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Pharm II: Exam 1 > Histamine > Flashcards

Histamine Flashcards

1
Q

Where are histamine located?

A

Found throughout many tissues, MAINLY in Mast cells (Highest amounts are found in the lung, skin, nasal; gastrointestinal mucosa)

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2
Q

How is Histamine synthesized and stored?

A

Formed by decarboxylation of the amino acid histidine and stored in granules

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3
Q

How are Histamines released?

A

Released along with several chemical mediators during episodes of trauma, allergies, anaphlyaxis, colds, bacterial toxins, bee sting venom, drugs

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4
Q

What are the two types of histamine release?

A
  1. Cytolytic: plasma membrane is damaged causing leakage of cytoplasmic contents (no energy dependent, no calcium required)
  2. Noncytolytic: exocytotic release from granules (no damage to mast cell, requires energy and calcium - IgE antibodies bind to antigen and release histamine)
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5
Q

What drugs are inducers of Cytolytic release of Histamine?

A
  • Phenothiazines
  • Narcotic analgesics
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6
Q

What substances and drugs stimulate Histamine release from Mast cells?

A
  • Radiocontrast media
  • D-Tubocurare
  • Mast cell degranulation protein (from bee venom)
  • Morphine
  • Codeine
  • Succinylcholine
  • Protamine
  • Doxorubicin
  • Vancomycin
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7
Q

What is Red Man Syndrome? What are associated S/Sx? How do you treat?

A

Related to reactions with Vancomycin may cause:

  • Flushing
  • Pruritus
  • Chest pain
  • Muscle spasm
  • Hypotension

Pretreatment with antihistamine attenuates the symptoms

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8
Q

Which drugs are Mast cells stabilizers (prevent noncytolytic degranulation and histamine release)?

A
  • Cromolyn
  • Nedocromil
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9
Q

How are Cromolyn and Nedocromil administered?

A

Inhalation of a powder

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10
Q

T or F: Cromolyn and Nedrocromil is useful in management of acute asthma attacks.

A

F; Only used prophylactically to BLOCK asthmatic reactions, DEC symptoms of allergic rhinistis, Effective only if used before a challenge not during.

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11
Q

How many types of histamine receptors are known? What are they?

A

4 different types:

  • H1: phospholipase C mechanism
  • H2: adenylyl cyclase mechanism parietal cell acid secretion
  • H3: inhibit the release of histamine on neurons (feedback inhibitions)
  • H4: Proinflammatory activity
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12
Q

What is histamines role in Allergies and Anaphylaxis?

A
  • Stimulation of secretions
  • Constriction of smooth muscle
  • Stimulation of sensory nerve endings
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13
Q

How does Histamine stimulate secretions at H1 receptors?

A

INCs mucus in nasal cavity and bronchi (results in respiratory symptoms)

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14
Q

How does Histamine stimulate secretions at H2 receptors?

A

Stimulates gastric acid secretion

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15
Q

How does histamine constitute constriction of smooth muscle?

A

H1 receptors constrict bronchi and intestines (causes cramps and diarrhea)

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16
Q

T or F: Healthy human’s histamine will causes hyperreactivity

A

F; healthy human’s histamine is not especially potent but in patients with asthma the bronchi are hyperreactive.

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17
Q

Which histamine receptor is responsible dilation of smooth muscle in blood vessels; How does histamine affect these processes?

A

H1; DEC blood pressure and INC nitric oxide (vasodilation)

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18
Q

Which histamine receptors stimulate heart rate and contractility? How does histamine affect these processes?

A

H1 & H2; Directly INCs via INC influx of calcium, Indirectly INC via baroreceptor-mediated INC in sympathetic tone

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19
Q

Where are catacholamines released from in the body?

A

Adrenal glands

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20
Q

Which histamine receptors are responsible for dilation and INC’d permeability of capillaries? How does histamine affect these processes

A

H1 & H2; causes endothelial cells to contract and expose permeable basement membrane (leaks protein and fluid)

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21
Q

What is the “Triple response of Lewis”?

A

Positive skin test, challenge with an allergen (bugbite, histamine, allergy test)

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22
Q

What are the three presentations of “Triple Response of Lewis”?

A
  • Red Line/Spot (Dilates arterioles where injected)
  • Flare (Histamine stimulates nerve endings which leads to dilation of arterioles)
  • Wheal (INC in capillary permeability due to local edema)
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23
Q

What are the principal targets in a hypersensitive reaction?

A
  • Mast cells
  • Basophils
24
Q

What happens in an allergic response?

A

Antigen produces formation of IgE antibodies bind with high affinity receptor specific for IgE and activate tyrosine kinase –> INC in intracellular calcium (triggers exocytosis of secretory granules in the mast cells)

25
Q

What other mediators of inflammation are released?

A

Phospholipase A2: produces leukotrienes (contract smooth muscles of the bronchi) and prostagladins

26
Q

What are the main differences are between allergic reactions and a anaphylatic response?

A
  • Releasing locations
  • Rates of release
27
Q

T or F; Response remains localized if histamine release is in a specific area.

A

T

28
Q

What will happen if histamine is released rapidly and diffuses into the blood?

