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Pathology > Resp Tract > Flashcards

Resp Tract Flashcards

1
Q

What is pneumonia?

A

Infxn of lung parenchyma

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2
Q

How do people become susceptible to pneumonia? Give 3 examples and explain why each would increase the risk of a person getting pneumonia.

A
  • Pneumonia occurs when normal defenses are impaired
  • Examples:
    1. Impaired cough reflex: Pt won’t be able to cough up organisms that may have gotten into the airways
    2. Mucociliary escalator: Resp. epith has cilia that beat upwards to push mucus in the conducting portion of lung up along the airway and into the throat so that we can swallow it
    3. Mucus plugging: whenever you have a block of a tube, you increase risk of infxn behind the block
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3
Q

How would a patient w/ pneumonia present clinically? (7 physical symptoms)

A
  1. Fever
  2. Chills
  3. Productive cough (yellow-green or rusty sputum)
  4. Pleuritic chest pain
  5. Tachypnea
  6. Decreased breathing sound
  7. Dullness to percussion
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4
Q

What causes the pleuritic chest pain seen in pneumonia?

A

Bradykinin and PGE2 are released during inflamm response, which sensitizes the sensory neurons for pain

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5
Q

What are 3 patterns of pneumonia that are classically seen on chest x-ray? Describe what changes in the lung would be seen in each type.

A
  1. lobar pneumonia: Consolidation of an entire lobe of the lung
  2. bronchopneumonia: Scattered patchy consolidation centered around bronchioles (often multifocal and bilateral)
  3. interstitial (atypical) pneumonia: Diffuse interstitial infiltrates
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6
Q

What is usually the etiology of lobar pneumonia? What are the most common causitive organisms?

A
  • Usually bacterial
  • Most common causes are: Strep pneumonia (~95%) and Klebsiella pneumoniae (~5%)
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7
Q

What is the causitive organism that is responsible for most community-acquired pneumonia cases? What patient population is generally affected?

A
  • Strep pneumoniae
  • Usually seen in middle-aged adults and elderly
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8
Q

What type of pneumonia (lobar, broncho, intersitial, or aspiration) would patients present with coughing up a jelly-like sputum? What is the causitive agent and why does it cause this type of presentation?

A
  • Lobar pneumonia
  • Klebsiella pneumoniae; Klebsiella has a thick mucoid capsule –> attracts water and makes it viscous –> Pt who cough this up will describe it as having a jelly-like consistency
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9
Q

What types of patients are most susceptible to lobar pneumonia caused by Klebsiella? Why?

A
  • Alcoholics and elderly in nursing homes
  • Klebsiella is normally found in the GI, but it can cause pneumonia if aspirated into the lungs –> Pt’s who are @ increased risk of aspiration would therefore be more susceptible to lobar pneumonia caused by Klebsiella
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10
Q

What are the 4 classic gross phases of lobar pneumonia? Explain how each arises.

A
  1. Congestion: inflammation increases leakiness of vessels –> leads to congested vessels and edema
  2. Red hepatization: Alveolar air space becomes filled w/ exudate + neutrophils + hemorrhage –> changes the lung from having a normal spongy consistency to one that is closer to the liver
  3. Gray hepatization: RBCs w/n the exudate begin to degrade –> changes the color from a dark red/blackish color to gray
  4. Resolution and healing: Healing is mediated by Type II pneumocytes, which act as the stem cells of the alveolar air sack
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11
Q

What is a complication of Klebsiella pneumoniae that commonly arises?

A

Abscess formation

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12
Q

What organism is the most common cause of bronchopneumonia?

A

Staph. aureus

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13
Q

What is secondary pneumonia? What are the most common organisms that cause secondary pneumonia?

A
  • Secondary pneumonia is bacterial pneumonia that is superimposed on an existing viral URI
  • Strep pneumoniae and Staph aureus
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14
Q

What organism is a common cause of secondary bronchopneumonia and pneumonia superimposed on COPD?

A

H. influenzae

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15
Q

What organism causes community-acquired pneumonia and pneumonia superimposed on COPD?

A

Moraxella catarrhalis

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16
Q

What is the most common cause of bronchopneumonia in cystic fibrosis patients?

A

Pseudomonas aeruginosa

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17
Q

What intracellular organism transmitted by water source causes community-acquired pneumonia, pneumonia superimposed on COPD, or pneumonia in immunocompromised states? How is it visualized?

A
  • Legionella pneumophila
  • Silver stain
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18
Q

Why is intertitial pneumonia also called atypical pneumonia?

A

Intersitial (atypical) pneumonia has “atypical” clinical symptoms in comparison to other forms of pneumonia. For example, Pts would present w/ mild upper respiratory symptoms (minimal sputum and low fever) than would be expected of Pts who have other forms of pneumonia

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19
Q

What is the most common cause of atypical pneumonia? What patient population is most affected by this organism?

A
  • Mycoplasma pneumoniae
  • Young adults (classically, military recruits or college students living in close quarters)
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20
Q

Mycoplasma pneumoniae is the most common cause of what type of pneumonia? What complications can arise in Pts who are infected with this organism?

A
  • Interstitial (atypical) pneumonia
  • Autoimmune hemolytic anemia: IgM-mediated (cold agglutinin) against I antigen on RBCs
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21
Q

What is the second most common cause of atypical pneumonia in young adults?

A

Chlamydia pneumoniae

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22
Q

Chlamydia pneumoniae causes what type of pneumonia? What patient population is most at risk?

