Respiratory Disorders Flashcards

1
Q

Asthma: Aetiology and Pathophysiology

A

characterised by airway constriction and/or inflammation
exposure to triggers, such as allergens, medications, stress, physical exertion, environmental factors can lead to obstruction of airflow during expiration

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2
Q

Exercise-induced Asthma

A

constriction of the bronchi due to exercise
manifests within 5-20 mins of physical activity
caused by increased breathing rates and loss of heat and water from the respiratory tract
leads to airway hyperresponsivity making breathing more difficult

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3
Q

Occupational Asthma

A

results from exposure to workplace substances and/or environmental conditions
can be allergen induced or non-allergen induced
allergen induced: due to allergens like dust and pollen
non allergen induced: due to irritants like smoke, fumes and gases

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4
Q

Asthma: clinical manifestations

A

high pitched, end-expiratory wheeze
dyspnea
non productive cough (dry cough)
chest tightness
hypoxia (not enough oxygen) -> activates SNS –> increases heart and breathing rates
nasal congestion
severe attacks –> excessive bronchoconstriction
respiratory muscle fatigue, and silent chest
severe signs include cyanosis and significant anxiety due to SNS activation

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5
Q

Asthma: Diagnosis

A

taking a thorough history to identify triggers and environmental factors (pet cohabitation, home routine cleaning, and any presence of mould)
physical exam with chest observation and auscultation
pulse oximetry from the start of an acute episode of asthma
chest x-rays and arterial blood gas analysis helps to rule out other conditions and assess respiratory changes
allergy testing and sputum analysis

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6
Q

Asthma: Management

A

apply high flow oxygen
position patient upright in high fowlers o semi-fowlers position
administer short acting beta 2 agonist (opens airways quickly and stops asthma) through nebulization
create a calm environment to reduce SNS activity
use corticosteroids (inhaled or oral) to control inflammation and bronchial hyperresponsiveness
educate on controlling environmental exposures
monitor physical activity and encourage indoor exercises
stop smoking and avoiding exertion in high pollution conditions
recommend avoiding certain drugs like aspirin and NSAIDS which can exacerbate Asthma symptoms

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7
Q

Chronic Obstructive Pulmonary Disorders (COPD)

A

characterised by irreversible airflow limitation
causes breathing difficulties

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8
Q

Chronic Bronchitis:

A

a productive (wet) cough lasting at least 3 months for two consecutive year
often coexists with emphysema due to shared risk factors like smoking
one of the most prevalent forms of COPD

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9
Q
A
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10
Q

Chronic Bronchitis: Clinical Manifestations

A

frequent productive cough
dyspnea and wheezing
signs of upper respiratory tract infections
increased breathing and heart rates during acute episodes
chronic issues: heart-related complications , pulmonary hypertension, peripheral oedema, R sided HF
can cause cyanosis in severe cases

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11
Q

Chronic Bronchitis: Diagnosis

A

through medical history and physical exam.
pulse oximetry to assess blood oxygen saturation
blood tests for additional info, especially for patients presenting fever symptoms
for patients with purulent productive cough, a sputum culture is typically advised
chest x-rays for chronic gas trapping and signs of heart failure
pulmonary function tests showing obstructive pattern
arterial blood gas analysis in severe cases for acidosis (acid in the blood) and gas levels

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12
Q

Chronic Bronchitis: Management

A

Focus on symptom relief and preventing acute exacerbations.
Use of bronchodilators and mucolytics.
Supplemental oxygen during hypoxic episodes.
Beta-2 agonists (a bronchodilator) to reduce wheezing and dyspnoea.
Staying well-hydrated to reduce secretion viscosity.
Avoid expectorant agents in acute bronchitis - they tend to increase mucus production
Quitting smoking is crucial.
Corticosteroids for inflammation reduction.
Antibiotics for secondary bacterial infections.

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13
Q

Emphysema: Background

A

Incurable condition often linked to smoking.
Leads to enlargement of terminal bronchioles and alveoli damage.
Results in loss of lung elasticity.

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14
Q

Emphysema: Aetiology and Pathophysiology

A

Arises from the imbalance of the enzyme that protects the alveoli
Destroys elastin and collagen, reducing lung elastic recoil and alveolar pressure.
Alveolar spaces become permanently enlarged.
Smoking initiates or worsens damage by triggering inflammation.

