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PHAR 300 > Drugs for inflammation/pain/surgery > Flashcards

Drugs for inflammation/pain/surgery Flashcards

1
Q

what are the two locations involved with sensation of pain?

A
  1. peripheral nervous system
  2. central nervous system: major site of action for opioids
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2
Q

what is the pain transmission pathway and the pain suppression pathway? what can cause pain suppression?

A
  • trans: spinothalamic tract (ascending–so starts in periphery)
  • supp: in dorsolateral funiculus (descending) and may be due to endogenous opioid peptides or ingested/exogenous opioids
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3
Q

compare opium, opiate, and opioid.

A
  • opium: what is crapped off the opium poppy and contains morphine, codeine, and heroin
  • opiate: alkaloids found in the opium poppy (mostly morphine but some codeine) - derived directly from plant
  • opioid: compound with morphine-like actions, which includes opiates
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4
Q

what are the types of opioids?

A
  1. morphine: ~10% of opium
  2. codeine (methylmorphine): ~0.5% of opium
  3. synthetic: drugs with morphine-like action
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5
Q

what are the endogenous opioids?

A
  • endorphins: used for pain relief
  • enkephalins: similar to morphine
  • dynorphins: acts on main receptor for pain relief
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6
Q

what is the efficacy/affinity of the following: morphine, buprenorphine, naloxone, pentazocine

A
  • mor: agonist
  • bu: weak agonist
  • nal: antagonist
  • pen: agonist-antagonist (has small effect but blocks receptor from more potent_
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7
Q

what are the two kinds of opioid analgesia? explain each.

A
  1. decrease pain signal:
    - presynaptic: blocks calcium channels, decreases transmitter release
    - postsynaptic: increase potassium channel, hyperpolarizes, so less likely to fire action potential
  2. increased inhibition:
    - increase in descending inhibition by decreasing GABA release presynaptically
    - descending inhibition enhanced by serotonin and noradrenaline release
    - decreases excitation by decrease release of neurotransmitters
    - combined effect is increase in pain threshold
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8
Q

what occurs with chronic use of opioids?

A
  • tolerance
  • number of receptors decrease
  • rapid desensitization as more phosphorylation and more rapid internalization
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9
Q

what are other effects of opiates (other than pain)? (on what other systems do they act on?)

A
  • limbic system: controls emotions to increase feelings of pleasure
  • brain stem: controls autonomic body functions and depresses breathing
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10
Q

what are the physiological effects of exogenous opioids?

A
  • analgesia
  • GI effects (constipation)
  • cough suppressant
  • euphoria (pleasure)
  • respiratory depression
  • miosis (pinpoint pupils)
  • motor effects (seizures)
  • nausea/vomiting (CTZ)
  • decrease urine
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11
Q

which opiate receptors are involved for the following: analgesia, GI, sedation, respiration

A
  • ana: mu, delta, kappa
  • GI/sed: mu, kappa
  • resp: mu
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12
Q

explain the pharmacokinetics of opiates.

A
  1. absorption:
    - GI absorption is slow and incomplete
    - oral: first-pass so slower onset but therapeutic effects last longer
    - IV: big peak right away but falls rapidly
    - IM: slower absorption, but decline is much lower
  2. distribution:
    - only 20% crosses BBB
    - much less lipid-soluble than heroin
  3. metabolism:
    - liver
    - T1/2: 2-4 hours
    - different metabolites for oral and parenteral
  4. excretion:
    - urine
    - two types of metabolites when injected – 3-glucuronide (60%) is inactive and half-life of 4 hours and 6-glucuronide (40%) is highly active and half-life of 3 hours
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13
Q

what metabolizes codeine? what is the metabolite produced?

A

CYP2D6 metabolizes into morphine

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14
Q

what is used to treat opioid withdrawal an doverdose?

A
  • withdrawal: weak agonist (methadone) – oral absorption, long-half-life, block withdrawal symptoms, don’t get high if take heroin
  • overdose: antagonist (naloxone/naltrexone)
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15
Q

what are corticosteroids and what do they do?

A
  • class of drug that lowers inflammation in the body, also reduce/shut-down immune system activity (immunosuppressants)
  • easy swelling, itching, redness, and allergic reaction (used to treat asthma and arthritis)
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16
Q

what are therapeutic uses of corticosteroids?

A
  • asthma
  • eczema
  • EVALI (e-cigarette or vaping induced lung injury)
  • allergic reactions
  • GI diseases
  • acute respiratory distress
  • infections
  • neurologic disorders
  • organ transplants
  • skin diseases
  • replacement therapy (for addison’s disease)
  • myeloproliferative diseases (aims to correct blood cell counts or other side effects – does not cure)
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17
Q

why does our body produce glucocorticoids?

A

to turn off the immune system

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18
Q

how are glucocorticoids signaled to be produced?