A
  • Intersitial (atypical) pneumonia
  • Young adults
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23
Q

What is the most common cause of atypical pneumonia in infants?

A

Respiratory syncytial virus (RSV)

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24
Q

What is the most common cause of atypical pneumonia in Pts w/ posttransplant immunosuppressive therapy?

A

CMV

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25
Q

What is the most common cause of atypical pneumonia in elderly, immunocompromised, and those w/ preexisting lung disease?

A

Influenza virus

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26
Q

What is the most common cause of mortality in Pts w/ atypical pneumonia due to influenza virus?

A

Superimposed S aureus or H influenza bacterial pneumonia is the most common cause of death in Pts w/ atypical pneumonia due to influenza virus

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27
Q

What organism is assoc w/ atypical pneumonia with a unique characteristic of causing high fever (Q fever) in Pts?

A

Coxiella burnetii

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28
Q

What patient population is most susceptible to pneumonia caused by Coxiella burnetii? What is unique to this organism in comparison to other organisms in the same genus?

A
  • Farmers and veterinarians (since the spores are deposited on cattle by ticks or are present in cattle placentas)
  • Coxiella is a rickettsial organism, but it is distinct from others in that:
    1. It causes pneumonia
    2. does not require an arthropod vector for transmission (survives as a highly heat-resistant endospore)
    3. does not produce a skin rash
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29
Q

What is aspiration pneumonia? What complication classically arises in this form of pneumonia?

A
  • Pts may aspirate into their lungs anaerobic bacteria of the oropharynx, which could cause pneumonia
  • Classically, this results in right lower lobe abscess
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30
Q

Give 3 examples of anaerobic bacteria present in the oropharynx that may cause aspiration pneumonia.

A
  1. Bacteroides
  2. Fusobacterium
  3. Peptococcus
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31
Q

How is tuberculosis (TB) transmitted?

A

TB is trasmitted via inhalation of aerosolized Mycobacterium tuberculosis

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32
Q

What microscopic changes are seen in primary TB? Clinically, how would the Pt present?

A
  • Primary TB results in focal, caseating necrosis in the LOWER lobe of the lung and hilar lymphnodes; fibrosis and calcification can also be seen subpleurally (Ghon complex)
  • Clinically, Pts will generally be asymptomatic, but will present with (+) PPD
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33
Q

How does Primary TB progress to Secondary TB?

A

Primary TB arises after initial exposure; Secondary TB arises due to reactivation of Mycobacterium tuberculosis due to AIDS or aging

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34
Q

What histological changes are seen in secondary TB of the lung? How would Pts present clinically?

A
  • Secondary TB would form foci of caseous necrosis @ the APEX of the lung (since there is relatively poor lymphatic drainage here and high O2). This may progress to miliary TB (tiny regions of TB which are scattered across the entire lung) or tuberculous bronchopneumonia
  • Pts would present w fevers and night sweats, cough w/ hemoptysis, and weight loss
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35
Q

In secondary TB, what complications may arise from the reactivation of TB and ongoing caseous necrosis?

A
  1. Miliary pulmonary TB (where tiny regions of TB are scattered across the entire lung)
  2. Tuberculous bronchopneumonia
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36
Q

What would a biopsy in secondary TB reveal? What type of stain could be used to visualize the baccili?

A
  • Caseating granulomas: would see central necrosis and surrounding it would be hisitiocytes
  • Acid-Fast-Bacilli (AFB) stain: would show as red rods
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37
Q

Systemic spread of secondary TB can involve any tissue. Give 4 examples of common sites.

A
  1. Meninges (meningitis; specifically affecting the meninges @ base of the brain)
  2. Cervical l.n.
  3. Kidneys (sterile pyuria)
  4. Lumbar vertebrae (Pott disease)
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38
Q

In COPD, what changes are seen in spirometry (FEV1:FVC ratio; TLC)

A
  • FEV1:FVC ratio decreases (both FEV1 and FVC decrease, but FEV1 decreases more since Pt is unable to effectively blow out air in COPD)
  • TLC: TLC increases b/c air trapping means more air will be present in the lungs than normal @ any given time
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39
Q

Copious amounts of mucus is coughed up in what particular COPD? What is the cause of this?

A
  • Chronic bronchitis
  • (highly assoc w/ smokers) Pts who smoke breathe in a lot more pollutants –> Mucinous glands in the submucosa layer of bronchus undergoes extensive hypertrophy/hyperplasia in attempt to better filter the air –> Copious amounts of mucus is produced, which travel up the airway and can be coughed out
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40
Q

What changes in the Reid index would be expected in chronic bronchitis?

A

Reid index measures the thickness of mucinous glands in relation to the thickness of the entire bronchial wall: normally, it is <40%, but in chronic bronchitis, it will increase to >50%

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41
Q

How can chronic bronchitis cause cyanosis?

A

Copious mucus production may travel down into airways and produce a mucus plug –> this traps CO2, thereby increase PACO2 and reducing PAO2 –> leading to a increase in PaCO2 and decreasing PaO2

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42
Q

“Blue Bloaters” is a HY word to describe cyanosis seen in what specific COPD condition?

A

Chronic bronchitis

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43
Q

What cardiovascular disease can be precipitated by COPD conditions? How does this happen?

A

In COPD conditions, hypoxia results from the inability to blow out air properly –> arterioles in the lungs vasoconstrict in an attempt to shunt blood to other parts of the lung that may be better oxygenated; however, in COPD, oxygenation is compromised in most areas of the lung –> this causes pulm. HTN –> RV has to pump against this increased pressure –> RV hypertrophy –> RH failure (cor pulmonale)

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44
Q

What is the physiological cause of emphysema?

A

There is destruction of alveolar air sacs due to loss of elastic recoil and collapse of airways during exhalation –> leads to obstruction and air trapping

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45
Q

Explain the physiological process by which there is air trapping and collapse of airways in emphysema.

A
  1. Air trapping: Normally, alveoli expand during inhalation and recoil in order to push the air out during exhalation. However, in emphesema, this elastic property is lost (“instead of having a bunch of small balloons, it’s like having a big shopping bag”) –> air is unable to be pushed out effectively
  2. Collapse of airways: As air goes from distal to proximal lung during exhalation, it gradually accelerates (“recall that area is related to velocity; although the terminal bronchioles may individually be smaller than larger bronchi, there are many more of them = much larger surface area”) –> this causes a drag force that tries to collapse the airway –> normally, this drag force is resisted in the upper airways by the cartilage and it is resisted in the lower airways by the recoil of alveoli that keep the airway open –> in emphysema, loss of elastic recoil means there is no counterbalancing force in the terminal bronchioles = airway collapse during exhalation
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46
Q

What is the molecular reason for emphysema?

A

There is always some underlying inflamm in the lower lungs due to debris in the air –> alveolar macrophages clean this debris, but in the process of inflammation, they release proteases (specific to emphysema is elastase) –> liver produces alpha1-antitrypsin (A1AT), which travels via blood into lungs and neutralizes the elastase and protects it from dmging the lung parenchyma

  • In emphysema, there is either excessive inflammation (increased protease) or lack of A1AT (genetic deficiency)
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47
Q

What is the most common cause of emphysema?

A

Smoking

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48
Q

What type of emphysema is characteristic of smokers?

A

Centriacinar emphysema that is most severe in upper lobes (as smoke comes down the airway, the first part of the acinous that gets hit with the brunt of it is the center; smoke travels upward, hence upper lobes is most severely affected)

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49
Q

What type of emphysema is characteristic of A1AT deficiency?

A

Panacinar emphysema that is most severe in lower lobes

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50
Q

What liver symptoms could be seen in panacinar emphysema? Why is this the case?

A
  • Liver cirrhosis
  • Panacinar emphysema is caused by A1AT deficiency. However, the disease is caused b/c there is insufficint levels of circulating A1AT, not b/c it is not being made in the liver. The liver is making misfolded A1AT, which is why it becomes sequestered in the ER –> accumulation of mutant A1AT results in liver dmg –> liver cirrhosis
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51
Q

In a Pt w/ panacinar emphysema, what would be seen on liver biopsy?

A

Pink, PAS-positive globules in hepatocytes (the pink/purple globules are the non-fxnal sequestered A1AT in the ER of hepatocytes)

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52
Q

What are the 2 most common alleles of A1AT?

A

PiM is the normal allele (2 copies are usually expressed: PiMM)

PiZ is the most common clinically relevant mutation that results in low levels of circulating A1AT and sequestration in ER

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53
Q

What COPD condition is associated w/ Pts having a “pink-puffer” presentation? Why do these Pts present this way?

A
  • Emphysema
  • “pink-puffer” is a description of how Pts w/ emphysema have pursed-lip breathing. Careful breathing with pursed lips increases back pressure –> keeps the walls of airways from collapsing
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54
Q

What changes in chest wall can be seen in Pts w/ emphysema? Why does this occur?

A
  • Barrel-chest can be seen (increase in anterior-posterior diameter of chest)
  • The chest wall has a tendency to want to expand out and the lungs have a tendency to want to collapse in. Normally, these two opposing forces are counterbalanced (fxnal residual capacity; think of it as Chest wall: Lung ratio). In emphysema, due to loss of elastic recoil, the opposing force by the lung is reduced –> FRC increases –> barrel chest
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55
Q

The clinical presentation of barrel chest is associated w/ what COPD condition?

A

Emphysema

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56
Q

What is asthma? What is it most often caused by?

A
  • Asthma is reversible airway bronchoconstriction (not spasm)
  • Most often due to allergic stimuli (atopic asthma; Hypersensitivity Type 1)
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57
Q

If asthma presents in childhood, what other comorbidities does it present w/?

A

Childhood asthma is often assoc w/ allergic rhinitis, eczema, and a family Hx of atopy

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58
Q

Explain the pathogenesis of atopic asthma.

A
  1. Allergens induce a TH2 CD4+ response in genetically susceptible individuals
  2. TH2 CD4+ cells secrete IL-4, IL-5, and IL-10 –> IL-4 mediates class switching to IgE; IL-5 attracts eosinophils; IL-10 potentiates TH2 response
  3. Reexposure to allrgen leads to IgE-mediated activation of mast cells (APCs w/ IgE will present a cross-linked allergen upon second exposure to mast cells) –> Acivated mast cells release preformed histamin granules (causes vasodilation and increased vascular permeability) and generate LTC4, LTD4, and LTE4 (causes constriction of smooth muscles = leads to increased vascular permeability by contracting pericytes and bronchoconstriction)
  4. Arrival of eosinophils exacerbates and perpetuates bronchoconstriction (late-phase of asthma reaction) via the release of major basic protein
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59
Q

What unique features are seen in the productive cough of asthmatic Pts?

