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Pharmacology (Winter) > Allergies > Flashcards

Allergies Flashcards

1
Q

What are the Allergic Disorders?

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

What is an Allergy?

A
  • Inflammatory disorder (immune response to allergens)
  • MALadaptive immune system response creating memory to antigens (b/c allergens are typ. not dangerous)
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3
Q

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

A
  • mast cells
    • basophils
    • eosinophils
    • dendritic cells
    • T-cells (naïve CD4+ and Th2)
    • B-cells
    • plasma cells

1st 3 are granulocytes

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4
Q

Innate vs Adaptive Immunity

A

Induces SAME exposure

vs.

Induces AMPLIFIED response

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5
Q

What are the Initial Steps in Developing Allergy:

A

Antigen presentation, has multiple steps:

  1. allergens (e.g. dust, mold, pollen, animal dander, foods) are taken up by dendritic cells (e.g. macrophages).
  2. These antigen presenting cells (APCs) present part of the allergen, antigen (typically a glycoprotein specific to this allergen) to T-cells (CD4+ naïve T-cells).
  3. T-cells identify it as “dangerous”, differentiate to Th2 cells that further present the antigen to B-cells.
  4. B-cells differentiate into plasma cells, which start to produce antibody (IgE) that recognizes specifically that antigen.

=> Development of memory (1-2 weeks)
Next time when the allergen is introduced, antigen specific IgE antibodies recognize allergen and IgE-antibody complex binds to receptors on mast cells (or other granulocytes) resulting in degranulation and release of inflammatory mediators.
=> Allergic response

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6
Q

What are Mast Cells?

A

Tissue cells of the immune system found in loose connective tissue, organs, vasculature, nerves, skin, respiratory tract, etc. (not present in epidermal cells, CNS, gastric mucosa)

Store histamine, proteases, serotonin, heparine and cytokines in their granules at cytoplasm.

Restock their granules and generate also other inflammatory molecules (e.g. cytokines, leukotrienes, prostaglandins, PAFs).

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7
Q

Granules released upon stimulation of allergen; degranulation:

A

=> increased blood flow and permeability of blood vessels
(i.e. inflammation and swelling)
=> contraction of smooth muscles (e.g. bronchial muscles)
=> increased mucus production & fluid secretion

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8
Q

What does Mast-cell activation & granule release do?

A

GIT:
- INCREASED fluid secretion, INCREASED peristalsis

Airways:
- DECREASED diameter, INCREASED mucus secretion

BV’s:
- INCREASED BF, INCREASED permeability

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9
Q

What sx’s do Histamine & Prostaglandins (PG) have?

A

Tickling
Itchiness
Nose rubbing
=> “Allergic salute”

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10
Q

What sx’s do Histamine & Leukotrienes have?

A

Sneezing
Runny nose (mucosal secretion)
Postnasal trip
Throat clearing

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11
Q

What sx’s do Histamine, Leukotrienes, Bradykinin, Platelet activating factor (PAF) have?

A

Nasal congestion
Mouth breeding
Stuffy nose (mucosal edema)
Congested airway => Snoring

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12
Q

What is Histamine?

A
  • an “autacoid” - self relief
  • stored in tissue mast cells and blood basophils
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13
Q

What does Histamine release triggered by?

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

Pseudo-allergic rxn (no previous exposure, no specific IgE)

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14
Q

H1 receptors:

A

important in allergic disorders; TARGET OF CLASSIC “antihistamines”

histamine receptor mediating (mainly)
- contraction; gastric and respiratory smooth muscle (H1)
- vasodilation (H1 and H2)
- increased vascular permeability (H1)
- pruritus “itching” (H1)
- increased bronchial secretions and viscosity (H1)

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15
Q

H2 receptors:

A

receptor stimulation mediates gastric acid secretion (H2)

receptor blockage decreases gut acidity (ranitidine)

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16
Q

H3 receptors:

A

inhibition of histamine synthesis and release, regulates neurotransmission (e.g. ↓ acetylcholin release); NEGATIVE

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17
Q

H4 receptors:

A

eosinophils, neutrophils, CD4 T cells; CHEMOTAXIS

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18
Q

Histamine - triple response when pricked onto skin:

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

What is Allergic Rhinits?

