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MS1 Spring > Respiratory Facts > Flashcards

Respiratory Facts Flashcards

1
Q

Mild hemoptysis amount?

A

5 to 10cc in 24 hours

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2
Q

Moderate hemoptysis amount?

A

Up to 100cc in 24 hours

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3
Q

Massive hemoptysis amount?

A

100-200cc in 24 hours

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4
Q

Seven causes of hemoptysis?

A

Very ITchy ITCH makes you cough

Vascular
Inflammatory
Trauma
Infection
Tumor
Cardiac
Hematological
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5
Q

Infections that lead to hemoptysis?

A

Bronchiectasis, bronchitis, tuberculosis, lung abscess, CF

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6
Q

Vascular causes that lead to hemoptysis?

A

Pulmonary infarction, arteriovenous malformation

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7
Q

Causes of inflammation that leads to hemoptysis?

A

Wegener’s, Goodpasture, Diffuse alveolar hemorrhage

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8
Q

Cardiac causes that lead to hemoptysis?

A

Mitral valve disease, acute left ventricular failure

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9
Q

Hematological causes that lead to hemoptysis?

A

Blood dycrasias (aka blood disorder), anticoagulation

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10
Q

Which circulation to the lung is to blame for most hemoptysis?

A

Bronchial (high pressure, comes from left ventricle)

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11
Q

What is bronchiectasis?

A

Dilated airways

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12
Q

Key questions to ask about cough?

A

Onset, duration, character, nocturnal, precipitating factors, relieving factors, sputum, hemoptysis, association

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13
Q

How long must a cough last to be chronic?

A

More than 8 weeks

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14
Q

What causes chronic cough?

A

Pertussis, TB, foreign body, asthma, drugs, bronchiectasis, interstitial lung disease (ILD)

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15
Q

What causes a dry cough?

A

GERD, Drugs (like an ACE inhibitor), acute epiglotitis

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16
Q

When do asthmatics tend to cough more?

A

Night and early morning

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17
Q

What are usual precipitating factors of a cough in asthmatics?

A

Emotion, weather (rain, wind, cold), dust, allergies, exercise, drugs

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18
Q

What do you want to consider when assessing sputum?

A

Color, volume, consistency, pattern

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19
Q

What associations with a cough are important to know?

A

Breathlessness, sputum, chest pain, wheeze, hoarseness, post-nasal drip

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20
Q

What are the three most common causes of chronic cough?

A

Asthma, GERD, and post-nasal drip (aka upper airway cough syndrome)

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21
Q

An FEV1/FVC ratio below what is considered obstructive?

A

70%

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22
Q

In using spirometry to diagnose asthma, we want to see what % increase in FEV1/FVC after bronchodilator use in order to diagnose? What mL improvement in FVC or FEV1?

A

12% in FEV1/FVC

200 mL in FEV1 or FVC

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23
Q

If you suspect someone has asthma but their spirometry does not confirm this diagnosis, what test do you perform next?

A

Methacholine challenge test. Administer small amount of methacholine and test reactivity then administer bronchodilator and assess if there is rebound

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24
Q

How do you treat GERD?

A

Conservatively you have the patient stop smoking and/or elevate the head of their bed

Or antacid therapy like a proton pump inhibitor or an H2 blocker

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25
Q

How long can a person normally have a cough post-infection?

A

Up to six weeks

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26
Q

What is a D-dimer test?

A

Looks for a small protein present in the blood after a clot is degraded

Best negative predicative value for a PE

BUT if its negative and the clinical suspicion of a PE is high (i.e. high Wells score) then order the CT

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27
Q

What does a Wells score assess?

A

The clinical probability that a patient has a PE

  • 3 pts for clinical symptoms of a DVT
  • 3 pts for diagnosis less likely PE
  • 1.5 pts for immobilization for more than 3 days or surgery in the last 4 weeks
  • 1 .5 pts for previous DVT/PE
  • 1 pt for hemoptysis
  • 1 pt for malignancy
  • 1 pt for HR over 100bpm
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28
Q

What is the most common finding on EKG in a person with a PE?

