Exam 1 Respiratory Flashcards

1
Q

Airway smooth muscle extends to

A

distal terminal bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Airway smooth muscles are influence by

A

PSNS and SNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Thoracic ganglia of the SNS innervate

A

smooth muscles of bronchi and pulmonary blood vessels

tracheobronchial blood vessels and glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sympathetic tone is

A

bronchodilation via beta 2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Vagus nerve of the PSNS system innervates

A

smooth muscles of bronchi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Beta adrenergic receptors located in the

A

smooth muscle of the blood vessels, skin muscle mesentary and bronchial smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

B2 adrenoreceptors cause

A

widening of airways (bronchodilation)

increase intracellular cyclic AMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Nonadrenergic non-cholinergic nerves (NANC)

A

influences on inflammation and smooth muscle tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

M3

A

mediate bronchoconstriction via the activation of IP3 which increases the intracellular Ca2+ concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Asthma causes recurrent episodes of

A
wheezing
breathlessness
chest tightness
cough (night and early am)
tachypnea
prolonged expiration phase of respiration
fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Asthma is

A

a chronic inflammatory disorder of the airways characterized by increase responsiveness of the tracheobronchial tree to a variety of stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Asthma creates airways that are

A

inflammed, edematous
bronchial hypersensitivity/reactivity to irritant stimuli
difficult with air outflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Degree of airway hyper-responsiveness and bronchoconstriction parallels

A

the extent of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Asthma is characterized by

A

inflammation
hyperreactivity
reversible airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

airway hyper-responsiveness and inflammation from allergen in bronchial mucosa leads to

A

activation of T2 lyphmocytes and cytokine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Asthma medications are aimed

A

at flattening the response to the mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Asthma mediators

A
eosinophils
mast cells
neutrophils
macrophages
basophils
T lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Probably mediators of acute bronchoconstriction

A

cytokines, interleukins
arachiddonic acid metabolites, leukotrienes and prostraglandins
histamine, adenosine and platelet activating factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Atopic Extrinisic asthama

A

produced by an allergen and IgE synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

COPD Factors

A
genes
smoking
age/gender
lung growth/development
exposure to particles: cigarette smoke, occupational dust and fumes, indoor air pollution
socioeconomic status
asthma/bronchial hyperactivity
chronic bronchitis
infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Neutrophils/marcophages

A

COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Esinophils/ mast cells

A

asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

COPD/Emphysema/Bronchitis

A

cell death of destruction of the alveoli, thickening of membrane air gas exchange over inflated alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Obstruction is either

A

not reversible or incompletely reversible by bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cell death is caused by

A

desctruction of alveoli due to lung parenchyma, degraded matrix and toxic actions of inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

COPD

A

results in enlargement of air spaces, fibrosis, and increase mucous production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Steroids have

A

limited effect on inflammation process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Inhaled corticosteroids help

A

reduce frequency of excerbations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Bronchodilators in COPD

A

best for patients with chronic breathlessness “worsened by exertion”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Steps of Airway Outflow Disorders

A
step 1: short acting bronchodilators
step 2: regular inhaled corticosteroids
step 3: long acting bronchodilators
step 4: PDE inhibitors, methyxanthines, leukotriene inhbitor
Step 5: oral corticosteroid
other- cromolyns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Bronchdilators

A

B2 agonist
anticholinergics
methylxanthines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Receptor selectivity to B2 is ____ more times more strongly than B1

A

200-400

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Short acting Beta agonist

A

terbutaline, albuterol, levalbuterol, salbutamol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Long acting beta agonist

A

salmeterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

MOA of Beta Agonist

A

Coupled to stimluatory G proteins
activate adenlyl cyclase which increases the production of cAMP which leads to bronchodilation, reduced Ca release and alters membrane conductance
inhibits mediator release from mast cells
increases mucous clearance by action of the cilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pharmacokinetics of B adrenergic agonist

