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Pharmacology > NSAIDS / Opiods / Asthma / COPD > Flashcards

NSAIDS / Opiods / Asthma / COPD Flashcards

1
Q

Aspirin (ASA)

MOA & PK

A

acetyl-salicylic acid –> met. to reactive acetyl group + salicylate

  • Effects due to salicylate moiety (binds to COXs)
  • 10x more potent on COX-1
  • covalently acetylate COXs –> inactivates irreversibly (due to acetyl effect on COX)
    • ​new COX synthesis req. to terminate action
  • ​**PK: **Oral, 325 mg, slows accumulation of free drug
    • ​rapidly hydrolyzed to salicylic acid + acetic acid
    • COVALENT acetylation may only occur near site of absorption (platelets, endothelial cells). Before acetyl group is hydrolyzed
    • ​​Low dose –> met by liver conjugation (1st order)
      • ​2-3 tabs –> analgesic & antipyretic
    • High dose –> excreted unmetabolized by kidneys
      • _​_4+ tabs –> anti-inflammatory dose
      • ​0 order (drug can build up, non-saturable)
    • ​High dose required for anti-inflammatory for COX-2 effect (toxic doses that take more time to eliminate)
    • Half-lives - 2 hr for low dose
      • 15-30 hr for high dose
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2
Q

Aspirin Therapy

A
  • Blocks PG synthesis and PG release
  • Analgesia
    • ​mild to moderate pain
    • PGs sensitize receptors for peptide mediators of pain (bradykinin, substance P)
    • Aspirin inhibition of PGs limits inflammation-related pain
  • ​Antipyresis
    • ​acts on hypothalamus to return thermoreg set-point to normal
  • ​Anti-inflammatory
    • ​double-dose
    • COX-2 effect, requires higher dose
    • for acute rheumatic fever, rheuatoid arthritis
  • _​_Unique use –> Reduce risk of MI and Stroke
    • ​reduce thrombus formation (after event or prophylactic)
    • effects on platelets = about 7 days
    • Shift balance to anti-thrombotic PGI (prosta**cyclin) **formation from endothelial cells (COX-2) -> sustained reduction in TXs
    • decreases clotting, increases bleeding time
  • ​Also beneficial in Colorectal Cancer, esp with FAP
    • ​COX-2 elevation
  • ​Closure in patent ductus arteriosus
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3
Q

Aspirin Adverse Effects

A
  • GI Effects:
    • ​PGs protect Gi mucose from acid damage, salicylates are acids
    • gastric irritation, bleeding, ulceration, ulcers
    • less irritation with enteric coated, use w/ PG analog or omeprazole
  • ​CV Effects
    • ​dilation of peripheral vessels with large doses
    • avoid in pts with blood-clotting disorders
  • ​Premature closure of Ductus Arteriosus (avoid in 3rd trimester)
    • ​patency mediated by PGs
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4
Q

Aspirin Toxicity

A
  • Low Therapeutic Dose - in balance
    • ​uncouple ox-phos in skeletal muscle –> Increase O2 consumption, CO2 production
    • Increase CO2 –> Increase respiration
  • ​Higher Dose - therapeutic or toxic
    • ​directly stim CNS resp center –> respiratory alkalosis
    • renal bicarb excretion compensates
  • ​Toxic Overdose
    • ​central vasomotor paralysis
    • decreased blood flow -> renal failure
      • ​leads to metabolic acidosis and hypokalemia
    • ​​respiratory paralysis –> resp acidosis. Plasma becomes acidic –> many organs fail
  • ​Mild Toxicity – Salicylism. Ringing in ears, dizziness, drowsiness, hyperventilatio –> reduce dose
  • Overdose Toxicity - children, large acute dose. GI duscurbances, CNS disturbances, skin eruptions, hyperpnea, then resp and metabolic acidosis
    • ​hospitalize and maintain vitals
    • prevent absorption with activated charcoal, whole bowel irrigation, volume repletion
    • Sodium Bicarb –> iorn trapping of salicylate in urine