A

Sputum of Pts w/ asthma would classically have: Curschmann spirals (spiral-shaped mucus plugs) and Charcot-Leyden crystals (crystal aggregates of major basic protein)

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60
Q

What is a fatal complication that can arise due to asthma?

A

Severe, unrelenting asthmatic attack can result in status asthmaticus (extreme bronchoconstriction), which can lead to death if not reversed

61
Q

What patient population is most affected by ASA-intolerant asthma? What clinical triad would be seen in these patients?

A
  • Adults w/ a Hx of asthma may present with asthmatic symptoms when taking aspirin
  • Clinical triad of aspirin-intolerant asthma include: Asthma + ASA-induced bronchospasms + nasal polyps
62
Q

What is bronchiectasis? How does it lead to air trapping?

A
  • Bronchiectasis is the permanent dilation of bronchi and bronchioles
  • Dilation of these airways lead to a loss of airway tone: when air flows through a larger tube, it loses its laminar flow and becomes turbulent –> when Pt breathes out, the air will not be able to flow effectively out through the dilated airways = air trapping/obstruction
63
Q

What gross changes of the lung would be seen in bronchiectasis?

A

There would be dilation of airways near the periphery. Normally, airways should get smaller as you go proximal (central) to distal (periphery) in the lungs.

64
Q

What is the underlying pathogenesis that precipitates bronchiectasis? Give 5 examples of possible causes.

A
  • Bronchiectasis is due to necrotizing inflammation that damages the airway walls. Hence, patients who get chronic infxn or inflammation w/n the airways will be most susceptible to bronchiectasis.
    1. Cystic fibrosis (high risk of pulm infxn due to viscous mucus)
    2. Kartagener syndrome (inherited defect of dynein arm = immobile cilia –> increased risk for pulm infxns); Kartagener syndrome is also assoc w/ sinusitis, infertility, and situs inversus
    3. Tumor or foreign body (tumor may physically block the tube and increase risk for infxn; foreign bodies may become a nidus for infxn or elicit an inflamm response)
    4. Necrotizing infxn from a high virulence organism
    5. Allergic bronchopulmonary aspergillosis (Hypersensitivity rxn to Aspergillus, which leads to chronic inflamm dmg; Pts w/ asthma or cystic fibrosis are particularly susceptible to developing this response to Aspergillus)
65
Q

Systemic amyloidosis can be seen in what COPD condn? How does this arise?

A
  • Bronchiectasis
  • Bronchiectasis is a condn due to chronic infxn/inflammation –> Acute-phase reactants, such as SAA, is upregulated during chronic infxn –> SAA can get converted to AA, which can then deposit as amyloid systemically
66
Q

What changes can be seen in spirometry in restrictive lung diseases (FEV1:FVC ratio, TLC)?

A

In restrictive lung disease, there is a problem with filling the lung (while as in COPD, there was a problem in emptying it)

  • Both FEV1 and FVC decrease in restrictive lung disease, but FVC decreases more (since there is less O2 to breath out) –> FEV1:FVC ratio increases
  • TLC decreases, since less O2 is able to enter the lungs
67
Q

What is the most common cause of restrictive lung disease?

A

Intersitial diseases of the lung are the most common cause of restrictive lung disease (Thickening of alveolar wall makes it difficult for gas exchange and to inflate w/ air)

68
Q

What is the pathogenesis of idiopathic pulmonary fibrosis?

A

Idiopathic pulmonary fibrosis is a restrictive lung disease of unknown etiology.

  • It is most likely due to cyclical lung injury (of unknown etiology), which causes cyclical healing response: TGF-Beta (an important fibroblast growth factor that initiates healing response) is released by injured pneumocytes –> induces fibrosis
69
Q

What are some secondary causes of pulmonary intersitial fibrosis?

A
  • Drugs (e.g. bleomycine and amiodarone)
  • Radiation therapy
70
Q

Describe the process of gross changes that would be seen via lung CT due to persistent pulmonary fibrosis (early to late stage).

A

Fibrosis would be seen on lung CT as subpleural patches –> eventually, it will become diffuse fibrosis w/ end-stage “honeycomb” lung

71
Q

What is the treatment for idiopathic pulmonary fibrosis?

A

Lung transplantation is the only way to treat pulmonary fibrosis (we have no other way to remove the fibrosis)

72
Q

What is pneumoconiosis?

A

Intersitial fibrosis due to occupational exposure; small particles that can bypass the mucus and ciliary filters will make it to the distal airways, where alveolar macrophages will engulf the particles and induce fibrosis

73
Q

What changes to the FRC would be seen in restrictive lung disease?

A

The FRC (chest wall: lung) would increase, as fibrosis of the lungs will increase the forces exhibited by the lung –> decrease A-P diameter of the chest

74
Q

Give 4 examples of pneumoconioses (Disease, Exposure, Pathologic findings, and Other Assoc. Findings)

A

“SCAB”

