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Pharmacology > Anticholinergics, Alpha and Beta Agents and Blockers > Flashcards

Anticholinergics, Alpha and Beta Agents and Blockers Flashcards

1
Q

what are the four “big” anticholinergic effects/side effects?

A

CAN’T SEE, CAN’T SPIT, CAN’T PEE, CAN’T SHIT

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2
Q

antihistamines, tricyclic antidepressants, and phenothiazine antipsychotics have strong ______ effects

A

anticholinergic

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3
Q

Atropine

Therapeutic uses

A

Bradycardia
Asthma/COPD

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4
Q

What are adverse effects of muscarinic antagonists/anticholinergic drugs?

A

CAN’T SEE - Blurred vision and photophobia, elevation of intraocular pressure (–> glaucoma)
CAN’T SPIT - