Acute bronchitis/flu/asthma Flashcards
Acute bronchitis
General and RF
Acute inflammation of the large airways of the lower respiratory tract, commonly accompanied by an upper respiratory tract infection
Among the top 10 conditions for which patients seek medical attention
Most commonly caused by a viral infection
More frequent during late fall and the winter months
♀=♂
Children/adolescents > adults
Risk factors:
Chronic lung disease (COPD, asthma)
Smoking
Chronic exposure to air pollution
acute bronchitis
patho
A virus or bacterium causes infection and inflammation of the cells of the tissue lining the bronchi
Irritation and inflammation cause:
Impaired ciliary function
Hyperemia and edema in the mucous membrane
Decreased bronchial mucociliary function
Increased mucus production → characteristic cough of acute bronchitis
Acute bronchitis
S/Sx
Cough(predominant symptom)
Productive with clear, yellow, or purulent sputum; may contain streaks of blood
Purulent sputum isNOTspecific to bacterial causes
Chest discomfort (frequent coughing)
Wheezing
Rhonchi (clears with coughing)
Subjective dyspnea
Malaise
Fever:
Uncommon, but possible
Often low grade if present
Should raise concern possible pneumonia or bacterial superinfection
Findings that are more consistent with pneumonia than acute bronchitis
Fever
Tachypnea
Rales
Dullness to percussion
Egophony: E → A
Tactile fremitus: ↑ in areas of increased lung density (consolidation)
acute bronchitis
Diagnosis
Made clinically based on history and physical examination
Suspected in patients with an acute onset of cough, which often follows a URI without findings to suggest pneumonia
Additional work-up can include:
Chest x-ray
Microbiologic testing
Rarely indicated because results do not normally change management
Indicated during suspected outbreaks
acute bronchitis
Chest X-ray indications
Obtained to rule out serious illness or pneumonia
Indications:
Signs of consolidation on exam:
Dullness to percussion
Egophony
Tactile fremitus
Abnormal vital signs:
Fever
Tachycardia
Tachypnea
↓ Oxygen saturation
Mental status or behavioral changes in the elderly (> 75 years of age)
Immunocompromised patients
Findings:
Usually normal in acute bronchitis
May show thickening of the bronchial walls in the lower lobes
Infiltrates/consolidation indicate pneumonia
acute bronchitis
Tx
Self-limiting condition
Usually requires only supportive care
Patient education
Explain why antibiotics areNOTindicated
Symptoms resolve spontaneously within 1‒3 weeks
Treatment of symptom reduction:
For cough
Nonpharmacological therapies
Hot tea, throat lozenges, honey
Antitussive agents
Given if cough is distressing or interfering with sleep
Dextromethorphan (Robitussin)
Guaifenesin (Mucinex)
Codeine → generally avoided due to addictive potential
acute bronchitis
Tx For malaise, myalgias, and fever
Analgesic antipyretics:
NSAIDs
Acetaminophen
Acute bronchitis
Tx For wheezing/ pts with asthma or COPD
For wheezing
beta-agonists (Albuterol)
For patients with underlying lung disease (COPD, asthma):
Prednisone
Consider antimicrobials in cases of known or suspected bacterial infections
Lifestyle modifications
Smoking cessation
Avoidance of allergens/pollutants
Influenza, Covid-19, and pneumonia vaccines according to standard guidelines
Influenza
Antigenic drift
Mutations accumulate in the viral genes that code for viral surface proteins resulting in new antigenic sites (HA or NA spikes); changes are generally minor
Epidemic
Antigenic shift
Two or more different strains of a virus combine to form a new subtype that is radically different; limited or no prior immunity
pandemic
flu
Transmission and Viral shedding
Transmission:
Airborne respiratory droplets
Person-to-person contact
Contact with contaminated items
Incubation period: 1–4 days
Viral shedding:
Begins with or just before the onset of symptoms (0–24 hours)
Lasts 5–10 days
Children and immunocompromised individuals tend to shed virus longer
flu
Clinical Presentation
Prodrome (3–24 hours)
Myalgia, malaise, headache, anorexia
