Exam 2 - pulmonary Flashcards

1
Q

Term: Ventilation

A

gas transport in and out of the lungs during inspiration and expiration

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2
Q

Term: respiration

A

gas exchanges across alveoli-capillary tissue

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3
Q

Term: perfusion

A

circulation of blood through tissues

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4
Q

Mech of ventilation: inspiration

A

all due to pressure changes
-inspiration = pressure in alveolar is LOWER than atmospheric

***diaphragm ACTIVELY lowers, thorax raises and expands

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5
Q

mech of ventilation: expiration

A

pressure changes result in air flow
- exhale = alveolar pressure is HIGHER than atmospheric

**diaphragm relaxes and PASSIVELY elevates, thorax lowers to resting position

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6
Q

mech of ventilation: compliance

A
  • distensibility of the lungs

- relates to ease of inflation and chest wall expansion during inspiration

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7
Q

mech of ventilation: elasticity

A
  • recoil, tendency to return to original size

- elastin and collagen fibers, surface tension

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8
Q

mech of ventilation: surface tension

A
  • contributes to elasticity by acting to collapse the alveoli
  • surfactant acts to reduce surface tension
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9
Q

Mech of ventilation: airway resistance

A
  • Flow = delta P / R
  • resistance = 8 micro l/(pi r^4)

upper airways - responsible for most airway resistance

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10
Q

bronchial smooth muscle innervated by

A

ANS

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11
Q

inhale vs exhale: airways open or close

A

inhale = airways are pulled open

Exhale = airways collapse and increase resistance

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12
Q

how does gas exchange occur in the lungs?

A

diffusion

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13
Q

diffusion of gases across alveolar membrane affected by??? (3 things)

A

1) pressure/concentration gradients (high to low)
2) surface area (total amount of alveolar-capillary interface)
3) thickness of membrane (thickness can impede exchange)

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14
Q

Ventilation perfusion ratio

A
  • gas exchange is optimized when ventilation matches perfusion
  • actual V:Q (ventilation:blood flow) = ~.8
  • gravity, position, and dysfunction affect ratio
  • generally, vent and perfusion are greatest in gravity dependent areas
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15
Q

Dead space (lungs)

A

when perfusion < ventilation (PE)

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16
Q

Shunting (lungs)

A

when perfusion > ventilation (alveolar collapse from secretions)

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17
Q

Gas transport: O2

A
  • dissolved in plasma (PO2)

- bound to hemoglobin (pulse ox toys! - ~97%)

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18
Q

Gas transport: CO2

A
  • dissolved in plasma (PCO2)
  • bound to hemoglobin (30%)
  • bicarbonate (60%)
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19
Q

Acid-base balance of breathing

A
  • breathing removes acid from blood in from of CO2
    (inc breathing = reduce CO2 = reduce H+ = increase in pH)
    (dec breathing = increase CO2 = increase H+ = dec pH)
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20
Q

Acid - base breathing equation

A

CO2 + H20 H2CO3 H+ +HCO3-

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21
Q

Neural - respiratory control

-automatic and voluntary

A
automatic = brainstem
voluntary = cerebral cortex
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22
Q

Chemical - respiratory control

A

chemoreceptors in carotids and aortic arch

- CO2, H+ ions, and O2

23
Q

Non-chemical (respiratory control)

A

-coughing, sneezing, bronchoconstriction, and mucus secretion occur in lungs as protective reflexes to irritants

24
Q

Restrictive dysfunction (gen def)

A

abnormal reduction in pulmonary ventilation

25
Q

Obstructive dysfunction (gen definition)

A

-diseases of the airways, producing obstruction to expiratory airflow

26
Q

Restrictive dysfunction: characterized by

A
  • decreased chest wall or lung compliance
  • dec lung volumes and capacities
  • inc work of breathing (inc pressures required for normal TV, inc energy expenditure, dec TV and inc RR)
27
Q

Signs and symptoms of restricted lung dysfunction

A
  • rapid, shallow breathing
  • tachypnea
  • hypoxemia
  • accessory muscle use
  • diminished breath sounds
  • dec lung vol and capacities
  • crackles
  • dyspnea
  • cough
  • weight loss
  • muscle wasting
28
Q

Restricted lung dysfunction eventually may lead to

A
  • pulmonary hypertension
  • cor pulmonale
  • severe hypoxia
  • ventilatory or cardiac failure
29
Q

Restrictive conditions (main categories)

A
pulmonary
connective tissue
musculoskeletal 
neuromuscular 
other (cancer, surgery, etc)
30
Q

Restrictive lung dysfunction TREATMENT

A
  • correct underlying cause if possible
  • supportive (supplement O2, antibiotic therapy, interventions for ventilation or prevent accum of secretions, good nutrition)
31
Q

