Pathology Tbl #6: Lung: Block Ii

Front 1

What is the normal PaCO2?

Back 1

40 mmHg

Front 2

What is the normal PaO2?

Back 2

80-100 mmHg

Front 3

What is the normal HCO3?

Back 3

22-26 (24) mmHg

Front 4

Which pressure gradient usually drives breathing? When is this not the case?

Back 4

PaCO2 usually drives breathing unless the patient is hypoxic or PaCO2 is chronically elevated as in obstructive lung disease.

Front 5

What is the main factor affecting PaCO2?

Back 5

The mechanical ability of the lungs to exchange gas - if there is a problem with CO2 gas is either not entering or not exiting the lung.

Front 6

How do the lungs compensate for hypercarbia (increased PaCO2)?

Back 6

By hyperventiliating the lung units that do work - this falls apart if the entire chest is hyperinflated.

Front 7

In patients with COPD, what is the effect on CO2 transport?

Back 7

Carbon dioxide cannot be blown off and thus is retained, making the patient acidotic.

Front 8

What is the effect on CO2 with patients who have an isolated segmental diffusion/perfusion defect (such as in a PE)?

Back 8

They have normal mechanical lung function and therefore no problem blowing off CO2. The lack of oxygen (hypoxic drive) caused the lung to be hyperinflated but cannot correct the underlying oxygen deficit.

Front 9

When lung segments are damaged, why cant the lung compensate for O2?

Back 9

Because each functional lung unit already produces 100% saturation of O2 even before hyperventillation and additional oxygen not bound to hemoglobin accounts for very little O2 delivery to tissues.

Front 10

What are the main facotrs that affect O2 delivery?

Back 10

Pure mechanical function and minute ventilation, the perfusion of the lung and the amount of diffusion membrane

Front 11

Which conditions increase membrane thickness, making O2 diffusion difficult?

Back 11

Pulmonary edema, ARDS, pulmonary fibrosis

Front 12

How would the PaCO2 and PaO2 change is diseases that primarily decrease ventilation?

Back 12

The PaCO2 would increase and the PaO2 would decrease.

Front 13

When can oxygenation defects for obstructive lung disease be overcome?

Back 13

When there is still enough diffusion membrane available and exposed for gas exchange.

Front 14

Name one disease that decreases ventillation segmentally.

Back 14

Chronic Bronchitis

Front 15

Which obstructive lung disease has normal PaCO2 and decreased PaO2?

Back 15

Chronic bronchitis

Front 16

Which obstructive lung disease has so many non-functional lung units due to mucus plugging, hyperinflation, and atelectasis that they cannot maintain a normal oxygen saturation but have preserved mechanical lung function allowing them to blow off CO2 with hyperventilation? What is the common term for their appearance?

Back 16

Chronic bronchitis - called "blue bloaters"

Front 17

In this condition the patient still has enough diffusion membrane to allow O2 delivery but failing mechanisms of ventilation causing CO2 retention that worsens with their attempts to hyperventilate:

Back 17

Emphysema

Front 18

Which conditions primarily decrease perfusion/diffusion and cause oxygenation defects?

Back 18

1. Pulomary Embolism
2. Interstitial Lung Disease
3. Pneumonia
4. Pulmonary Edema

Front 19

This disease is characterized by cycles of alveolar injury, idiopathic, chronic inflammation and fibroblastic proliferation.

Back 19

UIP or Idiopathic Pulmonary Fibrosis

Front 20

This disease is associated with TGF-beta inhibition of caveolin-1 which then causes fibrobalsts to increase.

Back 20

UIP or Idiopathic Pulmonary Fibrosis

Front 21

This disease presents with dry cough, DOE, cyanosis and clubbing (later). It causes a gradual decrease in lung function despite treatment and mean survival is 3 years. The only treatment is lung transplant.

Back 21

UIP or Idiopathic Pulmonary Fibrosis

Front 22

This disease is characterized by honeycomb lung, patchy fibrosis with temporal heterogeneity.

Back 22

UIP or Idiopathic Pulmonary Fibrosis

Front 23

This disease is characterized by uniform mild fibrotic patches with moderate inflammation. It is diffuse patchy fibrosis with No temporal fibrotic heterogeneity.

Back 23

Non-specific interstitial pneumonitis (NSIP)

Front 24

This disease presents with dyspnea and cough for several months and reponds well to steroids and can recover lung function.

Back 24

Non-specific interstitial pneumonitis

Front 25

How can one tell the difference between UIP and NSIP?

Back 25

Both have fibrosis with diffuse lung involvement but NSIP lacks temporal heterogeneity. NSIP has a much better prognosis than UIP.

