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Pharmacology > Week 3 ~ Central Nervous System > Flashcards

Week 3 ~ Central Nervous System Flashcards

1
Q

What are 2 kinds of Analgesics?

A

Opioids

Nonsteroidial Anti Inflammatory Drugs (NSAIDS)

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2
Q

What is the definition of pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage

ACUTE: sudden onset and subsides once treated

PERSISTENT: Lasts longer than 6 weeks and difficult to treat

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3
Q

10 Different Types of Pain

A
  • Somatic
  • Phantom
  • Visceral
  • Superficial
  • Referred
  • Vascular
  • Central
  • Cancer
  • Psychogenic
  • Neruopathic
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4
Q

What are the 4 processes of the Pain Transmission Gate Theory?

A

Transduction
Transmission
Perception
Modulation

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5
Q

What is the Pain Transmission Gate Theory?

A

How impulses from the damaged tissues are sensed by the brain

Pain Management drugs are aimed at altering this system

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6
Q

In Pain Transduction what does the tissue release?

A

*Bradykinin
*Histamine
*Substance P
*Prostaglandins
*Serotonin
*Leukotrienes
~These stimulate nerve endings and starts the pain process

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7
Q

What are the 2 main pain fibres in Pain Transmission?

A

A-Delta Fibres

C Fibres

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8
Q

What do A-Delta Fibres do?

A

Sensitive to mechanical and thermal pain.

Transmit local and sharp pain

Stimulate the sympathetic nervous system

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9
Q

What do C Fibres do?

A

Sensitive to mechanical, thermal and chemical stimuli

Transmit poorly localized and dull pain

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10
Q

What happens in the Pain Perception phase?

A

Complex behavioural, psychological and emotional factors

Is controlled by the single gene and opioid receptor gene

Perception is diminished when there are many receptions and exacerbated when there are too few or missing ones. Relatively minor pain stimuli may be perceived as painful

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11
Q

What are two types of endogenous neurotransmitters?

A

Enkephalins

Endorphins

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12
Q

What happens in Pain Modulation?

A

The body produces endogenous neurotransmitters:
Enkephalins
Endorphins——-> Produced to fight pain —-> Bind to opioid receptors —-> Inhibit transmission of pain by closing the gate

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13
Q

What is Pain Tolerance?

A

The amount of pain a person can insure without interfering normal function

  • Not a physiological function
  • Is the point beyond which pain becomes unbearable
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14
Q

What is a Pain Threshold?

A

The level of stimulus needed to produce the perception of pain

*Measure of the physiological response of the nervous system

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15
Q

3 Chemical Categories of Opioids?

A

Meperidine
Methadone
Morphine

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16
Q

Opioid Drugs under the Meperidine Category

A

Meperidine

Fentanyl

Sufentanil

Alfentanil

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17
Q

Opioid Drugs under the Methadone Category?

A

Methadone

Propoxyphene

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18
Q

Opioid Drugs under the Morphine Category?

A

Morphine

Heroin

Hydromorphone

Codeine

Hydrocodone

Oxycodone

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19
Q

Opioid Analgesics Mechanism of Action: Three Classifications based on Actions

A

-Agonist: Bind to opioid pain receptor in the brain. Cause an
Analgesic response
-Partial Agonist: Bind to pain receptor. Cause a weaker neurological
Response then a full agonist
Agonist-Antagonist or mixed agonist
-Antagonist: Reverse the effects of these drugs on pain receptors.
Bind to pain receptor and exert no response
Competitive Antagonist

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20
Q

5 Types of Opioid Receptors?

A 
Mu*
Kappa*
Delta*
Sigma
Epsilon
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21
Q

Indications for Opioid Analgesics

A

~Moderate to severe pain

~Used as adjuvant analgesic drugs to assist the primary drugs with pain relief:

          1. NSAIDS
          2. Antidepressants 
          3. Anticonvulsants
          4. Corticosteroids

Opioids are also used for cough centre suppression or diarrhea

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22
Q

Contraindications for Opioid Analgesics?

A

~Known drug allergy

~Severe asthma or respiratory insufficiency

~Pregnancy

~Elevated Intracranial Pressure

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23
Q

Adverse Effects of Opioid Analgesics

A 
Hypotension
Palpations
Flushing 
Nausea
Vomiting
Biliary Tract
Urinary Retention
Itching
Respiratory Depression
Aggravation of asthma
Wheat Formation
Sedation
Disorientation
Euphoria
Tremors
Lowered seizure thresholds
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24
Q

2 Opiate Antidote

A

Naloxone (Narcan)

Naltrexone (ReVia)
-Bind to opiate receptors and prevent a response
- Used for complete or partial reversal of opioid-induced
Respiratory depression

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25
Q

Opioid Tolerance

A

Common physiological result of chronic opioid treatment

Larger dose of opioids is required to maintain the same level of
Analgesia

Opiates cause a physical and psychological dependance

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26
Q

What are Analgesics?

