Bod: Respiratory: Pleural Disease

Front 1

What are the three regions of the parietal pleura?

Back 1

the diaphragmatic pleura, costal pleura, mediastinal pleura

Front 2

The visceral pleura and the parietal pleura meet at the _____ _____.

Back 2

The visceral pleura and the parietal pleura meet at the LUNG ROOT.

Front 3

The visceral pleura is supplied by the branches of the _______ artery.

Back 3

The visceral pleura is supplied by the branches of the BRONCHIAL artery.

Front 4

What is the only route by which fluid can leave the pleural space?

Back 4

Through stomas that connect the pleural space to the lymphatics of the parietal pleura.

Note that while there are abundant lymphatics in the visceral pleura, these lymphatics do not participate in the removal of particulate matter from the pleural space.

Front 5

True or false: the visceral and parietal pleuras are supplied by the bronchial arteries.

Back 5

False. The visceral pleura is supplied by the bronchial artery but the parietal pleura is supplied by the systemic capillaries.

Front 6

What is the cell type that makes up the visceral and parietal pleural membranes?

Back 6

Mesothelium (flat squamous) resting on submesothelium (a thin layer of connective tissue).

Front 7

What is the most significant cause of pleural effusion in congestive heart failure?

Back 7

Increased hydrostatic pressure in the microvascular circulation via an increase in the pulmonary wedge pressure (LA pressure)

Front 8

What are 5 different causes of pleural effusion?

(Hint: 3 are changes in the microvascular circulation, and 2 are more macro changes.)

Back 8

1. Increase in pulmonary capillary wedge pressure --> increased hydrostatic pressure in the microvascular circulation --> fluid leaks into intersitium --> fluid moves down pressure gradient into the pleural space.

2. Decrease in the oncotic pressure in the microvascular circulation. Low protein fluid in the pleural space --> pleural effusion. Usually gets cleared by lymphatics.

3. Increased permeability of the microvascular circulation. Leaky, damaged vessels can release particles that can clog stomata --> pleural effusion.

4. Impaired lymphatic drainage of the pleural space. Due to a tumor or due to fibrosis of the lymphatics.

5. Movement of fluid from the peritoneal cavity into the pleural space. Ascites in the peritoneal cavity --> moves down a pressure gradient accross the diaphragm.

Front 9

What is the differential diagnosis for transudative pleural effusion?

Back 9

1. Congestive heart failure
2. Cirrhosis
3. Pericardial disease
4. Nephrotic syndrome
5. Myxedema
6. Peritoneal dialysis
7. Pulmonary embolization

Front 10

What is the differential diagnosis for exudative pleural effusion?

Back 10

1. Infectious diseases
2. Bacterial infections
3. Tuberculosis
4. Fungal infections
5. Parasitic infections
6. Neoplastic diseases
7. Metastatic diseases

Front 11

Pneumothorax: pathology

Back 11

Mesothilial proliferation
Eosinophils
Fibrin/fibrosis
Small multinucleated giant cells (giant cells are larger in TB and rheumatoid disease)

The microscopic changes of pneumothorax are the same regardless of the etiology.

Front 12

What is the differential diagnosis for pneumothorax?

Back 12

1. Pulmonary eosinophilic granuloma.

2. Pleural changes due to cystic fibrosis.

Front 13

What are the pathological findings of pulmonary eosinophilic granuloma (part of the differential diagnosis of pneumothorax)?

Back 13

Will see large numbers of Langerhans' cells when stain with S100 protein and CD1a antigen.

Gross finidings are very similar to other forms of pneumothorax.

Front 14

What are the pathological findings of the pleura in cystic fibrosis?

Back 14

CF patients have small blebs of bullae. These may rupture and give rise to pneumothoraces. Most of the visceral pleura of a cystic fibrotic lung is structurally normal.

Vascular proliferation
Myxoid change
Subpleural air "cysts" (may be bronchiectatic cysts, interstitial cysts, and emphysematous bullae)

Front 15

List the diseases associated with secondary pneumothorax

Back 15

Pneumonia
Staphylococcal septicemia
Pneumocystis carinii (jiroveci, see in AIDS patients)
Lung abscess
Coccidiomycosis
Hyatid disease
COPD
Asthma
Sarcoidosis
Berylliosis
Idiopathic pulmonary fibrosis
Cystic fibrosis
Scleroderma
Histiocytosis X
Lymphphangioleiomyomatosis
Biliary cirrhosis
Marfan's syndrome
Ehlers-Danlos Syndrome
Idiopathic pulmonary hemosiderosis
Pulmonary infarction
Rheumatoid disease

Front 16

Pleural plaques may indicate what in a patient?

