respiratory Flashcards by Abby Hassett

forceful expulsion of air from the lungs

cough

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inflammation of the nasal mucosa

rhinitis

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inflammation of the nasal and paranasal sinus mucosa

rhinosinusitis

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inflammation of the paranasal sinuses

sinusitis

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improve both inflammation and bronchodilation; enhance pt adherence w/ asthma treatment

advair (combination therapy)

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used for patients w/ more severe asthma

leukotriene modifiers (montelukast)
monoclonal antibodies (omalizumab)

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cornerstone of long-term asthma control, may be used in COPD but only as combination/adjunct

inhaled corticosteroids (e.g. beclomethasone)

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last-line oral bronchodilators used in chronic asthma and copd

xanthines (theophylline)

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used for maintenance therapy, in COPD, and rescue and maintenance in asthma

anticholinergics (ipratroprium, tiotropium)

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management of status asthmaticus

Beta2-agonists in high doses are given every 20 minutes for up to 2 hours. High doses of systemic corticosteroids may be required for several days, given intravenously or orally.
Adrenergic bronchodilators (e.g., albuterol, levalbuterol) are the first-line treatment for acute asthma symptoms

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essential for asthma management

bronchodilators
anti-inflammatory drugs

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Include adrenergics, anticholinergics, and xanthines to relieve bronchoconstriction

bronchodilators

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orticosteroids, leukotriene modifiers, and mast cell stabilizers to reduce airway inflammation

anti-inflammatory drugs

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short acting rescue asthma medications

albuterol
levalbuterol
metaproterenol

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long acting asthma maintenance medications

salmeterol
formoterol
combined w/ inhaled corticosteroids for severe asthma control

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asthma stepwise management

inhaled corticosteroids are used early, often combined with a bronchodilator for severe cases.
long-acting beta2-agonists (LABAs) are added for long-term control but should always be combined with inhaled corticosteroids, not used alone

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involves the destruction of alveoli, reducing gas exchange and lung elasticity

emphysema

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characterized by mucus overproduction and airway inflammation, leading to cough and sputum production

chronic bronchitis

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progressive airway narrowing and dyspnea, often linked to smoking

COPD

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Exaggerated bronchoconstriction in response to stimuli.

airway hyperresponsiveness

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Genetic predisposition to allergic hypersensitivity reactions.

atopic sensitization

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constriction of the lung air passages d/t bronchial muscle contraction

bronchospasm

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severe asthma w/ blood eosinophil counts of ≥150/μL

eosinophilic phenotype

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Chemical mediators causing bronchoconstriction and inflammation in asthma.

leukotrienes

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Long-term beta2-agonists for controlling persistent asthma.

Maintenance inhalant medications

Cells releasing substances causing bronchoconstriction and inflammation.

mast cells

Short-acting beta2-agonists for quick relief of acute asthma symptoms

rescue inhalant medications

acute, severe asthma requiring urgent intervention

status asthmaticus

Environmental or physical factors that provoke asthma symptoms; Environmental allergens (pollens, dust mites, molds), viral infections, smoke, certain drugs, physical activity, and GERD.

asthma triggers

respiratory issues aggravated by work conditions

work-exacerbated asthma (WEA)

Promotes bronchodilation by inhibiting bronchoconstrictive mediators. However, in severe asthma, airway remodeling (structural changes) limits reversibility.

cyclic AMP

Plays a key role by activating mast cells, leading to the release of mediators (e.g., histamine, leukotrienes, cytokines) that cause bronchoconstriction and airway inflammation

IgE

In asthma, smooth muscle contraction in the airways narrows the lumen, exacerbated by inflammation, mucosal edema, and mucus production

bronchospasm

caused by a combination of genetic and environmental factors, high prevalence in urban areas, with atopic sensitization(an IgE-mediated allergic response) being the strongest predisposition.

asthma

Viral infection, mainly caused by rhinovirus, spreads through mucous membranes, airborne droplets, or contaminated surfaces. Most contagious period is 3 days after symptom onset.

common cold

Inflammation of sinus and nasal mucosa, often viral. Blocked sinus drainage causes infection, and oxygen reduction aids microorganism growth

rhinosinusitis

swollen nasal membranes from dilated blood vessels, leading to mucus secretion

nasal congestion

Protective reflex to clear irritants from the respiratory tract. Can be productive (with sputum) or nonproductive.

