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Lernmaterialien für Pharma an der Medical University Varna

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Non-selective inhibitors of cyclooxygenase (СОХ)


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Acetyl-salicyl acid (ASA)

Ibuprofen

Diclofenac 

Naproxen


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Toxicological characteristics of morphine

  • ADR
  • contraindication
  • acute intoxication
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ADR:

  • 􏰀  Respiratory depression )
  • 􏰀  Constipation (=Obstipation)
  • 􏰀  Nausea and vomiting
  • 􏰀  Sedation
  • 􏰀  Pruritus, urticaria, bronchospasm (histamine)
  • 􏰀  ↑ intracerebral pressure
  • 􏰀  Urine retention
  • 􏰀  Tolerance and dependence



Contraindication


  • Cranial trauma
  • Acute abdomen 
  • Bronchial asthma


Acute intox

  • 􏰀 Pinpoint pupils
  • 􏰀 Respiratory depression 
  • 􏰀 Coma → death
  • 􏰀 Treatment: naloxone IV



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Tolerance 

of opioid analgesics

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  • 􏰀 Rapid in development (days), but clinically manifested after 2-3 weeks
  • 􏰀  Dose escalation up to 30-50 fold in addicted persons
  • 􏰀  It is rarely a clinical problem (mostly a social phenomenon)
  • 􏰀  Cross tolerance (incomplete – allows switch to another analgesic)
  • 􏰀  Does not develop to: 
    • 􏰀 Miosis
    • 􏰀 Constipation


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Selective inhibitors of СОХ-2



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Celecoxib


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Clinical use of NSAIDs


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􏰀 Inflammatory conditions of the motor system and associated pain

􏰀 Acute or chronic pain of low to modest intensity – headache, toothache, dysmenorrhea, trauma, post-surgery pain


􏰀 In fever – ASA and ibuprofen
􏰀 Prevention of arterial thrombosis (AMI, stroke) –ASA at low doses



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TESTE DEIN WISSEN


ADRs to NSAIDs



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􏰀 Frequent and predictable АDRs (due to COX inhibition)

  - GIT
      ->Gastric discomfort, nausea, ulcers 

       ->Bleeding

􏰀 Renal and cardiovascular

  • -  Sodium and water retention – worsening of hypertension, heart failure

  • -  Thrombotic events (coxibs)

  • -  Reversible acute RF (=rheumatic fever)

          -  „Analgesic nephropathy“ – with chronic, long-term (years) use

􏰀 Bronchoconstriction in „Aspirin- sensitive asthma“


􏰀 Relatively uncommon ADRs 

    - Hepatotoxicity

        -> Nimesulide

         -> ASA – “Ray syndrome” – liver impairment + encephalopathy (in children with viral infections)


􏰀 CNS - ASA at high doses

􏰀 Bone marrow suppression

􏰀 Hypersensitivity reactions


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TESTE DEIN WISSEN


Pharmacodynamics of NSAIDs


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TESTE DEIN WISSEN


􏰀 Anti-inflammatory effect
   -> Reduced edema, swelling and    reddening (inhibition of PGs-induced

vasodilation)
􏰀 Antipyretic (anti-fever) effect

   -> Decrease of the temperature in fever (hyperpyrexia) 

􏰀 Analgesic effect

   -> Decrease of pain (reduced sensitization of nociceptive nerve endings) 

􏰀 Antiplatelet effect

  -> АSА at low doses (75-300 mg)
      - Selective irreversible inhibition of ТхА2 synthesis in platelets through

acetylation.

      - At higher doses АSА inhibits also the synthesis of PGI2 and the effect on platelet aggregation is nullified 


Lösung ausblenden
TESTE DEIN WISSEN


Cyclooxygenase(СОХ)


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TESTE DEIN WISSEN


􏰀 The enzyme responsible for the production of prostanoids from AA 

􏰀 Types of COX

    - СОХ-1: constitutive enzyme, involved in the physiological functions of prostanoids:

        -> Prostaglandins (PGs E1/2, F2α) effects:
            􏰀 In the stomach: PGE ↓ gastric acid secretion 

            􏰀 In the uterus: PGE/F cause contraction
            􏰀 In the kidneys PGs E: cause natriuresis

􏰀 Prostacyclin (PGI2)
   - In vascular endothelium: vasodilation, inhibition of platelet aggregation

􏰀 Thromboxane А2 (TxA2)
   - In platelets: aggregation, vasoconstriction

􏰀 СОХ-2:

  • 􏰀  Mainly inducible form, expressed in inflammation:

       - PGs E – edema, reddening, pain

  • 􏰀  Involved also in normal homeostasis (e.g. in the vascular endothelium, kidney, bones, brain)


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TESTE DEIN WISSEN


Analgesics antipyretics

(non-opioid analgesics)

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eg. Paracetamol (acetaminophen)

       metamizole (dipyrone)


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TESTE DEIN WISSEN

Analgesics antipyretics


Pharmacodynamics

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  • Analgesic effect – in mild to moderate pains

  • Antipyretic effect

  • No anti-inflammatory effect


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TESTE DEIN WISSEN

Analgesics antipyretics

Mechanism of action

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􏰀Central СОХ inhibition?
􏰀 Other possible mechanisms –

interaction with:

   - Endocannabinoid system

   - Opioid system

   - NO, monoaminergic, cholinergic systems


Lösung ausblenden
TESTE DEIN WISSEN


ADRs of NSAIDs

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TESTE DEIN WISSEN


􏰀 Antagonism with antihypertensive drugs
    􏰀 With АСЕ inhibitors and diuretics – risk of acute renal failure

(“Triple whammy”)
􏰀 Antagonism to the antiplatelet effect of ASA (ibuprofen, naproxen)

􏰀 With anticoagulants (vitamin K antagonists) – ↑ bleeding risk

(especially ASA)


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Beispielhafte Karteikarten für deinen Pharma Kurs an der Medical University Varna - von Kommilitonen auf StudySmarter erstellt!

