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Pharmacology FINAL (2nd sem) > B: 25-28 > Flashcards

B: 25-28 Flashcards

1
Q

Synthetic opiates

A
  • Fentanyl- (strong.) analgeisa and anesthetica
  • Merperidine- strong. analgesia , causes tachycardia bcz similar to atropine
  • Methadone (strong agonist): management of opoid withdrawal syndrome , maintenance program for addicts
    • Potent mui-receptor agonist
    • Potent NMDA antagonist
    • NE, SE reuptake inhibitor
  • Tramadol- (weak.) analgesia. also
    • inhibits 5HT, NE reuptake (serotonin syndrome)
    • analgesic use
  • Loperamide, Diphenoxylate- (weak agonist) anti diarrhea
    • loperamide has no cns effect
  • Dextromethorphan (weak synthetic agonist) - analgesic, anti-tussive, inhibit 5HT, NE reuptake
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2
Q

Opioid receptrors are coupled to

A

Gi protein

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3
Q

Opioid

A
  • Miu-
    • presynaptic
    • postsynaptic
      • increace K conductance. > IPSP
    • Endrophines>Enkephalin> dynorphin
    • Sedation, decrease respiration, decreased GI motility, analgesia
  • Delta-
    • presynaptic
    • enkephalin> endorphine> dynorphin
    • analgesia
  • Kappa-
    • presynaptic
    • dynorphin>> endorphins, enkephalin
    • analgesia, psichomimetic, GI motility decrease
  • All modulate hormone and NT release
    ALL are Gi coupled
  • ALL are Presynaptic
    • reduce Ca influx.
    • decrease transmitter release
    • increase K conductance
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4
Q

Opiates antagonists

A
  • Naloxone: strong antagonist of all opioid R
    • Semi-synthetic
    • used in case of opioid overdose ( IV )
    • T1/2= 1-2 hrs
    • stronger affinity for opioid R ; kicks opioid out!
  • methyl-Naltrexone( strong antagonist)
    • synthetic
    • management of opioid withdrawal syndrome (oral )
    • management of alcohol withdrawal syndrome
    • T1/2= up to 48 hrs

No relax zone

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5
Q

Natural opioids

A

Morphine- (strong agonist) Analgestic, anasthesia, acute pulm. edema

Codeine- (weak agonist) metabolised in the liver (CYP450) to produce morphine which is ten times more potent against the mu receptor.
Binding of codeine or morphine to the mu opioid receptor results in hyperpolarization of the neuron leading to the inhibition of release of nociceptive neurotransmitters causing an
analgesic effect and increased pain tolerance due to reduced neuronal excitability
Anti-tussive

Modulate transmission in many sites in the brain and spinal cord

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6
Q

endogenous Opioid peptides

A

Endorphine (u)
Enkephalin (Delta)
Dynorphine (Kappa)

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7
Q

Which are the semi synthetics opioids

A

Hydromorphone( strong agonist) - Analgesic use

Oxycodone (strong agonist)- Analgesic use

Dihydrocodeine (weak agonist)- Antitussive, analgesic

Buprenophine (Mixed activity : Partial u-agonist, Kappa-antagonist, deltaa-antagonist), maintenance programs for addicts, managing opioid withdrawal syndrome,

Nalbuphine (mixed activity) for spinal anasthesia

HOD -BN (hood black ni**a)

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8
Q

Teratogenicity of opoids

A
  • Respiratory depression
  • pre-eclampsia (pregnancy HTN +proteinurea)
  • fetal death
  • physical dependence –> Neonatal abstinence syndrome(NAS) = conditions caused when a baby withdraws from certain drugs he’s exposed to in the womb before birth. NAS is most often caused when a woman takes drugs called opioids during pregnancy
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9
Q

Acute toxicity opioids symtpoms and managements

A
  • pupillary constriction “pin point pupil”
  • respiratory paralysis
  • coma
  1. IV naloxone
  2. supportive
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10
Q

