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YSM Semester 2 > Anesthetics, Pain, Arthritis, Gout > Flashcards

Anesthetics, Pain, Arthritis, Gout Flashcards

1
Q

Desflurane, isoflurane, sevoflurane, nitrous oxide

A

inhaled anesthetics

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2
Q

describe the MOA of the inhaled anesthetics. What receptors do they act on?

A
  • fluranes, NO

MOA: alters neuronal ion channels:
- activates glycine + GABA receptors: inhibits postsynaptic receptors
- inhibits Na + K: inhibits presynaptic NT release
- inhibits nicotinic ACh + NMDA receptors: reduces excitatory postsynaptic receptors

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3
Q

What is minimum alveolar concentration? What is the target MAC?

A

potency of the drug
- concentration of the anesthetic at 1 ATM at which 50% of subjects move in response to noxious stimuli

target: 10-30% MAC

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4
Q

What are the side effects of NO ?

A

respiratory depression: can potentiate depressant effects in combination with other sedatives

diffusion hypoxia: concentration gradient between gases in the lungs and alveolar circulation rapidly reverses

postoperative NV

fever, pulmonary atelectasis, infectious complications

hyperhomocysteinemia: oxidizes cobalt in B12 = macrolytic anemia

subacute myeloneuopathy

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5
Q

What are the factors that influence the inhalation anesthetic bio-disposition?

A
  1. transfer of inhaled anesthetic to alveoli
    - inspired partial pressure
    - alveolar ventilation
    - characteristics of anesthetic breathing system
  2. transfer of inhaled anesthetic from alveoli to arterial blood
    - blood-gas partition coefficient
    - cardiac output
    - alveolar-to-venous partial pressure difference
  3. transfer of inhaled anesthetic from arterial blood to brain
    - blood-brain partition coefficient
    - cerebral blood flow
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6
Q

What is the MOA, kinetics, and elimination of etomidate

A

MOA: modulates action of the inhibitory NT GABA

Onset: 30-60 seconds
Duration: 3-5 minutes

elimination: hepatic + plasma esterase

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7
Q

What is the MOA, kinetics, and elimination of propofol

A

MOA: modulates the action of inhibitory NT GABA

onset: 30 seconds
Duration: 3-10 minutes

elimination: hepatic to inactive glucuronide + sulfate metabolites

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8
Q

What is the MOA, kinetics, and elimination of ketamine

A

MOA: NMDA receptor antagonist, dissociative anesthetic

onset: 1-2 minutes
duration: 5-15 minutes

elimination: hepatic, norketamine as active metabolite

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9
Q

How can you tell the difference between ester and amide local anesthetics. What is the amide and ester anesthetic?

A

esters have 1 I
- procaine, cocaine, tetracaine,

amides have 1 I’s
- lidocaine, bupivicaine, prilocaine

articaine

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10
Q

What is the MOA of local anesthetics?

A

procaine, lidocaine

MOA: reversibly blocks nerve conduction in peripheral and central NS without CNS depression or altered mental status

  • reduces the influx of Na ion at the nerve membrane by blocking voltage-gated Na channels
  • blocks sensory and motor neurons
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11
Q

What is the gas partition coefficient? How does it affect the speed and onset of anesthesia + recovery time?

A

gas partition coefficient: how readily an anesthetic dissolves in blood compared to partial pressure in alveolar air

solubility and uptake: higher blood/gas partition coefficient means more soluble in blood = greater amount that can enter the blood + brain

high blood/gas partition = slower rate of induction + offset

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12
Q

What are the factors that determine the susceptibility of nerve fibers to blockade

A

pH of the tissue - low pH = less effective
- e.g. inflammation
- use sodium bicarbonate to overcome acidity + increase efficacy

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13
Q

What are the major toxic effects of local anesthetics?