cough

Accumulation of mucus in respiratory diseases or post-surgery, potentially causing airway blockage or infections

bronchial secretions

Pseudoephedrine is the prototype drug, relieving nasal congestion by vasoconstriction. Caution is advised in children due to potential adverse effects.

nasal decongestants

adverse effects of nasal decongestants

* hypotension * dizziness * seizures * insomnia * urinary retention * thrombocytopenia

contraindications nasal decongestants

* patients with severe hypertension * coronary artery disease * narrow-angle glaucoma * caution is needed with other cardiovascular or metabolic conditions

* Dextromethorphan (Delsym), found in most OTC cough remedies, suppresses the cough center in the medulla or cough receptors in the respiratory tract * Goal of therapy: Suppress nonproductive coughing, not productive coughing. Indicated for dry, nonproductive coughs interfering with sleep.

antitussives

interactions antitussives

* MAOis * SSRIs * alcohol | serotonin syndrome or CNS depression

adverse effects antitussives

* typical: nausea, drowsiness, rash, difficulty breathing * excessive: hallucinations, dissociation, potential for recreational misuse

Peripherally acting antitussive, anesthetizes stretch receptors to decrease coughing. Should be swallowed whole to avoid mouth numbness.-->Used more in the hospital setting

benzonatate (tessalon perles)

Opioid antitussives used in low doses, risk of respiratory depression, especially in children with asthma.-->discouraged

* codeine * hydrocodone

* Guaifenesin (Mucinex), available alone or in combination with other cough/cold remedies, increases respiratory secretions and reduces their viscosity, making it easier to expel mucus. * purpose: iquefy respiratory secretions to ease their removal by making mucus less sticky and more fluid. Recommended for productive coughs to loosen mucus. ## Footnote safe for older adults and children, emphasize increasing fluid intake

expectorants

side effects expectorants

n/v, headache, skin rash

* Acetylcysteine (Acetadote, Cetylev), administered by inhalation or directly into the respiratory tract. * purpose: Liquefy mucus by breaking down protein bonds, allowing easier clearance from the respiratory tract, especially in conditions like cystic fibrosis, and as an antidote for acetaminophen overdose.

mucolytics

adverse effects mucolytics

* drowsiness * n/v * airway inflammation * bronchospasm

No better than placebo for treating colds in adults or children

echinacea

Mixed results on cold prevention and severity reduction; no strong evidence in children.

vitamin c

Oral zinc can reduce the severity and duration of colds in adults, but efficacy in children is unproven. Caution with nasal zinc due to risk of loss of smell.

zinc

Severe, whole-body allergic reaction causing a potentially life-threatening response.

anaphylactic reactions

Anaphylaxis-like reactions without prior sensitization or IgE involvement, possible upon first exposure to an allergen.

anaphylactoid reactions

Drugs that block histamine, particularly at H1 receptors, to alleviate allergic reactions. , reducing effects like bronchoconstriction, nasal congestion, and pruritus. H2 receptor antagonists, such as cimetidine, are used to treat peptic ulcers.

antihistamine

A chemical mediator in immune and inflammatory responses, primarily found in mast cells.

histamine

exaggerated immune responses causing tissue injury and potential serious disease

hypersensitivity

A type III hypersensitivity reaction with antigen-antibody complexes inducing acute inflammation in tissues.

serum sickness

the first mediator in immune responses, stored in mast cells and basophils, and released during allergic reactions. It affects smooth muscles, causing bronchoconstriction, cough, and mucus secretion, and increases capillary permeability, leading to edema and congestion.

histamine

Located in blood vessels and respiratory/GI tracts, responsible for symptoms like bronchoconstriction, cough, and nasal congestion.

H1 receptors

Primarily increase gastric acid secretion and affect the heart.

H2 receptors ## Footnote H2 blockers like cimetidine, ranitidine, famotidine, and nizatidine are unrelated to allergic reactions and are used to treat GI disorders

Found in the brain, regulating neurotransmitter release, with potential therapeutic use in CNS disorders

H3 receptors

Exaggerated immune responses to harmless environmental antigens, leading to tissue injury

hypersensitivity reaction

IgE-mediated allergic reaction (e.g., anaphylaxis, urticaria, rhinitis)

type I (immediate hypersensitivity)

cytotoxic rxns causing direct cell damage (e.g. hemolytic anemia)

type II hypersensitivity

Antigen-antibody complexes inducing inflammation (e.g., serum sickness).

