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AII week 1 > Pharmacotherapeutics > Flashcards

Pharmacotherapeutics Flashcards

1
Q

What are the 4 categories of steroid potency

A
  1. Lowest
  2. Low
  3. Intermediate
  4. High
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2
Q

When would you use the lowest/low potency in the treatment of allergies

A
  1. Usually used on dermatological problems on the face
  2. Most often used for maintenance and can be long term
    (Hydrocortisone, or triamcinolone (nasocort))
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3
Q

Contraindications of low potency steroids

A

hypersensitivity and does not penetrate mucous membranes well

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4
Q

When would you use an intermediate potency steroid

A
  1. Usually on the body and extremities
  2. Atopic dermatitis
  3. Severe dermatitis
  4. Usually short term
    (triaminolone - low potency in nasal steroids)
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5
Q

Contraindications of intermediate potency steroids

A

hypersensitivity and pediatric patients

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6
Q

When would you use a high potency steroid

A
  1. Psoriasis
  2. Severe poison ivy
  3. severe atopic dermatitis
  4. Only suitable for short term
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7
Q

Contraindications of high potency steroids

A

hypersensitivity and pediatric patients.

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8
Q

MOA of topical steroids

A

Steroids play a role in interfering with mast cell degranulation that results in decreased histamine and capillary permeability. (Also blocks phospholipase A2 which blocks prostaglandins and leukotrienes)

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9
Q

Examples of oral/topical corticosteroids used to treat allergic disorders

A
  1. Asthma - steroid inhalers, oral if severe (prednisone)
  2. Allergic rhinitis - Topical (in nose)
  3. Oral steroids useful in reducing eosinophils, prostaglandins, and other WBC involved in immune response
  4. Topical steroids for atopic dermatitis
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10
Q

Topical steroid affect on HPA axis

A

When topical steroids are absorbed, they tell your HPA axis that it does not need to make as much cortisol. Over time the cortisol production is dampened enough that the HPA forgets to make more steroid (HPA axis suppression). Takes 9-12 months to fully restore.

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11
Q

What adverse skin effects are associated with topical steroids

A
  1. Dermatitis
  2. Hypopigmentation
  3. Skin atrophy - most common
  4. Striae
  5. Infections
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12
Q

What is the main use of second generation antihistamines

A

Allergic rhinitis (and urticaria)

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13
Q

How do antihistamines work

A

They block H1 receptor sites to prevent the histamine reactions. They also inhibit the wheal and flare response on the skin so they must be stopped prior to skin testing

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14
Q

1st generation antihistamines

A

Highly sedative, because the cross into the CNS. And interact with other receptors (not just H1)

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15
Q

2nd generation antihistamines

A

Very little sedative reaction (do not cross into CNS). They interact and are specific to H1 receptors.

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16
Q

What types of allergies (general) do antihistamines work on

A

IgE mediated reactions - mast cells (not asthma or anaphylaxis)

17
Q

Types of 1st generation antihistamines

A
  1. Hydroxyzine
  2. Diphenhydramine (benadryl)
  3. Meclizine
  4. Chlorpheniramine
    DO NOT GIVE THESE TO ELDERLY!!!
18
Q

What is the correlation between topical nasal decongestants and rhinitis medicamentosa

A

Rhinitis medicamentosa is rebound nasal congestion caused by extended use of topical decongestants (oxymetazoline, phenylephrine).

19
Q

How do you treat rhinitis medicamentosa

A

Stop the nasal decongestant and start pt on nasal saline or a topical steroid if drug is still needed

20
Q

What is the new recommended daily max dose of acetaminophen

A

3grams. This is important to note because some nasal decongestants contain extra acetaminophen (tylenol) and the pt should not take extra tylenol.

21
Q

What drug is the leading cause of liver failure

A

Tylenol

22
Q

Which antihistamine class is used to treat anorexia (increases appetite)

A

Piperidines (cyproheptadine)

23
Q

What effect does aspirin have on a pt with asthma and nasal polyposis

A

Can cause aspirin exacerbated respiratory disease (AERD). When you combine aspirin with polyposis you can cause an acute upper and lower resp. tract reaction. (pseudo allergic because it is not IgE mediated)

24
Q

When do you use epi

A

Anaphylaxis, acute asthma, cardiac arrest

25
Q

MOA of epi

A

Direct acting adrenergic agonist. Binds with both alpha and beta adrenergic receptors to induce: Increased CO, Bronchodilator, vascular blood constriction

26
Q

Adverse effects of epi

A

CNS disturbances, cerebral hemorrhage, arrythmias, chest pain

AII week 1 (4 decks)

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