A

Sinus tachycardia

or S1/Q3/T3 (I have no idea what this means)

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29
Q

What is cardiac tamponade?

A

Accumulation of fluid in the pericardial sack; can cause pulmonary edema

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30
Q

What do pleural effusions do to structures in the mediastinum?

A

Push away from the effusion

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31
Q

What does lung collapse do to structures in the mediastinum?

A

It pulls toward it

NOTE: He said that a tension pneumothorax is not “collapsing” its high pressure pushing everything away like an effusion

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32
Q

Three bacterial causes of pharyngitis?

A
  1. Streptococcus pyogenes
  2. Neisseria gonorrhea
  3. Corynebacterium diphtheria (in unvaccinated)
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33
Q

Basic microbio of strep pyogenes

A

Gram + cocci in chains

Beta hemolytic

Group A carbohydrate, M protein, lipotechoic acid on surface. Also has hyaluronic capsule

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34
Q

What toxin causes scarlet fever?

A

SPE toxin (SPE-A to be specific) from strep pyogenes

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35
Q

How is the rash seen in Scarlet fever described?

A

“sandpaper rash”

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36
Q

Secondary complications from strep pyogenes?

A

Rheumatic fever (M protein cross reactivity with cardiac myosin). After pharyngitis form only.

Glomerulonephritis due to type III hypersensitivity (immune complexes). After pharyngitis or skin forms

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37
Q

What two strep pyogenes enzymes help it spread in a host?

A

Hyalurinidase and DNase B

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38
Q

What antibody do we look for to see if someone recently had a strep pyogenes infection/is at risk for rheumatic fever?

A

Anti-streptolysin O antibody

Streptolysin O is a hemolysin that lyses RBCs

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39
Q

Micro of corynebacterium diphtheria?

A

gram + rod (non-spore forming!)

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40
Q

Clinical manifestations that should clue you into diphtheria?

A

Pseudomembrane & bull neck (massive lymphadenopathy)

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41
Q

What is the diphtheria toxin? Where is it coded?

A

A-B type toxin encoded on a bacteriophage (lysogenic conversion)

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42
Q

Describe what the diphtheria toxin does

A

ADP ribosylates EF-2 (elongation factor 2) and inhibits protein synthesis. This obviously kills the cell

Damages heart, nerves, kidneys, etc by binding to Heparin-binding epidermal growth factor receptor

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43
Q

Microbio of bordetella pertussis

A

Gram - rod (coccobacillus)

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44
Q

Three stages of pertussis

A
  1. Catarrhal (cough, rhinorrhea)
  2. Paroxysmal (coughing spasms, whoop, cyanosis, vomiting)
  3. Convalescent (decreasing but continuing symptoms)
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45
Q

What stage of pertussis is a person most contagious?

A

Catarrhal

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46
Q

How does pertussis stick in our URT?

A

It adheres to ciliated epithelium via pili/fimbriae, pertactin, and filamentous hemagglutinin (FHA)

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47
Q

What type of agar plate is used for pertussis?

A

Bordet-gengou plates

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48
Q

What toxins does pertussis release?

A
  1. Pertussis Toxin - an A-B type toxin that ADP-ribosylates G protein and increases cAMP. Localized tissue damage and systemic toxicity
  2. Trachael Cytotoxin (TCT): a peptidoglycan building block derivative that destroys the ciliated epithelium and the mucociliary escalator
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49
Q

Systemic toxicity of the pertussis toxin?

A

Hypoglycemia, leukocytosis, neurological damage

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50
Q

What is in the current pertussis vaccine?

A

pertussis toxoid + FHA

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51
Q

If you see “sudden shaking chills episode” and “rust-colored sputum” in a question stem you should immediately think what?

A

Streptococcus pneumoniae

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52
Q

What pathogen is the most common cause of community acquired pneumonia?

A

Streptococcus pneumonia

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53
Q

What three pathogens typically cause atypical pneumonia?