type III hypersensitivity

Delayed hypersensitivity mediated by T cells (e.g., tuberculin test, contact dermatitis). FYI: from direct contact with sensitized antigens (e.g., poison ivy, cosmetics, metals)

type IV hypersensitivity

* Complex reactions affecting any tissue and may involve any hypersensitivity type. * Symptoms vary: skin rashes, drug fever, hematologic reactions, and liver involvement. * Allergic reactions often develop 7-10 days after initial exposure and may intensify with repeated exposures.

drug-induced immune rxns

common triggers for drug-induced anaphylaxis

penicillins, NSAIDs, radiocontrast media

Delayed hypersensitivity reaction, often caused by antimicrobials, with symptoms like urticaria, fever, and joint pain.

serum sickness

Caused by drugs like hydralazine, with symptoms mimicking systemic lupus erythematosus (SLE), though with less severe renal and CNS involvement.

drug-induced lupus

often an early sign of allergic drug reactions

fever

Mimic immune reactions but do not involve antibodies or T cells. Commonly triggered by drugs like radiologic contrast media, causing immediate and life-threatening reactions.

anaphylactoid rxns

* Inflammation of nasal mucosa caused by type I hypersensitivity reaction to allergens. Symptoms include nasal congestion, sneezing, itching, and watery discharge * a significant risk factor for asthma

allergic rhinitis

can lead to: Chronic fatigue Impaired daily functioning Sleep disturbances Sinus infections Postnasal drip Cough Headaches

untreated allergic rhinitis

Acute symptoms triggered by pollens

seasonal allergic rhinitis (hay fever)

Chronic symptoms caused by non-seasonal allergens like dust mites, animal dander, and molds

perennial allergic rhinitis

* Inhaled allergens trigger an IgE response, leading to histamine and other inflammatory mediators' release, causing nasal congestion, mucus secretion, and inflammation. * Repeated allergen exposure increases the number and reactivity of mast cells and basophils, leading to larger histamine release and more severe symptoms

allergic rhinitis

Effective for allergic rhinitis but not recommended for the common cold

antihistamines

allergic rhinitis first line treatment

* Second-generation H1 receptor antagonists (e.g., fexofenadine, desloratadine), which are more selective for peripheral receptors, leading to fewer side effects * Third-generation antihistamines are derivatives aimed at enhancing efficacy and reducing side effects

older, widely available, and inexpensive but have numerous adverse effects, including drowsiness and anticholinergic symptoms

first generation H1 receptor antagonists

* effective for allergic symptoms but lacks selectivity, affecting both central and peripheral H1 receptors, leading to CNS depression or stimulation * used for motion sickness, insomnia, and parkinsonism. * Absorbed well orally, acts within 15-60 minutes, and lasts 4-6 hours, Metabolized in the liver and excreted via urine within 24 hours. * Blocks histamine at H1 receptor sites, preventing smooth muscle constriction, reducing vascular permeability, and decreasing salivation and tear formation * Does not prevent histamine release, just blocks its effects

diphenhydramine (first generation H1 antagonists prototype)

Causes mild drowsiness but can impair psychomotor performance

chlorpheniramine

Used for nausea, vomiting, or sedation but with caution due to severe tissue irritation (especially promethazine)

* hydroxyzine * promethazine

contraindications benadryl

* Pregnant women * patients with narrow-angle glaucoma * prostatic hypertrophy * peptic ulcer * bladder neck obstruction

cautions for special populations benadryl

* children may experience paradoxical excitement; overdoses can cause hallucinations, convulsions, and death * Not recommended for newborns or children with chickenpox/flu * Older Adults: Increased risk of confusion, dizziness, hypotension, and anticholinergic effects like urinary retention * Caution in men with prostatic hypertrophy

adverse effects of benadryl

* CNS depression: Drowsiness, sedation, cognitive impairment * Anticholinergic effects: Dry mouth, urinary retention, constipation, blurred vision.

interactions benadryl

* alcohol * antidepressants * MAOIs

* **Mechanism:** These drugs do not readily cross the blood-brain barrier and bind primarily to peripheral H1 receptors, GI tract/blood vessels/respiratory system, reducing CNS-related side effects like drowsiness. * **Main Uses: **Treat allergic rhinitis, urticaria (pruritus), and atopic dermatitis. Beneficial for chronic asthma as well. Not as effective for nasal congestion compared to glucocorticoid nasal sprays. * **Absorption:** Rapidly absorbed, peak levels in 1 hour.

cetirizine (zyrtec allergy) [2nd gen h1 receptor antagonists]

* Available as nasal sprays. First-line treatment for allergic rhinitis, though less effective than corticosteroids * These can reduce nasal congestion significantly * Olopatadine produces less sedation than azelastine.

