Asthma Flashcards

Test 3

1
Q

Where is the greatest resistance in the lungs?

A

Medium bronchi

Has contraction from vagus nerves and ciliated cells

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2
Q

Describe smokers lungs

A

They lose cilliated cells that mutate to cells more adaptive to abrasions. This causes mucus to fall into lungs, and why they develop coughs, especially in the morning.

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3
Q

______ has cartilage, and ________ does not.

A

Bronchi

bronchioles

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4
Q

What is an obstructive disorder?

A

hyperactive airways

airway more collapsed
excessive mucous
airway overreacts to vagus nerve stimulation

-Asthma, Chronic bronchitis, emphysema, COPD

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5
Q

How do Obstructive disorders present?

A

Dyspnea
wheezing

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6
Q

Asthma is the most common in_____

A

Children

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7
Q

Describe the histamine challenge

A

In symptom-free adults with asthma, if you spray histamine in the air, you will see a decrease in exhale force

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8
Q

What is increasing obstructive diseases?

A

Infant second hand smoke
Worsening air quality
Hygiene hypothesis

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9
Q

What is hygiene hypothesis?

A

Not exposing children to enough, allergens and germs, therefore causing their immune system to not act normally

Also increasing the amount of auto immune diseases

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10
Q

Describe Asthma

A

S/S: Wheezing, breathlessness, chest tightness, coughing (esp. night/morning), airway inflammation, smooth muscle contraction, mucosal thickening.

-increased WBC, bronchoconstriction, mucosal edema, and mucus hypersecretion. even when airway is relaxed

triggers: allergens, respiratory infections, irritants, certain medications, exercise, gastroesophageal reflux disease, anxiety, and stress

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11
Q

How do you Dx Asthma?

A
  1. FEV1: Forced expiratory volume - Inhaled small concentration of histamine and compare exhale over 1 second to prior
  2. PEF: Peak expiratory flow - max flow of forced expiration based on sex/age
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12
Q

Dead space in lungs ______ with age

A

increase

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13
Q

What is the Tx for Asthma?

A

Beta-2 specific agonist

Anti-inflammatory as adjuncts

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14
Q

What are the 2 types of asthma?

A

Intrinsic: genetic factors/alleles more inclined to asthma

Atopic (extrinsic): reactions that occur when exposed to certain allergens

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15
Q

Describe what happens in an Atopic (extrinsic) reaction

A

Dendrite cells in the respiratory tract + allergen -> T Helper cell binds to the MHC2-R -> this produces IL4 -> IL4 binds with B cells -> These cells produce plasma cells or antibodies -> IgE which elicits an allergic response then binds to mast cells -> The next time this person is exposed to this allergen the mast cell will degranulate and cause allergic response including: mucus, secretion, capillary, dilation, allergic response, itching, hayfever, anaphylaxis

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16
Q

What mediators are responsible in asthma?

A

Early: Histamines, leukotrienes, prostaglandins = bronchoconstriction & vascular leakage

Late: Leukotrienes, platelet-activating factor, tryptase = sustained bronchoconstriction, cellular infiltration, and mucus hypersecretion

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17
Q

When does late response occur in asthma?

A

2-8 hours

18
Q

What cells produce mucous? and where are they located

A

Goblet cells

GI and respiratory tract

19
Q

What is mucous made of?

A

95% water
5% glycoproteins

20
Q

What does mucus do?

A

Grabs irritants before they go down into the lungs

21
Q

Describe the immune response to allergens as it pertains to the following cells: dendritic cells, T cells, B cells, plasma cells, mast cells, neutrophils, and eosinophils

A

Dendritic cells: Process and present allergen to T cells

T helper cells: Release IL-4 to activate B cells

B cells: Produce IgE antibodies that bind to mast cells

Plasma cells: Secrete IgE antibodies

Mast cells: Degranulate and release histamine, leukotrienes, prostaglandins

Neutrophils and eosinophils: Release proteases that contribute to inflammation

22
Q

List the primary pathways of the arachidonic acid cascade, and its main products

A

Lox pathway: Produces leukotrienes

Cox pathway: Produces prostaglandins

23
Q

Describe Coup

A

Common in 6mon - 5years

Viral RSV

Seal like barking cough

24
Q

How do you treat Croup?