Q:


Non-selective inhibitors of cyclooxygenase (СОХ)


A:

Acetyl-salicyl acid (ASA)

Ibuprofen

Diclofenac 

Naproxen


Q:

Toxicological characteristics of morphine

  • ADR
  • contraindication
  • acute intoxication
A:


ADR:

  • 􏰀  Respiratory depression )
  • 􏰀  Constipation (=Obstipation)
  • 􏰀  Nausea and vomiting
  • 􏰀  Sedation
  • 􏰀  Pruritus, urticaria, bronchospasm (histamine)
  • 􏰀  ↑ intracerebral pressure
  • 􏰀  Urine retention
  • 􏰀  Tolerance and dependence



Contraindication


  • Cranial trauma
  • Acute abdomen 
  • Bronchial asthma


Acute intox

  • 􏰀 Pinpoint pupils
  • 􏰀 Respiratory depression 
  • 􏰀 Coma → death
  • 􏰀 Treatment: naloxone IV



Q:


Tolerance 

of opioid analgesics

A:


  • 􏰀 Rapid in development (days), but clinically manifested after 2-3 weeks
  • 􏰀  Dose escalation up to 30-50 fold in addicted persons
  • 􏰀  It is rarely a clinical problem (mostly a social phenomenon)
  • 􏰀  Cross tolerance (incomplete – allows switch to another analgesic)
  • 􏰀  Does not develop to: 
    • 􏰀 Miosis
    • 􏰀 Constipation


Q:


Selective inhibitors of СОХ-2



A:


Celecoxib


Q:


Clinical use of NSAIDs


A:


􏰀 Inflammatory conditions of the motor system and associated pain

􏰀 Acute or chronic pain of low to modest intensity – headache, toothache, dysmenorrhea, trauma, post-surgery pain


􏰀 In fever – ASA and ibuprofen
􏰀 Prevention of arterial thrombosis (AMI, stroke) –ASA at low doses



Mehr Karteikarten anzeigen
Q:


ADRs to NSAIDs



A:


􏰀 Frequent and predictable АDRs (due to COX inhibition)

  - GIT
      ->Gastric discomfort, nausea, ulcers 

       ->Bleeding

􏰀 Renal and cardiovascular

  • -  Sodium and water retention – worsening of hypertension, heart failure

  • -  Thrombotic events (coxibs)

  • -  Reversible acute RF (=rheumatic fever)

          -  „Analgesic nephropathy“ – with chronic, long-term (years) use

􏰀 Bronchoconstriction in „Aspirin- sensitive asthma“


􏰀 Relatively uncommon ADRs 

    - Hepatotoxicity

        -> Nimesulide

         -> ASA – “Ray syndrome” – liver impairment + encephalopathy (in children with viral infections)


􏰀 CNS - ASA at high doses

􏰀 Bone marrow suppression

􏰀 Hypersensitivity reactions


Q:


Pharmacodynamics of NSAIDs


A:


􏰀 Anti-inflammatory effect
   -> Reduced edema, swelling and    reddening (inhibition of PGs-induced

vasodilation)
􏰀 Antipyretic (anti-fever) effect

   -> Decrease of the temperature in fever (hyperpyrexia) 

􏰀 Analgesic effect

   -> Decrease of pain (reduced sensitization of nociceptive nerve endings) 

􏰀 Antiplatelet effect

  -> АSА at low doses (75-300 mg)
      - Selective irreversible inhibition of ТхА2 synthesis in platelets through

acetylation.

      - At higher doses АSА inhibits also the synthesis of PGI2 and the effect on platelet aggregation is nullified 


Q:


Cyclooxygenase(СОХ)


A:


􏰀 The enzyme responsible for the production of prostanoids from AA 

􏰀 Types of COX

    - СОХ-1: constitutive enzyme, involved in the physiological functions of prostanoids:

        -> Prostaglandins (PGs E1/2, F2α) effects:
            􏰀 In the stomach: PGE ↓ gastric acid secretion 

            􏰀 In the uterus: PGE/F cause contraction
            􏰀 In the kidneys PGs E: cause natriuresis

􏰀 Prostacyclin (PGI2)
   - In vascular endothelium: vasodilation, inhibition of platelet aggregation

􏰀 Thromboxane А2 (TxA2)
   - In platelets: aggregation, vasoconstriction

􏰀 СОХ-2:

  • 􏰀  Mainly inducible form, expressed in inflammation:

       - PGs E – edema, reddening, pain

  • 􏰀  Involved also in normal homeostasis (e.g. in the vascular endothelium, kidney, bones, brain)


Q:


Analgesics antipyretics

(non-opioid analgesics)

A:

eg. Paracetamol (acetaminophen)

       metamizole (dipyrone)


Q:

Analgesics antipyretics


Pharmacodynamics

A:


  • Analgesic effect – in mild to moderate pains

  • Antipyretic effect

  • No anti-inflammatory effect


Q:

Analgesics antipyretics

Mechanism of action

A:



􏰀Central СОХ inhibition?
􏰀 Other possible mechanisms –

interaction with:

   - Endocannabinoid system

   - Opioid system

   - NO, monoaminergic, cholinergic systems


Q:


ADRs of NSAIDs

A:


􏰀 Antagonism with antihypertensive drugs
    􏰀 With АСЕ inhibitors and diuretics – risk of acute renal failure

(“Triple whammy”)
􏰀 Antagonism to the antiplatelet effect of ASA (ibuprofen, naproxen)

􏰀 With anticoagulants (vitamin K antagonists) – ↑ bleeding risk

(especially ASA)


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