A

Medications to relieve pain without causing loss of consciousness

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27
Q

Non-Opioid Analgesics: Acetaminophen

A

Has analgesic and antipyretic effects

Little to no anti inflammatory effects

Available OTC

Is a component of many combination products with opioids

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28
Q

Acetaminophen Mechanism of Action

A

Similar to the action of salicylates

Blocks pain impulses peripherally by inhibiting prostaglandins synthesis

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29
Q

Indications of Acetaminophen

A

Mild to moderate pain
Fever
Alternative for those who can’t take aspirin

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30
Q

Dosage of Acetaminophen

A

Healthy adults is 4000mg per day

Overdose causes hepatic necrosis or long term ingestion of large doses can cause nephropathy

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31
Q

What’s the antidote for Acetaminophen toxicity?

A

Acetylcysteine

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32
Q

Acetaminophen Drug Interactions

A

Dangerous interactions with alcohol

Other Hepatotoxic Drug

Liver Dysfunction

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33
Q

What are Anaesthetics?

A

Drugs that depress the central nervous system

~Depression of consciousness
~ Muscle relaxant
~Loss of responsiveness to sensory stimulation (including pain)

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34
Q

What is General Anaesthetic?

A

Drugs that induce a state in which the CNS is altered to produce varying degrees of:

 ~Depression of consciousness 
 ~ Skeletal mm relaxation
 ~ Visceral Smooth mm relaxation
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35
Q

2 Types of General Anaesthetics?

A

Inhaled Anaesthetics: Volatile liquids or gases that are
Vaporized in oxygen and inhaled

Injectable Anaesthetic: Administered Intravenously

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36
Q

Inhaled Anaesthetics

A

Inhaled Gas: Nitrous Oxide (“laughing gas”)

Inhaled Volatile Liquids
~Desflurane (Suprame)
~ Halothane

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37
Q

Injectable Anaesthetics

A

Ketamine (Ketalar)

Propofol (Diprivan)

Thiopental (Pentothal)
- Isoflurane (Forane)

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38
Q

Indications for Injectable Anaesthetics

A

Uses:
~ To induce or maintain general anaesthesia
~ To induce amnesia
~ To reduce anxiety
~ As an adjunct to inhalation-type anaesthetics

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39
Q

Adjunctive Drugs for Injectable Anaesthetics

A

Opioid Analgesics

Benzodiazepine

Anticholinergic

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40
Q

Opioid Analgesic Drugs

A

Alfentanil (Alfenta)

Fentanyl

Meperidine (Demerol)

Morphine

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41
Q

Benzodiazepine Drugs

A

Diazepam
Lorazepam
Midazolam

42
Q

Anticholinergic Drugs

A

Atropine

43
Q

What is the Overton-Meyer Theory?

A

When a sufficient number of inhalation anaesthetic molecules dissolve in the lipid cell membrane.

Effects:
1. Orderly and systematic reduction of sensory and motor CNS
Function
2. Progressive depression of cerebral and spinal cord functions

44
Q

General Anaesthetic Indications

A

Used during surgical procedures to create
Unconsciousness
Skeletal Muscular Relaxation
Visceral Smooth Muscle Relaxation

Rapid onset and quickly metabolized

45
Q

Contraindications of General Anaesthetic

A

Known drug allergy
Pregnancy
Narrow Angle Glaucoma
Known susceptibility to malignant hyperthermia

46
Q

General Anaesthetic Adverse Effects

A

Affect the heart, liver, kidneys, peripheral circulation, respiratory tract

Myocardial Depression

Malignant Hyperthermia

47
Q

What is Malignant Hyperthermia?

A

Sudden elevation of body temperature greater than 40c, tachypnea, tachycardia, muscular rigidity

48
Q

General Anaesthetic Drug Interactions

A

Anti hypertensives

B-Blockers

Tetracycline

49
Q

What is Local Anaesthetic used for?

