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Pathophysiology > Pulmonary Part 2 (Exam 3) > Flashcards

Pulmonary Part 2 (Exam 3) Flashcards

1
Q

Restrictive Lung Disease

A

thickened alveolar interstitial which leads to fibrosis
less oxygen in the lung and less gas exchange

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2
Q

fibrosis of the lung leads to decreased ____________ and reduces the ability for ________________

A

lung compliance

alveoli to recoil

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3
Q

in restrictive lung disease, collagen and elastic connective tissue ___________ and become _______

A

harden

unusable

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4
Q

Pulmonary fibrosis risk factors

A

occupational (farming/agriculture)
environmental (metal/wood dust)
dusts (organic/inorganic)
tobacco
comorbidities
chronic viral respiratory infections
genetic

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5
Q

what are the main types of medications that are risk factors for pulmonary fibrosis?

A

amiodarone
anti-cancer agents
macrobid

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6
Q

some DPLDs are ___________ in nature

A

idiopathic

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7
Q

typical wound process

A

fibroblasts and mesenchymal cells get to site of injury and repair the epithelium
cells undergo apoptosis

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8
Q

mesenchymal cells recruit

A

connective tissues and extracellular matrix proteins to make new connective tissue

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9
Q

connective cell molecules in the lungs

A

mesenchymal cells
collagen
elastin
leukocytes

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10
Q

major pathophysiology of restrictive lung disease

A

failed wound repair leads to scarring and fibrosis

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11
Q

In IPF, cells do not undergo ________ and just ___________ causing _____________ in the alveolar walls

A

apoptosis

accumulate

scarring

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12
Q

in a diseased lung what happens when mesenchymal cells reach the injury?

A

they accumulate and further contribute to tissue destruction

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13
Q

in restrictive lung diseases, lung volume capacity is ________ in setting of _________________

A

reduced

resistance to expansion

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14
Q

what happens to elastic resistance in restrictive lung diseases?

work of breathing?

A

increased

increased –> faster breathing to maintain ventilation requirements

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15
Q

diagnosis of pulmonary fibrosis can be by

A

CT imaging or surgical biopsy

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16
Q

does airflow resistance change in pulmonary fibrosis?

A

No!

only elasticity

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17
Q

what happens to the FEV1/FVC ratio in a restrictive pulmonary disorder?

A

it is preserved or increased

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18
Q

Clinical presentation of idiopathic pulmonary fibrosis

A

SOB gradually gets worse
dry cough
compensatory tachypnea
pulmonary HTN
crackles on inspiration
reduced lung volume
honeycombing
digital cyanosis and clubbing

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19
Q

honeycombing

A

seen in pulmonary fibrosis
fibrosis around airspaces

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20
Q

mutations in the CFTR lead to _____?

why?

A

production of thick and sticky secretions

there is a buildup of chord and bicarbonate ions in the cell

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21
Q

does CF just effect the respiratory system?

A

NO!

it also effects epithelial cells in the GI and reproductive tracts

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22
Q

pathophysiology of cystic fibrosis

A

small airways cause bronchiectasis –> airways widen and thicken
dehydration –> thick secretions
thick secretions –> permanent scarring and cysts in lungs