Front 26

This disease is characterized by subpleural or sub-bronchiole airway consolidation. There are loose connective tissue plugs within the bronchioles. There is not interstitial fibrosis or honeycombing in the lung.

Back 26

Crytogenic organizing pneumonia or BOOP

Front 27

This disease is triggered by inflammation or infection and presents with cough and dyspnea. There is no interstitial fibrosis or honeycombing and recovery can be spontaneous or is treated with steroids for 6 months.

Back 27

Crytogenic organizing pneumonia or BOOP

Front 28

This disease is common in african americans and non-smokers. CD4 cells are key in the pathogenesis of this disease and thus, granulomas result.

Back 28

Sarcoidosis

Front 29

This disease presents in young patients with dyspnea, interstitial infiltrate/fibrosis, hilar lymphadenopathy, and may have multisystem involvement (rash, erythema nodosum, blurry vision, hepatitis, enlarged salivary glands):

Back 29

Sarcoidosis

Front 30

In this disease, non-caseating granulomas are seen, with Schuamann bodies (laminated calcium) and stellate inclusions (asteroid bodies)

Back 30

Sarcoidosis

Front 31

In this disease skin lesions may occur and the eye (along with its glands) and salivary glands are often involved. There is a strong tendency for lesions to heal, so varying stages of fibrosis and hyaline change can be seen in the lungs.

Back 31

Sarcoidosis

Front 32

This disease has a wide spectrum of presentation, from asymptomatic to complicated and as the disease progresses it causes a decrease in ventilation. The underlying cause is activated macrophages filled with carbon.

Back 32

Coal workers pneumoconiosis (CWP)

Front 33

This disease is seen in coal workers with rheumatoid arthritis.

Back 33

CWP- Caplan Syndrome

Front 34

This is a complicated form of CWP that is seen after many years. It is considered a point of no return, even if exposure is stopped, leading to pulmonary HTN and cor pulmonale.

Back 34

Progressive Massive Fibrosis (PMF)

Front 35

This disease is characterized by many 2-10cm necrotic lesions filled with collagen and pigment. The lung many black scars on the surface.

Back 35

Progressive Massive Fibrosis

Front 36

This disease is seen most commonly in rock miners, stone cutters, etc. It causes release of free radicals, activates macrophages which release mediators. It can cause PMF, hypoxia and pulmonary HTN. Has acute and chronic presentations.

Back 36

Silicosis

Front 37

This disease is caused by exposure to silica and has a 10-30x increased risk of TB:

Back 37

Silicosis

Front 38

The acute form of this disease presents with diffuse alveolar lipoproteinaceous material with variable interstitial fibrosis and No classic nodules.

Back 38

Acute Silicosis

Front 39

The chronic form of this disease takes 20-40 years to develop and presents with nodules in the upper lung measuring 2-4mm and aggregates of tiny nodules of simple silicosis.

Back 39

Chronic Silicosis

Front 40

These are seen in people exposed to asbestos that and are not a precursor to cancer, are always benign, and can be seen on CXR.

Back 40

Asbestos related pleural plaques

Front 41

These are well circumscribed plaques containing collagen and calcium. They develop on the posterolateral aspects of the pleura, are benign, and do not have asbestos bodies.

Back 41

Asbestos related pleural plaques.

Front 42

Characteristics of this disease are dyspnea, cough with sputum, irregular linear densities on CXR (esp. in lower lobes), and honeycomb pattern in advanced stages.

Back 42

Asbestos related interstitial fibrosis

Front 43

This disease is characterized by diffuse pulmonary interstitial fibrosis with golden-brown fusiform or beaded rods.

Back 43

Asbestos related interstitial fibrosis

Front 44

What are the two types of asbestos particles? Which one is more pathogenic?

Back 44

Serpentines and amphiboles. Amphiboles are more pathogenic- allign themselves with airways and penetrate more deeply into the lungs

Front 45

Where does asbestos interstitial fibrossis start?

Back 45

Usually starts in the lower lobes/subpleural regions. Other pneumocoisis are in the upper lung.

Front 46

Which disease is characterized by ivory white pleural plaques?

Back 46

Asbestos related interstitial fibrosis.

Front 47

Which kind of cancer is caused by asbestos + smoking?

Back 47

Broncogenic Carcinoma

Front 48

Can act as tumor initiator and promoter, which is due to free radicals generated by their fibers.

Back 48

Asbestos

Front 49

This disease presents with pleural effusion, cannot be seen on a plain film, and kills by invading important local structures and by encasing and strangling the lung.

