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pulmonary pathology Flashcards

1
Q

Structure Of The Lung

A
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2
Q

bronchioles/lobe number for R/L lung, anlge?
importance?

A

3 for R and 2 for L
R bronchus is also more vertical: means that inspried object more liley to go right

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3
Q

compoents of trachea/ brocnhus

A

cartilage
and glands

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4
Q

bronchiole components

A

lack
cartilage and glands,
has smooth muscle for bronchoconstriction/dialtion

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5
Q

components of the alveolar wall

A

type 1 and 2 pneumocytes and pores of kohn

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6
Q
  • Type I pneumocyte –
A

flattened alveolar
lining cell

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7
Q
  • Type II pneumocyte – functions
A

surfactant, repair

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8
Q

pores of kohn allow?

A

passage of exudate between alveoli

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9
Q

IS cell found in alveoli?

A

alveolar macrophage

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10
Q

Surfactant

A

Surface active agent –reduces surface
tension

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11
Q

type 2 pneumo development, without this

A
  • Type II pneumocytes by 27-28th weeks of gestation
  • without this Hyaline membrane disease can occur and be fatal
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12
Q

Pleura

A
  • Visceral pleura (inner)
  • Parietal pleura (outer)
  • Mesothelial lining created by this
  • Pleural space –a potential space
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13
Q

implication?

pain receptors at lung/pleura

A
  • Pleura –pain receptors
  • Lung –few pain receptors
  • Pain is not a part of lung disease until the pleura is involved
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14
Q

lymphatics at lung

A

very rich, metatsis likely

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15
Q

forms?

Atelectasis

A

Collapsed Lung
* Resorption– Obstruction prevents air from reaching distal airway
* Compression– Fluid within pleural cavity
* Contraction– Local or generalized fibrotic changes

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16
Q

Scoliosis and Kyphosis pul effects

A

can add P onto lungs and reduce function

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17
Q

COPD

A

combination of two diseases: chronic bronchitis and emphysema

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18
Q

chronic inflamm where? resistance to?

  • Chronic bronchitis –
A

chronic inflammation of bronchi
–increases resistance to the outflow of air

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19
Q

Emphysema

A

destruction of elastic tissue, loss of surface area
–reduces the elastic recoil of the lung
and surface area

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20
Q

common in? rare in?

Chronic Obstructive
Pulmonary Disease

A
  • Common in cigarette smokers
  • Rare in non-smokers
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21
Q

portion of airway affected by chronic bronchitis?

A

proximal?

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22
Q

portion of airway affected by emphysema

A

distal

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23
Q

Pure Chronic Bronchitis vs
Pure Chronic Emphysema

A
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24
Q

clinical def of chronic bronchitis

A

persistent productive cough for 3 consecutive months in 2 consecutive years

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25
Q

forms of chronic brochitis

A

simple
asthmatic
obstructive

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26
Q

Simple chronic bronchitis

A

–airflow not obstructed

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27
Q

Chronic asthmatic bronchitis

A

–hyperreactive airways with bronchospasm and wheezing

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28
Q

Chronic obstructive bronchitis

A

chronic outflow obstruction

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29
Q

histo effects of chronic bronchitis

A

squamous metaplasia and thickening of the mucus layer

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30
Q

Chronic Bronchitis
* Inspiration vs Expiration

A
  • Inspiration –easy
  • Expiration - difficult
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31
Q

Emphysema

A
  • Abnormal permanent enlargement of the air spaces
  • Destruction of alveolar walls without fibrosis
  • Reduction in surface area for gas exchange
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32
Q

forms of emphysema

A

centrilobular and panacinar

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33
Q

centrilobular emphysema

A

affects res bronchiole
* Typically seen in
cigarette smokers

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34
Q

centrilobular emphysema

A

affects res bronchiole
* Typically seen in
cigarette smokers

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35
Q

panacinar emphysema

A

affect alveolus
* Most commonly seen in Alpha-1 Anti-trypsin Deficiency
* Seen in people without risk factors (smoking)

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36
Q

Alpha-1 Antitrypsin Deficiency

A
  • Causes a rare form of emphysema –panacinar emphysema
  • Protease-antiprotease imbalance
  • Oxidant-antioxidant imbalance
  • A1AT is anti-protease synthesized in the liver
  • A1AT scavenges proteases released by inflammatory cells (polys and macrophages)
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37
Q

COPD –“Pink Puffer” due to

A

Predominance of Emphysema

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38
Q

COPD –“Blue Bloater” due to

A

Predominance of Chronic Bronchitis

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39
Q

Bronchiectasis

A
  • A secondary disease; not a primary disease
  • Permanent dilation of bronchi and bronchioles caused by destruction of muscle and supporting tissue resulting from chronic necrotizing infections
  • Cough and expectoration of copious amounts of purulent sputum
    seen with CF
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40
Q

Brochial Asthma
symptoms?
diff with?
bronchi?
time frame?
tx?
Status asthmaticus?

