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Pharmacology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Where a.w smooth muscle extends to

A

Terminal bronchioles

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2
Q

SNS action and activation of which receptor

A

B2 adrenoreceptors mediate relaxation of smooth muscles in vessels, bronchi, uterus, bladder, and other organs. Activation= bronchodilation, increased cAMP

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3
Q

Non adrenergic, non cholinergic nerves

Do what to a/w

A

Relax smooth muscle by releasing NO and VIP

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4
Q

PSNS
Action
Receptors
Pathway

A

Stim vagus leads to bronchoconstriction. M3 receptors are pharmacologically most imp. In bronchial muscle, mediate constriction by activ of IP3 which increases intracellular Ca. Mediates mucus secretion

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5
Q

ANS impact on resp system through 2 things

A

Adrenergic B2: bronchial smooth muscle relaxation, bronchodilation
Cholinergic: smooth muscl contraction, increased gland secretion- constriction and inc mucus

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6
Q

Asthma results in what

S/s

A

Variable airflow obstruction that’s reversible.

Breathlessness, tight chest, wheeze, dyspnea, cough

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7
Q

What you’re addressing w drugs in asthma

2 main classes

A

Inflammation and bronchoconstriction

  1. Anti-inflammatories- steroids, prednisone
  2. Bronchodilators- B2 agonists, albuterol
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8
Q

Which drugs taken for asthma daily for long term control

A 
Anti inflammatories 
Inhaled corticosteroids 
Cromolyns 
Leukotriene inhibitors 
Anti IgE antibodies
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9
Q

Most important preventative tx for asthma

A

Glucocorticoids

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10
Q

Glucocorticoids

MOA

A

Suppress inflammation by altering genetic transcription

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11
Q

Glucocorticoids

Target

A

Glucocorticoids receptor alpha in cytoplasm of a/w epithelial cells.

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12
Q

Glucocorticoid transcription effects: 3

A

Inc transcription of genes for: B2 receptors/responsiveness, anti-inflammatory proteins
Decreases transcription of genes for pro inflammatory proteins: decreases mucus production and edema

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13
Q

Glucocorticoids

3 other effects than transcription

A

Induces apoptosis in inflammatory cells (eosinophils, th2, lymphocytes)
Indirect inhibition of mast cells over time
Reverses bronchial hyperreactivity

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14
Q

Glucocorticoids
Use, what it doesnt do
Usual route

A

Suppressive therapy, not a cure

Inhalation. (IV and oral also available)

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15
Q

Inhaled corticosteroids

Use

A

Long term prophylaxis in mod to severe asthma

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16
Q

Inhaled steroids

Which nebulized for who

A

Budesonide, kids too young to use MDI or DPI

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17
Q

Inhaled steroids

4

A

Budesonide
Beclomethasone
Triamcinolone
Fluticasone

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18
Q

IV steroids, use in asthma, 2

A

Hydrocortisone and methylprednisone, status asthmaticus

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19
Q

Corticosteroids

PO- for what, 2 ex

A

Acute exac, chronic severe asthma.

Prednisone and prednisolone

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20
Q

Inhaled corticosteroid
How much reaches airway, what increases concentration in lung
Conc in lung compared to PO
Adrenal suppression compared to PO/iv

A

10-20%, beta 2 agonist before inhalation
Higher
Mild

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21
Q

Inhaled corticosteroid

Side effects

A

Candidiasis
Hoarseness
Delayed growth kids
Osteopenia/porosis

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22
Q

Systemic corticosteroids AE
When minor
Long term effects

A

<10 days

Weakness, adrenal suppression, infection risk, growth suppression, PUD, wt gain, edema, hypokalemia, hyperglycemia

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23
Q

Systemic corticosteroids

Give extra when or what

A

IV or PO during physiologic stress (surgery, trauma, infection) or pt could die

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24
Q

Cromolyn

MOA

A

Stabilizes pulmonary mast cells. Inhibits antigen induced release of histamine, inflammatory mediators from: eos, neutro, mono, mac, lymph, Leuko. Inhib allergic response to antigen but not once its activated

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25
Q

Cromolyn

Principle use

A

Bronchial asthma prophylaxis, prevents exercise induced bronchospasm. Not a rescue inhaler.

