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Pharmacology > Immunopharm - Glucocorticoids/Asthma/COPD > Flashcards

Immunopharm - Glucocorticoids/Asthma/COPD Flashcards

1
Q

Overview of the adrenal cortex:

  1. Outer cortex is derived from ____ and the inner medulla is derived from?
  2. What are the three zones? What is produced in each?
A

Overview of the adrenal cortex:

  1. Outer cortex: mesoderm
  2. Inner medulla: neural crest cells
  3. Zona glomerulosa - mineralocorticoids
  4. Zona fasciculata - glucocorticoids
  5. Zona reticularis - androgens
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2
Q

Overview of the adrenal cortex:

  1. Function of mineralocorticoids?
  2. Function of glucocorticoids?
A

Overview of the adrenal cortex:

  1. Mineralocorticoids: H2O/electrolyte balance, active reabsorption of Na+ by kidneys, passive water reabsorption, and active secretion of K+ and H+
  2. Glucocorticoids: glucose metabolism and anti-inflammatory proterties
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3
Q

Overview of the adrenal cortex:

Glucocorticoid synthesis is regulated by _____ which is released from ___ cells in the ___ ____. Its synthesis is regulated by ____. A negative feedback inhibition occurs in that high ___ levels decrease the synthesis and release of ___ and ___ and thus the absence of ___ leads to atrophy of the zona ____ and zona reticularis.

A

Overview of the adrenal cortex:

Glucocorticoid synthesis is regulated by ACTH which is released from corticotroph cells in the anterior pituitary. Its synthesis is regulated by CRH. A negative feedback inhibition occurs in that high cortisol levels decrease the synthesis and release of CRH and ACTH and thus the absence of ACTH leads to atrophy of the zona fasciculata and zona reticularis

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4
Q

Synthesis of steroid hormones:

  1. What is the rate limiting step?
  2. What enzymes are needed to get from progesterone to aldosterone?
A

Synthesis of steroid hormones:

  1. Rate limiting step is the conversion of cholesterol to pregnenolone
  2. Progesterone –> 21 hydroxylase –> 11-hydroxylase –> aldosterone synthase –> aldosterone
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5
Q

Synthesis of steroid hormones:

  1. What enzymes are neeed to convert pregnenolone to cortosol?
  2. What are the steps from pregnenolone to testosterone?
A

Synthesis of steroid hormones:

  1. Pregnenolone –> 17 hydroxylase –> 21 hydroxylase –> 11 hydroxylase –> cortisol
  2. Pregnenolone –> DHEA –> androstenedione –> T
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6
Q

Drugs inhibiting steroid synthesis:

Why are these more systemically toxic?

Name 4 drugs.

A

Drugs inhibiting steroid synthesis:

More systemically toxic bc they inhibit CYP450

Mitotane, aminoglutethimide, ketoconazole, and metyrapone

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7
Q

Drugs inhibiting steroid synthesis:

Mitotane:

  1. Toxic to ____ cells and used as an ____ agent in adrenal tumors.
  2. MOA?
A

Drugs inhibiting steroid synthesis:

Mitotane:

  1. Toxic to adrenocortical cells and used as an antineoplastic agent in adrenal tumors
  2. MOA: unknown
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8
Q

Drugs inhibiting steroid synthesis:

Aminoglutethimide:

  1. Used to treat?
  2. MOA?
  3. Dose dependent __ and ___ side effects and rash, causes ___ insufficiency.
A

Drugs inhibiting steroid synthesis:

Aminoglutethimide:

  1. Use: breast cancer in postmenopausal women and metastatic prostate cancer
  2. MOA: blocks cholesterol side chain cleavage enzyme
  3. Dose dependent GI and neurological side effects and rash, causes adrenal insufficiency
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9
Q

Drugs inhibiting steroid synthesis:

Ketoconazole:

  1. ____ agent for?
  2. Second line treatment for?
  3. MOA?
  4. Major side effect?
A