Dependence of opoid symptoms and management

A
  • yawning
  • increased secretions: lacrimation, rhinorhhea, salivation
  • anxiety, sweating, hyperthermia
  • muscle cramps, spasm , CNS-originating pain
  • piloerection
  1. methadone, buprenorphine, naltrexone
  2. clonidine: decreases sympathetic symptoms ( sweating, hot flashes, watery eyes, and restlessness.)
  3. supportive
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11
Q

NSAID’s general drugs

A
  • Aspirin- irreversible COX inhibition (acetylation of serine OH group)
    • oral
    • Low dose: first order kinetics (T1/2= 3-5 hrs)
    • High dose: zero order elimination (T1/2= 15 hrs)
    • renal elimination
  • Allopurinol- Inhibits Xantine Oxidase–>decreased purine metab.–>decreased uric acid
  • Rasburicase- It is an Urate oxidase enzyme that metabolize uric acid into Allantoin
  • Colchicine- inhibits Microtubule assembly
    • binds tubulin > altered microtubular polymerization
    • decreased LTB4 > altered leukocyte and granulocyte migration
    • oral, parenteral
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12
Q

Aspirin- indications

A
  • Low dose (<300mg/dl)
    • Anti-platelet aggregation :
      • Post MI prophylaxis
      • reduce risk of CV events
  • Medium dose (300-2400 mg/dl)
    • analgesic
    • antipyretic
  • High dose (2400-5000 mg/dl)
    • Anti-inflammatory effect
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13
Q

aspirin SE

A
  • GI irritation ( PUD, gastritis, GI bleeding)
  • Renal damage ( AKI, interstitial nephritis)
  • tinnitus, vertigo, hearing loss
  • Increased bleeding time
  • chondrotoxic
  • Uric acid
    • high dose: uricosuria
    • low dose: hyperuricemia
  • NSAID induced asthma ( due to high LT)
  • hypersensitivity rxn ( due to high LT)
  • Hyperventilation ( respiratory alkalosis) early
  • metabolic acidosis, high anion gap (late)
  • dehydration, hyperthermia
  • collapse, coma , death
  • labor prolongation
  • rey’s syndrome in children treated with aspirin for viral infection –>
    • acute liver failure,
    • encephalopathy
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14
Q

Colchicine indication, administration

A
  • oral, parenteral
  • acute gout - high doses (use is limited due to severe diarrhea)
  • chronic gout - low doses
  • familial mediterranian fever
  • potential role in management of pericardial disease (pericarditis, pericardial effusion)
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15
Q

SE Colchicine

administration

A
  • Microtubule assembly inhibitor
  • oral, parenteral
  • acute:
    • severe diarrhea,
    • GI pain
  • chronic:
    • hematuria
    • alopecia
    • myelosuppression
    • gastritis
    • peripheral neuropathy
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16
Q

Acute gout

A

Acute attacks involve joint inflammation initiated by precipitation of uric acid crystals (monosodium urate)

Goal: to reduce inflammatory rxn

Give

  • Indomethacin (NSAID)
    • Reversibly inhibit COX-1 and COX-2 • reduce synthesis of prostaglandins
      • ORAL
      • 1st-line agent in managing acute attack
      • prescription drug
  • Naproxen(NSAID)
    • Reversibly inhibit COX-1 and COX-2 • reduce synthesis of prostaglandins
      • ORAL
      • less potent than indomethacin
      • OTC drug
  • Sulindac
    • NSAID
    • oral
    • less potent than indomethacin
  • Colchicine (Microtubule assembly inhibitor)
    • oral, parenteral
    • acute gout - high doses
    • chronic - low doses
  • Prednisolone (CS)
    • oral ( up to 5 days)
    • Intra-articular injection
    • treatment of acute gout where NSAIDS are CI or rarely 1st-line choice
17
Q

Chronic gout goal of treatment and what drugs

A
  • goal: reduce uric acid pool , either by
    • accelerating renal excretion
    • or by reducing endogenous production

