Chapter 15 - The Lung Flashcards

0
Q

Type of pneumocyte that makes surfactant

A

Type II

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1
Q

Causes of pulmonary hypoplasia

A
  • Compression
  • impede normal expansion
    1. oligohydramnios-not enough fluid to go in lungs and expand
    2. diaphragmatic hernia
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2
Q

Pneumocyte covering 95% of alveolar surface

A

Type I

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3
Q

Epithelium for most of respiratory tree & where is it not this?

A

Pseudostratified, tall, columnar, ciliated epithelial cells except for vocal cords (stratified squamous)

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4
Q
  • RESORPTION ATELECTASIS caused by? <– And what can cause this?
  • Reversible/irreversible?
  • Which way will mediastinum shift?
  • Why do alveoli collapse?
A
  • Complete obstruction of airway by mucous plugs post op, aspiration, neoplasms
  • shift towards affected lung
  • alveoli collapse because a lack of distal air and resorption of pre-existing trapped O2
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5
Q
  • COMPRESSION ATELECTASIS caused by?
  • why do alveoli collapse?
  • which way does the mediastinum shift?
  • reversible/irreversible?
A
  • pleural cavity is partially or completely filled by exudate, tumor, blood, air
  • pressure collapses small airways under the pleura
  • shifts away from affected lung
  • reversible
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6
Q
  • CONTRACTION ATELECTASIS caused by?

- reversible/ irreversible?

A
  • fibrotic changes cause prevent expansion

- irreversible :(

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7
Q

What are the 2 types of pulmonary edema?

A
  1. Hemodynamic pulmonary edema

2. Micro vascular injury

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9
Q

Hemodynamic pulmonary edema caused by and an example

A

Increased hydrostatic pressure, like left sided CHF

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10
Q
  • What do the lungs look like in hemodynamic edema grossly?

- histology?

A
  • heavy wet lungs
  • heart failure cells
  • alveolar capillaries engorged
  • intra-alveolar pink precipitate
  • eventually brown induration
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11
Q

Pathophysiology behind edema caused by microvascular injury

A

Primary injury to vascular endothelium/epithelial cells –> leakage of fluids and fluids into interstitial space –> leaks to alveoli –> can cause acute respiratory distress syndrome

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12
Q

Examples of edema caused by micro vascular injury

A

Infections (pneumonia, sepsis), aspiration, drugs

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13
Q

What is acute lung injury & and what’s it’s most severe form

A
  • Abrupt onset of hypoxemia and pulmonary lung infiltrates w/o cardiac failure
  • acute respiratory distress syndrome (ARDS)
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14
Q

Histology of ARDS

A

Diffuse alveolar damage, waxy hyaline membranes on alveoli

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15
Q

Pathophysiology of ARDS

A

Injury to endothelial/epithelial cells –> shift to pro-inflammatory state –> cytokine release –> neutrophil chemotaxis –> neutrophils damage alveolar epithelium –> dysregulation of coag system

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16
Q

Resolution and late findings in ARDS

A

Type II pneumocytes make surfactant and make more type I pneumocytes

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17
Q

Predisposing conditions to ARDS (10)

A

*Gram negative sepsis, *gastric aspiration, *trauma with shock, *pulmonary infections like SARS, heroin, smoke inhalation, acute pancreatitis, cardiopulmonary bypass, DIC, fat embolism

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18
Q

Physical findings for ARDS

A

Dyspnea, tachypnea, inspiratory infiltrates b/l, respiratory acidosis, unresponsive to O2, V/Q mismatch

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19
Q

Obstructive Lung Diseases (4) can’t get air in/out?

A

Can’t get air out:

  1. Bronchitis
  2. Bronchi ecstasies
  3. Asthma
  4. Emphysema
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20
Q

Types of emphysema (4)

A
  1. Centriacinar
  2. Panacinar
  3. Paraseptal
  4. Irregular
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21
Q

CENTIACINAR

  • What part does this affect
  • associated with what
  • what lobe
A
  • central/proximal acini
  • associated with smokers
  • upper lobes
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22
Q

PANACINAR

  • what part of alveoli?
  • associated with?
  • what part of lung
A
  • whole acinus from bronchioles to terminal alveoli
  • associated with alpha 1-anti trypsin deficiency
  • lower lung
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23
Q

Pathophysiology of emphysema

A

Cigarette smoke –> chemotactic for neutrophils and creates free radicals –> inactivates antiproteases (functional alpha1 antitrypsin deficiency) –> increase in neutrophil elastase <– congenital alpha1 antitrypsin deficiency

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24
Q

Genes involved in alpha1 antitrypsin deficiency!?!