Other Second-Generation H1 Receptor Antagonists: * Azelastine (Astelin, Astepro) * Olopatadine (Patanase)

* a metabolite of terfenadine * also Levocetirizine (Xyzal) * offer improved safety with minimal CNS effects, reducing sedation and drowsiness * Rapid absorption, peak serum levels in 2.5 hours * Excreted mostly unchanged in bile and urine * Effects last 12 to 24 hours.

Prototype: Fexofenadine (Allegra) [3rd gen H1 receptor antagonists

adverse effects allegra

Usually mild: Headache, nausea, vomiting, fatigue, and in women, dysmenorrhea, older adults caution cognitive function impairment

interactions allegra

* antifungals * macrolides can increase plasma levels * antacids * rifampin may reduce absorption * Fruit juice (apple, orange, grapefruit) can reduce drug absorption

cold incubation

5 days, most contagious after 3 days of sx onset lasts 7 days

part of lung is airless and collapses d/t secretions

atelectasis

mucus clear or white, gets better after 3-4days

viral infections

last or worsen over 10 days, sx continue to get worse for over t3 days or sudden worsening after initial improvement

bacterial infections

* IgE mediated, typically affects Histamine 1 receptor along smooth muscle cellls of bronchi, stimulating vagus nerves to cause bronchoconstriction * histamine released first in immune/inflammatory response * sx: nasal congestion, sneezing, pruritis, post-nasal drip, ocular discharge, loss of smell/taste, mouth breathing, swollen nasal canals, conjunctival swelling

allergic rhinitis

nonpharmacologic interventions for colds

* hydration * saline irrigations, steam or humidifier * lozenges * rest

# true or false: you should not use OTC products for more than 5-7 days w/o seeking medical care

true

how do we prevent asthma and copd exacerbations

* vaccines (COVID-19, influenza, pneumococcal) * lung cancer screening

* higher strength 4mg for those who smoke within 30 min of waking (>30min of waking should start at 2mg) * ADE: heartburn, nausea, indigestion, hiccups, mouth/throat irritation (don't use gum w/ dentures) * do not eat or drink anything except for water 15 min during and before * gum: chew and park, lozenge: disssolve over 20-30 min no chewing

nicotine gum or lozenges

* high strength 21mg/patch for those who smoke >10 cigs/day * less tahn that would start a 14mg/24h patch * ADEs: local skin irritation, insomnia, vivid dreams, remove at bedtime) * should be put on a clean, dry, hairless area btwn neck and waist rotate sites

nicotine patch

* depressed mood * insomnia * irritability * frustration, anger * anxiety * difficulty concentrating * restlessness * impatience * decreased HR * increased appetite

nicotine withdrawal

slow and deep breaths, hold for 10s wait 1-5 min between different inhalers

metered dose inhalers

fast and deep breaths wait 1-5 min between different inhalers

dry powder inhalers

how would we educate a pt on how to take care of their inhaler

* rinse mouth after ICS inhalers * learn how to clean * do not eat capsules * learn how to prime (at first and if not used for several days)

* Acetaminophen (Tylenol) * NSAIDs like Ibuprofen (Advil)

analgesics

* Oral: Diphenhydramine (Benadryl), Cetirizine (Zyrtec), Loratadine (Claritin), Fexofenadine (Allegra) * Nasal: Azelastine (Astepro), Olopatadine (Patanase)

antihistamines

* Budesonide (Rhinocort), * Fluticasone (Flonase), * Momentasone (Nasonex), * Triamcinolone (Nasacort)

nasal corticosteroids

* Pseudoephedrine (Sudafed) * Oxymetazoline (Afrin) * Phenylephrine (Vazculep, Sudafed PE)

decongestants

* Dextromethorphan (Delsym) * Benzonatate (Tessalon Perles) * Codeine products or Hydrocodone bitartrate (Hysingla, Zohydro ER)

antitussives

guaifenesin (mucinex)

expectorants

acetylcystine (acetadote)

mucolytics

max tylenol daily dose

4000mg/day

* max dose 1,200mg/day * Typically, 200mg or 400mg tablets * Can use Aleve (naproxen) alternative for fewer dosing throughout the day * caution in those with a cardiac history/htn/bleeding disorders/unstable disease states

advil (ibuprofen)

