Histamine Antagonists, Bronchospasm, And Pulmonary Pharmacology

Front 1

Is histamine a drug?

Back 1

no

Front 2

Why is histamine important?

Back 2

for it's physiological and pathophysiological actions

Front 3

What histamine drugs have therapeutic value?

Back 3

drugs that inhibit its release or block its receptors

Front 4

What does histamine mean?

Back 4

tissue amine

Front 5

What kind of compound is histamine?

Back 5

nitrogen

Front 6

What do Type 1 hypersensitivity reactions look like?

Back 6

rash on back

whelps on back

Front 7

What kind of amine is histamine?

Back 7

low molecular weight hydrophilic amine

Front 8

Histamines belong to a class of _______ receptors

Back 8

G-protein coupled receptors

Front 9

Histamine is an important mediator of?

Back 9

inflammation with allergies

Front 10

Does histamine cross the BBB?

Back 10

no

Front 11

Where is histamine found in the body?

Back 11

large amounts in the skin, lungs, GI tract, and basophils

Front 12

What is the precursor to histamine?

Back 12

histadine

Front 13

This is released in response to an antigen?

Back 13

stored histadine

Front 14

Stored histadine is released in response to an?

Back 14

antigen

Front 15

What is an antigen?

Back 15

any substance that causes your immune system to produce antibodies it. (cat dander)

Front 16

What s/s does local application of histamine cause?

Back 16

swelling, redness, and edema mimicking amild anti-inflammatory reaction.

Front 17

What changes do large systemic doses of histamine lead to?

Back 17

vascular changes similar to those seen after shock or anaphylaxis origin

Front 18

Within the body, the largest concentrations of histamine are found in?

Back 18

skin, lungs, GI tract

Front 19

How is histamine metabolized?

Back 19

Two ways

Pathway 1. methylaztion catalyzed by histamine-N-methyltransferase which is furter degraded by MAO.

Pathway 2. histamine undergoes oxidative deamination catalyzed by diamine oxidase.

Front 20

What happens to histamine once it is formed?

Back 20

it is either stored in mast cells or rapidly degraded by one of the two metabolic pathways

Front 21

Both routes of metabolism lead to a pharmacologically inactive metabolite that is excreted how?

Back 21

renal

Front 22

What are 3 conditions that release histamine?

Back 22

1. tissue injury

2. allergic reactions

3. drugs and other foreign compounds

Front 23

What causes a tissue injury?

Back 23

any physical or chemical agent that injures tissue, skin, or mucosa is particularly sensitive to injury and will cause the immediate release of histamine from mast cells.

Front 24

How does an allergic reaction cause the release of histamine?

Back 24

exposure of an antigen to a previously sensitized subject can immediately trigger allergic reactions.

Front 25

Name some drugs and foreign compounds that cause the release of histamine.

Back 25

morphine, dextran, antimalarial drugs, dyes, antibiotic bases, alkaloids, amides, quaternary ammonium compounds, enzymes (phospholipase C).

Penicillins, Tetracyclines

Basic drugs- amides, amidines, diamidines, Toxins, venoms, Proteolytic enzymes, Bradykinin, Kallidin, & Substance P

Front 26

What immunoglobulin plays a pivitol role in allergic conditions?

Back 26

IgE

Front 27

What are some mild or cutaneous symptoms associated with histamine release?

Back 27

urticaria (hives)

itching

erythema

Front 28

What are some mild to moderate symptoms associated with histamine release?

Back 28

skin reactions

tachycardia

dysrhythmias

mild respiratory distress

moderate hypotension

Front 29

What are some severe or anaphylactic symptoms associated with histamine release?

Back 29

ventricular fibrillations

bronchospams

respiratory arrest

severe hypotension

cardiac arrest

Front 30

Histamine 1 receptors cause what changes in the body?

Back 30

smooth muscle contraction in the GI and respiratory tract

Front 31

Histamine 1 receptors are associated with what body changes?

Back 31

sneezing and pruritus

Front 32

Histamine receptors are indicated in these s/s?

