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Biology 253 > Respiratory Disorders: Asthma > Flashcards

Respiratory Disorders: Asthma Flashcards

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1
Q

What is asthma?

A

chronic inflm of a/w with reversible episodes of a/w obstruction

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2
Q

Asthma is closely related to _______

A

COPD

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3
Q

What 2 response occur from chronic inflm of the a/w?

A
  1. hyper-response

2. recurrent, reversible bronchospasm

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4
Q

How are a/w hyper-responsive?

A

structures are easily irritated

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5
Q

What are known triggers? What happens when encountered?

A
  1. something that is known to set off an episodic a/w obstruction
  2. pt will react with bronchospasm and inflm
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6
Q

During a recurrent, reversible bronchospasm, the a/w is ___________ to other known _______

A

hyper-responsive

triggers

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7
Q

Bronchospasm involves the spontaneous _______ of the______ _______ and remains in that state until __________ _________ subsides

A

contraction

smooth muscle

asthmatic episode

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8
Q

The lumen is compromised d/t ________ _________ = ________ muscles

A

muscle hypertrophy = enlarged muscles

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9
Q

What is the difference if atopic and non-atopic forms?

A

Atopic = allergic conditions/disorders that are genetically based due to a genetic component

Non-Atopic = conditions/disorders similar to allergies that not genetically based

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10
Q

Atopic form is also known as _________ from?

A

Extrinsic Form

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11
Q

T or F: Non-Atopic is Extrinsic form

A

FFFFFFF!!!!!!

IINTRINSIC

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12
Q

Give an example of extrinsic form (atopic)?

A

allergic rhinitis, asthma, and atopic dermatitis (eczema)

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13
Q

Atopic form is typically associated with heightened ______ ________ to common ______ esp _______ allergens and _____ allergies

A

IR

allergens

inhaled

food

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14
Q

Asthma is largely _____ b/c there is type 1 ________

A

atopic

hypersensitivity

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15
Q

Etiology of Asthma (3)

A
  1. complex trait
  2. hypersensitivity to stimuli
  3. T2H cell differentiation
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16
Q

What is the complex trait etiology?

A

genetic component and environmental factors

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17
Q

Hypersensitivity/Hyper-response is related to ________ component. Pt w/ asthma are hypersensitive to triggers such as _____, strong _____, _____, and a/w _______.

A

genetic

allergens, strong odours, exercise/exertion, and a/w irritants

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18
Q

How does exercise trigger an asthmatic episode with inhaling an allergen? How does it present (2)?

A

places an increase burden in the compromised respiratory system

SOB and respiratory distress

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19
Q

Explain how T2H cell differentiation cause Asthma?

A

During differentiation of T cells, more T2H are formed than T1H cells in asthma.

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20
Q

Function of T2H vs T1H cells?

A

T2H cells: responds to allergens and intestinal parasites by stimulating differentiation of B cells into IgE-producing plasma cells acting as growth factors for mast cells and activating more eosinophils

T1H cells: responds to microbes and stimulate the differentiation of B cells into IgG- and IgM producing plasma cells

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21
Q

In an infection, what is the function of macrophage and T cells?

A

engulfs foreign microbe and presents to T cells

T cells produce clones to target bacteria

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22
Q

In respiratory infection , there is a shift to more _____ cells

A

T1H

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23
Q

In patho: the trigger –> increase _______—> 2 phase response. What are the phase called?

A

hypersensitivity

early phase and late phase

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24
Q

Fig 29.6: What happens in the early phase?

A

Allergens trigger T helper cells –> IgE are produced –> IgE binds to mast cells –> mast cells get sensitized and release mediators–> causing BRONCHOSPASM (parasympathetic receptors)

25
Q

In early phase, symptoms develop within ____-____ mins but can be inhibited/reversed by ______ such as __ _______ agonists

A

10-20

bronchodilators

Beta-2 adrenergic

26
Q

What are the effects of chemical mediators in early phase (3)?

A
  1. increase mucus secr.
  2. increase mucosal intercellular junctions
  3. bronchoconstriction
27
Q

What are the consequence of increased mucosal intercellular junction?

A

allows antigen (allergens) and sensitized mast cells to enter the submucosa into the muscle layers which are also impacted by bronchospasm

28
Q

Fig 29.6: What happens in the late phase?

A

allergens move into submucosa causing influx of inflm cells –> release more inflm mediators –> exacerbates bronchospasm and bronchoconstriction

29
Q

In late phase, what injuries occurs in submucosa layer (5)

A
  1. edema
  2. epithelial cell injury
  3. decreased mucociliary function
  4. accum. of mucus
  5. increased a/w responsiveness
30
Q

An individual suffers an asthmatic episodes from cig smokes and move out of building and inhale cool air the episode does not subside. WHY?

