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RESPIRATORY EXAM 2 > CUMULATIVE PATHOLOGY > Flashcards

CUMULATIVE PATHOLOGY Flashcards

1
Q

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

A

Hemodynamic pulmonary edema

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1
Q

Why would a person with emphysema get heart failure?

A

Because the lung disease can cause pulmonary hypertension = cor pulmonale

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1
Q

What is the cause of the type of emphysema that mostly affects the lower parts of the lungs?

A

This is Panacinar emphysema and is caused by homozygous A1AT deficiency

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2
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

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3
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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3
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.

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4
Q

When is pulmonary hypoplasia fatal?

A

If the disease is bilateral

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5
Q

What is the major complication of a bronchogenic cyst? Another name for these?

A

Infection; Foregut cyst

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6
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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7
Q

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

A

Scleroderma

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7
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

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7
Q

What are the late microscopic findings in chronic bronchitis (3)?

A

Goblet cell hyperplasia, increased Reid index, and squamous metaplasia

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8
Q

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

A

Goodpasture’s does not affect the URT

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9
Q

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

A

Fibrinous pleuritis; SPIRAL CT

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9
Q

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

A

c-ANCA reacting against Neutrophil Proteinase-3

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10
Q

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

A

Hypersensitivity angiitis, Wegener Granulomatosis, and SLE

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11
Q

What antibody isotype is present in lung disease caused by Aspergillus fumigatus? Name of disease?

A

IgE, Allergic Bronchopulmonary Aspergillosis

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11
Q

What kind of emphysema is caused by Coal Worker Pneumoconiosis? Why is this a weird form of emphysema?

A

Centriacinar emphysema, it is weird bc black lung also has fibrosis, which is atypical for emphysema

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12
Q

What is the clincial triad of Goodpasture Syndrome?

A

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

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13
Q

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

A

Oligohydramnios or decreased intrathoracic space

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13
Q

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

A

Primary Biliary Sclerosis

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13
Q

Which obstructive disease is most likely to result in lung cancer, why?

A

Chronic bronchitis because in late stages it can lead to squamous metaplasia to deal with the chronic inflammation, this predisposes to CA

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14
Q

What are the 4 general obstructive diseases of lungs? Which are COPD?

A

Chronic Bronchitis, Emphysema, Asthma, and Bronchiectasis. COPD = Chronic Bronchitis and Emphysema

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15
Q

Where do laryngeal cartilages come from? Airway cartilages?

A

Laryngeal cartilage is from neural crest (ectoderm) and airway cartilage is from splanchnic mesoderm

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16
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

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17
Q

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

A

Linear deposits on basement membranes of glomerulus and alveoli

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18
Q

What are the genetics of Kartagener Syndrome?

A

Autosomal Recessive

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20
Q

What is seen in long standing pulmonary edema?

A

Fibrosis of the alveoli

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21
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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21
Q

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

A

Acute cor pulmonale

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22
Q

Differentiate the implication of smoking in chronic bronchitis from centroacinar emphysema:

A

In centroacinar emphysema the issue is that the smoke is inhibiting antitrypsin and allowing elastase to destroy alveoli, in CB the smoke is killing off the cilia and producing inflammation.

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23
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.

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25
Q

What are the early microscopic findings in chronic bronchitis (2)?

A

Mucus in the airway, hypertrophy of submucosal glands

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26
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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27
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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28
Q

Fibrotic changes of lung and/or pleura are the major cause of this type of atelectasis

A

Restrictive Atelectasis

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29
Q

What is the deadly, unrefractory form of asthma?

A

Status asthmaticus

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29
Q

What exactly is a Charcot-Leyden crystal?

A

It is a crystal formed from EOSINOPHIL MEMBRANE PROTEIN, indicating eosinophils are present

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31
Q

What kind of edema is caused by near drowning?

A

Microvascular injury pulmonary edema

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31
Q

What are 3 REVERSIBLE microscopic signs of PHTN?

A

Medial hypertrophy, intimal thickening, and intimal hyperplasia

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32
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

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32
Q

What are the CXR findings in pulmonary embolus?

A

NORMAL, usually–that’s why you do spiral CT

32
Q

What lung pathology can Fen-Phen cause? Cardiac?

A

Pulmonary HTN; Phen-Fen valvulitis

32
Q

What kind of emphysema is caused by A1AT deficiency? Affects what aspect of lungs?

A

Panacinar emphysema, affects lower lobes

32
Q

Where is the cricothyroid muscle from? What innervates it?

A

Pharyngeal arch 4, superior laryngeal nerve

33
Q

What is the hallmark of ARDS?