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15
Q

Emphysema: Risk factors

A

Exposure to tobacco smoke, occupational dusts, pollution.
Male gender.
Age over 50 years.
Frequent respiratory infections.
Low socioeconomic status.
Poor nutrition.
Respiratory comorbidities

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16
Q

Emphysema: clinical manifestations

A

Gradual progression, often unnoticed until significant respiratory compromise.
Symptoms include frequent URIs, dyspnea, wheezing, tachypnoea, productive coughing.
Dyspnea initially during exertion, progressing to minimal effort.
Chronic gas trapping leads to barrel chest appearance.
Weight loss and fatigue due to chronic dyspnoea and increased respiratory effort.
Seasonal exacerbations can cause severe respiratory dysfunction.
Depression common due to social isolation and decreased mobility

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17
Q

Emphysema: Diagnosis

A

Detailed history and physical examination.
Blood tests for arterial blood gas (ABG) analysis and full blood count.
ABG analysis may show respiratory acidosis progressing to metabolic alkalosis, low blood oxygen, and high blood carbon dioxide levels.
X-rays reveal long lung fields and flattened diaphragm.
Lateral chest X-rays over time show barrel chest development.
Sputum samples and respiratory function tests reveal obstructive pattern in FEV1 (forced expiratory volume in 1 second)

18
Q

Emphysema: Management

A

Focuses on slowing disease progression and preventing exacerbations.
Key interventions include:
Stopping smoking.
Annual flu vaccinations.
Minimizing exposure to pollutants and passive smoking.
Oxygen therapy and diuretics.
Intermittent positive pressure ventilation in severe cases.
Managing weight loss and muscle wasting through diet and exercise.
Addressing osteoporosis risks, especially with corticosteroid use.

19
Q

Pulmonary Fibrosis: Aetiology and Pathophysiology

A

Condition where lung tissue becomes scarred and damaged, leading to breathing difficulties.
Damage from prolonged exposure to toxins like silica dust and asbestos fibres.
Can develop from medical conditions like dermatomyositis (muscle weakness and skin rash), scleroderma (hardening and thickening of skin), and pneumonia.
Certain chemotherapy drugs and medications can contribute to lung damage.
Lung tissue becomes thicker and stiffer, hindering lung function and causing shortness of breath.
Idiopathic pulmonary fibrosis has unknown causes, possibly linked to viruses, smoking, and genetics.
Key risk factors include:
Older age and male gender
Smoking habits.
Exposure to pollutants in work environments (e.g., mining, farming).
Previous cancer treatments.
Genetic predispositions.

20
Q

Pulmonary Fibrosis: Clinical Manifestations

A

Symptoms vary but often include:
Shortness of breath.
Persistent dry cough.
Fatigue and unexplained weight loss.
Muscle and joint aches.
Clubbing of fingers and toes.
Progression and severity differ among individuals.
Acute exacerbations can cause sudden, severe increases in symptoms like breathlessness

21
Q

Pulmonary Fibrosis: Diagnosis

A

Thorough physical exam and review of medical and family history.
Imaging tests: chest X-rays, CT scans, echocardiograms.
Pulmonary function tests, pulse oximetry, exercise capacity tests, and arterial blood gas analysis.
Invasive tests: lung biopsy, bronchoalveolar lavage, blood tests for liver and kidney function.

22
Q

Pulmonary Fibrosis: Management

A

Treatment aims to alleviate symptoms and enhance life quality.
Medications and therapies, including antibiotics and corticosteroids, during acute exacerbations.
Mechanical ventilation for severe cases.
Lung transplantation for certain individuals.

23
Q

Pulmonary Fibrosis: Complications

A

Possible complications include:
Pulmonary hypertension.
Right-sided heart failure.
Respiratory failure.
Lung cancer.
Pulmonary blood clots.
Pneumothorax.
Lung infections.

24
Q

Acute Bronchitis: Aetiology and Pathophysiology

A

Primarily caused by viral infections following an upper respiratory tract infection.
Bacterial infections can also cause acute bronchitis (more susceptible in individuals with chronic lung conditions e.g. emphysema)
Infection triggers an inflammatory response, increasing mucus production.
Leukocytes damage the ciliated epithelium in the bronchi, overwhelming the mucociliary escalator.
Leads to coughing fits and potentially bronchospasm, further obstructing the bronchi

25
Q

Acute Bronchitis: Clinical Manifestations

A

Often stems from a viral infection, preceded by symptoms like headache, fever, muscle ache, and malaise.
Common upper respiratory symptoms: sore throat, runny nose.
Lower respiratory symptoms: shortness of breath, wheezing, cough.
Chest discomfort or pain from coughing bouts (short periods of coughing)

26
Q

Acute Bronchitis: Diagnosis

A

Diagnosed by ruling out other conditions, as viral form can mimic asthma and bacterial form can resemble pneumonia.
Inves tigations similar to those for chronic bronchitis.
Chest X-ray may be necessary for severe symptoms to rule out bacterial pneumonia.
Spirometry can help exclude asthma.