Disease (7–10 days)
Fever
Range 37.8–40.0°C (100–104°F)
Lasts 1–5 days
Chills
Myalgias
Headache
Nonpurulent conjunctivitis
Nasal congestion or rhinorrhea
Sore throat
Mild cervical lymphadenopathy
Nonproductive/dry cough
Gastroenteritis symptoms:
Abdominal pain, vomiting, diarrhea
Flu
Dx
Key clinical findings
Typically madeclinically; rapid diagnostic tests if the results will influence management
Positive predictive value (80%–90%) of clinical diagnosis once the virus has been documented in the community
Key clinical findings:
Rapid onset of symptoms
Fever and symptoms of upper respiratory infection (URI)
Myalgias/headache
GI symptoms and high fever in children
flu
Virulent glycoproteins & Nucleoproteins
Hemagglutinin (HA):attaches to sialic acid-containing receptors on respiratory epithelial cells
Neuraminidase (NA):cleaves newly formed virions off the sialic acid-containing receptor, allowing the virus to exit cells
Nucleoprotein:helps distinguish between the 3 types of influenza viruses (A, B, and C)
Flu
Labs and imaging
Gold standards:
Viral culture (3–7 days)
Detects virus in nasopharyngeal or throat samples
RT-PCR (24 hours)
Identification of viral genomes
Rapid diagnostic testing:
ELISA (15–20 minutes)
Detection of antigens in throat and nasal swabs
Limited sensitivity and up to 98% specificity
Chest X-ray:
Obtained to rule out bacterial pneumonia
Should be obtained in the following cases:
Elderly
Patients at high risk due to medical comorbidities
Patients exhibiting signs/symptoms suggestive of pneumonia
Findings:
Bilateral symmetrical patch infiltrates
Ground-glass opacities
Focal infiltrates → bacterial pneumonia
flu
complications
Pneumonia
Viral
Suggested by a worsening cough, bloody sputum, dyspnea, and rales
Bacterial
Suggested by persistent or recurrence of fever and cough after the primary illness appears to be resolving:
Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Post-influenza encephalitis
Myositis
Flu
Tx
Majority of patients require only supportive care (rest, hydration, and antipyretics as needed)
Aspirin should be avoided in patients≤ 18 years
Recover without complications in 1-2 weeks
Pharmacotherapy
Antiviral drugs
Neuraminidase inhibitors
Interfere with release of influenza virus from infected cells and thus halt spread of infection
Recommended forhigh-risk patients(including all hospitalized patients)
Given within 48 hours of symptom onset
oseltamivir (Tamiflu),zanamivir (Relenza), andperamivir(Rapivab)
flu
prevention
Transmission prevention:
Cough etiquette
Use of facemasks
Frequent handwashing
Social isolation of infected individuals
Influenza vaccination: 50%–90% efficacy
Recommendedannuallyfor all individuals ≥ 6 months of age who do not have contraindications
Modified annually to include the most prevalent strains (often 2 strains of influenza A and 1 or 2 strains of influenza B)
flu
2 basic types ofinfluenza vaccine:
Inactivated influenza vaccine (IIV) - 70% efficacy
Trivalent or quadrivalent vaccine given by IM injection
Adverse effects: mild pain at the injection site; fever and myalgias (uncommon)
Live-attenuated influenza vaccine (LAIV) - 85% efficacy
Given intranasally
Used for healthy people aged 2 to 49 years; should not be given to children who are<5 years and have reactive airway disease
Adverse effects: rhinorrhea and mild wheezing
Both vaccines - children who are < 8 years and have not been vaccinated should be given a primary dose and a booster dose 1 month apart
Asthma
Chronic inflammatory respiratory condition characterized by bronchial hyperresponsiveness and airflow obstruction
- Involved cells: mast cells, eosinophils, neutrophils, T lymphocytes, macrophages
- Airflow obstruction is often reversible (spontaneously or with treatment)
Believed to result from the complex interaction of host and environmental factors
asthma
Predisposing Factors
Host risk factors:
Genetics
Studies of families show heritability of asthma (asthma in parents)
> 100 asthma susceptibility genes
Atopy
Genetic predisposition to produce immunoglobulin E (IgE) antibodies on allergen exposure