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26
Q

Cromolyn
Route
How much goes systemic
Take how often

A

Inhalation
8-10%
4 times daily

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27
Q

Cromolyn
SE
Comparison to other asthma meds
Route

A

Cough, bronchospasm, laryngeal edema, angioedema, urticaria, anaphylaxis
Safest of them all, SE rare
Neb or MDI

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28
Q

Leukotriene modifiers

How leukotrienes are synthesized, which we’re concerned about and why

A

From Arachidonic acid when inflammatory cells are activated. C4, D4, E4. Promote bronchoconstriction, eosinophils, mucus, and airway edema

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29
Q

Leukotriene modifiers
Comparison to glucocorticoids
Not effective for
Few what

A

Less effective
Acute attacks
Extrapulmonary effects

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30
Q

Leukotriene modifiers

3 ex

A

Zyflo (zileuton)
Accolate (zafirlukast)
Montelukast/singular

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31
Q

Zileuton
Class
Action
Uses

A

Leukotriene inhib.
Lipoxygenase inhib, blocks leukotriene synth from arachidonic acid
Bronchodilation, for asthma, long term improvement PFT

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32
Q

Zileuton
Metab
AE

A 
Low bioavailability and low potency 
Hepatotoxic- monitor LFT early 
Neuro: depression, anxiety, halluc, suicidal thinking 
Interacts w CYP450 
Not widely used
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33
Q

Montelukast

Action

A

Blocks bronchoconstriction and smooth muscle effects. Blocks binding to leukotriene 1 receptor. Improves bronchial tone, pulm function, and asthma symptoms

34
Q

Montelukast

Use in who

A

Asthma in <1 y/o, exercised induced bronchospasm >15 y/o, allergic rhinitis

35
Q 
Montelukast 
Adverse effects 
Max effect when 
Metab
What inc drug level
A

Placebo, rare psych effects
24 hrs after 1st dose
99% protein bound, by cyp 450, minimal interactions
Phenytoin

36
Q

Omalizumab
Class
Target

A

Anti IgE antibodies. Mouse monoclonal antibody.

IgE mediated allergic responses in asthma

37
Q

Omalizumab

Action

A

Binds to IgE and inactivates it. Decreases overall amt, prevents IgE binding to mast cells. Down regulates receptors on mast/baso/dendritic cells. Reduces stim T2 lymph.

38
Q 
Omalizumab 
Downside 
Route 
Taken when 
1/2 life
A

10k per year
Sq
Allergy induced asthma not tx by glucocorticoids
26 days

39
Q

Omalizumab

SE

A

Injection site rxn, viral infec, URI, sinusitis, HA, pharyngitis, CV (inc MI and CVA, HF, dysrhythmias, thromboembolism risk), possible inc risk cancer

40
Q

Omalizumab

Rare AE

A

Triggers anaphylaxis. Monitor 2 hrs after first three doses, then 30 min after all subsequent doses

41
Q

Bronchodilators

How they work

A

Symptomatic relief, dont tx underlying cause of inflammation.
Should also take glucocorticoids

42
Q

Bronchodilators

3 types

A

Beta adrenergic agonists
Anticholinergics
Methylxanthines

43
Q

B adrenergic agonists

MOA

A

B adrenergic receptors coupled to stim G proteins. Activate adenylyl cyclase which inc cAMP, then bronchodil. Dec Ca inc K. Dilates bronchi, smooth muscle relax, inhib mast cell and inc mucus clearance

44
Q

B adrenergic agonists

Most effective drugs for

A

Acute bronchospasm and prevention of exercise induced bronchospasm. Quick relief and long term control

45
Q

B adrenergic agonists
Receptor selectivity
Short v long acting types

A

B2 200-400x more than b1
Short: albuterol, levalbuterol
Long: salmetrol, terbutaline (po or iv)

46
Q

B adrenergic agonists
Onset
Routes

A

15-30 min. Short or long acting
Inhalation, aerosol
Powder, neb
Orally or sc

47
Q

B adrenergic agonists

SE

A

Minimized by inhalation route. Tremor, inc HR, vasodilation, hyperglycemia, hypokalemia, hypomagnesemia

48
Q

B adrenergic agonists

Oral preps excessive dose leads to

A

Angina and tacky dysrhythmias

49
Q

Albuterol

Doses

A

MDI: 100 mcg/puff. 2 puffs q4-6 h
Neb: 2.5-5 mg in 5 ml saline

50
Q

Albuterol
Duration
Isomers

A

4 hrs, up to 8 hrs.

R albuterol levalbuterol, more affinity B2.
S albuterol, more affinity b1.

