Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Pharm > Respiratory Drugs > Flashcards

Respiratory Drugs Flashcards

1
Q

What do the SNS fibers in the lung innervate and what do they do?

A

They pass from the thoracic ganglia to the lungs to innervate smooth muscles of bronchi and pulmonary blood vessels - they bronchodilate via B2ARs

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

What do the PSNS fibers innervate in the lung and what do they do?

A

innervates lung smooth muscle of the bronchi and pulmonary blood vessels and causes bronchoconstriction via muscarinic M3 receptors

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

beta 2 agonism causes and is morse sensitive to which NT

A
  • bronchodilation
  • increased intracellular cAMP
  • more sensitive to epi than NE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

M3 receptors do what

A

mediate bronchoconstriction and mucus secretion via the activation of IP3 which increases intracellular calcium concentration

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

What is asthma?

A

chronic inflammatory disorder of the airway characterized by increased responsiveness of the tracheobronchial tree to a variety of stimuli

creates airways that are inflamed and edematous

characterized by: irritation, hyper-reactivity, and REVERSIBLE airway obstruction (air outflow problem)

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

signs and symptoms of asthma

A 
wheezing
breathlessness
chest tight
cough (night and early AM)
tachypnea
prolonged expiratory phase
fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

primary histologic mediators for asthma

A

eosinophils, mast cells, cytokines, interleukins (3,4,5), leukotrienes, and histamine

**some asthmatics are atopic and have IgE synthesis = extrinsic asthma

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

primary histologic mediators for COPD

A

neutrophils, macrophages, and T lymphocytes

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

What is COPD?

A

Obstructive pulmonary disease that is not reversible

causes cell death and destruction of alveoli due to impaired lung parenchyma and toxic actions of inflammatory cells

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

Treatment steps for airway outflow disorders

A
  1. short acting bronchodilators
  2. regular inhaled corticosteroids
  3. long acting bronchodilators
  4. phosphodiesterase inhibitors, methylxanthines, leukotriene inhibitors
  5. oral corticosteroid
    other: cromolyns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name the three types of bronchodilators (classes)

A

beta-adrenergic agonists (increase cAMP = bronchodilation)
anticholinergics (inhibit Ach and PSNS response = bronchodilation/stop constriction)
methylxanthines (stop cAMP breakdown = bronchodilation)

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

How much more selective to beta2ARs than beta1ARS are our selective B2ARs?

A

200-400x more selective

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

MOA for beta adrenergic agonists

A

BARs = gpcrs
agonist activates adenlyl cyclase to INCREASE cAMP = bronchodilation
reduced intracellular calcium alters membrane conduction

WHAT HAPPENS?

  • smooth muscle relaxation and bronchodilation
  • inhibited mediator release from mast cells
  • increased mucus clearance by action on cilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

onset of action/duration of action of short acting beta adrenergic agonists

A

onset within minutes

duration 4-6 hours

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

side effects of beta adrenergic agonists

A

tremor, increased HR, vasodilation, metabolic changes (hyperglycemia, hypokalemia, hypomagnesemia)

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

Albuterol dosing

A

administered via metered dose

  • 100 mcg/puff
  • 2 puffs q4-6h

nebulizer = 2.5-5mg in 5ml of saline

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

anesthesia considerations for albuterol

A
  • has an additive effect with our VAs on bronchomotor tone
  • 4 puffs blunt airway response to tracheal intubation in asthmatic patients
  • remember that the medicine sticks to the tubes of the circuit so you have have to give more
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Metaproterenol-Alupent

  1. what is it?
  2. how is it administered?
  3. max dose?
A
  1. B2 agonist for asthma (less selective than Maxair)
  2. administered via metered dose
  3. not to exceed 16 puffs/day
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pirbuterol-Maxair

  1. what is it?
  2. dosing info
A
  1. beta 2 agonist (more selective than alupent)

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

20
Q

Terbutaline

  1. admin
  2. indication
  3. dose
A
  1. administered oral, subq, or inhalation
  2. used to treat asthma - subq admin resembles epi
  3. Doses
    - child subq = .01 mg/kg
    - adult subq = .25 mg q 15 min
    - metered dose inhaler = 16-20 puffs per day (1 puff = 200 mcgs)
21
Q

Long acting beta agonists

  1. what are they?
  2. why are they long acting?
  3. duration
A
  1. salmeterol (there is a combo drug with fluticasone and salmeterol also) and formoterol
  2. lipophillic side chain that resists degradation
  3. good for 12-24 hours but longer onset so not good for acute situations
22
Q