A

Anaphylatic reaction (systemic response)

29
Q

What will a patient presents with who is experiencing a hypersensitiveity reaction?

A
  • Intense warmth
  • Skin reddens
  • Marked effec on palms, hands, face, scalp and ears
  • Hives
  • Nausea
  • DEC BP
  • INC HR
  • Bronchospasm
  • Constriction
30
Q

How can (true) anaphylaxis reaction treated?

A

Epinephrine

31
Q

Which drugs are considered 1st Generation Histamine H1 Blockers?

A
  • Triprolidine
  • Diphenhydramine
  • Promethazine
  • Hydroxyzine
  • Chlorpheniramine
32
Q

Which drugs are considered 2nd Generation Histamine H1 Blockers?

A
  • Loratadine
  • Desloratadine
  • Azelastine
  • Cetirizine
  • Fexofenadine
33
Q

What are differences between 1st and 2nd generation H1 blockers?

A
  • 1st generation
    • anticholinergic
    • short-acting
    • CNS penetration
  • 2nd generation
    • no anticholinergic activity
    • Long-acting
    • no CNS penetration (does not cross BBB)
34
Q

What are characteristics of H1 blockers?

A

Antagonize all actions of histamine (reversible, competitive blockers of H1 receptors – action via H2 receptor still active) mainly blocking the effects of histamine on:

  • INC permeability
  • Edema formation
  • Itching
35
Q

T or F; H1 blockers have great effect on actions bronchoconstriction and vasodilation

A

F; these actions are predominantly caused prostaglandins and leukotrienes

36
Q

Does H1 Blockers have tolerance to suppressive effects on skin test reactivity to allergens? Tolerance to sedative effects?

A

No, concentration achieved at sites unknown with significant inhibition of wheal and flare response for 26 hours (residual suppression may last for up to 7 days after discontinuation of H1 blockers following 1-2 week regular use); Tolerance to sedative effects may occurs (theraputic effect may be restored with swith to another antihistamine class)

37
Q

What is the importance of active metabolites of 2nd generation H1 blockers?

A

Theraputic uses (Desloratadine=Clarinex, Fexofendaine=Allegra)

38
Q

T or F: All FDA-approved antihistamines do not prolong the QT interval

A

T

39
Q

What are theraputic uses for antihistamines?

A
  • Allergic reactions
  • Prevention of Motion Sickness
  • Prevention of Nausea/Vomiting
  • Sedative
  • Antiparkinsonism
  • Local anesthetic action
40
Q

How are antihistamines useful in preventing motion sickness?

A

Possibly related to anticholinergic effects; administered 1 hour prior to anticipated motion

41
Q

What antihistamine medications are available for prevention of motion sickness? Which are most effective?

A
  • Promethazine (most effective)
  • Scopolamine (most effective, non-antihistamine)
  • Diphenhydramine
  • Mecilizine
  • Cyclizine
42
Q

What antihistamine medications are available for prevention of nausea/vomiting? How do these medications work?

A

Block dopamine D2 receptors

  • Promethazine
  • Timeprazine
43
Q

What antihistamine medications are available as sleep medications?

A
  • Diphenhydramine
  • Doxylamine
  • Doxepin
44
Q

What is the limit for tolerance of antihistamines medications used for sedative purposes?

A

10 consecutive nights of use

45
Q

What antihistamine medications are available that have antiparkinsonism effects?

A
  • Diphenhydramine
46
Q

What antihistamine medications are available with local anesthetic actions? How do these medication have this effect?

A

Block sodium channels

  • Promethazine (sunburn preparation)
  • Magic Mouthwash (TX oral ulcers, infections, inflammation, and pain)
47
Q

What are all the actions of diphenhydramine?

A
  • H1 Blocker (1st Generation)
  • Motion Sickness
  • Sedative effects (Sleep medication)
  • Antiparkinsonism effects
48
Q

What are all the actions of Promethazine?

A
  • H1 Blocker (1st Generation)
  • Motion Sickness
  • Nausea/Vomiting
  • Local Anesthetic
49
Q

What are ADRs for Antihistamines?

A
  • Antimuscarinic
  • Sedative actions (absent/lower with 2nd generation H1 Blockers)
50
Q

What sedative effects might a patient present with when taking antihistamines?

A
  • Fatigue
  • Dizziness
  • Blurred vision
51
Q

What determines the CNS sedation of a person on Antihistamines?

A

Effect correlates with H1 receptor binding in the brain (i.e. Doxepin=50-90% CNS bound, Fexofenadine 0% bound)

52
Q

What antimuscarinic effects might a patient present with when taking antihistamines?

A
  • Dry mouth and nasal passages
  • Constipation
  • Blurred vision
  • Urinary retention
53
Q

T or F: Paradoxial excitation may occur in children taking antihistamines.

A

T

54
Q

What drug interactions are known with antihistamines (H1 blockers)?

A

Could potentiate other CNS depressants

55
Q

What are possible toxicities with antihistamines (H1 antagonist)?

A

OD is rare but acute poisoning is relatively common (esp. in children)

56
Q

What are acute poisoning effects experienced with antihistamines?

A
  • Initial excitement
  • Ataxia and convulsions
  • Coma and cardiorespiratory collapse

Pharm II: Exam 1 (7 decks)

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