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FPC2 Exam 7 > Allergy > Flashcards

Allergy Flashcards

1
Q

What are the three phases of the triple response to an allergen?

A

initial redness (vasodilation)
Flare @15sec (depolarization of sensory nerve ending-> itch)
Wheal @few min (vascular permeability ->swelling)

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2
Q

What are the clinically important components of anaphylaxis?

A

decreased blood pressure, edema (swelling lips, tongue, uvula), bronchconstriction

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3
Q

What is the main mediator of allergic responses

A

histamine

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4
Q

What are the effects of histamine at skin?

A

local response-> triple resopnse

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5
Q

What are the effects of histamine at bronchioles?

A

bronchoconstriction at high doses

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6
Q

What are the effects of histamine at brain?

A

sedation, appetite (satiety)

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7
Q

What are the effects of histamine at sensory nerve endings

A

depolarization-> pain and itch

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8
Q

What are the effects of histamine at vascular endothelium

A

contract endothelial cells-> extravasation of fluid->edema

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9
Q

What are the effects of histamine at arterioles (smooth muscle)

A

vasodilation (decrease BP)

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10
Q

What are the effects of histamine at heart?

A

increase heart rate-> direct and reflex

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11
Q

What are the effects of histamine at stomach?

A

acid secretion

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12
Q

What are the main sources of histamine (synthesis + metabolism)

A

mast cells + basophils
enterochromaffin cells in stomach
neurons in brain

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13
Q

What are things that trigger mast cells to release their stuffs

A

allergen, IgE, specific molecules (opioids, contract media, vancomycin)

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14
Q

What are some of the things that mast cells release?

A

histamine, tryptase, PAF, Lipid, proteases, chemokine, NO, endothelin
these all lead to inflammation

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15
Q

What are the function of histamine pathways of the brain?

A

sleep-wake cycle
appetite (satiety)
nociception?!?!

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16
Q

What is the process of histamine release into the stomach

A

vagus nerve -> enterochromaffin cells -> hist to parietal cells -> AC, cAMP, PKA -> Ca2+ release -> TV exocytosis into gastric acid

17
Q

How many histamine receptors are there? what type of receptor are they?

A

4

GPCR

18
Q

What does H1 receptor do? where is it located? what type of GPCR signaling?

A

vasodilation, edema, bhroncoconstriction, appetite, arousal.
Smooth muscle, endothelial, CNS
Gq IP3, DAG up

19
Q

What does H2 receptor do? where is it located? what type of GPCR signaling?

A

release stomach acid, VD, HR up
gastric parietal, cardiac, mast cells, CNS
G2, cAMP up

20
Q

What does H3 receptor do? where is it located? what type of GPCR signaling?

A

Inhibitory autoreceptor + heteroreceptors (appetite), arousal
CNS, myenteric plexus
Gi, cAMP down

21
Q

What does H4 receptor do? where is it located? what type of GPCR signaling?

A

chemotaxis, cytokine production
CNS, eosinophils, neutrophils, CD4 tcells
Gi, cAMP down

22
Q

Which are the two histamine targets that are used clinically?

A

H1 and H2

23
Q

What are the actions of drugs at H1?

A

Allergy- block edema, vasodilation, bronchoconstiction

24
Q

what are the actions of drugs at H2 (antagonists)

A

block stomach acid, some immune response

25
Q

What are some 1st generation histamine agonists? 2nd gen?

A

1st: Chlorpheniramine, diphenhydramine (Benadryl)
2nd: cetirizine (zyrtec), fexofenadine (allegra), loratidine (claritin), olopatidine (patanase), azelastine (astepro)

26
Q

What at some off target effects of H1 1st generation antagonists?

A

muscarinic antagonist, penetration of blood brain barrier, sedation
(drugs like diphenhydramine, chlorpheniramine, etc)

27
Q

Promethazine is used medically for

A

anti nausea, motion sickness

D3 antagonist properties

28
Q

What are glucocorticoids used for with allergies? What is MOA? what are some 1st and 2nd gen?

A

chronic inflammation, back migration and action of incoming immune cells, block cytokines

1st: beclomethasone, budesonide, flunisolide, triamcinonlone
2nd: fluticasone, ciclesonide, mometasone

29
Q

What is the mechanism of ipratropium and what is it used for?

A

Muscarinic antagonist (M3) -> block glandular secretion
runny nose
(this is an anticholinergic)

30
Q

What is montelukast used for? What is mechanism?

A

chronic allergy

leukotriene antagonist -> counter inflammation and VD produced by leukotriene release from mast cells

31
Q

What is the mechanism of nasal decongestants? what are examples?

A

α1 receptor agonist/NE releasers by heteroexchange

oxymetazoline, phenylephrine, pseudoephedrine

32
Q

Dimenhydrinate and cyclizine can be used for

A

motion sickness

33
Q

What do NE α1 do to arterioles?

A

constrict arterioles.

If taking while having HTN, raise BP. But it will dry up the runny nose so that’s good

34
Q

What is the advantage of nasal administration for decongestants?

A

nasal spray more effective and it avoids the systemic effects (BP up)

35
Q

Why do you use epinephrine for anaphylaxis?

A

bronchodilator, increase force and rate of heart, increase total peripheral resistance

36
Q

Why don’t you treat anaphylaxis with antihistamines?

A

slow onset of reversal, multiple mediators contribute to symptoms

FPC2 Exam 7 (4 decks)

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