  1. Silicosis:
    - Exposure: Silica; seen in sandblasters and silica miners
    - Findings: Fibrotic nodules in upper lobes of the lung
    - Other: Increased risk for TB, since silica impairs phagolysosome formation when it is ingested by macrophages
  2. Coal Worker’s Pneumoconiosis:
    - Exposure: Carbon dust; seen in coal miners
    - Findings: Massive exposure leads to diffuse fibrosis (“black lung”)
    - Other: Assoc w/ rheumatoid arthritis (Caplan Syndrome); Mild exposure to carbon (e.g. normal pollution in air) results in anthracosis (collection of carbon-laden macrophages), which is not clinically sig.)
  3. Asbestosis
    - Exposure: Asbestos; seen in construction workers, plumbers, and shipyard workers
    - Findings: Fibrosis of lung and pleura (plaques). Lesions may contain long, golden-brown fibers w/ associated Fe2+ (asbestos bodies).
    - Other: Increased risk for lung carcinoma and mesothelioma (moreso lung carcinoma than mesothelioma)
  4. Berylliosis
    - Exposure: Beryllium; seen in beryllium miners and workers in aerospace industry
    - Findings: Noncaseating granulomas in the lung, hilar ln, and systemic organs (very similar presentation to sarcoidosis)
    - Other: Increased risk for lung cancer; histologically similar to sarcoidosis
75
Q

What is sarcoidosis and how does it relate to lung disease? What patient population does it classically present in?

A
  • Sarcoidosis is a systemic disease characterized by noncaseating granulomas in multiple organs (esp. lung interstitium and hilar ln) –> this can thereby cause restrictive lung disease
  • African American females are classically affected
76
Q

What is the etiology of sarcoidosis?

A

Sarcoidosis has an unknown etiology; but it is most likely duie to CD4+ T-cell response to an unknown antigen

77
Q

What would biopsy show in a Pt w/ sarcoidosis? What is a characteristic finding?

A
  • Noncaseating granulomas (tons of epithelioid histiocytes and giant cells) would be seen in sarcoidosis
  • Asteroid bodies are a characteristic stellate inclusion that is often seen w/n giant cells of sarcoidosis granulomas (asteroid bodies are just a unique way giant cells in sarcoidosis look)
78
Q

What changes in serum Ca2+ levels would be expected in sarcoidosis? Is this a specific finding?

A
  • Hypercalcemia would be seen in Pts w/ Sarcoidosis b/c epithelioid histiocytes of granulomatous diseases express 1-alpha hydroxylase, which activates Vitamind D to its active form (1,25-calciferol)
  • This is not specific to sarcoidosis, as any granulomatous disease could cause this finding (e.g. berylliosis)
79
Q

What is the treatment for sarcoidosis?

A

Steroids or just spontaneous resolution w/o any treatment

80
Q

What is hypersensitivity pneumonitis?

A

Hypersensitivity pneumonitis is a granulomatous rxn to inhaled organic antigens (e.g. pigeon feces/feathers in pigeon breeders)

81
Q

How does hypersensitivty pneumonitis present? If this disease persists, what would happen?

A
  • Pt would present w/ fever, cough, and dyspnea hours after exposure to the organic antigen –> it resolves w/ removal of the irritating exposure
  • Chronic exposure would lead to intersitital fibrosis –> restrictive lung disease
82
Q

What is a characteristic finding in hypersensitivity pneumonitis?

A

Hypersensitivity pneumonitis is a granulomatous rxn to inhaled organic antigens. One important feature that differentiates this from other granulomatous causes of restrictive lung disease is the presence of lots of eosinophils w/ the granulomas

83
Q

What MAP of pulmonary circuit is considered pulm HTN? What is it normally?

A
  • MAP of >25 mmHg of pulmonary circuit is considered pulm HTN
  • Normal MAP of pulmonary circuit is 10 mmHg
84
Q

What 4 vascular changes are seen in pulmon. HTN?

A
  1. Atherosclerosis of pulm. trunk
  2. Smooth muscle hypertrophy of pulm. arteries
  3. intimal fibrosis
  4. Plexiform lesions (characteristic vascular change seen in severe long-standing pulm HTN, where capillaries grow in groups - probably to try to mitigate some of the increased pressure)
85
Q

How can pulmonary HTN be subclassified?

A

Pulmonary HTN is subclassified into Primary and Secondary pulm HTN depending on the etiology

86
Q

What is the etiology of primary pulm HTN? What patient population is classically affected by primary pulm HTN?

A
  • Etiology of primary pulm HTN is unknown; some familial forms are related to an inactivating mutation of BMPR2, which leads to proliferation of vascular smooth muscle
  • Classically this is seen in young adult females
87
Q

What are 3 underlying causes that may precipitate secondary pulm. HTN?

A
  1. Hypoxemia
  2. Increased volume in pulm circuit
  3. Recurrent pulm emboli (most PEs are clinically silent since they are small and b/c lungs have dual circulation –> however, repeated PE may cause thickening of vasc wall if it chronically obstructs vessels and thereby increase pressure)
88
Q

What is Acute Respiratory Distress Syndrome?

A

ARDS is diffuse dmg to the alveolar-capillary interface (diffuse alveolar dmg)

89
Q

Explain the pathogenesis of hypoxemia and cyanosis that occurs in Acute Respiratory Distress Syndrome.

A

In ARDS, there is diffuse alveolar dmg –> allows protein-rich fluid to leak into alveolar interstitium –> protein-rich fluid + necrotic epithelial cells forms hyaline membranes in alveoli –> hypoxemia and cyanosis occurs due to thickened diffusion barrier and collapse of air sacs (hyaline membranes increase surface tension = increase inward collapsing pressure of alveolar wall)

90
Q

Describe how the lungs would look on chest x-ray in ARDS.

A

ARDS leads to a characteristic “white-out” of the lungs (due to diffuse alveolar dmg that is filling w/ inflamm exudate/hyaline membranes)

91
Q

What is a common pathological process seen in the many diseases that precipitate ARDS?

