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Pathology II > Exam 1 Part 2 > Flashcards

Exam 1 Part 2 Flashcards

1
Q

what is bronchiectasis?

A

dilation of bronchus; large airway disease

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2
Q

what processes/diseases are associated with bronchiectasis?

A
  • congenital (cystic fibrosis)
  • TB, other bac & viruses
  • RA, SLE, IBD
  • bronchial obstruction due to tumor, foreign bodies or mucus plugs
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3
Q

how does bronchiectasis present clincally?

A
  • cough
  • fever
  • expectoration of copious amounts of foul smelling, purulent sputum
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4
Q

what is cystic fibrosis?

A
  • disorder of ion transport epithelial cells (CTFR gene disorder) which leads to excessive mucus in the lung
  • on skin Na stays outside epi cells, in airways it stays in epi cells
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5
Q

what 6 groups are mutations of CF in?

A
  • defective syn
  • abnormal folding
  • defective regulation
  • defective conductance
  • reduced abundance
  • altered regulation of separate ion channels
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6
Q

what is the main pathology associated with CF?

A

85-90% pancreatic insufficiency

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7
Q

what can the thick mucus and repeated infxns in CF lead to?

A

chronic bronchitis and bronchiectasis

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8
Q

what are the two diseases which lead to morbidity and mortality in CF pts?

A

cor pulmonale and COPD

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9
Q

what is fibrosing?

A
  • fibrosing of lungs following inflammation but absence of infectious organisms
  • perhaps autoimmune
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10
Q

how does a restrictive lung ‘feel’?

A

-if squeezed it it wouldn’t feel as spongy as a normal lung

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11
Q

what will an obstructive lung disease look like on an XR?

A

diffuse increased density and increased opacity

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12
Q

what is idiopathic pulmonary fibrosis?

A

chronic idiopathic inflammation of alveolar walls w/progressive fibrosis

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13
Q

pathophys of IPF?

A
  • alveolar MOs malfxn
  • lung epi cells produce abnormal amount of PDGF
  • alveolar glutathione reduced
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14
Q

how does IPF present clinically? on XR what is distinctive? tx?

A
  • progressive DOE
  • non-productive cough
  • crackles
  • cor pulmonale, clubbing of nails
  • XR: ‘honey-comb’ like appearance
  • tx: high dose steroids, cytotoxic drugs, supplemental O2, most die 4-6 yrs after dx
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15
Q

what is COP?

A

cryptogenic organizing pneumonia

  • idiopathic
  • bronhiolitis obliterans
  • often occurs in transplanted lung
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16
Q

what are the 3 collagen vascular dz?

A
  1. scleroderma
  2. RA
  3. SLE
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17
Q

what are the categories of pneumoconioses? obstructive or restrictive?

A
  • occupational
  • coal miners lung
  • dust or chemicals or organic material: coal, silica, asbestos, Be, FeO, hay, flax, bagasse, insecticides, etc
  • restrictive lung disease leading to fibrosis
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18
Q

the development of pneumoconiosis depends on what 4 factors?

A
  1. amount of dust retained in airways and lung
  2. size and shape of particulate matter
  3. solubility of particulate matter
  4. additional effects of other irritants (tobacco)
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19
Q

what range of size of particles are the most dangerous?

A

5 micrometers b/c 5 can be coughed up

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20
Q

what is silicosis due to?

A
  • inhalation of silicon dioxide crystals from sand blasters, foundry workers, stone cutters etc
  • IT IS THE MOST COMMON CHRONIC OCCUPATIONAL DX IN THE WORLD
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21
Q

where are fibrotic nodules from silicosis located in the lungs?

A

-initially confined to upper lobes

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22
Q

what is the pathognomonic sign?

A

eggshell calcifications of hilar lymph nodes

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23
Q

how fast does silicosis progress?

A
  • generally very slowly, yrs to decades
  • accelerated silicosis: 5-15 yrs
  • acute silicosis: weeks
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24
Q

how do pts with silicosis present?

A
  • sometimes asx or only complain of cough
  • SOB in late stages
  • may continue to worsen even w/o exposure
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25
Q

what is Caplan’s syndrome?