A

Used to a specific part of the body due to pain

Interferes with the nerve impulse transmitting to specific areas of the body. Doesn’t cause loss of consciousness

50
Q

2 Types of Local Anaesthetic?

A

Topical

Parenteral (Spinal Injection)

51
Q

2 Types of Parenteral Local Anaesthetic?

A

Central: Spinal or Intraspinal
Ie. Epidural or Intrathecal

Peripheral: Infiltration, nerve block, topical

52
Q

4 Types of Parenteral Anaesthetic Drugs?

A

Lidocaine

Mepivacaine

Procaine

Tetracaine

53
Q

Local Anaesthetic Drug Effects?

A

Paralysis ~

1st: Autonomic activity is lost
2nd: Then pain and other sensory functions are lost
3rd: Motor activity is lost

*As drug wears off the recovery occurs in reverse order
Motor –> Sensory –> Autonomic Acvitity

54
Q

Local Anaesthetic Indications?

A

Surgical/Dental and Diagnostic Procedures

Treatment of certain types of chronic pain

Infiltration anaesthetic or nerve block anaesthetic

55
Q

Infiltration Anaesthesia

A

Used in minor surgical or dental procedures

Given in a circular pattern

Injected intradermally, subcutaneously or submucosally across the
path of nerves supplying the targeted area

56
Q

Nerve Block Anaesthesia

A

Used for surgical, dental and diagnostic procedures

Therapeutic management of pain

Injected directly into or around the nerve trunks or nerve ganglia that supply the area to be numbed

57
Q

Local Anaesthetic Contraindications

A

Drug allergy

Spinal Headache

58
Q

What are Neuromuscular Blocking Drugs?

A

Prevent nerve transmission in certain muscles resulting in paralysis of the muscle

Used with anaesthetics during surgery

Paralyze respiratory and skeletal muscles and so the patient is unable to breath on their own

Do not cause sedation of pain relief!

59
Q

2 Types of Neuromuscular Blocking Drugs?

A

Depolarizing

Non Depolarizing

60
Q

How Neuromuscular Blocking Drugs affect the body?

A

First sensation is muscles weakness followed by total paralysis

Smaller rapidly moving muscles like fingers and eyes are affected first and then limbs, neck and trunk

Then intercostal muscles and the diaphragm are affected resulting in cessation of respiration

Recovery of muscular activity will occur in reverse order

61
Q

What are Sedatives?

A

Drugs that have an inhibitory effect on the CNS to reduce nervousness, excitability and irritability without causing sleep

62
Q

What are Hypnotics?

A

Causes sleep.

A sedative can become a hypnotic if it is given in larger doses

63
Q

What are Sedative-Hypnotics?

A

Dose dependant at low doses, they calm the CNS without inducing sleep and at high doses they calm the CNS to the point of causing sleep

Habit forming and have low therapeutic index

64
Q

What are the sleep stages?

A

Rapid eye movement (REM) sleep

Non rapid eye movement (non-REM) sleep

65
Q

4 Categories of Barbiturates?

A
  1. Ultrashort: Short surgical procedures
  2. Short: Sedative-hypnotic, control convulsive conditions
  3. Intermediate: Same as short
  4. Long: Sedative-hypnotic, epileptic seizures
66
Q

Name of an Ultra Short Barbiturate?

A

Thiopental (Pentothal)

67
Q

Name of a Short Barbiturate?

A

Pentobarbital

68
Q

Name of an Intermediate Barbiturate?

A

Butalbital

69
Q

Name of a Long Barbiturate?

A

Phenobarbital

70
Q

What’s a Therapeutic Index?

A

Dosage range which the drug becomes effective but above that range rapidly becomes toxic

Barbiturates have a very narrow therapeutic index!

71
Q

Barbiturate Mechanism of Action

A

Act primarily on the brain stem (reticular formation)

Inhibits gamma-aminobutyric acid (GABA)

Inhibit the nerve impulse travelling in the cerebral cortex

72
Q

Barbiturate Drug Effects?

A

Low Doses = Sedative

High Doses = Hypnotic effects and lower respiratory rate

Enzyme Inducers = stimulate liver enzymes that cause the metabolism
Or breakdown of many drugs and shorten duration
Of action

73
Q

Barbiturate Indications:

A

Sedative

Hypnotic

Anticonvulsant

Anaesthetics for surgical procedures

74
Q

Barbiturate Contraindications

A

Known allergy

Pregnancy

Severe liver disease

Significant respiratory difficulties

75
Q

Barbiturate Adverse Effects?

