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Pharmacology quiz 4 > Drugs and allergy > Flashcards

Drugs and allergy Flashcards

1
Q

List some allergic disorders

A
  • AR (hay fever)
  • Allergic conjunctivitis (pink eye)
  • Atopic dermatitis
  • Urticaria
  • Asthma (infl. of airways)
  • Anaphylaxis (multi-organ rxn)
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2
Q

What is an allergy?

A
  • inflammatory disorder (hyper immune response to allergens)

- Maladaptive immune system response creating memory to antigens

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3
Q

What are the key players / immune cells involved in allergic reactions?

A
  • IgE
  • mast cells
  • eosinophils
  • dendritic cells
  • T-cells (Th1&2)
  • B-cells
  • plasma cells
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4
Q

Describe mast cells

A
  • Tissue cells of the immune system found in loose connective tissues, organs, vasculature, nerves, skin, respiratory tract, etc. (not present in epidermal cells, CNS, gastric mucosa)
  • They store histamine, interleukins, proteoglycans (ex: heparin) and various enzymes in their granules at cytoplasm
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5
Q

When do mast cells release their stored enzymes from the granules? Describe this process

A

Granules are released upon stimulation of an allergen; process called degranulation. This causes:

  • increased blood flow and permeability of blood vessels (ie infl. and swelling)
  • contraction of smooth muscles (eg: bronchial muscles)
  • increased mucus production & fluid secretion
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6
Q

What are the effects of granule release in the GI tract?

A

Increased fluid secretion and peristalsis. This causes expulsion of GI tract contents (diarrhea, vomiting)

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7
Q

What are the effects of degranulation in the airways

A

Decreased diameter and increased mucus secretion. This causes:

  • congestion and blockage of airways (wheezing, coughing, phlegm)
  • swelling and mucus secretion in nasal passages
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8
Q

What are the effects of degranulation in the blood vessels?

A

Increased blood flow and permeability. This causes:

  • increased fluid in tissues causing increased flow of lymph to lymph nodes
  • increased cells and protein in tissues
  • increased effector response in tissues
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9
Q

Mediators of common allergy Sx: what Sx do histamines and prostaglandins (PGs) release from mast cells cause?

A
  • tickling
  • itchiness
  • nose rubbing
  • allergic salute
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10
Q

Mediators of common allergy Sx: what Sx do histamine and leukotriene release from mast cells, eosinophils, and basophils cause?

A
  • sneezing
  • runny nose (mucosal secretion)
  • post nasal drip
  • throat clearing
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11
Q

Mediators of common allergy Sx: what Sx do histamine, leukotriene, bradykinin, platelet activating factor (PAF) release from mast cells in the tissue, and eosinophils and basophils in the blood cause?

A
  • nasal congestion
  • mouth breathing
  • stuffy nose (mucosal edema)
  • snooring
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12
Q

Describe histamine

A
  • An “autacoid” (designed to exert its action near the site of release) for self relief
  • stored in tissue mast cells and blood basophils
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13
Q

Histamine is released by what?

A
  • antigens; allergic responses (immediate hypersensitivity)
  • drugs: morphine, succinylcholine, radio contrast media
  • insect venoms
  • physical factors: scratching, cold
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14
Q

Describe the histamine H1 receptor

A
  • important in allergic disorders: target of “classic” generation 1 anti-histamines
  • histamine receptor mediated (mainly) effects:
    • contraction: gastric and
      resp. smooth muscle
    • vasodilation (H1, H2)
    • increased vascular
      permeability (H1)
    • pruritis (H1)
    • increased bronchial
      secretions and viscosity
      (H1)
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15
Q

Describe the H2 receptor

A
  • receptor stimulation mediates gastric acid secretion (H2)

- receptor blockage decreases gut acidity (Ranitidine)

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16
Q

Describe the H3 receptor

A 
cholinergic neurotransmission (airway)?
- negative feedback mechanism: inhibit histamine, NA, and ACh release
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17
Q

Describe the H4 receptor

A

Found on eosinophils, neutrophils, TCD4 cells

  • Role in immune response regulation
  • Chemotaxis of mast cells, eosinophils, neutrophils, cytokine release from T and dendritic cells
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18
Q

