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Respiratory > Midterm - Pathology > Flashcards

Midterm - Pathology Flashcards

2
Q

at 15 weeks gestational age, the lungs are in this phase

A

pseudoglandular phase

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3
Q

by 24 weeks gestational age, the lungs are now in this phase

A

cannalicular phase

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4
Q

mature alveolar septa are composed of?

A

type 1 epithelium overlying endothelium with occasional type 2 epithelium (surfactant)

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5
Q

large ducts in the bronchial wall drain this

A

mucin from submucosal glands

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6
Q

what type of epithelium is found in the bronchi?

A

ciliated pseudocolumnar epithelium with goblet cells (that produce mucin)

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7
Q

in what direction do respiratory cilia beat?

A

upwards to remove debris

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8
Q

bronchiolar walls are lacking what two components found in the bronchi?

A

cartilage and glands

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9
Q

what separates type 1 epithelium and endothelium?

A

basement membrane, location of gas exchange

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10
Q

what is the purpose of type 2 epithelium?

A

produce surfactant which breaks water tension and prevents alveolar collapse, also pluripotent and can regenerate new type 1 cells

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11
Q

what type of cells are found in the pleura?

A

mesothelial cells

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12
Q

peribronchial and interstitial stroma supports airway and is rich is this component

A

elastin

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13
Q

where are the arteries and veins found within the secondary lobule?

A

arteries track with bronchioles, veins along interlobular septae

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14
Q

what is the purpose of pleura?

A

frictionless vaccuum system to keep lung inflated

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15
Q

name two genetic non-obstructive causes of bronchiectasis

A

cystic fibrosis, primary ciliary dyskinesia

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16
Q

pathology of bronchiectasis

A

permanent dilation of bronchi, peri-bronchial inflammation, and organization (fibroblastic proliferation)

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17
Q

radiology of bronchiectasis

A

airway dilation extending into periphery (seen on CT)

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18
Q

what is found in the dilated bronchi of a patient with CF?

A

muco-purulent debris plugging the bronchi

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19
Q

which microbial product leads to mucus hypersecretion and structural damage of airways in patients with CF?

A

elastase

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20
Q

what’s wrong with the cilia in CF?

A

nothing; just not mechanically strong enough to move abnormally thick mucus

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21
Q

which gene is mutated in CF, and what is the most common allele?

A

CFTR gene; delta F508

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22
Q

CF exhibits what inheritance pattern?

A

AR

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23
Q

what causes exceptionally thick mucus in patients with CF?

A

interrupted chloride pump leading to too much water absorption into the airway epithelium

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24
Q

this simple test is still used to diagnose CF in some patients

A

sweat test (measured chloridge levels in sweat, high in pts with CF)

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25
Q

what is the genetic abnormality in PCD?

A

loss of 1 or both dynein arms, leading to poor ciliary function

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26
Q

what would radiology of asthma show?

A

alternating atelectasis and overexpansion

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27
Q

pathology of asthma

A

edema, smooth muscle thickening, BM thickening, mucous cell hyperplasia, increased eosinophils, thickened mucus

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28
Q

what are the primary clinical features of asthma?

A

acute, usually reversible bronchial narrowing due to airway hyperresponsiveness, chronic inflammation of the airways

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29
Q

what are charcot-leyden crystals?

A

caused by high levels of eosinophils and found in asthma

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30
Q

what are curschmann spirals?

A

dehydrated mucus that causes mucus casts, seen in asthma

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31
Q

clinical definition of chronic bronchitis

A

productive cough at least 3 mo out of the year for 2 years or more

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32
Q

pathology of chronic bronchitis

A

mucus cellular and glandular hyperplasia + submucosal chronic inflammation

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33
Q

two major causes of COPD

A

cigarette smoking or alpha1-antitrypsin deficiency

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34
Q

emphysema from cigarette smoking leads to ______lobular destruction predominantly in the _____ lobes

A

centrilobular; upper lobes

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35
Q

emphysema from A1AT deficiency leads to ______lobular destruction predominantly in the _____ lobes

A

panlobular; lower lobes

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36
Q

emphysema pathology

A

dilation of distal airspaces due to septal destruction; increased elastase activity

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37
Q

smoking causes elastic damage by?

A

recruiting elastase-sereting leukocytes and inhibiting anti-elastase

38
Q

inheritance pattern of A1AT deficiency

A

AR

39
Q

at what age does A1AT deficiency present?

A

middle age, under 40

40
Q

A1AT is due to loss of function of this gene, and this allele leads to particularly severe disease

A

SERPINA1 gene; Z allele

41
Q

AIAT deficiency leads to disease of the lung and this organ

A

liver (Z protein aggregates in rER of hepatocytes)

42
Q

clinical presentation of BOOP/COP (organizing pneumonia)

A

acute onset cough, dyspnea, fever, malaise from drugs, infxn, coll-vasc dz

43
Q

treatment of BOOP/COP

A

corticosteroids WORK WELL

44
Q

pathology of BOOP/COP

A

patchy fibromyxoid plugs (fibroblastic prolif) in distal bronchioles and alveoli +/- endogenous lipid pneumonia

45
Q

peribronchovascular stroma is composed of what?

A

fibrous connective tissue rich in lymphocytes and macrophages

46
Q

interstitium

A

tissue separating alveoli

47
Q

pathology of sarcoidosis

A

tight, well-formed non-caseating granulomata

48
Q

granulomata are composed of these characteristic cell types

A

epithelioid histiocytes, occasional giant cells

49
Q

radiological findings in sarcoidosis

A

interstitial infiltrates in broncial tree + hilar LN adenopathy

50
Q

who is at greatest risk for sarcoidosis?