A

Normal M allele and homozygous ZZ allele which has an 80% chance of getting Panacinar emphysema

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25
Q

What are some symptoms of emphysema and when do they begin?

A
  • Dyspnea, coughing, wheezing, weight loss, barrel-chested, hunched over, breathing through pursed lips
  • clinical manifestations begin when at least 1/3 of pulmonary parenchyma is damaged
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26
Q

Where does para septal emphysema occur? Does it produce COPD? What is there an increase risk of?

A
  • distal acini
  • no COPD
  • increased risk of spontaneous pneumothorax with rupture of us pleural blebs
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27
Q

IRREGULAR EMPHYSEMA:

  • associated with?
  • COPD?
A
  • associated with scar tissue

- no COPD

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28
Q

CHRONIC BRONCHITIS definition?

A

Productive cough for at least 3 months for 2 years

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29
Q

Pathophysiology of chronic bronchitis

A

Irritation –> hypersecretion of mucous–> alterations in small airways of the lung, fibrosis

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30
Q

Histology of chronic bronchitis

A

Mucous gland hyperplasia in trachea + bronchi, Reid index of wall thickness to mucous gland layer (normal 0.4), goblet cell metaplasia

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31
Q

Long term Chronic bronchitis can lead to: (3)

A
  1. COPD
  2. Cor pulmonale and heart failure
  3. Atypical metaplasia/dysplasia (pre-cancerous)
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32
Q

Pink puffers

A

Emphysema

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33
Q

Blue bloaters

A

Chronic bronchitis

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34
Q

Symptoms of chronic bronchitis

A

Other than chronic sputum, dyspnea on exertion

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35
Q

Most common respiratory disease in kids

A

Asthma

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36
Q

Asthma with IgE mediated hypersensitivity, what will be a positive test

A

Atopic asthma, allergen sensitization, skin reaction positive

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37
Q

Asthma with no allergen sensitization and negative skin test result. What is its common trigger

A

Non-atopic asthma, viral respiratory infection

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38
Q

Pathophysiology of atopic asthma:

A

Initial sensitization –> IL-4 (switch to IgE) and IL-5 ( eosinophil chemotaxis) –> release mediators–> bronchoconstriction, mucous, leukocytes –> late phase 4-8 hours –> eotaxin (for eosinophils) –> eosinophils release mbp and damage epithelial cells and constrict airway

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39
Q

Status astmaticus

A

Unremitting attacks that result in fatality

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40
Q

Histology of asthma: (4)

A

Mucous plugs (curschmann spirals), eosinophils, Charcot Leyden crystals, airway remodeling

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41
Q

What is bronchiectasis? What does it destroy

A

Permanent dilatation of bronchi and bronchioles, destruction of cartilage and elastic tissue

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42
Q

What causes bronchiectasis? (4)

A

Cystic fibrosis, infections (TB is most common), bronchial obstruction (like a carcinoma), primary ciliary dyskinesia, aspergillosis

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43
Q

What is primary ciliary dyskinesia?

A

Absent dynein (ATPase for movement) arm in cilia, often have kartagener syndrome with it

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44
Q

What part of lungs does bronchiectasis affect

A

Lower lobes

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45
Q

Histology of bronchiectasis

A

Very dilated airways

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46
Q

Symptoms of bronchiectasis:

A

So much foul smelling sputum!, hemoptysis, dyspnea, orthopnea

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47
Q

Complication of bronchiectasis

A

Cor pulmonale

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48
Q

Causes of restrictive lung disorders (2)

A

Chest wall disorders, interstitial and infiltration diseases

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49
Q

Clinical and pulmonary symptoms of restrictive disease (5)

A

Dyspnea, tachypnea, end inspiratory crackles, b/l infiltrative lesions (nodules, irregular lines, ground-glass shadows), honeycomb lung (fibrosis in advanced stage)

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50
Q

What age group has interstitial pulmonary fibrosis?