* In many combination products labeled nighttime or sleepy * ADEs: Highly Sedating, anxiety, agitation, dryness. Children & older adults can have paradoxical excitement or hallucinations. Phenergan IV has a black box warning for chemical irritation and damage to tissue and respiratory depression in children (<2 yo).

first generation antihistamines * Diphenhydramine (Benadryl) * Chlorpheniramine (Aller-Chor) * Hydroxyzine pamoate (Vistaril) * Promethazine (Phenergan)

* anticholinergic properties * not great for cough/cold

antihistamines

max daily benadryl dose

100mg/day

Less blood-brain barrier penetration , mild benefit in asthma, long acting- once daily dosing

second generation antihistamines

less side effects and longer acting (1x daily dose)

third generation antihistamines * Fexofenadine (Allegra) * Levocetirizine (Xyzal)

* First Line for cough/cold: Possibly better than oral due to localized effect for mild disease Twice daily dosing ADE: Bitter taste, headache, sneezing, epistaxis, postnasal drainage, some drowsiness

Nasal Antihistamine * Azelastine (Astepro) 0.15% available OTC * Olopatadine (Patanase)

* OTC: Budesonide (Rhinocort), Fluticasone (Flonase), Momentasone (Nasonex), Triamcinolone (Nasacort) * RX: Beclomethasone (Qnasl), Triamcinolone * 2nd line for allergic rhinitis, most effective for mod/severe * May use scheduled daily-max effect in 2-4 weeks. Can use prn * ADE: headache, cough, pharyngitis, epistaxis

inhaled corticosteroids

* **MoA:** Adrenergic receptor sympathomimetic-indirect release of norepinephrine (directly on alpha receptor); Constricts arterioles and reduces blood flow to nasal mucosa- relives nasal congestion * Starts working in about 30 minutes and lasts about 4-8hrs * **Considerations:** Renally excreted, Older adults, Children, Pregnancy (C) * **ADEs:** Insomnia, Palpitations, increased BP, Irritability, Headache, Urinary retention * **Caution/Contraindications:** Hyperthyroidism, Diabetes, BPH, seizure disorders (CNS stimulation), Hypertension/CAD, Glaucoma, taking a TCA or MAO-Ai * **Drug-Drug interactions:** Caffeine, Digoxin, MAO-Ais and many others (Increase risk of dysrhythmias and vasoconstriction (hypertension))

nasal decongestants * Oral: Pseudoephedrine (Sudafed), Phenylephrine (Sudafed PE) * Nasal spray: Oxymetazoline (Afrin)-limit to 3 days due to rebound nasal congestion

* Goal is to liquefy secretions for removal * Works on gastric vagal receptors to stimulate respiratory tract fluid and reduce viscosity of secretions * Frequent dosing, generally safe, must hydrate

expectorants

* Inhalation or instillation (commonly nebulized)- quick action, short duration Use of a bronchodilator before increases effectiveness * **MOA:** Goal is to liquefy mucus; Disrupts disulfide protein bonds of mucus- works in lower/deeper portion of the lungs * Also used as acetaminophen overdose antidote * Watch for airway inflammation or bronchospasm due to inhibiting ciliary function in lungs. Looks like difficulty breathing, chest tightness * Given before meals and bedtime

acetylcystine (acetadote)

nursing considerations for respiratory medications

* topical: blow nose prior, awareness of admin frequency * do not crush/chew long-acting tablets/capsules * OTC use should not be more than a week

* Mix of genetics, environment and innate immunity * Unknown Cause: genetics, environmental exposures during immune system development * Chronic but Reversible (spontaneous or with treatment) * Inflammatory disorder * Episodic airflow limitation * Multiple symptoms: breathlessness, cough, wheezing, chest tightness * Worse at night or early morning * Can be exercise induced * bronchospasm and narrowing of airways, general hyperresponsiveness

asthma

what inhibits the release of bronchoconstrictive substances in asthma

cAMP

Influx of activated cells (including eosinophils and cytokine T cells) lead to Inflammation, mucosal edema, excessive mucus

IgE mediated

release substances that produce bronchoconstriction and inflammation

mast cells

major chemical mediator of bronchoconstriction and inflammation in asthma

leukotrienes ## Footnote others are acetylcholine, CGMP histamine, interleukins, prostaglandins, serotonin

