Pharmacotherapeutics Exam 2 Test Questions and Answers Graded A+
Bronchoconstrictor mediators such as:
1. Histamine
In asthma, mast cells release what three compounds that
2. Leukotriene D4
cause bronchoconstriction, microvascular leakage, and
3. Prostaglandin D2
plasma exudation?
HLP, my airways are constricting!
1. A characteristic feature of asthma is deposi- 1. A characteristic feature of asthma is collagen deposition
tion. ( ) (Fibrosis)
2. In hypersensitivity reactions, allergen-specific 2. In hypersensitivity reactions, allergen-specific IgE
bound to mast cells trigger the release of inflammatory bound to mast cells triggers the release of inflammatory
mediators. mediators.
1. In COPD, the release of PROTEASES results in alveolar
1. In COPD, the release of results in alveolar wall
wall destruction (EMPHYSEMA).
destruction ( ).
2. In COPD, mucus hypersecretion (Chronic Bronchitis)
2. In COPD, mucus hypersecretion ( ) air-
airway diseases have a dominant PARASYMPATHETIC over-
way diseases have a dominant overtone.
tone.
Increasing the number of MUCUS-SECRETING glands,
and reducing MUCOCILIARY function.
In COPD, larger airways respond via increasing the num-
ber of glands, and reducing function. Smaller airways go through repeated cycles of injury and
repair resulting in REMODELING / SCARRING / THICKEN-
Smaller airways go through repeated cycles of injury and ING
repair resulting in .
(we prob don't need to know all of those terms, just get
the general idea)
1. SABA: "-buterols", Albuterol, Levalbuterol, Pirbuterol
For the SABA medications, name the following:
1. Examples (or their suflx) 2. Used for acute inhalation of bronchospasms,
monotherapy for intermittent asthma or pretreatment be-
, Pharmacotherapeutics Exam 2 Test Questions and Answers Graded A+
fore exercise (NOT persistent asthma!)
2. Therapeutic uses
3. Their MOA (Activate enzyme, which increases 3. MOA:
production of ) - Activates adenyl cyclase, which increases cAMP produc-
tion (cAMP = smooth muscle relaxation)
Increase airflow within 3-5 minutes, Provide relief for 4-6
hours
SABAs increase airflow within minutes, and provide
relief for hours. SABA Toxicity: Skeletal musc tremor, Tachycardia, Increased
lactic acid, hypokalemia, hyperglycemia
What are some S/S of SABA Toxicity?
***Mnemonic: Saba Toxicity = S T = Skeletal tremor, Tachy-
cardia (just to remember a few)
1. TWO DRUGS: Formoterol Fumarate & Salmeterol Xinfo-
late
-Remember = Formoterol, Full agonist, Fast onset (FFF)
For LABA medications, name the following:
2. THEY DON'T CHANGE DISEASE PROGRESS, just help
1. The 2 drugs and the ditterences between them mask S/S
2. How they attect disease progress
3. Describe what they're used in combination with 3. Used in combo inhalers which combine LABA + corti-
costeroid for persistent asthma!
(Steroids upregulate the # of beta-2 receptors, probably
dont need to know that tho)
1. MOA: Inhibits phosphodiesterase (PDE), the enzyme
For Theophylline, name the following: that degrades cAMP to AMP (thus increasing cAMP)
1. MOA (inhibits what enzyme) 2. Target peak conc range: 10-15 mcg/ml
2. Target serum concentration values Unbound 6-12 mcg/ml (in patients with low levels of bind-
3. S/S of Theophylline Toxicity ing proteins)
, 3: Toxicity S/S: Severe headache, tachycardia, convulsions,
potentially fatal arrhythmias
1. Examples: Ipratropium Br, Tiotropium Br
For the anticholinergic agents, name the following: 2. MOA: Competitive antagonists of muscarinic receptors -
they block ACh from binding, which blocks airway smooth
1. Examples muscle contraction
2. Their MOA
3. Therapeutic uses 3. Ettective for COPD because cholinergic tone is in-
creased, response is based on strength of parasympathet-
ic tone
For the anticholinergic agents, name the following:
1. Not for acute bronchospasms because SLOW ONSET
1. Why they're not used for treatment of ACUTE asthma
2. Use with caution in pts:
bronchospasms
Narrow-angle glaucoma, prostatic hypertrophy, or blad-
der neck obstruction
2. Patients that should use them with caution (what con-
(the same exact 3 things go for antihistamines too)
ditions do they have)
1. Examples: Becomethasone, Fluticasone, Budesonide,
Flunosolide (BFBF)
2. MOA: inhibits cytokine production, adhesion protein
For Inhaled Corticosteroids (ICS), name the following: activation, decreases number of goblet cells
- Blocks late reaction to an allergen by lowering airway
1. Examples responsiveness
2. MOA (What does it inhibit/decrease?)
3. Toxicity S/S 3. Toxicity: Local (Candidiasis, hoarseness)
4. Dosing principles Systemic (Adrenal suppression in those taking high doses,
bone mineral density alteration)
4. Dosing - Based on clinician's judgement, not one size
fits all
Name some SYSTEMIC corticosteroids, and after how
many uses should treatment should be reevaluated?
