PATHOLOGY Flashcards

1
Q

How far down do the most inferior portions of a lung normally go?

A

They are usually level with the cardiac apex

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2
Q

When is pulmonary hypoplasia fatal?

A

If the disease is bilateral

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3
Q

What are the two general (major causes) of hypoplasia of the lung?

A

Oligohydramnios or decreased intrathoracic space

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4
Q

What are 4 causes of decreased intrathoracic space?

A

A diaphragmatic hernia (i.e. of Bochdalek/Morgnani), Cystic adenomatoid malformation, lethal form of osteogenesis imperfecta causing chest wall deformity, and chronic effusion such as hydrops fetalis

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5
Q

What is the lining of a foregut cyst? What are they from?

A

Pseudostratified columnar epithelium; detached part of embryonic foregut

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6
Q

What is the arterial supply/venous drainage of pulmonary sequestrations?

A

Both extralobar and intralobar are supplied by aorta NOT pulmonary artery, and drained by azygous system

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7
Q

Why is polydramnios an issue in utero? With which type of pulmonary sequestratant is it associated?

A

Because the excess volume can lead to strangulation; it is associated with EXTRALOBAR pulmonary sequestration

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8
Q

Differentiate the pleural linings of extralobar and intralobar sequestrants:

A

Extralobar are outside of the lung but have their own pleural lining, intralobar are within the lung and have the same pleural lining as the lung

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9
Q

What are the three types of atelectasis and in which way does the mediastinum shift?

A

Resorptive/Obstructive atelectasis shifts the mediastinum towards it; Compression atelectasis shifts the mediastinum away; and contraction atelectasis does NOT shift the mediastinum

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10
Q

In which way does the most common cause of atelectasis shift the mediastinum? What is the most common cause of this atelectasis?

A

Resorption/Obstruction atelectasis shifts mediastinum towards it; most common cause is EXCESSIVE SECRETION because it leads to a blockage

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11
Q

What are the treatments of the reversible causes of atelectasis?

A

Obstructive/resporption can be treated by removing the blockage and compression can be removed by sucking out the intrapleural compression (air, fluid, etc)

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12
Q

How long does it take to achieve an airless state in obstruction atelectasis and why?

A

It takes a few hours because the air that is in the aveolus will be absorbed by the blood vessels

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13
Q

A tension pneumothorax would shift the mediastinum in which direction?

A

Toward the healthy side, this is because tension pneumo is a form of compression atelectasis

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14
Q

What is the major cause of contraction atelectasis? What is the treatment?

A

Fibrotic changes of lung or pleura? No Tx.

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15
Q

What is the major cause of hemodynamic pulmonary edema?

A

Increased hydrostatic pressure, as in left heart failure

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16
Q

What kind of pulmonary edema can amphotericin B (amphoterrible) and heroin cause?

A

Microvascular injury pulmonary edema

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17
Q

What kind of pulmonary edema would be caused by an obstruction of pulmonary veins?

A

Hemodynamic pulmonary edema

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18
Q

What kind of edema is caused by near drowning?

A

Microvascular injury pulmonary edema

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19
Q

What is seen in long standing pulmonary edema?

A

Fibrosis of the alveoli

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20
Q

Why doesn?t administration of oxygen help in ARDS?

A

Because the hallmark of ARDS is hyaline change and hyaline is waxy/thick and creates a diffusion barrier in the blood-air membrane

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21
Q

Why are there more macrophages than neutrophils in Hamman-Rich syndrome?

A

Because this is ACUTE INTERSTITIAL PNEUMONIA–the lungs are NOT infected, this is a pnuemonia secondary to something somewhere else in the body like a liver laceration leading to hypovolemic or septic shock

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22
Q

Where is the most common origin of a pulmonary embolus? What kind of thrombus may form from an indwelling central catheter?

A

Most (95%) come from deep leg veins; an indwelling central catheter can cause a right atrial thrombus

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23
Q

Trousseau’s sign and protein C/S deficiency are risk factors for what? Why?

A

Pulmonary embolus (or any thrombotic event, really) because they indicate systemic hypercoagulability

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24
Q

What kind of heart failure will a patient with pulmonary embolism display? Sx?

A

ACUTE cor pulmonale (right heart failure)–JVD, peripheral edema, pulsatile liver, hepatic ascites (nutmeg liver)

