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PHAR370- Fundamentals of Pharmacology and Therapeutics > Module 2- Introduction to nervous system > Flashcards

Module 2- Introduction to nervous system Flashcards

Introduction to nervous system

1
Q

The Nervous System is the body’s…

A

control and communication system

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2
Q

The NS consists of…

A

brain, spinal cord, sensory organs, nerves

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3
Q

How does the NS function?

A
  1. Recognize: changes in internal or external environment
  2. Process and Integrate: perceives the changes in environment
  3. React: reacts to changes in the environment by producing a response or an action to counteract the change
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4
Q

Neurons

A

Functional unit of the brain and are nerve cells capable of generating and transmitting electrical signals

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5
Q

Neurotransmission

A

Process by which neurons communicate with each other

  1. electrical impulse travels down axon of a neuron
  2. when electrical impulse reaches the end of the presynaptic neuron, it causes the vesicles (containing neurotransmitters), to fuse w the presynaptic membrane –> releasing the neurotransmitters into synaptic cleft
  3. neurotransmitters then diffuse across synaptic cleft and bind w receptors on the post synaptic membrane
  4. activation of these receptors will cause a change in permeability of the membrane, allowing ions such as calcium to move into post synaptic neuron
  5. this changes electrical activity of the membrane, thereby generating an action potential or electrical impulse, which will then travel down the neuron’s axon
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6
Q

2 main systems of the nervous system

A
  1. CNS- brain and spinal cord
  2. PNS- contains all nerve fibers outside the CNS
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7
Q

Organization of PNS

A
  1. Sensory (afferent)- transmits sensory info from periphery to CNS
  2. Motor (efferent)- transmits motor controls from CNS to periphery
    a. somatic NS - voluntary control
    of skeletal muscle
    b. Autonomic NS- involuntary
    control of cardiac/smooth muscle
    i) Parasympathetic- rest/digest
    ii) Sympathetic- fight/flight
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8
Q

Autonomic nervous system

A

controls involuntary responses by influencing organs, glands, and smooth muscle and is often involved in maintaining a stable internal environment

Helps to control processes without conscious effort (i.e. blood pressure, heart rate, bowel movements, urinary output, sweating)

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9
Q

Neurons of ANS

A
  1. The first neuron’s cell body is in the CNS
  2. The second neuron’s cell body is in the ganglia
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10
Q

Preganglionic nerve

A

The neuron before the ganglia

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11
Q

Postganglionic nerve

A

The neuron after the ganglia

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12
Q

Parasympathetic NS

A

“Rest and Digest”- Activated under non-stressful conditions

i.e. pupil constriction, decreased heart rate, increased digestive intestinal activity

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13
Q

Sympathetic NS

A

“Fight or flight”- activated under conditions of stress

i.e. pupil dilation, increased sweating, increased heart rate, increased blood pressure

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14
Q

Parasympathetic neurons originate from what 2 places on the spinal cord?

A
  1. cranial, or brainstem region
  2. sacral, or bottom, region
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15
Q

All PNS nerve release what neurotransmitter?

A

Acetylcholine

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16
Q

Within PNS, acetylcholine binds to what 2 receptors

A
  1. Nicotinic receptors (Nn)
  2. Muscarinic receptors (M)
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17
Q

Termination of response

A

to terminate acetylcholine-mediated response within the PNS, acetylcholinesterase (AchE) breaks down acetylcholine in the synaptic cleft into acetate and choline

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18
Q

How can the PNS be activated

A
  1. Drugs can bind to and activate nicotinic receptors
  2. drugs can bind to and activate muscarinic receptors
  3. drugs can block the metabolism of acetylcholine (by inhibiting AchE) thereby increasing the concentration of acetylcholine in synaptic cleft
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19
Q

PNS activators

A

Drugs that stimulate the parasympathetic nervous system produce characteristics of rest and digest

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20
Q

Cholinomimetics

A

direct and indirect agents that mimic the actions of acetylcholine (at Nn or M receptors)

