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MSK Week 5 > ICL 3.6: Principles of PNS Pharmacology > Flashcards

ICL 3.6: Principles of PNS Pharmacology Flashcards

1
Q

what are NSAIDs?

A

NSAIDs = Non-Steroidal anti-Inflammatory Drugs

the nomenclature NSAID was given to this class of drug to distinguish them from the anti-inflammatory activity of glucocorticoids

NSAIDs are primarily used to treat inflammation in addition to mild or moderate pain and fever

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2
Q

what are the 3 therapeutic effects of NSAIDs?

A
  1. regulate body temperature
  2. reduce inflammation
  3. reduce pain
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3
Q

what is the immune response to tissue damage?

A

tissue damage is accompanied by the release of several biochemical mediators such as histamine, bradykinin, platelet activating factor, and a group of lipid materials known as prostaglandins and leukotrienes

histamine, bradykinin, and leukotrienes cause the swelling and redness of the inflamed area due to vasodilatation and increased capillary permeability

prostaglandins, on the other hand, increase tissue sensitivity to pain and cause elevation of body temperature

so NSAIDs are used in the treatment of inflammation, pain and fever!

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4
Q

what musculoskeletal disorders are NSAIDs used to treat?

A
  1. rheumatoid arthritis
  2. osteoarthritis

NSAIDs provide symptomatic relief from pain and inflammation

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5
Q

how do NSAIDs reduce pain?

A

they have analgesic activity that lowers prostaglandin levels by blocking their synthesis

normally, prostaglandins are increased in response to neuropeptides and cytokines associated with inflammation

so NSAIDs are effective against pain of low-to-moderate intensity

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6
Q

what kind of pain are NSAIDs useful for treating?

A

they are effective in treating somatic pain

they are also effective in treating menstrual pain, and a type of visceral pain associated with increased prostaglandin release

somatic pain comes from the skin. muscles, and soft tissues

visceral pain comes from the internal organs

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7
Q

how do NSAIDs reduce fever?

A

your body temperature is controlled by hypothalamus and during fever, the set point is elevated

this happens because cytokines increase prostaglandin E2 (PGE2) levels in circumventricular organs, leading to changes in hypothalamic function

NSAIDs block PGE2 synthesis!

NSAIDs reduce fever without impacting normal variations in temperature associated with the circadian rhythm

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8
Q

what is Reye’s syndrome?

A

Reye’s syndrome is characterized by encephalopathy, liver dysfunction and fatty infiltration of the liver

aspirin and other salicylates are associated with Reye’s syndrome so aspirin is contraindicated in children and adults under 20 years old that have a fever associated with a viral illness

NEVER prescribe aspirin to children and teenagers recovering from chickenpox or flu-like symptoms

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9
Q

which NSAID is a salicylates?

A

aspirin

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10
Q

which NSAIDs are propionic acids?

A
  1. ibuprofen (advil, motrin)

2. naproxen (alleve)

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11
Q

which NSAIDs is COX-2 inhibitors?

A

celecoxib

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12
Q

what are the categories of NSAIDs?

A
  1. salicylates
  2. propionic acids
  3. acetic acids
  4. oxicams
  5. fenamates
  6. COX2 inhibitors
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13
Q

what is the MOA of NSAIDs?

A
  1. injury to tissue
  2. phospholipase A2 acts on the phospholipids in the cell membrane and releases arachidonic acid
  3. arachidonic acid then makes leukotriene via the lipoxygenase pathway

or arachidonic acid can make prostanoids (prostacyclin, prostaglandin E2, or thromboxane) via COX1 or CO2 in the cyclooxyrgenase pathway

so what NSAIDs do is inhibit COX1 and COX2!

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14
Q

what is the function of COX1?