In a test, Histamine had a triple response when pricked onto skin. Describe

A
  1. RED area at the site of histamine injection - vasodilation
  2. WHEAL replaces red area - edema
  3. bright red FLARE - indirect vasodilation (axonal reflex)
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19
Q

Describe allergic rhinitis (AR)

A
  • rhinorrhea, plugged nasal passages, itching (eyes, nose, throat), tearing, fatigue, headache
  • Can be seasonal (airborne pollen) or perennial (animal dander, old, dust, etc)
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20
Q

Describe the prevalence of allergic rhinitis

A
  • North america: 20%
  • 40% of patients with rhinitis present with asthma
  • 70% of asthmatics experience rhinitis
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21
Q

AR Tx

A
  • AVOIDANCE
  • Pharmacotherapy
  • Immunotherapy
22
Q

List pharmacotherapy options for AR

A
  • Anti-histamines: Chlorpheniramine, diphenhydramine, cetirizine, loratadine, fexofenadine
  • intranasal glucocorticoids (fluticasone)
  • leukotriene modifiers (monteleukast)
  • decongestants (phenylephrine, pseudoephedrine)
  • mast cell stabilizers (cromolyn sodium)
  • anticholinergic (ipratropium)
  • anti-IgE therapy (omalizumab)
  • systemic steroids (not a preferred option)
23
Q

Describe immunotherapy for AR

A

Allergen specific immunotherapy; to develop a ‘resistance’ to a specific antigen

24
Q

Actions of H1 receptor antagonism

A
  • decreased itching
  • decreased vascular permeability
  • decreased bronchial secretions
  • relaxation of bronchial smooth muscle
  • decreased cough receptor stimulation
25
Q

What are additional effects of 1st generation anti-histamines?

A

Drug examples: diphenhydramine (Benadryl), chlorpheniramine (Chlor-Trimeton)
- 1st generation anti-histamines may also possess non-histamine blockage actions like sedation, atropinic, anti-emetic

26
Q

What are additional effects of 2nd and 3rd generation anti-histamines?

A 
Drug examples (2nd gen): Cetirizine, loratadine (Claritin)
Drug example (3rd gen): Fexofenadine (Allegra)
- These two types of anti-histamines also prevent mast cell release of mediators that cause inflammation
27
Q

Describe the pharmacokinetics of anti-histamines in AR

A
  • Administration rate may be flexible depending on the anti-histamine: oral (allergy), intranasal (allergy), or IV (only later in anaphylaxis; benefit questionable)
  • half-lives are variable (8-24h)
  • their concentration in breast milk parallels their concentration in plasma
  • best if they are taken before an anticipated allergic reaction
  • most are metabolized by CYP P450 system (CYP 3A4) and grapefruit juice may block metabolism
28
Q

Indication of anti-histamines

A
  • DOC for mild to moderate rhinitis
  • can relieve sneezing, itching, nasal discharge, and ocular Sx (itching, tearing, erythema)
  • best for exudative allergies (hay fever)
  • for seasonal rhinitis: 1st, 2nd, and 3rd gen anti-histamines are all effective
29
Q

Describe anti-histamine use in conjunction with a decongestant

A
  • may be given with a decongestant (pseudophedrine)

- for severe AR, use intranasal glucotoricoid

30
Q

Intranasal glucocorticoid drug example

A

Fluticasone

31
Q

How are 2nd and 3rd gen anti-histamines different than the 1st gen?

A

Lack sedative effects

32
Q

Adverse effects of 1st-gen anti-H’s (Chlorpheniramine, diphenhydramine)

A
  • atropinic, somnolence, problems with congnition, learning and memory, psychomotor, etc.
  • No longer approved in Canada for kids under 2. Use limited for kids under 6
  • not recommended during pregnancy (Although 2nd and 3rd gen are safe)
33
Q

Adverse effects of 2nd and 3rd gen anti-histamines (Cetirizine, loratidine, fexofenadine)

A
  • penetrate BBB poorly so sedation not an issue (although some with Cetirizine; 10% of patients)
  • fexofenadine is free of sedation
  • Cetirizine has demonstrated long-term safety in children
  • intranasal administration gives a rapid onset (Drug: Azelastine)
34
Q

Describe fluticasone

A
  • effective for nasal and ocular Sx, itching, sneezing, discharge, congestion
  • most effective for prevention and Tx
  • DOC for moderate to severe disase
  • dosing at plateau of dose-response curve (increasing the dose increases the SE’s but not the benefits)
35
Q

Describe the use of fluticasone (intranasal glucocorticoid)

A
  • effective used once daily

- may take 7 days to be maximally effective

36
Q

SE’s of fluticasone

A
  • might cause epistaxis (nose bleeds)
  • not well studied for SE’s associated with intranasal administration (newer ones safer?)
  • systemic glucocorticoids have effects on growth, bone density, cataract formation, intraocular pressure, etc.
37
Q

Leukotrienes are mediators of what effects?

