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Pharmacology Test 3 > CHAPTER 20 ASTHMA > Flashcards

CHAPTER 20 ASTHMA Flashcards

1
Q

What are ways to measure hyper-reactivity of someone who is asthmatic?

A

FEV1 and Peak Expiratory Flow

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2
Q

How is FEV1 Measured?

A

FEV1 is how much air we can push out in 1 second.

Histamine Challenge will measure Bronchial Hyper-reactivity. Histamine is inhaled into the lungs, there will be a huge decrease in forced expiratory volume or the amount of air they are able to draw in and force out within 1 second.

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3
Q

How is Peak Expiratory Flow Measured?

A

Maximum flow of forced expired air, now how air is coming out but how FAST it is coming out.

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4
Q

What does short term reliever target in asthma patients?
What type of drugs can do this?

A

Tighten smooth muscles in the airway.
Sympathomimetics: Beta 2 agonist will dilate smooth muscles, increase in cAMP in smooth muscles causing dilation. (Nebulizer Epinephrine)

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5
Q

What does long term controllers target in asthmatic patients?

A

Thicken airway d/t to inflammatory response from interleukine mediators (IL-4, IL5) and cytokines. Inflammatory mediators.

Corticosteroids.

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6
Q

What are the two types of asthma?

A

Intrinsic (genetic factors)- over 25 genes implicated and many involved inflammation

Extrinsic. (Atopic) - Type 1 Hypersensitivity Reactions

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7
Q

What is Type 1 Hypersensitivity Reaction?

A

Hyper-reactivity to an allergen.

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8
Q

What does the dendritic cell do?

A

Swallows up pathogen or allergens. Dendritic cell will process this first exposure and present the allergen peptide on its surface in a major histocompatibility type II complex (MHCII).

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9
Q

What does the Major Histocompatibility Complex Type II do?

A

MHCII proteins exist on the surface of antigen present cells as a way to present antigen to the immune cells (T-cells and B-cells).

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10
Q

Where does the dendritic cell migrate to when it has a first exposure allergen?

A

It will migrate to the closest lymph node in the area and present the antigen on its surface and activate T helper cell.

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11
Q

What two things happen when the T Helper cell is activated?

A
  1. The activation of the T-cell will cause proliferation of the cell resulting in long lived memory T-cells residing in the lymph nodes.
  2. Secrete IL4 which activates the B-cells.
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12
Q

What does the B-cells do when they are activated?

A

The dendritic cell can present it with the antigen or can interact with the antigen on its own.

The B-cells proliferate and become long live memory B-cells.

Most importantly they become Plasma Cells.

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13
Q

What are Plasma Cells and what do they produce?

A

They are antibody secreting cells.
They produce an antibody called IgE.
The IgE have receptors that bind to Mast Cells and Basophils

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14
Q

Where are the Mast Cells and Basophils located at?
What do they do during second exposure?

A

Mast cells and basophils are tissue dwelling cells, they stay in the mucous lining along the respiratory tract.

The second exposure to allergen will trigger a quick response from mast cells and basophils. The allergens will bind to the IgE antibodies and cause mast cell degranulation.

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15
Q

What are the granulations inside the Basophils and Mast Cells?

A

Chockablock full of Histamines, Leukotrienes, and Prostaglandins.

When allergens are expose to these cells for a second time that is what attributes to the airway clogging like mucous secretion, capillary dilation (more fluid into the airway), allergic response, itching, even anaphylaxis if it goes systemic.

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16
Q

What are the two components to an asthmatic response?

A

Early Response
Late Response

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17
Q

What is Early Response?

A

You breathe in whatever is going to cause this reaction that will trigger mast cell degranulation.

Histamine, Leukotrienes, PG, and Pro-inflammatory cytokines Released

Airway starts to close within 30 minutes to an hour.
Rescue inhaler used, FEV1 goes back to normal.

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18
Q

What is Late Response?
What is the cause of this?

A

This will usually occurs several hours later after an early response

Caused by WBC infiltration and inflammation.

