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RESPIRATORY EXAM 1 > PATHOLOGY > Flashcards

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
Q

When are small emboli in the lungs problematic?

A

Usually only if there is inadequate bronchial circulation or if there are a ton of them

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26
Q

What two systems are compromised in PE? Explain.

A

Respiratory compromise because the alveoli cannot exchange gas with an occluded vessel; Hemodynamic compromise from the increased resistance from the embolus.

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27
Q

Why is pulmonary infarction from a PE rare in young people? What wil you see in them?

A

Because they usually have adequate bronchial circulation. Infarction really only happens if inadequate circulation, BUT they will have hemorrhage.

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28
Q

Explain why a person with a saddle embolus has electromechanical dissociation (i.e. PEA)?

A

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
Q

What histopathologic type of pleuritis may result from PE? What is the diagnostic test of choice for PE?

A

Fibrinous pleuritis; SPIRAL CT

30
Q

What is the diagnostic test for deep vein thrombosis?

A

Duplex ultrasonography

31
Q

What are 4 methods of prophylaxis for PE?

A

Early ambulation post-op, IVC filter, compression stockings, and anticoagulation

32
Q

What are two treatment methods for PE?

A

Thrombolysis or anticoagulation

33
Q

Where do most PE’s occur anatomically? How do you distinguish a PE from a post-mortem clot?

A

In the lower lobes of lungs; LINES OF ZAHN–indicates that there was organization of the clot over time

34
Q

A pulmonary infarct with an intense neutrophilic reaction is most likely what?

A

A septic infarct from a septic embolus

35
Q

What are you most concerned with as a follow up to organization and dissolution of a PE?

A

The development of PHTN–> this is because scarring is a part of the organization process which increases resistance.

36
Q

What kind of congestion is seen in areas of pulmonary infarction?

A

PASSSIVE CONGESTION? Pulmonary infarct is seen as ischemic necrosis on background of passive congestion.

37
Q

What is the most likely etiology of a PE that looks like it has white holes in it histologically?

A

Fracture of a long bone–this is a fat embolus

38
Q

What does amniotic fluid look like histologically? Why?

A

Like a thumbprint because of the layers of fetal squames

39
Q

What is the most likely method of death in a patient with a sudden and large PE?

A

Acute cor pulmonale

40
Q

Why doesn?t PE cause atelectasis?

A

Because there is no obstruction of the airway

41
Q

What pressures define PHTN when at rest and exercise?

A

Greater than 25 mmHg at rest and greater than 30 with exercise

42
Q

What term best describes PHTN w/o underlying parenchymal disease of the lung?

A

Primary Pulmonary HTN

43
Q

How could endothelin dysfunction cause primary PHTN?

A

Because if prostacyclin/N2O are underproduced and endothelin is overproduced there is both vasoconstriction and vascular remodeling

44
Q

How could dysnfuctional potassium channels underlie primary PHTN?

A

By possibly affecting the resting membrane potential of the vessel leading to high intracellular [Ca] causing vasoconstriction

45
Q

What is the hallmark clinical sign of PHTN?

A

A progressive dyspnea that began with exertion and now occurs at rest–but can see that is not all that differenc from CHF

46
Q

What are 3 signs of PHTN seen on CXR? What is the utility of lung biopsy for the Dx?

A

1) increased cardiothoracic ratio 2) enlarged pulmonary arteries 3) right ventricular hypertrophy; lung biopsy is not helpful for Dx of PHTN

47
Q

What are 3 REVERSIBLE microscopic signs of PHTN?

A

Medial hypertrophy, intimal thickening, and intimal hyperplasia

48
Q

What are 3 IRREVERISBLE microscopic signs of PHTN?

A

Concentric laminar intimal fibrosis, fibrinoid necrosis, and plexiform lesions

49
Q

What are 3 things that nearly all etiologies of PHTN result in?

A

RVH, medial hypertrophy, and pulmonary atheromas

50
Q

What are plexiform lesions? What do they indicate about the severity of the disease? What vessels do they affect?

A

They are TUFTS of capillaries growing off of a parent artery; the indicate HIGH SEVERITY; they affect small vessels

51
Q

What heart defects are associated with pulmonary HTN, why?

A

Anything that involves a L-> R shunt, most commonly an ASD since it causes volume overload in the right heart

52
Q

What are 3 vasculitis-associated hemorrhages in the pulmonary system?

A

Hypersensitivity angiitis, Wegener Granulomatosis, and SLE

53
Q

What is the clincial triad of Goodpasture Syndrome?

A

Diffuse pulmonary hemorrhage, glomerulonephritis, and circulating anti-GBM antibodies

54
Q

What isotype is the antibody in Goodpasture’s? What is it actually against?

A

IgG; Type IV collagen of the basement membrane of glomeruli and lungs

55
Q

What is the main cause of death in Goodpasture’s? What is the Tx?

A

Uremia from Kidney failure; can Tx with plasma exchange and immunosuppressive Tx

56
Q

What is the morphology of the deposition of immunoglobulins in Goodpastures?

A

Linear deposits on basement membranes of glomerulus and alveoli

57
Q

What are c-ANCA and p-ANCA good for diagnostically?

A

They are commonly elevated in systemic vasculitides

58
Q

What is Anti-DNA topoisomerase I antibody useful for, diagnostically?

A

Scleroderma

59
Q

What is Anti-mitochondrial-antibody (AMA) useful for?

A

Primary Biliary Sclerosis

60
Q

How is Idiopathic Pulmonary Hemodiderosis different than Goodpasture’s?

A

There are no antibodies in the serum (it is idiopathic) AND there is no renal involvement

61
Q

What is the clinical presentation of of Idiopathic Pulmonary Hemosiderosis?

A

Intermittent hemoptysis and refractory anemia

62
Q

How is the cause of death different in Idiopathic Pulmonary Hemosiderosis than in Goodpasture’s?

A

IPH will be a pulmonary-related death whereas Goodpasture’s is usually uremia–a renal issue

63
Q

Describe the extent of necrosis and granuloma formation in Idiopathic Pulmonary Hemosiderosis:

A

There is no necrosis/granuloma formation, just capillary congestion with hemorrhage

64
Q

Though the etiology of of Idiopathic pulmonary hemosiderosis is unknown there is a favorable response to what Tx?

A

Immunosuppressives

65
Q

What 3 regions are affected by Wegener’s Granulomatosis? What term best describes the inflammation?

A

Upper Respiratory Tract, Lower Respiratory Tract and Kidneys; Necrotizing GRANULOMATOUS inflammation

66
Q

What marker is useful in Wegener’s? What does it seem to be reacting against?

A

c-ANCA reacting against Neutrophil Proteinase-3

67
Q

Describe how endothelial damage seems to occur in Wegener’s:

A

By having c-ANCA target the neutrophils (Neutrophil Proteinase-3) it ACTIVATES the neutrophil which selectively targets endothelium

68
Q

Regarding Wegener’s: 1) What is the typical lung lesion? 2) What is the typical renal lesion?

A

1) Necrotizing granulomatous alveolitis 2) Necrotizing glomerulonephritis

69
Q

How does Wegener’s differ from Goodpasture’s by location?

A

Goodpasture’s does not affect the URT

RESPIRATORY EXAM 1 (8 decks)

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