Pathologies Flashcards

1
Q

What is Bronchiectasis?

A

The permanent abnormal dilatation of one or more bronchi. Is a feature of CF although this describes non-CF bronchiectasis

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2
Q

Aetiology of Bronchiectasis?

A
  • Major cause of damage to the airways due to severe lower respiratory tract infections e.g., pneumonia, whooping cough or measles
  • Immunodeficiencies which affect the respiratory system, inhaled foreign bodies, gastric aspiration, primary ciliary dyskinesia, tuberculosis, and allergic bronchopulmonary aspergillosis
  • Also associated as a secondary manifestation of primary lung diseases such as COPD, sarcoidosis, and bronchiolitis obliterans
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3
Q

Pathophysiology of Bronchiectasis?

A
  1. The inflammatory processes related to acute or chronic lung infection damage the cilia, enabling bacteria to remain in the airway and colonize the mucus.
  2. These microorganisms stimulate a host inflammatory response, further inhibiting ciliary function, damages the elastic and muscular tissue of the bronchial walls and stimulate mucus production
  3. The loss of elastic and muscular tissue in the airway wall leads to dilatation of the bronchi
  4. A vicious cycle ensures where clearance of secretion from then dilated bronchi is impaired and secretions become chronically infected, producing a persistent host inflammatory response. This results in a progressive destructive lung disease
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4
Q

Clinical features of Bronchietasis?

A
  • Severe disease- cough productive of large amounts of purulent sputum, sometimes bloodstained
  • Severe exacerbations- chest pain, breathlessness, and fevers
  • Auscultation findings of localized or widespread inspiratory and expiratory crackles with occasional wheezing
  • Clubbing of fingers and/or toes may occur is severe disease
  • Exercise tolerance may be reduced
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5
Q

What is Asthma?

A

Characterized by hyperactive airways that respond to various stimuli by widespread inflammation and airway narrowing. Often reversible either spontaneously or with treatment

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6
Q

Aetiology of Asthma?

A
  • Predisposition to asthma if relatives are asthmatic
  • Environmental factors can trigger an attack of asthma, including allergens such as house dust mite; furred animals, pollens and moulds and chemical irritants such as tobacco smoke, air pollution or inhaled chemicals
  • Exercise (especially running in cold air), respiratory tract infections and some foods and drink can also be triggers
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7
Q

Pathophysiology of asthma?

A
  • Asthma triggered by allergens- the antigen-antibody reaction causes mast cells in the airways to degranulate, releasing substances that decrease cyclic adenosine monophosphate (AMP) in the bronchial smooth muscle, resulting in bronchoconstriction and increase capillary permeability and inflammation.
  • Mucous glands may be hypertrophied, releasing thick sticky mucus that can lead to mucous plugging of small airways
  • Inflammatory cells (eosinophils) in the mucus may give the appearance of infection due to yellow colour.
  • The pathophysiology changes of bronchoconstriction, airway inflammation and mucous secretion lead to narrowed airways and mucous plugging result in following clinical signs
  • Exercise-induced asthma- heat and water loss from the airways due to higher ventilation changes the osmolarity within the airway and induces mast cell degranulation with release of mediators that cause bronchoconstriction
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8
Q

clinical features of asthma?

A
  • Recurrent episodes of wheezing, cough, breathlessness, and chest tightness
  • Signs during an attack of asthma are wheeze on auscultation, obstructive pattern on spirometry, hyperinflation on chest X-ray and use of accessory inspiratory muscles of breathing
  • Children with asthma often have atopic (allergic) features such as eczema, food allergies, hay fever or urticaria
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9
Q

What is atherosclerosis?

A

A chronic and progressive inflammatory disease of the arterial endothelium. Atherosclerotic ‘plaques’ seen in coronary atherosclerosis resulting from a combination of intimal thickening and accumulation of lipids.
Coronary heart disease- form of ischemic heart disease caused by the build up of plaque in the coronary arteries that supply oxygen-rich blood to your heart. May result in angina or a heart attack. Other symptoms include shortness of breath and arrhythmias.

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10
Q

What is pulmonary tuberculosis? (TB)

A

TB is the worlds most lethal infection. 1/3 of the world’s population is infected by the TB bacillus which resides unobtrusively in immunocompetent hosts but may become active if defence mechanisms are impaired by poor living conditions, drug dependency or HIV infection.

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11
Q

Clinical features of TB?

Physiotherapy management?

A

Fever, night sweats, chest wall pain, weight loss, haemoptysis, and SOB

Usually confined to elicitin sputum specimens in a negative pressure room and devising way to encourage exercise in an isolation cubicle

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12
Q

What is CF?

A

It is a multi-system disorder of the exocrine glands, characterized by recurrent respiratory infections, pancreatic insufficiency, and malnutrition

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13
Q

Aetiology of CF?

A
  • Caused by mutations in a single gene called the ‘cystic fibrosis transmembrane conductance regulator (CFTR).’
  • The CFTR is a chloride channel in airway epithelial cells. Defects result in decreased secretion of chloride and water by airway epithelial cells, which leads to dehydrated mucus
  • The CFTR has other functions such as regulation of endosomal pH and adenosine triphosphate (ATP) transport and a receptor site for binding, endocytosing, and clearing bacteria
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14
Q

Pathophysiology of CF?

