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Last Minute Step 1 Facts > Respiratory Tract Pathology > Flashcards

Respiratory Tract Pathology Flashcards

1
Q

If you encounter a child with nasal polyps (which typically occur due to repeated bouts of rhinitis), you want to test them for…

A

Cystic Fibrosis

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2
Q

What is the major underlying association of adults that have nasal polyps?

A

Aspirin-induced asthma

Triad of: asthma, aspirin-induced bronchospasm, and nasal polyps

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3
Q

What is an angiofibroma?

A

Benign tumor of nasal mucosa composed of large blood vessels and fibrous tissue

Classically seen in adolescent males

Presents with profuse epistaxis

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4
Q

Describe nasopharyngeal carcinoma

A

Malignant tumor of nasopharyngeal epithelium

Biopsy usually reveals pleomorphic keratin-positive epithelial cells (poorly differentiated squamous cell carcinoma) in a background of lymphocytes

Associated with EBV

Classically seen in African children and Chinese adults

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5
Q

What is a vocal cord nodule?

A

A nodule that arises on true vocal cord consisting of degenerative (myxoid) connective tissue; presents with hoarseness; resolves with resting of voice

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6
Q

What is a laryngeal papilloma associated with? How does this differ between children and adults?

A

HPV 6 and 11

Papilloma are usually single in adults and multiple in children.

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7
Q

What is a laryngeal carcinoma?

A

squamous cell carcinoma usually arising from the epithelial lining of the vocal cord that is associated with alcohol and tobacco; rarely arises from laryngeal papilloma

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8
Q

What are the two key inflammatory mediators of pain?

A

Bradykinin and prostaglandin E2

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9
Q

What are the classic gross phases of lobar pneumonia?

A

Classic gross phases of lobar pneumonia

  1. Congestion- due to congested vessels and edema
  2. Red hepatization- due to exudate, neutrophils, and hemorrhage filling the alveolar air spaces, giving the normally spongy lung a solid consistency
  3. Gray hepatization- due to degradation of red cells within the exudate
  4. Resolution- due to the type 2 pneumocytes
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10
Q

What are the bacteria most commonly implicated in aspiration PNA?

A

Most often due to anaerobic bacteria in the oropharynx (e.g., Bacteroides,
Fusobacterium, and Peptococcus)

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11
Q

What are the five major bacteria implicated in bronchopneumonia?

A

S. aureus, H. flu, pseudomonas, moraxella, and legionella

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12
Q

MC cause of interstitial PNA

A

mycoplasma

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13
Q

2nd MC cause of interstitial PNA in young adults

A

chlamydia

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14
Q

MC cause of interstitial PNA in infants

A

RSV

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15
Q

What are the three unique features of coxiella?

A

Atypical pneumonia with high fever (Q fever); seen in farmers and veterinarians (Coxiella spores are deposited on cattle by ticks or are present in cattle placentas).

Coxiella is a rickettsial organism, but it is distinct from most rickettsiae because it (l) causes pneumonia, (2) does not require arthropod vector for transmission (survives as highly heat-resistant endospores), and (3) does not produce a skin rash.

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16
Q

Mycoplasma is grown on…

A

Eaton agar

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17
Q

What are the complications of mycoplasma

A

Complications include autoimmune hemolytic anemia (IgM against I antigen on RBCs causes cold hemolytic anemia) and erythema multiforme.

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18
Q

What are the three virulence factors of mycobacterium?

A
  1. trehalose dimycolate
  2. sulfatides
  3. catalase-peroxidase
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19
Q

MOA of TB virulence factor: trehalose dimycolate

A

aka cord factor

  • helps evade immune response
  • causes granuloma formation
  • triggers cytokine release
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20
Q

MOA of TB virulence factor:

sulfatides

A
  • glycolipids

- inhibits fusion of phagolysosomes

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21
Q

MOA of TB virulence factor:

catalase-peroxidase

A

-resists host cell oxidation

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22
Q

Where can TB systemically spread?

A

Systemic spread often occurs and can involve any tissue; common sites include
meninges (meningitis), cervical lymph nodes, kidneys (sterile pyuria), and lumbar vertebrae (Pott disease).

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23
Q

how can TB affect the heart?

A

constrictive pericarditis

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24
Q

reactivation TB is associated with what kind of spaces within the lung?

