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Respi Pathology > Chapter 8a > Flashcards

Chapter 8a Flashcards

1
Q

What is the difference between obstructive and restrictive lung diseases?

A

Obstructive (airway): Normal Total Lung Capacity, Reduced Expiratory Flow Rate

Restrictive (parenchymal): Total Lung Capacity Reduced, Expiratory Flow Rate Normal

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2
Q

What are 3 examples of obstructive lung diseases?

A
  1. COPD
  2. Bronchiectasis
  3. Asthma
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3
Q

What are 3 examples of restrictive lung disease?

A
  1. Chest Wall Disorders
  2. Diffuse Parenchymal Lung Disease
  3. Lung Scarring
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4
Q

How to distinguish between obstructive and restrictive disease?

A

Spirometry. Measures lung volume and flow rate

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5
Q

Pathogenesis of obstructive lung disease?

A

Problem with ventilation, usually at level of small branches of bronchial tree

  • exhalation affected more and requires effort
  • wheeze heard (air forced through small bronchi)
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6
Q

What is the pathogenesis of obstructive sleep apnea?

A

Episodes of partial or complete closing of the upper airways during sleep.

due to jaw and tongue falling backwards and obstructing airway

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7
Q

What are 3 consequences of obstructive sleep apnea?

A
  1. Pt wakes repeatedly to gasp for air
  2. Hypoxemia
  3. Poor sleep
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8
Q

In which group of people is obstructive sleep apnea more common?

A

Men, Obese

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9
Q

What is the pathogenesis of asthma?

A
  1. Exposure to precipitating factors
    - ‘atopic’ (foods, drugs, animal antigens etc)
    - ‘non-atopic’: hypersensitive airways and irritants may trigger attack ie exercise, air pollution, smoke)
  2. Previous sensitisation causes IgE mediated response causing activation of mast cells and direct stimulation of nerve receptors
  3. Mast cells release chemical mediators resulting in recruitment of eosinophils, bronchoconstriction, increase in vascular permeability, increase in mucus secretion
  4. Recruited eosinophils and T helper cells release further mediators which amplify and sustain inflammatory response
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10
Q

What is the consequence of repeated episodes of asthma?

A

Over-reactivity of airways & remodelling of airways

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11
Q

What is a condition of severe asthma?

A

Status Asthmaticus. Prolonged bronchospasm and mucus pluggingg results in respiratory failure

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12
Q

What are 5 structural changes seen in asthmatic patients?

A
  1. Hyperactivity and hypertorphy of smooth muscle of bronchus
  2. Hypersecretion of mucus
  3. Mucosal edema
  4. Infiltration of bronchial mucosa by eosinophils, mast cells, lymphoid cells and macrophages
  5. Deposition of collagen beneath bronchial epithelium in longstanding cases
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13
Q

In which patients are COPD seen in?

A

chronic smokers

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14
Q

What are two points that make COPD different from asthma?

A
  1. Airflow limitation is not fully reversible
  2. Disease is progressive
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15
Q

What is the progression of COPD?

A

stable for periods of time, but as normal lung function is lost, relatively mild concomitant illness (ie viral upper respiratory tract infection/ poor air quality). may cause sudden deterioration in symptoms and hospitalisation

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16
Q

What are 3 main underlying pathologies contributing to COPD?

A
  1. Emphysema (destruction of airspaces and loss of elastic recoil)
  2. Chronic Bronchitis (mucus hypersecretion and luminal narrowing of airways)
  3. Bronchiolitis (narrowing of small airways by inflammation and scarring)

*1. affects alveoli; 2. + 3. affects airways
*whilst emphysema and airways disease may exist individually, usually co-exist to differing degrees

17
Q

What is the definition of emphysema?

A

Permanent dilation of airspaces distal to the terminal bronchiole with destruction of tissue in absence of scarring

Destruction of alveolar walls results in loss of elastic recoil in lungs and reduction in gas exchange capacity

18
Q

What is the pathogenesis of emphysema?

A

Parenchymal destruction by extra-cellular proteases/elastases
- normally proteases secreted by inflammatory cells are inactivated by extracellular protease inhibitors in the lung (ie alpha-1-antitrypsin)

Smoking can inhibit these protease inhibitors, contain abundant free radicals which cause tissue damage, and that persistent irritation leads to increased inflammatory cells in the lung which themselves release mediators and enzymes
some pt have alpha-1-antitrypsin deficiency

these elastases then destory the alveolar wall causing emphysema

19
Q

What is 1 key pathological sign in emphysema?

A

Bullae

20
Q

What is chronic bronchitis?

A

Cough productive of sputum on most days for 3 months of year for 2 successive years

There is airway obstruction related to luminal narrowing and mucus plugging resulting in alveolar hypoventilation

21
Q

What is bronchiolitis?

A
  1. Inflammation of airways <2mm in diameter
  2. Macrophages and lymphoid cells infiltrate the airway wall
  3. May progress and lead to scarring and narrowing of airways, contributing to functional airway obstruction
22
Q

What are 3 risk factors for COPD?

A
  1. Smoking exposure
  2. Recurrent childhood infections
  3. Occupational exposure to dust
23
Q

What 2 things cause exacerbations of COPD?

A
  1. Infection
  2. Poor air quality
24
Q

How do COPD pts die?

A
  1. Respiratory Failure
  2. Secondary Right heart failure (cor pulmonale)
25
Q

State and explain two phenotypes of patients in advanced COPD.

A
  1. Pink puffers (lung damaged, airways ok)
    - pink complexion, obvious breathing efforts
    - emphysema is underlying pathology
    - patients compensates for less surface area for gas exchange by hyperventilating
    - few unventilated areas of lung, so carbon dioxide retention is not a major component
  2. Blue Bloaters (normal lung but cannot ventilate)
    - chronic bronchitis is underlying pathology
    - marked V/Q mismatch: unable to shift enough air, so blood leaving lungs is not oxygenated
    - poor ventilation results in combined hypoxemia and hypercapnia
    - heart works hard to try (in vain) to perfuse lung more so patients likely to have right heart failure
    - over time there is brainstem re-setting to tolerate levels of hypoxemia and hypercapnia that might usually be fatal
26
Q

What is the risk of advanced COPD ie pink puffers & blue bloaters

A

teetering at edge of respiratory failure; relatively mild concomitant illness (viral upper respi tract infection) may cause sudden deterioration in symptoms and hospitalisation

27
Q

How to treat COPD patients? What is the special consideration?

A

Treat cause (ie infection), give oxygen, bronchodilators, assist ventilation when necessary

in blue bloaters, there is dulling of CO2 driven breathing reflex, thus control of breathing is by oxygen levels, giving too much oxygen may reduce rate of ventilation further and exacerbate proble,s – greater need to control oxygen delivery and monitor closely

Respi Pathology (11 decks)

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