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Pulm > Path > Flashcards

Path Flashcards

1
Q

atelectasis

A

collapse of previously inflated lung resulting in relatively airless pulmonary parenchyma

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2
Q

ARDS/DAD

A

HYALINE MEMBRANE

EDEMA

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3
Q

emphysema

A

loss of elastic recoil of lung: abnormal PERMANENT enlargement of airspaces by destruction of their walls

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4
Q

centriacinar emphysema

A

HEAVY SMOKING

UPPER lobes

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5
Q

panacinar emphysema

A

alpha1-antitrypsin deficiency

LOWER lobes

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6
Q

paraseptal emphysema

A

underlies SPONTANEOUS PNEUMOTHORAX

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7
Q

chronic bronchitis

A

persistant cough with sputum at least 3 months in at least 2 consecutive years
increased REID index
large airway: submucosal gland hypertrophy
small airway: increase goblet cells
peribronchial fibrosis

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8
Q

asthma

A

chronic inflammatory disorder of airways: increased responsiveness to stimuli
inflammation damages and perpetuates bronchoconstriction
overinflation, mucous plugs
EOSINOPHILS
CURSCHMANN SPIRAL
CARCOT LYDEN crystals

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9
Q

bronchiectasis

A

permanent airway dilation with smooth muscle and elastic tissue destruction
repeated airway obstruction and inflammation lead to fibrosis

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10
Q

obstructive lung disease

A

lung does not empty

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11
Q

list of obstructive lung diseases (4)

A

emphysema
chronic bronchitis
asthma
bronchiectasis

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12
Q

Two functions of type II pneumocyte

A

surfactant

repair

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13
Q

resorption atelectasis

A

airway obstruction by mucous plugs, tumor
resorption of trapped O2 in dependent alveoli
mediastinum shifts TOWARD affected lung

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14
Q

compression atelectasis

A

filling of pleural cavity by tumor, blood, air
compression of pulmonary tissue
mediastinum shifts AWAY from affected lung

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15
Q

contraction atelectasis

A

fibrotic lung or pleura
prevention of full expansion
NOT reversible

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16
Q

COPD

A

combination of emphysema and chronic bronchitis

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17
Q

alpha1- antitrypsin deficiency

A

PANACINAR emphysema

LIVER CIRRHOSIS: PAS positive hyaline globules (misfolded protein accumulates in ER of hepatocytes)

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18
Q

alpha 1 antitrypsin

A

neutralize proteases (elastase) released by inflammatory cells

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19
Q

PiZZ

A

A1AT deficiency homozygote at risk for panacean emphysema and liver cirrhosis

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20
Q

PiMZ

A

A1AT deficiency heterozygote: low levels of A1AT; ok unless smoke

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21
Q

bullae

A

markedly enlarged subpleural airspaces

prone to rupture: results in pneumothorax

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22
Q

What is the role of smoking in chronic bronchitis?

A

chronic irritation from inhalation results in mucous hyper secretion

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23
Q

Reid index

A

ratio of thickness of the mucous gland layer to the thickness of the wall between the epithelial basement membrane and cartilage
normal: 0.4
increased in: chronic bronchitis

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24
Q

extrinsic asthma

A

type I hypersensitivity reaction to inhaled allergen
IgE
MAST cells

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25
Q

intrinsic asthma

A

non-immunologic reaction: precipitated by respiratory infection, stress, exercise, cold, drugs, etc.

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26
Q

histological aspects of asthma

A
  1. thickened BM
  2. submucosal gland hypertrophy
  3. bronchial wall smooth muscle hypertrophy
  4. eosinophils
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27
Q

causes of bronchiectasis

A
  1. cystic fibrosis
  2. Kartagener
  3. necrotizing pneumonia
  4. bronchial obstruction
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28
Q

cystic fibrosis

A

chloride transport defect results in thick obstructive secretions

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29
Q

Kartagener

A

immotile cilia syndromes: interferes with bacterial clearance

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30
Q

tracheoesophageal (T-E) Fistula

A

failure of fetal respiratory tract to separate from GI tract

FOREGUT

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31
Q

alveolar stages

A
  1. glandular: thick walls, lots of CT, cuboidal
  2. saccular: transition to flat, type I and type 2 alveolar cells
  3. alveolar stage: reduction of interstitial tissue and increase capillaries
    NOT histologically mature until: age 8
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32
Q

rhinitis

A

inflammation of nasal mucosa

rhinovirus: common cold or allergic (type I)
repeated: NASAL POLYPS

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33
Q

nasal polyps

A

edematous, inflamed nasal mucosa

causes: repeated rhinitis, CF, aspirin intolerant asthma

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34
Q

aspirin intolerant asthma

A

asthma
aspirin induced bronchospasm
nasal polyps

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35
Q

angiofibroma

A

benign tumor of the nasal mucosa composed of large blood vessels and fibrous tissue
Sx: profuse epitaxis

