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Pathology pulmonlogy > Pulmonary Pathology I > Flashcards

Pulmonary Pathology I Flashcards

1
Q

Developmental and Congenital Conditions

A
  • Congenital Anomalies
  • Atelectasis
  • Hyaline membrane disease
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2
Q

Vascular Lesions

A
  • ARDS/SIRS
  • Pulmonary edema
  • Pulmonary ischemia/infarction (PE)
  • Pulmonary hypertension
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3
Q

congenital cysts

A
  • associated with polycystic kidney disease
  • bronchogenic cysts; up to 5 cm
  • complications include infection, rupture
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4
Q

bronchopulmonary sequestration

A
  • presence of lobes or segments without a normal connection to the airway system – appear as masses
  • ventilation-perfusion mismatch
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5
Q

pulmonary hypoplasia

A

inadequate expansion (compression)

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6
Q

types of developmental and congenital conditions

A

congenital cysts
bronchopulmonary
pulmonary hypoplasia
hamartomas

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7
Q

Atelectasis

A
  • incomplete expansion OR
  • collapse of previously inflated lung tissue
  • reversible
  • reduces oxygenation and predisposes to INFECTION
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8
Q

obstructive Atelectasis

A

-airway obstruction with absorption of trapped air
*caused by excessive secretions, exudates, tumors,
foreign objects
*mediastinum may shift toward the atelectatic lung

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9
Q

compressive atelectasis

A 
external compression (pleural fluid, blood, etc.); also tension pneumothorax
-mediastinum shifts away from affected lung
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10
Q

patchy atelectasis

A

loss of pulmonary surfactant (hyaline membrane disease, ARDS)

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11
Q

Surfactant

A

surface active agent which reduces surface tension of a fluid
-secreted by type II alveolar epithelial cells

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12
Q

components of surfactant

A

dipalmitoyl lecithin (phospholipid), surfactant apoproteins, and calcium ions

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13
Q

Hyaline Membrane Disease

A

-insufficient surfactant synthesis in premature infant
-severe atelectasis
-development of respiratory distress within hours of
birth
-associated with prematurity, diabetes in the mother,
and non-elective cesarean section
-occurs in 60% or infant born at <5% after 37 wks

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14
Q

what does the respiratory distress in infants with hyaline membrane disease present with?

A
  • respiratory “grunt”, retraction of ribs

- eventual cyanosis only partially relieved with O2

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15
Q

fundamental defect in HMD

A

-deficiency of pulmonary surfactant

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16
Q

what happens to the alveoli in infants with HMD

A

-alveoli collapse with each successive breath; progressive atelectasis and reduced lung compliance
-alveoli are filled with a protein-rich, fibrin-rich exudates “hyaline membranes”
-necrosis of pneumocytes; paucity of inflammatory
reaction
-never seen in stillborn infants or babies who die within
hours

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17
Q

CO2 retention and hypoxemia in HMD

A
  • atelectasis and airway collapse result in decreased ventilation
  • exudate acts as barrier to gas exchange
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18
Q

how is fetal lung maturity assessed

A
  • by amniocentesis

- lecithin:sphingomyelin ratio

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19
Q

how is HMD treated?

A

-corticosteroids used to induce formation of surfactant

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20
Q

complications of oxygen therapy for HMD

A
  • bronchopulmonary dysplasia and retrolental fibroplasia (leading to blindness)
  • mechanical ventilation is associated with interstitial emphysema -forcing of air into interstitium
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21
Q

Adult Respiratory Distress Syndrome (ARDS)

A
  • rapid onset of severe life-threatening respiratory insufficiency, cyanosis, severe arterial hypoxemia refractory to oxygen therapy
  • poor aeration due to presence of pulmonary edema
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22
Q

what is ARDS associated with?

A

-non-cardiac, high-permeability edema(leaking of fluid from capillaries into alveoli 2° to capillary damage or increased vascular permeability)

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23
Q

what do capillaries fill with in ARDS?

