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Pulmonary drugs Flashcards

(52 cards)

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1
Q

Decongestants MOA

A

alpha 1 adrenergic agonists, increase SNS

Cause vasoconstriction

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2
Q

Decongestants AE

A

HA, CV irregularities (increased BP, palpations)

*can mimic the effects of increased sympathetic NS activity

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3
Q

Who shouldn’t use Decongestants

A

Hypertensive people and people who take a beta blocker b/c cancel each other and alpha agonist drugs

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4
Q

Antitussives uses and MOA

A

Cough suppression

decrease afferent nerve activity or decrease cough center sensitivity (Codeine)

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5
Q

Antitussives are helpful in treating in what kind of cough?

A

Dry cough but their use may not be justified in treating an active, productive cough

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6
Q

How codeine MOA and what kind of cough should avoid?

A

Act to suppress cough reflex centrally

Also thicken sputum, reduce clearance- don’t take if you have wet cough

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7
Q

Antihistamines (Benadryl) MOA

A

Block histamine receptors reducing:
Mucosal irritation
Decreases sneezing caused by histamine-associated sensory neural stimulation
Decrease nasal congestion due to vascular engorgement associated with vasodilation and increased capillary permeability

acts as a local anesthetic on the respiratory epithelium

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8
Q

Antihistamines AE

A

Sedation (most common AE) and Dizziness- especially with antihistamines

GI upset (especially with opioidsconstipation)

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9
Q

Histamines normally work on what receptor and normal response

A

H1 receptor

Cause vasodilation, increased vascular permeability, sneezing, nasal congestion

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10
Q

1st generation Antihistamines vs 2nd generation Antihistamines AE

A

1st generation cross blood brain barrier so you get sedation and fatigue feeling (Benadryl) while 2nd generation do not easily cross BBB

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11
Q

What kind of pathology can use Antihistamines

A

Asthma

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12
Q

Mucolytics MOA

A

MOA: split disulfide bonds
Drugs which decrease the viscosity of respiratory secretions (mucus)
In doing so, they loosen and clear mucus from the airways (makes mucous thinner)
Reduce the energy costs of coughing

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13
Q

Expectorants

A

Facilitate the production and ejection of mucus
Causes a thinning of the mucus
Lubricates the irritated respiratory tract
Promote a productive cough
Prevent the accumulation of thick, viscous secretions

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14
Q

What do you look out for when taking cold remedies and High Blood Decongestants can mimic effects of increased sympathetic activity
Vasoconstriction can increase blood pressure
Individuals with HTN should avoid OTC products that contain: endings with
-rine

A

Decongestants can mimic effects of increased sympathetic activity
Vasoconstriction can increase blood pressure
Individuals with HTN should avoid OTC products that contain: endings with
-rine

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15
Q

What drug class to treat COPD?

A

Inhaled beta agonists
Inhaled antimuscarinics
Inhaled corticosteroids

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16
Q

Inhaled Beta Agonists MOA

A

MOA: agonize β2 receptors = bronchodilation

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17
Q

Inhaled Beta Agonists drug endings?

A

-terol

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18
Q

Inhaled Beta Agonists AE

A

generally well tolerated; although fairly selective can cause tachycardia, tremor, hypokalemia

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19
Q

Inhaled Antimuscarinics (AKA: anticholinergics) MOA

A

primarily bind M3 in airway smooth muscle; antagonizes ACh actions at these sites = bronchodilation
Molecule structure ↓ systemic absorption = ↓ anticholinergic effects

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20
Q

Inhaled Antimuscarinics (AKA: anticholinergics) AE

A

dry mouth

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21
Q

Inhaled Corticosteroids uses

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A

COPD: typically used for exacerbations or more severe disease
Unclear safety if used >3 years
If inhaled steroid is stopped, monitor for worsening sx- increase SOB

22
Q

Inhaled Corticosteroids AE

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A

oral candidiasis- rinse out mouth, hoarse voice, skin bruising; elderly on high doses: osteoporosis, cataracts

23
Q

Why take combination bronchodilators?