A

COX-1 is responsible for the physiologic production of prostanoids = prostacyclin, prostaglandin E2, or thromboxane

it’s present in most tissues, especially in the GI tract; it maintains the normal lining of the stomach via mucous! –> this is why if you give too many NSAIDs you can cause stomach ulcers because you’re breaking down the stomach lining

it’s involved in kidney and platelet aggregation

COX-1 is “housekeeping enzyme” that regulates normal cellular process, such as gastric cytoprotection, vascular homeostasis, platelet aggregation, and kidney function

most NSAIDs target COX1

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15
Q

what is the function of COX2?

A

COX-2 causes the elevated production of prostanoids that occurs in sites of disease and inflammation

it’s present in macrophages and monocytes

it’s responsible for pain and inflammation

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16
Q

what class of drugs can inhibit COX2?

A

glucocorticoids!!

the structural differences between COX-1 and COX-2 permitted the development of COX-2 selective inhibitors

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17
Q

where is COX2 expressed in the body?

A
  1. brain
  2. kidney
  3. bone
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18
Q

what are the 2 mechanisms of aspirin?

A
  1. inhibits transcription of the COX-2 mRNA preventing more prostaglandin production
  2. aspirin is an acetylated form of salicylic acid
    and it *irreversibly alters the COX-1 or COX-2 enzyme responsible for production of prostaglandins by donating an acetyl group to a serine residue, thus inactivating COX-1 or COX-2
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19
Q

what are the uses of aspirin?

A
  1. regulates body temperature = aspirin inhibits cyclooxygenase activity which decreases the formation of prostaglandins (PGE2)
  2. anti-inflamatory
  3. anti-pain = decreases prostaglandin E2 synthesis which represses the sensation of pain usually arising from musculoskeletal disorders rather than that arising from the viscera
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20
Q

what are the uses of acetaminophen?

A

great of anti-pain and anti-fever but it is NOT good at anti-inflammatory effects

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21
Q

what respiratory effect does aspirin have?

A

at therapeutic doses, aspirin can increase ventilation

however, higher doses work directly on the respiratory center in the medulla, resulting in hyperventilation

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22
Q

what are the GI effects of aspirin?

A

normally, prostacyclin (PGI2) inhibits gastric acid secretion, whereas PGE2 stimulates synthesis of protective mucus in both the stomach and small intestine

in the presence of aspirin, these prostanoids are not formed resulting in increased gastric acid secretion and diminished mucus protection = stomach ulcers

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23
Q

what are the adverse effects of aspirin on the kidney?

A

COX-inhibitors prevent the synthesis of prostaglandins that are responsible for maintaining renal blood flow

decreased synthesis of prostaglandins can result in retention of sodium and water, and may cause edema and hyperkalemia

this is bad because this can in turn effect the heart!!

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24
Q

which conditions is aspirin used to treat?

A

salicylic acid derivatives are used in the treatment of gout, rheumatic fever, and osteoarthritis

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25
Q

which external applications does aspirin have?

A

salicylic acid is used topically to treat corns, calluses, and warts

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26
Q

how can aspirin be used to treat cardiovascular conditions?

A

aspirin is used to inhibit platelet aggregation so low doses are used prophylactically to:

  1. feduce the risk of recurring transient ischemic attacks and stroke
  2. feduce the risk of death in those having an acute myocardial infraction
  3. reduce the risk of recurrent nonfatal myocardial infraction

this is why people over 50 are recommended to take a baby aspirin!

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27
Q

what side effects can aspirin have on the GI system?

A
  1. abdominal pain
  2. nausea
  3. anorexia
  4. anemia
  5. diarrhea
  6. gastric erosions/GI hemorrhage

gastric damage produced by NSAIDs likely due to inhibition of COX-1 in gastric epithelial cells

selective COX-2 inhibitors are less likely to produce gastric ulcers! so some studies suggest fewer serious GI events (bleeding) if you use selective COX-2 inhibitors

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28
Q

what adverse effects can aspirin have on the CNS?

A
  1. headache
  2. dizziness
  3. confusion
  4. depression
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29
Q

what adverse effects can aspirin have on platelets?

A

inhibited platelet activation leads to a propensity for bruising and increased risk of hemorrhage

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30
Q

what adverse effects can aspirin have on the uterus?