Strongest identifiable risk factor for asthma
Perinatal factors
Prematurity at birth
Neonatal or early abnormality of lung function
Sex: ↑ in boys before puberty
Obesity: ↑ risk
Pollution:
Living close to a major road → nitrogen dioxide (produced from burning fuel) → ↑ asthma
Early exposure to pet allergens:
Varied results
Protects by decreasing sensitization to pet allergens
Asthma develops in some, but possibly influenced by other exposures (tobacco, pollution
asthma
Maternal factors
Decreased and increased risk
Maternal factors
Decreased risk of asthma:
Increasing maternal age at delivery (> 30 years)
Breastfeeding: ↓ wheezing in the first 2 years of life
Increased risk of asthma:
Maternal diet low in vitamin D and omega-3 polyunsaturated fatty acid
Poorly controlled maternal asthma
Prenatal exposure to maternal smoking
asthma
triggers
Inestablishedasthma, different triggers may exacerbate the symptoms
Environmental and drug-induced:
Allergens
Cold, dry air
Paints and fumes
Irritant gasses
Air pollution
Drugs
Behavioral and psychological:
Exercise
Hyperventilation
Stress
Other triggers:
Upper respiratory tract infections
Gastroesophageal reflux
Extrinsic (Immune)
Initial exposure to antigen:
Prompts naive T-cell differentiation to T helper (Th) 2 cells
Followed by production of IgE antibodies, which bind to mast cells and basophils (ready to respond to subsequent antigen exposure)
Extrinsic (Immune) Asthma Patho
Initial exposure to antigen:
T cells and production of igE that bind to MAST cells and basophils.
Early Phase:
Inhaled antigen → IgE-bound mast cells and basophils degranulate (early-phase reaction) → release of mediators (prostaglandin D₂, histamine, leukotrienes) → airway smooth muscle contraction → airway tightening and/or obstruction
Late phase:
Recruitment of inflammatory cells:Th2 cells → production of mediators and cytokines
Eosinophils (the most prominent cells) increase the release of inflammatory mediators
IL-3, IL-4, IL-5, IL-13
Differentiation of eosinophils (IL-5)
Prolonged survival of eosinophils (IL-3 and IL-4)
Production of IgE (IL-4)
↑ mucus glands, airway fibrosis (IL-13)
prostaglandin D₂, histamine, leukotrienes/eosinophils/
IL-3, IL-4, IL-5, IL-13
extrinsic asthma
During flares
The airways of most asthmatic patients are normal at baseline
During flares – often triggered by allergens:
Increased smooth muscle tone
Increased inflammation/edema
Increased mucus production leading to mucus “plugs”
Results in narrowed airways and restricted exhalation
Pathogenesis: Intrinsic (Non-immune) Asthma
Non-eosinophilic
No associated family history of asthma
Does not involve Th2 cells
Environmental factors (pollution, smoking, infections, allergens) →involve Th1 and Th17 cell responses → neutrophilic inflammation and airway hyperresponsiveness
Neutrophilic inflammation:
High sputum neutrophil counts
Associated with severe asthma exacerbations
Often difficult to treat (less responsive to corticosteroids)
typically more severe and more difficult to treat
asthma
Clin Man
Symptoms
Occur with characteristic triggers (allergens, cold air, exercise)
Recurrent wheezing
Dyspnea: chest tightness/heavy weight on the chest
Cough:
Dry or productive of sputum
Worse at night and in the early morning hours
Signs
Asymptomatic when under control
When symptomatic:
Tachypnea
Tachycardia
Hypoxemia
Expiratory ± inspiratory wheezing and rhonchi
Prolonged expiratory phase of respiration
Nasal flaring
Retractions
Use of accessory muscles to breathe
Asthma
PFT Dx
Pulmonary function testing – most useful diagnostic study
Recommended that bronchodilators be stopped before the test
Spirometry:
Maximal inhalation followed by rapid forceful exhalation (at least 6 seconds)
Measures:
FEV1 (forced expiratory volume in 1 second)
FVC (forced vital capacity or the maximal volume exhaled with maximally forced effort)
↓ FEV1 and FEV1/FVC ratio < 0.70 (suggests airway obstruction)
Bronchodilator response:
Nebulized or 2–4 puffs of bronchodilator given, then spirometry rechecked after 15 minutes