A

Nebulized Epi
Humidity

25
Q

Identify ANS effects on airwDesay diameter.

A

Parasympathetic (vagus nerve): Bronchoconstriction through vagal stimulation & Ach

Sympathetic: Bronchodilation through beta-2-R and relaxation of smooth muscle

26
Q

Describe the strategies of drug treatment of asthma and COPD and the two broad categories.

A

Short-term relievers (bronchodilators): Sympathomimetics like beta agonists

Long-term controllers (anti-inflammatories, antibodies, leukotriene inhibitors): Corticosteroids and other injectable medications

27
Q

List the major classes of drugs used in asthma and COPD

A

Short-term relievers: Beta-agonists, methylxanthines, anticholinergics/antimuscarinics

Long-term controllers: Corticosteroids, leukotriene inhibitors, antibodies

28
Q

What is COPD?

A

Chronic bronitis: cough & hypersecretion of mucus for 3 months of the year for 2 years

and Emphysema: enlargment of gas exchange airways, destruction of alveolar, loss of elastic recoil -> distended bronchioles and alveolus

29
Q

Describe the mechanisms of action of these drug groups

Beta-agonists, methylxanthines, anticholinergics/antimuscarinics, Corticosteroids, leukotriene inhibitors, antibodies

A

Beta-agonists: Relax airway smooth muscle and inhibit substances from mast cells

Methylxanthines: Inhibit phosphodiesterase, increase cAMP

Anticholinergics/Antimuscarinics: Block muscarinic receptors, inhibit bronchoconstriction

Anti-inflammatories (corticosteroids): Reduce inflammation by suppressing the immune response

Leukotriene inhibitors: Block leukotriene synthesis or receptors

Antibodies: Block cytokines/mediators (e.g. dupilumab blocks IL-4)

30
Q

Identify treatment considerations for specific patients with mild, moderate, or severe asthma and/or COPD.

A

Mild asthma: Short-term relievers as needed (i.e. rescue inhalers)

Moderate-severe asthma: Short-term relievers plus long-term controllers -> inhaled corticosteroids & PO leukotriene pathway inhibitor

COPD: Combination of bronchodilators and anti-inflammatories -> PO/inhaled corticosteroids, anti-IgE antibody

31
Q

List Beta-2 Specific Agonist

A

Albuterol: 30 mins - 4 hrs

Lipid soluble & up to 12 hr effects (LABA):
Salmeterol
Formotorol

32
Q

List Beta Agonist

A

Epinephrine - SQ or inhaled; max dilation in 15mins

Isoproterenol: not used much -> fatal arrhythmias

33
Q

How much of an inhaled dose actually gets into the airway? what is most important when taking an inhaler?

A

10-20% of dose gets to patient

training the patient to use an inhaler

34
Q

List Methylxanthines

A

Theophylline (tea or purified)
Theobromine (chocolate)
Caffeine (coffee)

35
Q

List Antimuscarinics

A

Atrovent/Atropine
Inhaled ipratropium bromide (longer acting than atrovent)

36
Q

Describe purified Theophylline

A

narrow therapeutic index (5-20mg/L)
used for COPD

37
Q

What route for steroids do you want to use and why?

A

Inhaled

targets lungs directly

38
Q

List Corticosteroids

A

Prednisone
Fluticasone (IM, aerosol)

Blocks transcription/translation

39
Q

What are adverse effects of corticosteroids?

A

Suppress immune system
Osteoporosis
Decrease growth in children
Oral yeast infection

40
Q

List Leukotriene pathway inhibitors

A

Montelukast

Improve aspirin induced asthma
Use as adjunct

Inhibits 5-lipoxygenase & receptor binding

41
Q

List Monoclonal antibodies to IgE

A

Omalizumab

Prophylaxis
Once a month - does not activate the IgE on mast cells

42
Q

What does a Nebulizer do?

A

Make particles small to get through to where they need to be