Drugs inhibiting steroid synthesis:

Ketoconazole:

  1. Antifungal agent for athletes foot, ringworm, and dandruff
  2. Second line for cushings
  3. Inhibits 17 hydroxylase and 14 demethylase
  4. SE: hepatotoxicity
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10
Q

Drugs inhibiting steroid synthesis:

Metyrapone:

  1. Used to treat?
  2. MOA?
A

Drugs inhibiting steroid synthesis:

Metyrapone:

  1. Hypercorticism from neoplasm
  2. Selective inhibitor of 11-hydroxylase
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11
Q

Glucocorticoids:

Cortisol:

Major ___ steroid. __ at the 11th position.

Function?

A

Glucocorticoids:

Cortisol:

Major endogenous steroid. Hydroxyl at the 11th position.

Functions: suppress immune system, increase gluconeogenesis, fat/protein/carbohydrate metabolism

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12
Q

Glucocorticoids:

Corticosterone:

Why is this inactive? What activates it?

A

Glucocorticoids:

Corticosterone:

Inactive because there is a carbonyl at the 11th carbon (instead of carboxyl) - becomes metabolized by 11 hydroxysteroid dehydrogenase to a hydroxyl at the 11th carbon

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13
Q

Glucocorticoids:

Prednisone is a prodrug converted to?

Fludrocortisone: level of glucocorticoid activity?

A

Glucocorticoids:

Prednisone is converted to prednisolone

Fludrocortisone: higher mineralocorticoid potency, higher glucocorticoid activity than cortisol but not overly high in comparison to others

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14
Q

Glucocorticoids:

Prednisolone/Methylprednisolone: ____ times more potent than cortisol for ______ activity. Low ____ activity.

Dexamethasone: Greater than ___ times more potent than cortisol with ___ mineralocorticoid activity.

A

Glucocorticoids:

Prednisolone/Methylprednisolone: 4-6 times more potent than cortisol for anti-inflammatory activity. Low mineralocorticoid activity

Dexamethasone: Greater than 18 times more potent than cortisol with no mineralocorticoid activity

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15
Q

Inhaled glucocorticoids:

Why are they better?

Name 4.

A

Inhaled glucocorticoids:

Deliver high concentrations to the lung with less systemic toxicity

Fluticasone, Beclomethasone, Flunisolide, and Triamcinolone

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16
Q

Glucocorticoids:

MOA: 90% is bound to ___ with the receptor for the ____ complex on the ____. ____ transport into the cell. Binds to ___ glucocorticoid receptor and _____. This ____ complex is transported to the ___ and regulates (either up or down) transcriptional expression of genes.

A

Glucocorticoids:

MOA: 90% is bound to CBG (corticosteroid binding globulin) with the receptor for the CBG-S complex on the surface. Active transport into the cell. Binds to T2 glucocorticoid receptor and dimerizes. This GR-S complex is transported to the nucleus and regulates (either up or down) transcriptional expression of genes

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17
Q

Glucocorticoids:

Metabolic effects:

  1. Antagonizes ___ action and promotes ____ (increases blood ____)
  2. What does it do to muscle?
  3. Augments growth hormone action on ____ (increased blood _____)
A

Glucocorticoids:

Metabolic effects:

  1. Antagonizes insulin action and promotes gluconeogenesis (increases blood glucose)
  2. Increases muscle catabolism
  3. Lipolysis (increased blood triglycerides)
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18
Q

Glucocorticoids:

Antiinflammatory actions of glucocorticoids? (3)

A

Glucocorticoids:

a. Decrease inflammatory response
b. Reduces cytokine release
c. Reduces production of eicosanoids

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19
Q

Glucocorticoids:

  1. Absorption?
  2. Binding of cortisol?
  3. Difference between binding of synthetics?
  4. Metabolism?
A

Glucocorticoids:

  1. Well absorbed in GI
  2. Cortisol is highly bound to cortisol binding globulin (CBG) and albumin
  3. Synthetics are much less bound
  4. Liver
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20
Q

Glucocorticoids:

Is the uce of prednisone during pregnancy safe? Why or why not?