A
  1. prolongation of gestation

2. inhibition of labor

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31
Q

which conditions are propionic acid derivatives used to treat?

A
  1. RA
  2. osteoarthritis

they have anti-inflammatory, analgesic, and antipyretic activity

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32
Q

what is the MOA of propionic acid derivatives?

A

they are reversible inhibitors of the cyclooxygenases

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33
Q

what are the potential side effects of propionic acid derivatives?

A

drugs can alter platelet function and prolong bleeding time

GI effects are generally less intense than those of aspirin

side effects involving CNS, such as headache, tinnitus, and dizziness

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34
Q

which NSAIDs are acetic acid derivatives?

A

tolmetin

also Indomethacin, Sulindac, and Etodolac

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35
Q

which conditions are acetic acid derivatives used to treat?

A
  1. gouty arthritis
  2. ankylosing spondylitis
  3. rheumatoid arthritis
  4. osteoarthritis

they have anti-inflammatory, analgesic, and antipyretic activity but they are NOT used to lower fever

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36
Q

what is the MOA of acetic acid derivatives?

A

reversibly inhibit cycloxygenase

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37
Q

which NSAIDs are oxicam derivates?

A
  1. piroxicam

2. meloxicam

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38
Q

which conditions are oxicam derivatives used to treat?

A
  1. ankylosing spondylitis
  2. rheumatoid arthritis
  3. osteoarthritis
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39
Q

what is the MOA of oxicam derivates?

A

meloxicam inhibits both COX-1 and COX-2, preferential binding for COX-2

at high doses, meloxicam is a nonselective NSAID, inhibiting both COX-1 and COX-2

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40
Q

which NSAIDs are fenamates?

A
  1. mefenamic acid
  2. meclofenamic acid

these drugs have no advantages over other NSAIDs as anti-inflammatory agents

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41
Q

what are the side effects of fenamates?

A

diarrhea can be severe

cases of hemolytic anemia have been reported!!

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42
Q

which NSAIDs are COX2 selective inhibitors?

A

celecoxib

also there’s valdecoxib and rofecoxib

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43
Q

what are COX2 selective inhibitors?

A

NSAIDS that are significantly more selective for inhibiting COX-2 that of COX-1

specifically inhibiting COX-2 to prevent or decrease chances of GI side effects normally caused by inhibition of COX-1

the inhibition of COX-2 is time dependent and reversible

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44
Q

what is the MOA of COX2 selective inhibitors?

A

COX-2 inhibitor binds its polar sulfonamide side chain to distinct hydrophilic side pocket region that is not present on the COX-1 isoform

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45
Q

which conditions are COX2 selective inhibitors used to treat?

A
  1. osteoarthritis
  2. RA
  3. acute pain
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46
Q

which COX2 selective inhibitors was discontinued and why?

A

Valdecoxib (Bextra®)

due to 5 fold increased risk of myocardial infraction and stroke!!

this is likely due to the increased risk of thrombosis

valdecoxib and rofecoxib were also withdrawn from the market

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47
Q

which NSAIDs commonly have upper GI side effects?

A
  1. aspirin (salicylate)

2. indomethacin (acetic acid)

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48
Q

which NSAID doesn’t have an antipyretic effect?

A

diflunisal (salicylate)

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49
Q

which NSAID is extremely potent and should only be used as a last resort?

A

indomethacin (acetic acid)

CNS disturbances are common

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50
Q

which NSAID has an increased risk for MI and stroke?

A

celecoxib (COX2 inhibitor)

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51
Q

which NSAIDs have decreased GI irritation in comparison to aspirin?

A
  1. diflunisal (salicylate)

2. celecoxib (COX2 inhibitor)

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52
Q

what is the function of acetaminophen?

A

aka tylenol

analgesic and antipyretic BUT weak anti-inflammatory properties

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53
Q

what is the MOA of acetaminophen?