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21
Q

Clinical use of activators

A
  1. Glaucoma- condition where the patient experiences in intraocular pressure due to poor drainage of the fluid in the eye
    - muscarinic receptor agonists increases PNS activation, leading to contraction of the ciliary body of the eye
  2. Poor muscle tone in bladder
    • admin of muscarinic agonists will cause bladder to contract, allowing patient to urinate
  3. Asthma- methacholine is a muscarinic agonist, and when inhaled it causes the bronchioles to constrict which inhibits breathing
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22
Q

PNS Inhibitors

A

Drugs that inhibit the activity of the PNS, and cause the effects of “fight or flight”

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23
Q

Anticholinergic drugs

A

Most common PNS inhibitors, drugs that antagonize or block M or Nn receptors

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24
Q

Ganglion blocking drugs

A

Drugs that specifically antagonize or inhibit the Nn receptors found in all autonomic ganglia

Limited clinical use due to broad range of adverse effects

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25
Q

Muscarinic receptor blockers

A

used much more commonly

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26
Q

Sympathetic neurons originate from which 2 places on the spinal cord

A
  1. Thoracic region
  2. Lumbar region
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27
Q

Organization of SNS

A
  1. short preganglionic neurons that release Ach at ganglia
  2. Ach binds/activates Nn receptors at sympathetic ganglia, conducting the signal to the long postganglionic neurons
  3. sympathetic postganglionic neurons predominately release norepinephrine at the target organ, which binds to alpha or beta receptors
  4. exception: the sympathetic postganglionic neurons that innervate sweat glands and renal vascular smooth muscle –> these neurons release ach which binds to M receptors, and dopamine which binds to D receptors
  5. Axons of SNS are highly branched and therefore influence many organs
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28
Q

The adrenal medulla

A

specialized organ that functions as a sympathetic autonomic ganglia, located in the centre portion of adrenal gland

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29
Q

What is the adrenal medulla innervated by

A

short sympathetic preganglionic fibres, when these fibres are activated they release Ach, which binds to Nn receptors on adrenal medulla

  • activation of the Nn receptors results in the release of predominately epinephrine and norepinephrine from adrenal medulla
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30
Q

Sympathetic neurotransmitters and receptors

A
  1. alpha receptors
    a. A1 receptors
    b. A2 receptors
  2. beta receptors
    a. B1 receptors
    b. B2 receptors
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31
Q

Alpha 1 receptors

A
  • Located post-synoptically, predominately on smooth muscle
  • Activation leads to contraction of muscle
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32
Q

Alpha 2 receptors

A
  • located post synoptically on smooth muscle and presynoptically on neuronal membrane
    - receptors
    presynoptically are
    autoreceptors
  • Activation leads to contraction
  • activation of a2 autoreceptors leads to a decrease in the release of norepinephrine from presynaptic nerve, decreasing sympathetic activation
33
Q

Beta 1 receptors

A
  • found predominately in heart and GI muscle
  • activation leads to increased force and rate of contraction of the heart, and relaxation of GI smooth muscle
34
Q

Norepinephrine in SNS

A

Postganglionic neurons release norepinephrine at the target organ and it binds to alpha or beta-1 receptors in the postsynaptic membrane to exert action

35
Q

Beta 2 receptors

A
  • found in lungs, blood vessels, GI muscle, and uterus
  • activation leads to muscle relaxation
36
Q

Cholinergic drugs

A

drugs that stimulate parasympathetic nervous system
- mimics the action of Ach binding to nicotinic or muscarinic receptors

37
Q

Adrenergic drugs

A

drugs that stimulate the sympathetic nervous system
- produce organ-specific effects due to receptor subtypes they bind to

38
Q

Activation of SNS

A

Drugs acting directly or indirectly on the SNS can mimic the actions of norepinephrine, increasing SNS activity

  1. direct stimulation- drugs bind directly to receptors and produce an effect
  2. indirect stimulation- drug increases the release of norepinephrine from presynaptic neuron
  3. combo of both- drug binds directly to receptor AND increases release of norepinephrine
39
Q

Clinical indications of Adrenergic drugs

A
  1. anaphylaxis
  2. cardiac applications
  3. nasal congestion
  4. ophthalmic
  5. pulmonary
40
Q

