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Anatomy and Phyisology > HLTH 2501: chronic obstructive pulmonary disease, restrictive disorders and vascular disorders > Flashcards

HLTH 2501: chronic obstructive pulmonary disease, restrictive disorders and vascular disorders Flashcards

1
Q

chronic obstructive pulmonary disease

A

is a group of common chronic respiratory disorders that are characterized by progressive tissue degeneration and obstruction in the airways of lungs

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2
Q

types of COPD

A

emphysema, chronic bronchitis, and acute asthma

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3
Q

restrictive lung diseases

A

silicosis, asbestosis, and farmer’s lung; these are restrictive because the irritant causes interstitial inflammation and fibrosis, resulting in loss of compliance or ‘stiff lung’

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4
Q

results of COPD

A

irreversible and progressive damage to the lungs and respiratory failure may result due to severe hypoxia or hypercapnia; can also lead to right-sided CHF

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5
Q

another name for right-sided CHF

A

cor pulmonale

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6
Q

emphysema

A

is destruction of the alveolar walls and septae, leading to large, permanently inflated alveolar air spaces

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7
Q

why do alveoli destruct in emphysema?

A

a deficiency of alpha 1 -antitrypsin, genetic factors, cigarette smoking, and air pollution

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8
Q

alpha 1-antitrypsin

A

is a protein that inhibits the activity of proteases which are destructive enzymes released by neutrophils during an inflammatory response; ex. elastase

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9
Q

what occurs in emphysema

A

alveolar wall breakdown, fibrosis and thickening of the bronchial walls, difficulty with expiration, and loss of tissue

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10
Q

what occurs when the alveolar walls breakdown in emphysema?

A

loss of SA for gas exchange, loss of pulmonary capillaries, loss of elastic fibres, altered ventilation-perfusion ratio, and decreased support for other structures like the small bronchi

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11
Q

how do the bronchial walls thicken and fibrosis in emphysema?

A

due to chronic irritation and the frequent infections associated with smoking and increased mucus production

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12
Q

result of fibrosis and thickened bronchial walls in emphysema?

A

narrowed airways, weakened walls. and interface with passive expiratory airflow

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13
Q

what is the result of progressing difficulty with expiration in emphysema?

A

air trapping, increased residual volume, overinflation of the lungs, fixation of the ribs in an inspiratory position, and the diaphragm will appear flattened on x-rays

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14
Q

what does loss of tissue in emphysema result in?

A

adjacent alveoli fuse, forming large air spaces; there may be holes in the lungs; tissue or pleural membrane may rupture, resulting in pneumothorax; hypercapnia occurs; infections develop often; and cor pulmonale may develop

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15
Q

blebs

A

air filled-spaces in the lungs cause by damaged alveoli fusing, forming air spaces

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16
Q

cor pulmonale in emphysema

A

this may develop as a result of loss of tissue because the pulmonary blood vessels are destroyed and hypoxia causes pulmonary vasoconstriction; the increased pressure increases resistance to the right ventricle, causing it to eventually fail

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17
Q

signs of emphysema

A

dyspnea, hyperventilation with a prolonged expiration, barrel chest position, anorexia, fatigue, clubbed finger, and secondary polycythemia

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18
Q

barrel chest

A

occurs with hyperventilation in emphysema and is a position of sitting and leaning forward to facilitate breathing

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19
Q

testing for emphysema

A

chest X-rays and pulmonary function tests (these looks at residual volume and total lung capacity)

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20
Q

treatment for emphysema

A

avoidance of respiratory irritants, immunization against influenza and pneumonia, appropriate exercise to facilitate breathing, learning breathing techniques (pursed lip breathing), adequate nutrition and hydration, bronchodilators, and lung reduction surgery

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21
Q

chronic bronchitis

A

is characterized by significant changes in bronchi resulting from chronic irritation from smoking or exposure to industrial pollution; this results in inflammation, obstruction, repeated infections, and chronic coughing

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22
Q

how does chronic bronchitis develop?

A

exposure to irritants causes the mucosa to be inflamed and swollen, causing hypertrophy and hyperplasia of the mucus glands and increased mucus secretion; fibrosis and thickening of the bronchial walls also occurs, causing obstruction

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23
Q

complications of chronic bronchitis

A

low O2 leads to cyanosis; dyspnea and fatigue interfere with nutrition and communication; and cor pulmonale may develop

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24
Q

causes of chronic bronchitis

A

cigarette smoking, urban area (air pollution), and sometimes asthma

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25
Q

signs of chronic bronchitis

A

constant cough (worse in the am), tachypnea with and shortness of breath, purulent and thick secretions, hypoxia leading to cyanosis, hypercapnia, secondary polycythemia, weight loss, and signs of cor pulmonale

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26
Q

treatment for chronic bronchitis

A

reducing exposure to irritants, influenza and pneumonia vaccines, antimicrobials, bronchodilators, chest therapy, and low-flow oxygen and nutritional supplements

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27
Q

bronchiectasis

A

is usually a secondary problem and is a irreversible dilation of the medium-sized bronchi

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28
Q

what may cause bronchiectasis?

A

CF, COPD, childhood. infection, aspiration of foreign bodies, of a congenital weakness in the bronchial wall

29
Q

two types of dilations in bronchiectasis

A

saccular or elongated (fusiform)

30
Q

how does bronchiectasis develop?

