Respiratory Illnesses Flashcards

1
Q

What is Asthma?

A

Inflammatory disease of the airways causing recurrent and variable airflow limitations which makes breathing difficult

  • Trigger coughing and wheezing when breathing out and shortness of breath
  • Bronchospasm can occur secondary to inflammation
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2
Q

What are the risk factors of asthma?

A

Can be a genetic component with >20 genes identified as linked to asthma, however, there typically needs to be a trigger to cause symptoms: allergens (pollen, dust mites, food, pets), drugs (beta-blockers and NSAIDs, aspirin and indomethacin), respiratory infections, exercise, emotional factors, and hormonal changes

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3
Q

What is the pathophysiology of Asthma?

A

The triad of effects associated with asthma include inflammation, bronchoconstriction and excess mucus secretion. Exposure to a trigger can lead to inflammation and a hyperactive airway

• Inflammation increases inflammatory cells (eosinophils, mast cells, neutrophils, T lymphocytes) in the bronchi = release inflammatory mediators (histamine, leukotrienes, enzymes) = further exacerbates the problem and may cause bronchoconstriction (typically short-lived and reversible in acute cases, however, can fatal)
• The inflammatory process triggers hypersecretion of mucus = block the airways = cause swelling of mucosa due to inflammation associated with vascular leakage and oedema = increased WOB, decreased ventilation and impaired gas exchange *In chronic severe asthma, there is remodelling of the airways to increase bronchial smooth muscle content = irreversibly narrow airway = limits the effectiveness of treatment
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4
Q

What are the types of triggers for asthma?

A
• Intrinsic: trigger for asthma may be intrinsic/ non-atopic (no external cause can be identified) = non-immune mechanisms and typically appear in adulthood and may not improve
		- Triggered by emotional factors, hormonal changes, exercise, respiratory infections, drugs (aspirin, indomethacin), occupational exposure (20% of working population) including isocyanates (present in industrial and polyurethane coatings) and fumes (welding or soldering) 
	• Extrinsic: trigger for asthma may be extrinsic/ atopic (identified though IgE mediated reaction of mast cells)
Primary mediator (histamine) or secondary mediators (leukotrienes, prostaglandin D2(PGD2)) are released in response to an outside trigger - exposure to dust mites, pollen or pet dander =  increase in vascular permeability and thus increased mucous secretions & bronchoconstriction
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5
Q

What are the morphological changes associated with bronchoconstriction? (4)

A

hyperinflation of the lungs, air trapping and mucus plugs= histological changes:
• Thickening of the basement membrane of the bronchial epithelium
• Inflammatory infiltration of the bronchial wall (oedema)
• Increased mucosal glands
• Hypertrophy of the bronchial smooth muscle (in the case of chronic asthma)

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6
Q

How do you diagnose Asthma?

A

based on patient history, physical examination, laboratory findings, pulmonary function tests (spirometry) and radiology
• Spirometry: measures ventilation of air exchanged in breathing - most likely reflect a decreased expiratory flow rate and forced expiratory volume
• ABG: moderate or severe cases of asthma = hypoxaemia
Chest X-rays: utilised to rule out other causes (e.g. pneumonia)

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7
Q

What is the pharmacological treatment for acute Asthma?

What are the pharmacological treatments for asthma aimed at and based on?

A

treated with drugs that reverse bronchoconstriction (inhaled bronchodilators) and relieve inflammation. May also require oxygen or oral corticosteroids

aimed at eliminating the causative agent and based on the severity of the asthma

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8
Q

What is the pharmacological treatment for chronic Asthma?

A

best treatment is prevention and to avoid known allergens/ triggers. Inhaled anti-inflammatory agents like corticosteroids:
• Long acting β2-agonists and ipratropium used to control persistent bronchospasm
• leukotriene receptor antagonists (montelukast and zafirlukast)
*Leukotrienes inflammatory mediators (LTC4, LTD4, LTE3) are associated with causing mucus secretion, airway wall oedema and bronchospasm

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9
Q

Define mild, moderate and severe asthma

A

Worsening of asthma control - just outside normal range for the individual:
More symptoms than usual, needing a reliever more than usual, waking up with asthma, asthma is interfering with usual activities
Tx:
• β2-agonist (salbutamol) is used as a reusable inhalant.
• Short course of inhaled corticosteroids may be appropriate