51
Q

Metaproterenol
Indic
Route
Max dose

A

Beta 2 agonist for asthma. MDI

16 puffs a day

52
Q 
Bitolterol 
Class 
Duration 
AE 
Dose
A

Selective B2 lasts longer than albuterol
Rare cv effects
Metered dose 16-20 puffs a day. Each dose 270 mcgs

53
Q

Terbutaline
Class
Routes
Indic

A

B adrenergic agonist
Oral, sc, inhalation
Treats asthma

54
Q 
Terbutaline 
Sc admin resembles 
Sc dose peds 
Sc dose adults 
Medi dose and amt
A 
Epi response 
0.1 mg/kg
0.25 mg q15 min 
16-20 puffs/day 
Each dose 200 mcgs
55
Q 
Salmetrol 
Class 
Other drug like it 
Duration 
For what 
Warning
A

Formoterol. Long acting b agonist
12-24 h, lipophilic side chains
Prevention not flare up
May inc risk of fatal asthma attack

56
Q

Methylxanthines
Class
MOA

A

Bronchodilators, phosphodiesterase inhib
Unclear. May inhib pdi isoenxymes and prevent camp degred in airway. Anti inflammatory. Possible adenosine receptor block

57
Q

Methylxanthines
Drug effect
Clinical applic
Types

A

Airway relaxation and bronchodilation
COPD and asthma
Theophylline and aminophylline

58
Q 
Methylxanthines 
Theophylline 
Downside 
Therap plasma level
When toxic 
1/2 life
A

Mult SE and narrow therapeutic index
10-20 mg/ml
>20 mg/ml
Wide variation, esp smokers who metab faster

59
Q

Methylxanthines

Drug interactions

A

Cimetidine, cipro, and antifungals inc levels (cp450 inhib)
Phenobarbital and phenytoin decrease levels
Caffeine can inc levels and be toxic to cns and cv

60
Q

Methylxanthines
Metab and excretion
Only in what form

A

Liver, kidney

Sustained release only

61
Q

Methylxanthines

SE

A

Cv arrhythmias
NV
Irritable, insomnia, seizures, brain damage, hyperglycemia, hypokalemia, hypotension,death from cv collapse

62
Q

Muscarinic receptor antagonists

MOA

A

Competitive antagonists at muscarinic acetylcholine receptors.
Promotes smooth musc relax and decreased mucus secretion

63
Q

Muscarinic receptor antag
Which subtype most imp
Uses

A

Muscarinic 3

Tx COPD, secondary line of tx for asthma in pts resistant to beta agonist or significant cv disease

64
Q

What m3 receptors do when stimulated

A

Drop inflammatory mediators

65
Q

Atropine
What it is
Indic
Dose

A

Naturally occurring alkaloid
Used to be 1st line for asthma
1-2 mg diluted in 3-5 ml saline via neb

66
Q

Atropine
Absorption
SE

A

Highly abs across respiratory epithelium

Systemic anticholinergic fx: tachycardia, nausea, dry mouth, gi upset

67
Q

Ipratropium bromide
What it is
What it does

A

Quaternary ammonium salt, deriv of atropine. Anticholinergic
Antagonists effect of ach at M3

68
Q 
Ipratropium 
Dose 
Onset 
Duration 
Absorption
A

40-80mcg MDI or in 2-4 puffs via neb
30-90 min
4-6 hours
Not absorbed as well as atropine. Inadvertent oral abs can lead to gi upset and dry mouth

69
Q 
Tiotropium 
What it is 
Class 
Absorption 
Approved for
A

Quaternary ammonium salt
Long acting anticholinergic
Not abs sig in resp epithelium, less SE
FDA approved for COPD

70
Q

Glucocorticoid/LAB2A combos
2 types
Indic for

A

Fluticason and salmetrol (advair)
Budesonide and formoterol (symbicort)
Long term maintenance in adults and kids. Reduces symptoms

71
Q

Glucocorticoid and LAB2A combos
Not for
Black box warning

A

Initial therapy. Many pts controlled on inhaled glucocorticoid
Asthma related death inc risk

72
Q

Lab2a stands for what

A

Long acting beta 2 agonist

73
Q

Asthma
Source of allergens
What can exac it

A

Dust mites, pets, cockroaches, mold

Tobacco Smoke, wood smoke, household sprays

74
Q

Drugs for severe asthma exac

A

Give o2 (hypoxia), Systemic glucocorticoid (inflam), neb high dose Saba (obstruc), neb ipratropium (obs)

75
Q

COPD
What drugs have ltd effect
What reduces exac freq
What modestly improves air outflow

A

Steroids
Inhaled corticosteroids
Bronchodilators- for pts w breathlessness worsened by exertion

76
Q

COPD

Monotherapy started which of 3

A

Long acting beta 2 (salmetrol)
Long acting anticholinergic (tiotropium)
Inhaled glucocorticoid (budesonide)
One of the 3. Bud- last choice

77
Q

COPD

If monotherapy doesnt work then what

A

Add a second class of drug. Usually laba and a steroid

78
Q

Roflumilast (daliresp)
For what
What it does

A

New COPD drug. Selective phosphodiesterase type 4 inhib, reduces exac

79
Q

Daliresp

Moa

A

Inc cAMP levels resulting in reduced cough, inflammation, and mucus

80
Q

Daliresp

SE

A

Diarrhea, wt loss, loss of appetite, nausea, HA, back pain, depression

Pharmacology (19 decks)

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