A

cavitations

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25
Q

when miliary TB goes to the brain, where does it specifically effect?

A

meninges at the base of the brain

26
Q

what is the most commonly involved organ in miliary TB?

A

kidney (gives sterile pyuria)

27
Q

what are the defining pressures of pulmonary HTN?

A

High pressure in the pulmonary circuit (mean arterial pressure > 25 mm Hg; normal is 10 mm Hg)

28
Q

what is the important path finding seen in those with pulmonary HTN?

A

plexiform lesions are seen with severe, long-standing disease

29
Q

what is the etiology of primary pulmonary HTN?

A

etiology is unknown; some familial forms are related to inactivating mutations of
BMPR2, leading to proliferation of vascular smooth muscle

30
Q

relate PE and pulmonary HTN

A
  • can have chronic long-standing PE that get reorganized
  • this reorganization leads to thickening of the vascular wall
  • leads to pulmonary HTN
31
Q

why does ARDS occur in so many diseases?

A

Activation of neutrophils induces protease-mediated and free radical damage of
type I and II pneumocytes.

32
Q

how is recovery complicated in ARDS?

A

-knocked out type II pneumocytes so….

interstitial fibrosis

33
Q

what types of mothers are at high risk for NRDS?

why do we give babies steroids?

A

Phosphatidylcholine (lecithin) levels increase as surfactant is produced; sphingomyelin remains constant

A ratio > 2 indicates adequate surfactant production

Caesarian section delivery: due to lack of stress-induced steroids; steroids increase synthesis of surfactant.

Maternal diabetes:
Insulin decreases surfactant production.

34
Q

What are the complications of neonatal RDS?

A

Complications

  1. Hypoxemia increases the risk for persistence of patent ductus arteriosus and necrotizing enterocolitis.
  2. Supplemental oxygen increases the risk for free radical injury. Retinal injury leads to blindness; lung damage leads to bronchopulmonary dysplasia.
35
Q

in a spontaneous pneumothorax, the trachea shifts to…

A

TO THE SIDE OF THE INJURY

36
Q

in a tension pneumothorax, the trachea shifts to…

A

TO THE OPPOSITE SIDE OF THE INJURY

37
Q

What are the three key risk factors of lung cancer?

A

Key risk factors are cigarette smoke, radon, and asbestos.

Radon is formed by radioactive decay of uranium, which is present in soil.
i. Accumulates in closed spaces such as basements
ii. Responsible for most of the public exposure to ionizing radiation; 2nd most
frequent cause of lung carcinoma in US
iii. Increased risk of lung cancer is also seen in uranium miners.

38
Q

small cell carcinoma is treated with ____.

non-small cell carcinoma is treated with ____.

A

small cell carcinoma is treated with chemo.

non-small cell carcinoma is treated with surgery.

39
Q

histology, location, and association of small cell lung carcinoma

A

Poorly differentiated small cells; arises from neuroendocrine (Kulchitsky) cells

Male smokers

Central

Rapid growth and early metastasis; may produce ADH or ACTH or cause Eaton-Lambert syndrome (paraneoplastic syndromes)

40
Q

histology, location, and association of squamous cell carcinoma of the lung

A

Keratin pearls or intracellular bridges

Most common tumor in male smokers

Central

May produce PTHrP

41
Q

histology, location, and association of adenocarcinoma of the lung

A

Glands or mucin

Most common tumor in nonsmokers and female smokers

Peripheral

42
Q

histology, location, and association of bronchioloalveolar carcinoma

A

Columnar cells that grow along preexisting bronchioles and alveoli; arises from clara cell

Not related to smoking

Peripheral

May present with pneumonia-like consolidation on imaging; excellent prognosis

43
Q

histology, location, and association of bronchioloalveolar carcinoma

A

Columnar cells that grow along preexisting bronchioles and alveoli; arises from clara cell

Not related to smoking

Peripheral

May present with pneumonia-like consolidation on imaging; excellent prognosis

44
Q

histology, location, and association of carcinoid carcinoma

A

Well differentiated neuroendocrine cells; chromogranin positive

Not related to smoking

Central or peripheral classically forms a polyp-like mass in the bronchus

Low-grade malignancy; rarely, can cause carcinoid syndrome

45
Q

FVC volume can be compared to

A
  • blowing out a candle on a birthday cake

- the amount of air you can maximally exhale

46
Q

what are the four major obstructive diseases?