Events that are troublesome or distressing to the patient - require a change in tx;
not life-threatening;
do not require hospitalisation
More symptoms than usual, increasing difficulty breathing, waking often at night with asthma symptoms
Tx: • Oxygen therapy may be required
• Salbutamol (5-10 mg; 8 puffs every 15 min for 3 doses)
Used initially with corticosteroids (50 mg oral prednisolone, 250 mg hydrocortisone) and then reviewed one hour after last dose

Require urgent action by the patient (or carers) and health professionals to prevent a serious outcome (hospitalisation or death)
Needing reliever again within 3 hours, difficulty with normal
Tx:
• Oxygen is required to maintain SpO2at >92%
• Continuous β2-agonists administered IV and corticosteroids/ipratropium
• Asthmaticus (asthma attacks follow one another without pause)intubation required

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10
Q

What is COPD?

A

COPD is an umbrella term for two pathological lung conditions that cause chronic and recurrent airflow obstruction: chronic bronchitis and emphysema

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11
Q

What is chronic bronchitis?

A

lining of the airways is constantly inflamed = lining to swell and produce more mucus making it hard to breathe

*clinical diagnosis that requires the presence of a chronic cough with sputum production for three months per year for at least two consecutive years

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12
Q

What is emphysema?

A

Pathological, permanent dilation of the respiratory bronchioles, alveolar ducts, and alveolar sacs - due to the destruction of the walls of the airways without fibrotic changes = disrupting gas exchange

*Clinical diagnosis characterised by the abnormal, permanent enlargement of the airspaces with alveolar wall destruction

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13
Q

What is the most common cause of COPD and other risk factors?

A

smoking; Expiratory airflow normally decreases with age, however, cigarette smoking accelerates this decline. Other risk factors and causes include genetic/hereditary (deficiency in α1-antitrypsin), occupational/environmental exposure (organic/inorganic dusts, gases, pollution), passive smoking and infections

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14
Q

What is the pathophysiology of chronic bronchitis?

A
• Inspired irritants/triggers (smoking/recurrent infections) increase mucus production and increase the size and number of mucous glands and goblet cells = sticky mucus makes it easy for bacteria to adhere and rapidly multiply in the airway secretion
	• Ciliary function is impaired = pulmonary infection and injury = inflammation
Persistent inflammation and oedema = bronchospasm, permanent narrowing of the airways, gas trapping = V/Q mismatch, hypoventilation, increased in PaCO2and hypoxemia
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15
Q

What are the clinical manifestations of chronic bronchitis?

A

• “blue bloater” - cyanosis: bluish colour of the lips and skin seen in patients who are ≥50 years - decrease in the amount of O2reaching the blood
• Ankles and legs may be swollen, distention of the neck veins, and the patient exhibits wheezing, dyspnoea, productive cough (smoker’s cough) and frequent pulmonary infections
Airway obstruction and decreased forced expiratory volume (FEV) accompanies a decrease in alveolar (minute) ventilation and a rise in PaCO2which may lead to hypoxemia, polycythaemia and cor pulmonale

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16
Q

How do you diagnose chronic bronchitis?

A
  • Hx of symptoms
  • Physical assessment: wheeze and barrel chest (increased anteroposterior dimensions of the chest)
  • Chest X-ray: determine structural problems
  • Pulmonary function tests (function of the lungs) and arterial blood gas sampling (oxygenation of blood) may be required
17
Q

What is the treatment of chronic bronchitis?

A
  • Prevention of pathology is irreversible: cease smoking , avoid irritants, immunisation for influenza and pneumococcal disease will assist to reduce the risk of exacerbations, oxygen therapy to prevent cor pulmonale, and antibiotics if there is a known and susceptibly to an infective source
    • Pharmacological treatment consists of bronchodilators and mucolytics, long-acting inhaled β2-agonists ipratropium, oral theophylline and corticosteroids in the later stages
18
Q

What is the pathophysiology of emphysema?

