CP Pharmacologic Interventions Flashcards

1
Q

What are 3 drug classes used to increase contractility

A

beta 1 agonists
phosphodiesterase Inhibitor
digitalis (foxglove)

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2
Q

what are 3 drug classes that decrease the heart’s workload via decreased contractility?

A

calcium channel blockers
centrally acting agents (also decrease HR)
beta 1 antagonists

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3
Q

what are 3 drug classes that decrease the heart’s workload via decreased afterload?

A

alpha 1 blockers
direct vasodilators
aldosterone blockers

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4
Q

what are 3 drug classes that decrease the heart’s workload via decreased preload?

A

diuretics (loop,thiazide, k-sparing)
ACE inhibitors
Angiotensin II Receptor Antagonists

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5
Q

what class of drugs increases myocardial bloodflow? What are the 3 types?

A

nitrates
-venodilators (preload), arteriodilaros (afterload) , organic nitrates (both)

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6
Q

what 2 classes manage hemostasis?

A

thrombolytics (clot busters-reactive) ) and anticoagulants (blood thinners-proactive)

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7
Q

Name the antiarrhythmic drug classes

A

I. Sodium Channel blockers (decrease excitability)
II Beta blockers-increase latency (decrease HR)
III-prolong repolarization (decrease HR)
IV- Calcium Channel Blockers (decreased excitability)

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8
Q

What is the most common treatment for hyperlipidemia? What are the PT considerations?

A

Statins
Myalgias + RHABDO!!
liver damage, intolerance, HA. GI and loass of CoenzymeQ10
+ increased risks of chronic conditions (cancers, DM, stroke, etc)

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9
Q

bronhi and bronchioles have an outer layer of cartilage and an inner layer of ___-hence pathologies related to these structures usually involve some sort of ____

A

smooth muscle, brohnchoconstriction

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10
Q

what are the 3 primary causes of bronchoconstriction?

A

abnormal tone (bronchospasms)
inflammation
mechanical obstruction

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11
Q

general characteristics of an acute brochospasm include:
smooth muscle _____
____ production
vascular _______

A

smooth muscle constriction, mucous production and vascular engorgement

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12
Q

T/F: Stimulation of the nucleotide cyclic AMP activates our beta-TWO receptors and produces bronchoconstriction as a parasympathetic response.

A

FALSE.
cAMP> beta 2 receptor stimulation> bronchodilation as adrenergic response

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13
Q

Stimulation of the nucleotide cyclic GMP activates ___ receptors causing parasympathetic ______.

A

muscarinic, bronchoconstriction

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14
Q

since cAMP and cGMP influence the ANS in opposite ways, meds interact with them differently to achieve the same goal.
____ promote bronchodilation via increasing cAMP, while ____ and ____ achieve brochodilation via inhibiting cGMP

A

beta- adrenergic agonists,

alpha-adrenergic antagonists + muscarinic antagonists

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15
Q

beta adrenergic agonists, are most commonly admistered via ____due to rapid onset and decreased concern about AEs related to receptor specificity.

A

inhalation

oral less common (HR/HTN AEs)
subcutaneous rare (many AEs)

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16
Q

why might a nebulizer be easier to administer than a metered dose inhaler? Why might someone prefer the latter?

A

the nebulizer req less coordination and the meds are mixed with saline for easy inhale

they are convenient and quick as compared to the neb that takes 10-15 min.

17
Q

list the 3 primary side effects related to beta adrenergic agonists.

A

receptor overreach (think BBB and cardiac irregularities from also hitting b1 recptors)

also
-developed tolerance
-airway irritation from excessive use

18
Q

T/F: Albuterol is an example of a short acting beta agonist and is thus most effectively used in rescue inhalers while LABAs are usually taken daily for maintenence.

A

true

19
Q

Why would aticholinergic/antimuscarinic drugs be prioritized for someone with COPD vs someone with asthma if both involve vasoconstriction?

A

these drugs target parasympathetic vagal tone/ACh release-not inflammation.

20
Q

SAMAs are ____ for COPD while LAMAs are for ____. Atropine is another option that is easily absorbed but rarely used due to AEs.

A

rescue inhalers, maintenance

21
Q

you remember our anticholinergic rhyme from pharm??

+ tachycardia and confusion

A

can’t see, can’t spit, can’t pee, can’t shit :)

22
Q

glucocorticoids by reversing what aspect of the inflammation cycle?

A

increase in vascular permeability

23
Q

T/F: An advantage of glucocorticoids for pulmonary pts is that they aren’t administered systemically but are inhaled instead–thus typical corticosteroid AEs are avoided.

A

false-AEs are decreased but not eliminated.

24
Q

____ (ex. theophylline, caffeine and theobromine) inhibit phosphodiesterase> increase cAMP> bronchodilation+antiinflammation.

found in coffee, chocolate and tea

A

Xanthine derivatives

25
Q

while xanthine derivatives allow for extended release, ____MUST be monitored in these pts as it has a low toxicity index.

A

blood pressure (HYPOtension)

++ other related AEs (confusion, restlessness,nausea,etc)

26
Q

Drug classes used to control respiratory secretions and treat respiratory tract irritations include: (4)

A

antitussives, decongestants, antihistamines, and mucolytics

27
Q

How do antitussives work? When would they NOT be indicated?

A

They either block receptors as topical anesthetics or increase the medulla’s cough threshold; they are not indicated for active and productive coughs.

28
Q

decongestants are usually from what class? What other effects might we expect?

hint: there is a reduction of bloodflow/outflow from capillaries

A

alpha 1 adrenergic agonists;
sympathetic responses (ex. CNS, CV excitation, rebound effects)

avoid long term use!!

29
Q

antihistamines are indicated for

A

sensorineurally-stim sneezing
increased mucous and congestion from vascular engorgement

30
Q

where are histamine receptors located?

hint: think about how the antihistamines impact the user

A

vascular smooth muscle and endothelial cells (vasodilation+ permeability)
CNS tissue throughout body

31
Q

this subclass of antihistamines does not cross the BBB, has fewer side effects and is preferred for asthma pts since it doesn’t dry out and further irritate their airways .

A

2nd generation

32
Q

T/F: Leukotriene Inhibitors (ex Singulair) are not safe for asthmatics because they trigger bronchial smooth muscle contractions.

A

false. leukotrienes trigger these and inhibition of these molecules is commonly used for seasonal allergies.

33
Q

what dynamic duo works best for mobilizing and removing secretions from the respiratory tract?

think Robitussin and Mucinex

A

mucalytics + expectorants

34
Q

what is a typical qualifier for supplemental O2?

A

SpO2 during a 6MWT</=90%

35
Q

what are some general complications of O2? for special populations?

A

general: skin irritation, fatigue, a.m. HA, explosion risk
COPD: hypoxic drive- don’t overdo it
infants: scarring in developing lungs

36
Q

list the 4 long term medications for asthma

A

LABAs
leukotriene modifiers
mast cell stabilizers
theophylline (xanthine derivative)

37
Q

list the 3 short term medications for asthma

A

SABA
anticholinergics
systemic corticosteroid