A
  • Severe dyspnea with wheezing
  • Difficulty with expiration
  • Bronchi constricted and filled with mucin and debris
  • Attacks last from one to several hours
  • Subside spontaneously or with therapy –usually bronchodilators and corticosteroids
  • Status asthmaticus –a severe paroxysm that does not respond to therapy and persists
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41
Q

what occurs in the airway with brochial asthma

A
  • Mucus accumulation
  • Goblet cell hyperplasia
  • Hypertrophy of submucosalmucous glands
  • Chronic inflammation
  • Basement membrane thickening
  • Smooth muscle cell hypertrophy and hyperplasia
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42
Q

Allergic Asthma
type od dx?
obstruction?
inflamm/cells involved?
smooth mm?

A
  • Allergic disease - repeated immediate hypersensitivity and late phase reactions
  • Intermittent and reversible airway obstruction
  • Chronic bronchial inflammation with eosinophils
  • Bronchial smooth muscle hypertrophy and hyper-reactivity
43
Q

Drug-Induced Asthma
what drug?
seen in?

A
  • Aspirin sensitivity –aspirin induces asthma attack
  • seen in pts with History of recurrent rhinitis, nasal polyps, urticaria and bronchospasm
44
Q

Metastatic Disease at lungs
* frequent site?
* The most common lung tumor?
* Lung metastases are present in about ______of all cancer deaths

A

Metastatic Disease
* The lungs are a frequent site of metastatic disease
* The most common lung tumor is metastatic
* Lung metastases are present in about 1/3 of all cancer deaths

45
Q

why are metasises so common at lung

A

Metastases to the lungs are more common even than primary lung neoplasms simply because so many other primary tumors can metastasize to the lungs

46
Q

carcinoma/sarcoma routes to lung

A
  • Carcinomas usually metastasize via the lymphatics
  • Sarcomas frequently metastasize via the hematogenous route
47
Q

Therapeutic Classification of
Bronchogenic Carcinoma

A
  • Small cell carcinoma (NE cells)
  • Non-small cell carcinoma (epi cells)
    both classes respond to dif tx
48
Q

Pathologic Classification of
Bronchogenic Carcinoma

A
  • Squamous cell carcinoma
  • Adenocarcinoma
  • Small cell carcinoma (oat cell carcinoma)
  • Large cell undifferentiated carcinoma
49
Q

Squamous Cell Carcinoma
* Most often seen in?
* Arises from where in lung?
* precursor lesion?
* Prognosis depends on?

A
  • Most often seen in cigarette smokers
  • Arises centrally from main bronchi close to the bifurcation
  • Squamous metaplasia precursor lesion
  • Prognosis depends on the stage
50
Q

Squamous Metaplasia of Columnar,
Ciliated Respiratory Epithelium

A
  • Smoking causes squamous metaplasia of respiratory epithelium
  • Creates “dead spots” in mucociliary escalator
  • Creates “fertile soil” for development of epithelial dysplasia leading to squamous cell carcinoma (most common type of bronchogenic carcinoma in smokers)
51
Q

Precursor Lesions of Bronchogenic
Squamous Cell Carcinoma

A
52
Q

what pigment can be seen with SCC

A

anthrcotic in the lesion due to smoke

53
Q

Small Cell Carcinoma
(Oat Cell Carcinoma)
* Arise where in lung?
* Aggressive?
* tx?
* origin?
* Frequent association with?

A
  • Arise centrally
  • Aggressive –metastasize early and widely, poor prognosis
  • Chemotherapy
  • Neuroendocrine origin
  • Frequent association with smoking
54
Q

pigmentation of oat cell carcinoma

A

can still see antrascotic pigment of lesion

55
Q

small cell carcinoma can cause ulceration where?

A

can see neutropenic ulceration in the oral cavity

56
Q

Adenocarcinomas arise where in lung

A

Arises peripherally in lung

57
Q

Large Cell Carcinoma

A
  • Undifferentiated epithelial tumors that lack the cytologic features of small cell carcinoma and glandular or squamous differentiation
  • poorly differentiated large cells= diagnosis of exclusion
  • can arise centrally of peripherally
58
Q

Bronchial Carcinoid
* origin?
* tx?

A
  • Neuroendocrine cell origin
  • Often resectable and curable
59
Q

Mass Effects of Lung Cancer

A
  • Obstruction (atelectasis)
  • Superior vena cava syndrome
  • Pancoast syndrome
  • Horner syndrome
60
Q

Superior Vena Cava Syndrome
* Obstruction of?
* Impaired?
* Edema and congestion?
* Upper extremity veins?