A
rapid onset of action (within minutes)
short DOA (4-6 hours)
good for use as a rescue inhaler
given: inhalation/aerosol
powder or nebulized
orally or injected (SC)
short or long acting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Side effects of Beta Adrenegic agonist

A
minimized by inhalation delivery
tremor
increased HR
vasodilation
metabolic changes (hypok, hyperg, hypomagnesmia)
38
Q

Albuterol

A

preferred selective beta 2 agonist

39
Q

Albuterol Dose

A

100mcg/puff
2 puff 4-6hrs
nebulizer 2.5-5mg in 5ml of saline

40
Q

DOA of albuterol

A

4 hours with some relief evident up to 8 hours

41
Q

R albuterol has more affinity

A

to beta 2

42
Q

S albuterol more affinity

A

to beta 1

43
Q

Albuterol has _____ effects with volatile anesthetics on bronchomotor tone

A

addictive

44
Q

Side effects of Albuterol

A

tachycardia, hypokalemia

45
Q

Anesthetic use of Albuterol

A

4 puffs blunt airway response to tracheal intubation in asthmatic patients

46
Q

Metaproterenol-alupent

A

beta 2 agonist for treatment of asthma
administered via metered dose
not to exceed 16 puff/day

47
Q

Pirbuterol-Maxair

A

beta two agonist
2 puffs (400mcg) via metered dose
not to exceed 12 inhalations/day

48
Q

Terbutaline

A

administered SC,oral, inhalation
treats asthma
SC administration resembles epi response

49
Q

Terbutaline SC dose for children

A

0.01mg/kg

50
Q

Terbutaline SC dose for adult

A

0.25mg q15 min

51
Q

Terbutaline Metered dose inhaler is and each dose is

A

16-20puff/day

200mcgs

52
Q

Long acting B agonist examples

A

salmeterol
combination with fluticasone
formoterol

53
Q

Long acting B agonist

A

have liphophic side chains that resist degradtion
duration 12-24 hours
good for prevention not flare up

54
Q

MOA of bronchodilators/anticholinergics

A

competitive antagonist at muscarinic acetylcholine receptors

55
Q

Uses of bronchodilators/anticholinergics

A

treatment of COPD

secondary line of treatment for asthma in patients resistant to beta agonist or significant cardiac disease

56
Q

Examples of Bronchodilators/Anticholinergics

A

atropine
ipratropium bromide
tiotropium

57
Q

Atropine

A

naturally occuring alkaloid
highly absorbed across respiratory epithelium
causes systemic anticholinergic effects (tachycardia, dry mouth, nausea, Gi upset)

58
Q

How is atropine dosed

A

1-2 mg diluted in 3-5 ml sof saline via nebulizer

59
Q

Ipratropium bromide

A

quaternary ammonium salt derivative of atropine

antagonizes endongenous ach at m3

60
Q

Dose of Ipratropium bromide

A

40-80mcg via metered dose in 2-4 puffs via nebulizer

61
Q

DOA and onset of Ipratropium bromide

A

slow onset 30 minutes

DOA 4-6 hours

62
Q

Compared to atropine, Ipratropium bromide is ____

A

not siginicantly absorbed

63
Q

S/E of Ipratropium bromide

A

inadvertent oral absorption

dry mouth and GI upset

64
Q

Tiotropium

A

quaternary ammonium salt
long acting anticholinergic
not significantly absorbed across resp epithelium= few side effects
approved by FDA for COPD

65
Q

COPD medications

A

tiotropium
Ipratropium bromide
atropine

66
Q

Examples of Methylxanthines- Phosphodiesterase Inhibitors

A

Theophylline, Aminophylline

67
Q

MOA of Methylxanthines

A

nonspecific inhibition of phosphodieterase isoenzymes (types 3 and 4) which prevent cAMP degradtion in airway smooth muscle as well as in inflammatory cells

68
Q

PDIs have multiple MOAs and are nonselective they have

A

various side effects and have a narrow TI

69
Q

theophylline

A

therapeutic plasma level of 10-20mcg/ml
toxic at >20mcg/ml
Susceptile to drug to drug interactions due to metabolism by CYP 450 (cimetidine and antifungals ie CYP 450 inhibitors)… increase level of drug
metabolized in liver excreted in kidney

70
Q

What drug do you have to caution with halothene?