A
  1. Mycoplasma pneumoniae
  2. Chlamydia pneumoniae
  3. Respiratory viruses like influenza, adenovirus, parainfluenza, and RSV
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54
Q

Haemophilus influenzae pneumonia is more common in what population?

A

smokers

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55
Q

What type of pneumonia do people get after influenza virus?

A

Staph aureus

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56
Q

What type of pneumonia do people with CF typically get?

A

Pseudomonas aeruginosa

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57
Q

Typical vs. atypical onset of pneumonia?

A

Typical is rapid onset, more severe symptoms, productive cough, purulent sputum and CXR with dense consolidation

Atypical slower onset, less severe symptoms (“walking pneumonia”), non-productive cough, a little white phlegm, and patchy interstitial infiltrates on CXR

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58
Q

Microbio of streptococcus pneumoniae

A

Gram + diplococci

alpha hemolytic

Carbohydrate capsule (target of vaccine)

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59
Q

Diseases caused by streptococcus pneumonia?

A

MOPS!

Meningitis
Otitis media
Pneumonia
Sinusitis

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60
Q

How does streptococcus pneumonia damage our cell membranes?

A

Releases pneumolysin, a toxin that binds cholesterol in our cell membranes

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61
Q

Four stages of pneumonia?

A
  1. Serous
  2. Early consolidation - numerous bacteria, few PMNs
  3. Late consolidation - numerous PMNs
  4. Resolution - effective Ab response, macrophages clear debris

No permanent damage if the patient survives

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62
Q

Microbio of Legionella pneumophila

A

Gram - rod

Stains irregularly and needs a silver stain or buffered charcoal yeast extract (BYCE) with iron and cysteine

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63
Q

Diseases caused by Legionella pneumophila?

A

Legionnarie’s disease

Pontiac fever (flu-like)

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64
Q

What is special about encountering the Legionella pneumophila pathogen?

A

It’s environmental only. Must be aerosolized in water for us to breathe in.

It goes directly into our alveoli

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65
Q

Is Legionella pneumophila contagious?

A

No, we’re a dead-end host

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66
Q

What medium is needed to diagnose Legionella pneumophila?

A

Buffered charcoal yeast (BCYE)

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67
Q

Where does Legionella pneumophila replicate?

A

Intracellularly in our macrophages (thus we need cell-mediated immunity)

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68
Q

Microbio of Mycoplasma pneumoniae

A

wall-less, lacks peptidoglycan

lacks definite shape

doesn’t gram stain

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69
Q

What disease does Mycoplasma pneumoniae cause?

A

Tracheobronchitis/atypical walking pneumonia

Typically in children and young adults

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70
Q

Where does Mycoplasma pneumoniae colonize?

A

URT - does not reach alveoli

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71
Q

What does Mycoplasma pneumoniae require for multiplication?

A

Our sterols

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72
Q

How do you treat Mycoplasma pneumoniae?

A

Erythromycin, doxycycline

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73
Q

What is special about Mycoplasma pneumoniae inflammation?

A

It’s monocytic, not neutrophilic

74
Q

How does Mycoplasma pneumoniae cause damage?

A

Peroxide and superoxide

Community-acquired respiratory distress syndrome (CARDS) toxin (similar to pertussis toxin –> leads to a broken mucociliary escalator)

Stimulation of autoimmune IgM that binds to RBCs –> diagnose with cold hemagluttinin

75
Q

Microbio of Pseudomonas aeruginosa

A

Gram - rod, aerobic

Opportunistic environmental pathogen

76
Q

What diseases does Pseudomonas aeruginosa cause?

A

Swimmer’s ear and infections in CF patient lungs

Systemic effects in immunocompromised and burn patients

77
Q

Why is Pseudomonas aeruginosa particularly bad in CF lungs?

A

It produces a mucus called alginate that normally makes an antiphagocytic biofilm… add that on top of lungs that already have thick mucus and you get a very bad situation

78
Q

What three endogenous pathogens cause acute sinusitis?

