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FMS Week 9: Pathology of Asthma Flashcards

1
Q

What is Asthma?

A

basically a reduction of airflow through a variety of processes that is

bronchoconstriction

airflow limitation

airway hyperreactivity

least partly reversible (in order to be asthma must be partly reversible)

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2
Q

Hallmarks of Asthma

A

*

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3
Q

Airway remodeling is?

A

Changes in the proportions of histologic constituents that make up the airways

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4
Q

Atopy classification

A

genetic predisposition towards IgE-mediated hypersensitivity reaction (eczema, allergic rhinitis, etc.)

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5
Q

Most common type of asthma

A
  • Atopic Asthma
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6
Q

Classic example of Type I IgE-mediated hypersensitivity reaction

A

Atopic Asthma

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7
Q

Atopic Asthma begins when?

A

Typically in childhood

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8
Q

Atopic Asthma is triggered by?

4 Listed

A

environmental allergens

  • pollen
  • dust
  • foods
  • animal dander
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9
Q

Does Atopic Asthma have a family history component?

A

Yes, often see a family history of asthma

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10
Q

Tests for atopic asthma

2 Listed

A

Weal and flare

RAST (Radioallergosorbent test)

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11
Q

RAST description and name

A

Identifies serum IgE specific for a panel of allergens

Radioallergosorbent test

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12
Q

Non-Atopic Asthma test

A

No evidence of allergen sensitization (negative RAST, skin test)

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13
Q

Non-Atopic Asthma family history component?

A

Less common than in atopic asthma

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14
Q

Non-Atopic Asthma underlying cause?

A
  • increased airway hyperirritability
  • viral respiratory infections are a common cause
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15
Q

Aspirin-sensitive asthma

A
  • seen in conjunction with recurrent rhinitis and nasal polyps
  • special type of non-atopic asthma
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16
Q

Occupational Asthma

A
  • A special type of non-atopic asthma
  • caused by dusts (wood, platinum), fumes, gases; generally occurs after repeated exposure
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17
Q

Asthma Pathogenesis

A

Pollen meets tissue dendritic cell to Th2 cell

Th2 cell activates B cell with IL-4

B cell produces IgE

IgE coats mast cells

IgE cross-linking on mast cells

degranulation recruits eosinophils

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18
Q

histopathologic changes in asthma

A
  • Type I hypersensitivity
  • A genetic predisposition + environmental triggers
  • thickening of the basement membrane
  • smooth muscle cells thickening
  • lamina propria macrophages, eosinophils, mast cells, neutrophils
  • goblet cell hyperplasia
  • eosinophils in the mucus
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19
Q

Atopic Asthma Early phase or immediate phase:

4 Listed

A
  • vagus nerve stimulated
  • vagus nerve parasympathetic nervous system
  • get bronchoconstriction
  • increased vascular permeability
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20
Q

Atopic Asthma: Late Phase

A
  • Increased inflammation
  • causes epithelial damage (raggedness and cell dropout of epithelial layer)
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21
Q

T cell environmental differentiation factors: Th1

5 Listed

A
  • Presence of older siblings
  • early exposure to daycare
  • viral infection
  • farm environment
  • Tuberculosis
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22
Q

T cell environmental differentiation factors: Th2

5 Listed

A
  • Widespread use of antibiotics
  • Western Lifestyle
  • Urban Environment
  • Diet
  • Aeroallergens
23
Q

Early Phase responses

4 Listed

A
  • Bronchial smooth muscle contraction
  • mucus secretion
  • vascular leakage
  • mucosal edema
24
Q

Late Phase response

3 Listed

A
  • Infiltration with eosinophils and neutrophils
  • increase inflammation
  • bronchial hyperreactivity
25
Q

Early and LAte Phase response effects

4 Listed

A
  • Obstruction of large and small airways
  • air trapping
  • respiratory acidosis
  • hypoxemia
26
Q

Genetics of Asthma

3 Listed

A
  • Multifactorial with environmental factors with multiple susceptibility genes
  • gene expression and the combination of various polymorphisms varies from patient to patient
  • more than 100 genes have a reported association in various mechanisms (immune response, tissue remodeling, disease severity, response to therapy)
27
Q

Specific examples of Genetics of Asthma

3 Listed

28
Q

Tissue/Pathology?

A

normal airway wall

29
Q

Tissue/Pathology?

A

Normal respiratory bronchiole

30
Q

Tissue remodeling in chronic asthma

At least 8

A
  • luminal mucous plugging
  • Epithelial goblet hyperplasia
  • Epithelial injury
  • Basement membrane thickening/fibrosis (AKA subepithelial fibrosis/subepithelial collagen deposition)
  • Increased airway vascularity
  • Smooth muscle hypertrophy
  • Mucous gland hypertrophy
31
Q

Airway remodeling summary

32
Q

Epithelial-mesenchymal trophic unit

36
Q

Additional characteristic findings in asthma

3 Listed

A
  • Creola Bodies
  • Curschmann spirals
  • Charcot-Leyden crystals
37
Q

Creola bodies Description

5 Listed

38
Q

Curschmann Spirals

5 Listed

39
Q

Charcot-Leyden Crystals Description

5 Listed

40
Q

What is this?

A

Creola Bodies

41
Q

What is this?

A

Curschmann Spirals

42
Q

What is this?

A

Creola Bodies

43
Q

What’s This?

A

Charcot-Leyden Crystals

44
Q

What’s this?

A

Charcot-Leyden Crystals

45
Q

What’s This?

A

Charcot-Leyden Crystals

46
Q

What’s This?

A

Charcot-Leyden Crystals

47
Q

Clinical features of Asthma

48
Q

Asthma Treatment

49
Q

Status Asthmaticus

50
Q

Status asthmaticus autopsy findings?

A

Obstructive: Difficulty expelling air

51
Q

Asthma summary 1

52
Q

Asthma Summary 2

53
Q

Asthma Summary 3

54
Q

Subepithelial fibrosis AKA

A

Basement membrane thickening

FMS (34 decks)

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