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271- F1 > ENT-2 > Flashcards

ENT-2 Flashcards

1
Q

Where is histamine stored?

A

Mast cells- tissue

Basophils (in granules)- Blood

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2
Q

Where are H1 receptors?

A

Smooth muscle
Endothelium
CNS

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3
Q

Where are H2 receptors?

A

Gastric parietal cells
cardiac muscle
mast cells
CNS

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4
Q

Where are H3, H4 receptors?

Importance?

A

H3- CNS, presynaptic
H4- Hematopoetic origin

*No drugs target

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5
Q

What are the effects of H1 receptor agonism?

A

Primary responsible for histamine’s allergic effects
Upregulated on endothelial cells increase vascular permeability
Copious watery rhinorrhea
Present on nociceptive nerve fibers to induce itching sensation

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6
Q

What are the effects of H2 receptor agonism?

A

Stomach acid production

Vasodilation and cardiac effect in anaphylaxis

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7
Q

What is the effect of H4 receptor agonism?

A

Induction of cellular shape change, chemotaxis

Secretion of cytokines and upregulation of adhesion molecules

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8
Q

Compare H1/H2 receptor time to effect

A

H1 receptors have higher affinity -> rapid and short-lived vasodilation -> lower sys BP
H2 receptors-> more slowly and sustained

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9
Q

What are the cardiac effects of H1 activation?

A

Increases cardiac force of contraction and HR
Directly slows AV (Atrioventricular) conduction (via H1) arrhythmias
+ inotrope
+ chronotrope
-dromotrope

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10
Q

What is the triple response of Lewis

A

Effects of Histamine intradermal:
Localized red spot – a few mm ~1min
Brighter red flush or “flare” – 1cm – developing more slowly
Wheal – 1-2min

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11
Q

What is the effect of histamine at peripheral nerve endings?

A

Epidermis -> itch

Dermis -> pain or pain accompanied by itching

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12
Q

What are the risk factors for allergic rhinitis?

A 
Family history
Elevated IgE levels
Higher socioeconomic class
Positive skin test results
Emigration into a Western industrialized environment
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13
Q

What are the sequelae of allergic rhinitis?

A

Sinusitis, obstructive sleep apnea

Otitis media, and nasal polyposis

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14
Q

What are the 1st line pharmacotherapies for allergic rhinitis?

A

Corticosteroids – nasal spray (NS)

Antihistamines – PO or NS

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15
Q

What are the second line treatments for allergic rhinitis?

A 
Decongestants
Mast cell stabilizers
Leukotriene receptor antagonists
Antimuscarinic (anticholinergic) agents
Saline
Monoclonal antibody
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16
Q

What Sx do IN steroids control?

A

Sneezing
Nasal itching
Rhinorrhea
Nasal congestion

17
Q

What are the newer IN steroids?

A

Flonase
Nasonex
Veramist
Omnaris

18
Q

What are the oder IN steroids?

A

Beconase AQ
Rhinocort aqua
Nasarel
Nasocort

19
Q

What are the SE of IN steroids?

A 
Drying of nasal mucosa
Burning, itching sensation
Sore throat
Epistaxis 
Headache
Slow growth in children
Esp. older products (i.e. higher systemic absorption)
DDI – Minimal effects due to limited systemic absorption
20
Q

What is the mechanism of H1 antihistamines?

A

All available H1-antagonists are inverse agonists
Binds to H1 receptors -> change conformation -> lock at inactive state (i.e. reduce constitutive activity of receptors) -> down regulation
Work only on the histamine receptors less effective than steroid

21
Q

What are the effects of H1 blockers?

A

Relieve mild to mod allergic rhinitis
Sneezing
Rhinorrhea
Nasal itching but not congestion

Inhibits most of the effects of histamine on smooth muscles constriction, BUT DOES NOT PREVENT RELEASE OF HISTAMINE

22
Q

What is the difference between 1st and 2nd gen antihistamines?

A

2nd less sedating

23
Q

What are the 1st gen antihistamines?

A

Chlorpheniramine (Chlor-Trimeton Allergy)

Diphenhydramine (Benadryl

24
Q

What are the second gen antihistamines?

A 
Loratidine (Claritin) 
Desloratidine (Clarinex) 
Fexofenadine (Allegra) 
Cetirizine* (Zyrtec) 
Levocetirizine* (Xyzal)
25
Q

What are the SE of 1st gen antihistamines?

A

Sedation
Impaired cognitive function
Decreased performance
Anticholinergic effects – blurred vision, dry mouth, urinary retention, and constipation
Dryness decrease running nose but increase thickness of secretion

26
Q

What are the disadvantages of 1st gen antihistamines?

A

Administer TID to QID
DDI with other sedative agents (i.e. additive effect)
Elderly more sensitive with SEs

27
Q

What are the advantages of 2nd gen antihistamines?

A

Much less sedation
Less anticholinergic
Require dosage adjustment in impaired renal function
Qday dosing improve adherence

28
Q

What are the DDI of 2nd gen antihistamines?

A

+ TCA (tricyclic antidepressants) -> additive anticholinergic effects, sedation
+ KCL tab -> slow passage through GI -> ulcerative/stenotic lesions
+haloperidol -> increase risk of QT prolongation
+MAOI (selegiline, rasagiline) -> prolong anticholinergic effects of antihistamines
+Cyclobenzaprine -> additive anticholinergic effects

271- F1 (7 decks)

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