A

• Loss of lung elasticity (proteases digest elastin and other alveolar wall components) and enlargement of airspaces - typically initiated by toxins in cigarette smokes = airway epithelial inflammation = infiltration of neutrophils, macrophages, lymphocytes
• Inflammatory cytokines cause an increase in protease activity and a decrease in antiproteases (α1-antitrypsin, inhibited by smoke) = imbalance leads to a breakdown of elastin in the alveolar septa = destruction of capillary beds = loss of elastic recoil and expiration becomes difficult:
- Hyperinflation of alveoli (bullae) and increased TLC
Blebs (air spaces adjacent to pleura) develop

19
Q

What are the classifications for emphysema ?

A
• Centriacinar (centrilobular)
	○ Upper lobes of the lung
	○ Smokers with chronic bronchitis
• Panacinar (panlobular)
	○ Lower lobes of the lung
Older and α1-antitrypsin deficient individuals
20
Q

What are the clinical manifestations for emphysema?

A
  • “pink puffer”- reddish complexion and the hyperventilation seen in patients (aged ≥60 years)
  • Tend to use accessory muscles, have pursed lips, are thin and tachypnoeic
  • Dyspnoea on exertion = progresses to severe, minor cough/sputum, barrel chest and decreased breath sounds
21
Q

How do you diagnose emphysema?

A
  • Pulmonary function test
  • Chest X-rays: flattened diaphragm and over-distention of the lungs
  • Atrial blood gas vary in the degree of hypoxaemia and/or hypercapnia
22
Q

What is the treatment for acute exacerbations of emphysema?
What is the treatment for chronic emphysema?

What is the pharmacological management of emphysema?

A

• Oxygen therapy (mechanical ventilation will depend on severity)
• Pharmacological management
• Administration of bronchodilators (inhaled)
Oral corticosteroids

• Smoking cessation
• Nutritional support
• Oxygen therapy
Pulmonary rehabilitation

• Inhaled anticholinergic medications and beta-agonists
COPD spectrum

23
Q

What is pneumonia?

A

• Acute inflammation and infection of the lung parenchyma (alveoli and bronchioles – lower respiratory tract) caused by bacteria, viruses, fungi (candida), protozoa and parasites
• Typically caused by gram-positive (Streptococcus pneumoniae (most common), Streptococcus pyogenes, Staphylococcus aureus) or Gram-negative (Pseudomonas aeruginosa, Enterobacter species, Klebsiella) bacteria
• Influenza and respiratory syncytial virus (RSV) can also cause pneumonia
**Upon auscultation - crackles

24
Q

What are the risk factors for pneumonia?

A

age (particularly older people), immunocompromised patients, underlying pulmonary disease/chronic diseases, alcoholism, smoking, malnutrition and prolonged immobilisation

25
Q

What are the classifications for pneumonia

A

• Causative agent
○ Typical - bacterial infection (most common)
○ Atypical - viral or mycoplasma infection (milder and less common)
• Distribution of infection
○ Lobar - consolidation of part or all of lung
○ Bronchopneumonia - consolidation in more than one lobe
• Setting
○ Community
Hospital

26
Q

What is the pathophysiology for typical pneumonia?

What is typical pneumonia usually caused by ?

A
  • Initiation of inflammatory and immune response = produce antibodies, complement activation, release of inflammatory cytokines = oedema
    • Oedema = where bacteria multiply and spread into adjacent portions of the lung = lobar consolidation
    • “Red hepatisation” = alveoli filled with RBC
    • “Grey hepatisation” = fibrin deposition, WBC and rapid phagocytosis
    • Resolution = increased macrophages, degeneration of neutrophils, fibrin and bacteria are digested and removed via the lymphatic vessels

streptococcus pneumonia

27
Q

What are the clinical manifestations of typical pneumonia?

A

depend on the age and general health status of the patient
• Previously healthy patients may experience a sudden onset:
○ Malaise, severe shaking, chills and fever (40-41°C)
○ Productive cough (sputum changes from watery to bloody)
○ Inspiratory crackles, dyspnoea and pleuritic chest pain
• Older people are less likely to have elevations in temperature:
○ Loss of appetite
○ Deterioration in mental status

28
Q

How do you diagnose typical pneumonia?

A

• Chest X-ray: infiltration
• WBC elevated
• Sputum Gram stain
• Sputum and blood cultures in hospitalised patients
For immunocompromised patients, lung biopsy and/or bronchoscopy

29
Q

What is the treatment of typical pneumonia?