A

analgesic action of acetaminophen is unclear

acetaminophen may inhibit a third enzyme, COX-3 in the CN

it’s is only a weak COX-1 and COX-2 inhibitor in peripheral tissues, which accounts for its lack of anti-inflammatory effect

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54
Q

what are the side effects of acetaminophen?

A

liver dysfunction if used at high doses

but otherwise well tolerated with few adverse effects; it also has reduced GI side effects

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55
Q

what are the 3 types of neurotransmitters in the CNS?

A
  1. amino acids
  2. amines
  3. peptides
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56
Q

which NTs are amino acids and what is their function?

A
  1. glutamate = excitatory
  2. gamma-aminobutyric acid (GABA) = inhibitory
  3. glycine
57
Q

which NTs are amines?

A
  1. ACh (not made from amino acids)
  2. norepinephrine
  3. dopamine
  4. serotonin
58
Q

which NTs are peptides?

A
  1. substance P
  2. dynorphin
  3. enkephalins
59
Q

what are glutametergic receptors?

A

glutamatergic receptors mediate much of the synaptic excitation in the CNS

60
Q

which glutametergic receptors are inotropic?

A
  1. AMPA
  2. NMDA
  3. Kainate
61
Q

how does the glutamate gated channel work?

A
  1. glutamate binds to the NMDA channel on the postsynaptic neuron
  2. the channel opens, but is “plugged” by a magnesium ion (Mg2+)
  3. depolarization of the postsynaptic membrane relieves the Mg2+ blockade and the channel opens to allow passage of sodium, potassium and calcium
62
Q

how do GABA-gated channels work?

A

the GABA receptor binds ethanol, benzodiazepines, barbiturates which facilitates the binding of GABA

this allows for an influx of Cl- which hyperpolarizes a cell and creates an inhibitory effect!

63
Q

what are nicotinic receptors? QUIZ QUESTION

A

a type of cholinergic receptor

nicotine is the agonist for this receptor and it mimics the action of the neurotransmitter ACh

curare on the other hand is the anatgonist for this receptor and blocks the action of both the NT and the agonist

nicotinic receptors are present in the skeletal muscle and the brain

64
Q

what are muscarinic receptors? QUIZ QUESTION

A

a type of cholinergic receptor

muscarine is the agonist for this receptor and it mimics the action of the neurotransmitter ACh

atropine on the other hand is the anatgonist for this receptor and blocks the action of both the NT and the agonist

muscarinic receptors are in the heart and brain

65
Q

what are the two types of skeletal muscle relaxants?

A

they’re both peripherally acting neuromuscular blockers

  1. non-depolarizing blockers
  2. depolarizing blockers
66
Q

what are the two types of spasmolytic drugs?

A

these drugs prevent muscle spasms

  1. centrally acting skeletal muscle relaxants
    ex. baclofen-diazepam
  2. direct acting skeletal muscle relaxants
    ex. dantrolene
67
Q

what is the MOA of a non-depolarizing blocker?

A

nondepolarizing blockers bind to the receptor to prevent opening of the channel and cause skeletal muscle relaxation

they’re competitive antagonists; they compete with ACh for the nicotinic receptors present in post-junctional membranes of motor end-plates

so the post-junctional membrane channel never even opens or depolarizes

these blockers are categorized as either short acting, intermediate acting or long acting

68
Q

what is the MOA of a depolarizing blocker?

A

the depolarizing blocker causes initial depolarization of the cell and then persistent depolarization of the channel

this will eventually lead to cause skeletal muscle relaxation

they combine with nicotinic receptors in post-junctional membrane of neuromuscular junction –> initial depolarization of motor end-plate –> muscle twitching –> persistent depolarization –> relaxation

these drugs have similar effect to acetylcholine on the motor end-plate receptors

they release histamine especially in larger doses**

ex. succinylcholine

69
Q

what are the uses of neuromuscular blockers?

A
  1. facilitate endotracheal intubation
  2. facilitate endoscopy

3, control convulsion –> electroshock therapy in psychotic patient

  1. relief of tetanus and epileptic convulsion
  2. as adjuvant in general anesthesia to induce muscle relaxation
  3. orthopedic surgery
70
Q

which non-depolarizing neuromuscular blockers are long acting?