Increase in FEV1 by > 12% and 200 mL (bronchodilator responsiveness)
80% of the FVC at 1 second
FEV1/FVC ratio 0.70 or greater
Normal spiro:
asthma
Bronchoprovocation testing
A stimulus (methacholine, exercise, histamine, inhaled mannitol) is tried, to trigger bronchoconstriction
≥ 20% reduction in FEV1 with challenge/testing (airway hyperresponsiveness)
asthma
Peak expiratory flow (PEF)
Used more for monitoring than for diagnosis
Maximal inhalation, then fast forceful exhalation (< 2 seconds) into peak flowmeter
A single peak flow is obtained during symptoms
Results compared with average normal values (based on height and age)
Post-bronchodilator administration (15 minutes after 2 puffs of a bronchodilator), improvement of > 20% suggests reversible airway obstruction
asthma
CXR
- Exclude other diagnosis (pneumothorax or pneumonia in exacerbations)
- Indicated for atypical presentation of asthma (fever, crackles, hypoxemia)
- Normal in mild asthma
- May show hyperinflation in severe asthma (flattened diaphragm, wide intercostal spaces)
asthma
Alpha-1 antitrypsin level
Alpha-1 antitrypsin level:detects alpha-1 antitrypsin deficiency (for patients with persistent airway obstruction)
asthma
Arterial blood gas
indications (3)
Arterial blood gas(in severe asthma exacerbation):
Obtain when oxygen saturation of < 94%, no bronchodilator response, mental status change(s)
What would you expect the ABG to be for a severe asthma exacerbation?
↓ pH – respiratory acidosis
↓↓ PaO2
↑ PaCO2
↓ HCO3
asthma
other labs
CBC
Complete blood count:may show eosinophilia (suggests atopic asthma)
Elevated IgE levels
Moderate-to-severe asthma
don’t need to memorize, know that it change
Early on in an acute episode, we will see hypocarbia (due to hyperventilation) → ↑ pH (respiratory alkalosis)
Severe asthma attack can lead to respiratory failure
asthma
Tx goals and non pharm Tx
Goals:
Control of symptoms and triggers
Reduce future risks and complications
Non-pharmacologic management
Patient education:
Asthma symptoms
Indications for and proper technique of bronchodilator and corticosteroid inhaler use
Discuss “written” asthma action plan (PEF monitoring and corresponding action)
Smoking cessation
Influenza, COVID-19, and pneumococcal vaccinations
asthma
rescue Tx
Used when symptoms occur
Begin working within minutes and can last several hours
Provide quick, short-term relief of asthma symptoms
Example:
Short-acting bronchodilators:
Albuterol
Levalbuterol
Long-acting bronchodilators:
Salmeterol
Formoterol
asthma
maintenance
Tx
Also known as maintenance medications
Used on a daily basis
Prevent the need to use rescue medications
Example:
Inhaled corticosteroids (ICS):
Budesonide
Fluticasone
Mometasone
Leukotriene receptor antagonists (LTRAs):
Zafirlukast
Montelukast (oral)
asthma
bronchodilators
Bronchodilators: Beta-2 Agonists
Short-acting beta-2 agonists:
Albuterol (inhalation, oral)
Levalbuterol (inhalation)
Long-acting beta-2 agonists:
Salmeterol (inhalation)
Formoterol (inhalation)
Mechanism of action and effects
Drug binds the β-2 receptor
Bronchial smooth muscle
Smooth muscle of the blood vessels
Effect
Smooth muscle relaxation → dilation of bronchioles
Decrease mast cell degranulation and histamine release
Inhibit microvascular leakage into the airways
Increase mucociliary clearance
SABA: onset within 5 minutes and duration of 4–6 hours
LABA: duration of up to 12 hours
asthma
Clinical use of Beta bronchodilators
Clinical uses
SABA:
Rapidly acting bronchodilator, used in acute asthma exacerbation
Prevention of exercise-induced asthma
LABA:
Used as acute symptom reliever for moderate to severe asthma
Prevention of nocturnal symptoms
Used only with inhaled corticosteroids, not as a monotherapy
Black Box Warning: monotherapy has an increased risk of asthma-related death
Side effects
β2-mediated skeletal muscle tremors (most common side effect)
Other effects:
Tachycardia (cardiac β receptor stimulation)
Hyperglycemia
Hypokalemia…administer albuterol Tx for hyperkalemia!
