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PHARMACOLOGY > 21-Drugs for Pulmonary Disorders > Flashcards

21-Drugs for Pulmonary Disorders Flashcards

1
Q

Bronchiolar smooth muscle input

A

controlled by ANS, sympathetic stimulates beta-2 adrenergic receptors (bronchodilation)

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2
Q

Major features of asthma (3)

A
  1. variable airway obstruction
  2. airway inflammation
  3. airway irritability
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3
Q

methacholine and histamine are responsible for __________ and increased ___________

A

airway inflammation

fall in FEV (forced expired volume)

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4
Q

common causes of asthma (5)

A
  • air pollutants
  • allergens
  • chemicals and food
  • resp infections
  • stress
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5
Q

what are the 2 goals of therapy for asthma?

A
  1. reduce the intensity and frequency of asthma symptoms

2. decrease the risk of adverse effects associated w asthma

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6
Q

reducing the intensity and frequency of asthma symptoms means:

A

reducing symptoms, need for short acting beta-agonist (<=2x/w), reduce night time awakening, optimize lung function, participate in formal activities

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7
Q

decreasing risk of adverse effects includes

A

preventing recurrent exacerbations and need for emergency/hospital c are, preventing poor lung development in children and loss of function in adults, optimizing pharmacotherapy w little to no adverse effects

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8
Q

2 strategies for pharmacological management of asthma and their drug classes:

A
  1. relievers
    - SA beta-adrenergic agonists
    - muscarinic antagonists
  2. controllers
    - glucocorticoids
    - LA beta-adrenergic agonists
    - leukotriene antagonists and lipoxygenase inhibitors
    - methylxanthines (PDE inhibitors)
    - IgE antibodies
    Mast cell stabilizers
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9
Q

briefly, how is histamine produced during asthmatic response

A

Allergen binds to IgE receptor, Gq receptor releases 2nd messenger, IP3 (cleaved by PIP2) and increases Ca, mast cell degranulation, and histamine release = bronchoconstriction

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10
Q

briefly, how are Leukotrienes produced during asthmatic response

A

Allergen binds to IgE receptor, Gq releases 2nd messenger IP3, cleaved by PIP2, releaseing Ca activating phospholipase A2
phospholipase A2 converts arachadonyl ester into AA, AA converts into leukotrienes via 5-lipoxygenase (and PGs through COX1 and 2)

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11
Q

when leukotrienes and histamine act on the receptors (Gq) of SM on bronchioles what occurs

A

bronchoconstriction

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12
Q

Beta 2 adrenergic agonists: action, routes, adverse

A

1st line therapy:
bronchodilator (SABA or LABA)
- binds to Gs proteins on SM of bronchioles to release cAMP and sequester Ca in endoplasmic reticulum (BONUS! hyperpolarize cell w K+ eflux)
PO (LABA), inh(SABA/LABA), neb (severe attack)
Adverse: tremor tachycardia (sympathetic syimulaiton)

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13
Q

Anticholinergic drugs: action, routes, adverse

A 
- muscuarining antagonists
2nd line therapy: (only works for 2/3 pt.s, good for COPD, chronic bronchitis)
- use w pt. w cardiovascular concern
- few adverse
can combine w SABA
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14
Q

Airway inflammation in asthma, main mediators

A

inflammatory cytokines from transcription factors produce eosinophils (increases production, recruitment, and survival and secretes cytotoxic, inflammatory, and bronchoconstrict)

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15
Q

glucocorticoids: action, use, adverse

A
  • suppress inflammation (inhibit COX2), hyper-responsiveness, obstruction, and prevent attacks
  • does NOT dilate bronchioles
  • ## works at cell membrane and DNA t bring to GCSr and GRE to downregulate gene producing mediators OR inactivate transcription factors
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16
Q

Leukotrienes Receptor Antagonists (LTRA): action,

A

competitive antagonist, induces bronchodilator and immunomodulatory effects
- can sue in combo w glucocorticoids, weaker than beta-2 adrenergic antagonists
PO, chewable form adverse: nausea, headache

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17
Q

Mast cell stabilizers: use

A
  • prevent allergen-induces A metabolization (decrease leukortienes) and prevents mast cell degranulation (decrease histamine and bronchoconstrictors)
  • no bronchodilatory effect, prevent constriction in response (take before exposure to antigen)
  • Martha’s damn cat
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18
Q

lipoxygenase inhibitor: action, adverse

A
  • inhibit formation of leukotrienes

- minimal adverse, contraindication: liver disease

19
Q

Methylxanthines: action, use, adverse

A
  • inhbit PDE (phosphodiesterase - degrades cAPM - no mast cell degranulaiton or IP3)
  • slow release, for nocturnal
    adverse: GI distress, irritability, insomnia, headache, nausea, vomiting
20
Q

IgE antibodies: use, considerations, adverse

A

subcut q2-4w for allergic asthma (reduces production of IgE, downregulates receptors, significant mast cell stabilizing effects)

  • v expensive, lots of tests, administered by HCP
    adverse: pain (arms, legs, ears), dizziness, fatigue, skin rash, anaphylaxis
21
Q

T/F: Drugs for asthma can be topically applied?

A

true

22
Q

What is the gold standard for relieving asthma attack?

A

beta adrenergic agonists

23
Q

What is used and is known as gold standard for prevention of attacks?

A
  • glucocorticoids
24
Q

How are glucocorticoids administered?

A

inhaled or orally

25
Q

COX enzymes convert arachidonic to

A

prostaglandins

26
Q

Lipoxygenase convert arachidonic to

A

leukotrienes

27
Q

Where are leuktrienes and histamines receptors found?

A

smooth muscle of lung

28
Q

t/f: with increase in Ca levels; contraction occurs

A

true

29
Q

Which are the most effective and rapid acting bronchodilator?

A

beta 2 adrenergic agonists

30
Q

Short and rapid acting beta 2 adrenergic agonists are known as

A

Salbutatomal and are relievers

31
Q

Long and slow acting forms of beta 2 adrenergic agonists are known as

A

salmeterol; LABA which is controller

32
Q

Routes of administration for beta 2 adrenergic agonists; which is short and long acting?

A

inhaler- short and long acting

oral- long acting

33
Q

Between inhaler or oral which one has the greatest increase of adverse effects

A

oral

34
Q

Adverse effects of B2 adrenergic agonists

A
  • tremor

- tachycardia

35
Q

Which types of patients are muscarinic relievers good for?

A

those with COPD and chronic bronchitis

36
Q

Function of muscarinic antagonists

A
  • blocks muscarinic receptors in smooth muscle of the bronchi
37
Q

Adverse effects of muscarinic antagonists

A
  • dry mouth
  • sedation
  • inappropriate inhalation
38
Q

Adverse effects for high and low dose glucocorticoid controllers

A
  • Low: throat irritation, oral candidiasis

- high: adrenal insufficiency, osteoporosis…

39
Q

Glucocorticoid controllers: route of admin for severe asthma

A

IV and PO

40
Q

Glucocorticoid controllers: route of admin for moderate to severe asthma

A

inhaled

41
Q

Which is a second line therapy for controllers; leukotriene or glucocorticoids

A

leukotrienes

42
Q

function of leukotriene receptor antagonists

A
  • competively bind to leukotriene receptors in bronchial smooth muscle
  • induce bronchodilation
43
Q

How are leukotrienes administered? and how often

A
  • orally; one daily
44
Q

Adverse effects of leukotriene receptor antagonists

A

Nausea and headache

PHARMACOLOGY (27 decks)

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