A

ARDS is secondary to a ariety of disease processes (e.g. sepsis, infxn, shock, trauma, aspiration, pancreatitis, DIC, hypersensitivity rxns, and drugs)

  • Common pathological process in all the diseases that cause secondary ARDS is: Activation of neutrophils –> induces protease and free-radical dmg of Type I AND Type II pneumocytes = unable to produce surfactant + unable to replace dmg’d resp epithelium
92
Q

What is the treatment for ARDS?

A
  1. Treat the underlying cause
  2. Ventilation w/ PEEP (positive end-expiratory pressure)
93
Q

What is positive end-expiratory pressure (PEEP)? What respiratory syndrome is it used for, and why is it useful?

A
  • PEEP is a form of ventilation, where a controlled amt of O2 is left in the lung during exhalation
  • It is used for ARDS; In ARDS, pts have an increased risk of airway collapse due to the hyaline membrane formation around alveoli –> if airway collapses, it takes great effort to reinflate during inhalation (initial inflation takes the most energy/stress) –> by leaving some O2 in the lung during exhalation, PEEP prevents complete collapse of the alveoli –> reduces stress of inhalation
94
Q

How may ARDS lead to intersitital fibrosis?

A

There is destruction of Type I and II pneumocytes in ARDS; Type II pneumocytes are the stem cells of lung parenchyma –> their destruction would mean fibrosis and scarring would be the only way to proceed in the healing response rather than replacement w/ lung tissue

95
Q

What is the etiology of neonatal respiratory distress syndrome (NRDS)?

A

NRDS is due to inadequate surfactant levels

96
Q

Explain the pathogenesis by which the respiratory symptoms in NRDS arise.

A
  1. Surfactant is made by Type II pneumocytes (surfactant is composed primarily of lecithin, aka phosphatidylcholine)
  2. Surfactant production may be interrupted (e.g. due to prematurity, C-section, or maternal diabetes)
  3. Lack of surfactant increases surface tension in the alveolar wall –> collapse of alveolar wall after expiration and increased resistance to reinflation –> hyaline membranes can form around the alveolar wall due to dmged resp epithelia + inflamm exudate
97
Q

What are 3 underlying causes that are associated w/ NRDS? Explain why each one may lead to NRDS.

A
  1. Prematurity: Surfactant production begins @ 28 weeks and adequate levels are not reached until 34 weeks.
  2. C-section delivery: Stress of birthing process normally increases steroids w/n the child –> steroids increases synthesis of surfactant; C-section removes this natural stress, which increases risk for NRDS
  3. Maternal diabetes: High maternal blood glucose will increase neonatal production of insulin in response to the high circulating blood glucose levels –> insulin inhibits surfactant synthesis
98
Q

What is an indirect measure for surfactant levels in neonates that are still in the mother’s womb? What numerical value would signify adequate surfactant production?

A
  • Lecithin (aka Phosphatidylcholine): Sphingomyelin ratio (“L:S ratio”) of the amniotic fluid can be used to screen for lung maturity
  • A L:S ratio >2 would indicate adequate surfactant production
  • Lecithin is the key component of surfactant; as lung matures and surfactant production increases, the lecithin levels should increase, while sphingomyelin levels remain pretty constant*
99
Q

What would be seen on chest x-ray in a nenoate w/ NRDS?

A

The lungs would appear diffusely grainy (“ground-glass” appearance of lungs; very similar to ARDS) due to the hyaline membrane formation and inflamm exudate

100
Q

What are some complications that can arise due to the hypoxemia assoc w/ NRDS?

A

Hypoxemia would inrease the risk for:

  • Patent ductus arteriosus (since PDS normally closes when lung infaltes and there is good oxygenation of blood)
  • Necrotizing enterocolitis, due to decrease oxygenated blood going to the gut
  • Think of it as the lungs are affected and the 2 other symptoms are things below it*
101
Q

Supplemental O2 is given to neonates suffering from NRDS to minimize the hypoxemia. However, what are some complications associated with O2 therapy?

A

Supplemental O2 increases risk for free radical dmg:

  • Retinal injury leads to blindness
  • Lung dmg leads to bronchopulmonary dysplasia (dmg to immature lung tissue in neonates precludes them from developing normal mature lungs)
102
Q

What are the 3 most common cancers in incidence (from most common to less common)?

A
  1. Breast/Prostate
  2. Lungs
  3. Colorectal
103
Q

What are the 3 most common cancers by mortality (from most common to less)?

A
  1. Lung
  2. Breast/Prostate
  3. Colorectal
104
Q

Give 3 examples of key risk factors for developing lung cancer.

A
  1. Cigarette smoke (Especially polycyclic aromatic hydrocarbons and arsenic)
  2. Radon
  3. Asbestos
105
Q

How do patients become exposed to radon?

A

Radon is formed by radioactive decay of uranium, which is present in soil. Normally, it is released into atmosphere, but it can become trapped in places where there is little ventilation (e.g. basements)

Radon is the 2nd most frequent cause of lung carcinoma in the US

106
Q

Imaging in a high risk Pt for lung cancer (e.g. smoker) may reveal what type of lesion? What would be the immediate next step if this lesion is found?

A
  • Imaging often reveals a solitary nodule (“coin-lesion”)
  • The next step would be to compare this imaging with prior imaging studies to see if the coin-lesion has changed or is a new finding
107
Q

What diseases could cause a coin-lesion that is benign (not carcinoma) on chest x-ray?