A

In late phase, there is an increase a/w responsiveness therefore a/w is hyper-responsive to new triggers eg cool air

31
Q

The late phase develops within ____-____ hours after exposure an asthmatic trigger.

A

4-8

32
Q

What are the symptoms of early phase (7)?

A
  1. type 1 H
  2. allergen binds to IgE on mast cells –> mediators –> inflm
  3. intercellular junctions open –> allergen enter submucosa
  4. increase permeability and mucus hypersec–> edema of a/w
  5. bronchospasm
  6. dyspnea and wheezing
  7. bronchoconstriction
33
Q

What is the duration of early response? How can relieve it?

A

less than 1 hour

a puffer

34
Q

Why is there an increase in permeability? and How?

A

inflm –> increase prod of mucus–>inflm cell release mediators–> mediators results in hyperemia and vasodilation

35
Q

Dyspnea and wheezing is present in severe ___________ ________

A

respiratory distress

36
Q

How is bronchoconstriction a compensatory mechanism? Give example

A

inhaled allergen (eg noxious fumes) cause bronchoconstriction b/c it prevents inhalation of more allergens

37
Q

In the late phase, what 2 things happen when there is an influx of inflm cells?

A
  1. decrease mucociliary blanket function

2. a/w become hyper-responsive

38
Q

Late response is in ____% of all cases and may last for ____ or _____ as it is a ____-_________ cycle of _______________

A

50%

days or weeks

self-sustained

exacerbation

39
Q

In late phase, a/w is responsive to ____ _______ and it is ________ and _____

A

responsive to new triggers

frequent and severe

40
Q

Which receptors cause bronchodilation when activated? What type of drugs and example?

A

beta adrenergic receptors

beta adrenergic agonists eg anticholinergic and ipratropium

41
Q

Which receptors cause Bronchoconstriction when activated? What type of drugs and example?

A

alpha adrenergic receptors

alpha adrenergic agonists eg. adrenaline (Epinephrine)

42
Q

________ _____ or _____ regulates the a/w smooth muscles. It is a _____ in many __________ processes in the body

A

Cyclic AMP or cAMP

mediator

physiological

43
Q

Theory suggests that asthma is d/t l/o _____ _______ ___________. There is a proposed problem with the ______ _________.

A

beta receptors stimulation

beta receptors

44
Q

Manifestations of Asthma (5)

A
  1. dyspnea
  2. wheezing and coughin
  3. bronchospasm
  4. increase respiratory effort
  5. Abn ABG profile
45
Q

What is the coughing type?

A

productive cough

46
Q

What 3 signs of increase respiratory effort?

A
  1. nasal flaring: nostrils open wide in effort to breathe
  2. purse-lip breathing: tunnel made with lips to suck in and breathe out air
  3. use of accessory muscle
47
Q

What does the abn ABG profile indicate (2)?

A
  1. hypoxemia

2. hypercapnia

48
Q

Diagnostic of Asthma (4)

A
  1. hx and px
  2. labs
  3. PFT
  4. Inhalation challenge test
49
Q

What is the inhalation challenge test?

A

To determine the allergen and trigger, the individual inhale potential allergens to confirm dx.

50
Q

What is a mucus plug?

A

Resembles the cast of respiratory tree of larger bronchus to finer a/w. It is expectorated in asthmatic attack. It is gel like.

51
Q

Treatment of Asthma (2)

A
  1. shift from episodic to long term management to prevent episode of asthma
  2. preventative:
    - avoid allergens and trigger
    - no smoking
52
Q

How many steps are in the stage based approach of drugs?

A

4 Stages

53
Q

What is stage 1 of stage based approach of drugs? route?

A

Step 1 = short acting bronchodilators –> inhaled PRN eg puffers and inhalers

54
Q

What is stage 2 of stage based approach of drugs? Why?

A

Add inhaled steroids to decrease inflm (localized effect)

55
Q

What is stage 3 of stage based approach of drugs?

A

add long acting bronchodilators

56
Q

What is stage 4 of stage based approach of drugs? What 2 drugs are used ?

A
  • Steroids PO short course: oral steroids for a week to deal with acute onset of inflm

AND

  • add 3rd drug to short acting bronchodilators, long-acting bronchodilators, and PO steroids

Examples = leukotriene receptor antagonists and theophylline

57
Q

T or F: Theophylline is a first line drug

A

F!!!!!!!

last line drug (not used earlier on in disease)

58
Q

What is the function of theophylline? Blood levels are required to achieve _______ dose not _____.

A

acts by relaxing bronchial smooth a/w

therapeutic

toxic

59
Q

What is leukotrienes? What do leukotriene receptor antagonists do?

A
  • A compound in the body that mediates inflm and allergic response to get the process going.
  • leukotriene receptor antagonist inhibit the binding of the compound and minimizes inflm and allergic response

Biology 253 (39 decks)

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