A
  • Emphysema
  • Chronic bronchitis
  • Asthma
  • Bronchiectasis
47
Q

what are the important numerical parameters of chronic bronchitis?

A

Chronic productive cough lasting at least 3 months over a minimum of 2 years; highly associated with smoking

Characterized by hypertrophy of bronchial mucinous glands –> leads to increased thickness of mucus glands relative to overall bronchial wall thickness (Reid index increases to > 50%; normal is< 40%).

48
Q

why do some people get emphysema?

A

the only way by which we can defend ourselves at the bottom of the lung is via the alveolar macrophages

overall, there is an imbalance between proteases and anti-proteases

Smoking is the most common cause of emphysema.

Pollutants in smoke lead to excessive inflammation and protease-mediated
damage.

Results in centriacinar emphysema that is most severe in the upper lobes

49
Q

when you lose the elastic recoil of the lungs and the chest goes out a bit, you reset the FRC because it…

A

increases

50
Q

What is seen histologically within the gunk of an asthmatic patient?

A

Productive cough, classically with spiral-shaped mucus plugs (Curschmann
spirals) and eosinophil-derived crystals (Charcot-Leyden crystals).

51
Q

histamine induced vasodilation occurs where?

where does the leaking of fluid occur?

A

histamine induced vasodilation occurs where?
arterioles

where does the leaking of fluid occur?
post capillary venules

52
Q

leukotrienes come super early in an allergic response or later?

A

in the second phase. get the bronchoconstriction from these. later, MBP is produced.

53
Q

what is bronchiectasis?

A
  • abnormal dilation of LARGE AIRWAYS
  • loss of tone
  • metaphor: blowing through a straw and feeling air come out on the other side vs blowing through a pipe
  • OBSTRUCTED from emptying the lung
54
Q

why do we get bronchiectasis?

A

Due to necrotizing inflammation with damage to airway walls.

Happens to patients that for some reason have chronic infections in these walls

Causes include

  1. Cystic fibrosis- thick secretions and block our large tubes
  2. Kartagener syndrome- can’t clear the mucus
  3. Tumor or foreign body
  4. Necrotizing infection
  5. Allergic bronchopulmonary aspergillosis-Hypersensitivity reaction to Aspergillus leads to chronic inflammatory damage; usually seen in individuals with asthma or cystic fibrosis
55
Q

what are the complications of bronchiectasis?

A

Complications include hypoxemia with cor pulmonale and secondary (AA)
amyloidosis.

56
Q

what is the overview of secondary amyloidosis

A

you have chronic inflammation that creates an acute phase reactant called SAA

gets overproduced in chronic inflammation

gets converted to AA

that is what deposits

57
Q

idiopathic pulmonary fibrosis overview idea

A

fibrosis of the interstitium that makes up the wall or outer portion of the alveolar air sac

cyclical lung injury with a cyclical healing response –> lots of TGF-beta

58
Q

exposure and pathological findings of coal workers lung

A

Carbon dust; seen in coal miners

Massive exposure leads to diffuse fibrosis (‘black lung’); associated with rheumatoid arthritis (Caplan syndrome)

Mild exposure to carbon (e.g., pollution) results in anthracosis (collections of carbon-laden macrophages); not clinically significant

59
Q

exposure and pathological findings of silicosis

A

Silica; seen in sandblasters and
silica miners

Fibrotic nodules in upper lobes of the lung

Increased risk for TB; silica impairs phagolysosome formation by macrophages.

60
Q

exposure and pathological findings of berylliosis

A

Beryllium; seen in beryllium miners and workers in the aerospace industry

Noncaseating granulomas in the lung, hilar lymph nodes, and systemic organs

Increased risk for lung cancer

61
Q

exposure and pathological findings of asbestosis

A

Asbestos fibers; seen in construction workers, plumbers, and shipyard workers

Fibrosis of lung and pleura (plaques) with increased risk for lung carcinoma and mesothelioma; lung carcinoma is more common than mesothelioma in exposed individuals.

Lesions may contain long, golden- brown fibers with associated iron (asbestos bodies)

Last Minute Step 1 Facts (16 decks)

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