asthma
muscarinic antagonists
Bronchodilators: Muscarinic Antagonists
SAMA: ipratropium bromide (inhalation)
LAMA: tiotropium bromide (inhalation)
Mechanism of action and effects
Relaxes bronchial smooth muscle through competitive inhibition ofmuscarinic (M3) cholinergic receptors, thereby preventing bronchoconstriction
Clinical uses
Less effective than β2-agonists for acute exacerbation, but provides additive benefit
Long-term maintenance treatment in children > 6 years of age and adults with severe symptomatic asthma uncontrolled with ICS
Side effects
Rare due to poor absorption into circulation
Blurry vision, dry mouth, dizziness, urinary retention
best result from saba with sama
Asthma
Antileukotriene Agents
Antileukotriene Agents
Leukotriene receptor antagonists (LTRAs): zafirlukast, montelukast (oral) (Singulair)
Mechanism of action and effects
Inhibit leukotriene receptors
Effects (by targeting leukotriene):
↓ smooth muscle contraction
↓ vascular permeability and mucus secretion
Reduced activation of inflammatory cells
Clinical uses
Exercise-induced bronchospasm
Mild persistent asthma + allergic rhinitis
Aspirin-exacerbated respiratory disease
Additive benefit for moderate-to-severe persistent asthma
Considered in patients with difficulty with compliance or inhaler technique (children)
Side effects
Headaches, fatigue, dyspepsia, hepatotoxicity
Drug interaction: increased warfarin effect
not the biggest player.. might not be on exam
asthma
corticosteroids
Corticosteroids
Inhaled corticosteroids (ICS): budesonide, fluticasone, mometasone
Systemic corticosteroids:
Oral: prednisone, prednisolone
IV: hydrocortisone, methylprednisolone
Mechanism of action and effects
Blocks the release of arachidonic acid, consequently halting the release of inflammatory mediators
Effects:
↓ airway hyperresponsiveness
↓ airway mucosal edema
↓ capillary permeability
↓ leukotriene release
Clinical uses
Drug of choice for long-term control of persistent types of asthma
Early systemic corticosteroids in acute exacerbations often abort the exacerbation, decrease the need for hospitalization, prevent relapse, and speed recovery
Short-term oral corticosteroid treatment (< 7 days) of acute severe exacerbations
Tapering required if oral corticosteroid > 2 weeks
asthma
side effects of corticosteroids
Side effects
ICS have less severe and fewer side effects than systemic steroids
Include:
Thrush, skin bruising, weight gain, hyperglycemia → diabetes, hypertension, immune suppression, ophthalmic changes, osteopenia/osteoporosis, respiratory infections, deceleration of growth velocity in children
way more symptoms with systemic steroids versus inhaled
asthma
Immunomodulators
Anti-IgE or IgE antibody (omalizumab)
IL-5 antagonist:mepolizumab, reslizumab
IL-5 Receptor antagonist: benralizumab
Anti-IL-4 receptor antagonist (dupilumab)
Clinical use
Management of moderate-to-severe asthma
script usually given by pulminologist or allergist
Asthma
Guidelines
National Asthma Education and Prevention Program (NAEPP)
Global Initiative for Asthma (GINA)
(preffered)
Asthma
Emergency management
severe asthma exacerbation
For severe asthma exacerbation
Oxygen therapy goal: 93%–95% oxygen saturation (adults)
Inhaled therapy:
High dose of SABA via nebulizer or spacer
Nebulized ipratropium (anticholinergic) if no response to beta-2 agonists
Intravenous medication(s):
IV corticosteroids:
If asthma does not improve consistently after SABA treatment
If exacerbation occurs despite ongoing daily oral steroid therapy
If exacerbation is recurrent after recent discontinuation of systemic steroids
Consider IV magnesium sulfate (bronchodilator activity)
2 g infused over 20 min; contraindicated in renal insufficiency
Status asthmaticus
emergency Tx
Status asthmaticus
Severe, intense, prolonged bronchospasm that is resistant to treatment
Endotracheal intubation and mechanical ventilation in case of impending respiratory failure:
- Mental status changes (confused, agitated, or drowsy)
- Silent chest on auscultation
- Respiratory fatigue (respiratory rate > 30/min, heart rate > 120/min, use of accessory muscles)
- Respiratory acidosis with increasing hypercapnia
- Low oxygen saturation (< 92%) despite high-flow oxygen