​

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5
Q

Ibuprofen / Naproxen

A
  • Propionic Acid Derivatives
  • **Therapy: **analgesic, antipyretic, anti-inflammatory
  • **MOA: **similar to aspirin
    • ​but reversible and competitive only
    • better than aspirin for dysmenorrhea
    • useful in treatment for gout
  • ​**Adverse: **GI concerns, prolongs bleeding time initially
    • ​not as long-lasting as aspirin
    • Binds to albumin –> displaces warfarin, other drugs
    • Cross-sensitivity w/ aspirin (dont use w/ allergy)
    • Ibuprofen - chronic use increase risk of MI and stroke, block effects of low-dose aspirin
    • Naproxen - greater ulcer risk
  • ​**Toxicity - **similar to aspirin
    • ​nausea, vomiting, Gi bleeds.
    • ​​treat with activated charcoal, monitor respiration and vitals
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6
Q

Indomethacin

A
  • Acetic Acid Derivative
  • 10-20x more potent than aspirin
  • mainly used in severe inflammation (rehumatoid arthritis, gouty arthritis), limited use for analgesia and antipyresis
    • ​also approved for PDA
      *
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7
Q

Celecoxib

A
  • Selective COX-2 inhibitor
  • most inflammation effects due to COX-2
    • ​many adverse effects are COX-1
  • ​**Therapy: **osteoarthritis, theumatoid arthritis, FAP
    • ​equal to naproxen for osteoarthritis and rheumatoid arthritis
    • pain relief, worse than naproxen after dental surgery
    • ​fewer problems for asthmatics than aspirin
  • ​Drug Interactions
    • ​metabolized by CYP-2C9, inhibts 2D6 in some pts
    • altered met of tricyclic and SSRI anti-depressants
  • ​**Adverse: **Edema is most common (dec kidney function)
    • ​GI problems
    • Cant use with Sulfa allergy
    • Not during pregnancy
    • increased risk of MI (tip balance to COX-1 –> increase TXs, platelet aggregation, risk of thrombosis, stroke)
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8
Q

Acetaminophen

A
  • Non-opioid analgesic -> not inflammatory
  • Inhibition of COXs and PG Synthesis
  • PK: well absorbed GI, metabolism in liver (CYP2E1)
  • **MOA: **analgesia and anti-pyresis (similar to aspirin)
    • ​no anti-inflammatory action
    • CNS effects - relaxation, drowsiness, euphoria
    • ​​safer alternative for pain and fever in children
  • ​Adverse: Differences from aspirin
    • ​No GI effects, No hematologic effects, No Reye’s syndrome, No CV effects, no acid-base effects
      • ​but no anti-inflammatory actions either
    • ​hepatic damage is major concern with chronic use
    • Alcohol increases liver damage risk
    • chronic abuse - nephrotoxicity
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9
Q

Acetaminophen Toxicity

A
  • GI Distress
    • ​nausea, vomiting, anorexia, abdominal pain
  • ​hepatotoxicity - major concern​ (occurs at 8 hours)
    • ​jaundice at 24-48 hrs, usually reversible
    • ​​formation of reactive electrophile –> modifies and inactivates liver proteins (unless adequately removed by glutathione (GSH)
    • ​CYP2E1 forms reactive electrophile
  • ​Treatment
    • ​remove drug –> activated charcoal, vomiting, gastric lavage in the first 4 hours
    • After 4 hrs –> N-acteyl-cysteine - reverse toxicity (reacts with AC toxic metabolite) and restores endogenous glutathione
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10
Q

Opiate Receptors

A
  • Mu - morphine-like. In CNS, periphery, spinal cord.
    • ​analgesia, anti-anxiety, resp depression
  • ​**Kappa - **petnazocine-like. CNS, spinal cord
    • ​Aanalgesia, miosis, sedation, dysphoria, hallucinations
  • ​Delta - Enkephalin-like. CNS, periphery
    • ​dependence, euphoria, analgesia

