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DT3- EXAM 2 > Drugs (IL)- Anti-histamines (3)- Leah* > Flashcards

Drugs (IL)- Anti-histamines (3)- Leah* Flashcards

1
Q

How is histamine synthesized?

A

histidine –> histamine via histidine decarboxylase

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2
Q

WHERE is histamine synthesized and stored?

#1? In blood? Other (3)

A
  • Mostly Masts
  • Basos in the Blood
  • Others: epidermal cells, ECL cells in the GI tract, and neurons
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3
Q

What are two urinary metabolites of histamine?

How are they synthesized?

A

Urinary metabolites:

  1. N methylhistamine (NMH)
  2. imidazole acetic acid
  3. histamine –>NMH (N meth. transferase–NMT)
  4. NMH –> imidazole acetic acid (Diamine oxidase)
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4
Q

What triggers mast cells/ basophils to release histamine/ other inflammatory mediators? (5)

A
  1. allergens
  2. morphine
  3. curare
  4. inflammatory mediators (*bradykinin, cytokines)
  5. venoms

“I.V. morphine Causes ALLERGies via histamine release”

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5
Q

What causes ECL cells to release histamine? (2)

A

gastrin; Ach

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6
Q

What are the 2 CNS effects of histamine?

What are the 2 Nerve Ending effects of Histamine?

A
  1. wakefulness 2.appetite suppression

1. Pain 2. Itching

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7
Q

How many histamine receptors are there?

Which are targeted by drugs?

A
  • H1-4
  • Only 1 +2 are currently drug targets.
  • H1:H2 determine effects of drugs
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8
Q

Location(3) and response (mechanism) of the H1 receptor

A

smooth muscle, endothelium, brain

works via Gq/IP3/DAG

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9
Q

Location (4) and response (mechanism) of the H2 receptor

A

cardiac/ gastric tissue, mast cells, brain

works via Gs/ ^^cAMP

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10
Q

What are the mechanisms for H3-4

A

both work through Gi to DECREASE cAMP

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11
Q

Name one H1 and one H2 agonist

A

H1: 2 methyl histamine
H2: dimaprit

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12
Q

Name the only important effect that needs to be correlated with the H2 receptor

A

gastric secretions

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13
Q

Name 3 cardio related effects of H1 receptors

A
  • Decreased TPR (via direct relaxation of sm muscle and short lived release NO / PG1)–>Flushing
  • increased HR
  • increased capillary permeability –>Swelling
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14
Q

Name 4 non-cardio effects of H1 receptors

A
  • bronchoconstriction
  • wheal and flare
  • wakefulness and appetite
  • pain/flushing/pruritis
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15
Q

How are “wheal and flare” responses mediated?

A

Both H1:
wheal- capillary permiability
flare- neuron reflex (vasodilation)

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16
Q

physiologic histamine antagonist?
mechanism?
use?

A
  • epinephrine
  • antagonizes histamine but works through NON HISTAMINE RECEPTORS!!!!
  • Gold standard for anaphylaxis
17
Q

Cromolyn and Nedocromil:

MOA?

A

Histamine RELEASE inhibitors (CROM drugs)

Block IgE/antigen interaction–> thus block Ag mediated histamine release

18
Q

What type of antagonists are 1st and 2nd gen antihistamines?

A

both are H1 REVERSIBLE, COMPETITIVE antagonists

19
Q

Where are H1 antihistamines metabolized?

Why does this matter?

A

HEPATIC METABOLISM:

  • kids metabolize faster
  • hepatic patients metabolize slower
20
Q

When might H1 anti-histamines cause uncharacteristic sleep changes? (2)

A

CNS stimulation in kids and H1 antag toxicity

CNS depression esp. with other depressants like alcohol

21
Q

What effects do anti-H1s fail to effectively block? (3)

A
  • effects on HR and bronchoconstriction is poor.
  • effects on pruritis are mild, corticosteroids more efficiently treat dermatitis
  • DO NOT suppress gastric secretions!!
22
Q

Typical H1 antihistamine uses (4)

A

Used in asthma, allergies, sedation and prophylaxis for motion sickness (promethazine)

23
Q

Which generation of anti-histamines cause drowsiness and why?

A
  • 1st gen because it readily enters the CNS

- 2nd gen doesn’t easily enter the CNS

24
Q

How long do gen 1 antihistamines last? gen 2?

A

1st gen: 4-6 hours

2nd gen: 12-24 hours

25
Q

What are 2nd generation anti-histamines a derivative of?
How do they compare to 1st gen in terms of activity?
Can thy cross BBB?
How are they metabolized?

A
  • they are metabolites of 1st gen. antihistamines
  • they are more active
  • CAN’T pass BBB
  • excreted unchanged.
26
Q

What are the 5 1st gen antihistamines?

A
  • diphenhydramine
  • dimethhydrinate
  • chlorpheniramine
  • hydroxyzine
  • promethazine
27
Q

What are the 3 2nd gen antihistamines?

A
  • loratadine
  • cetrizine
  • fexofenadine
28
Q

What is the only 2nd gen antihistamine with mild sedative effects?

A

Cetirizine

CCCCCetiri”zzzz”ine SSSSSedates you!!!

29
Q

Describe the ADRs of 1st gen antihistamines (3)

A

ALL cause EQUAL GI ADRs
ALL cause anti-muscarinic and sedative effects but THOSE are NOT EQUAL

  • anti-muscarinic=dry mouth/urinary retention/constipation
  • GI= N/V/D/anorexia
30
Q

Rank the anti-muscarinic properties of the 4 1st gen antihistamines

A

promethazine&raquo_space;> diphenhydramine&raquo_space; hydroxyzine= chlorpheniramine

31
Q

Rank the sedative properties of the 4 1st gen antihistamiens

A

promethazine&raquo_space;> diphenhydramine&raquo_space; hydroxyzine= chlorpheniramine

32
Q

Why can promethazine be used an motion sickness px?

A

because it has the most anti-muscarinic effects

33
Q

How is loratidine metabolized?

A

CYP3A4
Loratadine= Leah
OH LORd, LEAH hates the freaking CYPS!!!!!!!!!!!!!

34
Q

What kind of antagonists are the H2 antagonists?
How are they excreted?
Use?

A
  • competitive
  • renal excretion RENALLY ADJUST
  • used for GERD/peptic ulcer tx and px
35
Q

What are they 4 H2 antagonists?

A
  • ranitidine
  • cimetidine
  • famotidine
  • nizatidine
  • all end in “-tidine”, but be careful bc 2 H1-2ndGens end in “-dine”
36
Q

Which of the three H2 antagonists blocks P450?

A

-“C”imetidine blocks that stupid “CYP”450

–>increase pH and decreased drug metabolism

37
Q

What are the three most common side effects associated with H2 antagonists?

A

They are all typically mild:

- HA/ GI/ fatigue or drowsiness

DT3- EXAM 2 (19 decks)

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