Brainscape's Knowledge GenomeTM

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


See full index

Bloc F - Defense > Mar26 M3-Asthma > Flashcards

Mar26 M3-Asthma Flashcards

1
Q

asthma definition

A
  • reversible obstructive airway disease (COPD NOT reversible)
  • 12-15% improvement in FEV1 after bronchodilator
  • FEV1 drop of 20% with methacholine or histamine challenge
  • FEV1 drop 15-20% in std exercise challenge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

asthma and allergies association

A
  • TH2 system + allergies correlated with asthma
  • 70% of childhood asthmatics have allergies
  • 50% of adult asthmatics have allergies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

asthma signs and symptoms

A
  • dypsnea
  • cough
  • rapid breathing
  • wheeze on EXPIRATION (both insp and exp if very bad)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

pathology of airways with asthma

A
  1. constricted muscles (thick SM)
  2. filled with mucous and inflammatory cells (T, B, macrophages)
  3. denuded brush border, goblet cells, eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

3 main cytokines in asthma + kind of T helper cell they come from

A

IL-4, IL-5 and IL-13 (are from Th2 cells)

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

general fct of IL4,5,13

A
  1. help bring B cells and eosinophils

2. help predispose lung to IgE response

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

IL-4 action

A
  1. works on immune system and hematopoietic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IL-13 action

A
  1. works on immune system and hematopoietic cells (like IL-4)
  2. heps increase mucous prod, fibroblast prolif and SM hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3 phase response to inhaled Ag (in an ALLERGIC person who inhales an antigen, not asthmatics but allergic in general) + cells in each

A
  1. immediate phase (mast cells, epithelium)
  2. subacute phase (cell recruitment: chemokines, cytokines, innate immune cells)
  3. chronic phase (cellular invasion: innate and adaptive immune cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

substances and mediators involved in immediate phase of inhaled Ag allergic response

A

MAST CELLS release:

  • IgE
  • histamines
  • leukotriens
  • causes SM to constrict + cell recruitment for subacute phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

chronic phase of allergic resp to inhaled allergen what happens

A
  • dendritic cell picks up Ag for processing by T and mostly B cells
  • (already had IL-4 and IL-13 mediated rx by mast cells)
  • CD40L on T cells mediates how much IgE B cells will make
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

IgE found where in body + what happens in allergic rx

A
  1. mostly on eosinophils and basophils, out of circulation
  2. cross-links when bound by alergen
  3. mast cell releases histamine and leukotriene, vasoactive substances, chemokines and cytokines = lung is twichy and clamps down + cell recruitment (granulocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

bronchial challenge with an ALLERGEN: thing you notice in the FEV1

A
  1. intial drop of FEV1 by 30% and slowly recover (acute to subacute phase)
  2. 30% of people go in late phase rx bc cells migrate in allergy site. secondary resp 4-6 hours. continue to wheeze
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

consequence of not treating the inflammation in ASTHMA (and only treat cough and bronchoconstriction)

A

4x more mortality (lungs fill up with mcuous and cells)

NEED INHALED CS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

usual treatment of inflammation in asthma

A

(in over 80% of pts)

  • anti-inflam (inhaled or oral CS)
  • anti-mediator (anti-histamine or anti-leukotriene)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

less usual treatment of asthma (severe)

A

(in less 20% of pts)

  • anti-IgE (omalizumab)
  • anti-cytokines (multiple)
17
Q

effects of IL-4 and IL-13 released by TH2 T cells

A
  1. BOTH needed for IgE prod
  2. BOTH act on mast cells
  3. IL-4 recruits B cells
  4. IL-13 acts on structural cells
18
Q

redudancy in IL-4 and IL-13 Rs effect

A
  • Type 1 IL-4 R = for IL-4
  • IL-13 R = for IL-13
  • Type 2 IL-4 R = for IL-4 AND IL-13
19
Q

treatment found to act on IL-4 and IL-13 Rs pathways

A
  • dupilumab, human monoclonal Ab to the IL-4 Ralpha found on both type 1 and type 2 IL-4 Rs
  • blockage of JAK-STAT transduction pathway needed for IgE class-switch
  • blockage of IL-13 effect for less mucous prod + less SM prolif
20
Q

cells IL-4 and IL-13 Rs are expressed on

A

hematopoietic cells, activated SM, fibroblasts, eosinophils

21
Q

how good dupilumab is

A

greater effect than anti-IL4 or anti-IL13 alone

22
Q

dupilumab used where (how they’ll use it soon)

A

asthma

ectopic dermatitis

23
Q

dupilumab bad thing

A
  • don’t know long term effect on immune system (more infections? cancer risk?)
  • still less side effects than CSs
24
Q

what is periostin

A

marker of TH2 cytokines.

asthma pt with low periostin and no allergies = less IL-13 antagonist effect

Bloc F - Defense (57 decks)

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