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IPFC 2 Final > Asthma pathophys > Flashcards

Asthma pathophys Flashcards

1
Q

What symptoms sudden or persistent is associated with asthma (4)

A
  • Dyspnea (difficult breathing)
  • Chest tightness
  • Wheezing
  • Sputum production and cough
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2
Q

What is the main cause of asthma? What does this cause?

A

Inflammation
- bronchial hyper-resonsiveness/reactiveness

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3
Q

Is asthma reversible

A

Yes

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4
Q

Why is asthma still causing death? (4)

A
  1. Under-diagnosis of asthma
  2. Under-treatment of asthma
  3. Lack of public understanding and education of asthma
  4. Inadequate asthma supervision and poor monitoring
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5
Q

Asthma prevalence in boys vs girls and men vs women

A

More common in boys (children)
More common in women (adult)

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6
Q

T/F asthma is primarily an adult disease

A

False

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7
Q

Is life span affected with asthma patients?

A

No

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8
Q

What is considered a significant predisposing factor for asthma?

A

Atopy

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9
Q

What is the etiology of asthma (2)

A

Genetic factors + environmental risk factors/triggers

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10
Q

Define Atopy

A

The GENETIC tendency to develop IgE antibodies to encountered environmental allergens by natural exposure (pollens, grass)
- route of entry is mucosal surfaces and skin

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11
Q

When a patient experiences an intense immune response due to allergens.. what allergic diseases can it lead to? (5)

A
  • Allergic rhinitis
  • Asthma
  • Atopic dermatitis (eczema)
  • Hives
  • food allergies
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12
Q

Do all patients with atopy develop asthma?
Do all patients with asthma have atopy?

A

No
No

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13
Q

Explain the hygiene hypothesis

A

During pregnancy, women have more TH2 than TH1
- this is so she does not reject the fetus

The baby’s immune system must be rebalanced at birth to make TH2 = TH1 to decrease risks for atopy/asthma

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14
Q

What factors favour the Th2 phenotype which is not ideal (creating an imbalance) (5)

A
  • Antibiotics
  • Hand sanitizers
  • Urban environment
  • western lifestyle
  • Diet
  • Sensitization to house-dust mites
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15
Q

Which factors favour the Th1 phenotype (IDEAL)

A
  • presence of older siblings
  • Early exposure to day care
  • Tuberculosis, measles, or hepatitis A
  • Rural environment
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16
Q

What are some host factors that influence development of asthma?

A
  • Genetic
  • Obesity
  • Gender
  • Emotional factors/stress
  • Medical conditions
  • Perinatal factors (maternal smoking, maternal asthma)
  • Medical conditions (GERD, chronic sinusitis, URTI)
  • Exercise (cold air)
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17
Q

What are environmental factors that affect asthma

A
  • Allergens
  • Infections
  • Occupational sensitizers (paint fumes)
  • Tabacco Smoke (passive + active)
  • Outdoor/indoor pollution
  • Diet (food allergies like milk, soy, nuts, eggs, shellfish)
  • Medications (Aspirin or NSAID, use of beta-blockers)
18
Q

What is asthma caused by?

A

Bronchioal hyper-responsiveness
- bronchospasm, tissue edema, mucus hypersecretion
- narrowing airways

19
Q

Is asthma obstructive/restrictive

A

Obstructive

20
Q

What are 3 components that move debris out of lungs

A
  1. Cilia
  2. Sol layer
  3. Gel layer
21
Q

What are the 4 steps to allergic cascade?

A
  1. Sensitization to an allergen
  2. early/immediate phase response upon re-exposure to allergen (IAR)
  3. Late phase response to allergen (LAR)
  4. Chronic inflammation
22
Q

Explain how sensitization to allergen works

A
  1. Initial exposed to allergen
  2. If Atopic: T cells stimulate B cells to plasma cells to produce IgE antibodies for that antigen
  3. IgE antibodies bind to mast cells (mast cell-IgE complex)
  4. Allergen crosslinks IgE on mast cells

This complex is now sensitized (tiny ticking bombs). It is prepared to recognize and react to allergens

23
Q

When does Immediate Asthma response occur? How long does it last?