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36
Q

chronic interstitial/restrictive lung disease

A

heterogenous group
dyspnea and reduced lung capacity
results in diffuse scarring

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37
Q

honeycomb on CT

A

END STAGE of restrictive diseases

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38
Q

idiopathic pulmonary fibrosis (IPF)

A

patchy INTERSTITIAL fibrosis, lower lobe sub pleural distribution
Masson bodies, collagenized areas, mild lymphocytic inflammation
Sx: dyspnea on exertion, dry cough
Tx: NONE
must rule out secondary cause
TGF-B from injured pneumocytes: fibrosis
usual interstitial pneumonia (UIP): histologically

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39
Q

pneumoconioses

A

non-neoplastic lung rxn to inhaled dusts (coal, silica, asbestos, berylliosis, etc.)

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40
Q

hypersensitivity pneumonitis

A

prolonged exposure to inhaled dusts
type IV sensitivity: T cells (NO eosinophils)
GRANULOMA
to prevent fibrosis: remove environmental irritant
ex: farmer’s lung, bird fancier’s lung, etc.
interstitial fibrosis

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41
Q

Masson body

A

fibroblast foci

believed to be sites of recent injury

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42
Q

collagen vascular disease-associated lung disease

A

RA, scleroderma, mixed connective tissue disease

UIP histologically

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43
Q

cryptogenic organizing pneumonia (COP)

A

INTRA-ALVEOLAR: CT in bronchioles, alveolar ducts, and alveoli (all SAME AGE)
Tx: steroids

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44
Q

simple coal workers pneumoconiosis (CWP)

A

UPPER lobe
little or no pulm. dysfunction
coal dust macules (dust accumulation adjacent to respiratory bronchioles with/out dilated adjacent alveoli (emphysema)) and nodules (carbon-laden macrophages with collagen)

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45
Q

complicated coal workers pneumoconiosis (CWP)/ progressive massive fibrosis

A

lung function compromised
develops in those with simple CWP
black scars composed of pigment and dense collagen
associated with: RA

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46
Q

anthracosis

A

CWP

carbonaceous pigment in macrophages that accumulates in CT along lymphatics and in lymph tissue

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47
Q

silicosis

A

SANDBLASTERS, MINE WORKERS, STONE cutters
progressive nodular fibrosis
UPPER lobes and hilar nodes
macrophages: ingest silica and release fibrogenic mediators
collagenous nodules, birefringent silica particles
increased susceptibility to TB

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48
Q

beryllium

A

SPACE industry, MINERS
non-caseating GRANULOMA: lung, hilar lymph nodes, organs
increased chance of lung CA

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49
Q

non-neoplastic asbestos-related diseases

A
  1. diffuse pleural fibrosis
  2. benign pleural effusions
  3. plerual plaques
  4. parenchymal interstitial fibrosis (Asbestosis)
    MORE COMMON than cancer
50
Q

parenchymal interstitial fibrosis (asbestosis)

A

Sx: slowly progressive dyspnea
heavy ASBESTOS exposure: 20 yr latency
initial injury: respiratory bronchioles and alveolar ducts: results in fibrosis of adjacent alveoli

51
Q

drug/radiation pneumonitis

A

chemo (busulfan) or radiation to chest

52
Q

sarcoidosis

A 
AA female south
non-caseating GRANULOMA (hilar lymph nodes, lung, skin)
Sx: dyspnea, cough, non specific
Tx: steroids
CD4:CD8 ratio greater than 2.5
disease of EXCLUSION
53
Q

desquamative interstitial pneumonia (DIP)