A
  1. Streptococcus pneumoniae
  2. Non-typeable Haemophilus influnenzae
  3. Moraxella catarrhalis
79
Q

How do you treat sinusitis?

A

Antibiotics, anti-inflammatory agents, decongestants, fluids

80
Q

How does streptococcus pneumoniae evade host defenses?

A

Antiphagocytic capsule + sIgA protease

81
Q

Three manifestations of otitis media?

A
  1. Acute otitis media
  2. Chronic suppurative otitis media
  3. Otitis media with effusion
82
Q

What endogenous pathogens cause acute otitis media?

A

The same ones that cause sinusitis!

  1. Streptococcus pneumoniae
  2. Non-typeable Haemophilus influnenzae
  3. Moraxella catarrhalis
83
Q

Treatment for otitis media?

A

Antibiotics, surgery to remove adenoids (for recurrent cases), and myringotomy tubes in the tympanic membrane

84
Q

Microbio of haemophilus influenzae

A

Gram - coccobacillus

carbohydrate capsule (target of type B vaccine)

unencapsulated = nontypeable

85
Q

What does nontypeable haemophilus influenzae cause?

A

Otitis media, sinusitis, pneumonia

86
Q

What type of agar does haemophilus influenzae need?

A

Chocolate agar

87
Q

How does haemophilus influenzae evade host defenses?

A

Type B has an antiphagocytic capsule

Nontypeable has LPS (toxin)

Also sIgAse (not 100% effective as sIgA can still work)

88
Q

Major pathogen causing otitis externa (swimmer’s ear)?

A

Pseudomonas aeruginosa

89
Q

What causes chronic otitis externa?

A

Usually over cleaning of the ear canal

It’s itchy, and not painful

90
Q

What causes “malignant” otitis externa?

A

invasive Pseudomonas aeruginosa

91
Q

Where is Pseudomonas aeruginosa encountered?

A

In the environment! Water, soil, air, food, catheters, endotracheal tubes (why you can’t bring flowers into the ICU)

92
Q

What usually keeps Pseudomonas aeruginosa in check?

A

PMNs

So serious infections usually in those who are neutropenic

93
Q

Where does Pseudomonas aeruginosa multiply?

A

Simple requirements… can do it everywhere. Even in disinfectants and cleaning materials.

Does not ferment. For whatever that is worth.

94
Q

How does Pseudomonas aeruginosa cause damage?

A

Exotoxin A (similar to diphtheria toxin), type 3 secreted toxin, and numerous enzymes like phospholipase, protease, elastase

95
Q

Why is treating Pseudomonas aeruginosa problematic?

A

It’s highly resistant to numerous antibiotics

96
Q

What is the most common cause of lobar pneumonia in an otherwise healthy adult?

A

Streptococcus pneumoniae

97
Q

What are the characteristics of dimorphic fungi?

A

Yeast in body temperature (37*C); mold in environmental and culture temperature (“mold in the cold”)

98
Q

Your patient presents with cough and shortness of breath two weeks after exploring caves in the Mississippi River valley. What pathogen do you suspect?

A

Histoplasma

99
Q

Your patient is a truck driver who just came back New Mexico. He has diarrhea, fever, and dyspnea. What pathogen do you suspect?

A

Coccidioides

Valley Fever!

100
Q

What three diseases does aspergillus mold cause?

A
  1. Aspergilloma - colonization in a pre-existing cavity (“fungus ball”)
  2. Invasive pneumonia - very rare and in the immunocompromised
  3. Allergic Bronchopulmonary Aspergillosis (ABPA) - hypersensitivity rxn in asthmatics or CF patients
101
Q

What will be high in a patient with ABPA’s blood?

A

IgE and eosinophils

due to the hypersensitivity rxn to the mold

102
Q

A 24-year-old sex worker comes to you complaining of a four-week history of worsening cough, dyspnea, and fever. Her CXR shows diffuse infiltrates and her sputum sample shows “cotton candy” exudates. What pathogen do you suspect?

A

Pneumocystis

103
Q

What type of pathogen is most likely to cause pneumonia in alcoholics?

