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Pathophysiology > Obstructive Lung Disease > Flashcards

Obstructive Lung Disease Flashcards

1
Q

what is obstructive lung disease?

A

any disease that limits the movement of air out of the lungs

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2
Q

how do obstructive lung diseases broadly impact the lungs?

A

increase total lung volume

increase RV

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3
Q

obstructive lung disease can also be referred to as what general term?

A

Chronic Obstructive Pulmonary Disease

(COPD)

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4
Q

T/F: COPD is a specific medical diagnosis

A

FALSE

it refers to several disorders that can occur independently or in combo with one another

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5
Q

COPD include which disorders?

A
  1. Emphysema
  2. Chronic asthma
  3. Chronic bronchitis + small airway disease
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6
Q

what are some risk factors for COPD?

A
  1. exposure to air pollution
  2. secondhand smoke
  3. occupational dusts and chemicals
  4. heredity
  5. history of childhood respiratory infections and SES
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7
Q

what are the presenting signs of COPD?

A
  1. dyspnea
  2. sputum production
  3. chronic cough
  4. exertional dyspnea
  5. reduced function
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8
Q

what is one of the most important diagnostic criteria for COPD?

A

FEV/FVC ratio <0.70 after a bronchodilator has been given

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9
Q

what is emphysema?

A

a pathologic accumulation of air in the lungs

a disease of exhalation

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10
Q

what would you expect the diaphragm to look like in a patient with emphysema?

A

flattened

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11
Q

how does emphysema impact lung volume?

A

increase in residual volume (RV)

increase in total lung capacity

decrease in FEV/FCV ratio

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12
Q

what are the 2 main causes of emphysema?

A

genetic defect

smoking

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13
Q

what genetic defect results in emphysema?

A

alpha-1 antitrypsin (A-1AT) deficiency

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14
Q

what is the purpose of A-1AT?

A

blood protein synthesized in the liver

protects the lungs from degrading actions of powerful enzyme called neutrophil elastase (increases elastin degradation) and other proteases

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15
Q

how does smoking result in emphysema?

A

cigarette smoking inactivates A-1AT leaving the lung susceptible to damage

smoking also causes hyperinflammatory state which means that neutrophils are busy and a lot of elastase is produced

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16
Q

what is the collective anatomical/physiological effects of deficiency of A-1AT and cigarette smoking on the lungs?

A
  1. destruction of individual alveoli
  2. development of “super” alveoli
  3. destruction of CT supports for the very smallest airways allowing them to collapse during expiration
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17
Q

A-1AT deficiency can also result in _______

A

liver disease

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18
Q

what FEV/FCV ratio is “bad news”?

A

<0,5

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19
Q

what are the clinical manifestations of emphysema?

A
  1. SOB at rest (first complaint)
  2. apprehensive, anxious, addicted to O2
  3. thin, cachectic
  4. deformed chest w/prolonged expiration
  5. absent or non-productive cough
  6. accompanying cardiac problems (cor pulmonale)
  7. hypoxemia → can worsen to hypercapnia
  8. chronic pulmonary metabolic acidosis
  9. deconditioning
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20
Q

what is the prognosis of emphysema?

A

usually very poor

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21
Q

how is emphysema usually treated?

A
  1. reduce airway edema secondary to inflammation and bronchospasm
  2. facilitating the elimination of bronchial secretions
  3. preventing and treating respiratory infection
  4. increasing exercise tolerance
  5. avoiding airway irritants and allergens
  6. relieving anxiety and treating depression
  7. long-term O2 therapy potentially
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22
Q

what types of medications may be given to a patient with emphysema?

A
  1. Beta-2 agonists or anticholinergics
  2. anti-inflammatory agents
  3. antibiotics
  4. mucolytic expectorants
  5. mast cell membrane stabilizers
  6. antihistamines
  7. glucocorticoids
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23
Q

List some PT implications for patients with emphysema

A
  1. always use pulse oximeter
  2. monitor HR, RR, and BP frequently
  3. exercise program may include HITT or aerobic training
24
Q

what is hypoxic drive and how does it relate to emphysema?

A

emphysema → retain CO2 may have a decrease hypoxic drive

hypoxic drive → a form of respiratory drive in which the body uses O2 chemoreceptors instead of CO2 receptors to regulate the respiratory cycle

increasing O2 through a nasal cannula may prevent this mechanism

25
Q

pulmonary emphysema patients may be nicknamed ______

A

pink puffers

26
Q

chronic bronchitis patients may be nicknamed ______

A

blue bloaters

27
Q

what is required for the diagnosis of chronic bronchitis?

A
  1. productive cough lasting at least 3 months per year for 2 consecutive years
  2. FEV/FVC < 75%
28
Q

chronic bronchitis is characterized by what?

A
  1. inflammation
  2. excessive mucous production
  3. scarring of lining of bronchial tubes
  4. obstruction of bronchial air flow caused by increased mucous production/reduced mucous clearance
29
Q

how does chronic bronchitis develop?

A
  1. chronic exposure to irritants cause mucus hypersecretion and hypertrophy of mucus producing glands in the largest bronchi
  2. destruction of ciliary cells lining airway occurs
  3. smooth muscle hypertrophy and atrophy of epithelial cells
  4. decrease in radius
  5. airway collapses may occur leading to reduced alveoli ventilation, hypoxia and acidosis
30
Q

how would a patient with chronic bronchitis present throughout the day?

A

recurring productive morning cough

production of phelgm and chronic coughing increases over the course of the day

wheezing

31
Q

what can cause an exacerbation of chronic bronchitis?