A

40-70

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51
Q

Pathogensis of idiopathic pulmonary fibrosis

A

Unknown agent –> repeated cycles of epithelial injury/activation –> cytokine release –> alveolar interstitial fibrosis –> proximal dilation of small airways

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52
Q

Histology and gross morphology of lung in idiopathic pulmonary fibrosis

A

Usual interstitial pneumonia (patchy interstitial fibrosis), honeycomb fibrosis , grossly cobblestoned lung

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53
Q

What part of lung is affected in idiopathic pulmonary fibrosis

A

Lower lobes

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54
Q

what are heart failure cells?

A

Hemosiderin laden macrophages

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55
Q

Symptoms of idiopathic pulmonary fibrosis (3)

A

Dyspnea on exertion, dry cough, cyanosis/clubbing (late)

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56
Q

What are Masson bodies and in what disease can you find them?

A

Polyploid plugs of loose connective tissue in cryptogemic organizing pneumonia

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57
Q

Connective tissue diseases with pulmonary involvement (3)

A
  1. Rheumatoid arthritis
  2. Systemic sclerosis
  3. Lupus erythematosus
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58
Q

Characteristics of the lung in rheumatoid arthritis

A

Interstitial fibrosis with or without rheumatoid nodules, chronic pleuritic with or without effusion

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59
Q

4 main causes of pneumoconiosis

A
  1. Coal dust
  2. Silica
  3. Asbestos
  4. Beryllium
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60
Q

Most dangerous particle size in pneumonconiosis

A

1-5 micrometers –> reach terminal airways and sacs. If they are smaller than this they can reach the alveoli and be phagocytosis by the macrophages

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61
Q

Which is the mildest form of coal workers pneumoconiosis

A

Anthracosis

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62
Q

What size buildup in simple coal workers pneumoconiosis and what part of lung does it affect

A

1-2mm coal macules and larger coal nodules in upper lobes and upper portions of lower lobes

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63
Q

What can simple coal workers pneumoconiosis lead to

A

Centriacinar emphysema if coal deposits adjacent to respiratory bronchioles

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64
Q

Size of coal deposits in complicated coal workers pneumoconiosis, and what may happen in the middle of these deposits

A

Blackened scars greater than 2 cm, usually have a necrotic center

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65
Q

What can complicated coal workers pneumoconiosis lead to: (2)

A

Pulmonary HTN and cor pulmonale

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66
Q

What is the most common occupational disease in the world

A

Silicosis

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67
Q

What deposits in silicosis and where in lung

A

Crystalline silicone dioxide (Quartz), upper lung

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68
Q

Pathophysiology of silicosis

A

Macrophages eat the quartz and it causes them to release cytokines which stimulate fibrosis

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69
Q

What 2 things do you see on radiography in advanced silicosis

A

Nodular opacities that progress to hard collagenous scars and eggshell calcifications in hilar nodes

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70
Q

What disease is associated with silicosis

A

Increased susceptibility to tuberculosis

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71
Q

What 2 geometric forms of asbestos are there and what do they look like

A

Serpentine (curly and flexible) and amphibole (straight and rigid)

72
Q

Serpentine and Amphibole forms of asbestosis is associated with what diseases

A

Interstitial fibrosis (both), lung cancer (both), and mesothelioma (only amphibole form)

73
Q

What histology is associated with asbestosis (3)

A

Ferruginous bodies and asbestos bodies pleural plaques (most common)

74
Q

What are asbestos bodies

A

Golden brown beaded rods with a translucent center that consist of asbestos fibers coated with iron

75
Q

Asbestos related diseases (4)

A

Pleural plaques, diffuse interstitial fibrosis, bronchogenic carcinoma (risk lowers with smoking cessation), mesothelioma (not associated with smoking)

76
Q

What is berylliosis associated with

A

Nuclear aerospace industry

77
Q

Risks with berylliosis

A

Lung cancer, interstitial fibrosis with noncaseating granulomas

78
Q

Drugs associated with pulmonary disease (4)

A

Bleomycin, amiodarone, methotrexate, nitrofurantoin

79
Q

When can you get radiation induced lung disease and what can it turn into

A

1-6 months after radiation therapy –> chronic radiation pneumonitis

80
Q

Sarcoidosis etiology and is the pathologic finding

A

Unknown and non cascading grannnnnnuloooommaaaaas

81
Q

Pathophysiology of sarcoidosis

A

Cd4 th T cells interact with unknown Ag –> cytokine release –> non-case acting granulomas

82
Q

How do you diagnose sarcoidosis

A

Exclusion

83
Q

What are found in the granulomas of sarcoidosis and where are the granulomas in the lung located

A

Giant cells with Schaumann bodies (lamellar end calcium) and stellar inclusions (asteroid bodies), you find them in the interstitial and mediastinal and hilar nodes

84
Q

Other than the lung, what other organs does sarcoidosis mainly effect

A

Skin, eye (uveitis), liver, pituitary, salivary/lacrimal glands, bone, spleen

85
Q

How does sarcoidosis resolve, and really serious cases can lead to

A

On its own, cor pulmonale and death

86
Q

Types of hypersensitivity pneumonitis and what are their pathogens

A
  1. Farmers lung (humid warm hay - thermophilic actinoycetes)
  2. Pigeon breeders lung (proteins from bird feathers and feces)
  3. Air conditioner lung (thermophilic bacteria in heated water reservoirs)
87
Q

What histology do you find in hypersensitivity pneumonitis

A

Noncaseating granulomas

88
Q

Most common cause of pulmonary embolism

A

Thrombosis of deep leg veins

89
Q

Risk factors for thromboembolism

A

Blood flow stasis (bed rest), hypercoaguable state

90
Q

Clinical consequences of pulmonary embolism

A

Saddle embolus (large embolus), pulmonary infarction

91
Q

What does the embolism look like

A

Wedge shaped infarct, apex towards lung

92
Q

How can you distinguish a pulmonary embolus from a post mortem clot

A

Lines of Zahn in the thrombus

93
Q

You try CPR with pulmonary embolism and what happens

A

EKG will show activity but no pulses because no blood in pulmonary circulation

94
Q

Pulmonary embolism can lead to…

A

Cor pulmonale, pulmonary HTN, increased risk of another infarct (30%)

95
Q

Definition of pulmonary HTN

A

Pulmonary pressure reaches 1/4 of systolic levels

96
Q

Types of pulmonary HTN

A

Primary (mutation in BMPR-2,TGF-beta) or secondary (endothelial cell dysfunction)

97
Q

Diseases associated with pulmonary hypertension

A

COPD, heart disease (mitral stenosis), thromboemboli, connective tissue disease, obstructive sleep apnea

98
Q

Histology with pulmonary HTN

A

Medial hypertrophy of muscular and elastic arteries, plexiform lesions (tuft of capillaries)

99
Q

Good pasture syndrome etiology

A

Autoantibodies against collagen IV (basement membrane)

100
Q

What part of organs does good pasture syndromes affect

A

Basement membranes –> glomerulonephritis and pneumonitis

101
Q

Histology of good pasture syndrome 1.kidney 2. Lung

A
  1. Heavy lungs with red brown consolidation and hemosiderin laden macrophages
  2. Crescents, immunoglobulin deposits
102
Q

Most common cause of death with good pasture syndrome

A

Uremia

103
Q

Wagner granulomagosis has what kind of granulomas

A

Scattered and poorly formed unlike in sarcoidosis

104
Q

Most common cause of typical community acquired pneumonia

A

Streptococcus pneumoniae

105
Q

Most common bacterial cause of acute exacerbation of COPD

A

Hemophilus influenzae

106
Q

Common cause of typical pneumonia in elderly

A

Moraxella catarrhalis

107
Q

Most common gram negative cause of lobar pneumonia

A

Klebsiella

108
Q

Pneumonia in alcoholics

A

Klebsiella

109
Q

Is strep pneum part of indigenous flora?