​​Morphine acts at mu, kappa, & delta. All full agonists act at mu receptors

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11
Q

Morphine

A

Prototype for opioid drugs

  • Natural constituents of opium
  • **PK: **readily absorbed. Analgesia in 5-15 min. Duration 4-5 hrs
    • _​_EtOH can break down slow-release matrix
    • ​​Metabolism: conjugation with glucoronic acid - major
      • ​most inactive metabolites (3-B - seizures)
      • ​Excreted in urine as conjugate
    • ​Additional caution with impaired liver and renal function
    • ​Tolerance – develops to some effects, not others​
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12
Q

Morphine Actions

A
  • Analgesia –> without LOC at therapeutic doses
    • ​peripheral and spinal levels to block pain transmission and block response to pain
    • ​​more effective in continuous dull pain
    • Raises pain threshold - useful for moderate pain
    • Much more selective than anesthetics, barbituates, alcohol. Tolerance can develop
  • ​**Respiratory Depression - ** even at low doses
    • ​primary cause of death in overdose
    • increase in chemoreceptor sensitivity to CO2 levels (hypoxic response still present) (same for given level of analgesia between opioids)
    • Tolerance develops
  • ​Nausea & Vomiting - chemoreceptor trigger zone
    • ​Rapid Tolerance develops
  • ​GI Effects - constipation (decrease in propulsive contractions in LI and SI). No tolerance
  • **Drowsiness - **Tolerance develops
  • Miosis - diagnostic sign. No tolerance
  • Histamine release –> itching, hypotension
  • Inhibits immune system. Increase ACTH, PRL, ADH. Decrease TSH, LH
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13
Q

Morphine Therapy

A
  • Moderate to severe pain
  • Primarily in acute pain
    • ​Acute pain - injury/disease. Treat normally
    • Chronic - terminal -> disease. Continuous. Treat aggressively
    • Chronic - neuropathic -> treat carefully
  • ​First start with drugs for moderate pain (codeine, hydrocodone, codeine + aspirin), then morphine for moderate to severe pain (morphine)
  • Used in sickle cell crisis pain
  • Dyspnea in lung cancer (relax pt -> improve breathing)
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14
Q

Morphine Adverse

A
  • Dependence
  • Increased biliary and urinary tracts (worsen biliary colic and UTI)
  • Allergy
  • Neonates and elderly more sensitive
  • Limitations / Contraindications
    • ​Decreased resp reserves (asthma, emphy, cor pulmonale)
    • Head injuries (obscure important signs)
    • Pregnancy
  • ​Drug Interactions
    • ​Any CNS Depressant (sedative-hypnotics, MAO-I)
    • Sustained release are compromised by ethanol
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15
Q

Codeine

A
  • Structurally similar to morphine
  • More reliable when given orally (better first-pass metabolism)
  • ​Primarily to treat mild to moderate pain (30-60 mg)
    • ​moderate (combo w/ asprin or acetaminophen)
  • ​Effective for cough suppression
  • More constipation
  • Less potential for addiction compared to morphine
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16
Q

Methadone

A
  • Range of effects same as morphine, different PK
  • **PK: **very effective orally
  • Met by CYP3A4 slowsly (half life 15 hours) & 22 hours chronically
    • ​Chronic use: 6-8 hrs analgesia
  • **Therapy: **analgesia, treatment of drug dependence
  • **Adverse: **serious CV effects. (QT prolongation, Torsades)
    • ​Parenteral methadone - euphoria and dependence​
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17
Q

Fentanyl

A
  • Compared to Morphine
  • Analgesia - Short onset time. 15-30 min peak effects. Shorter duration of action
  • Produces suphoria, drowsiness, sedation, dependence
  • Similar respiratory and hormonal effects but does not induce histamine release
  • CV: less effect than morphine. Maintains cardiac stability
  • More likely to produce muscle rigidity of chest and abdomen
  • used in anesthesia
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18
Q

Hydrocodone / Oxycodone

A
  • Hydrocodone
    • Schedule II
    • Most commonly prescribe drug in US
    • CYP3A4
  • Oxycodone
    • More potent than codeine. Effective orally​. Abuse of timed release formation
    • CYP2D6
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19
Q