A

Glucocorticoids:

Yes. There is no 11b-hydroxysteroid dehydrogenase I in the fetal liver

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21
Q

Glucocorticoids:

Therapeutic uses? (6)

A

Glucocorticoids:

Therapeutic uses:

a. Replacement therapy - for adrenal insufficiency
b. Anti-inflammatory
c. Inhaled for asthma
d. Topical for psoriasis and dermatitis
e. Depot injections for arthritis or gout
f. immunosupression - trasplant rejection

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22
Q

Glucocorticoids:

  1. Why are they inhaled?
  2. What is topical dosing for?
  3. What are depot injections for?
  4. All are for ___ ONLY!
A

Glucocorticoids:

  1. Inhaled for asthma
  2. Topical dosing for psoriasis and dermatitis
  3. Depot injections for gout and arthritis
  4. *** TEMPORARY RELIEF ONLY!! NO change in underlying disease
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23
Q

Glucocorticoids:

Toxic side effects:

  1. Increased susceptibility to ___
  2. Increased ___ levels ( ____)
  3. Secondary ______ . This can lead to _____.
  4. Increased vascular permeability leading to ____.
A

Glucocorticoids:

Toxic side effects

  1. Increased suceptibility to infection
  2. Increased glucose levels (diabetes)
  3. Secondary hyperparathyroidism. This can lead to osteoporosis
  4. Edema
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24
Q

Glucocorticoids:

Toxic side effects:

  1. Suppression of ___ ___ growth in children
  2. Steroid ____
  3. ____ syndrome
  4. Withdrawl “rebound - ____ ____
  5. Muscular weakness - ____
A

Glucocorticoids:

Toxic side effects:

  1. Suppression of _linear bone _ growth in children
  2. Steroid psychosis
  3. CUSHINGS** **syndrome
  4. Withdrawl rebound - adrenal insufficiency
  5. myopathy
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25
Q

Primary adrenal insufficiency:

___ disease: self destruction of the ___ ___ by __ cell mediated autoimmune reaction. Insufficient ___ production. Requires lifelong treatment.

Symptoms?

A

Primary adrenal insufficiency:

Addisons disease: self destruction of the adrenal cortex by T cell mediated autoimmune reaction. Insufficient steroid production. Requires lifelong treatment.

SE: weakness, fatigue, hypotension, hypoglycemia, salt craving, dehydration, joint/muscle pain, and hyperpigmentation

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26
Q

Secondary adrenal insufficiency:

Decrease in ___ causes a decrease in cortisol and ____ production. This is due to an impairment of the ____ or ____. Can also be caused by sudden ___ of long term glucocorticoid therapy.

SE?

A

Secondary adrenal insufficiency:

Decrease in ACTH causes a decrease in cortisol and androgen production. This is due to an impairment of the pituitary or hypothalamus. Can also be caused by sudden withdrawl of long term therapy.

SE: weakness, fatigue, hypotension, hypoglycemia, salt craving, dehydration, and joint/muscle pain

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27
Q

Adrenal Excess: Cushings

  1. How is primary cushings brought about?
  2. What about iatrogenic cushings?
  3. Characterized by?
A

Adrenal Excess: Cushings

  1. ACTH secreting tumors = primary
  2. Excessive glucocorticoid therapy = iatrogenic
  3. Characterided by “apple” distribution of fat, hypertension, immunosupression, diabetes, “moon face” and excessive sweating
28
Q

Mineralocorticoids:

  1. Deficiency of aldosterone leads to?
  2. Hyperaldosteronism: cause? result?
  3. What drug is used for hypoaldosteronism?
A

Mineralocorticoids:

  1. Deficiency - salt wasting, hyperkalemia, and acidosis
  2. Hyperaldosteronism: cancers/tumors; edema and hypertension (due to Na/H2O retention) and hypokalemia (due to accelerated excretion of K+)
  3. Fludrocortisone
29
Q

Mineralocorticoids:

  1. 2 receptor antagonists?
  2. Classifications of asthma?
A

Mineralocorticoids:

  1. Spironolactone and eplerenone
  2. Mild intermittent, mild persistant, moderate persistant, and severe persistant
30
Q

Asthma

T helper cells: Allergen interacts with ____ cells and presents to ___ cells. Cytokines released to increase ___ production by __ lymphocytes. Cytokines increase __ cell proliferation and ___ recruitment.

