribution

A

Highly protein bound
Onset: 30 min (inflammation response takes days to weeks)
Half life: range from 1.5 to 50 hours

106
Q

NSAID metabolizes in the ____________

A

Liver

107
Q

NSAIDS get excreted through the _________

A

Kidney

108
Q

NSAID Adverse effects

A 
GI distress, ulcers, bleeding
Sedation, confusion
Rash, fever
Tachycardia
Acute bronchospasm
Renal: sodium and water retention; impairement
Head ache, dizziness
Tinnitus
109
Q

NSAIDS cautions

A 
Elderly may be more sensitive to adverse effects
Asthmatics
Ulcers or history of GI bleeds
Renal disease
Hepatic disease (Tylenol Bad)
Pregnant women should no use
Pts on anticoag therapy
Gout
Children with varicella or flu like symptoms
110
Q

NSAIDS drug interactions

A

Increase effects of anticoags and antiplatelets

Intereferes with metabolism of these drugs: digoxin, phenytoin, cyclosporine, fluconazole

111
Q

Aspirin Absorption

A

Occurs with 30 min depending on form gastric pH, presence of food
Mostly absorbed in small intestine
Suppositories are slower and have more variable absorption than oral forms.
Can give as a suppository

112
Q

Aspirin - Antipyretic effect

A

Works on hypothalamus which is the body’s temp regulator

113
Q

Aspirin - Anti-inflammatory effect

A

Inhibits prostaglandin synthesis

114
Q

Aspirin - Analgesic effect

A

Pain is mediated by prostaglandins that synthesize pain receptors
ASA inhibits COX 2 which decreases prostaglandins

115
Q

Aspirin - Anti-platelet effect

A

Has irreversible inhibition of throboxane A2

Which is a prostaglandin that indiced platelet aggregation

116
Q

ASA cautions

A

Contraindicated for peptic ulcer patients or other bleeding disorders
Do not give alcoholics
Do not give with anticoag therapy
Do not give to gout patients, renal (depends on how bad kidneys are functioning), or liver
Do not give to children with fever or flu like symptoms
Use in caution with smokers
ASA causes sodium retention; therefore harder on the kidneys.

117
Q

Nicotine is considered ____________; therefore do not give ASA’s

A

Ulceragenic

118
Q

ASA - Pregnancy Category

A

First and Second trimester: Category C

Third Trimester: Category D

119
Q

Salicylism is _______

A

Mild aspirin toxicity
Occurs with long term or high dose therapy
Signs and Symptoms: Headache, tinnitus, GI distress, resp stimulation, drowsiness or confused.
Treat by reducing the drug or stop therapy still together

120
Q

Absorption rate effected with suppositories

A

Due to diarrhea, constipation, fever

We never know how much gets absorbed

121
Q

Salicylate poisoning

A

Life threatening
No antidote
Signs and Symptoms are the same but more pronounced, occurs quickly.
Treat by gastric emptying and life support if needed. Charcoal

122
Q

Prostaglandin synthesase inhibitors

A

Ibuprophen (Motrin, Advil)

123
Q

Ibuprofen

A

Propoinic acids: fenoprofen, naproxen (ALEVE), fetoprofen

Acetic acids: indomethacin (Indocin), ketorolac (Toradol)

124
Q

Ibuprofen Absorption

A

Mostly GI system
Slower if taken with food
Analgesic and antipyretic effects take 2-4 hours
Inflammatory response takes a few days to weeks (Usually need higher doses)
Highly protein bound (Stays longer in the system)

125
Q

Ibuprofen Cautions

A

Ulcer, bleeding disorders
Contraindicated in heart patients
There may be a black box warning (May increase serious and potentially fatal cardiovascular thrombotic events, Serious GI events also listed)
Caution in renal patients (inhibition of renal prostaglandins can decrease renal blood flow)
Can increase BP
Can cause blurred vision and corneal deposits

126
Q

Selective COX 2 inhibitors

A

celecoxib (Celebrex)
Cant use with patients with sulfa allgery
Someone with history of GI bleed this would be the best drug to put them on

127
Q

Celebrex - Mechanism of action

A

Selectively inhibits the enztme COX 2

Inhibits prostaglandin synthesis

128
Q

Celebrex - Indications

A

Arthritis ad relieve dysmenorrhea
Category D in third trimester
Doesn’t effect kidneys
Increase INR

129
Q

Papa-aminophenol derivatives

A

Acetaminophen - ASA or APAP

130
Q

Acetaminophen mechanism of action

A

Fever - direct action on the hypothalamic heat regulating center
Inhibits the action of chemical that causes vasodilation and sweating
Pain - not completely clear how it works
No peripheral prostaglandin synthetase inhibition which means no anti-inflammatory effect or platelet aggretation inhibition

131
Q

Acetaminophen indications

A

Fever
Mild to moderate pain
Drug of choice for infants and children with flu or flu like symptoms and analgesic choice during pregnancy and lactation

132
Q

APAP Absorption

A

Rapid and completely absorbed orally

133
Q

APAP distribution

A

onset 30 min
peak 1-2 hours
Duration 4 hours

134
Q

APAP is metabolized in the ________

A

Liver

135
Q

APAP is excreted through the _______

A

Kidneys

136
Q

APAP adverse effects

A

Rare

Rash, uticaria, nausea, fever, neutropenia, throbocytopenia, Jaundice (Liver problems)

137
Q

APAP interactions

A

Use in caution with hepatic disease
Increased hepatoctoxicity with other drugs that cause liver damage
Major contraindication: hepatic disease, viral hepatitis, alcoholism
May exacerbate anemias

138
Q

APAP overdose

A

Can be fatal
It is partially metabolized into a toxic metaboliite that your body converts to a nontoxic form with the help of glutathione
In an overdose, glutathione is quickly depleted
Accumulation of toxic metabolite occurs, resulting in liver damage

139
Q

Mucomyst Acetylcysteine

A

Tylenol anecdote

140
Q

APAP symptoms of toxicity

A 
Anorexia, N/V, Pallor, Abdominal discomfort (RUQ pain in the first few days), Jaundice (Later stage)
#1 poisoning in children

Pharm (11 decks)

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