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Pathology > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

What kind of epithelia line the respiratory tract?

A

nasal cavity and paranasal sinuses = **cuboidal **

pharynx and larynx = **squamous **

trachea and bronchi = cuboidal

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2
Q

What are the main functions of the respiratory system?

A

primary = respiration

  1. voice
  2. immune (MALT & alveolar macrophages)
  3. metabolic, acid-base balance
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3
Q

Describe the respiratory defense system.

A

**MALT means mucosa-assoc. lymph tissue. **

  • forms tonsils in the nasopharynx and pharynx + lymphoid follicles in bronchi

Alveolar macrophages

  • phagocytic cells, can be found in sputum. Pulmonary capillaries mobilize leukocytes quickly to sites of infection.
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4
Q

What are the main respiratory diseases?

A
  • infectious disease
  • immune diseases
  • environmentally induced
  • circulatory disease
  • tumors
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5
Q

Compare the infections of the upper respiratory system with those of the so-called middle respiratory system.

A

**URI: **infection/inflammation of the nose, paranasal sinuses, throat, larynx . . .may spread to the middle ear, and tracheobronchial tree

**MRI: **larynx, trachea, extrapulmonary bronchi.

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6
Q

What could cause a “runny nose”?

A

Most URIs are viruses. In viral infections, lymphocytes, macrophages, and plasma cells infiltrate and cause congestion and edema.

Severe infections can cause ulceration of the mucosal epithelial lining, which allows entry of bacteria.

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7
Q

What is croup?

A

An acute life-threatening infection involving the **larynx. **

Inflammation causes swelling and laryngospasm. The vocal cords spasm and cause “barking cough”. Typically caused by _parainfluenza virus. _

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8
Q

Compare epiglotittis and bronchiolitis.

A

Epiglottitis = **h. influenzae

sudden loss of voice and hoarseness, pain with swallowing. edema and narrowing of the air passage. requires antibiotic therapy.

bronchiolitis = **RSV

wheezing, low-grade fever, SOB. virus invades epithelial cells of the bronchi and bronchioli, causing cell death and desquamation. Edema of airway and dead cells cause obstruction of the bronchi and bronchioli.

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9
Q

Compare alveolar and interstitial pneumonia.

A

aveolar

  • focal or diffuse
  • most often caused by bacteria
  • * often superimposed on pulmonary edema of CHF*

lobar

  • usually diffuse
  • often bilateral
  • most often caused by viruses
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10
Q

List the common causes of pneumonia and give specific characteristics about each of these forms of lung infection.

A

- upper respiratory flora

strep pneumo
H. influenzae
staph aureus

  • *- enteric saprophytes**
  • E. coli
    p. aeruginosa*

- extaneous pathogens
legionella
TB
herpesvirus, CMV

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11
Q

Compare lobar pneumonia and bronchopneumonia with interstitial pneumonia.

A
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12
Q

List 3 complications of bacterial pneumonia.

A
  1. pleuritis
    inflammation commonly >> pleural effusion.
    pus = pyothorax
    fibrous tissue = empyema
  2. abscess
    usually associated with highly virulent bacteria (Staph)
  3. chronic lung disease
    pus causes destruction and bronchial dilation (bronchiectasis).
    fibrosis >> honeycomb lungs
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13
Q

Compare community-acquired pneumonia and hospital-acquired pneumonia.

A

**primary (community-acquired) = **
affects previously healthy people

secondary (or nosocomial) =
affects those with pre-existing illness

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14
Q

What are the clinical signs of pneumonia?

A

systemic

  • fever, chills

local irritation

  • coughing, chest pain, expectoration

airway obstruction

  • dyspnea, tachypnea

inflammation

  • tissue destruction, bleeding
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15
Q

Explain the concept of atypical pneumonia and give specific examples of this clinicopathologic entity.

A 
**atypical** = pneumonias that **do not** present with classical symptoms
examples = *viruses, mycoplasma pneumo*
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16
Q

Compare primary and secondary tuberculosis.

A

Primary. . . occurs in a person not previously exposed.
symtoms = mild & lo fever

Secondary. . . is a reactivation of a dormant primary infection or a reinfection.

symptoms = dry cough, fever, loss of appetite, malaise, night sweats, weight loss

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17
Q

Which fungi cause pneumonia and under what circumstances?

A

community acquired = histoplasmosis, coccidiodomycosis

hosptial acquired (esp AIDS) = PCP, candida, aspergillus

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18
Q

Which pathogens cause pulmonary abscesses?

A

most common = s. aureus

less often = klebsiella, pseudomonas

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19
Q

Compare chronic obstructive pulmonary disease caused by chronic bronchitis and COPD caused by emphysema.

A

Chronic bronchitis = “blue bloaters”

  • bouts of coughing, purulent mucus, dyspnea
  • pulm. HTN, cor pulmonale

emphysema = “pink puffers”

  • no bronchial obstruction, no irritation (therefore no coughing)
  • tachypnea
  • barrel chest
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20
Q

What is bronchiectasis, and how does it develop?

A

a permanent dilation of the bronchi

result of persistent inflammation of the airways. Enzymes from bacteria and leukocytes + mechanical pressure + fibrous scars

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21
Q

Compare centrilobular and panacinar emphysema.

A
  • *centrilobular** = widening of the airspae in the center of a lobule and involves predominantly respiratory bronchioles
  • most common form of emphysema, smoking*
  • *panacinar **= airspaces distal to the terminal bronchioles
  • alpha-1AT deficiency*
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22
Q

List the most important immune diseases of the respiratory tract.

A
  1. sarcoidosis
  2. hypersensitivity pneumonitis
  3. bronchial asthma
  4. allergic rhinitis
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23
Q

Explain the pathogenesis of asthma.

A

increased responsiveness of the bronchial tree to stimuli

*allergens can trigger the release of mediators from mast cells, which act on the blood vessels and smooth muscle cells. Mediators released from chronic inflammatory cells in the wall of the bronchus also stimulate mucous secretion and contraction of the smooth muscle cells. *

24
Q

Compare extrinsic and intrinsic asthma.

A
  • *extrinsic**
  • exogenous allergens
  • type 1 hypersensitivity
  • *intrinsic**
  • nonimmune
  • hyperreactivity of the bronchial tissues
25
Q

What is sarcoidosis, and how does it affect the body?

A

= multisystemic ganulomatous disease

2x more common in AA women than men
10:1 (CD4:CD8)
may have dyspnea, cough, wheezing, low fever, lymphadeopathy

key = noncaseating granuloma

26
Q

List several important antigens that cause hypersensitivity pneumonitis.

A
  • *farmer’s lung**. . . moldy hay
  • *bagassosis**. . . sugar cane
  • *maple bark dx**. . . maple bark
  • *mushroom worker’s lung**. . . mushrooms
  • *humidifier lung**. . . contaminated fluid
  • *pigeon-breeder’s lung**. . . droppings
  • *furrier’s lung**. . . animal pelts
27
Q

Compare acute and chronic hypersensitivity pneumoitis.

A

acute
mediated by antibodies that react with inhaled antigens. will evolve over several hours
* sudden onset dyspnea

chronic
*T lymphocyte mediated. granulomas may from in alveolar septa and damages tissue (fibrosis).
* *chronic dyspnea, hyperventilation, ult resp failure

28
Q

What is pneumoconiosis?

A

= lung diseases caused by inhalation of mineral dusts, fumes, and other particulate matter

29
Q

How does inhalation of mineral particles damage the lungs?

A
  • Coal: less reactive, develops only after long exposure to high levels
  • silica: more reactive, produce prominent tissue injury
  • asbestos: insoluble, remain in lungs permanently
30
Q

Explain the effect of air pollutants on the lungs.

A

small particles = taken up by macrophages (<5 microm)
large particles = stay in nasal mucosa (>10)

macrophages stimulated by the ingested particles release cytokines (IL-1) and TNF, which promote inflammation and stimulate the proliferation of fibroblasts and the formation of collagen

31
Q

Explain the pathogenesis of coal-workers’ lung disease.

A

Particles are taken up by macrophages in alveoli. Particles are deposited in centrolobular zones and may be associated with fibrosis or centroacinar emphysema.

32
Q

What is silicosis, and how does it present pathologically?

A

Inhalation of silica (sand-blasting, mining, stone cutting)

  • causes fibronodular lesions in the lung parenchyma. Particles taken up by macrophages, which release silica crystals and stimulate fibroblasts to produce collagen*
  • **TB is a common complycation b/c silica-laden macrophages cannot effectively combat mycobacterial infections*
33
Q

Which lung diseases are related to exposure to asbestos?

A
  1. pulmonary fibrosis
  2. pleural fibrosis and pleural plaques
  3. lung cancer
  4. mesothelioma
34
Q

Explain the pathogenesis of dyspnea caused by various mechanisms.

A

large airway obstruction. . . laryngospasm

small airway obstruction. . . bronciolitis, asthma

intra-alveolar obstruction. . . pneumonia, edema

alveolar septal lesions

destruction. . . emphysema

increase in thickness. . . intersitital fibrosis

collapse. . . atelectasis

CNS causes. . . apoplexy of respiratory centers

35
Q

Compare the pathologic findings in wet drowning and dry drowning.

A

wet drowning: water prevents entry of air, death occurs within minutes

dry drowning: reflex laryngospasm closes glottis and prevents air/fluid

36
Q

List four main pathogenetic mechanisms of ventilatory failure and explain how they affect respiration.

A
  1. Neural control
    depends on CO2 content
    e.g. apoplexy
  2. Respiratory muscles
    striated muscles dependent on cranial/spinal nerves
    e.g. polio, tetanus, MG, MD
  3. Chest wall
    can restrict expansion
    e.g. kyphoscoliosis
  4. Airways
    alveolar hypoxia
    cystic fibrosis, laryngospasm
37
Q

List common causes of acute respiratory distress syndrome.

A

Shock

  • trauma
  • burns
  • acute cardiac failure

Pneumonia

  • bacterial
  • viral

Toxic lung injury

  • toxic fumes
  • cytotoxic drugs
  • bacterial endotoxins

Aspiration of fluids

38
Q

Describe the pathology of acute respiratory distress syndrome and explain its pathogenesis.

A

alveolar injury = initiating event in viral pneumonia or fumes

endothelial injury = initiating event in sepsis
regardless of initial injury, lesions are comprised of hyaline membranes, ruptured alveolar walls, and intra-alveolar edema

see pg. 185 in book

39
Q

What are the possible outcomes of acute respiratory distress syndrome?

A

1/3 die within days
+
1/3 die of pneumonia and heart failure within weeks
+
1/3 recover

40
Q

What is atelectasis, and what are its possible causes?

A

**atelectasis ****is the incomplete expansion or collapse of alveoli.

  1. deficiency of surfactant
  2. compression of the lungs from outside
  3. resorption of air distal to bronchial obstruction
41
Q

What are the most important neoplasms of the respiratory tract?

A

lung cancer + carcinoma of the larynx

42
Q

Correlate the pathology of carcinomas of the larynx with clinical findings and prognosis of the disease.

A

* all are squamous cell

  • linked with smoking and chronic alcohol
  • rare <40 yrs
  • can originate in any part of the larynx
  • present as nodules and ulcerations of the mucosa
  • patients present relatively early with hoarseness, stridor. 75% 5yr survival. *
43
Q

How common is lung cancer?

A

Most common malignant disease of internal organs and leading cause of cancer death in the US

44
Q

How is tobacco smoking related to lung carcinoma?

A

90% of patients with lung cancer are smokers!

Tobacco smoke has polycyclic hydrocarbons that initiate and promote malignant transformation of cells. Also contains procarcinogens.

45
Q

Explain the histogenesis of various histologic types of lung carcinoma.

A

*Columnar epithelium undergoes squamous metaplasia, which can progress to carcinoma in situ and invasive squamous cell carcinoma. *

adenocarcinomas = mucous/ciliated cells

small-cell = neuroendocrine cells

large-cell = anaplastic stem cells

46
Q

Compare hilar (central) and peripheral lung carcinoma.

A

Central = squamous, large-cell, small-cell

peripheral = adenocarcinomas

47
Q

Where do lung carcinomas metastasize?

A
  • Liver
  • Brain
  • Bone
  • Adrenals
48
Q

What are the clinical signs of lung cancer?

A
  • *- bronchial irritation/obstruction**
  • wheezing, dyspnea, hemoptysis*
  • *- local extension into the mediastinum or pleural cavity**
  • atelectasis, dysphagia*
  • *- distant mets**
  • HSM, neurologic symptoms, Addisons*
  • *- systemic effects**
  • weight loss, anorexia, malaise*
49
Q

What are the common paraneoplastic syndromes caused by lung carcinoma?

A

PTH >> hypercalcemia
ACTH >> Cushing’s

ADH >> hyponatremia

50
Q

Compare pneumothorax and hydrothorax.

A

pneumothorax = air in the pleural cavity

hydrothorax = fluid in pleural cavity

51
Q

Explain the pathogenesis of pleuritis.

A

Hallmark = exudate

bacterial pneumo >> fibrinous/purulent
viral >> serous
TB >> serous or fibrinous, NO PMNs
heart failure/edema >> transudate

52
Q

What is mesothelioma?

A

rare malignant tumor of the pleura

*often r/t asbestos

53
Q

What makes interstitial pneumonia unique?

A

Interstitial . . . inflammation affects the alveolar septa and does not result in exudation of PMNs into the alveolar lumen. Also viruses that cause interstitial pneumonia attach to respiratory epithelial cells >> cell necrosis = “reticular pattern” on x-ray

54
Q

How is pneumonia diagnosed?

A

- x-ray

- sputum studies

- peripheral blood studies

55
Q

What are some unique features of TB?

A
  • acid-fast bacillus (Ziehl-Neelsen)
  • TB does NOT attract PMNs, but forms granulomas
  • Ghon complex = parenchymal focus and hilar lymph node lesion
  • Ghon complex = central caseous necrosis surrounded by epithelioid cells, multinucleated giant cells, lymphocytes
56
Q

What is the defnition of chronic bronchitis?

A

excessive production of tracheobronchial mucus causing cough and expectoration for at least 3 months during **2 consecutive years. **

57
Q
A

Pathology (16 decks)

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