Eosinophils produce ____ which causes bronchoconstriction

A

Asthma:

T helper cells: Allergen interacts with dendritic cells and presents to Th2 cells. Cytokines released to increase IgE production by B lymphocytes. Cytokines increase mast cell proliferation and eosinophil recruitment

Eosinophils produce LTC4 which causes bronchoconstriction

31
Q

Asthma:

  1. What are airway constrictors?
  2. What are dilators?
  3. Note: ____ dont work for asthma!
A

Asthma:

  1. Constrictors: ACh, PNS, histamine, LTs, TxA2, serotonin, alpha agonists, decreased PCO2 in small airways
  2. Dilators: SNS, beta2 agonists, NO, increased PCO2 in small aiways, decreased PO2 in small airways
  3. Antihistamines dont work for asthma
32
Q

Drugs for asthma:

  1. Which cause bronchodilation?
  2. Which decrease inflammation?
A

Asthma:

  1. Bronchodilation: B2 agonists, methylxanthines, and muscarinic antagonists
  2. Inflammation: glucocorticoids, modulators of mast cell degranulation, LT antagonism, and Anti-IgE antibodies
33
Q

Bronchodilators:

Beta 2 Agonists:

  1. Which drugs are short acting?
  2. Which are long acting?
  3. Indications?
A

Bronchodilators:

Beta 2 Agonists:

  1. Short: albuterol, terbutaline, pirbuterol
  2. Long: salmeterol
  3. Acute exacerbation: short acting prophylaxis of exercise induced symptoms and oral for nocturnal issues
34
Q

Bronchodilators:

Beta 2 Agonists:

  1. Why are they not recommended for monotherapy?
  2. MOA?
  3. Combination with ____ boosts agonist effects
A

Bronchodilators:

Beta 2 Agonists:

  1. Doesnt actually reduce inflammation: just symptoms
  2. MOA: bronchodilation secondary to B2 receptor activation of cAMP in bronchial smooth muscle. Increased cAMP inhibits release of mast cells
  3. Combo with theophylline boosts effects
35
Q
A
36
Q

Bronchodilators:

Beta 2 Agonists:

  1. What are the side effects?
  2. Contraindications?
  3. Salmeterol can possibly increase ____ and decrease ____ of B2 receptor
A

Bronchodilators:

Beta 2 Agonists:

  1. SE: tachycardia, hypotension, tremor, anxiety, and insomnia
  2. Contraindications: heart disease or MAOIs
  3. Salmeterol can possibly increase wheezing and decrease regulation of B2 receptor
37
Q

Bronchodilators:

Beta 2 Agonists:

  1. Which drugs are best for symptomatic relief?
  2. Which is best prophylactically?
  3. Why is isoproterenol not used?
A

Bronchodilators:

Beta 2 Agonists:

  1. Symptomatic: short acting - albuterol, pirbuterol, terbutaline
  2. Prophylactic: long acting - salmeterol
  3. Potential toxicity
38
Q

Bronchodilators:

Methylxanthines:

  1. Drugs?
  2. Indications?
A

Bronchodilators:

Methylxanthines:

  1. theophylline and aminophylline
  2. Maintenance therapy for asthma/COPD: long acting bronchodilators
39
Q

Bronchodilators:

Methylxanthines:

  1. Side effects?
  2. Why is serum level monitoring required?
A

Bronchodilators:

Methylxanthines: (theophylline and aminophylline)

  1. SE: similar to caffiene - insomnia, aggitation, tachycardia, tremor, N/V, and seizures
  2. Serum is measured for toxicity reasons
40
Q

Bronchodilators:

Methylxanthines:

MOA: _____, nonselective, inhibition of ____. This causes increased cAMP and ____ which causes smooth muscle ____. In addition, ___ inhibition of ___ receptor to inhibit bronchoconstriction.