A
  • bronchiole constriction
  • mucous secretion
  • infl. of airway
38
Q

Prostacyclin, PGs, Thromboxanes are mediators of what Sx?

A
  • pain
  • fever
  • inflammation, etc.
39
Q

Corticosteroids inhibit what two pathways?

A

1) Inhibits Phospholipase A2 from converting membrane lipids into arachadonic acid (AA), thus leading to the formation of LT’s, PG’s, Prostacyclin, Thromboxanes
2) Inhibits the protein synthesis of COX-1 and -2 enzymes. Cylooxygenase leads to the formation of Prostacyclin, PG’s and Thromboxane

40
Q

Give a drug example of a Leukotriene receptor antagonist

A

Monteleukast

41
Q

Describe the purpose, use and effectiveness of Leukotriene receptor antagonists

A
  • LT’s are released during allergic infl. by mast cells, eosinophils, basophils, inflammatory cells
  • LT’s are involved in infiltration of inflammatory cells, mucus secretion, but also affect airway constriction
  • Monteleukast provides modest relief of congestion, itching and discharge
42
Q

LT-receptor antagonists (Monteleukast) are normally used with what?

A
  • Used with anti-histamine or intranasal glucocorticoid

- less effective than intranasal glucocorticoids

43
Q

What receptor does phenylephrine target for what effect?

A
  • targets alpha-1 receptor (agonist effect)

- leads to increased vasoconstriction and hence reduced nasal swelling

44
Q

Phenylephrine relieves what Sx?

A

relief of congestion only; not helpful for sneezing, itching, discharge.

45
Q

Compare phenylephrine and pseudoephedrine as decongestants

A
  • Phenylephrine has largely replased pseudoephedrine, which can’t be sold alone
  • many side effects: insomnia, nervousness, ,headache, palpitations, HTN, etc
  • topical intranasal application leads to fewer systemic effects
  • use for over 3 days can lead to rebound congestion
  • pseudoeph. proven to be effective, but not phenyleph.
46
Q

Drug example of a mast cell stabilizer

A

cromolyn sodium

47
Q

Describe mast cell stabilizers and their MOA, effects

A
  • Mast cell stabilizers inhibit degranulation and the release of infl. mediators (histamine, LT’s, PG, PAF)
  • less effective than intranasal corticosteroids
  • must be given before exposure
  • almost no local/systemic toxicity
48
Q

List an anticholinergic drug used in AR. What’s its MOA? Effects?

A

Drug: Ipratopium (anti-muscarinic)

  • reduces mucus secretion with no effect on inflammation (so no relief of sneezing, itching, congestion)
  • useful if primary Sx is nasal discharge
  • SE’s: atropinic-like effects (dry mucus membranes, urinary retention, etc.)
  • caution in glaucoma and prostatic hypertrophy
49
Q

Give a drug example of an anti-IgE antibody. What its MOA and effects?

A

Drug: Omalizumab

  • given as SC injection
  • selectively binds iGE
  • prevents igE from binding to cells and reduces free IgE in serum
  • anaphylaxis risk in 0.1% of patients (hours or days later)
50
Q

Immunotherapy is usually administered over what time period?

A
  • Initial build-up period where the patient goes for weekly then monthy injections for years
  • dose is increased until fewer Sx are achieved with natural exposure
  • once desired dose is established; monthly maintenance injections necessary
  • Administered over 3-5 years; benefit may continue when admin is discontinued
51
Q

Indications for immunotherapy

A
  • IgE in serum or skin sensitivity to allergen (cat, dog, pollen, etc)
  • poor pharmacotherapy response or side effects
  • patient preference
52
Q

When should you avoid immunotherapy?

A

in severe asthma, CV disease, high dose beta blockers.

- do not initiate Tx during pregnancy

Pharmacology quiz 4 (9 decks)

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