Back 32

tachycardia

hypotension

flushing

headache

Front 33

Histamine 1 receptors in the heart can cause what s/s?

Back 33

vasoconstriction in coronary epicardial vessels

decrease AV node conduction

Front 34

Histamine 1 receptors work on?

Back 34

smooth muscle, endothelium, & CNS causing bronchoconstriction and vasodilation??

pain

itching

allergic rhinitis

motion sickness

Front 35

How does the histamine 2 receptor affect the heart and GI system?

Back 35

stimulation results in increased GI hydrogen ion secretion

in the heart it increases myocardial contraction and HR

Front 36

How can histamine cause confusion when cimetidine is taken?

Back 36

histamine 2 is found in the CNS

Front 37

Where is histamine 2 found?

Back 37

CNS

gastric parietal cells

vascular smooth muscle

basophils

Front 38

What does histamine 2 regulate?

Back 38

gastric acid

Front 39

Where is histamine 3 expressed?

Back 39

CNS

Front 40

How does histamine work in the CNS?

Back 40

works presynaptically to inhibit the release of other neurotransmittes

Front 41

How do histamine 3 receptors play a role in control of satiety?

Back 41

It is thought that an increase in the hypothalamic concentration of histamine produces a reduction in food intake

Front 42

How many histamine receptors are there?

Back 42

4

Front 43

Histamine 4 receptors exhibit very restricted locations where?

Back 43

intestinal tissue

spleen

immune active cells

Front 44

Why were the first generation histamine blockers & anti-histamines developed?

Back 44

to counteract allergic symptoms

Front 45

What is the most common example of a 1st generation histamine blocker?

Back 45

benadryl

Front 46

What is a majot side effect of benedryl and other 1st generation anti-histamines?

Back 46

extreme sedation

Front 47

Do 1st generation antihistamines cross the BBB?

Back 47

yes

Front 48

What characteristic do 1st generation histamines possess that allows them to cross the BBB?

Back 48

they are lipophilic

Front 49

Do 2nd generation antihistimes cross the BBB?

Back 49

no

Front 50

Name some 2nd generation anti-histamines.

Back 50

Claritan (loratadine)

Allegra (fexofenadine)

Front 51

Do the 2nd generation antihistamines cause excessive sedation?

Back 51

no, they cause less sedation

Front 52

Where are histamine 2 receptors found?

Back 52

in the stomach lining

Front 53

Stimulation of histamine 2 receptors causes these s/s?

Back 53

increased digestion

stomach acid secretion

Front 54

Name some histamine 2 receptor blockers.

Back 54

Zantac (ranitidine)

Axid (nizatidine)

Pepcid (famotidine)

Tagament (cimetidine)

Front 55

What is the function of histamine 2 receptor blockers?

Back 55

to counteract excess stomach acid in PUD or GERD

Front 56

The histamine receptors on the basolateral membranes of the acid secreting gastric parietal cells are of hte histamine 2 type and are not blocked by _______ medications.

Back 56

histamine 1

Front 57

What are some clinical uses of histamine 1 blockers?

Back 57

motion sickness

n/v

toxicity

drug allergies

Front 58

What histamine 1 blockers have the greatest effectiveness in treating motion sickness?

Back 58

benadryl, phenergan

Front 59

What histamine 1 blockers have the greatest effectiveness in preventing motion sickness?

Back 59

scopolamine and certain 1st generation H1 blockers

Front 60

Name 2 other H1 blockers that are effective for motion sickness and are less sedating.

Back 60

meclizine and cyclizine (marezine)

Front 61

Are H1 blockers recommended for use in management of n/v in pregnancy? Why?

Back 61

No, due to difficulty in assessment of possible birth defects associated with H1 antagonists

known teratogenic effects of other H1 blockers

Front 62

How do H1 blockers help with toxicity?

Back 62

-excessive excitation and convulsions in children

-orthostatic (postural) hypotension

-Allergic responses

Front 63

H1 or H2 blockers are used for drug allergies and can be used topically?

