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Pathology > Pulmonary: Restrictive + Vascular + HTN + Miscellaneous > Flashcards

Pulmonary: Restrictive + Vascular + HTN + Miscellaneous Flashcards

1
Q

Restrictive lung disease are due to what?

A

Reduced lung compliance (Hard to fill lungs)

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2
Q

Restrictive
FVC?
FEV1?
FEV1/FVC

A

FVC: reduced
FEV1: Reduced
FEV1/FVC: Normal

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3
Q

Acute restrictive is defined by what symptoms (4)

A
  1. Acute dyspena
  2. Hypoxia
  3. Bilateral pulmonary infiltrates
  4. Absence of left heart failure
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4
Q

How are ALI and ARDS related?

A

ALI is like early stage ARDS

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5
Q

What are ALI/ARDS the most comon cause of?

A

Non-cardiogenic pulmonary edema

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6
Q

ALI/ARDS is due to what (2)

A
  1. Direct injury to lungs

2. Indirect injury due to systemic disease

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7
Q

Injury to lungs for ALI/ARDS is due to what? (3)

A
  1. Infections
  2. Toxins (Sepsis)
  3. Trauma
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8
Q

ALI/ARDS path?

A
  1. Endothelial injury
  2. Alveolar edema
  3. Type II pneumocytes injured
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9
Q

Cause of ALI/ARDS damage?

A

Imbalance of pro-inflammatory and anti-inflammatory cytokines

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10
Q

3 major morphologic changes in ARDS/ALI?

A
  1. Hyaline membrane formation2
  2. Hepatization of lungs
  3. Vascular congestion
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11
Q

End stage of ARDS/ALI?

A

Fibrosis and honey-combing

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12
Q

What do pathologists call ARDS/ALI?

A

DAD = Diffuse alveolar destruction

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13
Q

When do ARDS/ALI symptoms appear?

A

Within 72 hours of insult

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14
Q

What % die in ARDS/ALI?

A

30-40% (pretty high)

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15
Q

How well do ARDS/ALI survivors recover?

A

Complete regain of function within a year

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16
Q

Chronic restrictive lung disease end-stage? (2)

A
  1. Diffuse interstitial fibrosis

2. with or without Honeycombing

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17
Q

What data is important for chronic restrictive diagnosis? (2)

A
  1. Social

2. Occupational

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18
Q

Causes of chronic restrictive lung diseases? 7

A
  1. Asbestos
  2. Silicosis
  3. Coal
  4. Drugs
  5. Radiation
  6. High O2
  7. Immunologic
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19
Q

Definition of idiopathic pulmonary fibrosis?

A

Progressive interstitial fibrosis

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20
Q

IPF/UIP sex?
Age?
How is this diagnosed

A

Males
Elderly
Diagnosis of exclusion

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21
Q

How is the process of IPF/UIP in terms of morphology and age of fibrosis?

A

Heterogeneous

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22
Q

Main symptom of IPF/UIP?

A

Slow, continuous dyspnea

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23
Q

Sarcoidosis present how? 5

A

Lung problem in 90%
Noncaseating granulomas
Bilateral hilar and paratracheal lymphadenopathy (potato nodes)
Interstitial fibrosis

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24
Q

How do you diagnose sarcoidosis?

A

Diagnosis of exclusion of any other granuloma formers (Myco, Fungi)

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25
Q

Common complications of sarcoidosis besides lung? 2

A

Eye

Skin

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26
Q

Popuation of Sarcoidosis
Age
Ethnicies
Smoking

A

Younger than 40

Danes, Swedes, US Blacks &raquo_space;» Whites and Asians

Nonsmokers more common

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27
Q

The presumed cause of sarcoidosis?

A

Abnormal immune regulation in genetically predisposed people that are exposed to some enviromental stimuli

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28
Q

Genetic factors of sarcoidosis (2)

A
  1. Familial and racial clustering

2. Putative antigens like viruses, myco, pollen

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29
Q

Constitutional signs

A

Fever
Fatigue
Myalgias

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30
Q

What if sarcoidosis has uveoparotid involvement

A

Mikulicz syndrome

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31
Q

What test is elevated in granulomatous disorders and hence sarcoidosis? 2

A 
ACE elevated (granulomas)
Increased urine calcium (granulomas)
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32
Q

Hypersensitivity pneumonitis is defined how?

A

Immune mediated inflammatory disease of distal lung and alveoli due to sensitivity to inhaled antigens like mold, dust, chemicals

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33
Q

How does hypersensitivity pneumonitis affect the lung? (3)

A
  1. Decreased diffusion capacity
  2. Decreased lung compliance
  3. Decreased lung total volume
34
Q

acute form hypersensitivity pneumonitis presents how?

A

Fever, cough, dyspena 4 to 8 hours after exposure

Go on vacation, goes away, gets back to work

35
Q

Chronic form of hypersensitivity pneumonitis presents how?

A

Insidiously and not easy to diagnosis

36
Q

Evidence that suggests hypersensitivity pneumonitis is immune mediated?

