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Pharmacology B > Lecture 9 - Drugs & Allergy > Flashcards

Lecture 9 - Drugs & Allergy Flashcards

1
Q

List some Allergic Disorders that we discussed

A
  • Allergic Rhinitis (hay fever)
  • Allergic Conjunctivitis (pink eye)
  • Atopic Dermatitis (eczema)
  • Urticaria (hives)
  • Asthma (inflammation of airways)
  • Anaphylaxis (multi-organ allergic reaction)
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2
Q

Define what an allergy is

A
  • Inflammatory disorder (hyper immune response to allergens)

- Maladaptive immune system response creating memory to antigens

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3
Q

Maladaptive

A

not providing adequate or appropriate adjustment to the environment or situation

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4
Q

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

A
  • IgE
  • mast cells
  • basophils
  • eosinophils
  • dendritic cells
  • T-cells (Th1&2)
  • B-cells
  • plasma cells
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5
Q

What are mast cells?

A

Tissue cells of the immune system found in loose connective tissue, organs, vasculature, nerves, skin, respiratory tract, etc.

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6
Q

Where are mast cells not present?

A

in epidermal cells, CNS, gastric mucosa

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7
Q

What do mast cells store?

A

Store histamine, interleukins, proteoglycans (ex. heparin) and various enzymes in their granules at cytoplasm

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8
Q

When are mast cell granules released?

A

they are released upon stimulation an allergen; degranulation

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9
Q

What does mast cell degranulation cause?

A
  • increased blood flow and permeability of blood vessels (i.e. inflammation and swelling)
  • contraction of smooth muscles (ex. bronchial muscles)
  • increased mucous production & fluid secretion
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10
Q

What allergy symptoms do histamine and prostaglandin cause?

A
  • tickling
  • itchiness
  • nose rubbing
  • allergic salute
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11
Q

What allergy symptoms do histamine and leukotrienes cause?

A
  • sneezing
  • runny nose (mucosal secretion)
  • post nasal drip
  • throat clearing
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12
Q

What allergy symptoms do histamine, leukotrienes, bradykinin, platelet activating factor (PAF) cause?

A
  • nasal congestion
  • mouth breeding
  • stuffy nose (mucosal edema)
  • snoring
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13
Q

Histamine is an autacoid. What does autacoid mean?

A

self relief

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14
Q

Where is histamine stored?

A

-stored in tissue mast cells and blood basophils

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15
Q

What is histamine released by?

A
  • antigens; allergic responses (immediate hypersensitivity)
  • drugs; morphine, succinylcholine, radio contrast media
  • insect venoms
  • physical factors; scratching, cold
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16
Q

How many H (histamine) receptors are there?

A

4

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17
Q

Which H receptor is the most important for allergic disorder and is the classic target for “antihistamines”?

A

H1

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18
Q

What does binding to the H1 receptor cause?

A
  • contraction; gastric and respiratory smooth muscle (H1)
  • vasodilation (H1 and H2)
  • increased vascular permeability (H1)
  • pruritis “itching” (H1)
  • increased bronchial secretions and viscosity (H1)
  • bronchoconstriction
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19
Q

What does binding to the H2 receptor cause?

A
  • receptor stimulation mediates gastric acid secretion (H2)

- receptor blockage decreases gut acidity (ranitidine)

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20
Q

What does binding to the H3 receptor cause?

A
  • cholinergic neurotransmission (airway)

- negative feedback mechanism; inhibit histamine, NE and acetylcholine release

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21
Q

What does binding to the H4 receptor cause?

A

chemotaxis of mast cells, eosinophils, neutrophils. Cytokine release from T and dendritic cells

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22
Q

What happens when histamine is pricked onto skin?

A

It produces a triple response:
1 - RED area at site of injection (vasodilation)
2 - WHEAL replaces red area - edema
3 - bright red FLARE - indirect vasodilation (axonal reflex)

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23
Q

Allergic rhinitis is known as ?

A

hay fever bitches

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24
Q

List some symptoms of allergic rhinitis

A

-rhinorrhea (runny nose), plugged nasal passages, itching (eyes, nose and throat) tearing, fatigue, headache

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25
Q

List 2 branches of allergic rhinitis

A

1: Seasonal (airborne pollen)
2: Perennial (animal dander, mold, dust, etc.)