A
  • Obstruction of superior vena cava
  • Impaired venous return from the head and neck
  • Edema and congestion of face, neck and upper chest
  • Upper extremity veins fail to empty on elevation
61
Q

Horner Syndrome
* eyes?
* eyelid?
* pupils
* sweating?

A

Compression of the sympathetic
nerves to head and neck causing:
* Enophthalmos –retraction of
globe
* Ptosis of the upper eyelid
* Miosis - Pupillary constriction
* Anhidrosis –lack of sweating

62
Q

Pancoast Syndrome

A
  • Compression of the lower cervical and upper thoracic nerves causing shoulder pain radiating down the arm
63
Q

potnetial forms?

paraneoplasitc syndromes of lung cancer

A

Well Known for Causing Paraneoplastic Syndromes
* Small cell carcinoma –frequent ectopic hormone production

  • Cushing syndrome - ectopic secretion of an ACTH-like hormone
    – Patients present with Cushing syndrome
  • Hyperparathyroidism - ectopic secretion of a parathyroid-like hormone
    – Patients present with symptoms of hyperparathyroidism –parathyroids normal
64
Q

airway? metasis? paraneo? SVC? horner?

Effects of Bronchogenic Carcinoma
Summation

A
  • Local mass effects by blockage of airway
  • Metastasis
  • Paraneoplastic syndromes
  • Superior vena syndrome
  • Horner syndrome
65
Q

also increased risk of?

Mesothelioma

A

Mesothelioma
* Malignant neoplasm of pleura (pain occurs) associated with environmental asbestos exposure
* Asbestos also increases risk for squamous cell
carcinoma as well as mesothelioma

66
Q

Pulmonary Hamartoma

A

hyperproduction of lung tissue, benign

67
Q

Traditional Classification of
Pneumonia by Anatomic Distribution

A
  • classified based on Pattern of lung involvement
  • Bronchopneumonia –patchy involvement
  • Lobar pneumonia –entire lobe involved
68
Q

types of pneumonia?

A

lobular pneumonia

69
Q

Classification of Pneumonia by
Etiologic Agent or Clinical Setting

A
  • Specific etiologic agent –e.g. Streptococcus pneumoniae
  • Clinical setting
    – Community-acquired pneumonia
    – Nosocomial pneumonia (in hospital)
    – Aspiration pneumonia
    – Chronic pneumonia
    – Pneumonia in the immunocompromised host
70
Q

Pneumonia in Immunocompromised
Individuals spp?

A
  • Pneumocystis jiroveci(older name: Pneumocystis carinii)– Fungal organism of very low virulence in
    immunocompetent individials
  • Mycobacterium avium intracellulare (MAI)
71
Q

possible agents of pneumonia

A
  • Bacterial
  • Viral
  • Other
72
Q

bacterial agents of pneumonia

A

– Streptococcus pneumoniae
– Klebsiella pneumoniae
– Staphylococcus aureus
– Streptococcus pyogenes
– Legionella pneumophilia

73
Q

other agents of pneumonia

A

– Mycoplasma
– Chlamydia psittaci (psittacosis –parrot fever)

74
Q

viral agents of pneumonia

A

– Cytomegalovirus
– Roseola (measles)
– Varicella (chickenpox)

75
Q

Pneumonia in AIDS

A
  • AIDS patients are susceptible to all forms of pneumonia
  • Pneumocystis carinii pneumonia (PCP)
    – AIDS patients especially vulnerable to Pneumocystis carinii pneumonia (PCP)
    – Reclassified from a protozoan to a fungus
    – Name changed to Pneumocystis jiroveci
76
Q

Tuberculosis
caused by?
AIDS?
transmission?
inital lesion where? name?
course of events?

A
  • Caused by Mycobacterium tuberculosis hominis or bovis
  • In AIDS patients, Mycobacterium avium-intracellulare is a common pathogen
  • Transmitted from person-to-person by aerosolized droplets during coughing, sneezing and talking
  • Initial lesion in lung (Gohn focus/complex)
  • Following exposure the course of events is variable - may disseminate and cause systemic involvement
77
Q

Primary Tuberculosis histology

A
  • Granulomas form in the periphery of the lung
    (Gohn focus) followed by Gohn complex
  • The classic lesion is a caseating granuloma –a
    collection of activated macrophages (epitheliod
    histiocytes), sensitized lymphocytes, multinucleated giant cells and a collar of fibroblasts
78
Q
A

gohn complex of TB

79
Q

what necrosis occurs with TB

A

caseous

80
Q

Secondary Tuberculosis
* Lesions classically appear where? how?
* the result of?
* triggered by?