A

Hyaline membranes at the blood-air barrier

34
Q

What may cause non-bilious vomiting with an air bubble in the stomach?

A

Tracheoesophageal fistula

36
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

36
Q

When does alveolar fibrosis occur in pulmonary edema?

A

if the edema is long-standing, as in mitral stenosis

37
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

39
Q

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

A

RVH, medial hypertrophy, and pulmonary atheromas

41
Q

What are two treatment methods for PE?

A

Thrombolysis or anticoagulation

43
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

45
Q

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

A

Pseudostratified columnar epithelium; detached part of embryonic foregut

46
Q

This presents as a nodule with a pleural lining and served by the aorta

A

Extralobar sequestration

48
Q

What does amniotic fluid look like histologically? Why?

A

Like a thumbprint because of the layers of fetal squames

48
Q

What happened to a lung that weighs less than it should and has less alveoli than projected for gestational age?

A

Hypoplasia from oligohydramnios or decreased intrathoracic space

50
Q

What is the major cause of hemodynamic pulmonary edema?

A

Increased hydrostatic pressure, as in left heart failure

52
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

53
Q

What are 4 methods of prophylaxis for PE?

A

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

54
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

55
Q

Explain why chronic bronchitis and bronchiectasis lead to recurrent pneumonia:

A

Chronic bronchitis involves loss of cilia and bronchiectasis involves widening of bronchi so the cilia are not as effective at moving stuff up.

56
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

57
Q

What are 3 IRREVERISBLE microscopic signs of PHTN?

A

Concentric laminar intimal fibrosis, fibrinoid necrosis, and plexiform lesions

58
Q

A middle aged man presents with sinusitis, hemoptysis and hematuria. What test should you order?

A

c-ANCA, this is a classic presentation of Wegener’s Granulomatosis

59
Q

Essentially, how do you define chronic bronchitis?

A

Persistent cough with copious sputum for greater than 3 months over a period of 2 years

60
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

61
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

62
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

63
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

64
Q

What are the 2 general causes of bronchiectasis? End result?

A

Congenital malformation of bronchial tree, or post-infection? Either way it is a PERMANENT DILATION of the bronchus

65
Q

Which type of asthma has normal serum IgE, most common cause?

A

Non-Atopic asthma from infection, usually

67
Q

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

A

Primary Pulmonary HTN

68
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

69
Q

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

A

Immunosuppressives

70
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

72
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

73
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.

74
Q

Who are the blue bloaters? Who are the pink puffers?

A

Blue bloaters = chronic bronchitis and pink puffers = emphysema

75
Q

What differentiates asthma from COPD, in general?

A

Reversible bronchospasm

76
Q

Who gets Curshmann spirals and Charcot-Leyden crystals? What would a Charcot-Leyden crystal in a stool sample indicate?

A

Asthmatics; it would indicate a parasitic GI infection

78
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)

80
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.

82
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

83
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

84
Q

Which types of emphysema both predominately affect the upper lungs?

A

Centricacinar/Centrilobular caused by smoking and Distal Acinar/Paraseptal–bullous emphysema

85
Q

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

A

They are commonly elevated in systemic vasculitides

86
Q

What pressures define PHTN when at rest and exercise?

A

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

87
Q

Which obstructive disease is most likely caused by insipissated mucus? What is the cause for this mucus?

A

Bronchiectasis from cystic fibrosis

89
Q

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

A

A septic infarct from a septic embolus

91
Q

What is the diagnostic test for deep vein thrombosis?

A

Duplex ultrasonography

92
Q

What is the hallmark of acute interstitial pneumonia? AKA?

A

Diffuse damage with ridiculously thickened alveolar walls–lots of macro’s but few neutro’s b/c not infected? HAMMAN-RICH SYNDROME

93
Q

What is the clinical presentation of of Idiopathic Pulmonary Hemosiderosis?

A

Intermittent hemoptysis and refractory anemia

94
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

95
Q

Laryngeal muscles innervated by the recurrent laryngeal nerve are from which pharyngeal arch?

A

6

96
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

97
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

98
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)

99
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.

100
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

101
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

102
Q

What is the most common cause of resorption atelectasis?

A

Excess Secretion

103
Q

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

A

Microvascular injury pulmonary edema

104
Q

What happens to 1) Nearby lung tissue 2) Diaphragm and 3) Chest wall in a resorption atelectasis?

A

The nearby tissue distends, the diaphragm elevates, and the chest wall flattens

RESPIRATORY EXAM 2 (8 decks)

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