A

SMOKING
peribronchiolar
Tx: stop smoking, steroids

54
Q

respiratory bronchiolitis

A

SMOKING
peribronchiolar
Tx: stop smoking, steroids

55
Q

pulmonary langerhans cell histiocytosis

A 
YOUNG SMOKERS
rare
Tx: quit
BRAF mutation 
leads to alveolar damage and airway destruction
Langerin, S-100, CD1a
NO CD68
56
Q

pulmonary alveolar proteinosis

A

rare
defect in GM-CSF or macrophages: accumulation of surfactant
can be autoimmune, secondary (malignancy or immunodeficiency), or hereditary (infants)

57
Q

pneumocystis jirovecii

A

yeast fungus

IMMUNOCOMPROMISED: HIV

58
Q

pulmonary embolism

A

most from deep leg vein thrombi
immobilization, hypercoaguable states
adequate CV function: bronchial arterial supply sufficient to sustain distal lung tissue
inadequate pulmonary circulation (cardiac or pulmonary disease): infarction (10%)

59
Q

secondary pulmonary hypertension causes

A

cardiopulmonary conditions that increase pulmonary blood flow/pressure/vascular resistance or left heart resistance to flow

  1. chronic obstructive or interstitial lung disease
  2. cardiac disease
  3. recurrent thromboemboli
60
Q

primary pulmonary hypertension

A

female, 20s-40s
Sx: dyspnea, fatigue
inactivating BMPR2 mutation: proliferation of vascular sm. muscle

61
Q

How does chronic obstructive or interstitial lung disease lead to pulmonary HTN?

A

hypoxia and fewer alveolar capillaries from parenchymal destruction leads to increase pulmonary arterial resistance and pressure

62
Q

How does cardiac disease lead to pulmonary HTN?

A

mitral stenosis causes elevated left atrial pressure that increases pulmonary venous and arterial pressure

63
Q

How do recurrent pulmonary thromboemboli lead to pulmonary HTN?

A

decrease in functional area of pulmonary vascular bed leads to increased vascular resistance

64
Q

good pasture

A

male, teens, smokers
autoimmune disorder with Ab to alpha-3 chain of collagen IV
destruction of BM in kidney glomeruli and lung alveoli
Sx: pulmonary hemorrhage

65
Q

idiopathic pulmonary hemosiderosis

A

pulmonary hemorrhage disease

66
Q

lupus erythematosus

A

vasculitis with pulmonary hemorrhage

67
Q

wegener granulomatosis (polyangiitis with granulomatosis)

A

med. to small vessel vasculitis

Sx: necrotizing granulomas of respiratory tract, glomerulonephritis, pulmonary hemorrhage

68
Q

hemodynamic pulmonary edema causes

A
  1. increased hydrostatic pressure: left heart failure

2. decreased oncotic pressure: liver disease

69
Q

causes of pulmonary edema due to microvascular injury

A
  1. infection
  2. inhaled smoke and other gases
  3. shock
70
Q

acute lung injury/ ARDS (acute respiratory distress syndrome)

A

rapid onset of severe life-threatening respiratory insufficiency and hypoxia
caused by diffuse alveolar capillary damage
DECREASE COMPLIANCE
HIGH GRADE INFLAMMATION
high MORTALITY
HYALINE MEMBRANES, WHITE OUT CXR, non cardiogenic EDEMA
Sx: hypoxemia, cyanosis
Tx: underlying cause, PEEP, PRONE ventilation, diuresis as needed, NO (improves oxygenation, does NOT improve mortality)
SHUNT: does not respond to O2
complication: interstitial fibrosis (reduced DLCO), pneumothorax
death is due to: MULTI ORGAN FAILURE

71
Q

diffuse alveolar damage (DAD)

A

histological manifestation of ARDS and neonatal RDS

72
Q

neonatal RDS

A

preterm infants with deficient surfactant (28 weeks production, 34 weeks sufficient surfactant)
L:S ratio greater than 2: have enough surfactant
cause: premature, C-section, DM in mom
Sx: hypoxemia, cyanosis, tachypnea, increased respiratory effort, GROUND GLASS CXR
complications: patent ductus arteriosus, necrotizing enterocolitis
complications of supplemental O2: blindness, bronchopulmonary dysplasia

73
Q

Direct lung injury causes of ARDS

A

DIRECT injury:

  1. infection (pneumonia/ aspiration)
  2. injury: trauma, near drowning, burns
  3. inhaled irritants: O2 toxicity, smoke
  4. fat emboli
74
Q

pathophysiology of acute lung injury

A
  1. INFLAMMATORY MEDIATORS: macrophages release: IL-8, IL-1 and TNF
  2. NEUTROPHILS move from vasculature into alveolar space
  3. INCREASED PERMEABILITY: neutrophils release leukotrienes, oxidants, proteases, PAF that cause endothelial and epithelial injury
  4. PROTEIN RICH EDEMA in airspace, SURFACTANT INACTIVATION, hyaline membrane formation
  5. macrophage TGF-B and PDGF stimulate fibroblasts
75
Q

What happens in acute stage of acute lung injury?