A

CNS: sedation, visual + auditory disturbances, respiratory arrest, seizures

cardiovascular: decrease in electrical excitability, conduction rate, force of contraction; cardiovascular collapse

Methemglobinemia:
low: cyanotic appearance, unresponsive to O2
high: nausea, sedation, seizures, coma

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14
Q

If someone is having a cardiovascular collapse in response to a local anesthetic, how would you treat it?

A

ALCS - 1st line

lipid emulsion 20%
- lipid sink for anesthetic

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15
Q

define nociceptive pain

A

protective - indicates injury, deformity, inflammation

somatic: structural
- localized to site of injury
- ache, stabbing, throbbing

visceral - internal organs: diffuse, dull, pressure

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16
Q

define neuropathic pain

A

harmful - indicates neurologic damage

central - TBI, spinal injury, MS

peripheral - diabetic neuropathy, post herpetic neuroglia

burning, shooting, electrical shock

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17
Q

What are the non-pharmacologic treatments or pain?

A

PT/exercise
applications of heat/cold
transcutaneous electric nerve stimulation
psychotherapy

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18
Q

What is the WHO guidance for pain management. CDC?

A

Step 1: non-pharmacologic therapy, non-opioids, adjuvants
Step 2: add weak opioid
Step 3: add strong opioid

CDC: minimize risk of long-term opioid use
reassessment > 50 morphine units/day
soft limit of 90 morphine equivalents a day

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19
Q

Describe the MOA for NSAIDs

A

ibuprofen, diclofenac, indomethacin, naproxen, meloxicam

MOA: reversible inhibition of COX-1 and COX-2
- decreases prostaglandin synthesis

aspirin has the same MOA but IRREVERSIBLE

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20
Q

What are the AEs and contraindications for NSAIDs?

A

AEs:
gastric + duodenal ulcers, risk of GI bleed
increased risk of heart attack + stroke
renal function impairment
plastic anemia
increased risk of diverticulitis

contraindications:
gastroduodenal ulcers
acute hemorrhage
renal failure
surgery: discontinue NSAIDs 1-3 days before surgery
avoid during pregnancy

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21
Q

Describe the MOA of acetaminophen. What are it’s AEs?

A

MOA: reversibly inhibits COX, mainly in the CNS

AE:
APAP-induced hepatotoxicity: AST or ALT > 1000
acute liver failure can occur with acetaminophen overdose

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22
Q

What are the tricyclic antidepressants? What are their MOA? What indications does it have for pain?

A

amitriptyline/nortiptyline
imipramine/desipramine

MOA: inhibition of 5TH + NE reuptake in synaptic cleft = increased 5HT and NE

AEs:
orthostatic hypotension
cardiotoxic: Na channel inhibition = arrhythmia, QT interval prolongation
CNS: confusion, hallucinations, sedation, seizures

contraindicated in the elderly

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23
Q

What are the selective serotonin norepinephrine reuptake inhibitors? What are their MOA and AEs?

A

duloxetine, venlafaxine, minalcipran

MOA: inhibition of 5HT + NE reuptake in synaptic cleft = increased 5HT + NE

AEs:
early: NVD
late: sexual dysfunction, SIADH, serotonin syndrome

stimulant effect: increases BP, insomnia, can increase cholesterol + triglycerides

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24
Q

Describe carbamazepine. What is its MOA and what is its indication for pain? What are its AEs?