A
  • CF is a systemic disease affecting the respiratory tract, gastrointestinal tract, genitourinary tract, and hepatobiliary (liver, gallbladder, bile ducts or bile) tree. Obstruction of exocrine ducts by viscous secretions causes the pathogenesis of most of these manifestations
  • Changes in electrolyte transport cause a decrease in height of the periciliary liquid layer and formation of mucous plaques and plugs, adherent to the airway surface
  • Decreasing the efficiency of ciliary-dependent mucus clearance. The thickened mucus plaques provide an ideal environment for proliferation of bacterial microorganisms and the CF airway becomes chronically affected
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15
Q

Respiratory clinical features of CF?

A
  • Cough productive of sputum
  • Breathlessness on exercise, reduced exercise capacity and diminished physical activity
  • Clinical course- marked by acute exacerbations of lung disease occurring on a background of chronic airway infection
  • Pneumothorax (collapse of a lung) occurs in 5-8% of patients with CF
  • An acute exacerbation is defined as the presence of 2-4 out of 12 signs and symptoms of a respiratory exacerbation; change in sputum production, new/increased haemoptysis, increased cough, increased dyspnoea, malaise (general feeling of illness), fatigue, fever, weight loss, sinus pain/tenderness, changes in sinus discharge, loss of appetite
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16
Q

Non-respiratory clinical features of CF?

A
  • Pancreatic insufficiency causing maldigestion and malabsorption of fats and proteins
  • CF- related diabetes mellitus occurs in up to 50% of patients aged 30 years
  • Recurrent episodes of distal intestinal obstruction as a result of excessively viscid intestinal secretions
  • High incidence of gastro-oesophageal reflux contributing to deterioration in respiratory function
  • 17% of children and 24% of adults have clinically significant liver disease
17
Q

Musculoskeletal dysfunction clinical features of CF?

A
  • Spinal pain 43-94%
  • Chest pain 16-64%
  • CF arthropathy affects up to 9% of patients, resulting in joint pain, long bone pain, arthralgia, and joint effusions, particularly during exacerbations
  • Increased rates of long bone, rib and vertebral fractures have been reported
18
Q

what is COPD and aetiology?

A

A disease characterized by persistent airflow limitation that is usually progressive
• Most common cause is cigarette smoking.
• Smoking other types of tobacco, passive smoking, inhalation of organic and inorganic dusts, chemical agents, fumes from the burning of biomass fuels and outdoor air pollution increase rick of developing COPD.
• Childhood respiratory infections and long-standing asthma
• Risk factors- foetal and childhood exposure to smoke and low socio-economic status

19
Q

What is the pathophysiology of COPD?

A

The inhalation of noxious particles causes lung inflammation and results in the following changes within the lungs:

  1. Mucous gland hypertrophy with consequent increase mucus production
  2. Destruction of ciliated epithelial cells in the airway walls
  3. Chronic inflammatory changes and associated small airway fibrosis with consequent narrowing in the small airways.
  4. Increase in bronchial smooth muscle.
  5. Loss of alveolar walls with consequent destruction of capillary beds
20
Q

What is bronchitis?

A

increasing sputum production and reducing mucociliary clearance.
chronic cough and sputum expectoration
sputum expectoration on most days for at least 3 months of the year over 2 successive years

21
Q

What is emphysema?

A

the loss of alveolar walls

enlargement of the air spaces distal to the terminal bronchiole, with destruction of their walls

22
Q

Clinical features of COPD?

A

Main symptoms are progressive dyspnoea, cough, and sputum. On examination an individual with COPD may have the following signs depending on disease severity:
• Barrel chest- antero-posterior diameter of the chest wall in enlarged due to hyperinflation.
• Accessory muscle use, particularly the inspiratory accessory muscles. These are recruited due to the diaphragm being less available to contribute to ventilation as a consequence of hyperinflation.
• Chest radiograph showing signs of hyperinflation such as increased radio translucency (i.e., dark lung fields)
• Decreased breath sounds on auscultation due to loss of alveoli and hyperinflation. Maybe be coarse crackles if sputum is present in the airways.
• Reduced functional exercise capacity measured by a reduced distance walked in either the 6-minute walk test or incremental shuttle walk test.
• Oxygen desaturation during exercise. In severe disease oxygen saturation may be low at rest

23
Q

What is peripheral vascular disease?

A

PVD is a blood circulation disorder that causes the blood vessels outside of your heart and brain to narrow, block, or spasm. Common condition where a build-up of fatty deposits in the arteries restricts blood supply to leg muscles.

24
Q

symptoms of Peripheral vascular disease?

A

Symptoms
• Intermittent claudication- painful ache in their legs during walking, which usually disappears after a few minutes rest.
• Hair loss on legs and feet
• Numbness/weakness in the legs
• Brittle, slow-growing toenails
• Ulcers (open sores) on your feet and legs, which do not heal.
• Changing skin colour on legs, turning pale/blue
• Shiny skin
• In men, erectile dysfunction
• Leg muscle wasting

25
Q

causes and risk factors of Peripheral vascular disease?

A
  • Usually caused by atherosclerosis

* Risk factors- smoking, diabetes, high blood pressure, high cholesterol, and age