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19
Q

What does PGD2 and Pro-inflammatory Cytokines drawn in?

A

WBC to trigger Late Response/ Late Reaction

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20
Q

What kind of benefits do antihistamines have on asthma?

A

Little to no benefits. You want to target other inflammatory mediators like prostaglandins and leukotrienes.

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21
Q

What cells are responsible for the late reaction/ late response?
What do they do?

A

T-lymphocytes, Eosinophils, Neutrophils

These white blood cells will bring in a number of mediators that make the blood vessels more leaky and infiltrate the cells and overall increase the inflammatory response.

22
Q

How are early response and late response treated?

A

Early Response use Beta 2 agonist
Late Response use anti-inflammatory medication (corticosteroids)

23
Q

What does Histamine do?
How many types of histamines receptors are there?

A

Induces smooth muscle contraction (lungs) and bronchospasm.
It plays a role in mucosal edema and secretion.
H1, H2, H3, H4.

24
Q

What does H1 histamine receptors do?
What does an antihistamine do?

A

Bronchoconstriction and vasodilation

Antihistamine are H1 selective inverse agonist like Benadryl are useful in Type 1 hypersensitivity.

25
Q

What is PGD2?
What does it activate?

A

Pro-inflammatory mediator that binds to a GPCR to cause bronchoconstriction.

The play a part of the inflammatory response in asthma during the late response.

PG2 activates white blood cells in to increase inflammation.

26
Q

What are Leukotrienes (LTC4)

A

LTC4 is pro-inflammatory mediator during an inflammatory response (they are slow reacting)

LTC4 is liberated from the lungs during inflammation

LTC4 Bind to GPCR and cause: Bronchospasm, Mucous Secretion, Microvascular permeability, airway edema.

27
Q

Sympathetic Activity: Bronchiolar Smooth Muscles.
What’s the Action?
Whats the Receptor?

A

Action: Relax
Receptor: B2, increase cAMP smooth muscle relaxation

28
Q

Parasympathetic Activity: Bronchiolar Smooth Muscles.
What’s the Action?
Whats the Receptor?

A

Action: Contract
Receptor: M3

29
Q

How is the normal resting tone of airway smooth muscle maintained?

A

Vagal Stimulation from CN 10.

30
Q

Why is it not a good idea to scare someone with asthma?

A

Sympathetic Nervous System will kick in will open airway for a short amount of time.
The parasympathetic system will become overwhelming to bring you back to homeostasis.
The parasympathetic response in asthmatic patients can be significant.

31
Q

How does the CNS respond to an inhaled irritant?

A
  1. An inhaled irritant (dust) will trigger an autonomic response.
  2. The vagal afferent nerve will send a signal to the CNS
  3. CNS will send an impulse through the vagal efferent system and trigger a parasympathetic response.
  4. ACh is released and causes smooth muscle contraction.
  5. If the irritant is also an allergen, there will be mass cell degranulation contributing to smooth muscle constriction and leakiness in the blood vessels.
32
Q

How does circulating catecholamines help relax bronchioles?

A

There are B2 adrenergic receptors in the lungs, when catecholamine binds, it will produce bronchodilation.

For asthmatic patients it is best to inhale catecholamines, because circulating catecholamines can have a systemic effect like increase HR and BP. (Nebulizer Epi)

33
Q

What are the 3 categories of drugs used in Asthma?

A

Bronchodilators (Beta-2 agonist, Anti-muscarinic-block vagus response, Methylxanthines-PDE Inhibitors)

Anti-inflammatory Agents (Steroids, Antibodies-usually for unrelieved cases)

Leukotriene Antagonist (Lipoxygenase Inhibitors and Receptor Inhibitors)

34
Q

What specific receptors do we want the sympathomimetics to target for asthmatic patients? What will it do?

A

Beta2
Relax airway smooth muscle

And (anecdotal)
Inhibit some substance from mast cells
Inhibit microvascular leakage
Increase mucociliary transport

35
Q

What are the toxic effects of sympathomimetics?

Name some sympathomimetic B-2 selective drugs used for asthma.

