LO 18 - Part 1 Flashcards

Anti Histamines and Autocoids

1
Q

Define histamines

A
  1. Naturally occurring agents produced by many tissue types
  2. act locally only
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2
Q

Describe histamines

A
  1. Almost all mammalian tissues contain or can synthesize histamine
  2. Released as a result of immediate/allergy or inflammation
  3. Stored in mast cells & basophils
  4. Distribution of cells, eyes, nasal tissue, skin, GI
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3
Q

What are the 2 types of histamines

A
  1. H1 - Skin
  2. H2 - Only GI tract (to release HCL)
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4
Q

What are the clinical uses of HISTAMINES?

A

No clinical uses of histamine have been established - but H1 & H2 blockers aka antihistamines have great clinical applications

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5
Q

Describe Anaphylaxis

A
  1. Bronchoconstriction
  2. Vasodilation and increased capillary permeability - decreased blood pressure followed by shock and cardiovascular collapse
  3. Emergency tx - Epi-pen/epinephrine as direct β2-agonist
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6
Q

What are the 2 types of receptor-antagonist histamine ?

A
  1. RA-H1 - RA = receptor-antagonist
  2. RA-H2 - RA = receptor-antagonist
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7
Q

What are the pharm effects of old RA - H1 Sedatives such as Benadryl (generic: DPHA - diphenhydramine)

A
  1. Cross blood-brain-barrier
  2. RA-H1
  3. Anticholinergic (anti-SLUD)
  4. Anti-emetic
  5. CNS depression
  6. LA
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8
Q

What are the medical uses of old RA - H1 Sedatives such as Benadryl (generic: DPHA - diphenhydramine)

A
  1. seasonal allergy/hives Tx (RA-H1)
  2. motion sickness Tx (anti-emetic)
  3. post radiation tx (anti-emetic)
  4. Sleeping pills Nytol (CNS depressant/crosses BBB)
  5. Post-op sedation (CNS depressant/crosses BBB)
  6. Local anesthetic
  7. Tx of oral lesions
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9
Q

What are the adverse reactions of old RA - H1 Sedatives such as Benadryl (generic: DPHA - diphenhydramine)

A
  1. CNS depressant - no driving, no signing important docs, dizzy/fatigue/blurred vision
  2. GI - irritation, constipation, nausea/vomiting, anorexia (think Anticholinergic/anti-SLUD)
  3. Xerostomia
  4. Toxicity
  5. CV and Resp collapse
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10
Q

Describe new RA-H1 drugs

A
  1. Non-sedative
  2. Do not cross blood/brain/barrier
  3. no CNS depression/no sedation
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11
Q

Provide examples of new RA-H1 drugs

A
  1. Claritin
  2. Allegra
  3. Zyrtec
  4. Reactin
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12
Q

Describe RA-H2 drugs

A
  1. Suffix “tidine”
  2. Inhibit H2 → lower HCl production
  3. Med uses - Tx of GERD & Tx of gastric ulcers
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13
Q

List common RA-H2 drugs

A
  1. cimetidine (Trade: Tagamet)
  2. ranitidine (Trade: Zantac)
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14
Q

Describe Prostaglandins

A
  1. Members of a group of biologically active agents termed eicosanoids
  2. Produced in the body in response to many different stimuli and small quantities produce a large spectrum of effects on many different body systems

Pharm effects
1. Wide spectrum of action
2. Smooth-muscle effects: vascular smooth muscle may be relaxed or stimulated, depending on the specific PGs
3. Effects on reproductive organs: oxytocic action (stimulate and enhance uterine contractions)
4. PGs may be used for inducing mid trimester abortions
5. CNS: PGs increase body temperature
6. Other effects: increased heart rate and cardiac output

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15
Q

What are the dental implications of Prostaglandins?

A
  1. PGs have been implicated in periodontal disease
  2. At least two stages of periodontal disease may involve PGs - The first is inflammation of the gingiva with erythema, edema, and increase in gingival exudate; The second is the resorption of alveolar bone with tooth loss
  3. PG antagonist: NSAIDs
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16
Q

Describe Leukotrienes

A
  1. Another complex group of autocoids that are also derived from arachidonic acid
  2. Cause strong bronchoconstriction in humans
  3. They also contract other smooth muscle such as the uterus and GI tract
  4. LK antagonist is used in Tx of asthma (Singulair)
17
Q

Describe Kinins

A
  1. Polypeptides that are distributed in a great variety of body tissues
  2. Kallidin and bradykinin are found in plasma and may play a role in dental diseases - (pulpal caries pain)
  3. Antagonists: ASA and steroids