Asthma

Front 1

What are the 2 major pulmonary diseases

Back 1

COPD

Asthma

Front 2

2 subcategories of COPD, cuases, pathophysiology

Back 2

• Emphysema - Alveolar enlargement caused by tobacco smoke, air pollution.
• Chronic Bronchitis - Inflammation of airways

Front 3

Asthma is a 1 marked by 2 and 3

Back 3

1. Chronic Disease
2. Acute exacerbations (attacks)
3. Inflammation

Front 4

What are the signs of Asthma?

Back 4

• Shortness of breath
• Wheezing****
• Mucus Production
• Cough

Front 5

T/F Asthma is an obstructive disease

Back 5

T

Front 6

What R types are found in SM airways that are relevant to Asthma?

Back 6

Parasympathetic M receptors

Front 7

What is the most important muscarinic receptor?

Back 7

M3

Front 8

What activates M3 R and what does it cause?

Back 8

AcH

Bronchoconstriction

Front 9

What sympathetic R are found in bronchial SM?

Back 9

Beta R

Front 10

What does activation of Beta receptors in Bronchial Sm cause?

Back 10

Relax Bronchial SM

Front 11

In hyperressponsive asthma, what are the effects on Nocireceptor and Neuron involvement (6)

Back 11

1. Hypersecretion of mucus
2. Eosinphil products
3. C-fiber sensory neurons exposed
4. Neuropeptides released
5. Blood vessel leak** (Edema)
6. Smooth Muscle Contraction *

Front 12

Where do irritants act on the upper airway

Back 12

Myelinated fibers

Front 13

Where do irritants act on the lower airway

Back 13

C fiber receptors

Front 14

6 Common irritants of airways

Back 14

1. Cold air
2. Ammonia
3. Sulfur Dioxide
4. Cig smoke
5. Endogenous Inflam. mediators
6. Allergens

Front 15

Allergens are marked by what 2 types of responses

Back 15

Hypersensitivity

Hyperresponsiveness

Front 16

3 Characteristics of Asthma

Back 16

1. Inflammation
2. Bronchial Hyper-reactivity
3. Reversible airway obstruction

Front 17

T/F Asthma airway construction is completely reversible?

Back 17

T

Front 18

T/F COPD is completely reversible

Back 18

F; however partial reverse with Bronchodilators

Front 19

What T cells are activated in Asthmatic patients? Healthy individuals?

Back 19

Asthmatic - Th2

Healthy - Th1

Front 20

What inflammatory cells are activated in asthmatics, via Th2

Back 20

Eosinophil

Mast Cells

Plasma Cells

Front 21

What are 4 effects of inflammatory cells on airways

Back 21

1. Goblet Cell hyperplasia
2. Sub-epithelial fibrosis
3. Airway Edema
4. SM hyperplasia AND/OR hypertrophy

Front 22

*Airway SM contraction:

Hypersensitive vs Normal

Back 22

• Faster RXN
  
• Needs less stimulus
• Magnitude same as normal

Front 23

*Airway SM contraction:

Hyperreactive vs Normal

Back 23

• Similar amount of stimulus
• Magnitude is very High

Front 24

* Airway SM contraction:

Asthmatic/Hyperresponsive

Back 24

• Low stimulus
• High Magnitude

(double!)

Front 25

Pathophysiology of Asthma

Back 25

Increased Th2 in bronchial mucosa

Front 26

What 2 things happens when Th2 cytokines are released in bronchial mucosa

Back 26

1. Attract other inflammatory granulocytes
2. Promote IgE synthesis and changes responsiveness

Front 27

What does Omalizumab

Back 27

Blocks IgE from Plasma Cells for asthma cascade

Front 28

What are the 2 mechanisms for treating Asthma

Back 28

1. Enzyme Block
2. Receptor Blockers

Front 29

MOA of Zileuton

Back 29

5-Lipoxygenase Inhibitor

Front 30

What does Zileuton prevent the formation of

Back 30

LTA4

Front 31

MOA of Aspirin in Asthma

Back 31

Prevents formation of Prostaglandins from AA.

(COX Inhib)

Front 32

What is the major player in asthma

Back 32

Leukotrienes

Front 33

MOA of Montekulast/Zafirlukast

Back 33

LTE C4, D4, E4 R blocker

Front 34

What is the name of the R that Montekulast/Zafirlukast blocks

Back 34

CysLT1

Front 35

What is the role of LTB4 and where does it bind?

Back 35

BLT1 on Leukocytes

Chemotaxis

Front 36

Binding of LT on airway results in what 3 effects?

Back 36

1. SM contraction
2. Eosinophil migration
3. Airway edema

Front 37

Phase 1 of Asthma is also called

Back 37

Immediate Phase; initial response to antigen

Front 38

Mast cells release what 3 factors/mediators during the Immediate phase of Asthma

Back 38

1. Histamine
2. LT B4
3. PG D2

Front 39

T/F the Hyper-reactivity in asthmatic attacks occurs in the initial phase

Back 39

F; Late phase

Front 40

What causes the hyper-reactivity?

Back 40

• Progressing Inflammation
• IL induced damage/loss of epithelium
• *Irritant R and C fibers more accessible

Front 41

T/F It is best to use Non-selective COX or COX 1 inhibitors during Aspirin sensitive asthma

Back 41

F; COX2 Inhibitors

Front 42

Samter's Triad

Back 42

1. Rhinitis
2. Nasal Polyps
3. Aspirin Induced Asthma

Front 43

MOA of Aspirin induced asthma

Back 43

AA cascade --> increased LT

Front 44

3 Classes of Bronchodilators

Back 44

1. Anticholinergics
2. Beta Agonists
3. Methylxanthines

Front 45

3 Anti-Inflammation drugs (asthma)

Back 45

1. Corticosteroids
2. Cromolyns
3. LT pathway modifying agents

Front 46

2 Anticholinergic drugs

Back 46

1. Ipratropium Bromide**
2. Tiotropium

Front 47

MOA of Anti-chol drugs

Back 47

1. Quateranary Ammonium Salts

Front 48

T/F It is best NOT to combine B2 or when B2 contraindicated

Back 48

F; combination therapy best

B2 contraindicated during arrhythmia

Front 49

SE of Anti-chols

Back 49

Dry Mouth

GI

Front 50

T/F AcH causes bronchodilation

Back 50

F; bronchoconstriction

Front 51

ROA of Anti-chols

Back 51

Inhalation

Front 52

5 Beta Agonists.

Which is long acting?

Back 52

1. Epi
2. Isoproterenol
3. Terbutalin
4. Albuterol
5. Salmeterol (long acting)

Front 53

4 SE of Beta Agonists

Back 53

1. Tachycardia
   
2. Palpatations
3. Arrhythmias
4. Hypertension

Front 54

2 Phosphodiestersase Inhibitors

Back 54

1. Theopylline
   
2. Aminophylline

Front 55

MOA of Phosphodiesterase Inhibitors

Back 55

Inhibits Phosphodiesterase 3 and 4

Prevents degredation of cAMP

Front 56

4 SE of Phosphodiesterase Inhibitors

Back 56

1. Drug interactions with P450
   
2. Nausea
3. Diarrhea
4. Headache

Front 57

Anti-inflammatory/Immunosuppressive Agents:

3 Corticosteroids

Back 57

Corticosteroids

1. Beclomethasone
2. Fluticasone
3. Budesonide

Front 58

T/F Anti-inflammatory agents/Immunosuppressants are used for acute asthma attacks

Back 58

F; Beta agonists are

Front 59

MOA of Anti-inflams (Corticosteroids)

Back 59

Alter gene expression (ILs, TNF, COX, Phospholipase A2)

Front 60

4 SE of Anti-inflams (Corticosteroids)

Back 60

1. Osteoporesis (Long Term use)
   
2. Canadiasis
3. Insomnia
4. Supresses cortisol (stress hormone)

Front 61

Anti-inflammatory/Immunosuppressive Agents:

2 Cromolyns

Back 61

Cromolyn

Nedcormil

Front 62

Use of Cromolyn

Back 62

Prevent future asthma attacks

Front 63

MOA of Cromolyns

Back 63

Inhibit immediate effects; mast cell stabilizer

Front 64

SE of Cromolyns

Back 64

Local irritant; inhalant

Front 65

3 LT Pathway Modifying Agents

Back 65

Zileuton

Montelukast

Zafirlukast

Front 66

SE of LT Pathway Modifying Agents

Back 66

Fatigue, Dyspepsia, Headache

Front 67

When is it best to take inhaler for exercise induced asthma

Back 67

Before

Front 68

Best Treatment protocol for asthma

Back 68

Lung Function test: Peak Flows