Back 16

An exposure to asbestos, other pathogenic fibers, previous surgery, infection.

Front 17

Where are pleural plaques usually seen?

Back 17

On the parietal and diaphragmatic pleura.

Only occassionaly on the visceral pleura.

Front 18

What is a pleural plaque made up of?

Back 18

Mostly collagen and acellular material. Occasionally will see small foci of chronic inflammation. Maybe a single lining of mesothelial cells. Will not see any abestos bodies within the plaque. Plaques may calcify. Form between 10 and 20 years post-exposure.

Front 19

Amount of exposure needed to produce a pleural plaque vs. pulmonary fibrosis?

Back 19

The amount of asbestos exposure needed to cause plaques is significantly less than that required to produce pulmonary fibrosis.

Front 20

How long after exposure do mesotheliomas arise?

Back 20

15-25 years after.

Front 21

Where is asbestos actually found in people with mesotheliomas?

Back 21

In the distant airways of the lung parenchyma and not within the pleural tissue or within tumors themselves.

Front 22

Most mesotheliomas arise from the _____ pleura.

Back 22

Most mesotheliomas arise from the PARIETAL pleura.

Front 23

Benign or malignant: diffuse mesotheliomas

Back 23

Always malignant.

Front 24

Benign or malignant: localized mesotheliomas

Back 24

Most often benign.

Front 25

What are the three histological categories of mesothelioma?

Back 25

1. Epithelial (50%)
2. Fibrous (sarcomatous) (25%)
3. Mixed types (25%)

Front 26

What are two immunohistochemical tests that are hallmarks of mesothelioma?

Back 26

1. Postive calretinin
2. Negative CEA (carcinoembryonic antigen)

Front 27

Differential diagnosis of mesothelioma.

Back 27

Primary lung carcinoma
Metastatic adenocarcinoma into the pleura
Benign pleural tumors
Solitary fibrous tumors of the pleura

Front 28

Prognosis for patients with mesothelioma?

Back 28

Poor. Median survival is 1 year.

Front 29

What is Starling's law of transcapillary exchange?

Back 29

Q = L x A[(Pcap - Ppl) - σ(πcap - πpl)]

Q = the rate of fluid movement
L = the filtration coefficient.
A = the surface area of the membrane.
σ = the osmotic reflection coefficient for protein (a measure of the membrane's ability to limit the passage of large molecules.

Front 30

True or false: the pleural mesothelium makes a water-tight lining around the pleural cavity.

Back 30

False. The mesothelium is extremely permeable to water and protein. The endothelium of the pleural capillaries is the primary barrier to fluid movement.

Front 31

What are the general forces at work on the fluid in the pleural space?

Back 31

There is hydrostatic pressure is higher in the systemic capillaries of the parietal pleura, but the oncotic pressure is higher there. The net pressure gradient is INTO the pleural space.

Front 32

What are two potential routes by which fluid can be drained from the pleural space?

Back 32

1. Capillaries in the visceral pleura (low resistance, low hydrostatic pressure).
2. Lympatics in the parietal pleura (most important - can be augmented 20 to 30 fold).

Front 33

What is the list of causes of increased pleural fluid formation?

Back 33

- Increased interstitial fluid in the lung (LVF, pneumonia, PE)
- Increased intravascular pressure in the pleura (RVF, LVF, SVC syndrome)
- Increased pleural fluid protein level (increased microvascular permeability due to inflammation)
- Decreased pleural pressure.
- Decrease in oncotic pressure (hypoalbuminemia, nephrotic syndrome)
- Increased fluid in the peritoneal cavity (ascites, peritoneal dialysis)
- Disruption of the thoracic duct (lymphoma, trauma)

Front 34

What is the list of causes of decreased pleural fluid absorption?

Back 34

- Obstruction of the lymphatics draining the parietal pleura (malignancy, fibrothorax, infection)
- Elevation of systemic vascular pressures (SVC syndrome, RVF)

Front 35

What kind of ventilatory defect does having fluid in the pleural space cause?