A

BAL fluids with increased pro-inflammatory chemokines

  1. Increased CD4/CD8 ratio
  2. Serum Ab’s suggesting Type III
  3. Noncaseating granulomas suggesting Type IV
37
Q

Diffuse alveolar hemorrhage syndromes present how (3)

A
  1. Hemoptysis
  2. Anemia
  3. Diffuse pulmonary infiltrates
38
Q

Diffuse alveolar hemorrhage syndrome members

A

Goodpasture and Idiopathic Pulmonary Hemosiderosis

39
Q

Goodpastures syndrome definition (2)

A

Hemorrhagic interstitial pneumonitis and crescentis glomerulonephritis

40
Q

Goodpastures syndrome has what Ab’s?

A

IgG against BM and glomerulis suggesting Type II hypersenstivity

41
Q

Lungs in Goodpastures syndrome show what?

A

Focal necrosis of alveolar walls
Hemorrhage in alveoli
Hemosiderin laden macrophages

42
Q

Goodpastures syndrome treatment (2)

A
  1. Plasmapharesis

2. Immunosuppression

43
Q 
Idiopathic pulmonary hemosiderosis is similar to what?
Except for (2)
A

Presents the exact same as Goodpastures

  1. No Anti-Basement membrane Ab’s
  2. No renal disease
44
Q

Wegener Granulomatosis definition

A

Vasculitis

45
Q

Triad of wegener granulomatosis?

A
  1. URT crusting
  2. Lower respiratory disease
  3. Renal disease
46
Q

What is the mediator of Wegener granulomatosis?

A

Auto Ab’s against Type IV collagen in renal glomeruli and lung alveoli

47
Q

Two necrotizing features of Wegener granulomatosis?

A
  1. Necrotizing capillaritis

2. Necrotizing granulomas

48
Q

Radiographic changes in Wegener’s

A

Granulomas that cavitate and coalesce

49
Q

What is Wegener granulomatosis

50
Q

Collagen vascular disease can cause pulmonary disease, which members?

A

SLE
RA
Scleroderma
Dermatomyositis

51
Q

What do collagen vascular diseases most often cause?

A

Interstitial pneumonitis

52
Q

What is the worst ending for collagen vascular disease?

A

Progressive pulmonary fibrosis leading to end-stage honeycomb lung

53
Q

Accelerated pulmonary fibrosis in RA patients?

Exposure to what? (3)

A

Caplan syndrome

Coal, silica, asbestos

54
Q

Transplantation pulmonary

Acute rejection involves (3)

A

Fevers, Leukocytosis, Mimicking infections

55
Q

Pulmonary embolism that occludes pulmonary arteries at bifurcation?
Result?

A

Saddle embolus

Sudden death

56
Q

Most pulmonary emboli are what form?

57
Q

Studies for pulmonary emboli? (3)

A
  1. Doppler studies
  2. Radiography
  3. D-Dimer test (positive)
58
Q

Predisposing conditions for PE’s 7

A
  1. Prolonged bed rest
  2. Surgery to legs or knees
  3. Bone fractures in the leg
  4. CHF
  5. Pregnancy and oral birth control
  6. Inherited disease
  7. Mucinous adenocarcinomas
59
Q

What tests can you do in acute PE situations 2

A
  1. DNA analysis

2. Factor V test

60
Q

Why don’t we see infarctions often in PE?

Where will you normally see a PE infarct?

A

Dual blood supply

Distal, wedge-shaped, and involves the pleural

61
Q

How is the pain of a PE infarct described?

What will you hear?

A

Positional

Friction rub

62
Q

Most PE’s have what effect?

A

None, asymptomatic

63
Q

How does HTN occur with PE’s

A

Enough small PE’s block off enough arteries to raise resistance

64
Q

Patients with one PE have what risk for a second?

65
Q

Most often Pulmonary HTN is secondary to what two things?

A
  1. Decreased pulmonary vascular cross-sectional area

2. Increased pulmonary vascular blood flow

66
Q

Pulmonary HTN situations (3)

A
  1. COPD/Interstitial lung disease
  2. Recurrent PE’s
  3. Heart disease with left to right shunt
67
Q

Types of secondary pulmonary hypertension? (3)

A
  1. Plexiform pulmonary arteriopathy (most) convoluted tortuous path
  2. Thrombotic pulmonary arteriopathy
  3. Pulmonary venoocclusive disease
68
Q

If you see atheromas in pulmonary vessels you have to think what?

A

Pulmonary hypertension

69
Q

Morphology of PHTN? 2

A
  1. Atheromas

2. Intimal and medial thickening

70
Q

Patients with P-HTN the most?

A

Young females

71
Q

Only hope for pulmonary HTN patients?

A

Lung transplant

72
Q

Cancer types in lungs

A
  1. Small cell
  2. Squamous cell
  3. Adenocarcinoma
73
Q

Which cancer type in central in lungs?

74
Q

Adeno cancers tend to be where?

Two populations

A

Peripheral

Females and smokers

75
Q

Which cancer cavitates the most?

A

Squamous cell

76
Q

most common cancer with perineoplastic syndrome?

A

Small cell

77
Q

Hypercalcemia with lung cancer?

A

Squamous cell

78
Q

Asbestosis is what?

A

Fibrosis you get from asbestos exposure

79
Q

What is most common thing we see with asbestos?

A

Pleural plaques THEN fibrosis

80
Q

Most common malignancy with asbestosis?

A

Bronchogenic carcinoma

81
Q

Which cancer is most associated with asbestsos?

A

Mesothelioma

82
Q

Silicosis appears how? (3)

A

Concentric fibrosis with nodules
Refractory material
TB infection

Pathology (36 decks)

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