A

MOA: inactivates Na channels

indication: first line treatment trigeminal neuroglia

AEs: highly sedating, hepatic dysfunction, thrombocytopenia, hyponatremia

contraindicated in pregnancy

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25
Describe pregabalin. What are its MOA, indication, and AEs?
MOA: inhibition of presynaptic P-Q type Ca channels = decreased Ca flowing into the cell - decreased intracellular Ca = decreased glutamate release indication: neuropathic pain + neuralgia after herpes AEs: somnolence, nausea, ataxia, impaired vision, weight gain
26
Describe gabapentin. What is its MOA, indications, and AEs?
MOA: inhibition of presynaptic P-Q type Ca channels = decreased Ca flowing into the cell - decrease intracellular Ca = decreased glutamate release indications: postherpetic neuralgia, peripheral neuropathy AEs: dry mouth, somnolence, nausea, ataxia, dizziness, weight gain
27
How is pain management implemented as palliative care?
quality of life focused - emphasis of symptom management - frequent reassessment of therapy based on pt values - balance pain management with AEs
28
Describe the mu receptors. What is the endogenous peptide that works on it and what are its functions?
endorphins - work on mu receptors mu receptor functions: reward respiratory inhibition GI inhibition antitussive antinociceptive
29
describe the delta receptors. What is the endogenous peptide that works on it and what are its functions?
enkephalin - work on delta receptors delta receptor functions - antidepressant - anxiolytic - antinociceptive - antitussive
30
Describe kappa receptors. What is the endogenous peptide that works on it and what are its functions?
dynorphin - works on kappa receptors - antipruritic - antidepressant - diuresis - sedative
31
What are the effects that opioid peptides/agonists have on their receptors?
binding an agonist reduces synaptic transmission via: presynaptic inhibition: closing of the presynaptic Ca Channels = hyper polarization - decreases release of ACh, noradrenaline, 5HT, glutamate, NO, substance P postsynaptic inhibition: opening of postsynaptic K channels = hyperpolarization
32
What are the high potency opioid agonists?
sufenatil, fentanyl, buprenorphine
33
What are the medium opioid agonists?
methadone, oxycodone, morphine, ketobemidone, hydromorphone
34
What are the low potency opioids?
codeine, hydrocodone, tramadol, tapentadol
35
What re the opioid receptor antagonists?
full antagonists: naloxone, naltrexone, methyl naltrexone
36
What are the opioid mixed agonist-antagonists?
butoprophanol, nalbuphine, pentazocine
37
How does lipid solubility change the pharmacokinetics of opioid analgesics?
faster absorption through hydrophobic surfaces - allows for better crossing of the blood brain barrier
38
What are the routes of administration for opioid analgesics and how does it affect their pharmacokinetics?
sublingual/transmucosal - bypasses initial hepatic clearance subcutaneous - depot effect: longer duration epidural - quick penetration into the dura: rapid onset/offset - fentanyl: high potency/mu affinity - low doses avoid systemic absorption - morphine: no significant difference in AEs vs IV patent controlled - parameters set by provider, dose administered by pt
39
What are the main AEs of acute use of opioids?
pruritus - histamine release respiratory depression - TV + RR both decrease sedation NV - tolerance develops in 3-5 days constipation - do NOT develop tolerance
40
What are some ways to combat constipation in patients using opioid analgesics?
pts do NOT develop tolerance requires scheduled stimulant laxatives + stool softener routine can use peripheral acting mu-opioid receptor antagonists (PAMORA) - discontinue laxative - naloxegol + methylnaltrexone: consider in pts with constipation refractory to first line options
41
What are the long term AEs with opioid analgesics?
addiction overdose fractures breathing problems during sleep immunosuppression bowel obstruction myocardial infarction tooth decay secondary to xerostoma
42
What are the opioid antagonists and what are their clinical uses?