A

= hay fever
- rhinorrhea, plugged nasal passages, itching (eyes, nose and throat), watery eyes, fatigue, headache
- seasonal (airborne pollen) or perennial (animal dander, mold, dust, etc)
- prevalence in North America ~ 20%
- 40% of patients with rhinitis present with asthma
- 70% of asthmatics experience rhinitis

20
Q

What is the tx of Allergic Rhinitis?

A

Avoidance

Pharmacotherapy
- antihistamines (diphenhydramine, hydroxicine, cetirizine, - loratadine, desloratidine, fexofenadine, azelastine)
- intranasal glucocorticoids (fluticasone, mometasone)
- systemic steroids (not a preferred option)
- leukotriene modifiers (montelukast)
- mast cells stabilizers (cromolyn sodium)
- anticholinergic (ipratropium)
- decongestants (phenylephrine, pseudoephedrine)

Immunotherapy
- allergen specific immunotherapy

21
Q

What are Antihistamines?

A

= The therapeutic approach to block the effects of histamine

22
Q

What are the actions of antihistamines?

A

H1 receptor blockage
- Decreased itching
- Decreased vascular permeability
- Decreased bronchial secretions
- Relaxation of bronchial smooth muscle
- Decreased cough receptor stimulation

23
Q

What are the additional actions of antihistamines?

A

1st generation antihistamines (diphenhydramine “Benadryl”, dimenhydrinate “Gravol”, hydroxyzine “Atarax”) may also possess non-histamine blockage actions; SEDATION, ATROPINIC, ANTI-EMETIC

2nd generation (cetirizine “Zyrtec”, loratadine “Claritine”, desloratidine “Clarinex”, fexofenadine, “Allegra”, azelastine “Astelin” & “Optivar”) antihistamines also PREVENT MAST CELL RELEASE OF MEDIATORS that cause inflammation

24
Q

What are the Anti-histamines Pharmacokinetics?

A

administration rotes (depending on the antihistamine & symptoms)
- oral
- intranasal
- intraocular
- intravenous (only in anaphylaxis, but not as a 1st line treatment)

  • half lives variable (8 to 24 hrs)
  • [c] in breast milk parallels [c] in plasma
  • best if given before an anticipated allergic reaction
  • most metabolized by cytochrome P450 system (CYP3A4)
    – grapefruit juice may block metabolism
25
Q

What are the indications of Anti-histamines?

A
  • drug of choice for mild to moderate rhinitis
  • best for exudative allergies (hay fever)
  • relieves sneezing, itching, nasal discharge and ocular symptoms (itching, watery eyes, redness)
  • may be given with decongestant (ie. pseudoephedrine)
  • seasonal rhinitis; both 1st and 2nd generation antihistamines effective (e.g. diphenhydramine vs. loratidine)
    – 2nd generation drugs lack sedation
    severe allergic rhinitis - use intranasal glucocorticoid
    – e.g. fluticasone
26
Q

What are the AE’s of 1st gen Anti-histamines?

A

diphenhydramine, hydroxyzine
- Blood-brain-barrier permeable - CNS effects:
– atropinic, somnolence, problems with cognition (learning & memory), psychomotor, etc.
- 1st generation antihistamines no longer approved in Canada for children < 2 years, use limited for children < 6 years.
- 1st generation antihistamines not recommended during pregnancy or nursing, 2nd generation typically safe

27
Q

What are the AE’s of 2nd gen Anti-histamines?

A

; cetirizine, loratadine, fexofenadine are good alternatives:
- Poor blood-brain-barrier penetration - no CNS effects:
– sedation etc. not an issue (though some experience little sedation with cetirizine, but fexofenadine is free of sedation)
- cetirizine has demonstrated long term safety in children
- intranasal administration => rapid onset; azelastine

28
Q

What are the Intranasal Glucocorticoids?

A

Fluticasone, Mometasone
- effective for nasal and ocular symptoms; itching, sneezing, discharge, congestion
- most effective for prevention and treatment
- drug of choice for moderate to severe disease
- optimal dose at the plateau of dose response curve
- increasing dose => increasing side effects and not benefits effective once daily
- may take 7 days to be maximally effective

29
Q

What are the SE’s of Intranasal Glucocorticoids?