A

Klebsiella pneumoniae

current jelly sputum!

104
Q

What are two complications of S. aureus pneumo?

A
  1. Abscess

2. Empyema

105
Q

How do you diagnose Legionnarie’s Disease

A

Urine antigen

106
Q

If you see a multinucleated syncytial cell on gram stain what pathogen causing atypical pneumo should you suspect?

A

RSV - Respiratory Syncytial Virus

107
Q

If you see multiple species (mostly anaerobes) of multiple morphologies on gram stain, what type of pneumonia should you expect?

A

Aspiration pneumonia (organisms from the oral cavity are now in the lungs!)

108
Q

What organism causes Ghon complexes?

A

Mycobacterium tuberculosis

109
Q

What is Mycobacterium Avium-Intracellular Complex (MAC)?

A

Obtained from the environment; causes infections in many organ systems (example: diarrhea in HIV patients; lymphadenitis in children)

** Lady Windermere Syndrome because it affects healthy, older women

110
Q

What type of fungi is Pneumocystis jirovecci? What does it cause?

A

Opportunistic yeast that causes infection in immunocomprised patients (HIV, transplantation, those on long-term corticosteroids or TNF alpha inhibitors)

111
Q

What do you use to treat and prophylax HIV patients with to prevent P. jirovecci?

A

Bactrim (trimethoprim-sulfamethoxazole)

112
Q

If gram stain is descried as “cotton candy” exudate or silver stain is described as “crushed ping pong balls” what pathogen should you suspect?

A

Pnumocystis jirovecci

113
Q

What type of fungi is Cryptococcus? What does it cause?

A

Yeast associated with soil, bird droppings, chicken coops, barns

Causes “wax and wane” meningitis in immunocompromised

114
Q

Describe Cryptococcus morphology

A

Round, 5-15 um, surrounded by a thick, gelatinous capsule (**imp according to B&B); narrow based budding

115
Q

What type of fungi is Histoplasma? Where is it endemic to and how do we get it?

A

Dimorphic

Endemic to Mississippi River valley. Present in soil where growth is stimulated by bird and bat guano (high in caves!!)

116
Q

Describe Histoplasma morphology (yeast AND mold phases)

A

Yeast: very small (3-5um), narrow based budding, forms in macrophages (you will see tons inside a macrophage)

Mold: Characteristic tuberculate macroconidia (circular mold cells with spikes)

117
Q

If you see “tuberculate macroconidia” in reference to a fungi, which one is the question referencing?

A

Histoplasma

118
Q

Four B’s of blastomyces?

A

Broad
Based
Budding
Bone & skin (systemic effects)

119
Q

What type of fungi is Blastomyces? Where is it endemic to?

A

Dimorphic fungi

Endemic to Mississippi River Valley & Great Lakes

120
Q

Blastomyces morphology (yeast AND mold forms)?

A

Yeast: big (8-10um), thick refractile wall, broad based budding (**key)

Mold: Lollipop or pear-shaped microconidia

121
Q

What type of fungi is Coccidioides? Where is it endemic to and how do we get it?

A

Dimorphic

Endemic to Southern California and the Southwest US. Most cases occur in Arizona (“Valley Fever”)

Gets kicked up from soil in dust storms or wind and we inhale

122
Q

Describe Cocciodies morphology (yeast AND mold forms)?

A

Yeast: LARGE (250um) spherule filled with endospores

Mold: Barrel shaped conidia that alternate with empty cells (easily separated and aerosolized this way)

123
Q

What type of fungi is Aspergillus? Most common species?

A

Mold

Most common: A. fumigatus

124
Q

What is the morphology of aspergillus?

A

Thin septate hyphae; Y-shaped with branching at ~45 degrees

125
Q

What type of fungi is Zygomycetes? Three most common types?

A

Mold

Rhizopus, Mucor, Lichtemimia

126
Q

What predisposes someone to a Zygomycetes infection?

A

Neutropenia, diabetes mellitus, and corticosteroid usage

127
Q

What does Zygomycetes quickly cause?