Clinical indications of antiadrenergic drugs

A
  1. pheochromocytoma
  2. benign prostatic hyperplasia (BPH)
  3. angina and congestive heart failure
  4. glaucoma
  5. neurological diseases
41
Q

Somatic nervous system

A

Innervates skeletal muscle, under voluntary control and consists primarily of the muscles of posture and movement

42
Q

Organization of Somatic Nervous System

A

voluntary motor nerves extend from the CNS all the way to the skeletal muscle

  • at skeletal muscle, the neuron release Ach, which binds to nicotinic receptors on skeletal muscle (Nm)
  • receptor activation causes contraction of muscle
43
Q

Neuromuscular junction

A

The synapse between a motor neuron and skeletal muscle

  • when Nm receptors are activated, they cause muscle to contract
  • for them to contract, multiple Nm receptors on the muscle fibre have to be activated at once, causing depolarization of skeletal membrane followed by muscle fibre contraction
44
Q

Neuromuscular blocking drugs

A

drugs that target skeletal muscle act by interfering with neurotransmission at the neuromuscular junction

  1. Non-depolarizing neuromuscular blockers
  2. depolarizing neuromuscular blockers
45
Q

Non-depolarizing neuromuscular blockers

A
  • act like competitive antagonists, blocking the Nm receptors, thereby inhibiting the binding of Ach to the receptors
  • since less Nm receptors are available for acetylcholine to bind to, the muscle is unable to depolarize and muscle contraction is inhibited
46
Q

Depolarizing Neuromuscular blockers

A

Function like agonists, activating the Nm receptor, thereby initially causing muscle contraction

  • resistant to AchE breakdown and cause continual activation of the Nm receptors without allowing time for the muscle to repolarize, leading to muscle paralysis
47
Q

Example of Non-depolarizing neuromuscular blocker

A

Tubocurarine
- onset of action is about 4 mins, and pharmacological effects lasts 45-60 mins

48
Q

Example of depolarizing neuromuscular blockers

A

Succinylcholine
- rapid onset (30-60secs), short duration of action (5-10 mins)

49
Q

Why does succinylcholine have a short duration of action

A

It is metabolized by cholinesterase in the plasma of the blood, which is why the duration of action is short compared to non-depolarizing blocking agents

50
Q

Phases of depolarizing blockers action

A
  1. depolarizing phase
    • muscular fibres depolarize in a disorganized manner, resulting in muscular fasciculation (i.e. twitching)
    • once muscle fibres depolarize, they are unable to repolarize due to the continual presence of the drug activating the receptors, resulting in paralysis
  2. Desensitizing phase
    • once Nm receptors become desensitized to the depolarizing blocker, the Nm acts as if an antagonist is binding instead of an agonist
    • binding Ach no longer activates them
    • this desensitization, the effects of depolarizing blocks afents is prolonged by the use of AchE
51
Q

Adverse effects of depolarizing blockade

A
  1. Hyperkalemia- during sustained depolarization, potassium can rush out of the cell and into the blood (elevated potassium can lead to cardiac arrest)
  2. Muscle pain- use of depolarizing blockers are associated with postoperative pain
  3. Malignant hyperthermia- genetically linked condition that can occur after exposure to succinylcholine and manifests as a rise in body temp, tachychardia, and muscle rigidity
52
Q

Clinical indications of neuromuscular blockers

A
  1. surgery- to produce muscle paralysis as adjuncts to anesthetics OR to reduce spasticity- muscle relaxants for chronic back pain
  2. Endotracheal intubation- relaxation of tracheal and pharyngeal muscles, facilitating the insertion of an endotracheal tube
53
Q

What does parasympathetic nervous system release

A

acetylcholine from presynaptic neurons and postsynaptic neurons

54
Q

What does sympathetic nervous system release

A

acetylcholine from presynaptic neurons and norepinephrine from postsynaptic neurons

55
Q

Anesthesia

A

state of loss of sensation; purpose to protect patients from pain in surgery

56
Q

General Anesthesia

A
  1. hypnosis - loss of consciousness
  2. amnesia- loss of memory
  3. analgesia- loss of response to pain
  4. areflexia- loss of autonomic response
  5. relaxation- skeletal muscle
57
Q