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A

Combining bronchodilators may increase effect with lower AE as compared to increasing the dose of a single product

24
Q

Ex of SABA/SAMA drug

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A

albuterol/ipratropium (Combivent)

25
Ex LABA/ICS drugs (2)
formoterol/budesonide (Symbicort), salmeterol/fluticasone (Advair)
26
What if inhalers aren’t working?
Disease progression Incorrect inhaler or nebulizer use Nonadherence- need education on PRN vs maintenance meds, cost concerns
27
What if patient can produce enough inhalation force
Refer to the provider to discuss if a spacing device is needed or if a change from dry powder inhaler is needed
28
When do use antibiotics?
Used in acute exacerbations Extended treatment only in patients prone to exacerbations Azithromycin 250 mg daily or 500 mg three times per week x 1 year Erythromycin 500 mg twice daily x 1 year
29
Asthma short-term and long-term treatment
short-term: SABS | long-term: ICS and LABA
30
When would you use a LABA?
Only in combo with ICS for prn relief or long-term control Helps lower ICS dose to prevent ICS AE Do NOT use alone for acute symptoms
31
What are Leukotrines?
released from mast cells and eosinophils to play a role in airway edema, smooth muscle contraction, inflammatory process
32
Leukotriene receptor antagonist (LTRA) PO drugs and MOA
montelukast (Singulair), zafirlukast (Accolate) | MOA: competitively antagonize leukotriene receptors
33
Montelukast when do you take it for allergies and when do you take it for asthma?
Alllergies: AM Asthma: PM
34
Immunomodulators: Anti-IgE drugs and MOA
omalizumab (Xolair) prevents IgE binding to receptors on mast cells and basophils  limits activation and release of allergic response mediators
35
what to look out for when taking Immunomodulators: Anti-IgE
Very rare but anaphylactic allergic reaction may occur- must administer in provider’s office
36
How often can you use SABA?
up to 3 treatments at 20 minute intervals no relief go see medical treatment
37
Drug class to treat CF?
LABA, SABA, CFTR Modulators, Mucolytics, Inhaled/PO Antibiotics
38
CF transmembrane regulator role?
is a membrane protein, and chloride channel  regulates sodium and water which helps keep mucous thin
39
Genetic mutation of CF transmembrane regulator causes?
Genetic mutations cause closing and/or narrowing CFTR or stop CFTR from getting to the cell surface
40
CFTR Modulator drugs
tezacaftor/ivacaftor (Symdeco), lumacaftor/ivacaftor (Orkambi)
41
MOA Ivacaftor and Tezacaftor/ lumacaftor
facilitate trafficking of CFTR to the cell membrane surface = improved chloride transport. Improved regulation of sodium and water = mucous thinning
42
CFTR modulators must be taken with?
with high fat meal to ↑ absorption
43
AE for CFTR Modulators
dizziness, hypertension (Orkambi only)
44
Mucolytics Drug classes
Hypertonic saline and Donase alfa (Pulmozyme)
45
Hypertonic saline MOA
↑ hydration of airway mucus secretions, ↑ mucociliary function
46
Dornase alfa (Pulmozyme) MOA
MOA: cleaves DNA = ↓ mucous viscosity = improved airflow mucous has high levels of extracellular DNA that inhibit mucociliary function and may ↑ infection risk (“sticky” mucous
47
Inhaled Antibiotics dosage
Nebulized twice or three times daily x28 days on then 28 days off
48
Nutritional Support
Supplement vitamins A, D, E, and K (fat soluble vitamins have poor absorption) Digestive enzymes with H2-blocker or proton pump inhibitor (PPI) to maintain an alkaline environment
49
What additional complications with CF?
Cystic fibrosis related diabetes, bone disease, liver disease, lung transplant
50
How do you treat additional complications?
Cystic fibrosis related diabetes (CFRD)- scars pancreas, requires insulin Bone disease- vit D, vit K, calcium, bisphosphonates (ie: alendronate) Liver disease- Manage complications, may require liver transplant Lung transplant- Require antirejection meds and chronic steroids
51
Therapeutic Concerns with pulmonary drugs
Individuals with respiratory conditions typically have reduced exercise capacity muscle weakness, cardiac involvement, hypoxemia, etc Coordinate PT sessions with timing of respiratory medications
52
Therapeutic concerns with Anticholinergic Drug, Steroids, β2-agonists 
Anticholinergic Drug (ABCDs) Tachycardia HTN Dry mouth- have water for them to avoid dry mouth Steroids Inhaled drugs: Oral candidiasis and thrush Increased infection risk HTN Hyperglycemia- if the person is already dibetic Osteoporosis (more long-term effect) Muscle weakness, skin atrophy ``` β2-agonists  Tremor Tachycardia Hypokalemia Hyperglycemia ```

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