A
  1. CRH, which is a prohormone, released in hypothalamus
  2. then acts on GPCR in anterior pituitary where it stimulates synthesis of POMC
  3. POMC is processed to release ACTH
  4. ACTH regulates glucocorticoid synthesis in adrenal cortex, by increasing delivery of cholesterol to IMM and increase transcription of steroidogenic enzymes
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19
Q

how is cortisol synthesized?

A
  • cholesterol turns to pregnenolone, where it “committed” by CYP17
  • then, CYP11B1 converts to cortisol
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20
Q

how are glucocorticoids signaled off?

A

negative feedback to pituitary and hypothalamus

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21
Q

what are the anti-inflammatory effects of glucocorticoids?

A
  • changes in cell proliferation, survival, differentiation, and migration
  • decrease pro-inflammatory cytokines, interleukins, and prostaglandins
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22
Q

what is the metabolic effect of glucocorticoids?

A

general transcriptional activation
- increases blood glucose (for fight-or-flight)

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23
Q

what is the role of CBG?

A

binds and transports glucocorticoids BUT when bound, is biologically inactive

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24
Q

what are adverse effects of glucocorticoids?

A
  • not enough: hairiness, acne, greasy skin, irregular periods reduced fertility, tiredness, fatigue
  • too high: increases appetite, weight gain, muscle weakness, thin skin, easy bruising, high BP, osteoporosis , diabetes
  • thrush (when using inhalers)
  • HPA axis suppression
  • growth inhibition
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25
Q
A
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26
Q

What are the subdivisions of NSAIDs?

A
  • salicylates (e.g. aspirin)
    -non-salicylate (e.g. acetaminophen, ibuprofen, celecoxib)
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27
Q

What do NSAIDs target?

A

Prostaglandins

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28
Q

What are the roles of prostaglandins?

A
  • inflammation and pain signalling
  • protection of GI
  • effecting cardiovascular system
  • platelet aggregation and blood clotting
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29
Q

How are prostaglandins made?

A
  • arachnoid acid (part of membrane) is released by phospholipase A
  • acts on COX enzymes which make prostaglandins
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30
Q

What is the difference between COX1 and COX2?

A
  • 1: constitutive and involved in normal physiological functions / found in GI
    2: indicible and mostly involved in pain and inflammation BUT also has constitutive effect - important for platelet inhibition and vasodilatation / also channel is wider / found in brain, kidney, vasculature
31
Q

What do prostaglandins act on?

A

GPCRs called prostanoid receptors

32
Q

What are the therapeutic used of NSAIDs?

A
  • relieve mild to moderate pain
  • reduce inflammation
  • reduce fever
  • prophylaxis
33
Q

How is fever produced?

A
  • induced by endogenous pyrogens
  • go to brain and raise temperature set point in hypothalamus
  • temperature regulating center send signals via ANS leading to increase heat production and decrease heat loss
34
Q

What are side effects of NSAIDs?

A
  • upper GI ( upset stomach, ulcers, bleeding)
  • renal: dysfunction, failure
  • hypertension
  • heart failure
  • blood loss due to anti-platelet affect
35
Q

What is the mechanism of action of aspirin?

A
  • acetyl group of acetylsalicylic acid binds to serine group in COX active site
  • it acetylates it, which permanently inactivates cyclooxygenase
  • so body counteracts by making more enzyme (except in platelets)
36
Q

Explain the pharmacokinetics of aspirin.

A
  • T1/2: 3hrs (but can be up to 15hr à for high dose since switches to zero-order)
  • can become long since enzymes are easily saturated
  • metabolized to salicylic acid by P450s in liver then conjugated before being excreted
37
Q

What is a strategy in aspirin overdose?

A
  • to alkalinize the urine so that becomes ionized and will not be reabsorbed in kidney
38
Q

What are symptoms of aspirin toxicity?

A
  • tinnitus (ringing in ears)
  • headache, dizziness
  • confusion and drowsiness
  • sweating, hyperventilating
  • nausea, vomiting, …
39
Q

Why are children given acetaminophen instead of aspirin?

A
  • rare disease called Reye’s syndrome
  • affects nervous system, brain (severe inflammation), and liver
40
Q

What does ibuprofen do?

A

Blocks COX1 and COX2 reversibly (so cannot take with aspirin)

41
Q

what is the use of acetaminophen?

A
  • for pain and fever
  • NOT inflammation
42
Q

what is the pharmacokinetics of acetaminophen?

A
  • T1/2: 2-3 hours
  • CYP450 enzymes (1A2, 2E1, 3A4) create toxic metabolite (cellular necrosis - kills liver cells) which is quickly conjugated to allow for excretion
  • metabolized in liver
43
Q

why are alcoholics more vulnerable to toxicity of acetaminophen?

A

since ethanol induces the enzymes which breakdown acetaminophen, meaning that there will will more of the toxic metabolite

44
Q

what is an antidote of acetaminophen overdose?

A

glutathione precursor so that liver can conjugate the toxic metabolite (but needs to be given before liver damage)

45
Q

what was the first anesthesia used? why is it not used today?

