Asthma Flashcards by Delcie Remis

What factors affect ventilation?

1) Airway Resistance: contraction/relaxation

2) ANS input - widens airway

greatest resistance in medium bronchi

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Common obstructive disorders

1) Asthma
2) Chronic bronchitis
3) Emphysema

COPD→ chronic bronchitis + emphysema

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What happens with emphysema?

Alveoli walls are distended; blown out (;

cant suck as good (not enough gas exchange)

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Asthma s/s

Wheezing
Breathlessness
Chest tightness
Coughing

(Inc at night, early morning)

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Factors of airway obstruction in Asthma

Narrowing of airway- contraction of smooth muscle
Mucosal thickening
Mucous Plugs

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Airway tests for Asthma

FEV1
PEF

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FEV1

Testing bronchial hyperactivity testing

1) Have pt give a forced expiratory volume in 1 sec

2) Give histamine/ methacholine

3) Redo Forced expiratory volume

4) Asses how much value as fallen in that time

5) have rescue drugs ready

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PEF

Peak Expiratory Flow

Max flow of forced expiration

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Asthma Tx

Beta adrenergic agonist- SAB2A (B2- Albuterol)

Edema & cellular infiltration- Anti-inflam (Inhaled corticosteroids)

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Asthma Causes/Types

Intrinsic- genetic factors

Atopic (extrinsic) - Type 1 hypersensitive rx

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Explain first exposure to allergies

1) Dentrictic cells= bind to allergen = swallow= break it down

2) Antigen presenting cell leaves mucous of lungs= uses Major Histocompatibility Complex (MHC II) = takes allergen portion to lymph node

3) Present to T-helper cell= saying its bad for body

4) T- Helper= activates & proliferates = long-lived memory cells

5) T helper= Produce IL4= stimulates B cells

6) B cell= makes memory cells & plasma cell = antibody secreting factory

7) IgE made- F(c) domain of antibody binds to basophils (mast cells once they leave circulation) = tissue dwelling cells that hangout on mucous membrane & wait to see the allergen again

T Helper cells help the B cells secrete antibodies

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Explain 2nd exposure to an allergen.

After 1st exposure:

1) Allergen binds to tissue dwelling cell = mast cell degranulation occurs

2) Granules spill out of mast cells= releases histamine & leukotrienes

3) Histamine & leukotrienes= Mucous secretion, capillary dilation, allergic response, itching, etc

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How does dupixent work?

Blocks IL-4 in allergy response pathway

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List mediators released in early stages of asthma

Mast cell degranulation releases:

Histamines
Tryptase & Neutral Proteases: break down proteins
Leukotrienes
Prostaglandins

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Immunologic effect in EARLY rx

Mast cell degranulation= smooth muscle constriction & vascular leakage (fluid into area)

(NO INFLAMMATION YET)

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Histmines

Induce smooth muscle contraction & bronchospasms; role in mucosal edema & secretion

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Prostaglandins

Potent bronchconstricting agents
Enhances histamine effects

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Leukotrienes

Slow reacting substance of anaphylaxis
Liberated from lung during inflam

Produces: Bronchospasm, mucous secretion, microvascular permeability, airway edema

**INC IN LATE RX even though released by mast cells **

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Late Rx Mediators

2-8 hrs later - INC inflammation

1) Eosinophils
2) Neutrophils
3) T-Lymphocytes: T-Helper Cells

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How does the PNS effect the airway?

Vagus nerve innervates airway lining both efferent & afferent→ contraction (M3) would dec diameter of airway

Gives normal resting tone (constriction)= to help catch bacteria

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How does the SNS effect the airway?

Indirect effect through Epi= binds to B2 receptors in lungs = bronchodilation

Alpha1 in vessels of lungs= epi constricts blood vessels= beneficial (dec fluid & WBC) in asthma

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Croup S/s

RSV- rhinorrhea, sore throat, fever

Croup- Seal like barking cough

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What causes croup? Tx?

RSV causes hyper-reactivity of airway= seal barking cough

Tx: severe case- nebulized epi

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Drug classes:
Short term Relievers vs Long Term in Asthma

Short term

1) Bronchodilators: Beta agonist, anti-muscarinic, methylxanthines

Long term

1) Anti-inflam- steroids, antibodies

2) Leukotriene antagonists- lipoxygenase & receptor inhibitors

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Adrenergic receptor agonist - β2 Effect in Asthma

B2- relax airway smooth muscle -inhibit mast cells, dec microvascular leakage, inc mucociliary transport

Albuterol (SABA)

MOA- B2 selective Use- Rescue inhaler Effect- bronchodilation Duration- 3-4 hrs

Salmeterol & Formoterol

Long acting B2 agonist (duration- 12 hrs) -high lipid solubility, dissolve cell membrane, slowly release to receptor

Methylxanthines: Useful for? Drug Ex?