A

Tissue necrosis

128
Q

How does Zygomycetes disseminate throughout the body?

A

Hematogenously and by direct extension

129
Q

What is the morphology of Zygomycetes?

A

Broad, ribbon-like hyphea; pauci-septate (rare septations), and branches at ~90 degrees

130
Q

Does genetics play a role in susceptibility to fungal infections?

A

Yes, inflammatory cytokines, cell receptors, and clotting factors like plasminogen have been show to have variants that increase susceptibility to fungi

131
Q

What SNP in TLR-4 shows an increased susceptibility for invasive aspergillosis?

A

S4+

AND if the bone marrow recipient or donor was positive for Cytomegalovirus there was a slight increased risk (highest was S4+ with or with CMV+)

132
Q

What is our first line of defense against fungi entering the respiratory tract? The second?

A

First: mucociliary escalator

Second: Phagocytes

133
Q

What type of therapy increases the susceptibility of Coccidiomycosis reactivation?

134
Q

What type of immune cell is important for host defense against Coccidiomycosis?

A

T cell

DTH associated with recovery

135
Q

Key protective immune response against Histoplasma?

A

Macrophages (where they live!) and T cell immunity

136
Q

How are Crytopcoccus protected against phagocytosis?

A

Large capsule

+ other virulence factors like sialic acid and capsular polysaccharide

137
Q

What type(s) of immune cells are protective for Cryptococcus?

A

Innate, B, and T cell

138
Q

Radiologic findings in Pneumocystis jirovecci?

A

Infiltrates are characteristically diffuse

“ground glass” appearance

139
Q

When diagnosing acute invasive aspergillosis, at what stage do you want to Dx and begin treatment?

A

During the halo stage (less than 5 days)

140
Q

What is the progression of aspergillosis on CT scan?

A

Halo (5 days) –> increasing size and decreasing halo (1 week) –> stabilization –> air crescent

141
Q

Other clinical presentations of invasive aspergillosis?

A

Sino-orbital disease, cerebritis, cutaneous infection

142
Q

What kind of imaging do you want to obtain for an immunocompromised patient who you suspect has a lung infection?

A

CT

Much higher sensitivity and specificity than CXR for immunocompromised patients

143
Q

What two, non-invasive blood tests can help establish an aspergillosis diagnosis?

A
  1. Galactomannan (cell wall carbohydrate found in Aspergillus and Penicillium)
  2. B-glucan (present in the cell wall of most fungi except Cryptococcus and agents of Mucormycosis)
144
Q

Is and aspergillus PCR available?

A

No commercially in the US

Studies show that combining the non-commercial ones available with galactomannan testing may be a better screening than GM alone?

145
Q

Antigen testing can be used for the detection of which fungi?

A

Histoplasma, Blastomycosis, Cryptococcus

146
Q

B glucan testing can be used for which fungi?

A

Pneumocystis and Aspergillus

147
Q

What is a solitary pulmonary nodule?

A

Single, spherical, well-circumscribed radiographic opacity that measures up to 3cm in diameter

Completely surrounded by aerated lung.. No atelectasis, pneumonia, hilar enlargement or pleural effusion

148
Q

What percentage of lung masses over 3 cm are malignant?

149
Q

40% of solitary pulmonary nodules are what? 15% are what?

A

40% are inflammatory tissue (granulomas)

15% are bening neoplasms like hamartomas, lipomas, fibromas, cysts, etc

150
Q

What is the most common type of lung cancer?

A

Adenocarcinoma

151
Q

What is the most common type of benign tumor of the lung?

152
Q

What is a hamartoma?

A

Normal tissue that is disorganized. Composed of cartilaginous nests surrounded by connective tissue and mature fat cells

Can be parenchymal or central location

Fat is identified in 54% of lesions. Calcifications is identified in 15-30% of lesions

153
Q

What finding on CT scan is pathognomonic of pulmonary hamartoma?

A

“popcorn calcification”

154
Q

What is a bronchogenic cyst?