Give

  • Allopurinol:( xanthine oxidase inhibitor > decreased purine metabolism> decreased serum uric acid
    • oral
    • prodrug activated by xanthine oxidase
    • high doses: active metabolite acts as suicide inhibitor ( irreversible inhibition)
    • Drug interation: inhibits 6-MP
    • Chronic gout
    • adjunct to chemo and radiotherapy (tumor lysis sy- may precipitate gout attack)
  • Rasburicase: (Recombinant urate oxidase) - Urate oxidase catalyses metabolism of uric acid to allantoin (water soluble) > decreased serum uric acid , decreased uric acid precipitation
    • ​
  • Probenecid: ( Uricosuric agent = inhibit tubular resorption of uric acid > serum uric acid decreases)
    • Oral
    • ineffective when GFR <50 ml/min/1.73 m^2
    • Chronic gout
    • prolongs antimicrobial drug activity
18
Q

Probenecid SE and administraion

A
  • precipitation of acute gout attack or urate renal stone
  • Hypersensitivity rxn (sulfonoamide hyperssensitivty)
  • inhibits renal tubular secretion of weak acid drugs
    • penicillin
    • cephalosporin
    • MTX
  • oral
19
Q

Rasburicase administration, SE

A
  • IV
  • T1/2= 18hrs
  • anaphylactic rxn
  • methemoglobinemia in patient of G6PD defiency
20
Q

allupurinol SE , administration route

A
  • GI irritation
  • hypersensitivity rxn, SJS
  • bone marrow supression

drug interaction : inhibits metabolism of 6-MP

  • oral, prodrug activated by xanthine oxidase
21
Q

Dont give Allopurinol with

A

6MP ( inhibits 6MP metabolism)

22
Q

Non-selective NSAID’s (Non-aspirin)

A
  • Ibuprofen- Non-selective COX inhibitor ,
    • closes PDA
    • analgesic in children
  • Ketoprofen-
    • short T1/2. keto is a short diet
    • may also inhibit LOX (decreased LT)
  • Naproxen-
    • dysmmenorrhea, menstrual cramps. when you nap it helps with cramps
    • control of acute gout
    • long T1/2
  • sulindac (oral) - NSAID in acute gout
  • Indomethacin-
    • ​closure of PDA. indigo like blue blood bcs of PDA
    • control of acute gout
    • bone marro suppression ( thrombocytopenia, agranulocytosis)
  • Diclofenac-​ Dic like disc of vertabrae
    • Topical, oral
    • accumulates in Synovial fluid- pain of musculoskeletal origin (back pain, disc herniation, osteoarthritis)
    • prothrombotic risk
    • prescription-only drug
  • Metamizole- very hematotoxic( agranulocytosis). אני מתה מזה
    • limited use
  • Phenylbutazone- stop after 1 week
    • potent anti-inflammatory effect
    • severe se: Aplastic anemia
    • Pyrazolone derivative
  • Meloxicam- RA! COX2>COX1. so meloww
    • treat arthritis (Rheumatic disease, osteoarthritis)
  • Celecoxib- selective COX2. less bleeding. sulfa drug
    • Not more effective than non-selective cox-inhibitors
    • Oral
    • hepatic metabolism
    • Analgesic. antipyretic, anti-inflammatory
  • paracetamol(acetaminophen)
    • effective analgesic esp if adminitered IV
    • Anti-pyretic
    • analgesic
    • No anti-inflammatory effect
    • Hepatotoxicity due to acetaminophen overdose > leads to NAPQI build up ( N-acetyl-p-benzoquinone imine)
    • NAPQI > irreversible oxidative hepatocyte injury > liver cell necrosis
23
Q

Renal Aspirin SE

A

Anion gap metabolic acidosis

24
Q

Acetaminophen

A

Inhibit COX in brain so analgesia
When metab by CYP450 (10%), forms NAPQI that can cause acute liver failure

25
Q

Celecoxib- adverse effects

A

selective COX2.

  • GI irritation (miler than non-selective)
  • renal damage (= non selective)
  • prothrombotic effect > greater inhibitory effect on endothelial protacyclin (PGI2) which promotes vasodialation and inhibits PLT aggregation
  • sulfonamide hypersensitivity
26
Q

antidote for acetaminophen toxicity

A

N-acetyl cystein

Pharmacology FINAL (2nd sem) (37 decks)

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