Back 63

H1 blockers

Front 64

Overdose of a 1st generation blocker is similar to ________ overdose.

Back 64

atropine

Front 65

Overdose of a 2nd generation blocker may induce?

Back 65

cardiac arrhythmias

Front 66

Name some clinical uses of H2 blockers.

Back 66

Gastric ulcers

GERD (erosive esophagitis)

Hypersecretory diseases

Toxicity

Front 67

Is GERD treated with higher or lower doses of H2 receptor agonists as compared to gastric and peptic ulcer disease?

Back 67

higher doses

Front 68

Name some hypersecretory diseases.

Back 68

Zollinger-Ellison syndrome

Systemic mastocytosis

multiple endocrine adenomas

Front 69

How is Zollinger-Ellison syndrome characterized?

Back 69

acid hypersecretion which is caused y a gastrin secreting tumor.

It is often fatal, however H2 receptor antagonists often control the symptoms

Front 70

What is systemic mastocytosis and multiple endocrine adenomas?

Back 70

hypersecretory conditions in which H2 receptor antagonists often control the symptoms

Front 71

Are H2 receptor antagonists generally well tolerated?

Back 71

yes

Front 72

What are some side effects of H2 receptor antagonists toxicity?

Back 72

diarrhea

dizziness

somnolence

headache

rash

Front 73

What H2 blocker has the most adverse effects and what are they?

Back 73

cimetidine (tagament)

side effects: granulocytopenia, thrombocytopenia, neutropenia, aplastic anemia (extremely rare), hepatoxicity with reversible cholestatic effects, reversible hepatitis, liver enzyme test abnormalities

Front 74

Which H2 blocker has the fewest side effects?

Back 74

Axid (nizatidine

Front 75

What are some uncommon side effects of H2 blockers?

Back 75

CNS effects (except in the elderly where confusional states, delerium, and slurred speech may occur)

blood dyscrasias

Front 76

Endocrine effects are not associated with which H2 blockers?

Back 76

pepcid, zantac, axid

Front 77

Which of the following antihistamines is most likely to potentiate the effects of alcohol?

Back 77

a. phenergan

b. claritan

c. zantac

d. chlor-trimeton

Front 78

Rantidine (zantac), an H2 receptor antagonist is most likely to produce which of the following effects?

Back 78

a. inhibition of the "triple effect" of histamine

b. inhibition of gastric secretions

c. inhibition of nausea & vomiting

d. sedation

e. inhibition of salivary and bronchial secretion

Front 79

Which of the following statements about antihistamines are correct?

Back 79

a. antihistamines prevent histamine release

b. antihistamines produce their effects through

competition at the receptor

c. antihistamines promote histamine degradation

d. antihistamines prevent histamine synthesis

e. all of the above are correct

Front 80

Which of following effects is not associated with histamine

Back 80

a. triple effect

b. progressive fall in BP

c. headache

d. secretion of catecholamines from chromaffin cells in the adrenal medulla

e. sedation

Front 81

Which of the following drugs would be the best treatment for allergic rhinitis if you operated heavy machinery?

Back 81

a. benedryl

b. axid

c. phenergan

d. allegra

e. zantac

Front 82

Axid an H2 antagonist, can be effectively used for the control of ________?

Back 82

a. itching associated with insect bites

b. asthma

c. indigestion

d. the triple effect

e. insomnia

Front 83

Antihistamines acting at the ______ receptor are most likely to ________.

Back 83

a. H1 receptor; inhibit the triple effect of histamines

b. H2 receptor: inhibit the triple effect of histamines

c. H1 receptor: reverse anaphylaxis

d. H2 receptor: reverse anaphylaxis

e. H1 receptor; block gastric secretions

Front 84

Which of the following effects is most commonly associated with histamine?

Back 84

a. progressive increase in BP

b. progressive decrease in BP

c. decrease in gastric secretions

d. triple effect

e. sedation

Front 85

This drug is a 1st generation, sedating, oral antihistamine.