A
  • Epistaxis
  • Mild side effects compared to oral glucocorticoids
30
Q

What are the Oral Glucocorticoids?

A
  • oral administration is last resort because systemic delivery can cause major side effects
  • intranasal is the best choice
31
Q

What are Leukotrienes the mediators of?

A
  • bronchiole constriction
  • mucous secretion
  • inflammation of airway
  • etc
32
Q

What are Prostaglandins the mediators of?

A
  • pain
  • fever
  • inflammation
  • etc
33
Q

What are the Leukotriene Receptor Antagonists?

A

Leukotrienes released during allergic inflammation by mast cells, eosinophils, basophils, inflammatory cells

Leukotrienes involved in infiltration of inflammatory cells, mucous secretion, but also affect airway (bronchiolar) constriction

34
Q

What is Montelucast?

A

leukotriene receptor antagonist
- modest relief of congestion, itching, discharge
- less effective than intranasal glucocorticoids
- normally used with antihistamine or intranasal glucocorticoid

35
Q

What are the Mast-cell stabilizers?

A
  • mast-cells are activated by response to allergens
  • activated mast cells release inflammatory mediators (e.g. histamine, leukotrienes, PG, PAF, etc)
36
Q

What is Cromolyn Sodium?

A

inhibits mast cell degranulation and release of mediators
- less effective than intranasal corticoid steroids
- must be given BEFORE exposure
- almost no local/systemic toxicity

37
Q

What is Ipratropium?

A

antimuscarinic
- reduces mucus secretion, no effect on inflammation,
i.e. no relief of sneezing, itching or congestion
- useful if primary symptom is nasal discharge

38
Q

What are the AE’s of Anticholinergics?

A

Adverse effects are atropinic
- dry mucous membranes, urinary retention, etc.
- caution in glaucoma and prostatic hypertrophy
- intranasal administration limits systemic adverse effects
and the atropinic effects are beneficial in nostrils.

39
Q

What is Pseudoephedrine?

A

1) α1-adrenergic receptor agonist
=> increased vasoconstriction; reduced nasal swelling

2) non-adrenergic effect
=> Increased mucociliary clearance; more liquidy mucus
relief of congestion only, not helpful for sneezing, itching and discharge

DECONGESTANT

40
Q

What is Phenylephidine?

A

1) α1-adrenergic receptor agonist
Replacing pseudoepherine, which use is reduced from market due to street use for illicit purposes
- efficacy of phenylephrine < pseudoephedrine

DECONGESTANT

41
Q

What are the AE’s of Decongestants?

A

; insomnia, nervousness, headache, palpitations, hypertension, urinary retention, etc.

  • topical intranasal application has fewer systemic effects
  • not for people taking MAO inhibitors, caution when given to people with heart disease or high blood pressure, diabetes, glaucoma, thyroid disorder or enlarged prostate.
  • intranasal decongestants not to be used longer than 3 days; potential rebound congestion
  • oral decongestants not to be used longer than 7 days
  • often given within antihistamine
42
Q

Which Allergic Rhinitis has the best response?

A

Oral/Intranasal Antihistamines
- sneezing
- itching
- congestion
- rhinorrhea
- eye sx’s

43
Q

What is Allergen Specific Immunotherapy?

A
  • Subcutaneous (sc) allergen immunotherapy
  • administer increasing doses of a solution of allergens to which
    patient is shown to be sensitive (skin tests)
  • may also be given sublingually

Build up period; weekly then monthly injections for 3-6 months
- dose increased so that symptoms remain within injection area, but do reduce symptoms with natural exposure
- once desired dose established; monthly maintenance

Maintenance period; monthly with desired dose for 3-5 years
- reduced symptoms with natural exposure
- benefit may continue when therapy discontinued

44
Q

What are the indications for immunotherapy?

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

avoid in severe asthma, cardiovascular disease, high dose β
adrenergic receptor blocker, do not initiate during pregnancy

requires multiple visits; patient compliance important
- poor compliance associated with systemic reactions

thought to be as effective as intranasal glucocorticoids
may add endogenous glucocorticoid production (additive)

Pharmacology (Winter) (23 decks)

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