A

theophylline

71
Q

Side Effects of PDI

A
headache
N/V
irritability/restlessness
insomnia
cardiac arrthymias
seizures
SJS
72
Q

Anti-Inflammatory agents

A

inhaled corticosteroids
cromolyns
leukotriene inhibitors
anti- IgE antibodies

73
Q

Examples of Inhaled corticosteroids

A

beclomethasone
triamcinolone
fluticasone
budensonide

74
Q

Pre-op Considerations with inhalated corticosteroids

A

may consider use of corticosteroid administration 1-2 hours preop
they prolong the response of beta agonist
may consider 5 day course of combined corticosteroid and albuterol to minimize the risk of intubation evoked bronchospasm

75
Q

Inhaled corticosteroids

A

reduce the number of inflammatory cells in the airways and the damage to airway epithelium
vascular permeability is reduced which decreases airway edema
overall reduction in airway hyper-sensitivity

76
Q

inhaled corticosteroids are considered the most

A

important drug in management of asthma

major preventative treatment for patients with asthma

77
Q

MOA of Inhaled Corticosteroids

A

alters gene transcription
increases transcription of genes for beta 2 receptor and anti-inflammatory proteins
decreases transcription of genes for pro-inflammatory proteins
induce apoptosis in inflammatory cells (esinophils, TH2, lymphocytes)
indirect inhibition of mast cells over time
reverses many ft of asthma
used as suppressive therapy not a cure

78
Q

Side Effects of Corticosteroids

A
oropharyngeal candidiasis
osteopenia/osteoporosis
delayed growth in children
hoarseness
hyperglycemia
79
Q

Cromolyn

A

stabilizes mast cells

80
Q

MOA of Cromolyn

A

inhibits antigen-induced release of histamine
including release of inflammatory mediators from eosinophils, neutrophils, monocytes, macrophages, lymphocytes, and leukotrienes form pulm mast cells
inhibits allergic response to antigen but not the allergic response once it has been activated

81
Q

Administration of Cromolyn

A

inhalation 8-10% enters the systemic circulation

take 4x daily

82
Q

How much inhaled dose reaches oropharynx is swallow of inhaled corticosteroids

A

80-90%

83
Q

How much inhaled corticosteroid reaches airway

A

25%

84
Q

Principle use of cromolyn

A

prophlaytic therapy of bronchial asthma

85
Q

Cromolyn does not

A

relieve allergic response after initiation

not a rescue inhaler

86
Q

S/e of cromolyn are

A

laryngeal edema
angioedema
uticaria
anaphylaxis

87
Q

Leukotriene Inhibitors

A

synthesized from arachidonic acid when inflammatory cells are activatd
not effective in the treatment of acute asthma attacks
few extrapulmonary effects

88
Q

Leukotriene Inhibitor examples

A

zileuton

montelukast

89
Q

Zileuton

A

lipoxygenase inhibitor which blocks the biosynthesis of leukotrienes from arachiondic acid
produces bronchodilation, improves asthma symptoms and has shown long term improvements in PFTs
low bioavailability, low potency and significant adverse effects
hepatotoxic
no widely used

90
Q

Montelukast-singulair

A

leukotriene receptor antagonist block the mechanism of bronchoconstriction and smooth muscle effects
blocks the ability of leukotrienes to bind to cysteinyl-leukotriene 1 receptor
improve bronchial tone, pulm function, and asthma symptoms

91
Q

Montelukast-singulair with warfin

A

can result in prolonged PT

92
Q

Omalizumab

A

monoclonal antibody derived from DNA
given in the early and late phase of asthmatic response
given SC 2-4 parenterally infused
high cost and incovenience
binds to igE (decrease IgE circulating quantity and prevent IgE from binding to mast cell)
down regulation of receptors
adverse effet: triggering of immune response