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IHO Week 5 AJL > Anti-inflammatory Drugs- Regal > Flashcards

Anti-inflammatory Drugs- Regal Flashcards

1
Q

Explain the general process of inflammatory process

A

Injury —-> Mediators —-> Inflammation: redness, swelling, heat, and pain

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2
Q

These cause redness/vasodilation

A

Histamine, PGE2, PGI2, kinins

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3
Q

These cause swelling/increased vascular permeability

A

Histamine, peptido leukotrienes (LTC4, LTD4, LTE4)

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4
Q

These cause pain

A

PGE, PGI, LTB4, kinins

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5
Q

These are chemotactic/direct migration of WBC

A

LTB4 (neutrophils, etc), peptido leukotrienes (eosinophils)

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6
Q

These cause fever

A

PGEs induce fever!

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7
Q

These cause airway constriction

A

histamine, peptido leukotrienes, kinins, PGD2

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8
Q

These cause hypotension

A

Kinins, histamine

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9
Q

What happens with oral administration of histamine?

A

Nothing, it’s inactivated by enzymes in the intestinal wall or liver after ingestion.

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10
Q

What happens with intracutaneous administration of histamine?

A

“Triple response” Itching, pain, wheal and flare

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11
Q

What causes (1) Localized redness (2) Flare (3) Localized edema or wheal formation?

A

(1) Arteriolar dilation
(2) nerves dilating neighboring arterioles
(3) Increased capillary permeability with leakage of the postcapillary venules

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12
Q

Symptoms of intranasal histamine?

A

Intense itching, sneezing, hypersecretion, nasal blockage

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13
Q

Symptoms of IV histamine?

A

Hypotension, tachycardia, broncoconstriction, flushing, headache, wheal and flare, stimulation of mucus secretion and gastric acid secretion

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14
Q

Stimulation of the H1 receptor causes what?

A 
Bronchoconstriction
Contraction of GI smooth muscle
Inc. capillary permeability (wheal) 
Pruritis (itch) and pain
Release of catecholamines from the adrenal medulla
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15
Q

Stimulation of the H2 receptor causes what?

A

Gastric acid secretion
Inhibition of IgE-mediated basophil histamine release
Inhibition of T lymphocyte mediated cytotoxicity
Suppression of Th2 cells and cytokines

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16
Q

Does first or second generation antihistamines have affinity for P-glycoprotein in the CNS?

A

Second generation has affinity for P-glycoprotein in CNS……Prob why the second generations are non-sedating…

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17
Q

What side effect did one of the first non-sedating antihistamine have that has now been fixed in the newer drugs?

A

Cardiotoxicity with overdose

18
Q

What are the second generation antihistamines we need to know?

A

Cetirizine (OTC)
Fexofenadine
Loratidine (OTC)

19
Q

What effect do the first gen antihistamines have that the second gens don’t?

A

Second generation antihistamines don’t have any anticholinergic properties…..first gens have a little, but not as much as Atropine

20
Q 
Diphenhydramine (OTC)
MOA
ADME
TU and Common Side effects
Toxicities
A

H1 antagonist (histamine)

A – good oral
D – widely, even CNS (no P-glycoprotein)
M – liver
E –urine

Ophthalmic solutions
Motion Sickness (Diph.)

Sedation, dry mouth, GI disturbances (anti-cholinergic action)

21
Q 
Chlorpheniramine 
MOA
ADME
TU and Common Side effects
Toxicities
A

First generation – block H1, muscarinic, α-adrenergic, 5HT receptors

Ophthalmic solutions
Motion Sickness (Diph.)

Sedation, dry mouth, GI disturbances (anti-cholinergic action)

Suitable for day time use - ↓ sedation

22
Q

Cetirizine (Zyrtec) OTC
MOA
ADME
TU and Common Side effects

A

H1 antagonist (histamine), Second generation

D - Able to cross BBB – have affinity for P-glycoprotein (efflux)

  • Less sedation than 1st generation (P-glyco)
  • Do NOT potentiate effects of CNS depressants
23
Q

Fexofenadine
MOA
ADME
TU and Common Side effects

A

H1 antagonist (histamine), Second generation

D - Able to cross BBB – have affinity for P-glycoprotein (efflux)

  • Less sedation than 1st generation (P-glyco)
  • Do NOT potentiate effects of CNS depressants
24
Q

Loratadine [Claritin] (OTC)
MOA
ADME
TU and Common Side effects

A

H1 antagonist (histamine), Second generation

D - Able to cross BBB – have affinity for P-glycoprotein (efflux)

  • Less sedation than 1st generation (P-glyco)
  • Do NOT potentiate effects of CNS depressants
25
Q 
Zileuton
MOA
ADME
TU and Common Side effects
Toxicities
A