A

upper and lower respiratory infections

exposure to environmental irritants such as dust, fumes or air pollution

32
Q

describe what “blue bloater” means

A

chronic bronchitis patient, has the following:

  1. decreasing ventilation
  2. increasing RV and decreasing expiratory flow
  3. terrible V/Q mismatch
  4. hypoxemia, hypercapnia, cyanosis, polycthemia
  5. cor pulmonale secondary pulmonary HTN
33
Q

list some PT implications for patients with chronic bronchitis

A
  1. reduce exposure to irritants
  2. bronchodilators (B-2 agonsits)
  3. mucolytics
  4. no evidence for use of antibiotics, oral corticosteroids, expectorants, or postural drainage
  5. NSAIDs
34
Q

what is asthma?

A

episodic, reversible, obstructive lung disease characterized by bronchospams resulting from an exaggerated inflammatory response of the airway smooth muscle to various stimuli (allergens)

Bronchial hyperactivity

35
Q

what are the clinical manifestations of asthma?

A

episodic dyspnea

coughing and wheezing

36
Q

what are the 2 main types of asthma?

A

Intrinsic (nonallergic/non-immune cause)

Extrinsic (allergens)

37
Q

what is extrinsic asthma?

A

results from an allergic reaction to specific triggers

mast cells, sensitized by IgE antibodies, degranulate and release bronchoactive mediators after exposure to a specific antigen

38
Q

what is intrinsic asthma?

A

how no known allergic cause or trigger

adult onset

most often secondary to chronic or recurrent infections of the bronchi, sinuses, or tonsils and adenoids

39
Q

what are some other recognized types of asthma?

A
  1. adult-onset
  2. exercise-induced (can be outgrown)
  3. aspirin sensitive
  4. Aspergillus-hypersensitive
  5. Occupational asthma
40
Q

describe the pathogenesis of asthma

A

there is an inflammatory response consisting of:

  • cellular infiltration
  • epithelial disruption
  • mucuosal edema
  • mucous plugging of airways
41
Q

what is the product of inflammatory mediators in asthma?

A
  1. bronchial smooth muscle spasm
  2. vascular congestion
  3. increased vascular permeability
  4. edema formation
  5. production of thick, tenacious mucus
  6. impaired mucociliary function
42
Q

T/F: there is difficulty with breathing air in during asthma

A

FALSE
difficulty with expiration

results in air trapping in distal alveoli and hyperinflation

43
Q

T/F: asthma results in an increase in blood pH?

A

FALSE

a decrease (acidosis) due to more retention of CO2 (hypercapnia)

44
Q

what should you ensure your asthmatic patient always has?

A

their rescue inhaler

45
Q

what is an exercise-induced bronchospasm in an asthmatic patient?

A

acute, reversible, usually self-terminating airway obstruction that develops 5-15 minutes after vigorous exercise

usually the episode subsides spontaneously in 30-60 minutes

be sure to warm up

46
Q

T/F: Cystic fibrosis can be considered an obstructive lung disease

A

TRUE

almost all persons w/cystic fibrosis develop obstructive lung disease assocaited with chronic infection that leads to progressive loss of pulmonary function

47
Q

what is a cystic fibrosis?

A

genetic disease that causes a disorder of ion transport (sodium and chloride) in the lungs and in exocrine glands of the liver, pancreas, digestive, and male reproductive organs

characterized by secretion of a thick mucous which is very difficult to move

48
Q

how does cystic fibrosis impact ion exchange?

A

CFTR proteins are incorrectly manufactured which results in Cl- not being transported to epithelial surfaces and remains trapped in cells

Cl- is necessary for water to move, without the movement of water, mucus becomes thick and hard to expel

49
Q

what is the result of thickened mucus production in cystic fibrosis (for more than just the lung)?

A
  • reduced movement of cilia in the bronchiole tubes
  • obstructs the tubular network in the pancreas which reduces release of digestive enzymes and insulin
  • obstruction of the terminal ileum by thick meconium in new borns
  • results in biliary fibrosis and portal hypertension
50
Q

give a more detailed description of how mucous in cystic fibrosis impacts the lungs

A

increase in mucous results in bronchial obstruction which predisposes the lungs to infection and causes patchy atelectasis

disease can progress to bronchitis, followed by bronchiectasis, pneumonia, fibrosis and formation of large cystic dilations

51
Q

what is patchy atelectasis?

A

a complete or partial collapse of the entire lung or area (lobe) of the lung

52
Q

how has the prognosis for cystic fibrosis changed in the last 60 years?

A

1938 → 6 months to live, couldn’t distinguish CF from celiac disease

Now → median survival is 36.8 years

53
Q

what is the most common cause of death from cystic fibrosis?

A

pulmonary failure

54
Q

how is cystic fibrosis diagnosed?

A
  1. genetic screening
  2. sweat test
  3. pancreatic elastase (marker for pancreatic insufficiency)
  4. pulmonary function tests
    • FEV1
    • VC
  5. assessed for DM
55
Q

how are digestive problems from CF managed?

A
  1. digestive enzymes, vitamin supplementation
  2. enemas and mucolytic agents to treat intestinal blockages
  3. Diets rich in proteins and calories
  4. PT interventions
56
Q

how does CF impact the musculoskeletal system?

A
  1. Osteoporosis risk increases
  2. muscular dysfunction
  3. thoracic cage deformation → reduced capacity for posture and thoracic cage movement and altered spinal movement results in reduced total lung capacity
  4. poorer postural control
  5. reduced ventilation capacity
57
Q

how is CF treated?

A
  1. Pharmacologically
    • bronchodilator
    • hypertonic saline solutions
    • pancreatic enzymes
    • high dose NSAIDs
    • prophylactic antibiotics
  2. Treatment
    • TherEx
    • airway clearance techniques
    • lung transplants

Pathophysiology (18 decks)

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