A

pneumoniosis coexisting with RA usually due to asbestosis, silicosis or coal worker’s pneumoconioses
-lg distinct pulmonary nodules often develop w/center that cracks open

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26
Q

where would one be exposed to asbestos?

A
  • insulation fabrication
  • mining
  • break lining fabrication
  • asbestos removal workers
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27
Q

what do asbestos crystals do to the lungs?

A

transverse the lung, enter the interstitium and impale the pleural lining

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28
Q

what are ferruginous bodies?

A

asbestos fibers coated by proteins w/in lungs

29
Q

what kind of parenchymal disease is asbestosis?

A

-diffuse

30
Q

signs usually appear where first?

A

-pleural and sub-pleural fibrosis usually precede any signs of pulmonary fibrosis

31
Q

what are pleural plaques?

A
  • large dense plaques that form on both sides of pleural surface
  • appear first at base then surround lung
  • seen on CXR
32
Q

what greater risks in relation to cancer do asbestos workers have? smokers?

A
  • 5x greater risk of bronchogenic carcinoma in asbestos workers
  • mesothelioma, rare tumor of pleura almost always associated with asbestos exposure
  • smoking + asbestos exposure raises risk of developing bronchogenic cancer from 5-55x
  • smoking + asbestos doesn’t seem to raise risk for developing mesothelioma
33
Q

where does one get exposed to berylliosis?

A

-aerospace, nuclear & defense industries

34
Q

is coal worker’s pneumoconiosis a serious respiratory problem? what is the more mild form called and where is it found?

A
  • NO not unless additional pathology is present (TB, emphysema)
  • anthracosis: milder form of deposition often found in urban pops, tobacco users
35
Q

what is black lung disease? becoming more or less common?

A
  • CWP progressing to more severe diffuse pulmonary fibrosis

- becoming more common b/c of ppls lack of adherence to safety regulations

36
Q

what is siderosis?

A

-consequence of inhalation or iron oxide dust

37
Q

what are the 3 types of granulomatous dz?

A
  1. sarcoidosis
  2. non-caseating granulomas (idiopathic)
  3. hypersensitivity
38
Q

what is sarcoidosis?

A
  • multi-system granulomatous disorder of unknown etiology
  • lungs common to be affected, but can occur elsewhere
  • non-caseating
39
Q

who gets sarcoidosis?

A

20-40 yo african american women

40
Q

how does a pt w/sarcoidosis present clinically? what is the most common skin sx?

A
  • often asx
  • 1st sign may be dyspnea
  • often found incidentally on XCR
  • erythema nodosum is most common skin lesion
41
Q

what happens if sarcoidosis affects the liver or heart?

A
  • hepatic granulomas present in 70% of pts but usually no sxs
  • heart rarely affected but if affected about 50% will die of cardiac complications
42
Q

what labs might you find with a pt with sarcoidosis? what is a diagnostic thing you might find in a biopsy?

A
  • elevated vit D; alveolar MOs can synthesize calcitriol
  • hypercalcemia & elevated angiotensin converting enzyme
  • asteroid bodies!! truly diagnostic but hard to find
43
Q

what does organic pneumoconiosis develop in response to?

A
  • allergic rxn to inhaled organic dusts
  • type I (IgE), III (IgG) or IV (delayed)
  • abnormal sensitivity or heightened rxn to an antigen
  • usually more acute response than other pneumoconioses
44
Q

what is farm worker’s lung in response to? what is bagassosis?
what is byssinosis? what are the sxs?

A

-farm worker’s lung: actinomycetes spores (damp harvested hay)
-bagassosis: hypersensitivity rxn to mold found in sugar cane
-byssinosis: allergic response to airborne fibers of cotton, linen, flax & hemp
SXS: similar to bronchial asthma with coughing and wheezing, prolonged exposure= chronic bronchitis and emphysema

45
Q

what is DIP?

A
  • desquamative interstitial pneumonia
  • cigarette related
  • 100% survival
  • M»F
46
Q

what is PAP?

A
  • pulmonary alveolar proteinosis
  • very rare, usu acquired
  • exudate in alveoli
  • like PE but exudate
47
Q

what are the three types of ‘vascular’ lung diseases?