A

Skeletal tremors (Nebulizer Epinephrine)

Drugs Beta-2 Selective: Terbutaline, Formoterol, Salmeterol (no cardiac effect)

36
Q

Name a short acting Beta 2 agonist (SAB2A)
Name a long acting Beta 2 agonist (LAB2A)

A

Albuterol - short acting (3-4 hours)
Salmeterol and Formoterol - long acting (12-24 hours)

37
Q

When using an inhaler, where does the medication need to get to in the airway for it to be effective?

A

Medium size bronchi

38
Q

Why are particle size important when it comes to inhalers? Why does size matter?

A

The fine particles will be breathed into the lungs, but don’t bind. They are breathed right back out.

The medium size particles get to the medium size bronchi will bind and have an effect.

The larger particles just end up in the oral cavity.

39
Q

Where does 80-90% of the inhaled medication end up?

A

End in the mouth, pharynx, or breathed right back out.

Only 10-20% of the medication goes to target.

40
Q

What drugs are in the Methylxanthine group?
What is the primary action of Methylxanthine?

A

Caffeine, Theophylline (most effective, found in tea), Theobromie
Primary Action is to inhibit PDE, thus keeping cAMP activate and contributing to smooth muscle relaxation in the lungs.

41
Q

What are two chemicals/NTs that can cause bronchoconstriction?

What agents can block these receptors?

A

Acetylcholine (Vagus Nerve) and Adenosine

Theophylline can block adenosine receptors
Anticholinergics (muscarinic antagonist) can block ACh receptors.

42
Q

What are two ways to increase cAMP so that bronchial tone can stay dilated?

A

Beta agonist can activated adenylyl cyclase and convert ATP to cAMP.

Methylxanthine can inhibit PDE and prevent the breakdown of cAMP to AMP.

43
Q

Pharmacodynamics of Methylxanthines

A

Mild Bronchodilation (Tea)
CNS-stimulation (trouble falling asleep)
Kidney (diuretic action)
Cardiac Muscle (pos. chronotropic and inotropic)
Skeletal muscle tremor

44
Q

How does muscarinic antagonist work as a short term reliever?

A

They are effective bronchodilators that block the contraction of smooth muscles and prevent mucous secretions.

Parenteral: Atropine

45
Q

What drug is valuable for asthmatic patients who are intolerant of a beta agonist?

A

Ipratropium Bromide - selective than atropine
No CNS effects, does not cross BBB
Use in COPD patients (tiotropium can be used to)

46
Q

Which group of people show less of a response to corticosteroids?

A

COPD and Emphysema patients
Corticosteroids treat inflammation.

47
Q

Pros and Cons of Corticoid Steroids

A

Pro:
Reduce bronchial activity, increase airway caliber, reduce frequency of asthmatic exacerbation, improve quality of life

Con:
Osteoporosis with long term therapy, slow growth rate in kids, oropharyngeal candidiasis (suppress immune response in oral cavity)

48
Q

How do Leukotriene Pathway Inhibitors work?
Give examples.

A

LPI works by interrupting synthesis pathway by inhibiting 5-Lipoxygenase (Zileuton) the enzyme that produce LTC or inhibiting the leukotriene receptors (Zafirlukast/Montelukast/Singulair).

49
Q

If you are loaded and have severe allergies what can you get? How does it work?

A

Get Anti-IgE monoclonal antibody (Omalizumab/Xolair)

They work by targeting portions of IgE that binds to mast cells and prevent them from degranulating.

Lessens asthma severity, decrease corticosteroid requirements, reduce hospitalization, $500-2000/shot (multiple shots/maintenance shots).

50
Q

What to do with a severe asthma attack?

A

O2
Frequent/Continuous Inhalation of beta-2 agonist (nebulizer)
Systemic steroids (Prednisone/Methylprednisone).

51
Q

Bronchitis + Emphysema =. _______

A

COPD

52
Q

What drug can be given for COPD patients?

A

Ipratropium Bromide (Anticholinergic), Brochodilator

Pharmacology Test 3 (6 decks)

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