Loperamide HCl (Imodium)

A
  • Potent anti-diarrheal agent.
  • Full opioid agonist that crosses mucosal membranes poorly
    • ​Limited to GI tract
    • Not a scheduled drug
20
Q

Dextromethorphan

A
  • Antitussive
  • Full opioid agonist
  • Effective cough-suppressant
  • Abuse is increasing
  • No analgesia effects
21
Q

Pentazocine

A
  • Partial Opioid Agonist
    • ​Kappa receptor agonist (not as efficacious as full agonist, antagonist effect when on-board with full agonists)
  • ​Analgesia, sedation, resp depression similar to morphine
    • ​resp depression and analgesia plateau
    • High doses –> produce dysphoria
  • ​May increase BP and Heart Rate
  • May precipitate withdrawal in opioid depednent pts due to antagonist action
    • ​Very reliable orally
  • ​Use: analgesia in moderate to severe pain (not in high dose because of dysphoria and hallucinations
    *
22
Q

Buprenorphine

A
  • Partial agonist at Mu receptors
  • Antagonist at kappa receptors
    • ​Ceiling for producing analgesia, resp depression, euphoria
  • ​Similar morphine effects on eyes, GI tract, high dose may prolong QTc
  • Uses: analgesia – only IV
    • ​Treatment of opioid dependence
    • Treatment of cocaine abuse
23
Q

Tramadol

A
  • Very weak partial opioid agonist
    • Weak Mu Partial Agonist plus inhibits NE and 5HT transport
    • Can produce dependence, difficult withdrawal
  • ​Adverse: Seizures, serotonin syndrome
24
Q

Naloxone (Narcan)

A
  • Opioid Antagonist
    • ​Blocks opiate receptors (more effective vs full agonists than partial agonists) at mu receptors (competitive antagonist)
  • ​Use: Little to no effect on its own
    • ​to counteract the effects of opioids (resp depression after surgery, overdose, drug abuse)
  • ​Short acting (1-4 hrs)
  • Will precipitate withdrawal when physical dependence is present
    • ​Cannot treat resp depression due to non-opioid effects
25
Q

Acute Opioid Overdose

A
  • Diagnosis
    • ​Resp depression
    • Miosis
    • Coma
  • ​Treatment
    • ​Support respiration, intubate
    • Prevent further absorbance
    • Naloxone –> to reverse resp depression (partial agonists are not very responsive)
26
Q

Albuterol

A
  • Short Acting Beta-2 Selective Agonist (SABA)
  • Treating acute bronchoconstriction and exercise-induced asthma
  • PK: Inhalation - onset within 1-5 minutes, duration 2-6 hrs
    • ​Longer duration orally
  • ​Adverse: Tachycardia, palpitations.
    • ​CNS stimulatory
    • Receptor desensitation with chronic drug use
    • Inhalation reduces systemic effects
27
Q

Salmeterol

A
  • Long-acting beta-2 selective agonist (LABA)
    • ​most widely used
  • ​High B-2 selectivity, long-lasting action
    • ​Exosite on B-2 receptor –> persistent & repeated activation of receptor
  • ​**Therapy: **Useful for maintenance and patients with nocturnal symptoms
    • ​Inappropriate for acute bronchoconstriction
  • ​Always used together with anti-inflammatory steroid
    • ​Fixed-combo dose in inhalers​
28
Q

Formoterol

A
  • Maintenance and Prevention of exercise-induced bronchospasm
  • Long-action due to lipophilicity
    • ​More rapid onset than salmeterol
    • ​**Always together with ** anti-inflammatory steroid
  • ​LABAs also used in COPD
    • ​safe alone for COPD
  • ​Oral therapy less effective –> for children who cannot use inhaler or with severe asthma
29
Q