27
Q

Acute Bronchitis: Management

A

Acute bronchitis is typically self-limiting and doesn’t require medical intervention or hospital admission.
Preventive measures: avoid respiratory irritants like smoke, sudden temperature changes, heavy pollution.
Bed rest advised due to fatigue from viral infection and coughing spells.
NSAIDs can relieve chest pain.
Chest splinting during coughing can reduce discomfort.
For high-risk individuals: smoking cessation programs, annual flu vaccinations, avoiding contact with people with respiratory infections.
Maintaining good nutrition, body weight, and a balance of rest and exercise is important.

28
Q

Pneumonia: Aetiology and Pathophysiology

A

Characterized by inflammation of the alveoli, impacting gas exchange.
Caused by bacteria, viruses, fungi, or other pathogens, and non-infectious factors like harmful substances or aspiration of gastric contents.
Pathogens entry into the respiratory system leads to multiplication and release toxins, causing an inflammatory response.
Results in alveolar oedema, vascular congestion, epithelial cell damage, and debris accumulation in alveoli, decreasing lung compliance.
Can affect entire lobes, specific regions, or cause patchy inflammation and small, diffuse lesions.
Can be acquired in hospitals, aged-care facilities, clinics, or in the community.

29
Q

Pneumonia: Risk Factors

A

Chronic illness, advanced age, lung cancer.
Abdominal or thoracic surgery, viral infections.
Chronic respiratory diseases, smoking, malnutrition, alcoholism.
Exposure to harmful gases, aspiration, immunosuppressive therapy, premature birth.

30
Q

Pneumonia: Clinical Manifestations

A

Common symptoms: shortness of breath, rapid breathing, cough, fast heart rate, increased sputum, fever, chest pain, malaise, fatigue.
Severe hypoxia may lead to confusion or agitation.

31
Q

Pneumonia: Diagnosis

A

Comprehensive history and physical exam.
Focus on risk factors, oxygen saturation monitoring, vital sign assessment

Chest X-ray to identify affected areas.
Blood examination may show increased white blood cell count.

32
Q

Pneumonia: Management

A

Supplemental oxygen for shortness of breath and rapid heart rate.

Antimicrobial therapy for bacterial or fungal infections, and secondary bacterial infections after viral pneumonia.

Paracetamol for pain and fever management, considering fever and inflammation as natural defense mechanisms.

33
Q

Influenza: Aetiology and Pathophysiology

A

Viral respiratory infection affecting upper and lower respiratory tracts.
Causes inflammation in sinuses, nasal cavity, pharynx, tonsils, epiglottis, larynx, trachea, and bronchioles.

34
Q

Influenza: Clinical Manifestations

A

Rapidly developing symptoms: fever above 38°C, headache, nasal congestion, chills, sweats, Dry cough, fatigue, and muscle aches.

35
Q

Influenza: Diagnosis

A

Rapid onset of fever, nasal congestion, and dry cough suggest influenza.
Confirmed via PCR test using a nose and throat swab.

36
Q

Influenza: Management

A

Antibiotics are ineffective; antiviral drugs effective if started early.
Management includes rest, isolation to prevent spread, paracetamol or NSAIDs for symptom relief.

37
Q

Lung Cancer: Aetiology and Pathophysiology

A

Lung cancer includes various malignancies in the respiratory system.

Classified into two types: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC).

NSCLC is the most common, responsible for 80% of lung cancers, usually starting in bronchi and smaller airways.

SCLC accounts for 20%, typically beginning in central lung locations.

Caused by disordered cell growth and failure of immune surveillance, allowing abnormal cells in bronchi, bronchioles, and alveoli to mutate and proliferate.

Major cause is smoking, with risk increased by genetic predisposition and exposure to carcinogens like asbestos.

Risk factors include early smoking, age, frequency and duration of smoking, with smokers having up to 25 times higher risk than non-smokers.

38
Q

Lung Cancer: Clinical Manifestations

A

Local effects: chest pain, cough, dyspnoea, coughing up blood.
Regional effects: complications in metabolic, endocrine, hematological, neurological, and renal systems.

39
Q

Lung Cancer: Diagnosis

A

Thorough history, focusing on smoking behaviors and exposure to carcinogens.
Initial imaging studies: chest X-ray, CT scan to determine presence and location of lesions.
Conclusive investigations to determine cancer type

40
Q

Lung Cancer: Management

A

Treatment plans based on cancer stage.
Options include surgery to remove lesions (not possible for all types), radiotherapy, and chemotherapy to reduce or control cancer size