A
  • pulmonary embolism (usu w/o infarct)
  • pulmonary HTN, leading to cor pulmonale
  • hemorrhagic syndrome (good pasture, hemosiderosis, wegener granulomatosis)
48
Q

when do PEs develop? where do they come from? what is the triad it correlates to? do they infarct?

A
  • develop secondarily to debilitated states
  • usually from deep leg veins
  • virchow’s triad: 1. flow problems 2. endothelial disruption 3. hypercoagulability
  • usually don’t infarct, when do it is hemorrhagic
49
Q

is a PE a problem with diffusion or perfusion?

A

PERFUSION, ventilated but not perfused

50
Q

what are some causes of a thromboembolism? what lungs are move involved?

A
  • DVT from legs or pelvis
  • long standing IV line catheters
  • pro-thrombogenic blood diseases
  • lung cancer
  • lower lungs 4x more involved
51
Q

what are the two outcomes of a PE?

A

-in non-fatal PE’s embolus lyses within several days-weeks
OR
-cardiogenic shock: emboli occludes >50% of arterial supply, death in 1-2 hrs possibly; saddle embolus= death in minutes

52
Q

what are the factors that will lead to PE mortality? with pre-existing condition? without tx? with anticoagulant tx?

A
  • emboli size and location and pt’s pre-existing cardiopulmonary status
  • pre-existing cardiopulmonary status= 25% mortality
  • w/o tx= reoccurs 50% of the time, with 50% fatality
53
Q

what are two other types of emboli and what type of circulation do they block? Sxs?

A
  • fat emboli
  • amniotic emboli
  • block microciruclation–> may initiate Adult Respiratory Distress Syndrome (ARDS)
  • sxs: sudden onset of tachypnea, dyspnea, tachycardia
54
Q

what is a pulmonary infarction? what % of PE’s progress to a PI?

A
  • complete occlusion of blood supply

- PI

55
Q

what is the gross morphology of a PI?

A
  • hemorrhagic consolidation
  • necrosis of lung tissue
  • classic wedge or pie shape
  • tissue fibrosis
  • cough
  • hemoptysis
  • pleuritic chest pain
  • fever
  • friction rub
  • severe hypotension will occur in the case of cardiogenic shock
56
Q

are CXRs helpful in diagnosing a PE?

A

NO, they are the least helpful thing to do if assuming a PE

57
Q

what can cause pulmonary HTN?

A
  • COPD or CIPD
  • CHD
  • recurrent PE’s
  • autoimmune
58
Q

in primary PH it is arterial thickening and obliteration of what sized arteries? more or less common?

A
  • medium & small pulmonary arteries

- less common

59
Q

in secondary PH what walls are thickening? usually due to what?

A
  • wall thickening may be through entire arterial system
  • usu due to other cardiac or pulmonary conditions
  • recurrent thromboemboli can cause PH
60
Q

in primary and secondary PH what is damaged, what thickens, what is there dysfunction of and what is diminished?

A
  • damaged endothelial cells
  • thickening of smooth muscle cells
  • dysfunction of endothelial cells= less NO
  • diminished oxygenation
61
Q

PH leads to what in the heart?

A

persistent elevated P leads to right ventricular enlargement

62
Q

what is cor pulmonale?

A

right ventricular failure secondary to lung pathology

63
Q

what are risks of PH?

A
  • alveolar hypoxemia
  • ARDS
  • sleep apnea
  • pulmonary edema at high altitudes
  • emphysema
64
Q

is tx for PH usu very successful?

A

NO lung transplant usu necessary, death in 1-5 yrs usu

65
Q

what are the hemorrhagic syndromes?

A
  • goodpasture syndrome
  • idiopathic pulmonary hemosiderosis
  • wegener granulomatosis
66
Q

what is goodpasture syndrome?

tx?

A
  • multi-system disease involving lungs & kidneys
  • Abs to alveolar & glomerular basement membrane–> hemoptysis & hematuria
  • tx= steroids, plasma phoresis but may be resistant & lead to death in days to weeks
67
Q

what is wegener granulomatosis?

A
  • vasculitis that affects lungs, kidneys & other organs

- end-organ damage= serious disease that can require immunosuppression

68
Q

what does IPH have that CHF does not have?

A
  • IPH: hemosiderin in alveoli

- CHF: no hemosiderin

Pathology II (6 decks)

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