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Pathophysiology > Asthma > Flashcards

Flashcards in Asthma Deck (60):
1

Is asthma acute or chronic?

chronic

2

What cells are involved in asthma?

-mast cells
-eosinophils
-T-lymphocytes
-macrophages
-neutrophils
-epithelial cells

3

What symptoms are associated with asthma?

-wheezing
-breathlessness
-chest tightness
-coughing

4

When are symptoms more common/worse?

at night or in early morning

5

Who does asthma affect the most?

the children

6

If we control asthma, we prevent _____ ?

COPD people!

7

What does natural history of a disease mean?

It means we let the disease run it's course and do not intervene in any way.

8

What are predictors of adult asthma persistence?

*ON EXAM
*Slide 8

-diagnosis during school age
-presence of atopy (genetic tendency to develop allergic diseases)
-BHR (bronchial hyper reactivity)

9

What are 2 non-modifiable risk factors associated with asthma?

-genetics (atopy or BHR)
-gender (more common for males in childhood and females in adulthood)

10

What are modifiable risk factors associated with asthma?

-lower socioeconomic status
-family size
-obesity
-exposure to second-hand smoke
-respiratory syncytial virus exposure
-reduced exposure to childhood infectious agents

11

What is the hygiene hypothesis?

Basically if you keep your kid too clean and don't allow it to do shit, it will never be exposed to things that will strengthen it's immune system. Then when it finally is exposed, it's immune system is so weak which makes it harder to fight infections.

12

What type of cells cause the inflammation in asthma?

mast cells

13

What are factors that can trigger asthma symptoms?

-respiratory tract infections
-allergens
-environment
-food additives
-exercise
-drugs/preservatives
-occupation
-emotion

14

Explain why asthma makes it hard for a patient to breathe.

The muscles of the bronchial tubes tighten and thicken and the air passages become inflamed and mucous-filled, making it hard for air to move.

15

What are the hallmarks of asthma pathology?

1. BHR
2. airway inflammation
3. airway remodelling
4. some degree of airflow obstruction

16

Describe BHR

-twitchy lungs
-increased tendency of bronchospasm
-exposure to irritants can trigger great spasmodic rxn

17

What type of antibodies bind to receptors on mast cells which produce inflammation?

IgE

18

After all the inflammation occurs, Type 2 helper cells are activated which produce ??

B cell activation which makes more IgE antibodies

19

What does chronic airway inflammation result from?

repeated exposure to the allergen

* we don't want this bc it can lead to other lung probs

20

Explain mast cells.

-found in walls of respiratory tract
-increased number in pt's with allergic asthma

-when exposed to allergen - mast cell degranulation
-allergen binds to IgE then mast cells release:
-bronchoconstrictors (histamine, leukotrienes, etc.)
-eosinophil and neutrophil chemotactic factors (attract more mast cells to area to make it worse)

21

Explain eosinophils

-once activated they release inflammatory mediators such as leukotrienes and granule proteins to injure airway tissue

22

Explain T-lymphocytes

-release cytokines that mediate the allergic rxn
-increase TH2 activity

23

Explain macrophages

-scavengers that engulf and digest bacteria
-release inflammatory mediators such as platelets activated factor and leukotrienes
-release neutrophil chemotactic factor and eosinophil chemotactic factor which amplify the inflammatory process

24

Explain epithelial cells

-can be activated by IgE dependent mechanisms, viruses, pollutants, histamine
-normally - clear mucocilliary and removal of noxious agents but in chronic asthma - epithelial shedding occurs

25

What are 3 types of inflammatory mediators?

-histamine
-arachadonic acid
-PAF (platelet activating factor)

26

Describe histamine

-released by lung mast cells
-induces smooth muscle constriction and bronchospasm

27

Describe arachadonic cells

Mast cells activate arachidonic cells to form:
-prostaglandin D2 and F2 (bronchoconstrictors)
-prostacyclin (vasodilators)
-thromboxane (bronchoconstriction, airway inflammation, and BHR)

28

Describe PAF

-mediation of bronchospasm, inflammation, anaphylaxis, etc.