naloxone: opioid overdose + reversal of respiratory depression associated with opioid use = emergency naltrexone: opioid relapse, alcohol use disorder, smoking cessation, weight management + bupropion methylnaltrexone - PAMORA for opioid induced constipation
43
What are the opioid antagonists and what is their MOA?
naloxone, naltrexone, methylnalterxone blocks 1 or more receptors in central/peripheral NS MOA: central: competitive inhibitors, highest affinity for mu receptors - displaces opioid agonists from receptors - stimulates respiratory drive, increases alertness, terminates analgesia + eurphoria
44
What are the two opioids used as an antitussive and the one used as an antidiarrheal?
cough suppressants - codeine - dextromethorphan - weak opioid agonist, NMDA receptor agonist diarrhea - loperamide cannot cross BBB - low abuse potential - inhibits propulsive peristalsis, increases sphincter tone, inhibits intestinal fluid secretion
45
What are the functions of COX?
COX - oxidizes arachindonic acid into: prostaglandins - mediator of inflammation + anaphylaxis thromboxane - modifies leukocytes + alters vascular permeability prostacyclin - vasodilatory, active during acute inflammation
46
Describe the specific functions of COX 1 and COX 2
COX 1 - expressed in most cells for housekeeping - important for cytoprotective of gastric epithelium COX 2 - upregulated by cytokines, stress, growth factors - principle prostaglandin during inflammation
47
Describe aspirin. What are its MOA and indications?
MOA: irreversibly attaches to COX - COX1 - inhibits thromboxane synthesis in platelets = prevents aggregation COX 1 + 2 - inhibits prostacyclin and prostaglandin synthesis - antipyretic - anti-inflammatory - analgesic indications: acute MI acute ischemic stroke angina management of ASCVD primary prevention of ASCVD + colorectal cancer giant cell arteritis prevention of stent thrombosis after revascularization procedures pain
48
What are the toxicities of aspirin?
GI: due to decreased prostaglandins = decreased mucus + bicarbonate - dyspepsia - gastric ulceration + bleeding coagulopathy: increased bleeding time tinnitus - can affect verstibulocochlear nerve renal: AKI, acute interstitial nephritis salicylate poisoning: mostly in children, fatal - activated medulla = hyperventilation = respiratory alkalosis
49
describe the MOA and indications for nonselective NSAIDs. What are the medications?
ibuprofen, diclofenac, naproxen, meloxicam, indomethacin MOA - reversibly inhibits COX - including platelets - prevents conversion of arachidonic acid into prostaglandins, thromboxane, and prostacyclin indications - acute/chronic pain - fever - indomethacin: closure of patent ductus arteriosus
50
What are the toxicities of nonselective NSAIDs?
BLACK BOX WARNINGS - CV thrombotic events: contraindicated in CABG - GI bleeding, ulcerations, perforations: contraindicated in elderly, hx of PUG or GI bleed CNS - headache, tinnitus, dizziness CV - fluid retention, HTN, edema, MI, CHF GI - abdominal pain, NV, ulcers, bleeding - decreased mucus, bicarbonate, gastric blood flow hepatic - elevated LFTs pulmonary - asthma, bronchospasm renal - decreased GFR, hyperkalemia, proteinuria, renal insufficiency/failure
51
What are the selective COX 2 inhibitors and what are their MOA and indications?
celecoxib, meloxicam MOA: reversibly inhibits COX-2 production of prostacyclin in vascular epithelium decreased risk of GI irritation NO impact on platelet aggregation + cardioprotective effects indication: patients concerned for GI bleed, but has greatest CV toxicity
52
What are the toxicities for the COX 2 selective inhibitors?
BLACK BOX WARNING - CV thrombotic events: contraindicated in CABG - GI bleeding, ulcerations, perforation: elderly pts, hx of PUG, GI bleeds cardiovascular - stronger association of MI and stroke due to favored formation of thromboxane renal toxicities similar to non-selective NSAIDs
53
Describe methotrexate. What is its MOA and indications?
MOA: folate antagonist/antimetabolite - inhibits folate acid synthesis - inhibits purine synthesis = prevents DNA synthesis = cytotoxic - anti-inflammatory: suppresses AICAR transformylase indication - first line treatment for RA - psoriasis/psoriatic arthritis, ankylosing spondylitis, SLE