A

• Adequate ventilation and oxygenation, adequate hydration and pulmonary hygiene
• Antibiotics (broad spectrum)
○ ß-Lactams (penicillins and cephalosporins)
○ Macrolides (erythromycin)
Fluoroquinolones

30
Q

What are some complications of typical pneumonia?

A

• Pleurisy – inflammation of pleura
• Pleural effusion – present in 20-60% of patients with typical pneumonia; reabsorbs in approximately 1-2 weeks but in severe cases, thoracentesis (drainage) is required
• Atelectasis with mucus/sputum plugging
• Lung abscess – necrosis of lung tissue (rare, linked to aspiration)
• Empyema – purulent exudate within pleural cavity (less common, requires chest drain and antibiotics)
• ARDS, pericarditis, endocarditis, meningitis (systemic spread of the organism)
Multi-organ dysfunction syndrome – severe pneumonia can lead to systemic organ dysfunction/failure - high mortality

31
Q

What are some vaccinations relating to pneumonia?

A

• Hib vaccine: mainly children for Haemophilus influenzae type B
• Flu vaccine: older people, smokers and people with chronic illness and weakened immune system
Pneumococcal vaccine: Chronic illness, asplenic patients, transplant recipient

32
Q

What is the pathophysiology of atypical pneumonia?

A

• Lack of lung consolidation and alveolar exudate
• Moderate amount of sputum or dry cough
• Destruction of ciliated mucosa, goblet cells and mucus glands - prevents mucociliary clearance
Bronchial wall becomes oedematous and infiltrated with WBC (increased WBC)

33
Q

What are the clinical manifestations of atypical pneumonia?

A

• Fever, headache, muscle aches and pain

Cough may be dry/non-productive or productive

34
Q

How do you diagnose atypical pneumonia?

A

• Patient History
• Physical examination
Chest X-ray

35
Q

What is the treatment of atypical pneumonia?

A

• O2therapy, hydration (IV fluids), fever management (antipyretic therapy) and possibly macrolides.
Antiviral agents for severe infections and immunocompromised patients (famciclovir)

36
Q

What is community acquired pneumonia?
What is the diagnosis and tx for community acquired pneumonia?
How to reduce community-acquired pneumonia?

A
• Defined as an infection that begins outside the hospital or is diagnosed within 48 hours after admission in a patient who has not resided in a long-term care facility for at least 14 days prior to admission or onset of symptoms
Typically bacterial (S. pneumoniae) or viral (influenzae, RSV)

Diagnosis:
• Age, severity, coexisting pathological conditions
• <65 years without coexisting medical problems – patient hx, physical examination, CXR, knowledge of pathogens
• Sputum and blood cultures – patients requiring hospitalisation

Treatment:
• Usually does not require hospitalisation but may require broad spectrum antibiotics
• Higher mortality rates for older people and smokers

Reduce host factor vulnerability:
• Vaccination
• Gardening precautions – legionella (gram-negative bacteria) contactable in soil, fertilizers, mulch, water-tanks (harmful when inhaled)
• Caution handling animals
• Improvement in poor dental hygiene
• Reduce exposure to anaerobes
37
Q

What is hospital acquired pneumonia?

A
  • Lower respiratory tract infection that was not present or incubating on admission: occurs > 48 hours after admission
  • 2nd most common cause of hospital-acquired infections - mortality rate of 20-50%
  • Usually occurs in ICU patients (mechanical ventilation/intubation), immunocompromised patients (chemotherapy/radiation, transplants, prolonged corticosteroids), chronic lung disease patients or other conditions
  • Most are bacterial
  • Organisms present in the hospital environment are Pseudomonas aeruginosa, Staphylococcus aureus, Enterobacter and Klebsiella species - more difficult to treat than community-acquired infections because of acquired antibiotic resistance
38
Q

What is aspiration pneumonia?

A

inhaling pathogenic material from the oropharynx; common cause of pneumonia in 5-15% cases; can occur due to a loss of consciousness (gag and cough reflex depressed)

39
Q

What is aspiration pneumonitis?

A

inflammatory chemical injury of the tracheobronchial tree and pulmonary parenchyma due to inhalation of sterile gastric contents - Gastric juices are irritants that causes parenchyma injury with infection a secondary event (48-72 hours later). The pathogen is usually one of the normal oropharyngeal flora