Pulmonary Diseases and Conditions Flashcards Preview

Block 2: Cardio, Renal, and Respiratory > Pulmonary Diseases and Conditions > Flashcards

Flashcards in Pulmonary Diseases and Conditions Deck (26)
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Obstructive lung disease (within COPD)

Destruction of the alveolar-capillary membranes distal to terminal bronchioles, resulting in dilatation of terminal air spaces, and this reduces surface area of the lung

Lose elasticity/recoil of lungs, taking you to higher FVC

EPP moves farther along airways to alveoli, causing ariway collapse

Tau (R x C) is increased so can't count on passive exhalation anymore and have to use accessory muscles

Barrel chest, difficulty breathing out, increasing expiratory flow does NOT prevent airways from collapsing

Emphysema worse in upper lobes than in lower lobes


Examples of obstructive lung disease



Upper airway?


Examples of restrictive lung disease

Pulmonary fibrosis

Chest wall deformity

Neuromuscular weakness


Lung volumes in obstructive lung disease

TLC, FRC, RV increased

FEV1/FVC ratio is decreased (normal is 80%)

Remember: hyperinflation, air trapping


Lung volumes in restrictive lung disease

TLC, FRC, RV decreased because lungs are smaller

FEV1/FVC same or larger

Lungs are less compliant and thus more elastic



Viral disease that causes muscle weakness that leads to restrictive lung disease

Iron lung was a negative pressure ventilator to aid patients in breathing


Interstitial fibrosis

Stiff lungs

Can result in mechanical problems (alveolar hypoventilation) but also thickening can cause diffusion abnormality because of thickening of alveolar walls

On exercise PaO2 falls because of inadequate time for oxygen diffusion (this doesn't happen very commonly)


High altitude

Lower barometric pressure, so therefore 21% O2 concentration is lower O2 pressure, so you get lower PAO2 because of altitude

Also at high altitude, CO will increase (widening pulse pressure)

Also pulmonary arteries will constrict (hypoxic pulmonary vasoconstriction)


Pulmonary embolism

Happens in people who are immobile for a long time, previously healthy, estrogen therapy, "bad cold" at onset of symptoms is actually PE, causes rapid deterioration

Pulmonary vascular resistance is increased

If no pulmonary infarction, PE can even be asymptomatic, or difficult to diagnose



Necrotizing infection of bronchi

Dilated bronchi that have destruction of muscle and elastic tissue

Green/yellow sputum

Smokers, CF, congenital, poor ciliary motility, breathing in food particles

Obstructive lung disease


Honeycomb change

Multiple abnormal airspaces surrounded by dense collagen (pink)

Thick wall spaces

Seen in end stage pulmonary fibrosis, life expectancy only 3 years once you see honeycomb change



Chronic Obstructive Pulmonary Disease

Two components: emphysema and airway inflammation

Lungs and chest get big--barrel chest

Lungs very gray/black because of anthrocrotic pigment

Destruction of alveoli

Emphysema worse in upper lobes than lower lobes


Diseases caused by smoking


Chronic bronchitis

Respiratory bronchiolitis

Desquamative interstitial pneumonia

Eosinophilic granuloma



Chronic bronchitis

Airway inflammation causes increased glands and secretions (mucous in the airway)


Interstitial lung disease (ILD)

200 different diseases with different causes but similar symptoms (inflammation and fibrosis)

Not that common

Most important is Usual Interstitial Pneumonia, usually affects lower lobe (spatially and temporally heterogeneous)


Acute Lung Injury

Adult Respiratory Distress Syndrome (see hyaline membranes: pink lining that represents necrotic epithelial cells in alveolar septae and plasma proteins deposited from leakage of capillaries)


Diffuse Alveolar Damage (first see edema on x-ray, then hyaline membranes 24 hours later)



Exudate, inflammatory cells that eventually turn white and harden

Seen in pneumonia


Virchow's triad of things that increase the probability of thromboemboli

1) Vascular injury

2) Stasis

3) Hypercoagulable state

Note: people who have just had surgery more at risk for PE because of these 3 things


Major types of lung cancer

1) Adenocarcinoma

2) Squamous cell carcinoma

3) Small cell carcinoma (neuroendocrine/Kulchitsky cell)

4) Large cell undifferentiated carcinoma



Tumor encasing/surrounding lung

Associated with asbestos exposure (can even have secondary asbestos exposure via clothes etc as a cause)


Mechanism of damage caused by smoking

Activation of leukocytes that induce chronic inflammation and structural injury by release of enzymes and ROS's

Inactivates anti-proteases, causing tissue destruction


D-dimer test

D-dimer is a fibrin degradation product

Used to diagnose PE

High sensitivity (people who have PE WILL have high D-dimer) but low specificity (many false positives, so people with no PE may easily still have high D-dimer)


Chronic hypercapnia/Chronic lung disease

Chronic respiratory failure causes increased PaCO2, low PaO2, acidic pH --> CO2 goes into CSF, H+ gets into kidney tubule, causes excretion of H+ and retention of HCO3- --> HCO3- actively transported out of BBB to try to reduce pH changes --> reduces H+ in CSF --> reduced stimulus for chemoreceptors to increase ventilation (bad!)

Compensated respiratory acidosis with chronic hypoxemia, hypercapnia, renal HCO3- retention, normal blood pH

Patients insensitive to chronically elevated PaCO2, so ventilation stimulated by hypoxia!

Dejor effect says: Don't give 100% O2 to person with chronic hypercapnia because that decreases ventilation more (peripheral carotid bodies turned off!) and increases PCO2 even more

Patient develops pulmonary hypertension, edema, in response to hypoxemia which can lead to right side heart failure


Sleep apnea

Cessation of breathing for more than 10 seconds

Caused by obstruction of hypopharyngeal airway or disturbance of ventilatory control during sleep

Leads to sleep disruption, nocturnal hypoxemia, early morning hypercapnia, sleepiness during day


How can you tell if someone has diaphragm paralysis?

When they breathe in, their abdomen will be sucked INWARD

Thoraco-abdominal paradox

Have to use their accessory muscles to expand ribcage due to floppy diaphragm and this causes abdomen to be sucked in


Why is emphysema considered obstructive?

Airways collapse because less elastic recoil moves EPP closer to alveoli, so can't get air out