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Pathology > 2nd Exam: Lung Disease 1 > Flashcards

2nd Exam: Lung Disease 1 Flashcards

1
Q

partial or complete collapse of the lung:

A

atela

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2
Q

fulmninant:

A

severe and sudden in onset.

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3
Q

Normal bronchus is lined by;

A

ciliated epi, cartilage for support

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4
Q

These divide alveoli:

A

septae containing many caps

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5
Q

prototype of immune-mediated d.:

A

asthma

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6
Q

asthma is one of __ types of immune response:

A

4

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7
Q

asthma:

A

long lasting, begins 1st-2nd decade, 1-2h episodes, stress, inhaled irritants, cold air, exertion, bronchial tube mm. tighten, thicken, inflamed walls, mucus filled airways

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8
Q

Pathogenesis of asthma:

A

type 1 hypersensitivity, exposure to antigen, it binds IgE, this activates inflammatory cells, mediators are released that cause the symptoms and inflammation

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9
Q

mediators released in asthma attack:

A

PG, leukotrienes, histamine, bradykinin

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10
Q

Types of inhaled irritants:

A

microbes, allergens, pollutants, oxidants, irritants

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11
Q

inhaled irritants that attract and activate macs, PMNs, and eosinophils:

A

CCL2, 5, 11, Il-6, 8, TNF-a, GM-CSF

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12
Q

Pwy antigen presentation to naive T-cell:

A

activate Th17 OR Th2 (routes) 1: eosinophil, cytokines, chemokines, cytotoxic products, lipid mediators 2. B cell w IgE, Mast cells and/or basophils, histamine, leukotrienes, PGD2, cytokines

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13
Q

IL required for Th2 cells to activate eosinophiis;

A

IL-5

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14
Q

IL’s required for Th2 cells to activate B cells

A

IL-4, 13

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15
Q

Eosinophils activate:

A

cytokines, chemokines, cytotoxic products, lipid mediators

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16
Q

mast cells and/ or basophils activate:

A

Leukotrienes, PGD2, cytokines

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17
Q

TF? Airflow is only restricted TO the lungs in asthma.

A

F. Both to and from

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18
Q

Asthma pathology:

A

vasod, mucus plus, desquamation of epi, mucus gland hyperplasia, sm hypertrophy and hyperplasia, thickened BM and sm, edematous submucosa w infiltration of granulocytes, infiltration of bronchi and para bronchial tissues w monocytes and lymhpos, thick mucus, inflammation

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19
Q

Prominent cell in response to asthma:

A

eosinophil

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20
Q

What do the eosinophils that respond to asthma secrete:

A

major basic protein, damaging

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21
Q

Diagnostic marker of asthma:

A

Charcot-Leyden crystals (eosinophil proteins)

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22
Q

What are Charcot-Leyden crystals?

A

eosinophilic proteins

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23
Q

Emphysema is aka:

A

COPD, centrilobular emphysema

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24
Q

Emphysema

A

common, chronic, progressive, mainly smokers, over 60 it gets severe, dyspnea, shortness of breath, cyanosis, disability, lungs hyperinflated, dilated air spaces in form of cysts/ blebs

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25
Q

Causes of tissue damage in emphysema:

A

ROS, inc mac elastase and metalloproteinases

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26
Q

These lead to ROS formation:

A

neutrophils, tobacco

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27
Q

Transport ROS to the blood stream:

A

IL-8, LTB4, TNF (8 Before tnf)

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28
Q

Role of neutrophils in emphysema:

A

create ROS, inc neutrophil elastase

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29
Q

These can increase neutrophil elastase:

A

neutrophils, congenital a1AT deficiency

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30
Q

3 roles of ROS in emphysema:

A

tissue damage, inactivation of antiproteases (essentially activating protease) (“functional: a1AT deficiency”, go to blood stream

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31
Q

Alveolar Type II cell:

A

septal cell, make surfactant

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32
Q

Alveolar Type I cell:

A

form wall

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33
Q

Some sm cells of the alveolar septum

A

knob cells

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34
Q

What happens with COPD?

A

septae destroyed, airspaces enlarged, O2 exchange reduced, fewer caps, loss of elasticity, can’t contract normally

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35
Q

Differential Dx of post-op dyspnea:

A

pulmonary emboli, pneumonia, diffuse alveolar damage (DAD)

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36
Q

Lines the wall of pts w acute lung injury (DAD):

A

hyaline mem

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37
Q

Causes of DAD (ARDS)

A

shock, trauma, surgery, burns, sepsis, oxygen therapy, smoke from house fire, drugs, aspiration, uremia (kidney failure), viral infection, newborn (surfactant)

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38
Q

ARDS sf:

A

Acute respiratory distress syndrome

39
Q

Premature:

A

less than 37 wks gestation or under 2500 grams

40
Q

Babies are more likely to be born preterm if:

A

maternal illness (GU tract infection), uterine incompetence-cervix dilates, multiple pregnancies, placental problems, premature labor, lack of prenatal care

41
Q

Consequences of preterm birth for baby:

A

Death, immature organs vulnerable to many complications esp in lungs (RDS/HMD)

42
Q

Appearance of HMD lungs :

A

firm, airless, dark red

43
Q

Are HMD or normal newborn lungs crepitant?

A

normal

44
Q

Greater than 50% of newborns are born under __ wks.

A

28

45
Q

When ratios of this are less than 2:1 in the amniotic fluid, the risk of RDS is greater:

A

Lecithin, sphingomyelin

46
Q

A large increase in lecithin happens at this wk of gestation:

A

35th

47
Q

Pathologic lung changes that result from RDS:

A

atelectasis and hyaline membranes

48
Q

TF? synthesis, storage, and release of surfactant are all reduced in HMD:

A

T

49
Q

Does alveolar surface tension increase or decrease w dec alveolar surfactant?

A

Decreases

50
Q

increased alveolar surface tension leads to:

A

atelectasis

51
Q

atelectasis can lead to:

A

uneven perfusion, hypoventilation

52
Q

Both uneven perfusion, hypoventilation can lead to

A

hypoxemia, Co2 retention, acidosis

53
Q

Factors that lead to reduced surfactant synthesis, storage and release:

A

hypoxemia, CO2 retention, acidosis

54
Q

Acidosis leads to:

A

pulm vasoc and reduced surfactant synthesis, storage and release

55
Q

Pulm vasoc leads to:

A

hypoperfusion

56
Q

pulm hypoperfusion leads to:

A

epi/ endo damage, blood leaks into alveoli, fibirin and necrotic cells (hyaline mem)

57
Q

What is hyaline mem?

A

fibrin and necrotic cells

58
Q

This is prominent in HMD:

A

lecithin

59
Q

When are alveoli mature?

A

greater than 2:1, L:S ratio

60
Q

Ischemia in HMD babies leads to:

A

cap perm, plasma leaks into alveoli, hyaline membrane formation (fibrin, necrosis)

61
Q

Pneumonia can be:

A

bacterial, fungal, viral

62
Q

Lung abscesses are usually due to:

A

bacterial infection

63
Q

Pulmonary defense mechs:

A

nasal filtration, mucociliary escalator, macs, BALT, IgA, anti-proteases, anti-oxidants

64
Q

The mucociliary escalator is in:

A

tracheobronchial tree

65
Q

Where are macs found in the lungs?

A

alveoli

66
Q

Immunologic pulmonary defense mechs:

A

BALT, IgA

67
Q

Biochemical defense mechs:

A

anti-protease, anti-oxidants

68
Q

Sources of acute pneumonia:

A

CON: Community acquired, nosocomial, opportunistic

69
Q

Main organisms that cause community acquired pneumonia:

A

S. pneumoniae, H. influenze, influenza virus

70
Q

Main organisms that cause nosocomial pneumonia:

A

Staph areus, gram negatives

71
Q

Main organisms that cause opportunistic pneumonia:

A

CHAPP: CMV, herpes, adenovirus pseudomonas, pneumocystis,

72
Q

Pop more prone to contracting opportunistic pneumonia:

A

elderly, immunosuppressed

73
Q

Tissue site for bacterial pneumonia infection:

A

distal lung parenchyma

74
Q

Bacterial pneumonia:

A

purluent exudate and consolidation (solidification) of lung, fever, shaking chills, productive cough, dullness to percussion, rales, chest x-ray infiltrates

75
Q

Pt w productive cough, think:

A

bacterial pneumonia

76
Q

Pathogenesis of bacterial pneumonia:

A

loss or suppression of cough reflex (anesthesia, coma), injury to mucociliary apparatus, inc secretions, impaired phagocytic activity of alveolar macs, alcohol, smoking, immune suppresision, previous lung injury (COPD, viral pneumonia), old age, exposure to cold

77
Q

Factors that lead to impaired phagocytic activity of alveolar macs:

A

alcohol, smoking

78
Q

Previous lung injury that can cause bacterial pneumonia:

A

COPD, viral pneumonia

79
Q

Airway routes for spread of bacterial infection:

A

inhaled aerosols (env or person to person), aspirated vomit

80
Q

Sources of bacterial infection in lungs:

A

airway, hematogenous (infection at other site)

81
Q

Stages of bacterial infection in lung:

A

acute, resolving, organizing

82
Q

Char’s of the acute phase of bacterial infection in lung:

A

polys in alveoli

83
Q

Char’s of resolving stage of bacterial infection in lung:

A

no polys, many macs, infiltrates are cleared, alveolar walls intact

84
Q

Char’s of organizing stage of bacterial infection in lung:

A

granulation tissue, fibrosis (terminal bronchioles and alveoli)

85
Q

Anatomic patterns of bacterial pneumonia:

A

bronchopneumonia, lobar pneumonia

86
Q

bronchopneumonia:

A

polys in distal airways

87
Q

Risks for acquiring aspiration pneumonia:

A

caries, pd, poor oh, debilitation, alcohol abuse, loss of consciousness, surgery, vomiting, reflux, diminished gag reflex, abnormal swallowing

88
Q

apiration pneumonia results in:

A

chemical injury and bacteria

89
Q

This type of aspiration pneumonia may lead to abscess formation:

A

necrotizing, fulminant

90
Q

Aspiration is more common here:

A

R bronchus, larger, shorter, more vertical

91
Q

These cells react to foreign material in aspiration pneumonia:

A

giant cells

92
Q

cxr:

A

chest x-ray

93
Q

Lung abscess, routes of infection:

A

aspiration, previous pneumonia, bacteremia, from another organ

Pathology (23 decks)

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