A

diffuse capillary/alveolar damage with collection of
fibrin-rich exudate in alveoli (hyaline membranes) and
subsequent interference with gaseous exchange

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24
Q

ARDS complications

A

-direct injury to lungs: infections, oxygen toxicity, inhalation of toxins, irritants; aspiration of gastric contents
-systemic conditions: septic shock, shock associated with
trauma, hemorrhagic pancreatitis, burns

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25
Q

what is the final common pathway in ARDS

A

-diffuse damage to the alveolar and/or capillary walls
-edema, fibrin exudation, and formation of hyaline membranes
-neutrophil and inflammatory mediator-induced damage
to capillary walls

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26
Q

morphology of ARDS

A
  • acute, edematous stage: lungs are heavy, firm , red, and boggy; interstitial and intra-alveolar edema, inflammation
  • fibrin deposition leads to hyaline membrane formation including necrotic epithelial cells
  • rarely resolves; organization of exudate with intra-alveolar fibrosis
  • (pulmonary edema resolves without scarring)
27
Q

what HMD result from?

A
  • results from atelectasis and associated formation of hyaline membranes
  • ?mechanical damage to alveoli
  • No intrinsic pathology of interstium or capillaries
  • No inflammation
28
Q

what does ARDS result from?

A

ARDS results from formation of hyaline membranes

secondary to alveolar damage (with inflammation)

29
Q

how does ARDS result from SIRS?

A

-In SIRS, ARDS results from a systemic inflammatory
response and subsequent increased vascular permeability
(cytokine storm)

30
Q

Pulmonary Edema

A
  1. Hemodynamic - transudate
  2. Inflammatory – exudate (infiltrate)
  3. Mixed (i.e., tumors)
31
Q

pulmonary edema: Hemodynamic - transudate

A
  1. increased hydrostatic pressure
    -congestion of vessels with microhemorrhages
    -chronic CHF – heart failure cells
  2. left-sided congestive heart failure
    -obstruction of outflow – mitral valve stenosis, aortic
    valve stenosis, ischemic heart disease
  3. decreased oncotic pressure
32
Q

pulmonary edema pathophysiology

A

heavy, wet lungs
-fluid accumulation initially in basal regions of lower
lobes
-alveolar capillaries are engorged and an intra-alveolar
pink precipitate is seen
-alveolar microhemorrhages with hemosiderin-laden
macrophages
-long-standing disease is associated with fibrosis and
thickening of the alveolar walls (lungs become firm
and brown or brown induration)

33
Q

key features of Pulmonary edema

A
  • vascular congestion
  • edema
  • fluid in airways mixed with air – productive cough
  • fluid collection gravity dependent (sitting vs. lying down)
  • lungs are wet and heavy
34
Q

edema in pulmonary edema causes

A

widening of the alveolar walls

  • fluid accumulation within the alveoli
  • transudate – pink, granular fluid without infiltrate
  • few red cells
35
Q

PE

A

occlusions of the pulmonary arteries by blood clots are almost always embolic in origin

36
Q

occurrence of PE

A
  • deep vein thrombosis - 95%
  • (rare in situ thrombosis - pulmonary hypertension, atherosclerosis, heart failure)
  • > 50,000 deaths per year
  • sole or major contributing factor in 10% of adults dying acutely in hospitals
37
Q

causes of PE

A

-associated with underlying disorder - ie. cardiac disease, cancer, etc.
-also immobilization, hypercoagulable states
(primary or secondary)
-indwelling central lines - right atrial thrombus, PE

38
Q

primary PE cause

A

antithrombin III deficiency, protein C deficiency

39
Q

secondary PE cause

A

obesity, recent surgery, cancer, oral contraceptives, pregnancy

40
Q

large PE

A
  • main pulmonary artery or bifurcation
  • acute cor pulmonale and right heart failure
  • sudden death due to blockage of pulmonary circulation (saddle embolus) - electromechanical dissociation
41
Q

small PE

A

travel more distally; transient chest pain, cough, hemorrhage without infarction

  • about 10% cause infarction
  • travel into smaller vessels
  • called great mimicker: mimics an acute MI
42
Q

issues of PE

A

-pulmonary hypertension, obstruction to cardiac flow; ventilation-perfusion mismatches
*(old) perfusion scan may reveal ventilation-perfusion (V/P)
mismatches; now CT

43
Q

what do small PE presage?

A

large ones
-30% have chance of developing second embolus
-multiple small emboli over protracted course:
pulmonary HTN, sclerosis, cor pulmonale

44
Q

how are PE resolved?

A

contraction and fibrinolysis

45
Q

what protects against infarction or hemorrhage

A
  • protected by secondary (bronchial) circulation

* when infarcts occur, may be hemorrhagic

46
Q

infarcts happen in

A
  • in pre-existing heart or lung disease
  • about 10% of PE cause infarction
  • 3/4 in lower lobes; over 50% - multiple
47
Q

can hemorrhages happen without infarction?

A

yes

48
Q

what shows on an XRAY with an infarct?

A

-may show wedge shaped infiltrate at 12-36 hours

49
Q

pathology of infarct

A
  • wedge-shaped, hemorrhagic
  • raised, red-blue area in early stages
  • after 48 hours, RBC’s lyse and infarct becomes pale
  • as hemosiderin produces, becomes red-brown
  • can get fibrosis
50
Q

pathology of infarction/hemorrhage

A

-gradual fibrous replacement: begins at margins
and forms contracted scar
-septic infarcts are accompanied by inflammatory reaction and exudate

51
Q

Pulmonary Hypertension and Cor Pulmonale

A

-pulmonary pressures reach 1/4 of systemic (normally 1/8)
-usually secondary to structural or cardiopulmonary
conditions
-reversible changes occur with vasoconstriction
secondary to hypoxia

52
Q

secondary to structural or cardiopulmonary

conditions for PHTN

A
  • longstanding COPD, interstitial lung disease/fibrosis
  • congenital or acquired heart disease
  • recurrent PE’s
53
Q

primary or idiopathic pulmonary hypertension

A
  • middle-aged women (20 to 40)
  • associated with mutation in bone morphogenetic protein receptor type 2 (BMPR-2, bone morphogenic protein receptor)
  • progressive hypertension; requires lung transplant
  • can have them inhale nitrous gas-> vasodilator
54
Q

secondary forms of pulmonary hypertension

A

-increased shear and mechanical injury from increased pressures
-dysfunction of pulmonary vascular endothelium
*decreased prostacyclin, increased endothelin, decreased nitric oxide
-release of growth factors and cytokines: migration and
replication of vascular smooth muscle cells, elaboration of
extracellular matrix
-get hyperplastic fibrosis

55
Q

P-HTN: vessel changes involve entire arterial tree

A
  • arterioles/small arteries: striking increases in muscular thickness -concentric hyperplasia
  • most severe cases - atheromatous deposits (lesser degree than system atherosclerosis)
  • intimal fibrosis and luminal narrowing: IRREVERSIBLE
56
Q

plexogenic pulmonary arteriopathy in P-HTN

A
  • primary pulmonary hypertension or congenital heart disease with left to right shunts
  • tuft of capillary formations is present producing network or web that spans lumina
57
Q

Clinical Course of P-HTN

A
  1. symptoms evident with advanced arterial disease
    -chest pain, dyspnea and fatigue
    -right ventricular hypertrophy
    2.death from decompensated cor pulmonale with
    superimposed thromboembolism and pneumonia
    (2 to 5 years in 80%)
58
Q

treatment for P-HTN

A

vasodilators, nitric oxide, antithrombotic medications

59
Q

Diffuse Pulmonary Hemorrhage Syndromes

A
  1. Goodpasture’s Syndrome
    2 Wegener’s granulomatosus
  2. Idiopathic Pulmonary Hemosiderosis
60
Q

Idiopathic Pulmonary Hemosiderosis

A
  1. hemorrhage into alveolar spaces with resulting interstitial fibrosis and hemosiderosis
  2. occurs in children and younger adults
  3. similar to Goodpasture’s in presentation, but NO anti-basement membrane antibodies
  4. productive cough, hemoptysis, anemia, weight loss and diffuse pulmonary infiltrations
61
Q

PE tend to cause

A

hemorrhagic emobli

62
Q

what is done to detect presence of emboli?

A

perfusion scan

63
Q

is P HTN reversible?

A

no

-need lung transplant

Pathology pulmonlogy (5 decks)

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