A

Nausea/vomiting

Diarrhea/constipation

Drowsiness/lethargy

Vertigo

Mental Depression

Respiratory Depression/Apnea

Bronchospasms/cough

Hypotension

Reduced REM sleep resulting in agitation

76
Q

Barbiturate Toxicity and Overdose

A

Respiratory Arrest

CNS depression ranging from sleep to coma and death

77
Q

Barbiturate Additive Effects

A

If ingested with the following it will intensify the CNS depression

Alcohol

Antihistamines

Opioids

Benzodiazepines

78
Q

Barbiturate Inhibited Metabolism

A

Mono amine oxidase inhibitors (MAOIs) will prolong effects of barbiturates

79
Q

Barbiturate Increased Metabolism

A

Reduces anticoagulant response leading to possible clot formation

80
Q

What are Benzodiazepines?

A

Most commonly used sedative-hypnotic because of their favourable adverse effect

81
Q

2 Classifications of Benzodiazepines?

A

Sedative-Hypnotic

Anxiolytics (Relieves Anxiety)

82
Q

Benzodiazepine Sedative-Hypnotic Types

A

Long Acting:
Flurazepam (Apo-Flurazepam)

Short Acting:
Temazepam (Restoril)
Triazolam (Halcion)

83
Q

Benzodiazepines Mechanism of Action

A

Depress CNS activity

Affect hypothalamic, thalamic and limbic systems of the brain

Activate Benzodiazepine receptors

Doesn’t suppress REM and doesn’t increase metabolism of other drugs!

84
Q

Benzodiazepines Drug Effects

A

Calming effect on CNS

Useful in controlling agitation and anxiety

Reduce excessive sensory stimulation, inducing sleep

Induce skeletal muscle relaxation

85
Q

Benzodiazepine Indications

A

Sedation

Sleep Inducing

Anxiety Relief

Depression

Skeletal muscle relaxation

Alcohol withdrawal

Epilepsy

Balanced Anesthesia

Moderate or conscious sedation

86
Q

Contraindications of Benzodiazepines?

A

Known drug allergy

Pregnancy

Narrow angle glaucoma

87
Q

Benzodiazepines Adverse Effects?

A 
Mild/Infrequent:
     Headache
     Vertigo
     Drowsiness/Dizziness
     Lethargy

Fall hazard in frail elderly

88
Q

Benzodiazepine Drug Interactions

A

Grapefruit and grapefruit juice alter drug absorption

Kava and Valerian further CNS depression

Other CNS depressants further CNS depression

89
Q

Drugs under the Nonbarbiturate or Non Benzodiazepine Sedatives:

A

Buspirone
`Chloral Hydrate

Tizanidine

Paraldehyde

90
Q

What is a Seizure?

A

Brief episode of abnormal electrical activity in the nerve cells of the brain

91
Q

What are convulsions?

A

Involuntary spasmodic contractions of any or all voluntary muscles throughout the body including skeletal and facial muscles

92
Q

What is Epilepsy?

A

Chronic and recurrent pattern of seizures

93
Q

2 Types of Epilepsy’s?

A

Primary (Idiopathic)
` No apparent cause (50% of cases)

Secondary
` Distinct cause identified ie trauma, infection

94
Q

Classification of Epilepsy

A
  1. Partial
    ` Simple
    ` Complex
  2. Generalized
  3. Unclassified
  4. Status Epilepticus
95
Q

What are Anti-Epileptic Drugs?

A

*Also known as anti-convulsants

Control and prevent seizures while maintaining quality of life and to minimize adverse effects

Usually lifelong

Serum drugs need to be measured

96
Q

Anti-Epileptic Drugs Mechanism of Action

A

Exact mechanism is unknown and thought to alter the movement of sodium, potassium and calcium ions across nerve cells in the brain

Prevent degeneration

Spread of excessive electrical discharge from abnormally functioning nerve cells and protect surrounding normal cells

Reduce nerve stimulation and transmission of impulses from one nerve to the next

97
Q

Anti-Epileptic Drug Adverse Effects?

A

Drowsiness

Vision Problems

Narrow Therapeutic Index

98
Q

Anti-Epileptic Drug Interactions?

A

Increased bone marrow toxicity

Decrease in half life

Increase CNS depression

Breakthrough seizures

Increased or decreased drug levels

99
Q

First Choice Anti-Epileptic Drugs

A

Carbamazepine

Phenobarbital

Phenytoin

Primidone

Valproic Acid

100
Q

Some Second Choice Anti-Epileptic Drugs

A

Clonzepam

Levetiracetam

Clorazepate

Pharmacology (6 decks)

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