Fluticasone / Budesonide

A
  • Inhaled Corticosteroids (ICS)
  • **MOA: **Do not relax airway smooth muscle –> little effect on acute bronchoconstriction
    • ​Inhibit inflammation
    • Bind to agonist transcription factors - stimulate anti-inflammatory products
    • Modulate cytokine / chemokine production - inhibit basophils, eosinophils, other leukocytes
  • ​**Therapy: **moderate persistent asthma & severe asthma
    • ​Used prophylactically
    • Control symptoms, prevent irreversible airway changes
  • ​**PK: **Inhaled - enhanced therapeutic index. Longer durations action, higher affinities and selectivities for GC receptors
  • **Adverse: **Mostly free of toxicity - localized
    • ​Hoarseness and pharyngeal candidiasis due to inhalation - rinse mouth after delivery
    • Other GC effects (HPA, decreased bone density, cataracs)
  • ​Combo with LABA (salmeterol + fluticasone)
30
Q

Prednisone

A
  • Systemic Glucocorticoid
    • ​used for acute exacerbations of asthma unresponsive to inhaled dilators
    • Sometimes for chronic, severe asthma
  • ​Much greater concern for GC toxicity
    • ​increased BP, Glucose intolerance, osteoporosis, cataracts, and glaucoma, HPA suppression
31
Q

Long-term asthma control

A
  • Mild intermittent –> None
  • Mild persistent –> low-dose inhaled steroid
  • Moderate persistent –> low-dose inhaled steroid + LABA. Or medium steroid
  • Severe persistent –> high dose inhaled steroid plus LABA or oral steroid

Quick relief –> always SABA

32
Q

Theophylline

A
  • Methylxanthine - Bronchodilators for asthma
    • ​structural analog of caffeine
    • Orally, short duration of action​
      • ​Not inhaled
  • ​​**Therapy: **weak bronchodilator (not useful for acute)
  • mainly used as adjunct for long-term preventative therapy
  • Decrease freq and severity of symptoms (especially nocturnal)
  • **MOA: **Phosphodiesterase inhbition - cAMP elevation
    • ​PDE3 - bronchodilation
    • Antagonist at bronchoconstrictor adenosine receptors
    • Calcium release in muscle contraction
  • ​**Adverse: **Higher dose: nausea, nervousness, anxiety, headache
    • ​Toxic: vomiting, hypokalemia, hyperglycemia, tachy, seizures
    • Many drugs and foods can increase concentrations
33
Q

Montelukast / Zileuton

A
  • Leukotriene Modifiers
  • LT increase eosinophil migration, mucus production, airway wall edema, bronchoconstriction
  • **Use: **Decrease LT levels
    • ​Alternatives to inhaled steroids in mild-persistent asthma
    • Add-on therapy in moderate-persistent asthma
    • ​​Use in aspirin-sensitive asthma (NSAIDS shift PG-LT balance to favor LTs)
    • Limited for acute attacks - no major dilation effect
  • ​**Adverse: **Mild ehadache, GI disturbance
    • ​Reversible liver toxicity with zileuton
    • risk of psychosis or depression with montelukast
  • ​​Comparisons
    • ​oral is convenient for children
  • Montelukast - only one LT receptor (antagonist of CysLT1) - LTD4 receptor (LT bronchoconstriction, CYP450)
  • Zileuton blocks All LT actions. (inhibitor of 5-lipoxygenase enzyme). More anti-inflammatory than montelukast
34
Q

Omalizumab

A
  • Recomb human monoclonal antibody against IgE
    • ​Administered SC injection every 2-4 weeks
  • ​Use for moderate to severe asthma whose asthma is due to reactivity to allergens and not controlled with steroids
  • **Adverse: **skin irritation / recation at injection site
    • ​Occaisonal anaphylactic reactions upon injection
35
Q

Cromolyn Sodium

A
  • Mast Cell Stabilizer
  • ​​**MOA: **prevent release of mast cell mediator
  • **Use: **decrease airway hyperresponsiveness –> prevent asthmatic attacks in mild to moderate asthma
    • ​Not useful in acute attacks (limited use overall)
  • ​**PK: **Inhaled powder or aerosol, short duration of action
  • **Adverse: **bronchospasm, reflex wheezing, throat irritation, cough, dry mouth
    • ​joint swelling and pain, headache, rash
36
Q

