Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

bio253 > Asthma > Flashcards

Asthma Flashcards

1
Q

asthma

A

chronic disease w/ acute, reversible episodes of air way obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

reversible episodes of airway obstruction d/t what

A
  • muscle hyperactivity (bronchospasm)

- inflm (exudate + swelling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

chronic inflm of the a/w (URT) d/t what

A
  • hyper-responsive a/w

- “known” trigger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hyper responsive a/w

A

structures are easily irritated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

“known” trigger

A

recognizable trigger that would cause an episode of a/w obstr –> bronchospasm, inflm & hyper-responsive to unknown triggers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

bronchospasm

A

reversible + recurrent spasm where a/w locks in constricted state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

extrinsic (atopic) form

A
  • genetic tendency to develop allergic diseases (ex. allergic rhinitis, asthma, dermatitis)
  • commonly assoc w/ heightened IR to common allergies, esp inhaled + food allergens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

intrinsic (non-atopic) form

A

responses to triggers that are not genetically based

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

etiology

A
  • complex trait –> genetic factors + enviro factors

- hypersensitivity to triggers (hyper-responsiveness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

trigger examples

A

allergen, strong odor, a/w irritant, exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

patho

A

a/w become more hyper-responsive to other allergens/triggers + leads to bronchospasm & airflow limitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

early phase of asthma

A

release of chemical mediators –> inc mucus prod from goblet cells –> creates mucosal intercellular junctions (gaps b/w epith cells) once allergen is exposed to mast cell –> bronchospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

late phase of asthma

A

allergen moves in –> influx of inflm cells into submucosa that release more inflm mediators, epith cell injury w/ dec mucociliary Fx & accum of mucus, inc vascular permb & edema; results in dec a/w patency d/t bronchospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

acute phase response

A
  • can last upto 1h
  • inhaled allergen –> prev sensitized mast cells degranulate & IgE mediated release inflm mediators –> irritation of inflm cells & bronchospasm (limiting airflow) but the inflm cells do not move into the submucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

acute phase response sequence

A
  1. prior sensitization to allergen (T1 HS)
  2. subsequent exposure = IgE Abs bind to sensitized mast cells
  3. mast cells on mucosa (surface of a/w) release inflm mediators
  4. intercellular junctions open –> allergens enter submucosa
  5. inc cap permb (d/t inflm) and inc mucus secretion (exudate & edema in a/w)
  6. bronchospasm reflex (via PNS)
  7. bronchoconstriction to compensate but not beneficial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

late phase response

A
  • can last hrs-wks
  • a/w is inflamed further –> edema, inflm damage & hypersecretion of mucus –> dec mucociliary Fx –> further limits airflow (peaks 4-8h post-exposure)
  • pt becomes hyperresponsive to new triggers
  • causes influx of inflm cells
  • beta-adrenergic receptors cause bronchodilation (inc breathing)
  • alpha-adrenergic receptors cause bronchoconstriction
17
Q

influx of inflm cells causes what

A
  • inflm damage to epith cells (difficult to regen new epith cells)
  • compromises mucociliary blanket (dec defences –> inc susceptibility to infect)
  • hyperresponsive a/w to new triggers
  • every response inc chance of responding again, every subsequent rxn gets more severe
18
Q

binding to beta and alpha-adrenergic receptors mediated by what

A

cAMP

19
Q

mnfts

A
  • dyspnea w/ wheezing & coughing
  • hunched over during attack
  • inc ventilatory effort (accessory muscle use)
  • pursed-lip breathing
  • nasal flaring (to inc air flow)
  • barrel chest (develops over time)
  • altered resp status & ABGs during attack (hypoxemia & hypercapnia)
20
Q

Dx

A
  • Hx, Px (resp & cardiac)
  • pulmonary Fx tests
  • labs (CBC, ABGs)
  • CXR (exlude COPD)
  • distinguish asthma vs COPD
21
Q

how to distinguish asthma from COPD diagnostic test

A

inhalation challenge tests to assess a/w responsiveness to different substances

22
Q

inhalation challenge test

A

pt exposed to specific agent to see what reaction occurs (gold standard in asthma Dx)

23
Q

Tx

A
  • control w/ minimal amount of meds possible
  • prophylactic management
  • pharmacologic agents (stage-based)
24
Q

what does prophylactic management include

A
  • cessation of smoking

- avoid triggers

25
Q

pharmacologic agents and stages

A
  1. short-acting beta-agonist inhaled prn (bronchodilators)
  2. add inhaled steroid (dec inflm –> local
  3. add long-acting bronchodilator (inhaled)
  4. short course of steroids
26
Q

when is leukotriene receptor antagonist or theophylline added

A

during fourth phase with short course of steroids

27
Q

leukotrienes action

A

inhibits inflm mediators involved in allergic response

28
Q

theophylline is added to which drugs

A

to the inhaled long-acting bronchodilators and the PO steroids

bio253 (68 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions