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Anesthesia Pharm I > anaphylaxis > Flashcards

anaphylaxis Flashcards

1
Q

What are the roles and functions of histamine?

A
  • mediator of allergic reactions and inflammatory processes
  • affects gastric secretion
  • neurotransmitter
  • neuromodulator
  • found in plants, animals, insects
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2
Q

how is histamine stored?

A
  • tissue histamine is bound into vesicles in mast cells or basophils (inactive in bound form)
  • mast cells found in nose, mouth, feet, internal body surfaces, blood vessels
  • non-mast cell histamine found in the brain as an endogenous neurotransmitter
  • stored and released from enterochromaffin-like cells of the fundus of the stomach (activate acid production from parietal cells)
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3
Q

describe histamine release

A

major pathophysiologic mechanism of mast cell and basophil histamine release is immunologic

  • cells have IgE antibody attached to membrane; when antigen is exposed to cell, degranulation of cell occurs causing release of histamine and other mediators
  • initial exposure antibodies form, 2nd exposure histamine release
  • negative feedback from H2 receptors found in skin and basophils (NOT IN LUNGS) limits reaction in skin and blood
  • bronchoconstriction not limited
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4
Q

how do amine drugs affect histamine?

A 
amine drugs (morphine, tubocurarine) compete with histamine for sites within cells and displaces it
*effects are the same but not r/t mast cells releasing
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5
Q

describe H1 receptors

A

similar to muscarinic receptors

  • located postsynaptic in the brain
  • located in endothelium, smooth muscle cells, nerve endings (brain)
  • effects: bronchoconstriction, slowed conduction through AV node, coronary artery vasoconstriction
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6
Q

describe H2 receptors

A

similar to 5-HT1 receptors

  • located postsynaptic in the brain (where neurotransmitter histamine acts in brain to cause PONV)
  • located in the gastric mucosa, cardiac muscle cells, and some immune cells
  • effects: CNS stimulation, increased myocardial contractility and HR, bronchodilation, increased secretion of H+ ions by gastric parietal cells
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7
Q

describe H3 receptors

A

similar to H4 receptors

  • located in the heart presynaptic postganglionic sympathetic nervous system: decreases NE release
  • decreases synthesis and release of histamine
  • H2 blockers also have some block on H3, so more histamine is produced and released; if on chronic H2 blocker, something causing histamine release can have exaggerated effects
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8
Q

describe H4 receptors

A

similar to H3 receptors

-located in the blood cells in the bone marrow and blood (eosinophils, neutrophils)

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9
Q

what are CV effects of histamine at both H1 and H2 receptors?

A
  • decrease in SBP and DBP d/t vasodilation of arterioles and precapillary sphincters (cause skin wheels)
  • increase HR d/t direct stimulation, reflex, and release of NE, E from adrenal medulla
  • vasodilation d/t release of nitric oxide (flushing)
  • coronary vasoconstriction (H1) opposed by vasodilation (H2)
  • edema from separation of endothelial cells in the microcirculation allowing leakage of fluid and small proteins into tissue (hives)
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10
Q

what are direct effects of histamine on the myocardium?

A
  • increased contractility
  • increased rate
  • result of H2 receptor stimulation
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11
Q

how does histamine effect H1 and H2 receptors differently r/t CV effects?

A
  • H1 receptors are stimulated at lower concentration to cause rapid onset but transient vasodilation (doesn’t last long)
  • H2 receptors have a slower onset, but more sustained vasodilation
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12
Q

what are pulmonary effects of histamine?

A
  • bronchoconstriction at H1 receptors (outweighs dilation)
  • bronchodilation at H2 receptors
  • asthma patients have 100 - 1000x greater sensitivity
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13
Q

what are GI effects of histamine?

A
  • excessive secretion of gastric fluid with a low pH

* caused by plasma histamine levels so low that no hemodynamic effect is evident

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14
Q

what are CNS effects of histamine?

A

CNS stimulation at H2 receptors

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15
Q

what are the effects of drugs on histamine?

A

histamine receptor blockers do not inhibit the release of histamine

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16
Q

what are specific effects of H1 blockers?

A
  • prevent activation of H1 receptors by histamine (competitive antagonist)
  • may activate muscarinic cholinergic, 5-HT3, alpha-adrenergic receptors
    drugs: diphenhydramine (Benadryl), dimenhydrinate (Dramamine), meclizine (Bonine), promethazine (Phenergan)
17
Q

what are the specific effects of H2 blockers?

A
  • prevent increase in intracellular cAMP which would activate the proton pump of the gastric parietal cell to secrete hydrogen ions
    drugs: cimetidine (Tagamet), famotidine (Pepcid), ranitidine (Zantac)
18
Q

what drug prevents the release of histamine?