29

What is PAF produced by?

neutrophils, monocytes, and macrophages

30

How are leukotrienes formed?

arachidonic acid metabolized by 5-lipooxygenase (5-LO) to form leukotrienes

31

What does excess production of leukotrienes cause?

bronchospasm and promote histamine release from mast cells

32

leukotrienes are ____

bronchoconstrictors

* they also increase mucous production which reduces clearance of aggravating allergen

33

T or F: it is ok to give Cox 1 inhibitors to asthmatics

FALSE - as Namaka said - you might as well give up your license now if you're gonna do that lol

Can never give Cox 1 inhibitors such as aspirin or ibuprofen to asthmatics!!!!

*Be sure to see slide 32

34

T or F: a cox 2 inhibitor helps with asthma

TRUE

35

T or F: a leukotriene inhibitor will help with asthma

also TRUE

36

T or F: 5-LO inhibitors are used in treating asthma

False. (As dwight k. schrute would say it) - used for allergic rhinitis and nasal congestion

37

T or F: antihistamines help in treating asthma

True

38

What is the #1 cause of COPD in adults?

smoking

39

What is airway remodelling?

altered repair process in response to chronic inflammation leading to fibrosis and increase in smooth muscle cells, number of blood vessels, and increase in mucous glands

40

What factors lead to varying degrees of airway obstruction?

-mucous production
-smooth muscle of airways
-neuronal control and neurogenic inflammation

41

What does ACh cause?

Bronchoconstriction

42

T or F: an anticholinergic will treat asthma

True - it will cause bronchodilation making it easier for air to pass through

43

Norepinephrine affects alpha receptors which causes ?

Bronchoconstriction

44

Epinephrine affects beta receptors which causes ?

Bronchodilation

* Therefore you would never want to use a beta blocker on an asthmatic because it will prevent bronchodilation making it harder for the pt to breathe.

45

Would an alpha agonist be used in asthma?

no way

46

Would a beta agonist be used in asthma?

yes way

47

Would smooth muscle relaxants be used in asthma?

yes

48

Are corticosteroids used in asthma?

Yes - steroids reduce inflammation and swelling

49

When are oral corticosteroids used?

In acute asthma attacks

50

When are inhaled corticosteroids used?

Used for prophylactic control of asthma

*prophylactic means it is intended to prevent disease

51

How is asthma diagnosed?

-history
-measurement of lung function
-spirometry
-peak expiratory flow rate
-airway responsiveness testing
-allergy testing to assess for triggers

52

What two things can be measured through spirometry that we talked about in class?

FVC
FEV1

53

What is FVC?

Forced vital capacity - volume delivered during an expiration made as forcefully and completely as possible starting from fully inspired

54

What is FEV1?

Forced expiratory volume in 1 second - volume delivered in the first second of an FVC manoevre

55

What ratio do we care about that is used to measure airflow limitation?

FEV1/FVC ratio
normal is greater than or equal to 0.70 (70%)

less than 70% ratio indicates there is some form of airway obstruction

56

What is PEF? What does it measure?

Peak Expiratory Flow - measures maximum speed of expiration
-expressed as L/min

*useful mainly for monitoring therapy

57

What are some asthma triggers?

-methacholine
-histamine
-cold air
-exercise

58

What are the 2 parts to pharmacologic therapy for asthma?

1. Relievers - use as needed to quickly reverse bronchoconstriction and relieve symptoms
2. Controllers (prophylactic medications used to prevent the disease) - inhaled steroids - use daily to prevent symptoms and flare ups

59

What are symptoms of an asthma episode?

-dyspnea (trouble breathing)
-chest tightness
-cough
-wheeze

60

What are treatment targets for asthma?

-bronchoconstriction
-inflammation