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Pulmonary > Asthma > Flashcards

Asthma Flashcards

1
Q

What is the definition of asthma?

A

chronic (1) inflammatory disorder of the airways that is characterized by (2) episodic reversible bronchospasm resulting from an exaggerated response to a stimulus

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2
Q

What cells play major roles in asthma?

A

mast cells, eosinophills, and T cells

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3
Q

What is the long term consequence of chronic inflammation (this is what leads to the obstruction)?

A

remodeling of the airway

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4
Q

T or F: Asthma is curable

A

F: very manageable

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5
Q

Describe the epidemiology of asthma

A
  • -2-7% of the pop has it
  • -overall female > male but in childhood male > female
  • -blacks > risk of asthma death
  • -30-50% of kids will “outgrow” asthma
  • -20-30% of adult onset asthma will experience remission
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6
Q

How is asthma classified?

A

intermittent = 1-2 episodes/year
persistent = > 1-2 episodes/year
-mild, moderate, severe

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7
Q

How is mild persistent asthma treated?

A

inhaled steroids

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8
Q

How is moderate persistent asthma treated?

A

inhaled steroids and long acting beta agonists (LABAs)

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9
Q

How is severe persistent asthma treated?

A

inhaled steroids, long acting beta agonists (LABAs), and leukotreine modifiers

*leukotreines cause constriction

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10
Q

What type of asthma treatment is assc with an increased in mortality?

A

LABA

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11
Q

What is the rescue medication for an acute asthma attack?

A

LABA

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12
Q

What is the most common type of asthma? What age group is it most common in?

A

extrinsic and kids

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13
Q

What is the pathophys of extrinsic asthma?

A

type I HS reaction: IgE response to environmental allergens

Triggering of response:
Ag recognized by Th2 cell which makes IL-5 and IL-5 and IL-13.
–IL-4 activates B cells to make IgE against Ag. IgE binds FcR and coats Mast cells. Mast cells degranulate and make IL-5 when exposed to Ag
–IL-13 promotes mucous production.
–Mast cell and Th2 cell IL-5 recruit and activate eosinophils.

Early/immediate response: minutes
-mast cell and eosinophil granule contents either directly or through neuronal reflexes… induce bronchospasm, increase vascular permeability and mucus production, and recruit additional mediator-releasing cells from the blood

Late phase: hours
the arrival of recruited neutrophils, eosinophils, basophils, lymphocytes, and monocytes are active and release more inflam mediates that cause more inflammation, mucous prduction, bronchoconstriction, and damage to epithelium in airways

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14
Q

What are common environmental allergens that cause extrinsic asthma?

A

house dust mites
cockroaches
pets (cell debris in their saliva)
mold

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15
Q

How is extrinsic asthma diagnosed?

A

wheal-and-flare reaction

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16
Q

T or F: infections can trigger extrinsic asthma

A

T

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17
Q

What triggers intrinsic asthma?

A

respiratory infection (rhinovirus, parainfluenze) and inhaled air pollutants (sulfur dioxide, ozone, nitrogen dioxide)

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18
Q

what is the epidemiology of intrinsic asthma

A

adult onset

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19
Q

Are skin tests + or - in intrinsic asthma?

A

negative

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20
Q

What is the pathophys of intrinsic asthma?

A

not sure but know that eosinophils are involved bc it is treated the same as extrinsic asthma

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21
Q

How can intrinsic and extrinsic asthma be differentiated?

A

IgE levels are only elevated in extrinsic also intrinsic is not allergen mediated so a skin test will be negative

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22
Q

What drugs can induce asthma

A

aspirin

NSAIDS

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23
Q

How does drug induced asthma present?

A

recurrent rhinitis and nasal polyps, urticaria, and bronchospasm

24
Q

What is the suspected mechanism behind drug induced asthma?

A

aspirin and NSAIDS inhibit the COX pathway without affecting the lipoxygenase pathway. it is thought that this shifts the balance of production towards leukotrienes which cause bronchial spasm

25
Q

What is the Tx for drug induced asthma?

A

leukotriene antagonists

26
Q

How is occupational asthma differentiated from non-occupational/all other asthmas/?

A

pts feel better on vacations and on weekends

27
Q

What causes occupational asthma?

A

exposure to fumes (epoxy resins, plastics), organic and chemical dusts (wood, cotton, platinum), gases (toluene)

28
Q

Occupational asthma is (IgE or non-IgE) mediated reaction/

A

both

29
Q

When does exercise induced bronchospasm occur?

A

usually AFTER not during exercise

30
Q

What is the mechanism of exercise induced bronchospasm?

A

cooling and mucosal drying of airways during exercise is thought to trigger mast cell release of histamine

31
Q

Howe is exercise induced bronchospasm treated?

A

pre-treatment with B agonist or cromolyn is effective

*slow warm-ups also help

32
Q

T or F: coughing can be the only presenting symptom of athma

A

T: it is called Cough-Variant Asthma

33
Q

Describe the history of a person with cough-variant asthma

A

history of chronic cough and exposure to irritants (smoke, fumes, exercise)

34
Q

How is cough variant asthma diagnosed?