MOA anticholinergics/muscarinic receptor antagonists

A
  • competitive antagonists at mAChR
  • M1 and M3 subtypes are the targets of the antagonists to mediate smooth muscle relaxation and decreased mucus secretion
  • drugs antagonize endogenous Ach
23
Q

what are the common uses for muscarinic antagonists

A
  1. COPD treatment

2. Second line treatment for asthma in patients resistant to beta agonist or patients with significant cardiac disease

24
Q

Atropine

  1. what is it
  2. how is it administered/dosed
  3. PK highlight
  4. SE
A
  1. naturally occuring alkaloid, muscarinic receptor antagonist (anticholinergic), used now for COPD
  2. administered 1-2mg in 3-5ml saline vie neb
  3. highly absorbed across respiratory endothelium
  4. tachycardia, nausea, dry mouth, GI upset
25
Q

ipratropium bromide

  1. MOA
  2. Dose
  3. onset/DOA
  4. PK highlights
  5. SE
A
  1. antagonizes effect of Ach at M3 receptor
  2. MDI 40-80mcg in 2-4 puffs via neb
  3. onset = 30 min/DOA = 4-6 hours “short acting”
  4. not as well absorbed compared to atropine (This is a good thing because less systemic side effects)
  5. accidental oral admin = dry mouth and GI upset
26
Q

tiotropium

  1. What is it?
  2. PK highlights
  3. use
A
  1. long acting anticholinergic
  2. not well absorbed across resp epithelium, so less side effects
  3. FDA approved for COPD
27
Q

rank the anticholinergics for COPD

A
  1. tiotropium
  2. ipratropium
  3. atropine
28
Q

Methylxanthines - Phosphodiesterase Inhibitors

  1. MOA
  2. clinical applications
  3. types and routes
A
  1. nonspecific inhibition of phosphodiesterase isoenzymes to prevent cAMP degradation in airway smooth muscle cells as well as in inflammatory cells leading to airway relaxation and bronchodilation
  2. clinical applications = copd and asthma
  3. theophylline = PO/aminophylline = IV
29
Q

what are the big problems with methylxanthines-phosphodiesterase inhibitors

A

they have multiple MOAs and are nonselective so they have multiple side effects and a tight therapeutic index
TOX LEVELS
- theophylline = therapeutic level = 10-20mcg/ml
-TOXIC at >20mcg/ml

they are metabolized by CYP450, so be careful with drugs that are inhibitors
renal excretion

caution with halothane?

30
Q

side effects of PDIs

A 
headache
N/V
irritability/restlessness
insomnia
arrhythmias
seizures - lowers threshold
SJS
31
Q

what are the mechanisms of bronchodilation?

A

agonistic effects on beta2ARs = increase cAMP
antagonistic effects to Ach at M3 receptor sites = increased cAMP
inhibiting breakdown of cAMP via targeting phosphodiesterase = increased cAMP

32
Q

Inhaled corticosteroids

  1. use
  2. MOA
A
  1. major preventative treatment for patients with asthma
  2. MOA = alter gene transciption by increasing B2ARs and anti-inflammatory proteins, decreasing pro-inflammatory proteins, inducing apoptosis in inflammatory cells, inhibits mast cells indirectly over time

SUPPRESSIVE THERAPY - not a cure

33
Q

what is the major preventative treatment for patients with asthma/their most important drug in asthma management

A

inhaled corticosteroids

suppressive therapy = not a cure

34
Q

what are the 3 major actions of inhaled corticosteroids

A
  1. decrease inflammatory cells and thereby damage to lungs
  2. decreases vascular permeability = less airway edema
  3. reduces airway hyper-responsiveness
35
Q

what are the types of inhaled corticosteroids?

A

beclomethasone
triamcinolone
fluticasone
budesonide

36
Q

inhaled corticosteroid considerations for surgery (3)

A
  1. administer 1-2 hours preop
  2. may prolong response of beta agonists
  3. may consider 5 day course of combined corticosteroid and albuterol to minimize the risk of intubation evoked bronchospasm
37
Q

how much of your inhaled coricosteroid reaches the airway

A

25%

38
Q

side effects of inhaled corticosteroids

A
  1. thrush
  2. osteopenia/osteoporosis
  3. delayed growth in kids
  4. hoarseness
  5. hyperglycemia
39
Q

Cromolyn MOA

A

stabilized mast cells by inhibiting release of histamine and other inflammatory mediators

***it inhibits immediate allergic response to antigen, but does not stop an allergic response that has already been activated

40
Q

administration of cromolyn

A

administered by inhalation
8-10% enters systemic circulation
give 4x a day

41
Q

what do we use cromolyn for

A

prophylactic therapy of bronchial asthma

NOT FOR RESCUE OR TO STOP AN ALLERGIC RESPONSE ALREADY STARTED

42
Q

cromolyn side effects

A

laryngeal edema
angioedema
urticaria
anaphylaxis

43
Q

leukotriene inhibitors

A

used for bronchial asthma (not for acute attack)
MOA: leukotrienes are synthesized from arachadonic acid when inflammatory cells are activated, these drugs inhibit that pathway

montelukast, zileuton

44
Q

Zileuton

A

leukotriene inhibitor that blocks biosynthesis of leukotrienes from arachiodonic acid to produce bronchodilation and improve asthma symptoms

shown long term improvement in PFT

HEPATOTOXIC - not commonly used

45
Q

montelukast

A

leukotriene inhibitor that blocks the leukotriene receptors (antagonists) to stop bronchoconstriction

caution with co-administration of warfarin, because could result in prolonged PT

46
Q

Anti-IgE Antibodies

A

by removing these antibodies from circulation, you mitigate acute response of inhaled allergen

47
Q

Omalizumab

A

monoclonal antibody derived from DNA (anti-IgE antibody)
binds to IgE to decrease quantity of circulating IgE
down regulation of receptors

RARE adverse effect = triggers immune response

Advanced Pharm (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions