Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology II PCC > Chapter 12 for exam II > Flashcards

Chapter 12 for exam II Flashcards

1
Q

What cancer causes the most cancer related deaths in males and females?

A

lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is an acinus?

A

found distal to terminal bronchiole

berry shaped, contain alveolar duct –> alveolar sac –> alveolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the major pneumocyte found on the alveolar surface?

What is the major pneumocyte found in surfactant?

A

type I makes up 95% of alveolar surface

Type II is in surfactant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is atelectasis? what happens to the blood?

A

Atelectasis is a collapsed lung– failure to expand

decrease in oxygenated blood is shunted, hypoxemia to hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the categories of atelectasis?

A

resorption

compression

contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Details about resorption atelectasis?

A

airway obstruction that prevents air from reaching distal airways

MC: mucopurulent plug: bronchial asthma, bronchiectasis, chronic bronchitis

single lobe or entire lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Details about compression atelectasis

A

aka passive atelectasis

pleural cavity fills with serous fluid, blood, air

CHF is the MC cause

may follow pleural effusion

pneumothorax: air accumulation around lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Details about contraction atelectasis

A

aka cicatrization atelectasis

Scarring of the lungs (interstitial fibrosis, pleural fibrosis)

decreased inhalation– decreased expansion/distention, limits alveolar opening = collapse

Recovery is limited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is acute respiratory distress syndrome?

A

severe trauma or infection causes diffuse alveolar damage & bilateral vascular and epithelial damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

with ARDS, what leads to hypoxia?

A

inflammation prevents gas exhange which leads to hypoxemia then hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

obstructive pulmonary diseases

A

airflow resistance

decreased expiratory flow rate = wheezing

emphysema, chronic bronchitis, bronchiectasis, asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

restrictive pulmonary diseases

A

decreases lung expansion: chest wall disorders (pleura, NMS) & Intersititial lung diseases (fibrosis)

decreased forced vital capacity, normal expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is emphysema?

A

permanent pulmonary destruction– destruction of alveolar septa and enlarged acini

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

is there fibrosis found with emphysema?

A

No!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What accumulates with emphysema?

A

inflammatory cells: increase in proteases and ROS, decrease in anti-protease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are they types of emphysema?

A

Centriacinar/centrilobar

panacinar/panlobular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

details about centriacinar emphysema

A

20x MC than panacinar

destroys central acini

spares distal lobule

MC in lung apices

risk: chronic smokers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

details about panacinar emphysema

A

acini are uniformly affected/destroyed

MC in lower lungs

risk: alpha-antitrypsin deficiency = increased protease activity

smoking accelerates destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Smoking contributes to emphysema in what way?

A

ROS from the smoke and from the WBC’s brought by the inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

‘pink puffer’ refers to…

A

emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

symptoms of emphysema

A

progressive dyspnea (forced expiration)

cough

hyperventilation

wheezing

weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

emphysema is: obstructive or restrictive?

A

obstructive because there’s wheezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the hallmark of chronic bronchitis?

A

hypersecretion of mucus

in trachea and bronchi

hypertrophy/hyperplasia of mucous glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

who is most at risk for chronic bronchitis?

A

males

25% are between 40-65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Symptoms of chronic bronchitis

A

pronounced & productive cough lasting > or equal to 3 consecutive months in > or equal to 2 consecutive years

sputum production is yellow/green

dyspnea, wheezing, cyanosis, cor pulmonale, recurrent lung infxns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

chronic bronchitis is a risk for what?

A

a secondary microbial infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

blue bloater refers to

A

chronic bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

chronic bronchitis is almost always complicated by what other condition?

A

emphysema

Chronic obstructive pulmonary disease (COPD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

T/F: The airflow obstructions associated with COPD are reversible

A

False, the airflow obstructions associated with COPD are IRREVERSIBLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is a risk factor for emphysema, chronic bronchitis and COPD?

A

cigarette smoking (MC)

air pollution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

T/F: The airway obstruction associated with asthma is reversible

A

True, asthma airway obstruction is REVERSIBLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What physiologically occurs during asthma?

A

reversible bronchoconstriction– smooth muscle hypertrophy & hyperreactivity

inflammation & increased mucous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are curschmann spirals and charcot-leyden crystals associated with?

A

Asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the symptoms associated with asthma?

A

wheezing, dyspnea, cough or chest tightness

difficulty inhaling & exhaling**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Where is asthma most prevalent?

A

westernized world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Atopic vs. Non-atopic asthma

A

atopic: (MC) Type I hypersensitivity, Allergens

Non-atopic: bronchial hyper-responsiveness, various non-allergic stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

details about atopic asthma

A

aka extrinsic asthma

MC type: 70% of all cases

childhood onset, family Hx

triggered by environmental antigens

associated with additional allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

details about non-atopic asthma

A

aka intrinsic asthma

idiopathic–no allergen sensitization, not genetic

bronchial inflammation & hyper- responsiveness

various stimuli (stress, exercise, cold air, aspirin, inhaled irritants)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the differences between normal and bronchial asthma histology?

A

increased: mucus, WBCs, goblet cells, fibrosis present, smooth muscle, submucosal glands and increased submucosal vascularity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

chronic asthma is obstructive or restrictive?

A

obstructive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what occurs with chronic asthma?

A

bronchial narrowing

thickened airway wall– hypertrophy of bronchial smooth muscles & submucosal glands –> mucous plugs

fibrosis & increased submucosal vascularity

progressive hyperinflation of the acini–dysfunctional expiration

may be lethal

NO response to bronchodilators or steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is permanent dilation of the bronchial tree?

A

bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

is bronchiectasis restrictive or obstructive?

A

obstructive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

when does bronchiectasis occur?

A

it is a necrotizing infection

occurs with lung cancer, TB, chronic bronchitis, foreign bodies

impacted mucus: asthma, cystic fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

T/F: during bronchiectasis, there is connective tissue and musculature destruction

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

location of bronchiectasis? if localized or if bilateral, what does it mean caused it?

A

MC in lower lobes

if localized: caused by foreign body

if bilateral: cystic fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What causes bronchiectasis/necrotizing pneumonia?

A

Klebsiella spp. and Staph. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What characterizes chronic intersititial lung diseases?

A

decreased compliance

MC bilateral and chronic

dyspnea, pulmonary HTN and hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What do chronic interstitial lung diseases progress into?

A

respiratory failure, pulmonary HTN and cor pulmonale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What type of fibrosing chronic intersititial lung disease produces velcro-like crackles, an insidious non-productive cough, dyspnea and cyanosis?

A

idiopathic pulmonary fibrosis, it also produces bilateral/patchy interstitial fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Who will most likely develop idiopathic pulmonary fibrosis?

A

men > 60 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the hypothesis for idiopathic pulmonary fibrosis?

A

repeated endothelial activation

faulty repair –> progressive fibrosis

53
Q

What produces pneumoconiosis?

A

inhalation of particulates – MC workplace exposures

pulmonary alveolar macrophages create fibrosis

54
Q

What are the types of pneumoconioses?

A

Coal dust

silica

asbestos

55
Q

Which of the three pneumoconiosis does NOT increase risk of lung cancer?

A

Coal dust/coal workers pneumoconiosis

56
Q

Silicosis can be caused by what occupations?

A

sandblasting

rock mining

rock quarries

ceramics

cutting stone

57
Q

What is the most common pneumoconiosis worldwide?

A

silicosis

58
Q

What pneumoconiosis increases the risk for malignant mesothelioma?

A

Asbestosis

59
Q

What professions cause asbestosis?

A

asbestos insulation

mining

milling

60
Q

What are the types of coal workers pneumoconiosis?

A
  1. Anthracosis
  2. Simple coal worker’s pneumoconiosis (CWP)
  3. Progressive massive fibrosis
61
Q

What is anthracosis? Who’s most at risk?

A

pigment accumulates in lungs

NO inflammation or dysfunction

asymptomatic

Most city dwellers & smokers are at risk

62
Q

What is simple coal worker’s pneumoconiosis? What is the hallmark?