A

Yes nasopharynx

110
Q

Major cause of meningitis in kids

A

Hemophilus

111
Q

Three most common causes of otitis media in kids

A
  1. H. Influenzae, M. cattarrhalis, S. pneumoniae
112
Q

Pneumonia in drug users

A

Staphylococcus aureus

113
Q

Characteristic sputum of klebsiella

A

Thick gelatinous currant jelly sputum

114
Q

Pneumonia in cystic fibrosis

A

Pseudomonas aeruginosa

115
Q

Organ transplant recipients are susceptible to pneumonia by what

A

Legionella

116
Q

Where does legionella thrive

A

Aquatic environments, ie water cooling towers

117
Q

What type of pneumonia?

  1. Patchy consolidation
  2. Consolidated areas of acute suppurative inflammation
A

Bronchopneumonia

118
Q

What type of pneumonia?

1. Fibrinosuppurative consolidation of large portion of lobe

A

Lobar pneumonia

119
Q

Stages of inflammation in lobar pneumonia (4)

A
  1. Congestion (heavy boggy lung)
  2. Red hepatization (neutrophils and RBCs)
  3. Gray hepatization (fibrinosuppurative exudate)
  4. Resolution (digestion –> granular debris)
120
Q

Atypical pneumonia caused by

A

Viruses and mycoplasma and Chlamydia

121
Q

Some types of atypical pneumonia

A

Mycoplasma, influenzae, MPV (kids elderly immuno compromised), SARS (civet cats in china)

122
Q

Where is the inflammation in atypical pneumonias

A

Within walls of alveoli interstitially

123
Q

Common causes of hospital acquired pneumonia

A

Gram negative rods like pseudomonas and also staph aureus

124
Q

Who gets aspiration pneumonia

A

Alcoholics, comatose

125
Q

Histologic change in lung abscess

A

Suppurative destruction of lung parenchyma within the central area of cavitation

126
Q

3 causes of chronic pneumonia

A

Histoplasmosis, blastomycosis, coccidiodomycosis

127
Q

Geographical Location of histoplasmosis,
What part of lung does it attach to,
Histological appearance,
Vector

A

Ohio, MS, Caribbean
Intra cellular parasite of macrophages
Tree bark calcium yeast forms
Bird or bat droppings

128
Q

Where is blastomycosis found?
What part geographically?
Features of this bug

A

In soil in central nd southeast us

Suppurative granulomas, a yeast with thick double cell wall with lots of nuclei

129
Q

Where is coccidiodomycosis found, pathophysiology, vector,

A

Delayed type hypersensitivity, southwestern and western us, arthroconidia

130
Q

Most common cause of cancer mortality in the world

A

Lung cancer

131
Q

Most common cause of lung cancer

A

Cigarette smoking

132
Q

Other potential causes of lung cancer: (5)

A

Uranium, indoor air pollution (radon), asbestos, high dose ionizing radiation, second hand smoke

133
Q

Primary lung cancers in decreasing incidence (5)

A

Adenocarcinoma, squamous cell carcinoma, small cell carcinoma, large cell carcinoma, bronchial carcinoid

134
Q

Lung cancers with the greatest relation to smoking

A

Squamous and small cell lung carcinomas

135
Q

Lung cancer with the weakest association to smoking

A

Adenocarcinoma

136
Q

Which lung cancers are most responsive to initial chemotherapy

A

Small cell carcinomas, as opposed to non small cell

137
Q

Which lung cancers are more likely to metastasize

A

Small cell carcinomas as opposed to non small cell carcinomas

138
Q

Most common type of lung cancer in women. This is also the most common in what other category of people

A

Adenocarcinoma, also most common lung cancer in non-smokers

139
Q

Where is an Adenocarcinoma located in the lung. Are they larger or smaller lesions?