Inhibits 5-LO (prevents synthesis of all leukotrienes)

M – Cyp P450

Chronic asthma

Drug interactions
Monitor for hepatic toxicity

26
Q 
Zafirlukast
MOA
ADME
TU and Common Side effects
Toxicities
A

CysLTR1 (LTD/C/E4) receptor antagonists

M – Cyp P450

Chronic asthma
Montelukast used more due to once/day admin

Drug-drug interactions

27
Q 
Montelukast
MOA
ADME
TU and Common Side effects
Toxicities
A

CysLTR1 (LTD/C/E4) receptor antagonists

Chronic asthma
Montelukast used more due to once/day admin

28
Q 
Acetylsalicylate (aspirin, OTC)
MOA
ADME
TU and Common Side effects
Toxicities
A

IRREVERSIBLY acetylates COX1

  • GI ulceration (due to PG synthesis inhibition)
  • Secondary anemia
  • Prolonged gestation
  • ↓ Renal function
  • Abnormal Hepatic function
  • Increased bleeding time
  • Hypersensitivity-like reaction due to increased LT production
    (3-10% of asthmatics)
  • Reye Syndrome following viral infection in children
29
Q 
Ibuprofen [Advil] (OTC)
MOA
ADME
TU and Common Side effects
Toxicities
A

Inhibit both COX1 &2

A – oral
D – good bioavailability – cross BBB; PPB
E – glucuronidation; urine

  • GI ulceration (due to PG synthesis inhibition)
  • Secondary anemia
  • Prolonged gestation
  • ↓ Renal function
  • Abnormal Hepatic function
  • Increased bleeding time

Fewer GI issues

30
Q 
Naproxen [Aleve] – long-acting ibuprofen (OTC)
MOA
ADME
TU and Common Side effects
Toxicities
A

Inhibit both COX1 &2

A – oral
D – good bioavailability – cross BBB; PPB
E – glucuronidation; urine

  • GI ulceration (due to PG synthesis inhibition)
  • Secondary anemia
  • Prolonged gestation
  • ↓ Renal function
  • Abnormal Hepatic function
  • Increased bleeding time

Fewer GI issues

31
Q 
Ketorolac
MOA
ADME
TU and Common Side effects
Toxicities
A

Inhibit both COX1 &2

A – oral
D – good bioavailability – cross BBB; PPB
E – glucuronidation; urine

  • GI ulceration (due to PG synthesis inhibition)
  • Secondary anemia
  • Prolonged gestation
  • ↓ Renal function
  • Abnormal Hepatic function
  • Increased bleeding time

Fewer GI issues

32
Q 
Indomethacin
MOA
ADME
TU and Common Side effects
Toxicities
A

Inhibit both COX1 &2

A – oral
D – good bioavailability – cross BBB; PPB
E – glucuronidation; urine

  • GI ulceration (due to PG synthesis inhibition)
  • Secondary anemia
  • Prolonged gestation
  • ↓ Renal function
  • Abnormal Hepatic function
  • Increased bleeding time
33
Q

Ketorolac

A

Promoted primarily for analgesia but is also anti-inflammatory

34
Q

Ketoprofen

A

ibuprofens goofy cousin……?

35
Q

Sulindac

A

????

36
Q

Piroxicam

A

Once a day administration….can cause dose related serious GI bleeding

37
Q

Celecoxib
MOA
Uses
Side effects

A

COX2 Inhibitor – theoretically beneficial since COX1 protects GI mucosa

Safe in aspirin-hypersensitive individuals

Thrombotic CV events with chronic use

38
Q 
Acetaminophen (Tylenol) OTC 
MOA
ADME
TU and Common Side effects
Toxicities
A

Weak inhibitor of COX (esp. in brain); minimal anti-inflammatory effects…..antipyretic and analgesic

A – oral
D - ???
M – liver (Cyp P450)
E – urine

Toxic when used in conjunction with alcohol—> N-acetyl-p-benzo-quinone

Tx: N-acetylcysteine

39
Q

Kinin Inhibitors, C1IHN
MOA
TU and Common Side effects
Toxicities

A

Inhibits kallikrein

Nasal allergies, rhinitis associated with rhinoviral infections; dental pain

Since Kinin, complement, coagulation, and fibrinolytic pathways have a interrelationship, perturbing one pathway disrupts another

40
Q

Four key enzymes for kinin inhibitors?

A

Four key enzymes: HFa, C1 esterase, kallikrein, plasmin

41
Q

Where do you find COX 1 and COX 2?

A

COX1 – platelets, other cells (protect GI mucosa)

COX2 – Constitutively expressed in brain and kidney; induced in other tissues in response to inflammation

IHO Week 5 AJL (2 decks)

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