A

recurrent inflammation and infection in the airways leads to the weakening of the muscle and elastic fibres in the bronchial wall, in which fibrous adhesions may pull the wall outward, dilating it

31
Q

infections and bronchiectasis

A

in dilated and ballooning areas, large amounts of fluid collect and become infected; the infections can cause a loss of cilia and metaplasia in the epithelium, causing additional fibrosis

32
Q

what organisms often cause infection in bronchiectasis?

A

streptococci, staphylococci, pneumococci, and H influenzae

33
Q

signs of bronchiectasis

A

chronic cough, copious production of purulent sputum, rales and rhonchi, foul breath, dyspnea, hemoptysis, weight loss, anemia, and fatigue

34
Q

treatment for bronchiectasis

A

antibiotics, bronchodilators, and chest PT

35
Q

restrictive lung disorders

A

a group of diseases in which lung expansion is impaired and total lung capacity is reduced

36
Q

restrictive lung disorders two groups

A

those in which an abnormality of the chest wall limits lung expansion and those in which lung disease impairs expansion

37
Q

restrictive disorders in which an abnormality of the chest wall limits expansion

A

includes conditions like kyphosis, scoliosis, poliomyelitis, ALS, muscle dystrophy, or botulism

38
Q

botulism

A

respiratory muscle paralysis

39
Q

restrictive disorders in which lung disease impairs expansion

A

is when the tissues providing the supportive framework are effected; includes idiopathic pulmonary fibrosis, pulmonary edema, and occupational disease from inhaled irritants

40
Q

pneumoconioses

A

are chronic restrictive diseases resulting from long-term inhalation of irritating particles like asbestos

41
Q

how does pneumoconiosis develop?

A

the normal defence in the upper tract cannot handle the overload of foreign material with long-term exposure; inflammation and fibrous tissue then develop, causes loss of function and frequent infections

42
Q

types of pneumoconiosis

A

coal workers disease, silicosis, asbestosis, and farmer’s lung

43
Q

coal workers disease

A

is caused by coal dust in mines

44
Q

silicosis

A

is caused by silica in stone-cutting, sand-blasting and mines

45
Q

farmers lung

A

is caused by fungal spores from hay

46
Q

effects of asbestos fibres

A

frequent cause pleural fibrosis and increase the risk of lung cancer

47
Q

signs of pneumoconiosis

A

dyspnea, effort for inspiration, and cough

48
Q

pulmonary edema

A

refers to fluid collecting in the alveoli and instersital area; this reduces gas exchange

49
Q

why does excess fluid develop in pulmonary edema?

A

inflammation in the lungs (increases capillary permeability), low plasma proteins (decreases plasma osmotic pressure), and pulmonary hypertension

50
Q

results of pulmonary edema

A

inference of gas exchange, hypoxemia, decreased action of surfactant, difficulty expanding lungs, capillary rupture, and blood sputum

51
Q

causes of pulmonary edema

A

left sided CHF, hypoproteinemia (caused by kidney or liver disease), inflammation from inhalation of toxic gases or tumors, or blocked lymphatic drainage from fibrosis

52
Q

signs of mild pulmonary edema

A

cough, orthopnea, and rales

53
Q

signs of severe pulmonary edema

A

hemoptysis, frothy and bloody sputum, labored breathing, hypoxemia, cyanosis, and paroxysmal nocturnal dyspnea

54
Q

treatment for pulmonary edema

A

treating causative factors, positive pressure mechanical ventilation, and upper position elevated position

55
Q

pulmonary embolus

A

is a blood clot or mass of other material that obstructs the pulmonary artery or a branch of it, blocking the flow of blood through the lung tissue

56
Q

what are most pulmonary embolus a result of?

A

are thrombi or blood clots originating from the deep leg veins; this may be caused by phlebothrombosis or thrombophlebitis

57
Q

effects of a small pulmonary emboli

A

are often silent or asymptomatic but multiple small ones can be dangerous

58
Q

signs of a small pulmonary emboli

A

chest pain, cough, and dynspea

59
Q

effects of a medium sized pulmonary emboli

A

can cause respiratory impairment and pulmonary infarction; reflex vasoconstriction also occurs, obstructing the vessel further

60
Q

signs of a medium sized emboli

A

chest pain, tachypnea, dyspnea, hemoptysis, fever, and hypoxia

61
Q

effects of a large sized pulmonary emboli

A

can cause right sided CHF, decreased CO (shock), and sudden death

62
Q

signs of a large size emboli

A

severe crushing chest pain, low BP, rapid weak pulse, and loss of consciousness

63
Q

risk factors for thrombi forming in the legs

A

immobility, trauma or surgery to the legs, childbirth, CHF, dehydration, and cancer

64
Q

fat emboli

A

occur from loss of bone marrow resulting from a fracture of a large bone (ex. femur)

65
Q

types of emboli

A

thrombi from the leg veins, fat emboli, vegetations resulting from endocarditis in the right side of the heart, amniotic fluid, tumor cells, or air

66
Q

signs of a fat emboli

A

show separate signs like acute respiratory distress, a rash on the trunk, and neurologic signs like confusion

67
Q

diagnosis for pulmonary edema

A

X-ray, lung scan, MRI, and pulmonary angiography; the source can be identified using doppler ultrasound or venography

68
Q

treatment of pulmonary edema

A

includes assessing risk factors, compression stockings, filter surgically inserted in the inferior vena cava, heparin to remove clots, or mechanical ventilation

Anatomy and Phyisology (94 decks)

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