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Flashcards in Pathology II Deck (26):
1

What type of inflammation accompanies chronic bronchitis?

lymphocytic inflammation, along with the cardinal symptom of excessive mucus production (as opposed to eosinophillic infiltrate in asthma

2

Describe the type of collagen that is laid down in basement membrane thickening during asthma.

type I and III are deposited instead of the normal type IV

3

What are Curschmann spirals and Charcot-Leyden crystals? What disease are they characteristic of?

whorls of shed epithelium in mucus plugs

4

Classify and describe Loffler Syndrome.

simple pulmonary eosinophilia with transient pulmonary lesions, peripheral (blood) eosinophilia, benign course

5

Describe the symptoms and clinical data associated with acute eosinphilic pneumonia with respiratory failure.

rapid onset of illness of unknown cause presenting with fever, dyspnea and hypoxemic reparatory failure which responds to corticosteriods

BAL >25% eosinophils, CXR shows diffuse infiltrates

6

Define bronchiectasis by describing the symptoms and mechanism(s) of disease. What are some possible causes?

permanent dilation of bronchi/bronchioles caused by destruction of muscle and elastic tissue due to repeated bouts of inflammation, associated with chronic necrotizing infection (TB, Staph, Aspergillus)

Causes: obstruction by tumor or foreign body, hereditary dysfunction of mucus (CF) or kartageners (cilia).

7

What defect causes primary cilia dyskinesia?

AR defect in dyne in arms of cilia (present in ½ patients with Kartageners syndrome: bronchiectasis, sinusitis, situs inversus)

8

CRTR is a ______ channel but regulates multiple ion channels including facilitating the movement of ____ ions.

chloride, Na+

9

What are the 3 striking pathological features of CF lung?

mucus plugging, bronchiectasis, consolidation (due to infection), pseudomonas is a common infection and causes green color from metabolite

10

Name 4 common causes of pulmonary fibrosis.

chronic injury or recurrent acute injury
interstitial lung disease

11

What is the key mediator that is released from injured type I alveolar epithelial cells in IPF?

TGF B1
it is an important inhibitor of caveolin (natural inhibitor of collagen deposition) AND acts to reduce telomerase

12

Name two pathologic characteristics of a section of IPF lung.

temporal heterogeneity (key feature of UIP) consists of both:
new (active) fibrosis called fibroblastic foci
old (collagenized) dense fibrosis

13

Discuss the two geometric forms of asbestosis and how their characteristics modulate disease risk.

amphibole: more pathogenetic because it is more aerodynamic (penetrates deeper in lung) and is less soluble

serpentine: less pathogenic because of curly shape (less penetrant) and is more soluble (able to be removed from lung)

14

Asbestos fibers become coated with iron and calcium which is why it is often referred to as a ______ ______.

ferrugeinous body

15

What two qualities of a mesothelioma can be used to confirm by lab test that the growth is mesothelioma?

mesothelioma does not produce TTF-1 thyroid transcription factor like lung tissue does

mesothelioma will be Cal-retnin positive

16

What is egg-shell calcification on x-ray a classic symptom of?

silicosis (affects the upper lobe primarily), can increase susceptibility to TB

17

What are lines of Zahn?

created by the layering effect of thrombus forming in a vessel with blood flow (an alternating pattern of platelets, fibrin and RBC)

is important in identifying ante-morem thrombosis v. post mortem clot

18

Discuss possible causes of pulmonary HTN.

COPD/ILD causing hypoxia and loss of capillaries
congenital (shunts) or acquired heart disease (MS)
recurrent tromboemboli (obstruction causes increase in PVR)
connective tissue disease (systemic sclerosis)
obstructive sleep apnea (with obesity_
idiopathic PAH

19

What gene is connected to familial pulmonary arterial hypertension? What is its inheritance pattern?

BMPR 2: bone morphogenic protein receptor type 2, lack of signaling by this receptor causes an increase in proliferation and a decrease in apoptosis of endothelial cells ("gate keeper" of # endothelial cells)

AD with 10-20% entrance, follows two-hit hypothesis

20

What morphological changes occur in response to pulmonary hypertension?

increase atherosclerotic plaques, and medial hypertrophy (smooth muscle proliferation causing onion like pattern)

plexiform lesions: proliferation of SM form multiple channels within the capillary

21

Pulmonary edema can be divided into types based on their etiology, what are those two types?

Hemodyanmic (increased hydrostatic pressure-CHF; decreased oncotic pressure- protein loss)

microvascular injury (increased vascular permeability due to injury, infection, sepsis, trauma, shock and drugs)

22

What is pulmonary alveolar proteinosis? What causes it?

granular precipitate of surfactant that can fill alveoli; it is most often caused by a anti GM-CSF antibody (autoimmune) and secondarily by hemopoietic disease or malignancy

23

How are ALI, ARDS and DAD related?

acute lung injury: hypoxemia and infiltrates without heart failure

acute respiratory distress syndrome: severe hypoxema and infiltrates without heart failure

diffuse alveolar damage: histologic manifestations of ALI and ARDS characterized by hyaline membranes that impair gas exchange and consist of fibrin rich edema and cytoplasmic and lipid remnants of necrotic cells

24

What are the reproducible phases of DAD?

exudative, transition, proliferative, fibrotic

25

Goodpasture syndrome is an autoimmunity disease that occurs against type ____ collagen in the basement membrane which is damaged in a type ___ reaction.

antibody against type IV collagen in the basement membrane, damage due to type II reaction

note death commonly mediated by uremia in renal failure and tx. includes plasmapheresis to remove antibody (linear pattern of antibody deposition)

26

What systems does Wegener Granulomatosis effect?

necrotizing granulomatous vascultitis involves the airways (upper and lower) and the kidneys and is mediated by cANCA (anti protenase-3) in 95% of patients causing granulomas and vasculitis