Pulmonary Pathophysiology- Restrictive Lung Disease Flashcards

1
Q

What is the general characteristic of restrictive lung disease?

A

can’t get air in mainly due to decreased chest and lung compliance

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2
Q

In RLD what must increase as a response to decreasing Vt?

A

RR, which causes increase in metabolic demand to breath

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3
Q

What happens if you begin to lose your lung compliance?

A

more inspiratory muscle are needed to pull the lungs open

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4
Q

What is the general theme with the LFT value’s?

A

All values will decrease but ratios will stay the same because all values are decreasing

Vt very last value to decrease

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5
Q

Which LFT is much more decreased in restrictive than obstructive?

A

DLCO

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6
Q

What is interstitial pulmonary fibrosis?

A

an overwhelming inflammatory process involving all parts of the alveolar wall

life expectancy after diagnosis is less than 6 years

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7
Q

What is pathogenesis of IPF?

A

likely an inflammatory trigger

ex. cigarette smoke, viral/bacteria infection

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8
Q

What is pathophysiology of IPF?

A

initial changes due to inflammation but then this destroys lung parechyma allowing fibrin to enter alveoli and leads to scarring

this clogs alveoli making it harder to pull lungs open

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9
Q

What happens due to thickening of alveolar walls?

A

leads to less gas exchange, decreased elasticity and lung compliance and increases work of breathing

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10
Q

Why does DLCO drop on IPF?

A

increased distance to get to alveoli, increased alveoli size, loss of capillaries, fibrin interferes with gas exchange

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11
Q

What will you see on chest x ray in pts with IPF?

A

reticulonodular patterns (lines with nodes)

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12
Q

What are main clinical signs of IPF?

A
  1. breath sounds- diminished with fine crackles (sounds like velcro)
  2. Dyspnea- initially on exertion but progresses to rest- progression is key sign
  3. weight loss- due to increased work of breathing
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13
Q

What are other potential clinical signs of IPF?

A

cough- dry and non mucus clearing

hypoxia- decreased SpO2, cyanosis, constriction of vessels

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14
Q

Tx of IPF?

A

drugs, oxygen, nutrition, lung transplant

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15
Q

Will aerobic conditioning help patients with IPF?

A

No, b/c it changes muscle ability to efficiently use O2 therefore you need lessO2 to perform

however in IPF you are not getting a lot of air into to begin with an aerobic conditioning can’t help that

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16
Q

What is sarcoidosis?

A

mutlisystem disease caused by granulomas in different organs- most common in lungs

these granulomas infiltrate alveolar walls and cause fibrosis and inflammatory response

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17
Q

What are other characteristics of sarcoidosis?

A

fatal in only 5-10% of pts, uncommonly seen and 25% of pts wont seen lung function drop

treat like IPF

18
Q

What is broncholitis?

A

fibrotic lung disease that affects small airways due to necrosis of respiratory epithelium causing inflammatory response similar to IPF

uncommon but seen in pts under 2 and after lung transplants

tx: similar to IPF

19
Q

What are three groups of occupational lung disease?

A
  1. toxic fumes-
  2. mineral dusts- silica, coal dust, asbestos
  3. organic dusts- mostly farm or animal related
20
Q

What are signs of OLD?

A

chronic cough, weight loss, DOE, declining PFT

tx: similar to IPF mostly supportive, try and remove trigger

21
Q

Why is obesity a RLD?

A

subcutaneous fat decreases chest wall compliance and increases work of breathing

22
Q

What is scleroderma?

A

progrssive systemic connective tissue disease

if in lungs presents as IPF

23
Q

What is atelectasis?

A

loss of volume of lung tissue due to lack of expansion of structures in respiratory zone, basically collapsing of alveoli

24
Q

Can you find atelectasis in healthy patients?

A

Yes this is why we yawn and take deeper breaths unconsciously at times

25
What is primary atelectasis?
lack of expansion due to decreased inspiration, caused by diseases with chest wall compliance, respiratory muscle weakness, or loss of surfactant or bed rest
26
What is secondary atelectasis?
common in obstructive pulmonary disease
27
What type of patient is likely to have both primary and secondary atelectasis?
post op pt: primary- bed rest and splinting secondary- due to irritation from anesthesia cure: mobility!
28
What are clinical signs of atelectasis?
increased sputum, fever, crackles, dimished breath, SOB/DOE, increased RR but decreased Vt
29
What is main tx of atelectasis?
mobility! plus pain control and incentive spirometer
30
What is pneumonia?
from atelectasis leads to this- inflammatory process of the lungs that begins with infection can be community or hospital acquired can be restrictive or obstructive
31
What are stages of pneumonia?
1. intro of bacteria 2. outpouring of edema 3. active inflammatory process 4. fibrin is laid down at site 5. day 5 specific antibodies fight infection
32
Main causes of pneumonia?
aspiration: food, gastric contents, or foreign objects community/hospital acquired- bacteria, viral etc.
33
Clinical signs of pneumonia?
increased RR, fever, tachycardia, hypoxia, frequent productive cough, dark mucus, myalgias
34
What is pulmonary edema?
extra fluid getting into alveoli, decreasing lung compliance goes hand in hand with heart failure
35
What is pathophysiology of pulm edema?
increased intravascular pressure, decreased integrity of blood vessels
36
What are causes of pulm edema?
left heart failure- back up of plumbing other causes the decrease endothelium integrity- trauma, shock, meds
37
What are signs of pulm edema?
fine crackles at lower lobes, increased RR, V/Q (perfusin off not vent), pink frothy sputum, pallor, orthopnea (cant lie prone bc cuts off most dependent areas)
38
What is a pneumothorax?
free air leaks in pleural space, this cause positive pressure within lung and it collapses
39
What is tension pneumothorax?
medical emergency, lungs letting air into pleural space but not out life threatining as each breath increases positive pressure
40
What can cause a traumatic pneumothorax?
GSW, stabbing, rib fracture, MVA Iatrogenic- think Bergeron