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pharm drugs > Pulmonary drugs > Flashcards

Pulmonary drugs Flashcards

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

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

A

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

23
Q

Why take combination bronchodilators?

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

A

albuterol/ipratropium (Combivent)

25
Q

Ex LABA/ICS drugs (2)

A

formoterol/budesonide (Symbicort), salmeterol/fluticasone (Advair)

26
Q

What if inhalers aren’t working?

A

Disease progression

Incorrect inhaler or nebulizer use

Nonadherence- need education on PRN vs maintenance meds, cost concerns

27
Q

What if patient can produce enough inhalation force

A

Refer to the provider to discuss if a spacing device is needed or if a change from dry powder inhaler is needed

28
Q

When do use antibiotics?

A

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
Q

Asthma short-term and long-term treatment

A

short-term: SABS

long-term: ICS and LABA

30
Q

When would you use a LABA?

A

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
Q

What are Leukotrines?

A

released from mast cells and eosinophils to play a role in airway edema, smooth muscle contraction, inflammatory process

32
Q

Leukotriene receptor antagonist (LTRA) PO drugs and MOA

A

montelukast (Singulair), zafirlukast (Accolate)

MOA: competitively antagonize leukotriene receptors

33
Q

Montelukast when do you take it for allergies and when do you take it for asthma?

A

Alllergies: AM
Asthma: PM

34
Q

Immunomodulators: Anti-IgE drugs and MOA

A

omalizumab (Xolair)

prevents IgE binding to receptors on mast cells and basophils  limits activation and release of allergic response mediators

35
Q

what to look out for when taking Immunomodulators: Anti-IgE

A

Very rare but anaphylactic allergic reaction may occur- must administer in provider’s office

36
Q

How often can you use SABA?

A

up to 3 treatments at 20 minute intervals no relief go see medical treatment

37
Q

Drug class to treat CF?

A

LABA, SABA, CFTR Modulators, Mucolytics, Inhaled/PO Antibiotics

38
Q

CF transmembrane regulator role?

A

is a membrane protein, and chloride channel  regulates sodium and water which helps keep mucous thin

39
Q

Genetic mutation of CF transmembrane regulator causes?

A

Genetic mutations cause closing and/or narrowing CFTR or stop CFTR from getting to the cell surface

40
Q

CFTR Modulator drugs

A

tezacaftor/ivacaftor (Symdeco), lumacaftor/ivacaftor (Orkambi)

41
Q

MOA Ivacaftor and Tezacaftor/ lumacaftor

A

facilitate trafficking of CFTR to the cell membrane surface = improved chloride transport.

Improved regulation of sodium and water = mucous thinning

42
Q

CFTR modulators must be taken with?

A

with high fat meal to ↑ absorption

43
Q

AE for CFTR Modulators

A

dizziness, hypertension (Orkambi only)

44
Q

Mucolytics Drug classes

A

Hypertonic saline and Donase alfa (Pulmozyme)

45
Q

Hypertonic saline MOA

A

↑ hydration of airway mucus secretions, ↑ mucociliary function

46
Q

Dornase alfa (Pulmozyme) MOA

A

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
Q

Inhaled Antibiotics dosage

A

Nebulized twice or three times daily x28 days on then 28 days off

48
Q

Nutritional Support

A

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
Q

What additional complications with CF?

A

Cystic fibrosis related diabetes, bone disease, liver disease, lung transplant

50
Q

How do you treat additional complications?

A

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
Q

Therapeutic Concerns with pulmonary drugs

A

Individuals with respiratory conditions typically have reduced exercise capacity
muscle weakness, cardiac involvement, hypoxemia, etc
Coordinate PT sessions with timing of respiratory medications

52
Q

Therapeutic concerns with Anticholinergic Drug, Steroids, β2-agonists

A

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

pharm drugs (10 decks)

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