A

positive clinical response to treatment

Methacholine challenge test

35
Q

What is nocturnal asthma? What is the pathophys?

A

asthma symptoms predominate at night during sleep due to decline in circulating catecholamines and cortisol (vagal tone predominates)

36
Q

What is ABPA?

A

allergic bronchopulmonary aspergillosis = asthma due to asperigillus fumigatus via a type III IgE mediated response

37
Q

What are the criteria for diagnosis of ABPA?

A
  1. poorly controlled asthma
  2. eosinophillia
  3. IgE > 1000ng/ml
38
Q

What is the treatment for ABPA?

A

prednisone

39
Q

What is airway hyperresponsiveness?

What does it lead to?

A

exaggerated bronchoconstrictive response by the airway to a variety of stimuli. It leads to
1. Airway inflammation
2. epithelial injury
3. neural mechanisms
4. intrinsic airway smooth muscle function
=AIRFLOW OBSTRUCTION

40
Q

What mediators cause airway constriction?

A

Major Basic Protein (released by eosinophils)
Eosniphillic Cationic protien
Histamine (mast cells and eosinophils)
Leukotrienes and prostaglandins

41
Q

What happens to the epithelium lining the airway in asthma?

A
  • disruption of epithelium with loss of cilliated cells (denudation)
  • increased permiability –> hyperresponsiveness
  • transudation of fluids
  • increased mucous and respiratory secretions
42
Q

T or F: asthmatics have increased vagal tone with reflexive bronchocontriction

A

T: according to Muthiah….

43
Q

What causes permanent narrowing of the airways?

A

airway remodeling (subepithelial fibrosis)

44
Q

What determines the diameter of the airway?

A 
edema
mucous
ASM contraction and hypertrophy
inflam cell infiltrate
airway remodeling
45
Q 
How does asthma and COPD compare?
Onset
Type of inflammation
relevate lymphocytes
relevant interleukins
allergy history?
reverisbility of bronchospasm 
during exacerbation
A

Asthma / COPD:

younger / older
eosionophillic / neutrophillic
CD4 / CD8
IL-5 / IL-8
usually present / not usual
reverisble / varible and limited reversibility
neutrophillic / eosinophillic
46
Q

When a middle aged pt presents to you and their response is mainly neutrophillic, are you thinking asthma or COPD?

A

asthma

47
Q

When a middle aged pt presents to you and their response is mainly eosinophillic, are you thinking asthma or COPD?

A

COPD

48
Q

What are the symptoms of Asthma?

A 
wheezing
chronic cough
noctournal cough/wheeze
chest tightness 
sputum production
SOB or wheezing that is seasonal/after exposure to allergens
49
Q

What can exacervate asthma?

A

allergens, GERD, URI, exercise

50
Q

What may cause a post infectious bronchial hyperresponsiveness for up to 6 weeks?

A

viral tracheobronchitis

51
Q

What are signs of life threatening asthma?

A 
accessory muscle use on presentation
pulsus paradoxus
signs of R heart strain (P-pulmonale on EKG)
hypoxemia 
hypercapnia
52
Q

What is the cause of death for a pt with asthma?

A

mucous plugging of airways = suffocation

53
Q

When during the day is peak expiration flow rate (PEFR) normally highest? Why?
How is this different in an asthmatic?

A

highest at 4 PM due to increased levels of catecholamines and cortisol and lowest at 4AM due to lower levels of catecholamines and cortisol

in asthamtics the daily PEFR differs by > 20%… does this mean that there is greater than 20% change between morning and nighttime readings??? bc PEFR should not increase in asthmatics… CONFUSING SLIDE GRRRR

54
Q

Describe the tests results that can be used to diagnose asthma

**this slide of his was super confusing

A
  1. spirometery: dec FEV1 and FEV1/FVC and FEF25-75 (all of which will reverse with admin of bronchodialtors)
  2. reversibility criteria: 12% improvement (in what? I dont know) with 200cc increase in FEV1 and/or FEC
  3. lung volumes: hyperinflation suggested by elevated RV, FRC, RV/TLC, and TLC
  4. gas exchange would be normal
55
Q

Describe the Methacholine Challenge Test.

A

The patient breathes in nebulized methacholine to provoke bronchoconstriction via the M3 receptor. The degree of narrowing can then be quantified by spirometry. People with pre-existing airway hyperreactivity, such as asthmatics, will react to lower doses of drug.

HIgh negative predictive value = if you are negative you do probably do NOT have asthma

56
Q

What are the asthma relievers?

Conrollers?

A

relievers = short acting B2 agonsits and anticholinergic

controllers (from 1st to last choice)

  • inhaled corticosteriods
  • inhaled LABA
  • LT modifiers
  • systemic steroids
  • Anti IgE

Pulmonary (31 decks)

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