How does increased pleural fluid affect diaphragm function?

Back 35

It causes a restrictive defect. TLC decreases.

Increased fluid in the pleural space causes the diaphragm to operate as a disadvantageous portion or the length-tension curve.

Front 36

What are the two types of pneumothoraces? (PTX)

Back 36

1. Spontaneous pneumothorax
2. Traumatic pneumothorax

Front 37

Spontaneous PTX in males and females?

Back 37

Males: 6-7/100,000/year
Females: 1-2/100,000/year

Front 38

What is the pathogenesis of the majority of cases of spontaneous pneumothorax?

Back 38

Ruptured subpleural blebs (usually apical).

Front 39

Development of subplural blebs is strongly associated with what?

Back 39

With cigarette smoking.

Front 40

Spontaneous PTX is more likely to happen during large swings in what?

Back 40

Barometric pressure.

Front 41

What can sudden chest compression with a closed glottis cause?

Back 41

Pneumothorax

Front 42

When a PTX occurs, what will happen to the lung and the chest wall?

Back 42

The chest wall will expand and the lung will collapse.

Front 43

What are the main physiologic consequences of a PTX?

Back 43

- Decrease in vital capacity.
- V/Q mismatch (increased A-a gradient)
- Decrease in PaO2

Front 44

What will happen to a healthy individual who gets a spontaneous pneumothorax?

Back 44

The PTX will actually be well tolerated!

Front 45

What is a radical therapy for those with recurrent pneumothoraces?

Back 45

Pleural "abrasion"

Insert something into the pleural space that causes inflammation --> the pleural membranes stick together (these will NEVER come apart!) --> thoracic surgery becomes impossible.

Front 46

What is a common physical finding of someone with "subcutaneous emphysema?"

Back 46

Feel in the anterior triangle of the neck --> feels like "rice crispies"

Front 47

What causes "pneumo-everywhere?"

Back 47

Being on a ventilator. This is not a real problem, surprisingly.

Front 48

Tiny PTX: treatment?

Back 48

Not a huge problem, just give 50% oxygen.

Front 49

Tension PTX: hallmarks

Back 49

Involves some type of one-way valve process that allows air in during inspiration, but closes during expiration.

Front 50

The onset of tension PTX is usually heralded by what?

Back 50

Cardiopulmonary status deterioration (primarily the result of a decreased cardiac output due to impaired venous return).

Front 51

What is BAPE?

Back 51

Benign asbestos pleural effusion.

Front 52

Pleural plaques: symptoms

Back 52

None

Front 53

Pleural plaques: risk for future disease?

Back 53

10 fold increase in risk for mesothelioma

Slightly increased risk of lung cancer in patients that continue to smoke.

Front 54

What adverse effects can blood in the pleural space cause?

Back 54

Blood, if not drained, will cause fibrosis.

Front 55

Diffuse pleural fibrosis: causes

Back 55

- End result of exposure to asbestos.
- Drugs (methysergide, bromocriptine, ergotamine)
- Collagen vascular disease (rheumatoid pleuritis, systemic and drug-induced lupus erythematosus)
- Infectious diseases
- Idiopathic causes

Front 56

What is a fibrothorax?

Causes?

What is notable about the amount of pleural disease present versus the clinical presentation?

Treatment?

Back 56

A thick peel around the lung.

- Hemothorax
- Tuberculosis
- Bacterial lung infections

The clinical presentation is much worse than the degree of pleural disease present.

Decortication (removal of the pleural surfaces).

Front 57

What are the common symptoms of a pleural effusion?

Back 57

Cough
Chest pain (usually respirophasic)
SOB

Front 58

True or false: both pleura of the lung are innervated.

Back 58

False: Only the parietal pleura is innervated.

Front 59

What can shoulder pain indicate when presenting with cough, chest pain, SOB?

Back 59

Involvement of hte diaphragmatic portion of the parietal pleura.

Front 60

Pleural effusion: findings on physical exam.

Back 60

Pleural friction rub (not heard if effusion is large). This is a course, creaking, leathery sound that is loudest on inspiration.

Breath sounds on the affected side will be diminished and will be dull to percussion. Increased transmission of whispered pectoriloquy and egophony may be appreciated.