Ideal anesthetic

A

induce anesthesia quickly, while allowing for prompt recovery after its administration has stopped

high therapeutic index and have no adverse effects

58
Q

Anesthesia Mechanisms of Action

A
  1. facilitation of GABA-mediated inhibition at GABA receptor chloride channel
  2. antagonism of glutamic acid excitation of NMDA channel receptor
59
Q

Inhaled anesthesia route of admin

A
  • inhaled
  • reaches alveoli of lungs, transferred into blood, and travels to brain
  • increased pulmonary ventilation will increase the speed of anesthetic uptake
60
Q

Two types of inhaled anesthetics

A
  1. nitrous oxide- low potency and produces incomplete anesthesia
  2. volatile anesthetics (i.e. isoflurane, halothane)- potent drugs that produce unconsciousness
61
Q

intravenous anesthetics

A

administered directly into the blood, and travels to brain to exert effects

  • patient awakes after given a bolus of a drug often because of redistribution of the drug
62
Q

Types of intravenous anesthetics

A
  1. Propofol - most frequent
  2. Ketamine- provides analgesia and is the choice for compromised blood flow
63
Q

Local anesthesia

A

Loss of sensation that is confined to a discrete area of the body (blocking sensory nerve conduction)

The unionized local anesthetic enters the cell, where it becomes ionized and blocks the voltage-gated sodium channels, which inhibits nerve transmission

64
Q

Local anesthetics and the ANS

A

not only blocks pain, but also blocks autonomic function, temp sensation, light touch sensation, proprioception, and motor function

65
Q

Clinical application of local anesthetics

A
  1. topical
  2. local infiltration (injection in area of terminal nerve endings)
  3. spinal
  4. epidural
66
Q

Allergies

A

most “allergies” are not allergies to anesthetic itself, but are due to added preservatives in the solution

67
Q

System toxicity

A

occurs to excessively high blood vessels of the local anesthetic and is associated with drug overdose or accidental intravascular injection

68
Q

what is SUD stand for?

A

Substance use disorder

69
Q

SUD criteria

A

Min of 2…

  1. social impairments
  2. risky use
  3. impaired control
  4. withdrawal
  5. tolerance
70
Q

Factors influencing SUD

A
  1. genetic factors
  2. pre-existing disorders
  3. environmental factors
  4. developmental factors
71
Q

Potential for misuse of a drug

A
  1. nature of drug
  2. route of administration
  3. amount/frequency of use
  4. availability
  5. inherent harmfulness
72
Q

Drug tolerance

A
  1. a state in which repeated administration of a given dose has progressively less pharmacological effect
  2. a state in which the dose of a drug must be increased to obtain the same magnitude of pharmacological effect as was produced by the original dose
73
Q

Extent of drug tolerance

A

expressed as shortened duration of action and a decreased magnitude of effect

74
Q

Cross tolerance

A

resistance or tolerance to one drug because of the resistance or tolerance to a pharmacologically similar drug

75
Q

Withdrawal

A

abnormal physiological state produced by repeated administration of a drug that leads to the appearance of a withdrawal syndrome when drug administration is discontinued or the dose is decreased

76
Q

Withdrawal symptoms

A

Usually the opposite to the effects of the drug (i.e. withdrawal from amphetamine (CNS stimulant) would manifest sleepiness (CNS depressant)

Severity of symptoms increases with the speed of withdrawal

77
Q

Drug addiction

A

A state in which stopping or abruptly reducing the dose of a given drug produces non-physical symptoms

78
Q

The dopamine hypothesis

A

commonly misused drugs increase dopamine in the reward systems of the brain

the dopaminergic systems are also responsible for natural rewards such as food and sex, as well as stimulus-related rewards (i.e. video games + gambling)

79
Q

Characteristics of addictive drugs

A
  1. Increase dopamine (in brain reward systems)
    • CNS stimulants
    • opioids
    • other drugs (alcohol +
      cannabis)
  2. Produce novelty
  3. reduce anxiety
    • CNS depressants

PHAR370- Fundamentals of Pharmacology and Therapeutics (5 decks)

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