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26
Q

___% of patients with rhinitis present with asthma

A

40

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27
Q

__% of asthmatics experience rhinitis

A

70

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28
Q

Allergic Rhinitis prevalence in North America = ___%

A

20

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29
Q

3 treatment options for AR are?

A
  • Avoidance
  • Pharmacotherapy
  • Immunotherapy
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30
Q

What pharmacological options are available for the treatment of AR?

A
  • antihistamines
  • intranasal glucocorticoids
  • leukotriene modifiers
  • decongestants
  • mast cell stabilizers
  • anticholinergic
  • anti-IgE therapy
  • systemic steroids (not preferred)
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31
Q

List some antihistamines

A
  • chlorpheniramine
  • diphenhydramine
  • cetirizine
  • loratidine
  • fexofenadine
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32
Q

List an intranasal glucocorticoid

A

-fluticasone

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33
Q

List a leukotriene modifier

A

-montelukast

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34
Q

List some decongestants

A
  • phenylephrine

- pseudoephedrine

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35
Q

List a mast cell stabilizer

A

-cromolyn sodium

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36
Q

List an anticholinergic

A

-ipratropium

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37
Q

List an anti-IgE therapy

A

-omalizumab

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38
Q

What is Immunotherapy?

A

allergen specific immunotherapy

39
Q

What is the action of antihistamines?

A

block H1 receptor

40
Q

What kind of symptom relief do we see with antihistamines for the treatment of AR?

A
  • decreased itching
  • decreased vascular permeability
  • decreased bronchial secretions
  • relaxation of bronchial smooth muscle
  • decreased cough receptor stimulation
41
Q

List some 1st gen AH

A
  • diphenhydramine

- chlorpheniramine

42
Q

Side effects/other actions of 1st gen AH

A
  • sedation
  • anticholinergic effects (dry mouth, constipation, dry eyes)
  • anti-emetic
43
Q

List some 2nd gen AH

A
  • cetirizine

- loratidine

44
Q

List the 3rd gen AH

A

fexofenadine

45
Q

What are the administration routes of antihistamines?

A
  • Oral (allergy)
  • Intranasal (allergy)
  • Intravenous (used only later in anaphylaxis but benefit ?)
46
Q

Half-lives of antihistamines?

A

Variable: 8-24 hours

47
Q

Are antihistamines present in breast milk?

A

Yes - the conc in plasma = conc in breast milk

48
Q

When is the optimal time to take antihistamines?

A

Best if given before an anticipated allergic reaction
**Remember, antihistamines do not get rid of existing released histamine, only prevent further histamine from binding to H1 receptors.

49
Q

Most antihistamines are metabolized by ______ enzymes

A

CYP 3A4

50
Q

Knowing that antihistamines are metabolized by CYP 3A4, what is a beverage that you would suggest patients stay away from when taking them?

A

grapefruit juice as it may block metabolism

51
Q

What is the indication for antihistamines?

A
  • DOC for mild to moderate rhinitis
  • relieves sneezing, itching, nasal discharge and ocular symptoms (itching, tearing, erythema)
  • may be given with decongestant (i.e. pseudoephedrine)
  • best for exudative allergies (hay fever)
52
Q

For seasonal mild AR, recommend ??

A

1st, 2nd, or 3rd generation AH

53
Q

What do you recommend for severe AR

A

intranasal glucocorticoid (ex. fluticasone)

54
Q

Adverse effects of 1st gen AH?

A

-anticholinergic (dry mouth, dry eyes, constipation) , somnolence (sleepiness/drowsiness), problems with cognition, learning and memory, psychomotor, etc.

55
Q

Who are 1st gen AH approved for?

A

Anyone over 2

*Use limited for children under 6

56
Q

Which gens of AHs are safe in pregnancy?

A

2nd and 3rd gen

57
Q

Would you recommend a 1st gen AH in pregnancy?

A

No - recommend a 2nd or 3rd gen instead

58
Q

Adverse effects of 2nd and 3rd gen AH’s?

A
  • penetrate brain poorly

- sedation is NOT an issue (except maybe a little with cetirizine)

59
Q

Fexofenadine is free of _____

A

sedation

60
Q

Is cetirizine safe in children?