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25
When are small emboli in the lungs problematic?
Usually only if there is inadequate bronchial circulation or if there are a ton of them
26
What two systems are compromised in PE? Explain.
Respiratory compromise because the alveoli cannot exchange gas with an occluded vessel; Hemodynamic compromise from the increased resistance from the embolus.
27
Why is pulmonary infarction from a PE rare in young people? What wil you see in them?
Because they usually have adequate bronchial circulation. Infarction really only happens if inadequate circulation, BUT they will have hemorrhage.
28
Explain why a person with a saddle embolus has electromechanical dissociation (i.e. PEA)?
Because their heart generates a rhythm but no blood can get past the pulmonary trunk, so no blood goes systemically either producing pulseless electrical activity.
29
What histopathologic type of pleuritis may result from PE? What is the diagnostic test of choice for PE?
Fibrinous pleuritis; SPIRAL CT
30
What is the diagnostic test for deep vein thrombosis?
Duplex ultrasonography
31
What are 4 methods of prophylaxis for PE?
Early ambulation post-op, IVC filter, compression stockings, and anticoagulation
32
What are two treatment methods for PE?
Thrombolysis or anticoagulation
33
Where do most PE's occur anatomically? How do you distinguish a PE from a post-mortem clot?
In the lower lobes of lungs; LINES OF ZAHN--indicates that there was organization of the clot over time
34
A pulmonary infarct with an intense neutrophilic reaction is most likely what?
A septic infarct from a septic embolus
35
What are you most concerned with as a follow up to organization and dissolution of a PE?
The development of PHTN--\> this is because scarring is a part of the organization process which increases resistance.
36
What kind of congestion is seen in areas of pulmonary infarction?
PASSSIVE CONGESTION? Pulmonary infarct is seen as ischemic necrosis on background of passive congestion.
37
What is the most likely etiology of a PE that looks like it has white holes in it histologically?
Fracture of a long bone--this is a fat embolus
38
What does amniotic fluid look like histologically? Why?
Like a thumbprint because of the layers of fetal squames
39
What is the most likely method of death in a patient with a sudden and large PE?
Acute cor pulmonale
40
Why doesn?t PE cause atelectasis?
Because there is no obstruction of the airway
41
What pressures define PHTN when at rest and exercise?
Greater than 25 mmHg at rest and greater than 30 with exercise
42
What term best describes PHTN w/o underlying parenchymal disease of the lung?
Primary Pulmonary HTN
43
How could endothelin dysfunction cause primary PHTN?
Because if prostacyclin/N2O are underproduced and endothelin is overproduced there is both vasoconstriction and vascular remodeling
44
How could dysnfuctional potassium channels underlie primary PHTN?
By possibly affecting the resting membrane potential of the vessel leading to high intracellular [Ca] causing vasoconstriction
45
What is the hallmark clinical sign of PHTN?
A progressive dyspnea that began with exertion and now occurs at rest--but can see that is not all that differenc from CHF
46
What are 3 signs of PHTN seen on CXR? What is the utility of lung biopsy for the Dx?
1) increased cardiothoracic ratio 2) enlarged pulmonary arteries 3) right ventricular hypertrophy; lung biopsy is not helpful for Dx of PHTN
47
What are 3 REVERSIBLE microscopic signs of PHTN?
Medial hypertrophy, intimal thickening, and intimal hyperplasia
48
What are 3 IRREVERISBLE microscopic signs of PHTN?
Concentric laminar intimal fibrosis, fibrinoid necrosis, and plexiform lesions
49
What are 3 things that nearly all etiologies of PHTN result in?
RVH, medial hypertrophy, and pulmonary atheromas
50
What are plexiform lesions? What do they indicate about the severity of the disease? What vessels do they affect?
They are TUFTS of capillaries growing off of a parent artery; the indicate HIGH SEVERITY; they affect small vessels
51
What heart defects are associated with pulmonary HTN, why?
Anything that involves a L-\> R shunt, most commonly an ASD since it causes volume overload in the right heart
52
What are 3 vasculitis-associated hemorrhages in the pulmonary system?
Hypersensitivity angiitis, Wegener Granulomatosis, and SLE
53
What is the clincial triad of Goodpasture Syndrome?
Diffuse pulmonary hemorrhage, glomerulonephritis, and circulating anti-GBM antibodies
54
What isotype is the antibody in Goodpasture's? What is it actually against?
IgG; Type IV collagen of the basement membrane of glomeruli and lungs
55
What is the main cause of death in Goodpasture's? What is the Tx?
Uremia from Kidney failure; can Tx with plasma exchange and immunosuppressive Tx
56
What is the morphology of the deposition of immunoglobulins in Goodpastures?
Linear deposits on basement membranes of glomerulus and alveoli
57
What are c-ANCA and p-ANCA good for diagnostically?
They are commonly elevated in systemic vasculitides
58
What is Anti-DNA topoisomerase I antibody useful for, diagnostically?
Scleroderma
59
What is Anti-mitochondrial-antibody (AMA) useful for?
Primary Biliary Sclerosis
60
How is Idiopathic Pulmonary Hemodiderosis different than Goodpasture's?
There are no antibodies in the serum (it is idiopathic) AND there is no renal involvement
61
What is the clinical presentation of of Idiopathic Pulmonary Hemosiderosis?
Intermittent hemoptysis and refractory anemia
62
How is the cause of death different in Idiopathic Pulmonary Hemosiderosis than in Goodpasture's?
IPH will be a pulmonary-related death whereas Goodpasture's is usually uremia--a renal issue
63
Describe the extent of necrosis and granuloma formation in Idiopathic Pulmonary Hemosiderosis:
There is no necrosis/granuloma formation, just capillary congestion with hemorrhage
64
Though the etiology of of Idiopathic pulmonary hemosiderosis is unknown there is a favorable response to what Tx?
Immunosuppressives
65
What 3 regions are affected by Wegener's Granulomatosis? What term best describes the inflammation?
Upper Respiratory Tract, Lower Respiratory Tract and Kidneys; Necrotizing GRANULOMATOUS inflammation
66
What marker is useful in Wegener's? What does it seem to be reacting against?
c-ANCA reacting against Neutrophil Proteinase-3
67
Describe how endothelial damage seems to occur in Wegener's:
By having c-ANCA target the neutrophils (Neutrophil Proteinase-3) it ACTIVATES the neutrophil which selectively targets endothelium
68
Regarding Wegener's: 1) What is the typical lung lesion? 2) What is the typical renal lesion?
1) Necrotizing granulomatous alveolitis 2) Necrotizing glomerulonephritis
69
How does Wegener's differ from Goodpasture's by location?
Goodpasture's does not affect the URT