A
  1. d-tubocurarine

2. pancuronium

71
Q

which non-depolarizing neuromuscular blockers are intermediate acting?

A
  1. atracurium
  2. cisatracurium
  3. vecuronium
  4. rocuronium
72
Q

which non-depolarizing neuromuscular blockers are short acting?

A

mivacurium

73
Q

how are non-depolarizing neuromuscular blockers broken down in the body?

A

they’re polar compounds which are inactive orally

they have to be taken parenterally = IV, IM, subcutaneous

they are metabolized by the kidney or liver

they don’t cross the placenta or CNS

74
Q

what degrades mivacurium?

A

acetylcholinesterase

mivacurium is a short acting non-depolarizing neuromuscular blockers

75
Q

what degrades atracurium?

A

spontaneous degradation in blood

it’s an intermediate acting non-depolarizing neuromuscular blockers

76
Q

what are some of the side effects of non-depolarizing neuromuscular blockers? which specific ones cause these side effects?

A
  1. release histamine and produce hypotension:
    d - Tubocurarine
    atracurium
    mivacurium
  2. tachycardia = pancuronium
77
Q

what is d-tubocurarine? what are some its side effects?

A

long acting non-depolarizing neuromuscular blocker = 1-2 hours

dliminated by kidney 60%; liver does other 40%

it releases histamine which causes bronchospasm, hypotension and tachycardia

78
Q

what is pancuronium? what are some its side effects?

A

long acting non-depolarizing neuromuscular blocker

it’s 6 times more potent than curare (nicotinic antagonist)

excreted by the kidney 80% of the time

side effects = hypertension and tachycardia –> this is because it has antimuscarinic action and blocks parasympathetic action which normally slows heart rate

79
Q

what is atracurium?

A

intermediate acting non-depolarizing neuromuscular blocker = 30 minutes

it’s eliminated by non-enzymatic chemicals or degraded in plasma due to spontaneous hydrolysis at body pH

80
Q

what is atracurium used for?

A

DOC for liver and kidney failure

it releases histamine which leads to transient hypotension!

81
Q

what is vecuronium?

A

intermediate acting non-depolarizing neuromuscular blocker

metabolized mainly by the liver

82
Q

what are the side effects of vecuronium?

A

few side effects

no histamine release and no tachycardia!

83
Q

what is mivacurium? what is a potential side effect?

A

short acting non-depolarizing neuromuscular blocker = 15 minutes

longer duration in patient with liver disease or genetic cholinesterase deficiency

releases histamine so could cause transient hypotension

84
Q

what are the pharmacological actions of depolarizing neuromuscular blockers on the body?

A
  1. initial contraction followed by relaxation of skeletal muscles
  2. hyperkalemia which could lead to cardiac arrest
  3. increased intraocular pressure in the eye
  4. arrhythmias
85
Q

what are the pharmacokinetic of depolarizing neuromuscular blockers?

A

fast onset of action = 1 minute

short duration of action = 5-10 minutes

they’re metabolized by pseudocholinesterase in plasma

their half-life is prolonged in neonates, elderly and pseudocholinesterase deficient patients (liver disease)

86
Q

what are the side effects of depolarizing neuromuscular blockers?

A
  1. hyperkalemia**
  2. CVS arrhythmia
  3. increased intraocular pressure = glaucoma
  4. can produce malignant hyperthermia
  5. may cause succinylcholine apnea due to deficiency of pseudocholinesterase
87
Q

what is malignant hyperthermia?

A

it’s the inability to bind calcium by sarcoplasmic reticulum in some patients due to genetic defect

increased Ca+2 release leads to intense muscle spasms and hyperthermia

it’s a a rare inherited condition that can occur upon administration of drugs such as depolarizing neuromuscular blockers like suxamethonium or general anesthesia like halothane

88
Q

what are spasmolytics?

