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
intrinsic asthma
non-immunologic reaction: precipitated by respiratory infection, stress, exercise, cold, drugs, etc.
26
histological aspects of asthma
1. thickened BM 2. submucosal gland hypertrophy 3. bronchial wall smooth muscle hypertrophy 4. eosinophils
27
causes of bronchiectasis
1. cystic fibrosis 2. Kartagener 3. necrotizing pneumonia 4. bronchial obstruction
28
cystic fibrosis
chloride transport defect results in thick obstructive secretions
29
Kartagener
immotile cilia syndromes: interferes with bacterial clearance
30
tracheoesophageal (T-E) Fistula
failure of fetal respiratory tract to separate from GI tract | FOREGUT
31
alveolar stages
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
32
rhinitis
inflammation of nasal mucosa rhinovirus: common cold or allergic (type I) repeated: NASAL POLYPS
33
nasal polyps
edematous, inflamed nasal mucosa | causes: repeated rhinitis, CF, aspirin intolerant asthma
34
aspirin intolerant asthma
asthma aspirin induced bronchospasm nasal polyps
35
angiofibroma
benign tumor of the nasal mucosa composed of large blood vessels and fibrous tissue Sx: profuse epitaxis
36
chronic interstitial/restrictive lung disease
heterogenous group dyspnea and reduced lung capacity results in diffuse scarring
37
honeycomb on CT
END STAGE of restrictive diseases
38
idiopathic pulmonary fibrosis (IPF)
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
39
pneumoconioses
non-neoplastic lung rxn to inhaled dusts (coal, silica, asbestos, berylliosis, etc.)
40
hypersensitivity pneumonitis
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
41
Masson body
fibroblast foci | believed to be sites of recent injury
42
collagen vascular disease-associated lung disease
RA, scleroderma, mixed connective tissue disease | UIP histologically
43
cryptogenic organizing pneumonia (COP)
INTRA-ALVEOLAR: CT in bronchioles, alveolar ducts, and alveoli (all SAME AGE) Tx: steroids
44
simple coal workers pneumoconiosis (CWP)
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)
45
complicated coal workers pneumoconiosis (CWP)/ progressive massive fibrosis
lung function compromised develops in those with simple CWP black scars composed of pigment and dense collagen associated with: RA
46
anthracosis
CWP | carbonaceous pigment in macrophages that accumulates in CT along lymphatics and in lymph tissue
47
silicosis
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
48
beryllium
SPACE industry, MINERS non-caseating GRANULOMA: lung, hilar lymph nodes, organs increased chance of lung CA
49
non-neoplastic asbestos-related diseases
1. diffuse pleural fibrosis 2. benign pleural effusions 3. plerual plaques 4. parenchymal interstitial fibrosis (Asbestosis) MORE COMMON than cancer
50
parenchymal interstitial fibrosis (asbestosis)
Sx: slowly progressive dyspnea heavy ASBESTOS exposure: 20 yr latency initial injury: respiratory bronchioles and alveolar ducts: results in fibrosis of adjacent alveoli
51
drug/radiation pneumonitis
chemo (busulfan) or radiation to chest
52
sarcoidosis
``` 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
desquamative interstitial pneumonia (DIP)
SMOKING peribronchiolar Tx: stop smoking, steroids
54
respiratory bronchiolitis
SMOKING peribronchiolar Tx: stop smoking, steroids
55
pulmonary langerhans cell histiocytosis
``` YOUNG SMOKERS rare Tx: quit BRAF mutation leads to alveolar damage and airway destruction Langerin, S-100, CD1a NO CD68 ```
56
pulmonary alveolar proteinosis
rare defect in GM-CSF or macrophages: accumulation of surfactant can be autoimmune, secondary (malignancy or immunodeficiency), or hereditary (infants)
57
pneumocystis jirovecii
yeast fungus | IMMUNOCOMPROMISED: HIV
58
pulmonary embolism
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
secondary pulmonary hypertension causes
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
primary pulmonary hypertension
female, 20s-40s Sx: dyspnea, fatigue inactivating BMPR2 mutation: proliferation of vascular sm. muscle
61
How does chronic obstructive or interstitial lung disease lead to pulmonary HTN?
hypoxia and fewer alveolar capillaries from parenchymal destruction leads to increase pulmonary arterial resistance and pressure
62
How does cardiac disease lead to pulmonary HTN?
mitral stenosis causes elevated left atrial pressure that increases pulmonary venous and arterial pressure
63
How do recurrent pulmonary thromboemboli lead to pulmonary HTN?
decrease in functional area of pulmonary vascular bed leads to increased vascular resistance
64
good pasture
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
idiopathic pulmonary hemosiderosis
pulmonary hemorrhage disease
66
lupus erythematosus
vasculitis with pulmonary hemorrhage
67
wegener granulomatosis (polyangiitis with granulomatosis)
med. to small vessel vasculitis | Sx: necrotizing granulomas of respiratory tract, glomerulonephritis, pulmonary hemorrhage
68
hemodynamic pulmonary edema causes
1. increased hydrostatic pressure: left heart failure | 2. decreased oncotic pressure: liver disease
69
causes of pulmonary edema due to microvascular injury
1. infection 2. inhaled smoke and other gases 3. shock
70
acute lung injury/ ARDS (acute respiratory distress syndrome)
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
diffuse alveolar damage (DAD)
histological manifestation of ARDS and neonatal RDS
72
neonatal RDS
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
Direct lung injury causes of ARDS
DIRECT injury: 1. infection (pneumonia/ aspiration) 2. injury: trauma, near drowning, burns 3. inhaled irritants: O2 toxicity, smoke 4. fat emboli
74
pathophysiology of acute lung injury
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
What happens in acute stage of acute lung injury?