Bronchoconstrictor mediators such as:
1. Histamine
In asthma, mast cells release what three compounds that
2. Leukotriene D4
cause bronchoconstriction, microvascular leakage, and
3. Prostaglandin D2
plasma exudation?
HLP, my airways are constricting!
1. A characteristic feature of asthma is deposi- 1. A characteristic feature of asthma is collagen deposition
tion. ( ) (Fibrosis)
2. In hypersensitivity reactions, allergen-specific 2. In hypersensitivity reactions, allergen-specific IgE
bound to mast cells trigger the release of inflammatory bound to mast cells triggers the release of inflammatory
mediators. mediators.
1. In COPD, the release of PROTEASES results in alveolar
1. In COPD, the release of results in alveolar wall
wall destruction (EMPHYSEMA).
destruction ( ).
2. In COPD, mucus hypersecretion (Chronic Bronchitis)
2. In COPD, mucus hypersecretion ( ) air-
airway diseases have a dominant PARASYMPATHETIC over-
way diseases have a dominant overtone.
tone.
Increasing the number of MUCUS-SECRETING glands,
and reducing MUCOCILIARY function.
In COPD, larger airways respond via increasing the num-
ber of glands, and reducing function. Smaller airways go through repeated cycles of injury and
repair resulting in REMODELING / SCARRING / THICKEN-
Smaller airways go through repeated cycles of injury and ING
repair resulting in .
(we prob don't need to know all of those terms, just get
the general idea)
1. SABA: "-buterols", Albuterol, Levalbuterol, Pirbuterol
For the SABA medications, name the following:
1. Examples (or their suflx) 2. Used for acute inhalation of bronchospasms,
monotherapy for intermittent asthma or pretreatment be-
, Pharmacotherapeutics Exam 2 Test Questions and Answers Graded A+
fore exercise (NOT persistent asthma!)
2. Therapeutic uses
3. Their MOA (Activate enzyme, which increases 3. MOA:
production of ) - Activates adenyl cyclase, which increases cAMP produc-
tion (cAMP = smooth muscle relaxation)
Increase airflow within 3-5 minutes, Provide relief for 4-6
hours
SABAs increase airflow within minutes, and provide
relief for hours. SABA Toxicity: Skeletal musc tremor, Tachycardia, Increased
lactic acid, hypokalemia, hyperglycemia
What are some S/S of SABA Toxicity?
***Mnemonic: Saba Toxicity = S T = Skeletal tremor, Tachy-
cardia (just to remember a few)
1. TWO DRUGS: Formoterol Fumarate & Salmeterol Xinfo-
late
-Remember = Formoterol, Full agonist, Fast onset (FFF)
For LABA medications, name the following:
2. THEY DON'T CHANGE DISEASE PROGRESS, just help
1. The 2 drugs and the ditterences between them mask S/S
2. How they attect disease progress
3. Describe what they're used in combination with 3. Used in combo inhalers which combine LABA + corti-
costeroid for persistent asthma!
(Steroids upregulate the # of beta-2 receptors, probably
dont need to know that tho)
1. MOA: Inhibits phosphodiesterase (PDE), the enzyme
For Theophylline, name the following: that degrades cAMP to AMP (thus increasing cAMP)
1. MOA (inhibits what enzyme) 2. Target peak conc range: 10-15 mcg/ml
2. Target serum concentration values Unbound 6-12 mcg/ml (in patients with low levels of bind-
3. S/S of Theophylline Toxicity ing proteins)
, 3: Toxicity S/S: Severe headache, tachycardia, convulsions,
potentially fatal arrhythmias
1. Examples: Ipratropium Br, Tiotropium Br
For the anticholinergic agents, name the following: 2. MOA: Competitive antagonists of muscarinic receptors -
they block ACh from binding, which blocks airway smooth
1. Examples muscle contraction
2. Their MOA
3. Therapeutic uses 3. Ettective for COPD because cholinergic tone is in-
creased, response is based on strength of parasympathet-
ic tone
For the anticholinergic agents, name the following:
1. Not for acute bronchospasms because SLOW ONSET
1. Why they're not used for treatment of ACUTE asthma
2. Use with caution in pts:
bronchospasms
Narrow-angle glaucoma, prostatic hypertrophy, or blad-
der neck obstruction
2. Patients that should use them with caution (what con-
(the same exact 3 things go for antihistamines too)
ditions do they have)
1. Examples: Becomethasone, Fluticasone, Budesonide,
Flunosolide (BFBF)
2. MOA: inhibits cytokine production, adhesion protein
For Inhaled Corticosteroids (ICS), name the following: activation, decreases number of goblet cells
- Blocks late reaction to an allergen by lowering airway
1. Examples responsiveness
2. MOA (What does it inhibit/decrease?)
3. Toxicity S/S 3. Toxicity: Local (Candidiasis, hoarseness)
4. Dosing principles Systemic (Adrenal suppression in those taking high doses,
bone mineral density alteration)
4. Dosing - Based on clinician's judgement, not one size
fits all
Name some SYSTEMIC corticosteroids, and after how
many uses should treatment should be reevaluated?