# symptoms * Triggers lead to airway inflammation * Hypersecretion of mucus * Airway muscle constriction * Swelling of bronchial membranes * Narrowing Breathing Passages * Wheezing * Cough * SOB * Tightness in chest

asthma ## Footnote diagnosed by sxs and spirometry

* May not respond to usual treatment * Life-threatening- respiratory failure * Chest tightness, agitation, confusion * Lack of wheezing/coughing indicates impaired gas exchange * Does not change the natural progression of asthma but overtime severe asthma can become less reversible due to airway remodeling (fibrosis, enlarged glands/ muscle cells)

status asthmaticus

indicator of expiratory airflow limitation

spirometry

* preventable progressive disease with no cure * Persistent airflow limitation * Includes emphysema and chronic bronchitis * 3rd leading cause of death worldwide * History of asthma/childhood lung infections * COPD exacerbation is the acute worsening of respiratory symptoms from baseline * Usually results in change in treatment regimen * mainly caused by tobacco smoking (1o, 2o, or 3o)

COPD

how do we calculate pack per day hx

ppd = # cigarettes per day/20 x smoking years

* Dyspnea (SOB) that worsens over time and w/ exercise, persistent * Talks in short sentences, “air hunger” * Chronic Cough * Chronic Sputum Production * Wheezing (recurrent) * Chest Tightness * Recurrent lower respiratory infections * Diagnosis requires: Symptoms + known risk factors and Pulmonary function Rule out other causes: test (Spirometry)

COPD

risk factors for poor asthma outcomes

* Exacerbations * Medication side effects * Fixed airflow limitation

severe asthma tx

* Needs moderate to high dosing with or without adjuncts

moderate asthma tx

low daily dose ICS/LABA

Total volume you can forcibly blow out

forced vital capacity (FVC)

forced expiratory volume in 1 second (first second of FVC)

FEV1

confirms presence of persistent airflow limitation (COPD) | exceptions based on hx

Post-Bronchodilator FEV1/FVC <0.7

indicates reversibility of asthma

FEV1 % change > or = 12 ## Footnote * Post-Bronchodilator actual minus Pre- Bronchodilator actual divided by Pre- Bronchodilator actual * Poor descriptor of COPD or differentiating from asthma and does not necessarily affect treatment in COPD

goals of asthma tx

* symptom control * risk reduction

mild asthma tx

Well controlled with prn low dose ICS/Formoterol or daily ICS ## Footnote everyone requires a reliever inhaler that may be a PRN low dose ICS/Formoterol or SABA

what is COPD tx used for even though disease is progressive

* reduce frequency and severity of exacerbations * improve QOL/health status * improve exercise tolerance

spirometry result indicating very severe COPD

FEV1 < 30%

spirometry result indicating severe COPD

30% ≤ FEVQ < 50%

spirometry result indicating moderate COPD

50% ≤ FEV1 < 80%

spirometry indicating mild COPD

FEV1 ≥ 80%

what initial pharmacologic tx would a group of COPD pts had greater than or equal to 2 moderate exacerbations or greater than or equal to 1 leading to a hospitalization

LABA + LAMA ## Footnote consider LABA + LAMA + ICS if blood eosinophil ct is ≥ 300

how would we treat a pt w/ COPD that has had 0-1 moderate exacerbations (not leading to hospital admission | mMRC 0-1, CAT < 10

bronchodilator

how would we treat a patient w/ COPD w/ 0-1 moderate exacerbations (not leading to hospital admission | mMRC ≥ 2, CAT ≥ 10

LABA + LAMA

bronchodilator tx in asthma

* Use of SABA and LABA (preferably in combo with ICS) * LAMA only used as add on in severe cases, never used as monotherapy

bronchodilator tx in COPD

LAMA and LABA given as mainstay and central to sx management ## Footnote Improvement in lung function, SOB and reduce exacerbations: LAMAs > LABAs

use of what improves FEV1 and asthma/copd sx

SABA + SAMA

* **MoA:** Sympathomimetic→ Stimulates B2 adrenergic receptors→ increasing cAMP→ triggers K+ and decreases CA2+ hindering muscle contraction → bronchodilation→ relax airway smooth muscle * **ADEs:**Tachycardia (palpitations), excitement, Hypokalemia, Tremor in geriatric patients, “jitters” * Typical prn relief, MAX 8 inhalations a day * Onset in 5 minutes, duration 4-6 hours * No advantage of levalbuterol over albuterol * (Albuterol used off label for COPD)