A
  1. Granulomas: Often due to TB or fungus (esp. Histoplasma if Pt is from midwest)
  2. Bronchial hamartomas: Benign tumor of normal lung tissue (hamartomas are malformation of normal tissue that grows in a disorganized way)
108
Q

What 2 categories can lung carcinoma be divided into? How does this dictate treatment modalities?

A
  1. Small cell carcinoma (15%): Not able to surgically resect; Pt is treated early w/ chemo
  2. Non-small cell carcinoma (85%): Treated upfront w/ surgical resection; these cancers do not respond well to chemo
109
Q

What are some examples of non-small cell carcinomas? (Name 5)

A
  1. Adenocarcinoma (40% of NSCC)
  2. Squamous cell carcinoma (30% of NSCC)
  3. Large cell carcinoma
  4. Carcinoid tumor
  5. Bronchioalveolar carcinoma
    * NSCCs Are Still Like Cancer Bro*
110
Q

Explain the histological findings, associated risk factors, location of tumor, and other assoc symptoms for: Small Cell Carcinoma

A

Histological finding: Poorly differentiated small cells of neuroendocrine (Kulchitsky) cell origin

Assoc risk factors: Male smokers

Location: Central

Assoc Symptoms: Rapid growth/metastasis and Paraneoplastic Syndromes (e.g. Cushing Syndrome due to the cells releasing ADH or ACTH and Eaton-Lambert Syndrome)

111
Q

Explain the histological findings, associated risk factors, location of tumor, and other assoc symptoms for: Adenocarcinoma

A

Histological finding: Glands or mucin

Assoc risk factors: Most common tumor in nonsmokers and female smokers

Location: Peripheral

Assoc Symptoms: None

112
Q

Explain the histological findings, associated risk factors, location of tumor, and other assoc symptoms for: Squamous Cell Carcinoma

A

Histological finding: Keratin pearls or intercellular bridges (intercellualr bridges is due to desmosomes that normally connect squamous epith)

Assoc risk factors: Most common tumor in male smokers

Location: Central

Assoc Symptoms: May in a small subsect of Pts produce PTHrP (which essentially acts like PTH) –> hypercalcemia

Recall, cancers of Lungs that start with S (i.e. small cell carcinoma and squamous cell carcinoma) are associated w/ Smokers and are found S(c)entrally and have associated Syndromes

113
Q

Explain the histological findings, associated risk factors, location of tumor, and other assoc symptoms for: Large Cell Carcinoma

A

Histological finding: Poorly differentiated large cells w/o defining features of other lung carcinomas (no keratin pearls, no intercellular bridges, glands, or mucin) - Basically this is a broad term given if the cells are poorly differentiated and large and it doesnt fit into other categories

Assoc risk factors: Smoking

Location: Central or Peripheral

Assoc Symptoms: Poor prognosis

114
Q

Explain the histological findings, associated risk factors, location of tumor, and other assoc symptoms for: Carcinoid tumor

A

Histological finding: Well differentiated neuroendocrine (Kulchitsky) cells. They grow in nests, which is a characteristic growth pattern of differentiated neuroendocrine cells.

Assoc risk factors: Not related to smoking

Location: Central or peripheral; If central, it will form a polyp-like mass in the bronchus

Assoc Symptoms: Cells will stain chromogranin positive (since they are differentiated neuroendocrine cells). This is a low-grade malignancy, but rarely, can cause carcinoid syndrome (where excess serotonin is over-produced due to neuroendocrine origin of the carcinoid tumors)

115
Q

Explain the histological findings, associated risk factors, location of tumor, and other assoc symptoms for: Bronchoalveolar carcinoma

A

Histological finding: Thin epithelium of bronchioles and alveoli are replaced by columnar cells; These arise from Clara (aka Club) cells, which act as the stem cells in the bronchiolar epithelium

Assoc risk factors: Not related to smoking

Location: Peripheral

Assoc Symptoms: Pt may present w/ pneumnonia-like consolidation on imaging; This disease has excellent prognosis

116
Q

Pleural involvement is seen classically in what type of lung cancer?

A

NSCC (specifically adenocarcinoma)

117
Q

What is Superior Vena Cava Syndrome and how does it present? (in reference to lung cancer)

A

SVC syndrome is where the lung tumor may obstruct the SVC –> leads to distended head and neck veins w/ edema and blue discoloration of arms and face

118
Q

Involvement of what structures would cause hoarseness and diaphgragmatic paralysis in lung cancer?

A

Involvement of the recurrent laryngeal nerve or phrenic nerve would lead to hoarseness and diaphgramatic paralysis, respectively

119
Q

How could Horner syndrome arise in lung cancer? Where (anatomically) is the lung cancer usually located if it causes Horner Syndrome?

A
  • Compression of the sympathetic chain due to the lung cancer would lead to Horner Syndrome (ptosis, miosis, and anhidrosis)
  • Usually due to an apical (Pancoast) tumor
120
Q

What is the major reason for which lung carcinoma generally have poor prognosis (15% 5-year survival)?

A

There is no effective screening method and the disease presents late (since pleural cavity is large, the cancer would have to have grown to a large size to present clinically)

121
Q

What are the most common sites that lung carcinomas metastasize?

A

LABB (Liver, Adrenal Glands, Brain, Bone)

122
Q

What are the most common primary tumors that metastasize to lung? What would be seen on imaging?