A

endothelial: vasculature leakage
epithelial: cell sloughing
edema, hyaline membrane, atelectasis

76
Q

What happens in the organizing stage of acute lung injury?

A

type II cell proliferation

interstitial inflammation: recovery, interstitial fibrosis, death

77
Q

congestion stage of pneumonia

A

vascular engorgement and edema
few PMN
numerous bacteria

78
Q

red hepatization stage of pneumonia

A

massive congestion

abundant PMNs and fibrin

79
Q

gray hepatization stage of pneumonia

A

disintegration of RBC, macrophages

fibrinopurulent exudate

80
Q

resolution stage of pneumonia

A

enzymatic digestion

resorption by macrophages

81
Q

aspiration pneumonia

A

risk: alcoholic, comatose, drugs
anaerobic from oropharynx
RIGHT LOWER lobe abscess

82
Q

bronchogenic cysts

A

arise from abnormal detachments of primitive foregut and usually present with compression of nearby structures or are found incidentally

83
Q

pulmonary sequestration

A

discrete area of lung tissue that lacks connection to the airway system and has an abnormal blood supply arising from the aorta

84
Q

hamartoma

A

benign nodules of overgrowth mature connective tissue (in normal location)
karyotype: 6p21 or 12q14-15

85
Q

causes of primary lung carcinoma

A
  1. smoking (number 1)
  2. industrial: radiation, uranium
  3. asbestos: synergistic with smoking
  4. air pollution
  5. radon (number 2)
86
Q

small cell carcinoma

A

presents at advanced stage

Tx: chemo, radiaiton

87
Q

Non-small cell carcinoma

A

more resistant to chemo
Tx: surgery with/out chemo, radiation
operate on I, II, IIIA (not past lung, involves structures that can be removed)
IIIb, IV (out of chest): not operable

88
Q

lung adenocarcimona

A 
most common: female, non-smoker
PERIPHERAL
GLANDS, MUCIN
sometimes pneumonia like consolidation
lepidic pattern
horner syndrome sometimes
stain: TTF-1 positive, CK-7 positive
89
Q

squamous cell carcinoma

A 
males, SMOKERS
CENTRAL
central necrosis/CAVITATION
KERATIN PEARLS, INTRACELLULAR BRIDGES
PTHrP: HYPERCALCEMIA
Stain: p40
90
Q

large cell lung carcinoma

A

PERIPHERAL
large nuclei with prominent nucleoli and vesicular chromatin
POOR PROGNOSIS

91
Q

small cell lung carcinoma

A

SMOKING
high grade NEUROENDOCRINE
CENTRAL: with mediastinal lymphadenopathy
AGGRESSIVE, RAPID growth with widespread metastases
more chemo/radiosensitive: good response, but comes back (high mortality)
abundant mitoses, small blue cells with scant cytoplasm and granular (SALT and PEPPER) chromatin
ADH: hyponatremia
ATCH: cushings
Lambert-Eaton syndrome: muscle weakness
stain: CHROMOGRANIN, SYNAPTOPHYSIN
MEDICAL disease, limited vs extensive

92
Q

carcinoid tumor

A 
50-70, often incidental finding
low grade NEUROENDOCRINE carcinoma
central or peripheral
bland cells with granular chromatin, dense core granules 
CHROMOGRANIN
93
Q

what does prognosis of lung carcinoma depend on?

A

stage (TMN)
T: size (invasion of pleura, bronchus, etc., distance from carina)
N: nodes
M: metastases

94
Q

K-ras mutation

A

25% of ADENOCARCINOMA in SMOKERS

95
Q

EGFR mutations

A

10-25% of ADENOCARCINOMAS

non-smoker, FEMALE, ASIAN

96
Q

ALK mutations

A

ADENOCARCINOMA

mucin stain?