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23
Q

in CF, once cells in lungs are damaged, they further recruit

A

more inflammatory cells and become necrotic

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24
Q

continuous inflammation in CF causes

A

permanent damage and invites persistent infection and additional damage

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25
why are natural defenses diminished in CF?
pH of the airway becomes acidic due to reduced bicarbonate secretion
26
why are bacterial infections persistent in CF?
thick/sticky mucus is retained in the lower airways, preventing inhaled bacteria from being cleared
27
signs and symptoms of CF
cough wheezing nasal congestion headache and inflammation clubbing (advanced)
28
how to treat CF?
airway clearance therapy
29
airway clearance therapy steps
1. bronchodilators - open airway 2. inhaled mucolytics - break up and thin mucus 3. inhaled antibiotics - clear mucus secretions
30
types of inhaled mucolytics
dornase alpha hypotonic saline
31
hypotonic saline
pulls water out of epithelial cells and into mucus secretions
32
pulmonary edema
excessive fluid in the alveolar space or interstitium
33
hallmark symptom of pulmonary edema
dyspnea (SOB)
34
normal movement of fluid in the lungs
fluid flows out of the blood vessels into the interstitial space because pressure in the capillaries is higher than the interstitial space
35
how to alveoli protect themselves from interstitial fluid?
barrier formed by the epithelium epithelial cells transport sodium out of alveolar space gradient allows alveoli to function properly pulmonary lymphatic system
36
what does the pulmonary lymphatic system do?
removes excessive fluid in the interstitial space
37
due to negative pressure, fluid accumulates _______ from the airspaces and gets ___________ back into the blood vessels
away reabsorbed
38
Pulmonary edema types
increased permeability pulmonary edema (non-cariogenic) increased hydrostatic pulmonary edema (cariogenic) impairment of lymphatic drainage pulmonary edema
39
pulmonary embolism
embolus is dislodged somewhere in circulation and it moves to pulmonary circulation, gets stuck, blockage of the vessel and obstructing perfusion
40
what can cause pulmonary embolism?
air during surgery amniotic fluid fat from long bone fracture foreign body septic emboli DVT tumor
41
risk factors for venous thromboembolism
venous stasis increased coagulopathy vascular injury
42
dead spaces
ventilated well with fresh oxygen but not all perfused so carbon dioxide can't be removed
43
in pulmonary embolism, pulmonary vascular resistance and pulmonary arterial pressure both ___________ which can cause ___________ into the right ventricle and can severely ___________ cardiac output
shoot up circulatory backup limit
44
clinical presentation of pulmonary embolism
chest pain dyspnea hemoptysis sinus tachycardia inspiratory crackles due to atelectasis
45
can there be evidence of DVT in the lower extremity when someone has a pulmonary embolism?
yes, but not all the time warm, red, tender and swollen calf
46
tuberculosis
macrophages eat bacteria --> bacteria replicates in macrophage --> granuloma forms --> if one bursts they can multiply
47
region of the lungs TB typically infects
posterior apical region (deep lung infection)
48
cycle of TB infection continues until the mycobacteria
disseminates in the intravascular space
49
pulmonary symptom of TB
cough
50
what can be visualized on chest imaging when someone has TB?
patchy and nodular infiltrates
51
how does the body fight the TB infection?
form granulomas around the microorganism and T lymphocytes induce apoptosis
52
can TB evade detection and lysis of apoptosis?
yes and they can become dormant
53
how can someone contract pneumonia?
inhalation of infectious particles aspiration of oropharyngeal contents hematogenous spread from other side of infection
54
risk factors of pneumonia
immunocompromised primary lung infection alcohol consumption and narcotic use comorbidities
55
how can alcohol consumption and narcotic use lead to pneumonia?
they depress mucociliary transport
56
clinical presentation of pneumonia
pulmonary infiltrates on chest imaging fever cough increased sputum production SOB
57
how does lung cancer develop?
normal bronchial epithelial cells acquire multiple genetic mutations over time
58
mutations of lung cancer include
activating proto oncogenes inhibiting tumor suppressor genes production of self stimulating growth factors
59
biomarkers identified as drivers of tumor growth and survival can serve as
targets for drug therapy
60
most common mutated genes in lung cancer
EGFR KRAS BRAF HER2 (not as much as the other 3)
61
risk factors of lung cancer
smoking respiratory exposure to asbestos, arsenic and benzene genetics history of COPD
62
types of lung cancer which is more prevalent?
Small cell lung cancer (SCLC) non small cell lung cancer (NSCLC) - more prevalent
63
different types of infiltrates seen on chest imaging and which lung disease they correlate to
pulmonary infiltrates - pneumonia nodular/patchy infiltrates - TB honeycombing - pulmonary fibrosis

Pathophysiology (18 decks)

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