Front 61

What are the two major classifications of pleural effusions?

Back 61

Transudates and exudates

Front 62

What are the characteristics of an exudate pleural effusion?

Back 62

Loss of integrity of the pleural capillary endothelium and/or disruption of the lymphatic clearance mechanisms. Marked by HIGH pleural fluid protein concentrations.

Treatment of an exudate is more difficult than that of a transudate.

Front 63

What are the characteristics of a transudate pleural effusion?

Back 63

Usually involves an imbalance of Starling forces such that low-protein content pleural fluid is increased.

Very much reversible

Front 64

What are the clinical criteria for a transudate? (3)

Back 64

1. A pleural fluid to serum total protein ratio < 0.5.
2. A pleural fluid to serum lactate dehydrogenase (LDH) ratio < 0.6.
3. A pleural fluid LDH that is < 2/3 of the upper limits of normal for the serum LDH.

If any of the above are not met, then it is not a transudate.

Front 65

What is the list of diseases that are "virtually always" transudates?

Back 65

- CHF (acute diuresis may result in a "pseudoexudate")
- Cirrhosis (rate without clinical ascites)
- Nephrotic syndrome (usually bilateral and subpulmonic)
- Atelectasis (caused by increased negative pleural pressure)
- Hypoalbuminemia (edema fluid rarely isolated to the pleural space???)
- Peritoneal dialysis (transudate develops within 48 hours of initializing dialysis)
- Urinothorax (caused by ipsilateral obstructive uropathy)
- Constrictive pericarditis (bilateral effusions)
- Trapped lung (a result of remote or chronic inflammation)
- SVC obstruction (may be due to acute systemic venous HTN or acute blockage of thoracic lymph flow).

Front 66

What is the list of diseases that are "classic"" exudates that can be transudates?

Back 66

- Malignancy (due to early lymphatic obstruction, obstructive atelectasis, or concomitant disease. 10 to 20% are transudates.)
- Pulmonary embolism (due to atelectasis, > 20% are transudates)
- Hypothyroidism (see transudates secondary to hypothyroid heart disease)
- Sarcoidosis (rare. Seen in stage II and III disease.)

Front 67

What are some of the major pathogenic processes that cause exudative pleural effusions?

Back 67

- Infections
- Noninfectious inflammations
- Malignancies
- Chronically increased negative intrapleural pressure
- Iatrogenic
- Connective tissue disease
- Endocrine disorders
- Lymphatic disorders
- Movement of fluid from the abdomen to the pleural space

Front 68

What are the three major disease processes that cause exudative pleural effusions?

Back 68

- Infection
- Malignancies
- PE

(the above cause about > 80% of exudative pleural effusions)

Front 69

What is the most common cause of transudative pleural effusion?

Back 69

CHF (1/3 to 2/3 of all pleural effusions)

Front 70

What is the most common cause of exudative pleural effusion?

Back 70

Most likely pneumonia

Front 71

Patients with an exudate over the age of 60 will likely have what etiology to their exudative pleural effusion?

Back 71

Malignancy (often adenocarcinoma of the lung or breast/liver mets)

Front 72

What type of PTX should be expected if the patient has a pulse over 140/min, is hypotensive, diaphoretic, cyanotic, or has electro mechanical dissociation?

Back 72

A tension pneumothorax.

Electromechanical dissociation is now called PEA (pulseless electrical activity), meaning that they have PQRS, but you can't feel a pulse.

Front 73

Tension PTX: findings on PE

Back 73

Pulse over 140/min, hypotensive, diaphoretic, cyanotic, electro mechanical dissociation, breath sounds diminished on affected side, percussion is hyperresonant. Tactile fremitus will be absent. Trachea may be shifted to unaffected side.

Front 74

Any PTX patient has the ability to quickly develop what?

Back 74

A tension PTX.

Front 75

What is one of the only reasons to do an "open biopsy" of the lung

Back 75

When you suspect mesothelioma.

Front 76

Transudates: treatment

Back 76

Minimal. Use diuretics, afterload reducers.

Front 77

What is the risk that someone with spontaneous PTX develops a second PTX? A third?

Back 77

50% --> 60% --> 80%

Front 78

Do you get a CXR in a patient with a tension PTX?

Back 78

No! Get a tube in their pleural space as soon as possible!