endothelial: vasculature leakage epithelial: cell sloughing edema, hyaline membrane, atelectasis
76
What happens in the organizing stage of acute lung injury?
type II cell proliferation | interstitial inflammation: recovery, interstitial fibrosis, death
77
congestion stage of pneumonia
vascular engorgement and edema few PMN numerous bacteria
78
red hepatization stage of pneumonia
massive congestion | abundant PMNs and fibrin
79
gray hepatization stage of pneumonia
disintegration of RBC, macrophages | fibrinopurulent exudate
80
resolution stage of pneumonia
enzymatic digestion | resorption by macrophages
81
aspiration pneumonia
risk: alcoholic, comatose, drugs anaerobic from oropharynx RIGHT LOWER lobe abscess
82
bronchogenic cysts
arise from abnormal detachments of primitive foregut and usually present with compression of nearby structures or are found incidentally
83
pulmonary sequestration
discrete area of lung tissue that lacks connection to the airway system and has an abnormal blood supply arising from the aorta
84
hamartoma
benign nodules of overgrowth mature connective tissue (in normal location) karyotype: 6p21 or 12q14-15
85
causes of primary lung carcinoma
1. smoking (number 1) 2. industrial: radiation, uranium 3. asbestos: synergistic with smoking 4. air pollution 5. radon (number 2)
86
small cell carcinoma
presents at advanced stage | Tx: chemo, radiaiton
87
Non-small cell carcinoma
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
lung adenocarcimona
``` 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
squamous cell carcinoma
``` males, SMOKERS CENTRAL central necrosis/CAVITATION KERATIN PEARLS, INTRACELLULAR BRIDGES PTHrP: HYPERCALCEMIA Stain: p40 ```
90
large cell lung carcinoma
PERIPHERAL large nuclei with prominent nucleoli and vesicular chromatin POOR PROGNOSIS
91
small cell lung carcinoma
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
carcinoid tumor
``` 50-70, often incidental finding low grade NEUROENDOCRINE carcinoma central or peripheral bland cells with granular chromatin, dense core granules CHROMOGRANIN ```
93
what does prognosis of lung carcinoma depend on?
stage (TMN) T: size (invasion of pleura, bronchus, etc., distance from carina) N: nodes M: metastases
94
K-ras mutation
25% of ADENOCARCINOMA in SMOKERS
95
EGFR mutations
10-25% of ADENOCARCINOMAS | non-smoker, FEMALE, ASIAN
96
ALK mutations
ADENOCARCINOMA | mucin stain?
97
local effects of lung cancer spread
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
horner syndrome
PANCOAST tumor: just above lung sympathetic nerve ganglion invasion Sx: one sided: mild ptosis (drooping), miosis, lack of sweating, red half of face
99
Lambert-Eaton syndrome
Ab to voltage gated Ca channels | muscle weakness
100
common origins of metastatic lung cancer
MOST COMMON site of metastatic tumors carcinoma (lymph): breast, colon, lung, melanoma sarcomas: blood
101
common origins of metastatic pleural tumors
MORE common than primary | lung, breast
102
malignant mesothelioma
``` 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
histologic types of malignant mesothelioma
1. epithelioid (most common): can resemble metastatic adenocarcinoma 2. sarcomatoid: resembles sarcoma 3. biphasic: mix of both
104
how do you distinguish mesothelioma from adenocarcinoma? 1. histochemical stain 2. immunohistochemical stain 3. electron microscopy
``` mesothelioma 1. hyaluronic acid 2. calretinin 3. long slender microvilli Adenocarcinoma 1. mucin 2. CEA (carcinoembryonic antigen) 3. stubby microvillus rootlets ```
105
nasopharyngeal carcinoma
malignant epithelial cancer EBV association cervical lymph nodes are often involved
106
laryngeal papilloma
benign: papillary lesion of vocal cord HPV 6 and 11 single in adults multiple in children
107
laryngeal carcinoma
squamous cell carcinoma arising from vocal cord | risk: ALCOHOL, TOBACCO
108
Primary lung cancer vs. Secondary lung cancer
primary: one nodule secondary: multiple nodules lung adenocarcinoma: colonic adenocarcinoma metastasis: taller longer cells, dirty necrosis
109
CK20
stain positive if origin of cancer is below the waist ex: colonic that metastasize to lung
110
CK7
stain positive if origin of cancer is above the waist ex: originate from lung
111
p40
stain | squamous cell lung carcinoma
112
CA19
stain | pancreatic adenocarcinoma
113
CDX2
stain | colonic adenocarcinoma
114
performance status
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
Tx of NSCLC by stage of cancer
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
adjuvant tx
surgery, then chemo
117
neoadjuvant tx
radiation to shrink, then surgery
118
Indirect lung injury causes of ARDS
INDIRECT injury: 1. SEPSIS 2. chemical injury: heroin overdose 3. shock (hypoperfusion) 4. hematologic: multiple transfusions: TRALI (transfusion related acute lung injury) 4. cardiopulmonary bypass 6. acute pancreatitis
119
Causes of ARDS in unknown category
1. hypersensitivity rxn | 2. uremia
120
4 stages of ARDS and their time frames
1. exudative (acute): 0-4 days 2. proliferative: 4-8 days 3. fibrotic: greater than 8 days 4. recovery
121
factors that increase the risk of death in ARDS
1. chronic liver disease 2. non-pulmonary organ dysfunction 3. sepsis 4. old age
122
When is pneumothorax after ARDS most prevalent?
after 2 weeks of ARDS onset