short-acting B2 agonists * albuterol * levalbuterol

* **MoA:** Sympathomimetic→ Stimulates B2 adrenergic receptors→ increasing cAMP→ triggers K+ and decreases CA2+ hindering muscle contraction → bronchodilation→ relax airway smooth muscle * **ADEs:** Tachycardia (palpitations), excitement, Hypokalemia, Tremor in geriatric patients, “jitters” * Scheduled dosing (NOT PRN) * Longer duration (more lipophilic and selective) BID or daily dosing **BLACK BOX WARNING:** increased risk of asthma related deaths as monotherapy

long acting B2 agonists (LABA) * formoterol * indacaterol * salmeterol * vilanterol * olodaterol * afrometerol

* **MoA:** Muscarinic receptor antagonist →(Competitive and reversible) blocks acetylcholine at parasympathetic sites → Depletes cGMP → reduced contractility → relax airway smooth muscle and reduces mucous secretions * **ADEs:** Dry mouth (xerostomia), Constipation * PRN for quick relief, MAX 12 Inhalations a day * Onset within 15 mins, duration ~8 hours * Can be used in combo with a SABA but not with a LAMA

short-acting muscarinic antagonist (SAMA) * Atrovent (Ipratropium) * Combo with SABA Ipratropium/Albuterol- DuoNeb or Combivent

* **MoA:** Muscarinic receptor antagonist →(Competitive and reversible) blocks acetylcholine at parasympathetic sites → Depletes cGMP → reduced contractility → relax airway smooth muscle and reduces mucous secretions * **ADEs:** Dry mouth (xerostomia), Constipation * Scheduled dosing * BID or daily dosing * Maximum benefits take 4-8 weeks

long acting muscarinic antagonists (LAMA) * Spiriva (Tiotropium) * Tudorza (Aclidinum) * Incruse (Umeclidinium) * Seebri (Glycopyrrolate)

* **MOA:** Non-selective phosphodiesterase inhibitor → smooth muscle relaxation (unclear); Enhanced Calcium uptake by adenosine mediated changes →enhanced inspiratory muscle function * Narrow Therapeutic Index (5-15 mcg/ml) -Risk of toxicity increases with age and impaired renal/hepatic fx -Based on ideal body weight and serum concentration * Dose related toxicity (benefit from drug only occurs near toxic doses).: Fatal arrhythmias, Seizures, Geriatric max of 400mg/day unless serum con <10 mcg/ml * Multiple Drug-Drug Interactions with CYP1A2, 3A4, P450, 3A3 substrates -Increase serum conc: Macrolides, ciprofloxacin, fluvoxamine, cimetidine, azole antifungals, amiodarone, etc -Decrease serum conc: Smoking, charcoal broiled meats, carbamazepine, phenytoin, rifampin, etc * **Adverse effects:** Headaches, Insomnia, Nausea/heartburn * Evidence of modest effect especially in combination with Salmeterol in COPD | NOT A FIRST LINE OPTION, less effective and less tolerated

bronchodilator methylxanthines * theophylline

* **MoA:** Agonist at glucocorticoid receptor → inhibits mast cells, eosinophils, etc → inhibits histamine, cytokines, leukotrienes (mediators of inflammation) → Local antiinflammatory activity * **Adverse Effects:** Oral candidiasis (must rinse after use), Hoarse voice, Increased risk of pneumonia * Asthma: Preferred long-term/chronic control, used for maintenance and prophylactic treatment; Dosing can be low, medium or high (most benefit seen at low dose) * COPD: 3rd line option for those at high risk of exacerbations. If blood eosinophil counts ≥300 or those with a history of asthma. Never use on it’s own due to limited responsiveness and it does not modify mortality.

inhaled corticosteroids * Fluticasone (Flovent) * Budesonide (Pulmicort) * Mometasone (Asmanex), Belomethasone (Qvar) * Ciclesonide (Alvesco) * Flunisolide (Aerospan) | budesonide preferred in pregnancy

what would we use as asthma adjuncts

* mast cell stabilizers * leukotriene modifiers * injectibles (omalizumab - xolair, mepolizumab - nucala, reslizumab - cinqair, benralizumab fasenra)