A

Macrophages and little-to-no dysfunction

Hallmark is coal macules & nodules

63
Q

What is progressive massive fibrosis? What can it lead to?

A

massive black scars

extensive fibrosis and decreased lung function

pulmonary HTN leads to cor pulmonale

64
Q

What part of the lung does coal workers pneumoconiosis affect?

A

MC affects the upper lobes

65
Q

What is both the MC occupational disease worldwide and the MC pneumoconiosis?

A

silicosis

66
Q

Why does silicosis cause so much damage?

A

the inhalation of silica crystals (quartz) activates macrophages and increases ROS

67
Q

what does silicosis increase the risk of?

A

TB and lung CA

68
Q

What does silicosis destroy?

A

alveoli which leads to hypoxia

nodular scarring occurs

pulmonary HTN and cor pulmonale

69
Q

where in the lungs does silicosis occur?

A

in the upper lung near hilar lymph nodes

70
Q

How is silicosis most likely detected?

A

MC detected on routine x-ray of asymptomatic patients

71
Q

Which pneumoconiosis has whorled appearance on histology?

A

silicosis

72
Q

Asbestos exposure may cause:

A

fibrotic pleural plaques (MC)

mesothelioma

73
Q

Which pneumoconiosis has interstitial fibrosis, failed phagocytosis and progressive dyspnea and cough?

A

Asbestosis

74
Q

where does asbestosis occur in the lung?

A

begins in the lower lungs/pleura

75
Q

ferruginous bodies are associated with what?

A

asbestosis, they are remants of asbestos that was failed to be phagocytized

76
Q

Asbestosis increases the risk of what cancers?

A

bronchogenic cancer

mesothelioma

77
Q

What is the hallmark of sarcoidosis?

A

noncaseating granulomas!!

affects hilar lymph nodes (lungs)

affects skin: erythema nodosum

78
Q

T/F: Sarcoidosis is a multisystem inflammatory disorder

A

true, affects lungs, skin, eyes, liver, spleen

79
Q

What’s another name for sarcoidosis?

A

bilateral hilar lymphadenopathy

80
Q

what populations is sarcoidosis MC in?

A

african americans

young adults 20-40 years

MC among non-smokers

81
Q

Do people with sarcoidosis typically recover?

A

yep, 70% recover

82
Q

what are most pulmonawry emboli caused by?

A

95% from DVT

83
Q

T/F: only 20-30% of pulmonary emboli are diagnosed prior to death

A

True– there are a small amount that are small enough not to kill you but big enough to cause symptoms

84
Q

Consequences of pulmonary emboli

A

depend on size

  1. increase pulmonary artery pressure–HTN
  2. tissue ischemia & infarction
85
Q

sudden pulmonary HTN causes….

A

diminished cardiac output –>acute cor pulmonale –>hypoxia/death

cardiogenic shock

86
Q

T/F: infarction from embolus is quite common

A

FALSE– infarction from embolus is RARE

87
Q

What has dula blood supply?

A

pulmonary & bronchial arteries

88
Q

What is a large pulmonary embolism referred to as?

A

a saddle embolism

occlusion of >or equal to 60% of pulmonary arterial supply

89
Q

What percentage of PE are clinically silent?

A

60-80%

90
Q

What arteries sustain lungs?

A

bronchial arteries

91
Q

infarction caused by a pulmonary embolism is referred to

A

hemorrhagic: it is raised and red-blue

92
Q

What are the symptoms of non clinically silent pulmonary emboli?

A

MC: sudden onset dyspnea

chest pain worse with breathing

cyanosis

collapse

93
Q

pulmonary HTN is diagnosed as a systemic BP…

A

> or equal to 30/20

94
Q

Pulmonary HTN is MC secondary to what diseases?

What happens physiologically?

A

fibrosis, recurrent emboli and heart disease

decreased cross-sectional area of pulmonary vessels

increased blood volume due to a left-to-right shunt (VSD), congestion is secondary to mitral valve stenosis

95
Q

What age does pulmonary HTN develop?

