Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > respiratory drugs > Flashcards

respiratory drugs Flashcards

1
Q

Respiratory stimulant

A

Doxapram (Respiram)
-supposedly direct stimulation of respiratory center
-used in neonatal animals and anesthesia

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

Depression of respiration

A

Many drugs that negatively impact respiration
= OPIATES **reversed by Naloxone
=Any highly active sedatives= Barbiturates

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

Coughing

A

Protective reflex, not necessary a pathological sign.

Productive (mucus and debris in airway) vs. non-productive cough (irritation, but not there)

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

Contributors to coughing

A

-Glottis/trachea/bronchi pathology

-Mechanical stimuli

-inflammation

-pulmonary edema and left sided Heart Failure

-drug adverse events (ACE inhiibition)

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

Mechanism of coughing

A
  1. stimuli
  2. stimulates larynx, trachea, bronchi
  3. Afferent limb and vagal nerves to the Cough center in Medulla Oblongata
  4. Efferent limb motor nerves to the laryngeal and respiratory systems
  5. COUGH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Antitussive drugs

A

Opioids- suppress cough center in medulla. Mediated through mu and K receptors

  1. mu agonists
    -Morphine
    -Codeine (increased oral bioavailabiliy, decreased analgesia compared to morphine)
    -Hydrocodone
  2. K agonists
    -Butorphanol (formerly approved in Canada)
    1, 5mg oral tablets
    -poor oral availability, so higher dose than used for equine IV injection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Topical analgesics

A

Work on preventing stimulation affecting the larynx, trachea, bronchi

“sooth the throat”

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

Expectorant

A

increase mucus hydration to volumes more easily expectorated by coughing

eg. Guaifenesin- muscle relaxant

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

Mucokinetics

A

-increase mucus transportability by coughing

eg. ambroxol

-no evidence that it works

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

Mucolytics

A

-reduce mucus viscosity by cleaving mucin disulfide bonds

-no evidence that they work

eg. N-actylcysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mucoregulators

A

-reduce mucus hypersecretion

-no evidence they work

-Anticholinergics

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

Airway inflammation

A
  1. infectious
  2. non-infectious
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Infections inflammatory airway disease

A

-bacterial or viral

-consider antibiotics (anti-virals)

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

non-infectious inflammatory airway disease

A

-can occur without infection
-typically some form of allergic disease
-typically use bronchodilators and anti-inflammatories

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

Goals of therapy for inflammatory airway disease

A
  1. maintain near normal pulmonary function
  2. prevent recurrent episodes of dyspnea and reduce emergency visits
  3. provide optimal pharmacotherapy with min adverse effects
  4. improve QOL for animal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

feline asthma

A

-linked with mast cells and feline airway is therefore responsive to serotonin

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

Canine bronchitis and Equine RAO

A

-responsive to cyclo-oxygenase pathway products (PGE inhibition)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Species specific effective therapy for inflammatory airway disease

A

May be species specific due to inflammatory mediators causing bronchoconstriction
**differences in airway reactivity

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

Treatment of inflammatory airway disease

A

Combination of anti inflammatories and bronchodilators together!

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

Inflammatory disease

A
  • Easy to breath in, difficult to breath out (EXPIRATION is issue!)
    >more they try and breath out, more that airways collapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Airway resistance

A

Resistance and airflow are inversely proportional
*resistance is determined by radius of tube (decrease radius=increased resistance)

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

Physiology of airway constriction during airway disease

A

Inflammatory mediators increase= increase in Ach= constriction and mucus= BAD

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

Physiology of normal relaxation of airways

A

Beta 2 agonists= muscle relaxation= GOOD

Beta 2= Bronchodilation!

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

Beta 2 adrenergic receptor agonists and effects on smooth muscle

A

Bronchial smooth muscle is innervated by beta 2 adrenergic receptors

Results in increased activity of adenylate cyclase= increase in cyclic AMP which leads to relaxation of bronchial smooth muscle

25
Q

Beta 2 agonists impact on mast cells and mucus

A

Mast cells
-beta agonists stimulate beta receptors on mast cells leading to decreased release of inflammatory mediators (but not other inflammatory cells)

Increased Mucociliary clearance

26
Q

Epi

A

Stimulates both alpha and beta receptors, producing vasopressive and cardiac effects

-reserved for emergency treatment of life threatening bronchoconstriction (eg. anaphylaxis)

27
Q

Why not use Epi for chronic therapy of respiratory inflammatory conditions?

A

-side effects (nonspecific stimulation of alpha 1 and beta 1 receptors)
-short duration of action

28
Q

Clenbuterol (Ventipulmin)

A

-Oral syrup

-beta 2 agonist approved for RAO in horses

-mostly effects airways in horses, not much on cardio system

-opens airways, but does not deal with the allergy. Open airways mean more of what horse is allergic to can enter
Therefore conflicting evidence of efficacy when used as sole therapy for treating RAO.