A

Peripherally, smaller lesions (cigarette filters take away the larger carcinogens slowing the smaller ones to get into the periphery -rapid review)

140
Q

What Histologic characteristic do you see in adenocarcinoma

A

Glands/mucin

141
Q

Where does the carbon pigment end up in anthracosis

A

Interstitial tissue and hilar nodes

142
Q

What is a subtype of adenocarcinoma

A

Bronchioloalveolar carcinoma

143
Q

What cell type is found in bronchioloalveolar carcinoma and what are they composed of

A

Clara cells, mucin secreting

144
Q

What might bronchioloalveolar carcinoma on chest radiograph

A

Can look like lobar pneumonia

145
Q

What part of the lung does squamous cell carcinoma usually infect?

A

Central parts

146
Q

What does histology show for squamous cell carcinoma

A

Keratin pearls and intercellular bridges

147
Q

What lung carcinoma is most associated with the p53 mutation

A

Squamous cell carcinoma

148
Q

What can squamous cell carcinoma secrete? And what may it lead to?

A

PTH, hypercalcemia

149
Q

What type of cells are associated with small cell carcinoma

A

Kulchitsky cells (neuro endocrine)

150
Q

What part of the lung does small cell carcinoma affect

A

Central

151
Q

What may small cell carcinoma secrete

A

ADH or ACTH

152
Q

Why is small cell carcinoma so dangerous (2)

A

It’s rapidly growing and it metastasizes early

153
Q

What part of the lung does large cell carcinoma typically affect

A

Central or peripheral

154
Q

What do you see histologically with large cell carcinomas, what types of cells are associated

A

Nothing much because it is poorly differentiated, large nuclei in cells

155
Q

Symptoms associated with lung cancer (4)

A

Cough, weight loss, chest pain, dyspnea

156
Q

Common sites for lung metastasis in decreasing incidence

A

Hilar lymph nodes, adrenal gland, liver, brain, bone

157
Q

Is metastatic or primary lung tumor more common?

A

Metastatic

158
Q

Cancers most likely to metastasize to the lung

A

Breast, colon cancer, renal cell carcinoma

159
Q

What is a pancoast tumor

A

Cancer goes to extreme apex of the lung, destroys superior cervical ganglion resulting in ptosis, miosis, and anhydrosis

160
Q

What secondary pathology is possible from lung cancer

A

Pancoast tumor (sympathetic effects), superior vena cava syndrome, emphysema, Atelectasis, pleuritis, paraneoplastic syndromes

161
Q

What is lambert eaton syndrome

A

Antibodies against calcium channel in muscle that result in muscle weakness

162
Q

Which lung cancers have the better prognosis?

A

Adenocarcinoma and squamous cell

163
Q

What part of he lunch does a bronchial carcinoid tumor affect

A

Central or peripheral

164
Q

Where does a bronchial carcinoid originate from?

A

Neuroendocrine

165
Q

What kind of mass does a bronchial carcinoid form

A

Polyp like mass by the bronchus

166
Q

Collar button lesion associated with:

A

Carcinoid tumor of lung if it goes peripherally

167
Q

What is carcinoid syndrome

A

Intermittent attacks of diarrhea, flushing, and cyanosis

168
Q

Carcinoid tumor of lung is benign or malignant?

A

Benign

169
Q

Where is a bronchial harmatoma most likely located in

A

Peripheral 90% and central the rest of the time

170
Q

Why does spontaneous pneumothorax occur?

A

Rupture of a emphysematous bleb

171
Q

What kind of people does a spontaneous pneumothorax occur in, what will happen to the trachea

A

Young tall people, trachea shifts toward the affected lung

172
Q

What causes a tension pneumothorax

A

Penetrating injury

173
Q

Pathophysiology of tension pneumothorax, how do you treat it

A

A flap forms that allows air to enter during inhalation but does not let the air out –> need a chest tube

174
Q

Asbestos workers that also smoke are most likely to die from

A

Lung carcinoma, not mesothelioma

175
Q

Mesothelioma has the most correlation with

A

Asbestos exposure

176
Q

Cancer will arise in patients with asbestos exposure approximately how many years after exposure

A

20/25(lung carcinoma/mesothelioma) - 40 (for mesothelioma)

177
Q

Histology of bronchioloalveolar carcinoma, growth pattern

A

No invasion, grows along pre-existing structures without destruction of alveolar architecture –> Lepidic like butterflies on a fence (what?)