A

any age

mechanisms vary by age: pulmonary or cardiac

96
Q

vascular alterations that can cause pulmonary HTN

A

atherosclerosis

smooth muscle hypertrophy

97
Q

what is primary pulmonary HTN?

A

when there is no pulmonary pathology

idiopathic

MC sporadic

98
Q

primary pulmonary HTN is caused by what? who’s it most common in?

A

endothelia dysfunction– smooth muscle cell proliferation

young adult females

99
Q

What are the symptoms of primary pulmonary HTN?

A

dyspnea, fatigue, exertional syncope, angina

possible severe respiratory insufficiency/cyanosis

cor pulmonale decompensation

poor prognosis

100
Q

What is diffuse alveolar hemorrhage syndrome?

A

a group of immune-mediated diseases– pulmonary hemorrhage

101
Q

What is the classic triad associated with diffuse alveolar hemorrhage syndrome?

A

hemoptysis (coughing up blood)

anemia

diffuse pulmonary edema

102
Q

Goodpasture syndrome is associated with what? what is it?

A

associated with classic DAHS

Lung & kidney involvement –type II hypersensitivity

progressive–hemoptysis & hematuria

anemia

103
Q

Does DAHS have granulomas or sinuses?

A

NOPE that’s Wegners

104
Q

What makes up 1/6 of all US death?

A

pulmonary infection

Pneumonia

105
Q

What are the sources of pulmonary infections?

A
  1. Contaminated air
  2. Aspiration of nasopharyngeal flora–alcoholics (Klebsiella pneumoniae)
  3. various comorbid lung pathologies
106
Q

What are some extrinsic factors that contribue to pulmonary infections?

A

smoking: decreases mucociliary clearance & decreases immune cell mobilization

Alcohol: decreases cough & epiglottic reflexes

107
Q

What are some intrinsic factors that contribute to pulmonary infections?

A

defects in cell-mediated immunity

defects in humoral immunity

108
Q

Where does pneumonia infections most commonly occur within the lungs?

A

withing the alveoli

109
Q

What are the two types of acute bacterial pneumonia?

A
  1. Bronchopneumonia– multiple lobes
  2. lobar pneumonia– one lobe
110
Q

90% of lobar pneumonia results from infection with what organism?

A

Strep. pneumoniae

111
Q

What is community acquired acute pneumonia? what is the main symptom?

Who acquires it?

A

**MC bacterial: strep. pneumoniae **

not recently hospitalized

mucopurulent sputum: yellow-greenish sputum

acquired by high-risk patients: diabetes, CHF, COPD, immunosuppressed, those with decreased/absent splenic function

112
Q

How does community acquired acute pneumonia typically present itself on xray?

What organism causes community-acquired acute pneumonia?

A

lobar

Strep. pneumoniae

113
Q

What are the additional community acquired pneumoniae besides Strep. pneumoniae?

A
  1. *Staph. aureus: *secondary viral URTI, children (MC)
  2. Klebsiella pneumoniae: alcoholics/debilitated
  3. Pseudomonas aeruginosa: secondary to burns, chemo and cystic fibrosis
  4. *Leginella pneumophila: *aquatic–inhalation or aspiration
114
Q

What are the two community-acquired acute pneumonia caused by Legionella pneumophila?

A
  1. Legionnaire disease– aggressive, possible hospitalization, immunocompromised
  2. Pontiac Fever– limited to an URTI, NO lung involvement, spontaneously resolves
115
Q
A
116
Q
A

Acute respiratory distress syndrome

117
Q
A

Asbestosis

118
Q
A

Bronchiectasis

119
Q
A

Chronic interstitial lung diseases

120
Q
A

coal workers pneumoconiosis

121
Q
A

Emphysema

122
Q
A

Ferruginous body, asbestosis

123
Q
A

silicosis

124
Q
A

whorled appearance

silicosis

125
Q
A

picture on right is emphysema

126
Q
A

centriacinar emphysema

127
Q
A

panacinar emphysema

128
Q
A

Pathology II PCC (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions