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Pathology Pre-Midterm > Module 7 pulmonary > Flashcards

Module 7 pulmonary Flashcards

1
Q

What is Asthma?

A

The only reversible airway bronchoconstriction,most often due to allergic stimuli (type I HSR)

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2
Q

There are different types of asthma and the order of the cards will follow the different types. The first type is Atopic (Extrinsic) Asthma, what are some features?

A

Much more common and is episodic
based on a familial predisposition to type I HSR to dust, pollen, animal dander and foods
Causes bronchial asthma, allergic asthma, allergic rhinitis and eczema (ectopic dermatitis)

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3
Q

What happens with the first exposure to a trigger in a person with atopic extrinsic asthma?

A

Sensitization: so antigen presentation and isotype switching from THO to TH2 because of IL4 and IgE production.
IgE binds to the surface of mass cells and basophils and you get mast cell degranulation

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4
Q

What happens with the second exposure to a trigger in a person with atopic extrinsic asthma?

A

Re-exposure to antigen induced cross linking of IgE on mast cells and basophils – brochoconstriction

  • –production and activation of eosinophils (stimulated by IL-5), PMNs and T cells
  • -epithelial cells are activated and recruit more TH2 cells and eosinophils = damage resp epithelium —- amplifies bronchospasm and edema
  • -produces histamine, leukotrienes and Prostoglandins that cause bronchoconstriction and bronchospasms
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5
Q

Review: What are the TH2 cytokines?

A

IL4-stimulates IgE production by turning THO to TH2 (isotype switching)
IL5: activates eosinophils
IL-13: stimulates mucus production and promotes IgE production by B cells IgE coats mast cells = degranulation with Ag exposure

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6
Q

Review: What two diseases are associated with Eosinophils?

A

Asthma

Churg Strauss

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7
Q

Patients with extrinsic bronchial asthma are at risk of developing what disease if exposed?

A

Allergic bronchopulmonary aspergillosis: which is a type I and III HSR

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8
Q

What do patients with both types of bronchial asthma present with?

A

Expiratory wheeze, chest tightness, productive cough (Sputum), and SOB

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9
Q

In sputum cytology what do you see on a patient with atopic extrinsic asthma? pics on slide 5b

A 
Curschmann Spiral (shredding of bronchial epithelial cells) (pseudostratified) 
Charcot layden crystals: MBP and eosinophilic cationic protein
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10
Q

On CXR what do you see in a patient with atopic extrinsic asthma?

A

Hyperinflated lung fields

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11
Q

What do you see on pulmonary function test and ABG for extrinsic asthma?

A

Pul function test: decreased FEV:FVC ratio and Increased TLC:RV
ABG: low O2 and Low CO2 and elevated pH because you are hyperventilating. If CO2 becomes high and patient becomes acidotic then patient is decompensating (getting tired) and about to die.

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12
Q

Now on histology, slide 5a, what do each of the arrows represent?

A

Green Arrow: Goblet cell hyperplasia no metaplasia
Black Arrow: thick BM
Yellow Arrow: eosinophils (inflammatory cells)
Blue arrow: bronchial SM hypertrophy

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13
Q

What is reversible and irreversible in atopic bronchial asthma?

A

So the changes seen on histology are irreversible
but the symptoms are reversible
—remember only reversible obstructive disease
—remember REID index is normal

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14
Q

How chronic bronchitis different from bronchial atopic asthma?

A

Chronic Bronchitis: no eosinophils, REID elevated, squamous metaplasia (Because cig smokers)

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15
Q

The next type of asthma is non atopic bronchial asthma Intrinsic. What are the causes?

A

Most common is viruses

and then aspirin

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16
Q

Explain how viruses cause non atopic bronchial asthma

A

Lower the threshold of the vago receptors (vago receptors bind acetylcholine and that increases PS response — bronchoconstriction
–give Albuterol (B2 agonist)–stimulates sympathetics — bronchodilation (but you can also give this to atopic bronchial asthma as well)

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17
Q

Explain how aspirin can cause non atopic bronchial asthma?

A

Inhibits COX and favors lipooxygenase — increases leukotrienes — bronchoconstriction

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18
Q

What are some differences in atopic and non atopic bronchial asthma

A

NO IgE
No family history
NO CHARCOT LEYDEN CRYSTALS
BUT DO SEE CURSCHMAN SPIRALS AND PMNs

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19
Q

What are the complications of both types of bronchial asthma?

A

Status Asthmaticus: severe persistent bronchial asthma, the get mucus plugs, resorptive atelectasis and does not respond to albuterol only responds to intubation.
–more common with extrinsic

20
Q

Eosinophilic Granuloma as called pulmonary histiocytosis X and pulmonary langerhan cell histiocytosis (PLCH), occur when?

A

Pulmonary diseases in the adult almost exclusively involves smokers, treatment centers on cessation

  • -results in dyspnea and cough, interstitial nodular and fibrocystic, disease, obstructive and restrictive changes on spiro.
  • -culprit cell in the langerhans cell, not the eosinophil, contain Birbeck granules on EM
21
Q

The last obstructive lung disease bronchiectasis. What is bronchiectasis?

A

Permanent/ irreversible dilation of bronchi to pleural surface

22
Q

Bronchiectasis is not a primary disease but a secondary disease, what factors predispose an individual of getting bronchiectasis?

A
  1. Congenital or Hereditary Conditions: CF is most common cause of bronchiectasis, also immunodeficiency states and Kartagener syndrome
  2. Obstruction and Chronic Infection: Obstruction with either tumor or foreign body
  3. Necrotizing/suppurative pneumonia: virulent organisms like S. aureus and Klebsiella
23
Q

What is the pathogenesis for bronchiectasis?

A

Obstruction hampers clearance — secondary infection — damaged/weakened bronchial walls — bronchiectasis

24
Q

What is the pathogenesis for a tumor/foreign body in bronchiectasis?

A

Impairs clearance of secretions, providing favorable substrate for superimposed infection
—centrally located tumors (bronchial carcinoid, squamous and small cell carcinoma)

25
Q

What is the pathogenesis for CF in bronchiectasis?

A

Widespread and severe bronchiectasis results from obstruction caused by the secretion of abnormally viscid mucus thus predisposing to infection of the bronchial tree

26
Q

What is the pathogenesis for Kartagener syndrome?

A

Is a rare autosomal recessive disorder that is frequently associated with bronchiectasis and sterility in males. In this condition structural abnormalities of the cilia impair mucocilliary clearance in the airways, leading to persistent infections and reduce mobility of spermatozoa.

27
Q

Bronchiectasis favors what lobes?

A

affects lower lobes bilaterally particularly those air passages that are most vertical
when causes by tumors or aspiration of foreign bodies the involvement may be localized to a single segment of the lungs

28
Q

What are the symptoms you see for a patient with bronchiectasis?

A 
Fevers 
Halitosis (bad breath)
Productive cough with foul smelling sputum 
Finger Clubbing (Due to hypoxia)
Hemoptysis (coughing up blood)
29
Q

What do you see on CXR and cytology in a patient with bronchiectasis?

A

CXR :train track appearance (due to the dilation of the bronchi all the way to the pleura)
Cytology: mixed flora of anaerobes (foul smelling) and aerobes

30
Q

What are some complications of bronchiectasis?

A
  1. Can lead to resp failure
  2. Cor pulmonale (Enlargement of right side of heart due to a secondary pul condition)
  3. Decreased FEV: FVC and Increased TLC:RV
  4. Metastatic abscesses (from lung and brain)
  5. Sepsis (if travels to blood)
  6. Resorption atelectasis due to obstruction of bronchial lumen
  7. AA amylodiosis due to chronic inflammatory condition – leading to restrictive cardiomyopathy
31
Q

Now bronchiectasis mimics a lung abscess, point out some differences between the two?

A

Lung Abscess: Spike fever (Abscess in general have this feature) and Cavity with air fluid level (all pus in that cavity)
Bronchiectasis: just fever and train track appearance on CT or xray

32
Q

Now moving onto restrictive lung diseases, what are some general characteristics of restrictive lung diseases?

A

Heterogenous group of disorders
Bilateral, patchy chronic lung involvement
Involves the interstitium of alveolar walls
may involve the intra alveolar space
Fibrosis therefore decreased lung compliance = increased work to breathe = dyspnea
Progression to resp failure with pul HTN and cor pulmonale

33
Q

There are 5 main categories of restrictive lung diseases the first is fibrosing, what are the 4 diseases in this category?

A
  1. IPF/UIP
  2. NSIP
  3. COP
  4. CVD
34
Q

The first fibrosing restrictive lung disease is Idiopathic pulmonary fibrosis (IPF) also called usual interstitial pneumonia (UIP), what are some features?

A

UIP is the pattern seen on histology
Involves fibrosis of the lung interstitum
Involves more Males over Females are over 60 years old and are smokers

35
Q

Why is IPF/UIP considered a diagnosis of exclusion?

A

because we dont know the etiology ( idiopathic)

36
Q

What is the pathogenesis for IPF/UIP?

A

TGFbeta responsible for IDF (macrophages and type I pneumocytes make TGFbeta) and they bring in fibroblasts which bring in collagen and hence fibrosis

37
Q

There are two types of heterogeneity involved in UIP, geographic and temporal, explain the differences

A

Geographic or spatial: favors the lower lobe first

Temporal: indicates new and old fibrosis so you will have acellular type I HSR and cellular fibroblasts

38
Q

On microscopy slide 7, how do you differentiate the new and old fibrosis?

A

Temporal
so old would be the pink acellular spots
new fibrosis is the cellular or fibroblast foci

39
Q

What other disease, that we have discussed does heterogeneity?

A

Polyarteritis Nodosa

–displaced temporal heterogenity: old (fibrosis) and new (PMNs and fibrinoid necrosis) inflammatory changes

40
Q

What is the presentation for UIP/IPF?

A

Dry cough (Nothing in alveolar space) with dyspnea on exertion, finger clubbing, pulmonary fibrosis

41
Q

What does the CXR and gross specimen for patients with UIP/IPF look like?

A

CXR: bilateral reticular nodular shadowing
Gross: honey comb parachyma (distention of lungs) lined by type II pneumocytes (pleural cobblestone)

42
Q

What is the course and treatment for UIP/IPF?

A

Progressive and relentless —- need a lung transplant

  • -alot of times too old to get a transplant
  • -most patients die about 3 years after dx
43
Q

What are the complications of UIP/IPF?

A
  1. Contraction atelectasis (fibrosis)
  2. Cor pulmonale (fibrosis)
  3. AIP (Acute interstitial pneumonia, is the acute accelerated phase, like an acute on chronic thing) (looks like ARDS)
44
Q

What is the histological appearance of UIP/IPF?

A

Diffuse alveolar damage with hyaline membrane with AIP (also called Hamman Rich) on top of UIP

45
Q

What is AIP also known as hamman rich syndrome?

A
  • -very aggressive form of interstitial lung disease
  • –may also occur as an acute phase of accelerated IPF( so like an acute on chronic thing)
  • -presents with diffuse alveolar damage and hyaline membranes, similar to those found in the acute resp distress syndrome ARDS and Diffuse Alveolar Damage (DAD)
  • if there is no known cause of ARDS then called acute interstitial pneumonia

Pathology Pre-Midterm (35 decks)

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