A

Bronchodilators:

Methylxanthines:

MOA: competitive, nonselective, inhibition of PDE. This causes increased cAMP and cGMP which causes smooth muscle relaxation. In addition, nonselective inhibition of adenosine A2 receptor to inhibit bronchoconstriction

41
Q

Bronchodilators:

Muscarinc receptor antagonist:

  1. Drugs?
  2. Indications?
A

Bronchodilators:

Muscarinic receptor antagonists:

  1. Ipratropium and tiotropium
  2. COPD, used for asthma with other bronchodilators
42
Q

Bronchodilators:

Muscarinic receptor antagonists:

MOA: receptor antagonist/_____ inhibitor of ___. This decreases the activity of ____ receptors (____ antagonist) in smooth muscle of the lung. It also decreases ____, inhibits bronchoconstriction and ____ secretion.

A

Bronchodilators:

Muscarinic receptor antagonists:

MOA: receptor antagonist/competitive inhibitor of ACh. This decreases the activity of muscarinic receptors (cholinergic antagonist) in smooth muscle of the lung. It also decreases cGMP, inhibits bronchoconstriction and mucous secretion.

43
Q

Bronchodilators:

Muscarinic receptor antagonists:

  1. Ipratropium bromide: quaternary so it minimizes ____ side effects.
  2. SE?
  3. Useful in patients who cannot take ___ ____. Examples?
A

Bronchodilators:

Muscarinic receptor antagonists:

  1. Ipratropium bromide: quaternary so minimizes CNS side effects
  2. SE: dry mouth, blurred vision, nausea, HA, and tachycardia
  3. Useful for those who cant take B2 agonists. Examples: patients on MAOIs, with cardiac arrhythmias, or unstable angina
44
Q

Anti-inflammatory drugs:

Glucocorticoids:

  1. Drugs?
  2. Indications?
A

Anti-inflammatory drugs:

Glucocorticoids:

  1. Beclomethasone and fluticasone
  2. SEVERE asthma attacks resistant to therapy with bronchodilators
45
Q

Anti-inflammatory drugs:

Glucocorticoids:

  1. Why not useful for chronic systemic use?
  2. Beclomethasone ___\_ used in inhaler to suppress ___.
A

Anti-inflammatory drugs:

Glucocorticoids:

  1. Side effects
  2. Beclomethasone dipropionate used in inhaler to suppress inflammation
46
Q

Anti-inflammatory drugs:

Glucocorticoids:

  1. MOA: suppress release of ___/___ by inhibiting ___/___
  2. Side effects?
  3. Concern with daily use of systemic absorption: what should be done to minimize?
A

Anti-inflammatory drugs:

Glucocorticoids:

  1. MOA: suppress release of LT/PGs by inhibiting PLPA2/PLPC
  2. SE: hoarse voice, oral candidiasis, systemic at high doses: osteoporosis
  3. Rinse mouth or use a spacer to minimize absorption
47
Q

Anti-inflammatory drugs:

Inhibition of mast cell degranulation:

  1. Drug?
  2. Inhibiting degranulation –> inhibit __/__ synthesis
  3. Used by inhalation for?
A

Anti-inflammatory drugs:

Inhibition of mast cell degranulation:

  1. Cromolyn
  2. Inhibit degranulation –> inhibit LT/PG synthesis
  3. Inhalation to prevent mild to moderate asthma attacks by reducing airway reactivity
48
Q

Anti-inflammatory drugs:

Inhibition of mast cell degranulation:

  1. Cromolyn is often used with?
  2. Minimal SE?
  3. DOES NOT relieve?
A

Anti-inflammatory drugs:

Inhibition of mast cell degranulation:

  1. Cromolyn is often used with glucocorticoids
  2. SE: bad taste, cough, wheezing, bronchospasm, HA
  3. Does NOT relieve acute asthmatic symptoms
49
Q

Anti-inflammatory drugs:

Leukotriene Receptor Antagonists:

  1. Drugs?
  2. MOA: prevents actions of ___ leukotrienes (___, ___, ___) at ___ receptors by binding to it
A

Anti-inflammatory drugs:

Leukotriene Receptor Antagonists:

  1. Montelukast and zafirlukast
  2. MOA: prevents actions of **cysteinyl **leukotrienes (LTC4, LTD4, and LTE4) at CysLT1 receptors by binding to it
50
Q

Anti-inflammatory drugs:

Leukotriene Receptor Antagonists:

  1. Administered ____ for?
  2. Inhibits ____. This increases ___ by 60%. Not used for acute asthma because of MOA.
A

Anti-inflammatory drugs:

Leukotriene Receptor Antagonists:

  1. Administered orally for prophylactic treatment of mild asthma –> decreases bronchoconstriction
  2. Inhibits CYP450!!!!! This increases warfarin by 60%!
51
Q

Anti-inflammatory drugs:

Leukotriene Receptor Antagonists:

  1. Side effects?
  2. Who is this particularly ok for?
A

Anti-inflammatory drugs:

Leukotriene Receptor Antagonists: Montelukast/Zafirlukast

  1. SE: RARE - pulmonary infiltrates, neuropathy, skin rashes, and vasculitis
  2. This is USED IN CHILDREN
52
Q

Anti-inflammatory drugs:

5-Lipoxygenase Inhibitor:

  1. Drug?
  2. MOA?
A

Anti-inflammatory drugs:

5-Lipoxygenase Inhibitor:

  1. Zileuton
  2. Inhibits formation of ALL 5-lipoxygenase products including LTB4/C4/D4/E4
53
Q

Anti-inflammatory drugs:

5-Lipoxygenase Inhibitor:

  1. Administration? Use?
  2. Contraindication? Why?
A

Anti-inflammatory drugs:

5-Lipoxygenase Inhibitor:

  1. Oral; prophylactic treatment of mild asthma
  2. Contraindicated in patients with active liver disease because it can elevate liver enzymes in 5% of patients
54
Q

Anti-inflammatory drugs:

Humanized Monoclonal Anti-IgE Antibody:

  1. Drug?
  2. Humanized ____ antibody that binds free ___, thus prevents ___ from interacting with receptor and blocks release of ____ and ___.
A

Anti-inflammatory drugs:

Humanized Monoclonal Anti-IgE Antibody:

  1. Omalizumab
  2. Humanized IgG1k antibody that binds free IgE, thus prevents IgE from interacting with receptor and blocks release of histamine and leukotrienes
55
Q

Anti-inflammatory drugs:

Humanized Monoclonal Anti-IgE Antibody:

  1. Administration?
  2. Reduces? Decreases need for?
  3. Concerns? SE?
A

Anti-inflammatory drugs:

Humanized Monoclonal Anti-IgE Antibody:

  1. Subcutaneous or IV (once every 2-4 weeks)
  2. Reduces airway responsiveness and decreases need for other asthma drugs
  3. Concern: cost; SE: potential infection, pain on injection, and small risk for anaphylaxis
56
Q

Asthma: I - Intermittent:

  1. Taken when?
  2. Drug class of choice? Drugs?
A

Asthma: I - Intermittent:

  1. Taken as needed
  2. Drug class: B2 agonists - albuterol, salmeterol, pirbuterol, and terbutaline
57
Q

Asthma II - Mild persistant:

Inhaled ______. Drugs?

What other 2 drug classes? Drugs?