A

drugs that reduce muscle spasms in spastic states

89
Q

which drugs are spasmolytics?

A
  1. baclofen
  2. diazepam
  3. dantrolene
  4. tizanidine
90
Q

what is baclofen?

A

a centrally acting spasmolytic

it’s a GABA-B agonist that acts on the spinal cord

91
Q

what is diazepam?

A

a centrally acting spasmolytic

it facilitates GABA-A action on the CNS aka it’s a GABA-A agonist

92
Q

what is dantrolene? what’s it used to treat?

A

a direct acting spasmolytic

it directly acts on skeletal muscles by acting as a receptor antagonist to the ryanodine receptor and decreasing free intracellular calcium concentration

aka it interferes with the release of calcium from its stores in skeletal muscles in the sarcoplasmic reticulum

ryanodine receptors are huge ion channels that are responsible for the release of Ca2+ from the sarco/endoplasmic reticulum and normally cause muscle contractions

used in treatment of malignant hyperthermia

93
Q

what is tizanidine?

A

a spasmolytic that’s a central alpha-2-adrenergic receptor agonist

it’s a short-acting muscle relaxer used to treat muscle spasms caused by certain conditions such as multiple sclerosis, amyotrophic lateral sclerosis, or spinal cord injury

94
Q

what conditions can the botulinum toxin be used to treat?

A
  1. focal dystonia
  2. cerebral palsy

injections are repeated approximately every 3 months for focal dystonia

adverse reactions include pain at the injection site and excessive weakness

95
Q

what’s the MOA for how the botulinum toxin is used to treat spastic disorders?

A

it inhibits acetylcholine release from nerve terminals

botox binds presynaptically to high-affinity recognition sites on the cholinergic nerve terminals and decreasing the release of acetylcholine, causing a neuromuscular blocking effect.

96
Q

what’s the function of local anesthetics?

A

local anesthetics produce a transient and reversible loss of sensation in a circumscribed region of the body WITHOUT loss of consciousness

the process is completely reversible

97
Q

what’s the chemical structure of local amides?

A

aromatic group + amide or ester link + amine

most are weak bases

98
Q

which local anesthetics are esters?

A
  1. benzocaine
  2. procaine
  3. proparacaine
99
Q

which local anesthetics are amides?

A
  1. bupivacaine
  2. levobupivacaine
  3. lidocaine/Lignocaine
  4. mepivacaine
100
Q

how do local anesthetics gain access to the inner axonal membrane?

A
  1. traversing sodium channels while they are more often in an open configuration

or

  1. directly through the plasma membrane
101
Q

what is the MOA of local anesthetics?

A

they block Na+ channels which inhibits the initiation and propagation of action potentials

102
Q

what are the effects of local anesthesia on the body?

A
  1. sympathetic block (vasodilatation)
  2. loss of pain and temperature sensation
  3. loss of proprioception
  4. loss of touch and pressure sensation
  5. loss of motor function
103
Q

how long do local anesthetics work for?

A

they’re effective within 5 min but only last 1-1.5 hours

they have increased action in acidic pH environment

104
Q

how are local anesthetics cleared from the body?

A

esters are cleared by hydrolysis via cholinesterase

amides are cleared by metabolism via hepatic enzymes

105
Q

what are some clinical uses for local anesthesia?

A
  1. nerve blocks
  2. IV
  3. epidurals*
  4. spinal anesthesia
  5. surface anesthesia**
106
Q

what is a nerve block?

A

inject a local anesthetic around the nerve and you anesthetize a whole region

107
Q

what are epidurals?

A

thoracic, lumbar, or sacral injection of local anesthesia that acts on nerve roots

there’s no hypotension

epidural drugs such as bupivacaine, chloroprocaine, or lidocaine might be given in combination with opioids or narcotics such as fentanyl and sufentanil.

108
Q

what is spinal anesthesia?

A

local anesthesia that is injected into the cerebrospinal fluid in the lumbar spine to anesthetize nerves that exit the spinal cord

spinal anesthesia blocks sympathetic nerves

hypotension is a common side effect!

