Acute bronchitis/flu/asthma Flashcards

1
Q

Acute bronchitis

General and RF

A

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

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2
Q

acute bronchitis

patho

A

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

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3
Q

Acute bronchitis

S/Sx

A

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

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4
Q

Findings that are more consistent with pneumonia than acute bronchitis

A

Fever
Tachypnea
Rales
Dullness to percussion
Egophony: E → A
Tactile fremitus:
↑ in areas of increased lung density (consolidation)

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5
Q

acute bronchitis

Diagnosis

A

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

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6
Q

acute bronchitis

Chest X-ray indications

A

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

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7
Q

acute bronchitis

Tx

A

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

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8
Q

acute bronchitis

Tx For malaise, myalgias, and fever

A

Analgesic antipyretics:
NSAIDs
Acetaminophen

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9
Q

Acute bronchitis

Tx For wheezing/ pts with asthma or COPD

A

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

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10
Q

Influenza

Antigenic drift

A

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

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11
Q

Antigenic shift

A

Two or more different strains of a virus combine to form a new subtype that is radically different; limited or no prior immunity

pandemic

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12
Q

flu

Transmission and Viral shedding

A

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

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13
Q

flu

Clinical Presentation

A

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

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14
Q

Flu

Dx
Key clinical findings

A

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

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15
Q

flu

Virulent glycoproteins & Nucleoproteins

A

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)

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16
Q

Flu

Labs and imaging

A

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

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17
Q

flu

complications

A

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

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18
Q

Flu

Tx

A

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)

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19
Q

flu

prevention

A

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)

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20
Q

flu

2 basic types ofinfluenza vaccine:

A

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

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21
Q

Asthma

A

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

22
Q

asthma

Predisposing Factors

A

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

23
Q

asthma

Maternal factors
Decreased and increased risk

A

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

24
Q

asthma

triggers

A

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

25
Q

Extrinsic (Immune)
Initial exposure to antigen:

A

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)

26
Q

Extrinsic (Immune) Asthma Patho

A

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

27
Q

extrinsic asthma

During flares

A

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

28
Q

Pathogenesis: Intrinsic (Non-immune) Asthma

A

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

29
Q

asthma

Clin Man

A

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

30
Q

Asthma

PFT Dx

A

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:

31
Q

asthma

Bronchoprovocation testing

A

A stimulus (methacholine, exercise, histamine, inhaled mannitol) is tried, to trigger bronchoconstriction
≥ 20% reduction in FEV1 with challenge/testing (airway hyperresponsiveness)

32
Q

asthma

Peak expiratory flow (PEF)

A

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

33
Q

asthma

CXR

A
  • 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)
34
Q

asthma

Alpha-1 antitrypsin level

A

Alpha-1 antitrypsin level:detects alpha-1 antitrypsin deficiency (for patients with persistent airway obstruction)

35
Q

asthma

Arterial blood gas
indications (3)

A

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

36
Q

asthma

other labs
CBC

A

Complete blood count:may show eosinophilia (suggests atopic asthma)

Elevated IgE levels
Moderate-to-severe asthma

37
Q

don’t need to memorize, know that it change

A

Early on in an acute episode, we will see hypocarbia (due to hyperventilation) → ↑ pH (respiratory alkalosis)

Severe asthma attack can lead to respiratory failure

38
Q

asthma

Tx goals and non pharm Tx

A

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

39
Q

asthma

rescue Tx

A

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

40
Q

asthma

maintenance
Tx

A

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)

41
Q

asthma

bronchodilators

A

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

42
Q

asthma

Clinical use of Beta bronchodilators

A

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!

43
Q

asthma

muscarinic antagonists

A

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

44
Q

Asthma

Antileukotriene Agents

A

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

45
Q

asthma

corticosteroids

A

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

46
Q

asthma

side effects of corticosteroids

A

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

47
Q
A

way more symptoms with systemic steroids versus inhaled

48
Q

asthma

Immunomodulators

A

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

49
Q

Asthma

Guidelines

A

National Asthma Education and Prevention Program (NAEPP)

Global Initiative for Asthma (GINA)
(preffered)

50
Q
A
51
Q

Asthma

Emergency management
severe asthma exacerbation

A

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

52
Q

Status asthmaticus
emergency Tx

A

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