54
What are methotrexate toxicities?
bone marrow suppression: anemia, thrombocytopenia, leukopenia GI: nausea, mucosal ulcers, stomatitis, GI ulcerations Hepatic: increased LFTs renal failure: GFR 10-50; < 10 contraindicated alopecia teratogenic - contraindicated in pregnancy
55
What is hydroxychloroquine MOA and indications?
MOA: suppresses T lymphocytes response to mitogens (proteins that enhance rate of cell division) - inhibits leukocyte chemotaxis - inhibits DNA/RNA synthesis - impairs complement-dependent antigen-antibodies reactions indications - anti-malarial - some efficacies in rheumatic diseases
56
What are the toxicities of hydroxychloroquine?
hyperpigmentation retinopathy NVD, abdominal pain rash/pruritus
57
Describe sulfasalazine. What is its MOA, indication, and toxicities?
MOA: metabolizes into sulfapyridine + 5-aminosalicylic acid in the colon - anti-inflammatory + immunosuppressant properties indications: RA, psoriatic arthritis, IBD toxicities - requires gradual titration to help avoid AEs - headache - NVD, anorexia - rash - blue discoloration - contraindication in pts with sulfa/salicylate allergies
58
Describe leflunomide. What is its MOA, indications, and toxicities?
MOA: prodrug of teriflunomide - inhibits pyrimidine synthesis: decreases T cell proliferation + B cell antibody production - anti-inflammatory + immunomodulatory indication: RA toxicities BLACK BOX WARNING: pregnancy - need (-) pregnancy test + 2 forms BC; 2 years after discontinuation diarrhea LFT elevation - contraindicated in severe HI HTN rash nausea abdominal pain back pain alopecia
59
Describe tofacitinib. What is its MOA, indications and toxicities?
MOA: JAK inhibitor - mainly JAK 1 and 3 - decreases transcription pathway for pro inflammatory genes indication - RA toxicities BLACK BOX WARNINGS - serious infections (TB) - increased risk for lymphomas + malignancies AEs diarrhea increased lipids URTI severe hepatic impairment
60
Describe TNA-a inhibitors. What is their MOA, indication, and toxicities?
MOA: TNA-a important in orchestrating inflammatory process in RA indication: adjuvant to MTC; mono therapy for severe RA toxicities BLACK BOX WARNINGS - TB, HBV, HCV - must test prior to treatment - risk for malignancy: lymphomas, melanomas AEs - exacerbation of new-onset HF - pancytopenia + aplastic anemia - rash, injection site reactions - URTIs
61
What are the major toxicities of acetaminophen?
non-selective COX inhibitor well tolerates < 4 g daily hepatic necrosis - single ingestion 10-15 mg - doses > 20-25 g fatal
62
What are the 3 main treatment strategies for gout management? Acute and chronic
Acute - NSAIDs - Corticosteroids (PO + IA) - colchicine chronic rate-lowering therapy: - Allopurinol - uricosurics - recombinant uricase
63
Describe indomethacin. What is its MOA, indication, and toxicities?
MOA: COX inhibitor - decreased prostaglandin synthesis indications: pain, RA, ankylosing spondylitis, osteoarthritis, bursitis, gouty arthritis, patent ductus arteriosus toxicities - headache, dizziness, dyspepsia, nausea - elevated LFTs, jaundice - neurologic: tinnitus, vertigo, depression, dizziness, headaches - renal insufficiency - cardiac: acute respiratory distress, pulmonary edema, CHF
64
Describe colchicine. What is its MOA, indication, and toxicities?
MOA: binds to tubular + prevents polymerization into microtubules - inhibits leukocyte migration + phagocytosis - reduces expression/formation of cytokines + receptors indication: PPX for gout flares; familial mediterranean fever toxicity - NVD, abdominal pain - requires renal dose adjustment in renal impairment, hepatic failure
65
Describe allopurinol. What are its MOA, indication and toxicities?
MOA: competitive inhibition of xanthine oxidase - hypoxanthine/xanthine not degraded into uric acid indication: preferred first-line for chronic gout toxicity contraindications: HLA B5801 - Han Chinese, Korean, Thai AEs - maculopapular rash - GI intolerance: NVD - bone marrow suppression, aplastic anemia, hepatotoxicity - Stevens-Johnson syndrome/Toxic epidermal necrolysis

YSM Semester 2 (10 decks)

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