Pulmonary fibrosis (what it is)

A

Interstitial lung disease

  • inflam process involving alveolar wall
  • leads to progressive scarring (fibrosis)
  • progressive, stead decline in lung funct, often with acute exacerbations
  • poor prognosis
32
Q

Pulmonary fibrosis (what causes it)

A
  • idiopathic (2/3 of cases. risk factors = environmental, genetic, age over 50 usually)
  • other causes: infectious agents, environ and occupational inhalants, drugs, healing scar tissue
33
Q

Pulmonary Fibrosis TREATMENT

A
  • lack of evidence supporting most treatments
  • response to treatment is unpredictable
  • lung transplant is the ONLY definitive therapy
34
Q

Pneumoconiosis (general and risk severity)

A

-lung diseases resulting from inhalation of industrial substances (dusty lungs)

risk depends on many things (type/duration/intensity of exposure, presence of underlying pulmonary disease, smoking history, particle size and water solubility)

35
Q

Pneumoconiosis (most common population)

A
  • among miners, sandblasters, stonecutters, asbestos workers, insulators, and agriculture workers
36
Q

Pneumoconiosis (pathogenesis)

A
  • variable
  • may be rapid onset or last years without clinical manifestations
  • dust particles taken up by macrophages
  • may activate and/or damage macrophages causing release of mediators
  • macrophages containing particles may accumulate in nodules or lesions in the lung, connective tissue, and lymphatic tissues.
  • can lead to excessive fibrosis and scarring of lung tissue
37
Q

Systemic sclerosis or scleroderma (what it is)

A
  • autoimmune disease
  • excessive collagen deposition in the skin, but can affect internal organs including the lungs
  • inflammation leads to fibrosis
  • with progression of fibrosis, capillaries become involved causing pulmonary hypertension and cor pulmonale
38
Q

systemic sclerosis or scleroderma (disease course, treatment)

A
  • unpredictable disease course
  • treatment = immunosuppressive medications and drugs targeting pulmonary HTN (although could be bad drugs)
  • lung transplant may be an option for some
39
Q

Most common cause of death from scleroderma

A

Lung disease

40
Q

Atelectasis (definition)

A

collapse/incomplete expansion of alveoli in part or all of a lung

obstructive.
non-obstructive (collapse, compression)

41
Q

Atelectasis (what does it result from)

A
  • hypoventilation or ineffective secretion clearance
  • inactivity
  • thoracic or abdominal incisional pain
  • compression of lung
  • diaphragm weakness/paralysis
  • pneumonia
  • foreign body obstruction
42
Q

Types of lung cancer

A

-small cell lung cancer (20%)

-non-small cell lung cancer (80%
squamous cell, adenocarcinoma = most common, large cell)

43
Q

Most common type of non-small cell lung cancer

A

adenocarcinoma

44
Q

Most cases of lung cancer are linked to what?

A

cigarette smoking (~80%)

45
Q

Most common site of lung cancer metastases?

A

Adrenal

**also the lungs are a common site of metastases from other types of cancer

46
Q

Lung cancer (symptoms)

A

symptoms = productive cough, dyspnea, hemoptysis, recurrent infection
May also have fatigue, weight loss, weakness (vague systemic symptoms) or bone pain, headaches, jaundice (metastasis)

47
Q

Lung cancer (treatment and prognosis)

A

Treatment and prognosis depends on stage

treatments can be: chemotherapy, radiation, surgery, and hormone therapies

48
Q

Pulmonary edema: inc pulmonary capillary hydrostatic pressure

A

L sided heart failure
PE

= transudate

49
Q

Pulmonary edema: inc pulmonary capillary membrane permeability

A

ARDS
pna
infection

=exudate

50
Q

Pulmonary edema: dec plasma protein

A

liver cirrhosis

=transudate

51
Q

Pulmonary edema: inc fluid accum in interstitial space and alveoli

A
  • inc hydrostatic pressure
  • inc membrane permeability
  • dec plasma protein
  • altered lymphatic function
52
Q

ARDS

A

“Acute respiratory distress syndrome”

  • acute respiratory failure that follows systemic or pulmonary insult (severe trauma, sepsis, burns, aspiration, embolism, etc)
  • diffuse alveolar damage
53
Q

ARDS clinical manifestations

A
  • respiratory distress
  • dyspnea
  • hyperventilation
  • atelectasis
  • hypoxia and cyanosis
54
Q

ARDS treatment

A
  • first aimed at underlying pathology (sepsis, pneumonia)
  • supportive therapy (ventilation)
  • high mortality rate (>40%)
  • **many recover pulmonary func but may have physical or cognitive impairments (some get scarring and interstitial fibrosis)