Back 85

benadryl

Front 86

This medication is an excellent topical anesthetic, effective for local anesthesia as an injection and has anti-pruritic effects.

Back 86

benadryl

Front 87

Benadryl has a __ dimensional structure, which is similar to other anesthetic drugs.

Back 87

3

Front 88

This drug is not really a 1st line anesthetic, but can be used to help with sedation in a pt with a regional anesthetic.

Back 88

benadryl

Front 89

In patients who are allergic to local anesthetics, a local injection of _____________ provides adequate anesthesia for _______ % of people within _____ minutes. The duration of anesthesia is between 15 minutes and 3 hours, which is adequate for dermatology procedures.

Back 89

1% benadryl

80%

5 minutes

Front 90

Bronchodilators are the therapeutic mainstay for patients with ______.

Back 90

COPD

Front 91

In COPD, bronchodilators have been consistently shown to induce long term improvements in?

Back 91

symptoms

exercise capacity

airflow limitation (even when there is no spirometric improvement following a single test dose

Front 92

How can bronchodilators be administered?

Back 92

inhalation

orally

SC

IV

Front 93

Name 3 pulmonary bronchodilators.

Back 93

beta agonists

anticholinergics

theophylline

Front 94

All symptomatic COPD patients should be prescribed this medication?

Back 94

short acting bronchodilator to be used on as as needed basis

Front 95

What should be added to the medication regimen if COPD symptoms are inadequately controlled with short acting bronchodilator therapy or if the pt is at risk for poor outcomes?

Back 95

a regularly scheduled long acting bronchodilator

Front 96

What is the recommended method of delivery of medications in COPD patients? Why?

Back 96

inhalation

because it maximizes the bronchodilators direct effect on the airways, while minimizing the systemic effects

Front 97

How can medications be delivered by inhalation?

Back 97

MDI

DPI

SMI

nebulizer

Front 98

Can SABA and anticholinergics be used alone, in combination, or both.

Back 98

both

Front 99

True or False: All short acting broncohdilators improve lung function and symptoms?

Back 99

True

Front 100

Why is combination therapy often preferred when treating COPD?

Back 100

because the combination of a SABA plus a short acting anticholinergic achieves a greater bronchodiator response that either one alone

Front 101

In COPD, is monotherapy with SABA or short acting anticholinergics acceptable?

Back 101

yes

Front 102

Name some short acting bronchodilators.

Back 102

albuterol and levabuterol

Front 103

What is the first decision that most clinicians face when managing a patient with COPD?

Back 103

deciding which short acting bronchodilator is most appropriate in a pt with mild intermittnet symptoms

Front 104

What is the advantage of SABA?

Back 104

their rapid onset of action

Front 105

Short acting bronchodilators alone or in combination may be ________ to control symptoms and are not considered to be _______ therapies.

Back 105

insufficient

maintenance

Front 106

What asthma medications are the most potent and rapid acting?

Back 106

beta adrenergic agonists

Front 107

How do beta agonists interact with beta adrenergic receptors. Name 5 ways.

Back 107

1. relax bronchial smooth muscle

2. decrease mast cell mediator release

3. inhibit neutrophil, eosinophil, and lymphocyte functional responses

4. increase mucociliary transprot

5. affect vascular tone and edema formation

Front 108

What are the acute s/s of asthma?

Back 108

SOB

coughing

wheezing

chest tightness

Front 109

What is the primary use of SABA?

Back 109

quick relief of acuteasthma symptoms

Front 110

Are SABA prescribed for use on an as needed basis or routine basis?

Back 110

as needed

Front 111

What is the DOC for asthma exacerbations?

Back 111

SABA

Front 112

Do short acting anticholinergics improve lung function?

Back 112

yes

Front 113

Name 2 antichoinergic medications.

Back 113

atrovent (ipratopium)

budesamide (formorterol)

Front 114

Are SABA permitted for relief of acute dyspnea?

Back 114

yes

Front 115

How do albuterol and atrovent compare to one another?