A
  • Lesions classically appear at the apices of the lungs and are cavitary
  • This form of tuberculosis usually is the result of reactivation of dormant organisms in old, silent lesions of primary tuberculosis
  • Reactivation is usually triggered by immunosuppression
81
Q
A

milliary tuberculosis of the spleen, can occur with dessimination thru lymphatics

82
Q

Pneumoconioses

A

Lung scarring from inhaled particulate matter

83
Q

forms of Pneumoconioses

A
  • Silicosis –silica
  • Asbestosis –asbestos
  • Berylliosis –Beryllium
  • Anthracosis –coal dust: Coal worker’s pneumoconiosis, Black lung disease
84
Q

Silicosis increases risk of? what is seen in histo

A
  • Increased risk for tuberculosis= Silico-tuberculosis
  • silica crystal seen
85
Q

from? risk for? will form?

Asbestosis

A
  • Environmental hazard
  • Risk for mesothelioma
    forms a fibrous pleaural plaque
86
Q

progressive? what pigments are seen?

Coal Worker’s Pneumoconiosis

A
  • Black lung disease
  • Progressive massive fibrosis
    will see an anthracotic pigment
87
Q

IV drug use Lung effect

A

Talc Crystals form in Lung

88
Q

Nasopharyngeal Carcinoma
* Strong epidemiologic link?
* High frequency in?
* Three histologic variants?
* variant most common?
* Radiosensitive?

A
  • Strong epidemiologic link to Epstein Barr
    virus
  • High frequency in Chinese
  • Three histologic variants:
    – Keratinizing SCCa
    – Non-keratinizing SCCa
    – Undifferentiated carcinoma
  • Undifferentiated carcinoma variant most
    common
    – “Lymphoepithelioma” (a misnomer) due
    to the influx of mature lymphocytes
  • Radiosensitive –50% 5-year survival rate
89
Q

what dx are associated with HHV-4

A
  1. Infectious Mononucleosis
  2. Lymphomas –NHL and HL
    e.g. Burkitt lymphoma (NHL)
  3. Nasopharyngeal Carcinoma
  4. Oral Hairy Leukoplakia
90
Q

Most common presenting symptom of laryngeal lesions is?

A

Most common presenting symptom of laryngeal lesions is hoarseness

91
Q

hoarseness of larynx seen with

A

Vocal cord nodules (singer’s nodes, polyps) –chronic irritation
* Laryngeal papillomas –squamous papilloma - HPV

92
Q

squamous? recurrent? inherited?

  • Laryngeal papillomas
A

Squamous papilloma - HPV
– Solitary in adults
– Multiple in children

    • Recurrent respiratory papillomatosis (RRP)
    • HPV types 6 and 11 (vaccination) –vertical transmission from infected mother- Spontaneously regress at puberty
93
Q

demo? associated with? most common sign?

Laryngeal Squamous Cell Carcinoma

A
  • Adult males (7:1)
  • Strong association with cigarette smoking
  • Persistent hoarseness is most common symptom
94
Q

forms of laryngeal SCC

A

glottic
supraglottic
subglottic

95
Q

confined? when are symptoms? prognosis?

  • Glottic tumors
A
  • Glottic tumors (directly on vocal cords) most common
    – Most confined to larynx at diagnosis
    – Cause symptoms early in course of disease
    – Best prognosis –sparse lymphatics
96
Q
  • Supraglottic tumors
A
  • Supraglottic tumors (above the vocal cords)
    – Rich in lymphatics –likely to metastasize to regional (cervical) lymph nodes
97
Q
  • Subglottic tumors
A
  • Subglottic tumors (below the vocal cords) least common
    – Remain subclinical and present with advanced disease
98
Q

Toxic Pulmonary Effects of
Chemotherapy

A

Pulmonary Fibrosis will occur
* Pulmonary function tests (PFTs) normal at start of chemotherapy
* One year later PFTs, 19% of lung function remaining
* Continuous 100% oxygen therapy
* Confined to wheel chair

99
Q

where can lung cancer metastisize too that we will see?

A

oral cavity, gingiva

100
Q

what pul. fungal infection can be seen orally on occasion

A

histoplasmosis, diagnosed with biopsy, would see red dots in macrophages

101
Q

radiographic app of metasises in oral

A

presents as a luceny

102
Q

what sarcoma can be seen orally

A

karposi sarcoma

103
Q

how can this be avoided?

what oral infection can occur with corticosteroid inhalers?

A

candidasis, do not touch inhaler to mouth and rinse with water after use

Pathology (19 decks)

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