A

You bet your ass it is :D

61
Q

Intranasal 2nd or 3rd gen AH = ____ onset

A

rapid

62
Q

Give an example of an intranasal 2nd or 3rd gen AH

A

azelastine

63
Q

Fluticasone is an example of ??

A

an intranasal glucocorticoid

64
Q

Is fluticasone for prevention or treatment?

A

BOTH

65
Q

Does increasing dose of fluticasone increase benefits?

A

No - it increases side effects and not benefits

66
Q

Effective dosing of fluticasone?

A

once daily

67
Q

Fluticasone:

May take _____ to be maximally effective

A

7 days

68
Q

Fluticasone:

Could cause ___

A

epistaxis (nose bleed)

69
Q

What do systemic glucocorticoids have effects on?

A

growth, bone density, cataract formation, intraocular pressure

70
Q

Where do corticosteroids act?

A
  • Act on phospholipase A2 so prevents formation of Arachidonic acid
  • Acts on protein synthesis so prevents synthesis of COX1 and COX2
71
Q

When are leukotrienes released?

A

During allergic inflammation by mast cells, eosinophils, basophils, inflammatory cells

72
Q

What are leukotrienes involved in?

A

Infiltration of inflammatory cells, mucous secretion, but also affect airway (bronchiolar) constriction

73
Q

Give an example of a leukotriene receptor antagonist

A

montelukast

74
Q

What kind of symptom relief does montelukast provide?

A
  • modest relief of congestion, itching, discharge
  • less effective than intranasal glucocorticoids
  • normally used with antihistamine or intranasal glucocorticoid
75
Q

MOA of Montelukast?

A

block leukotriene receptor

76
Q

Phenylephrine is a ______

A

decongestant

77
Q

Phenylephrine is a __________ agonist

A

alpha 1

78
Q

MOA of phenylephrine (decongestant)?

A

-increased vasoconstriction, reduced nasal swelling

79
Q

SE of phenylephrine (decongestant)?

A

insomnia, nervousness, headache, palpitations, HTN, urinary retention

*nasal decongestants have WAY LESS side effects

80
Q

Why should you only use phenylephrine for less than 3 days?

A

potential rebound congestion

81
Q

How does chromoly sodium work?

A

It is a mast cell stabilizer:

-Inhibits mast cell degranulation and release of mediators

82
Q

Why are mast cell stabilizers not really helpful?

A

MUST BE GIVEN BEFORE EXPOSURE

-hard to do

83
Q

How does Ipratropium work?

A

It is an anticholinergic:

  • Reduces mucus secretion
  • No effect on inflammation
  • No relief of sneezing, itching or congestion
84
Q

When is Ipratropium v useful?

A

if primary symptom is nasal discharge

85
Q

SE of Ipratropium?

A

Other anticholinergic effects:

-urinary retention, dry eyes, dry mouth

86
Q

When is Ipratropium not recommended?

A

-caution in glaucoma and prostatic hypertrophy

87
Q

Omalizumab is a _________

A

anti-IgE antibody

88
Q

Describe the administration and MOA of Omalizumab

A
  • given SC, selectively binds human immunoglobulin E (IgE)

- prevents IgE binding to cells and reduces free IgE in serum

89
Q

When are oral glucocorticoids recommended?

A
  • oral administration of glucocorticoids is last resort due to major side effects
  • intranasal is best choice
90
Q

chart on slide 29 = good stuff

A

cool

91
Q

Describe Allergen Specific Immunotherapy

A
  • SC allergen immunotherapy
  • administer increasing doses of a solution of allergens SC to which patient is shown to be sensitive (skin tests)
  • may also be given SL
  • build up period…weekly then monthly injections for years, dose increased until fewer symptoms with natural exposure
  • once desired dose is established, there is monthly maintenance
  • administered over 3-5 years
  • benefit may continue when this therapy is discontinued
92
Q

Indications of Immunotherapy

A
  • IgE in the serum or skin sensitivity to allergen (cat, pollen, dog, etc)
  • poor pharmacotherapy response or side effects
  • patient preference
93
Q

When should you avoid Immunotherapy?

A

severe asthma, CV disease, high dose B blockers, do not initiate during pregnancy

Pharmacology B (21 decks)

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