Back 115

they both improve lung function to a similar degree

side effects are minimal

Front 116

The degree of bronchodilation achieved by SABA and anticholinergics is _________, especially when submaximal doses of each agent are combined.

Back 116

additive

Front 117

In COPD, are anticholinergics or SABA superior?

Back 117

anticholinergics (atrovent)

Front 118

Atrovent (ipratropium) may result in improvement in ______.

Back 118

quality of life

Front 119

These medications are used in combination with inhaled glucocorticoids for patients with moderate or severe asthma whose symptoms are inadequately controlled on inhaled glucocorticoid therapy alone, especially when nocturnal symptoms are problematic.

Back 119

Long-acting beta agonists (LABAs), formoterol and salmeterol

Front 120

LABAs have ________ effects with inhaled glucocorticoids (LAG) when the two agents are used in combination

Back 120

additive

Front 121

______ should NEVER be prescribed as monotherapy for asthma

Back 121

LABA

Front 122

A regularly scheduled ________ is added in patients, who have more advanced disease. What two medications are acceptable to prescribe?

Back 122

long-acting inhaled bronchodilator

LABA or long acting anticholinergic

Front 123

Initial selection of a long acting bronchodilator is often based on what criteria?

Back 123

patient specific needs, co-morbidities, and side effects

Front 124

What is the dose of epinephrine to treat acute asthma/bronchospasm exacerbation?

Back 124

0.01 mg/kg to a max dose of 0.3 mg

Front 125

How can epinephrine be administered?

Back 125

IM or SC (according to the ppt)

guess she forgot about IV access

Front 126

Epinephrine is reserved for times when?

Back 126

nebulized therapy is either unavailbale to ineffective clinically

Front 127

Is nebulized epinephrine usually more for croup or bronchospasm?

Back 127

croup

Front 128

What is the MOA of epinephrine in asthma?

Back 128

Epinephrine constricts pre-capillary arterioles in the upper airway mucosa, DECREASING capillary hydrostatic pressure, leading to fluid resorption and improvement in airway edema

Front 129

Does epinephrine increase or decrease hydrostatic pressure in asthma?

Back 129

decreases

Front 130

Anticholinergics are derivatives of?

Back 130

atropine

Front 131

What condition are anticholinergics only approved for? But also used in _____?

Back 131

COPD

asthma

Front 132

How do anticholinergics work?

Back 132

reduce bronchospasm and mucus

Front 133

Name 3 anticholingeric medications used for COPD and asthma.

Back 133

Atrovent (ipratropium)

combivnet (combo of atrovent and albuterol)

spiriva (tiotropium)

Front 134

What is the onset time for atrovent? How long does it last? How is it adminisered?

Back 134

30 minutes

6 hours

MDI or nebulizer

Front 135

What other condition can combivent be use for? What route is it administered?

Back 135

allergic rhinitis

intranasally

Front 136

What are the effects of glucocorticoids?

Back 136

Decreases release of inflammatory mediator
Decreases infiltration and action of WBC’s
Decreases airway edema
Decreases airway mucus production
Increases number of beta-2 receptors
Increases sensitivity of beta-2 receptors

Front 137

What are some characteristics of systemic glucocorticoids?

Back 137

stronger effects

more side effects, esp with long term therapy

action is UNAFFECTED by lung restriction

Front 138

What are some characteristics of inhaled glucocorticoids?

Back 138

1. localized action

2. fewer side effects; some absorption occurs

3. action AFFECTED by lung restriction (disease may prevent penetration of drug to affected areas

Front 139

Name some inhaled corticosteroids?

Back 139

Fluticasone (Flovent) MDI

-Advair Diskus DPI (combo fluticasone with salmeterol)

-Flunisolide (Aerobid) MDI

-Budesonide (Pulmicor Turbohaler) DPI, neb

-Beclomethasone QVAR (MDI)

-Triamcinolone (Azmacort) MDI

-Almost all of these also have intranasal preparations for allergic rhinitis