A

diethyl ether, which is a good anesthetic but not used since is highly flammable

46
Q

what replaced diethyl ether?

A

halothane

47
Q

what are the properties of general anesthisia?

A
  • blockage of pain and consciousness
  • amnesia
  • relaxation of skeletal muscle and suppression of reflexes (somatic, autonomic, and endocrine)
48
Q

what are the different types of drugs given for general anesthesia? What are each used for?

A
  • premedication: relax, decrease pain, reduce saliva/mucosa
  • induction agents: rapidly induce unconsciousness
    -anesthesia gases: maintain surgical anesthesia
  • analgesics: pain
  • muscle relaxants: eliminate motion
  • reversal agents: reverse muscle relaxation
49
Q

what are two types of anesthetics? give examples for each.

A
  • inhalation: isoflurane
  • IV: propofol
50
Q

which anesthetics are used for long and short procedures?

A
  • long: inhalation
  • short: IV
51
Q

how do you determine the rate of delivery for inhalation anesthetics?

A
  • by the partial pressures of the anesthetic in the gas (since gas is mix of gases)
  • also partial pressure is directly proportional to concentration
  • also have to consider the solubility of the gas (more soluble will take longer since some retained in blood)
52
Q

what drives the gases in inhalation anesthetics to go into the blood?

A

the partial pressure

53
Q

what occurs during induction and recovery for inhalation anesthetics?

A
  • induction: gas goes to alveoli, to arterial blood vessels, then mostly to brain (a little other tissue)
  • recovery (stop administering): most drug will be coming out of brain then go to venous system and will be expired
54
Q

how are inhalation anesthetic metabolized?

A

most are not metabolized, they are cleared by exhalation

55
Q

can inhalation anesthetics cross the BBB?

A

yes since is lipid soluble

55
Q

what is the minimum alveolar concentration?

A

concentration where anesthesia is seen in 50% of patients

55
Q

why is artificial depression usually done in surgery?

A

since inhalation anesthesia causes respiratory depression due to increases pCO2, which decreases minute ventilation

55
Q

how do inhalation anesthetics affect the cardiovascular system?

A
  • all cause cardiovascular depression (blood pressure declines)
  • CO changes but is variable with different gases
56
Q

is nitrous oxide a good anesthetic? why or why not?

A
  • no
  • huge MAC
  • but still put in mixture since good analgesic with minimal side effects (compared to opioids)
57
Q

why was halothane replaced and what did we replace it?

A
  • replaced since small amount metabolized by liver, creating unwanted effects and causes sensitization of the cardiovascular system to arrythmia
  • replaced with isoflurane since no cardiac sensitization, is a good muscle relaxant, and no toxic metabolites
58
Q

what is an advantage of IV anesthetics over inhalation?

A
  • less respiratory and cardiovascular depression
  • can be used without complicated equipment
59
Q

what are some pharmacokinetics on IV anesthesia?

A
  • very stable
  • rapid onset
  • short duration of action (for short procedures)
  • non-toxic
  • water soluble
60
Q

what is used for concious sedation?

A

Midazolam with opioids

61
Q

what is a disadvantage of using opioids as anesthesia?

A

it depresses respiration

62
Q

what is neurolept analgesia? what is used?

A
  • to relieve stress but not have patient unconscious
  • fentanyl + droperidol
63
Q

What drugs are used for total IV anesthesia?

A
  • propofol for induction
  • an opioid
  • drug for amnesia
  • short-acting muscle relaxant
64
Q

What are the advantages and disadvantages of ketamine?

A
  • advantage: stimulates cardiovascular system instead of depressing it
  • disadvantage: patient goes into dissociative anesthesia (dysphoria), can cause intense hallucinations, delirium, anxiety, and irrationality during recovery
65
Q

What are the main sites of actions of anesthetics and what are their usual effects?

A
  • act at synapses
  • presynaptically: decrease neurotransmitter release by blocking calcium channels
  • postsynaptically: effect on ligand gated ion channels
  • they increase inhibition and decrease excitation
66
Q

What are the uses of neuromuscular blocking agents during surgery?

A
  • allow for intubation and ventilation (not fighting it)
  • reduce muscle fasciculation and motion
67
Q

What are the two types of neuromuscular blocking agents? Compare them.

A
  • depolarizing non competitive: rapid onset and short duration of action (short half life)
  • non-depolarizing competitive: compete for binding with acetylcholine and there exists one that are short, intermediate, and long acting
  • both don’t cross BBB
68
Q

What do local anesthetics target? And how do they work?

A

Target Voltage-gated channels along the axon, and block sodium influx to stop AP propagation

69
Q

What substance are local anesthetics usually injected with? Why?

A

Adrenaline since it increases the duration of action (causes vasoconstriction)

70
Q

Why does inflammation lower the effect of local anesthetics?

A

Since it decreases the pH of tissue, so less are in unionized form and can cross the membrane

PHAR 300 (12 decks)

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