A
  • Breast and colon carcinoma
  • Multiple “cannon-ball” nodules on imaging
123
Q

What is a pneumothorax?

A

Accumulation of air in the pleural space

124
Q

How do spontaneous pneumothorax occur?

A

Spontaneous pneumothorax occur due to rupture of an emphysematous bleb

125
Q

What would be seen on chest xray in spontaneous pneumothorax?

A

Collapse of affected lung would be seen with a shift of the trachea towards the side of collapse

(Kind of like the spontaneous pneumothorax is sucking it towards that side)

126
Q

How do tension pneumothorax arise?

A

Usually arise w/ penetrating chest wall injury

127
Q

What is the mechanism by which tension pneumothorax causes clinical disease?

A

Penetrating chest wall injury allows air to enter the pleural space, but it cannot exit when you expire –> As more air enters and accumulates, it compresses down the lung and pushes the trachea to the opposite side of injury

128
Q

How is tension pneumothorax treated?

A

Chest tube, which allows air to drain out from the pleural space

129
Q

What is mesothelioma? What risk factor is it associated with?

A
  • Malignant neoplasm of mesothelial cells
  • Highly associated w/ occupational exposure to asbestos
130
Q

Where are mesothelial cells found in the lung? What is its fxn in the lung?

A
  • Mesothelial cells line the parietal and visceral pleura (in general, mesothelial cells line these visceral coverings, like pleura, peritoneum, epicardium, etc.)
  • Mesothelial cells secrete fluid that lubricate the pleural space to facilitate movement of lung against chest wall during breathing
131
Q

What clinical symptoms would a patient with mesothelioma present with (3)?

A
  1. Recurrent pleural effusion (since mesothelial cells normally secrete fluid)
  2. Dyspnea
  3. Chest Pain
132
Q

How would the gross appearance of the lung be in a Pt w/ mesothelioma?

A

The tumor would encase the lung (lung would be collapsing due to the massive mesothelial tumor that encases it)

133
Q

In a Pt being treated for small cell carcinoma, what complication can arise that would cause fever, tachypnea, leukocytosis, and chest X-ray that shows a distinct cavity w/ an air/fluid level distal to the tumor?

A

Pulm. abscess due to dstruction of lung parenchyma (either by chemo or tumor)

air/fluid refers to the pus and air found in the abscess cavity

134
Q

What is Diffuse Alveolar Damage? What would be seen histologically?

A
  • DAD is a nonspecific pattern of rxn to injury of alveolar epith/endothelial cells from a variety of acute insults
  • Hyaline membrane formation and interstitial inflammation
  • (DAD is essentially a less severe form of ARDS)*
135
Q

What is atelectasis?

A

Fancy word for Collapse of lung

136
Q

What is chylothorax?

A

Fancy word for accumulation of lymphatic fluid w/n pleural space

137
Q

What is Alveolar proteinosis? What would it show histologically and how is it treated?

A
  • Alveolar proteinosis (aka lipoproteinosis) is a rare condn where alveoli are filled w/ a granular proteinaceous/eosinophilic material
  • Histologically, you will see acellular eosinophilic material that fills the alveoli
  • It is treated w/ repeated bronchoalveolar lavage to remove the material
138
Q

What is pulmonary eosinophilic granuloma? What is a major risk factor for this disease and what would it look like histologically?

A
  • Pulmonray eosinophilic granuloma is a type of Langerhans Cell Histiocytosis
  • Virually all the patients who get isolated forms of this are cigarette smokers
  • Histologically, you’d see a granuloma w/ Langerhan cells (specialized dendritic cells that are APCs) + lymphocytes + eosinophils + macrophages
139
Q

What histological changes would be expected in Pts who expired from status asthmaticus?

A

A bronchus w/ luminal mucous plug (Curshmann Spirals); submucosal gland hyperplasia; basement membrane thickening; and increased number of eosinophils (Charcot-Leyden Crystals)

140
Q

What is Homan’s Sign? What does this suggest? What pulm complication is this Pt susceptible to develop?

A
  • Physical exam technique, where Pt feels pain in the calf muscle upon dorsiflexion of foot w/ leg extended
  • DVT
  • Pulmon emboli
141
Q

What patient population is most affected by lymphangioleiomyomatosis?

A

Women of childbearing age

142
Q

What histological changes would be seen in lymphangioleiomyomatosis?

A

Widespread proliferation of smooth muscle in the lung, mediastinal & retroperitoneal l.n.’s, and the major lymphatic ducts

143
Q

How would lymphangioleiomyomatosis present on gross exam?

A

Bilateral, diffuse enlargement of the lungs + cystic changes similar to emphysema

144
Q

In Goodpasture Syndrome, what is the target of the autoantibodies produced?

A

Noncollagenous domain of type IV collagen (found on basement membranes)

145
Q

What would be seen histologically in Cryptogenic Organizing Pneumonia?

A

Loose fibrous tissue in the alveoli and bronchioles (compared to DAD, which would have INTRA-alveolar fibrous tissue [hyaline membranes])

146
Q

What type of cancers are primarily seen in the larynx? What patient population is most likely affected?

A
  • Squamous cell carcinoma makes up the vast majority of laryngeal carcinomas
  • Primarily seen in smokers
147
Q

A coin lesion found on chest x-ray with the characteristic of having a “popcorn” pattern of calcification indicates what disease?

A

Pulmonary hamartoma

148
Q
A

Pathology (5 decks)

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