109
Q

what can you do to prolong a surface local anesthetic?

A
  1. add vasoconstrictor – adrenaline
  2. can use a larger dose

do NOT give to fingers, toes,
nose, or penis

110
Q

what are some of the side effects of local anesthetics?

A
  1. vasodilatation at site
  2. toxicity related to rate of absorption via blood flow
  3. blockage of voltaged-gated Na+ channel affects action potential propagation throughout the body
111
Q

what are the effects of local anesthetics on the body?

A
  1. excitation = anxiety, agitation, restlessness
  2. convulsions
  3. reduced myocardial contractility
  4. vasodilation
112
Q

what is general anesthesia?

A

reversible, drug-induced state marked by the following:

  1. loss of consciousness (sleep)
  2. analgesia (loss of pain sensation)
  3. amnesia (inability to remember)
  4. inhibition of reflexes (autonomic and sensory-motor)
  5. reduced skeletal muscle tone
113
Q

what are the stages of undergoing general anesthesia?

A

STAGE I: analgesia; disorientation

STAGE II: excitement; delirium: eyelash reflex disappears. Coughing, and vomiting may occur, irregular respiration with breath holding.

STAGE III: surgical anesthesia: It is divided into four planes:

Plane I – Eyelid reflex lost, swallowing reflex disappears, marked eyeball movement may occur, conjunctival reflex is lost at the end.

Plane II – Laryngeal reflex lost, corneal reflex disappears, secretion of tears increases, respiration is automatic and regular.

Plane III – Diaphragmatic respiration persists, progressive intercostal paralysis, pupils dilated and light reflex is abolished.

Plane IV – intercostal paralysis, diaphragmatic paralysis (apnea).

STAGE IV: Medullary depression with respiratory arrest and vasomotor collapse. Pupils are widely dilated and muscles are relaxed

114
Q

what is balanced anesthesia?

A

typical situation, in which multiple drugs are used to induce and maintain general anesthesia

  1. preanesthetic medication(s) may include – anti-muscarinic agent, benzodiazepine, opioid
  2. neuromuscular blocking agent (“muscle relaxant) – such as succinylcholine, vecuronium
  3. induction agent – such as thiopental, methothexital, propofol
  4. maintenance – such as isoflurane plus nitrous oxide, i.v. propofol, opioids, others
115
Q

which inhalation agents can be used for general anesthesia?

A
  1. gas: NO
  2. volatile liquids
desflurane
sevoflurane
isoflurane
enflurane
halothane
116
Q

which IV agents can be used for general anesthesia?

A
  1. barbiturates
  2. propofol
  3. etomidate
  4. opioids
  5. benzodiazepines
  6. ketamine
117
Q

what are inhalation anesthetic agents?

A

nonselective CNS depressants

118
Q

what’s the MOA of inhalation anesthetic agents?

A

prominent effects to potentiate GABA actions at GABA(A) receptors

actions involving ligand-gated ion channels for other neurotransmitters, such as glutamate receptors, glycine receptors.

nitrous oxide (N2O) seems to act mainly via NMDA receptors

119
Q

what is the MAC of a general anesthetic?

A

MAC = Minimal Alveolar Concentration

it’s a measure of potency of inhaled anesthetics

MAC is the concentration necessary to prevent responding in 50% of population

MAC is achieved when inhaled air includes just few % of the anesthetic

N2O can not produce anesthesia by itself

120
Q

what do the pharmacokinetics of inhaled anesthetics depend on?

A
  1. the amount that reaches the brain –> this is based on lipid solubility aka oil:gas ratio
  2. solubility of the gas into the blood

the lower the blood:gas ratio, the more anesthetics will arrive at the brain

121
Q

how does the solubility of the gas into the blood of an anesthetic effect recovery?

A

LOW solubility in blood= fast induction and recovery

HIGH solubility in blood= slower induction and recovery

122
Q

what are the general effects of inhaled anesthetics on the body?