29
Q

Adverse effects of clenbuterol

A

1.tachycardia and muscle tremors
-beta 2 seletive initially, then becomes beta 1 (increase HR, lipolysis)

  1. Tocolytic= uterine relaxation
  2. Banned in food animals.
    -Residues in food can cause cardiotoxicity in humans
    -residues detected in tissues up to yrs later
    -Fat breakdown, muscle build lead to a lot of misuse of the drug =non steroidal anabolic drug
30
Q

Why would someone misuse Clenbuterol in food animals?

A

-increased skeletal muscle blood flow
-lipolysis

**non steroidal Anabolic drug but not an anabolic steroid

31
Q

Compounded clenbuterol

A

-Very risky
-variation with the potency of the drug can lead to many sick animals and deaths

32
Q

Salbutamol aka albuterol

A

-blue inhaler
-Aerosol route= very rapid onset, little systemic effect
-often used in cats and horses
-intended for acute bronchoconstriction events

33
Q

Why is salbutamol/albuterol not intended for repeated chronic use?

A

-Can lead to beta receptor down regulation resulting in less bronchodilation effects

-The S-enantiomer may also exacerbate airway inflammation in cats

34
Q

Ideal drug use for respiratory

A

beta 2 Drugs work in the lungs with minimal systemic effects
-problem is that animals cannot time the puff

35
Q

Nebulization

A

Creating tiny drug droplets that can be inhaled in lungs

36
Q

Puffers

A

metered dose inhalers

37
Q

Masks/spacing chambers

A

-nebulized particles inhaled over multiple breaths
-less drug deposited on oropharynx
-animal use!

38
Q

Theophylline

A

-widely used in humans
-injectables, aqueous solutions, elixirs, tablets, capsules
-smilar to beta 2 agonists
-use disappeared

39
Q

Anticholinegics goal

A

-inhibit vagally mediated bronchial smooth muscle tone= bronchodilation

40
Q

anticholinergics Use

A
  1. Asthmatic humans may have excessive cholinergic stimulation
  2. Experimental feline asthma- long term antigen exposure can increase muscarinic receptor response to Ach
41
Q

Anticholinergic options

A
  1. Atropine
  2. Glycopyrrolate
  3. Ipratropium bromide
42
Q

Atropine

A

-use for RAO in horses
-side effects: colic and ileus
increased HR and mydriasis

43
Q

Glycopyrrolate

A

-mostly used during anesthesia
-bronchodilation=decrease in BP

44
Q

Glucocorticoids

A

Historic therapy for horses, dogs and cats
-high dose chronic oral glucocorticoids with the beta 2 agonists

45
Q

Why use steroids?

A

BLUNT INFLAMMATORY RESPONSE:
-suppress generation of cytokines
-decrease recruitment of airway eosinophils (decreased leukotrienes)

46
Q

Benefits of glucocorticoids on airway

A
  1. decreased severity of airway inflammatory symptoms
  2. decreased airway response to ongoing allergens
  3. possibly prevent airway wall remodelling

**increase effective airway radius=increased airflow

47
Q

Concerns of using glucocorticoids

A

-side effects
*use lowest effective dose!

48
Q

Inhalent Glucocorticoids

A

-less systemic absorption, decreased HPA suppression

-Options: Fluticasone (most potent), Ciclesonide

49
Q

Fluticasone

A

-Flovent
-most potent, longest acting glucocorticoids
-available as puffer

50
Q

Ciclesonide

A

-for horses
-enzymatically converted to the pharmacologically active metabolite
-expensive

51
Q

How is ciclesonide administered?

A

-In horses left nostril
-use intranasal inhaler
-8-12 actuations per dose
-343 mcg ciclesonide/puff

52
Q

Side effects of Ciclesonide

A

-coughing
-nasal discharge

**note: a lot of the medication gets stuck in nose rather than reaching airway… likely absorbed by mucosa

53
Q

Efficacy of Ciclesonide

A

-52% vs 33% (placebo) improvement in respiratory scores

-73% vs 43% (placebo) after 10 days

54
Q

Purpose of using bronchodilator for inflammatory airway disease

A

Treatment of inflammatory airway disease signs
-BUT causes downregulation of beta2 receptors with chronic use

**only use as needed for rescue therapy when clinical signs flare up

55
Q

Purpose of steroid use for inflammatory airway disease

A

Prevention of airway inflammation
-used chronically even when clinical signs not apparent

56
Q

Steps for using both glucocorticoids and bronchodilators together

A

Use together for best results
-use bronchodilator first to maximize absorption by dilating airways
-use aerosolized steroid second which will be more readily absorbed

57
Q

Environmental modifications for airway disease

A

For RAO: hay nets, moisten feed, outdoor vs indoor housing
eg. moldy hay

For small animals: indoor air quality, allergens

58
Q

Anti-leukotriene drugs

A

-used in human asthma
-used as chronic therapy of inflammation, not acute bronchoconstriction

**Note: leukotrienes do not cause bronchoconstriction in cats, so drug often no effect

59
Q

Cyproheptadine

A

-blocks H1 receptor and serotonin receptor
-may be used in cats who are sensitive to serotonin induced respiratory inflammation

Pharmacology (33 decks)

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