Back 49

Malignant Mesothelioma

Front 50

This disease is characterized by ensheathment of the lungs and invasion into local structures with thick, gelatinous, greyish pink, invasive tumor.

Back 50

Malignant Mesothelioma

Front 51

This disease is often associated with smoking because it inhibits alpha-1-antitrypsin leading to digestion of the walls of the lungs.

Back 51

Emphysema

Front 52

This disease presents with dyspnea, cough, weight loss, wheezing, slowed forced expiration, a barrel chest, and tripod stance.

Back 52

Emphysema

Front 53

What is the PO2 in emphysema? When does it change?

Back 53

The PO2 in patients with emphysema is normal until so much of the diffusion is lost that it begins to decrease. This marks the terminal stage of emphysema.

Front 54

This disease is characterized by voluminous upper 2/3 of the lungs, bleb formation and flat diaphragm on CXR.

Back 54

Emphysema

Front 55

This disease is characterized by septal wall destruction and distened alveolar spaces.

Back 55

Emphysema

Front 56

This obstructive disease is characterized by increased pressure on expiration due to compromised outflow, a decreased FEV1, and enlargement of airspaces distal to terminal bronchioles.

Back 56

Emphysema

Front 57

90% of this disease is seen in smokers and is characterized by persistent cough with sputum production, DOE, hypoxemia and decreased PO2.

Back 57

COPD- Chronic Bronchitis

Front 58

In this disease chronic irritation, recurrent infections and smoking cause airflow obstruction due to inflammation, fibrosis and narrowing of the bronchus. Will also see hypersecretion of mucus.

Back 58

COPD- Chronic Bronchitis

Front 59

This disease is characterized by excessive mucus on epithelial surfaces, increased size of mucus glands and increased number of goblet cells.

Back 59

COPD-Chronic Bronchitis

Front 60

This type of asthma is caused by respiratory tract infections, cold, exercise, and stress.

Back 60

Intrinsic Asthma

Front 61

This type of asthma is caused by atopic, occupational and allergic reactions.

Back 61

Extrinsic Asthma

Front 62

What do the early and late phases of asthma look like?

Back 62

Early has bronchoconstriction and increased mucus production and late has neutrophils and eosinophils.

Front 63

This disease is characterized by reversible bronchial airway constriction, overdistended lungs with bronchial mucus plugs and Curshman's spirals

Back 63

Asthma

Front 64

Which type of asthma has increased IgE?

Back 64

Extrinsic- is typical hypersensetivity Type I reaction

Front 65

This disease has curshman's spirals, charcot-leyden crystals, thickened basement membrane, inflammation and hypertrophy of the bronchial wall muscles and increased mucosal glands

Back 65

Asthma

Front 66

This is not a primary disease but associated with bronchial obstruction (like by a tumor), CF, kartagener's necrotizing pnuemonia, and impaired immunity:

Back 66

Bronchiectasis

Front 67

Characterized by severe persistent or paroxysmal cough with excessive sputum production, episodic URIs, may have dyspnea, cyanosis or cor pulmonale, less frequently presents with brain abcess and clubbing.

Back 67

Bronchiectasis

Front 68

Chronic necrotizing infections of bronchi and bronchioles leading to permanent dilation of airways:

Back 68

Bronchiectasis

Front 69

Chracterized by dilated airways usually in lower lobes that extend almost to pleura, filling of ectatic airways with purulent secretions

Back 69

Bronchiectasis

Front 70

In this secondary disease inflammation, metaplasia, fibrosis, ulcerated mucosa and possible abcesses can be seen. Sputum cx have mixed flora with pseudomonas, staph aureus, and haemophilus species

Back 70

Bronchiectasis

Front 71

This autosomal recessive disease is due to a delta 508 deletion

Back 71

Cystic Fibrosis

Front 72

This disease is tested for on the newborn screen and presents with thick, sticky mucus with persistent recurring infections of the respiratory tract.

Back 72

Cystic Fibrosis

Front 73

This disease involves nasal polyps, chronic sinusitis, bronchiectasis involving all lobes, and can be diagnostically confirmed with sweat test:

Back 73

Cystic Fibrosis

Front 74

This disease is caused by abnormal sodium transport leading to thickened mucus secretions, chronic infections of the respiratory tract causing progressive respiratory insufficiency and death

Back 74

Cystic Fibrosis

Front 75

Characterized by mucus plugs, bronchiectasis, and airways filled with pus.

Back 75

Cystic Fibrosis

Front 76

This disease can present in newborns with meconium ileus, jejunal-ileal atresia or bowl obstructions later in life:

Back 76

Cystic Fibrosis