A

Epinephrine

*drug of choice for anaphylaxis treatment

19
Q

what are the effects of Epi?

A
  • acts on different receptos
  • opposite effect on smooth muscles
  • prevents release of histamine (Cromolyn and beta 2 agonists) by decreasing the degranulation of mast cells that occurs with immunologic triggering
20
Q

what is anaphylaxis?

A

severe immediate hypersensitive reaction mediated by IgE antibodies formed in response to a foreign antigen

21
Q

what is anaphylactic shock?

A

the cardiovascular collapse that results from anaphylaxis

22
Q

what are anaphylactoid reactions?

A

non IgE mediated reaction that clinically resembles anaphylaxis

23
Q

what are the mast cell mediators involved in anaphylaxis?

A
  • histamine 1: contracts bronchial smooth muscle, vasodilation
  • histamine 2: vasodilation, mucous secretion, increased HR and contractility
  • kinins: increases vascular permeability, vasodilation; contracts smooth muscle including bronchoconstriction
  • heparin: intravascular coagulation
  • leukotrienes: inflammatory injury, constriction of smaller airways, coronary vasospasm, increase vascular permeability, myocardial depression
  • platelet-activating factor: increase vascular permeability; contract smooth muscle; wheal
  • prostaglandins: coronary vasospasm
  • serotonin
24
Q

what are physiologic manifestations of anaphylaxis?

A
  • bronchospasm
  • tachycardia, hypotension
  • edema, urticarial
  • excessive respiratory/ GI secretions
  • inflammation
  • abdominal pain, nausea, vomiting, diarrhea
25
Q

what are signs of anaphylaxis?

A
  • cutaneous: urticarial, angioedema, erythema, periorbital and facial edema
  • respiratory: coughing, sneezing, hoarseness, intraoral edema, laryngeal edema, stridor, cyanosis, tachypnea, WHEEZING, decreased pulmonary compliance, pulmonary edema, acute respiratory distress
  • CV: diaphoresis, hypotension, tachycardia, arrhythmias, decreased SVR, cardiac arrest, pulmonary hypertension
  • other: vomiting, diarrhea, acute intravascular coagulation
  • *under anesthesia, only sign may be CV collapse (LATE SIGN)
26
Q

what are risk factors for anaphylaxis?

A
  • receiving IV drugs
  • history of allergies or atopy
  • history of asthma
  • women 2.5x r/t cosmetics and cleaning chemicals with quaternary ammonium structures
  • history of previous anesthetic
27
Q

what are some drugs associated with anaphylaxis?

A
  • muscle relaxants (succs, roc)
  • morphine, Demerol, codeine
  • induction agents: pentothal, ketamine, benzo, propofol
  • local anesthetics: esters > amide, preservatives
  • antibiotics
  • blood products
  • protamine
  • LATEX, vascular graft material, methylmethacrylate bone cement
28
Q

how do you treat anaphylaxis?

A

-remove offending agent
-aggressive airway management (100% FiO2, epi aerosol, intubation)
-circulatory management (40% loss to interstitial space)
IV fluids (volume expansion; 25-50 ml/kg or 2-4 L); epi, vasopressin
-discontinue anesthetic agents (vasodilates)
-adjunctive drugs

29
Q

what dose of epinephrine is used with anaphylaxis?

A
  • 10-100 mcg for moderate hypotension
  • 1-3 mg for circulatory collapse/pulseless
  • infusion: 4-10 mcg/min
  • start epi with small doses (too much r/t death)
30
Q

what are adjunct drugs for anaphylaxis treatment?

A
  • antihistamines (H1-benadryl 1mg/kg max 50 mg; H2 Pepcid 20 mg)
  • glucocorticoids (hydrocortisone 5 mg/kg or 50-150 mg)
  • aminophylline (load 5-6 mg/kg; infusion 0.4-0.9 mg/kg/hr) for bronchoconstriction
  • epi infusion (0.02-0.05 mcg/kg/min)
  • dopamine infusion (5-20 mcg/kg/min) hemodynamic support
  • norepinephrine infusion (0.05 mcg/kg/min) needed vasoconstriction
  • NaBicarb 0.5-1 mEq/kg initially, then titrate to ABGs (acidosis from poor perfusion)
31
Q

how can anaphylaxis be prevented?

A
  • avoid risky patterns of practice
  • careful history taking
  • intradermal skin testing
  • RAST test
  • leukocyte histamine release test
  • pharmacologic prophylaxis (Benadryl, decadron, ranitidine 1-2 mg/kg)

Anesthesia Pharm I (28 decks)

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