A
  1. depressed respiration and response to CO2
  2. depression of renal blood flow and urine output
  3. high enough concentrations will relax skeletal muscle
  4. generalized reduction in arterial pressure and peripheral vascular resistance

isoflurane maintains CO and coronary function better than other agents**

  1. increased cerebral blood flow and decreased cerebral metabolism
123
Q

what is the MOA of nitrous oxide?

A

it’s an inhalation anesthetic that acts as an NMDA receptor antagonist and facilitates GABAA action

it’s a widely used, potent analgesic but it does not depress the respiration/vasomotor center

124
Q

what is the MOA of halothane?

A

it’s an inhalation anesthetic that activates GABA(A) and glycine receptors, NMDA receptor antagonist, inhibits voltage-gated sodium

125
Q

what are the potential side effects of halothane?

A
  1. myocardial depressant (sinoatrial node), sensitization of myocardium to catecholamines –> can cause arrhythmias
  2. transient hepatic damage; liver necrosis with repeated exposure
126
Q

what’s the MOA of enflurane?

A

it’s an inhalation anesthetic that activates GABAA and glycine receptors, antagonist for NMDA, AMPA and kainate receptors

it was introduced as replacement for halothane

127
Q

what’s the MOA of isoflurane?

A

it’s an inhalation anesthetic that binds to GABAA receptor, glutamate and glycine receptors (similar to Enflurane)

most widely employed – no reports of hepatotoxicity or renotoxicity

128
Q

what’s the MOA of IV general anesthetics?

A

most exert their actions by potentiating GABAA receptor or blocking NMDA receptor

129
Q

what are the commonly used IV general anesthetics?

A
  1. Propofol
  2. Thiopental sodium
  3. Ketamine
130
Q

what are the effects of IV general anesthetics on organs?

A
  1. most decrease cerebral metabolism and intracranial pressure
  2. most cause respiratory depression
  3. may cause apnea after induction of anesthesia
131
Q

what’s the MOA of thiopental sodium?

A

it’s an IV general anesthetic that’s a GABAA receptor agonist = it opens Cl- channel

it also inhibits GABA transaminase which is the enzyme responsible for inactivation of GABA

it blocks glutamate receptors at low doses and it can block K and Na channels at higher doses

132
Q

how long does thiopental sodium last in the body?

A

rapid onset (20 sec) and short-acting

effect terminated not by metabolism but by redistribution so you need repeated administration or prolonged infusion approached equilibrium at redistribution sites

this can lead to a build-up in adipose tissue = very long emergence from anesthesia

133
Q

what are the potential side effects of thiopental sodium?

A
  1. hypotension
  2. apnea
  3. airway obstruction
134
Q

what is the MOA of propofol?

A

potentiation of GABAA receptor activity (agonist)

short acting and used for maintenance of general anesthesia and sedation

it is highly protein bound in vivo and is metabolised by conjugation in the liver

135
Q

what are the side effects of propofol?

A
  1. pain on injection
  2. hypotension
  3. transient apnoea following induction
136
Q

what’s the MOA of ketamine?

A

NMDA Receptor Antagonist

it usually stimulates rather than depress the circulatory system

it’s a dissociative anesthesia so patients will have cataleptic appearance with their eyes open and reflexes in tact –> people will say they have vivid dreaming extracorporeal (floating “out-of-body”) experience misperceptions, misinterpretations, illusions

may be associated with euphoria, excitement, confusion, fear

137
Q

what are the 3 components of balanced anesthesia?

A
  1. sensory

N20, opioids, ketamine for analgesia

  1. cognitive

produce amnesia, and preferably unconsciousness; either inhaled or IV

  1. motor

muscle relaxants

138
Q

what is the function of atropine?

A

atropine injection is given before anesthesia to decrease mucus secretions, such as saliva

during anesthesia and surgery, atropine is used to help keep the heart beat normal.

atropine can be given at the end of surgical procedure to prevent activation of cardiac muscarinic receptors

MSK Week 5 (7 decks)

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