97
Q

local effects of lung cancer spread

A
  1. tumor obstruction of airway: pneumonia, abscess, collapse
  2. recurrent laryngeal nerve invasion: hoarse
  3. superior vena cava compression: superior vena cava syndrome
  4. sympathetic ganglion invasion: horner syndrome
98
Q

horner syndrome

A

PANCOAST tumor: just above lung
sympathetic nerve ganglion invasion
Sx: one sided: mild ptosis (drooping), miosis, lack of sweating, red half of face

99
Q

Lambert-Eaton syndrome

A

Ab to voltage gated Ca channels

muscle weakness

100
Q

common origins of metastatic lung cancer

A

MOST COMMON site of metastatic tumors
carcinoma (lymph): breast, colon, lung, melanoma
sarcomas: blood

101
Q

common origins of metastatic pleural tumors

A

MORE common than primary

lung, breast

102
Q

malignant mesothelioma

A 
parietal or visceral pleura
ASBESTOS
long latency:20 + years
SIMIAN virus 40 assoc.
Chromsome deletions: 1p, 3p, 6q, 9p, 22q common
Sx: chest pain, dyspnea, effusion
rapid course: 50% die in less than a year
Tx: surgery, chemo/radiation
103
Q

histologic types of malignant mesothelioma

A
  1. epithelioid (most common): can resemble metastatic adenocarcinoma
  2. sarcomatoid: resembles sarcoma
  3. biphasic: mix of both
104
Q

how do you distinguish mesothelioma from adenocarcinoma?

  1. histochemical stain
  2. immunohistochemical stain
  3. electron microscopy
A 
mesothelioma
1. hyaluronic acid
2. calretinin
3. long slender microvilli 
Adenocarcinoma
1. mucin
2. CEA (carcinoembryonic antigen)
3. stubby microvillus rootlets
105
Q

nasopharyngeal carcinoma

A

malignant epithelial cancer
EBV association
cervical lymph nodes are often involved

106
Q

laryngeal papilloma

A

benign: papillary lesion of vocal cord
HPV 6 and 11
single in adults
multiple in children

107
Q

laryngeal carcinoma

A

squamous cell carcinoma arising from vocal cord

risk: ALCOHOL, TOBACCO

108
Q

Primary lung cancer vs. Secondary lung cancer

A

primary: one nodule
secondary: multiple nodules
lung adenocarcinoma: colonic adenocarcinoma metastasis: taller longer cells, dirty necrosis

109
Q

CK20

A

stain
positive if origin of cancer is below the waist
ex: colonic that metastasize to lung

110
Q

CK7

A

stain
positive if origin of cancer is above the waist
ex: originate from lung

111
Q

p40

A

stain

squamous cell lung carcinoma

112
Q

CA19

A

stain

pancreatic adenocarcinoma

113
Q

CDX2

A

stain

colonic adenocarcinoma

114
Q

performance status

A

poor (status 3 or 4): can’t tolerate surgery, chemo, or radio
respectability also depends on if patient can survive removal of whole lobe or the lung
0: perfect
1: less than 25% have to rest/nap during day
2: less than 50%
3: less than 75%
4: have to rest entire day
5: dead

115
Q

Tx of NSCLC by stage of cancer

A

I: surgery
II: surgery (radiation if unable to under go surgery), then chemo (adjuvant)
III: radiation and chemo
IV: chemo, immune Rx, palliative radiation

116
Q

adjuvant tx

A

surgery, then chemo

117
Q

neoadjuvant tx

A

radiation to shrink, then surgery

118
Q

Indirect lung injury causes of ARDS

A

INDIRECT injury:

  1. SEPSIS
  2. chemical injury: heroin overdose
  3. shock (hypoperfusion)
  4. hematologic: multiple transfusions: TRALI (transfusion related acute lung injury)
  5. cardiopulmonary bypass
  6. acute pancreatitis
119
Q

Causes of ARDS in unknown category

A
  1. hypersensitivity rxn

2. uremia

120
Q

4 stages of ARDS and their time frames

A
  1. exudative (acute): 0-4 days
  2. proliferative: 4-8 days
  3. fibrotic: greater than 8 days
  4. recovery
121
Q

factors that increase the risk of death in ARDS

A
  1. chronic liver disease
  2. non-pulmonary organ dysfunction
  3. sepsis
  4. old age
122
Q

When is pneumothorax after ARDS most prevalent?

A

after 2 weeks of ARDS onset

Pulm (11 decks)

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