Useful for COPD- due to higher tox risk (not worth it for asthmatics) Theophylline, Theobromine, Caffeine

Methylanthines MOA

Inhibits phosphodiesterase Inhibits adenosine receptors- kidneys Anti-inflammatory

Theophylline has a _____ therapeutic index. Therapeutic Monitoring level

Extracted/ Purified= LOW; high risk for toxicity Therapeutic: 5-20 Toxic: >20

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

1) Disturbance= phospholipids converted into Arachidonic acid 2) LOX- leukotrienes liberated from lung during inflammation Produce (GPCR): bronchospasm, mucous secretion, microvascular permeability, airway edema 3) COX- Enhance histamine effects Potent bronchoconstricting agent (GPCR) Products: 1) Prostaglandins 2) Thromboxane 3) Prostacyclin

Causes of Asthma attack

Allergens, Resp infection, stress/anxiety, irritants

Chronic Bronchitis: Factors, S/S

Factors: Hyper secretion of mucus, mucus thicker than normal, irritants inc mucus production S/S: chronic productive cough lasting at least 3 mo of year and for at least 2 consecutive years

Emphysema: Factors, S/S

Factors: Abnormal PERMANENT enlargement of alveoli (scar tissue), loss of elasticity S/s- Dyspnea, cough

Adrenergic receptor agonist - β2: Drug Ex? Toxic Effect

Toxic- Skeletal muscle tremor Drugs- Terbutaline, albuterol, salmeterol, Epi, Isoproterenol

If you give epi for an asthma attack, how would the route of the medication given effect your further treatment?

Inhalation- 60-90 min duration Must monitor for late reaction & tachycardia, arrhythmias due to B1 stimulation as well as B2 (nonspecific)

Explain isoproterenol given for asthma (SABA)

Non- specific Potent bronchodilator-- but high doses = arrhythmias so replaced by albuterol

What medication is available parenteral for asthmatics?

Terbutaline- B2

Which particles from the inhales are producing effect in the airway?

Intermediate particles

Theophylline effect on body & toxic S/S

Body effects: CNS stimulation, Inc HR, skeletal muscle (tremors) Toxic S/s: HA, N/V, tremors, seizures **Monitor with Liver

What are muscarinic antagonist commonly used for?

COPD

Atropine for COPD

Lower dose than normal for cardiac parasympathetic blockade (Short Acting Muscarinic Antagonist)

Ipratropium bromide for COPD- Drug class, Pharmackinetics

Long Acting Muscarinic Antagonist (LAMA)- more selective than atropine when inhaled Synergistic w beta-2-agonist A: poorly absorbed, no CNS effects

Tiotropium: Drug class, duration, common use?

Drug class: Muscarinic antagonist (LAMA) Duration: Longer acting (24hrs) Uses- COPD (limited in asthma)

Who are long term corticosteroids more useful for?

Asthma over COPD

Describe the glucocorticoid pathway.

1) Binds to glucocorticoid receptor 2) Translocates into nucleus 2) Binds to area of DNA called glucorticoid response elements 3) Stimulates transcription/translation of proteins ALSO 1) Causes Transrepression= repression of transcription/translation of proteins 2) Supreses NFkB (proinflammatory) = dec inflammation

What does phospholipase A2 do?

Converts phospholipids into arachidonic acid

Explain what transrepression does with glucorticoid binding

Binds to proteins that will supress NF-KB= dec inflammation

Overall effect of corticosteroids

Reduces symptoms Improves pulmonary function Reduces need for oral steroids Reduces bronchial reactivity

What are the potential bad effects of corticostreroids?

Osteoporosis with long term therapy Slow rate of growth in children

What is a common side effect of long term inhaled corticosteroid use cause?

Thrush- oropharyngeal candidiasis

What else can you do besides taking long term corticosteroids? Ex?

Injection of IgE monoclonal antibodies Ex: Xolair (Omalizumab)

How do anti-IgE monoclonal antibodies work?

Targets IgE portion on mast cells - prevents degranulation of mast cell & allergen from binding to it - lessens asthma severity -dec corticosteroid requirement - reduce hospitalizations

Zileuton: Drug Class, MOA

Drug Class- Leukotriene pathway inhibitor MOA- inhibits 5-lipoxygenase

Which meds inhibit leukotrienes from binding to their receptors ?

Zafirlukast Montelukast

TX for Mild Asthma

Beta Receptor agonist prn (SAB2A)

Tx moderate asthma

Inhaled Corticosteroids Oral Leukotriene receptor antagonist (LAB2A) (usually combine short term w longer term tx)

Know Diff in Tx of asthma & COPD.

TX for severe acute attacks

1) Oxygen 2) Beta-2 agonist (nebulizer) 3) Systemic steroids- prednisone 4) Intubation

What are the 3 things that glucorticoids increase?

1) Annexin-1 = suppression of phospholipase A2= dec WBC to site/inflammation 2) Secretory Leukoprotease Inhibitor = suppress tissue damage/inflam 3) IL-10 Immunosupressive= inc anti-inflammatory

What do proteases do?

Secreted by WBC; Protein enzymes that break down proteins = will degrade proteins & surrounding tissues to get into areas= can inc inflammation

Asthma Flashcards

(62 cards)