A

Asthma II - Mild persistant:

Inhaled glucocorticoids: beclomethasone and fluticasone

a. Inhibitors of mast cell degranulation - Cromolyn
b. CysLT1 receptor antagonists: monelukast and zafirlukast

58
Q

Asthma III - Moderate Persistant:

3 drug classes and accompanying drugs that are best for moderate persistant asthma.

A

Asthma III - Moderate Persistant:

a. Inhaled glucocorticoids: beclomethasone and fluticasone
b. Long acting B2 agonist: salmuterol
c. Methylxanthines: theophylline

59
Q

Asthma IV - Severe Persistant:

5 drug classes and the drugs associated.

A

Asthma IV - Severe Persistant:

a. Inhaled glucocorticoids: beclamethasone and fluticasone
b. Long acting B2 agonist: salmuterol
c. Methylxanthines: theophylline
d. Systemic glucocorticoids
e. Human Anti-IgE Ab: Omalizumab

60
Q

COPD:

Indicators are not diagnostic themselves but helpful:

  1. Age?
  2. ___ that is progressive: worse with exercise and described as “____”
  3. Chronic ____, may be intermittent or even ____
  4. Chronic ____ prouction
  5. ___ of exposure to risk factors: examples?
A

COPD

  1. OVER 40
  2. Dyspnea that is progressive: described as “gasping”
  3. Chronic cough, may be intermittent or nonproductive
  4. Chronic sputum production
  5. History of exposure to risk factors: ***Smoking or working with dusts/chemicals
61
Q

Therapy of COPD:

Reduce of Risk Factors:

Host risk factors include ___ ___ deficiency, _____ airways, and both sex and ___. (highest prevalence in the ___ ___ population).

Therapy?

A

Therapy of COPD:

Reduce of Risk Factors:

Host risk factors include alpha1 antitrypsin deficiency, hyperresponsive airways, and both sex and ethnicity. (highest prevalence in the white male population)

Therapy: quit smoking - nicotine replacement

62
Q

COPD MAnagement:

  1. Use of combination therapy is recommended as COPD advances beyond Stage __.
  2. Good to give long-acting muscarinic receptor antagonists: ___ and ___.
  3. At what stage is O2 therapy usually introduced?
A

COPD management:

  1. Combination: Stage II
  2. Muscarinic receptor antagonists: ipratropium and tiotropium
  3. O2 therapy - stage III
63
Q

COPD Management:

  1. What is combivent therapy?
  2. Who is it indicated for?
  3. Contraindications?
A

COPD Management:

  1. Combivent: ipratropium with albuterol
  2. COPD patients who were not controlled with a single therapy
  3. Contraindicated in patients with soy allergy
64
Q

COPD Management:

Drugs that are not recommended:

  1. ___ cell stabilizer: ___
  2. LT modifiers: ___, ___, and ____
A

COPD Management:

Not recommended

  1. mast cell stabilizer: cromolyn
  2. LT modifiers: Zileuton, Zafirlukast, and Montelukast
65
Q

COPD Management:

  1. 2 Contraindications? Why if reason given?
  2. Benefits of mucolytic agents?
A

COPD Management:

  1. Antitussives
  2. Narcotics: because of respiratory depression and potential to worsen hypercapnia
  3. Mucolytic agents show small, if no, overall benefits
66
Q

COPD Management:

What to give for:

  1. Stage 1 mild COPD?
  2. Stage 2 COPD?
A

COPD Management:

What to give for:

  1. Stage 1: flu vaccine + short acting bronchodilator when needed
  2. Stage 2: ADD long acting bronchodilator and rehabilitation
67
Q

COPD Management:

What to give for:

  1. Stage 3 COPD?
  2. Stage 4 COPD?
A

COPD Management:

What to give for:

  1. Stage 3: ADD (to stage 2) inhaled glucocorticosteroids
  2. Stage 4: ADD long term O2 and consider surgery

Pharmacology (24 decks)

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