A

An abnormal detachment of the primitive foregut

Clinical presentation varies from respiratory distress in a newborn to an incidental finding in an adult

Benign lesions that do not metastasize

155
Q

What is a carcinoid tumor?

A

A low-grade neoplasm of neuroendocrine cells

May arise centrally or peripherally

156
Q

How do carcinoid tumors present?

A

With cough, hemoptysis, secondary post-obstructive pneumonia (recurrent in the same location)

Sometimes symptoms related to the secretion of compounds can cause diarrhea, flushing (serotonin secretion causing carcinoid syndrome)

157
Q

What is carcinoid syndrome?

A

Diarrhea and flushing caused by the secretion of serotonin from carcinoid tumors

Usually only if metastatic or huge

158
Q

How does a carcinoid tumor usually look on bronchoscopy?

A

“like a raspberry”

very red, very vascular

159
Q

How do carcinoid cells appear on histology?

A

Tumor cells are arrange in small groups and nests

In typical carcinoid tumors there are no mitotic figures or necrosis present

160
Q

Carcinoid tumor cells can be identified by using immunohistochemistry chemistry for what two markers?

A

Synaptophysin and Chromogranin

161
Q

How do carcinoid tumor nuclei appear on histology?

A

“salt-n-pepper”/speckled light and dark appearance

162
Q

What type of lung tumor is most common in women and those who never smoked?

A

adenocarcinoma

163
Q

Where in the lung does adenocarcinoma develop?

A

The periphery

164
Q

What gene mutations are associated with adenocarcinoma?

A

EGFR and ALK

very low percentage though

165
Q

What is the growth pattern of adenocarcinoma in situ?

A

it spreads along the alveolar spaces on the lung and does not invade the stroma/vessels or pleura

166
Q

How does adenocarcinoma in situ normally present?

A

“Pneumonia” that doesn’t resolve

But generally asymptomatic

167
Q

How does adenocarcinoma in situ appear on CT?

A

Ground glass opacity

168
Q

What are the two types of adenocarcinoma in situ?

A

Mucinous and serous

169
Q

Thyroid Transcription Factor 1 (TTF-1) is normally expressed in what two types of lung tumors?

A

Small cell and adenocarcinoma

NOT typical for squamous cell

170
Q

What type of lung cancer is highly associated with smoking?

A

Squamous cell carcinoma & small cell carcinoma

171
Q

Where in the lung is squamous cell typically found?

A

Central (think where the smoke gets!)

172
Q

What features are key identifies are squamous cell carcinoma?

A

Intercellular bridges and keratinization (keratin pearls!)

173
Q

What are the pre-cursor intra-epithelial dysplasia steps seen in squamous cell carcinoma of the lung?

A

Normal –> squamous metaplasia –> dysplasia –> carcinoma in-situ –> invasive carcinoma

174
Q

What is the most aggressive type of lung cancer?

A

Small cell carcinoma

175
Q

Small cell carcinoma is derived mostly from what cell type?

A

Neuroendocrine cells that line the airways

176
Q

Where does small cell carcinoma arise in the lung?

A

Centrally

Generally non resectable

177
Q

How does small cell lung cancer appear on histology?

A

Small, high N:C ratio, cells stream & mold against each other

178
Q

What is a paraneoplastic syndrome?

A

Clinical syndrome that occurs in patients with malignancies, often due to compounds secreted by the tumor

Often predate the clinical appearance of the tumor

179
Q

What is Lambert-Eaton Syndrome?

A

Antibody against pre-synaptic Ca2+ channels that blocks the release of Acetylcholine

Main symptom is weakness (similar to Myasthenia Gravis)

180
Q

What two hormones does small cell carcinoma release? What are the effects of this?

A

Antidiuretic hormone (ADH) –> hyponatremia

Adrenocorticotropic hormone (ACTH) –> Cushing’s syndrome (too much cortisol)

181
Q

What hormone does squamous cell carcinoma release? What is the effect of this?

A

Parathormone, PTH-like peptide

Causes hypercalcemia

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