A
  • Occurs within minutes with re-exposure
  • lasts a few hours
24
Q

How does Immediate-phase asthma response work (IAR)? What is the result

A
  1. Incoming allergen binds to IgE on mast cells creating a cross linking of IgE antibodies
  2. With sufficient cross-linking, mast cells explode and degranulate
    - release histamine + inflammatory mediators
  3. The inflammatory mediators will cause
    - bronchoconstriction
    - vasodilation (edema)
    - increase mucous secretion
    - induce plasma exudation (leaking) into airways

Result:
- thickened, edematous airways & narrowing of airway lumens

25
Q

What is the solution to IAR?

A

Can spontaneously reverse on its own OR
with inhaled B2-agonist

26
Q

When does late Asthma response occur (LAR)? How long does it last?

A

Occurs within several hours
- can last 3-10 hours (sometimes 24+ hours)

Starts at the SAME TIME as IAR but takes longer to fully manifest

27
Q

How does late asthma response work (LAR)? What is the result?

A
  1. Recruits and activates immune cells (eosinophils, basophils, neutrophils, macrophages, Th cells)
  2. Immune cells release more inflammatory mediators
  3. Inflammatory mediators cause MORE activation of EOSINOPHILS

Result: Damage to epithelial cells and further bronchoconstriction

28
Q

What is the solution to LAR

A

corticosteroids
- difficult stage to reverse with bronchodilators

29
Q

How does chronic asthma occur. What is the result

A
  1. Repeated exposure to allergens and allergic response
  2. Permanent damage occur in lung tissue

Result
- airway remodelling
- scarring over time

30
Q

Is chronic asthma curable?

A

No
- it is treatable AND preventable

31
Q

What are the effects of chronic inflammation on airways? (6)

A
  • epithelial damage –> airway hyper-reactivity
  • Loss of relaxant factors –> exposure of sensory nerves
  • FIBROSIS: thickening of basement membrane due to sub-epithelial fibrosis + deposition of collagen below the basement memrbane
  • Hypertrophy and hyperplasia of airway smooth cells (inc # of cells = thickened = not functional)
  • Increased sensitivity of smooth muscle cells (from chemical mediators)
  • increased mucous: from goblet cells
32
Q

Explain aspirin induced asthma? What is the triad? What occurs? What is the solution?

A

Triad =
- Asthma + aspirin sensitivity + nasal polyps

How
1. Single dose during 30-40s can provoke an acute asthma exacerbation,
- + rhinorrhea, conjunctival irritation, flushing of head and neck
2. leads to overproducing leukotrienes

Treatment
- avoid these meds BUT
- leukotriene receptor antagonists can work (montelukast) OR
- desensiztization to ASA

33
Q

What is the role of mast cells?

A

INITIATE (happens 1st) the acute bronchoconstriction to allergens
- allergens combine with IgE antibodies to sensitize mast cells then release mediators

34
Q

What is the role of macrophages?

A

Amplify inflammatory response via release of cytokines

35
Q

What is the role of dendritic cells?

A

Take allergen to introduce to the rest of the body to fight it
- interacts with undifferentiated Th cells and stimulate more Th2 –> leads to formation of ANTIBODIES and MORE EOSINOPHILS

36
Q

What is the role of T lymphocytes

A
  • release specific cytokines that drive eosinophils to the inflammation and maintenance of mast cells
37
Q

What is the role of B lymphocytes?

A

Secrete IgE antibodies

38
Q

What is the role of eosinophils? (3)

A

secrete proteins that:
- damage epitheliel cells
- cause epithelial remodelling
- airway hyper-reactivity

39
Q

What is the role of neutrophils?

A

Seen in COPD

40
Q

What are the 4 structural cells? What are their roles?

A
  1. Epithelial cells
    - interact with inhaled allergen to secrete Thymic Stromal Lymphopoietin (TSLP) to acitvate dendritic cells

Endothelial cells, smooth muscle cells, fibroblasts

41
Q

What are the chemical mediators?

A

Cytokines (most important are interleukins)
- IL-3, 4, 5, 8, 13

Chemokines
- Attract th2 to the bronchioles

Arachidonic acid
- leukotrienes: important mediator for cytokine function
- inc. mucous secretion, recruit more inflammatory cells etc.. (look at table with 6)

IPFC 2 Final (6 decks)

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