Indacaterol

A
  • **Inhaled LABA **for COPD use only
    • ​NOT indended for asthma or acute COPD exacerbations
  • ​Once-daily maintenance for airflow obstruction in chronic bronchitis and emphysema
37
Q

Ipratropium / Tiotropium

A
  • Muscarinic Antagonist (Tiotropium - LAMA)
  • ​**​MOA: **derivatives of atropine
    • ​non-selective blockade of M1-M5 receptors (M3 blockade - main target for bronchodilation
  • ​Block only part of bronchoconstriction that is mediated by acetylchoine release
    • ​Prevent constriction, not actively dilate
    • ​​dilation occurs more slowly and less intense. Also reduce mucus hypersecretion
  • ​**Clinical Use: **Only for COPD and emphysema
  • **PK: **Inhalation. Ipratropium - short acting
    • ​Tiotropium - long (24 hr)
  • ​**Adverse: **Some dry mouth and pharyngeal irritation
    • ​increase ocular pressure in glaucoma patients
    • Anti-chol effects: constipation, tachycardia, blurred vision, urinary retention
38
Q

Roflumilast

A
  • PDE4-selective inhbitor
    • ​Orally effective
  • ​Specifically for reducing exacerbations in adults with severe COPD assoc. with chronic bronchitis & history of exacerbations
    • ​Reduces inflammation but NOT bronchoconstriction
  • ​NOT a bronchodilator and should NOT be used for bronchospasm
  • **Adverse: **Diarrhea & nausea
    • ​Insomnia, anxiety, depression
    • weight loss
    • should not be used in liver impairment
39
Q

Dephenhydramine (Benadryl)

A
  • First Generation H1-Receptor Antagonist
  • ​​Oral & topical preparation for allergic symptoms
  • **Use: **Allergic rhinitis, derm pain and itching, Sleep Aid, motion sickness (anti-muscarinic effect)
  • **Adverse: **due to anti-muscarinic effects
    • ​​​Sedation is prominent
    • ​topical allergic responses (dermatitis)
    • may reduced lactation / enters breast milk
    • Avoid in narrow angle glaucoma
40
Q

Chlorpheniramine (Chlor-Treimetron)

A
  • First Generation H1-antagonist
  • Oral preparation
  • **Use: **Allergic rhinitis, derm pain and itching, OTC cold remedy
  • **Adverse: **Sedation (less than diphenhydramine)
    • ​less effects at muscarinic receptors than diphenhydramine, but similar side effects (glaucoma, reduced lactation)
41
Q

Promethazine

A
  • First Generation H1-antagonist
  • Oral preparation
  • **Use: **in similar fashion to diphenhydramine / chlorpheniramine
    • ​Antiemetic agent (for nausea and vomiting)
  • ​**Adverse: **similar to antihistamines
    • ​also photosensitivity
42
Q

Meclizine

A
  • First generation H1-antagonist
  • Used for vertigo, preventing motion sickness
  • _Less sedating _ than other 1st generation antihistamines
43
Q

Doxylamine

( + pyridoxine = Diclegis)

A
  • First generation anti-histamine
  • Approved for Morning Sickness in Pregnancy
44
Q

Fexofenadine (Allegra)

A
  • Second Generation H1-Antagonist
  • Oral prep. Do not take with fruit juice (reduced absorption via OATPs)
  • **Use: **Allergic rhinitis
    • Derm pain and itching (better if before onset of symptoms)
  • ​**Adverse: **generally not sedating
    • ​nausea, vomiting, dysmenorhea, drowsiness, enters breast milk
45
Q

Cetirizine (Zyrtec)

A
  • Second Generation H1-antagonist
  • Oral prep. Long duration of action
  • **Use: **allergic rhinitis, derm pain and itching
  • **Adverse: **relatively sedating for a 2nd-gen
    • ​Weak anti-musc. effects (dry mouth)
  • ​Metabolized by CYP3A4

Pharmacology (2 decks)

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