* **MOA:** Inhibits release of Inflammatory mediators from mast cells * **ADEs:** Well tolerated; Some: drowsiness, burning in nose, nausea, congestion * Cromolyn (Gastrocrom): Nebulizer Inhalation solution up to four times a day

mast cell stabilizers

* **MOA:** Mainly interact with the receptor to prohibit leukotriene formation * **Adverse Effects:** Well tolerated; CNS effects seen in children: agitation, mood changes, irritability, insomnia

leukotriene modifiers *montelukast (singulair)*

Monoclonal Antibody Injections for specific allergen patients >12yo with severe & persistent stage 5 asthma, take weeks for max benefit

injectable asthma adjuncts omalizumab (xolair) | **BB WARNING FOR ANAPHYLAXIS**

* **MOA:** Anti-inflammatory by unknown mechanism, prevents pneumonia in COPD pts * Algorithm: Add on to triple therapy in those who are former smokers (not current smokers) * **Contraindications**→ History of cholestatic jaundice or hepatic dysfunction with prior azithromycin use * **Adverse effects:** Nausea, diarrhea, Impaired hearing, QTc prolongation

macrolides *azithromycin* | 250mg 1 tablet daily or 500mg tablet 3x/wk ## Footnote Long term use of Azithromycin therapy reduces exacerbations over one year (no data beyond 1 year of use because most die by that point)

* **MOA:** Inhibit PDE4 →Inhibit breakdown of cAMP → reduces inflammation; Additional suppression of cytokines and inhibition of neutrophils and leukocytes * Algorithm: Add on to triple therapy in those with an FEV1 < 50% predicted + chronic bronchitis (especially with at least one hospitalization) Ideally in exacerbations requiring corticosteroids - Improves lung function (including those with chronic bronchitis) - Delays mucocilliary malfunction and pulmonary remodeling- Reduces future exacerbations * **Contraindications:** Hepatic impairment → Child-Pugh B and C * **Adverse Effects** *May diminish over time***:** Nausea, diarrhea, abdominal pain; Reduced appetite leading to weight loss; Sleep disturbances and Mood changes-anxiety, depression * **Drug interaction:** Increased levels with CYP3A4 and or CYP1A2 inhibitors

phosphodiesterase-4 (PDE4) inhibitors *Daliresp (Roflumilast)* ## Footnote 500mcg 1 tablet daily (250 mcg for first 4 weeks)

COPD adjuncts

* macrolides * phosphodiesterase-4 (PDE4) inhibitors

* Progressive lung dysfunction: symptoms of SOB, cough, wheezing, chest tightness; Cause typically viral infections, seasonal or general allergens, poor adherence * Mild/Moderate (able to talk but clearly agitated SABD every 20 minutes for an hour with or without oral corticosteroid & oxygen * Severe (confused, silent chest) Requires hospitalization; SABA+ SAMA nebulization and oral corticosteroid

asthma exacerbations and how we treat

what does a history of copd exacerbation do to a pt's exacerbation risk

increases it

when to call 911 when pt is having a COPD exacerbation outside of a hospital

* Increased intensity of symptoms (ie Resting dyspnea) * Cyanosis (blue lips or nails) * Comorbidities that can worsen exacerbation (ie Heart failure) * Past exacerbation frequency * Severe underlying COPD * Lack of home support

* Worsening of respiratory symptoms beyond day-to-day variations; dyspnea, cough, sputum, Typically respiratory infection * Non-Pharmacological Strategies: Oxygen Therapy * Pharmacological Strategies * **Mild:** Short Acting Bronchodilators (SABD=SABA and/or SAMA) * **Moderate:** SABD PLUS Antibiotic (augmentin, azithromycin, doxycycline); Only if there is increased Sputum pruluence (yellow/green) with either increased volume or SOB - Always if there is mechanical ventilation AND/OR SABD PLUS Oral corticosteroid - Short term prednisone for 5-7 days in outpatient setting - Corticosteroids help shorten recovery and improve lung function- better in those with high eosinophils * **Severe:** Hospitalization for possible acute respiratory failure and differentiation of other comorbidities (ACS, CHF,PE, Pneumonia) - IV Corticosteroids may be used

copd exacerbation and how we treat

what is the most important step in asthma/copd management

follow up * yearly assessment of lungs via spirometry * optimize pharmacotherapy (evaluate adherence, monitor for ADEs, exacerbations should prompt adjustments, ASSESS INHALER TECHNIQUE ALWAYS)

respiratory Flashcards

(181 cards)