A

adults, black > white, females > males

51
Q

hypersensitivity pneumonia (HP) is also known as?

A

extrinsic allergic alveolitis (EAA)

52
Q

what causes hypersensitivity pneumonia?

A

organic dusts, animal proteins, synthetic organic chemicals, hot tubs, AC, hay, sugarcane, maple bark

53
Q

pathology of HP

A

patchy peri-bronchiolar and interstitial chronic inflammation and loosely formed granulomata; visible lymphocytes

54
Q

pneumoconioses are caused by?

A

inorganic dusts from occupational or environmental exposure –> lung fibrosis

55
Q

three major causes of pneumoconiosis

A

silica, asbestos, coal

56
Q

why do inorganic dusts cause fibrosis of the lung?

A

body cannot metabolize them; digested by macrophage, gives off cytokines that promote a fibrogenic response

57
Q

early silicosis is rich in?

A

macrophages

58
Q

late stage silicosis shows?

A

fibrotic nodules (pink on slide)

59
Q

asbestosis causes this unique pathological finding

A

asbestos fibers; crystals less than 7mm that are brittle and undigestible; surrounded by iron released by macrophages –> ferruginous bodies

60
Q

fibrosis caused by asbestos is usually patchy and confined to the ______ region

A

sub-pleural

61
Q

coal-worker’s pneumoconiosis leads to?

A

coal dust macules, black lung, no interference with gas exchange

62
Q

usual interstitial pneumonia is also known as?

A

idiopathic pulm fibrosis

63
Q

what is the prognosis of UIP?

A

poor; avg survival 3-5 yrs after dx

64
Q

UIP can resemble what other diseases radiologically?

A

asbestosis, autoimmune dz (all three cause patchy subpleural infiltrates

65
Q

important pathological finding that suggests UIP

A

temporal heterogeneity: alternating between fibroblasts, mature fibrosis, and normal tissue

66
Q

late stage sub-pleural fibrosis resembles?

A

honeycomb change

67
Q

diffuse alveolar damage (DAD)

A

shock –> fibrin rich alveoli –> after 1 week the fibrin is cleared, leading to lung remodeling –> decreased pulm compliance –> impaired mechanical ventilation

68
Q

prognosis of DAD

A

50% mortality

69
Q

pathology of DAD

A

interstitial +/- intra-alveolar fibroblastic proliferation in sites of fibrin accumulation (uniform fibrosis)

70
Q

major difference between UID and DAD

A

both cause interstitial fibrosis, but with DAD it is temporally uniform and occurs predictably after shock

71
Q

pathology of a hamartoma

A

solitary, lobulated, cartilagenous benign tumor made up of normal tissue in excess/disarray (can have popcorn calcification)

72
Q

who presents with hamartomas?

A

adolescence to adulthood (never congenital)

73
Q

what are the 4 types of malignant epithelial neoplasms in the lung (carcinomas)?

A

squamous cell, adenocarcinoma, large cell undiff, small cell undiff

74
Q

what is the 5 year survival rate of lung cancer (unspecified subtype)?

A

15%; very high mortality

75
Q

what % of lung carcinoma deaths occur in cigarette smokers?

A

more than 85%

76
Q

cigarette smoking causes death by what three main disease outcomes?

A

lung cancer, ischemic heart disease, COPD

77
Q

what % of tobacco particulates are cleared by cilia?

A

50%; the remainder are phagocytosed and transported through the lymphatics –> tatooing

78
Q

describe the cause, location, pathological findings, and paraneoplastic phenomena assoc. with squamous cell carcinoma

A

cause: SMOKING, location: central (usually bronchi due to increased turbulence), path: desmosome bridges, keratin pearls; secretes PTH-like compound –> hypercalcemia

79
Q

what are the three stages of adenocarcinoma

A

ACIS/BAC (less than 3cm, noninvasive); MIA (less than 3cm w/ small invasion), invasive (greater than 3cm OR large invasion)

80
Q

describe the cause, location, pathological findings, and paraneoplastic phenomena assoc. with adenocarcinoma

A

can occur in non-smokers, peripheral, path: glands and/or mucin

81
Q

how to detect mucin

A

PASd stain; mucin looks red

82
Q

what is unique about BAC?

A

can be multifocal –> must distinguish from mets; not associated with smoking; butterfly-like growth pattern; VERY TREATABLE

83
Q

how about large cell undiff?

A

carcinoma negative for all of the traits assoc with squamous cell and adenocarcinoma

84
Q

prognostic variables for NSCLC

A

stage, performance status, weight loss (NOT age, histology)

85
Q

describe the cause, location, pathological findings, and paraneoplastic phenomena assoc. with small cell carcinoma

A

20%; undifferentiated neuroendocrine carcinoma that presents late stage with rapid, necrotic growth of a primary central mass and metastasis to LN and liver; commonly causes SIADH leading to water retention and hyponatremia

86
Q

therapy for small cell carcinoma

A

chemo/RT; very responsible initially but cancer always comes back and kills the patient

87
Q

prognostic variables for small cell lung cancer

A

stage, performance status, women do better than men

88
Q

mesothelioma

A

malignant neoplasm of the pleura caused by asbestos; deeply invasive growth pattern; immuno positive for keratin & calretinin, long microvilli; can appear epithelial, spindle cell, or biphasic

89
Q

metastatic carcinomas that end up in the lung

A

breast, GI, renal, head/neck

90
Q

metastatic melanoma is unique in that?

A

it can appear to be a primary cancer of the lung since it is often difficult to find to primary cancer

Respiratory (15 decks)

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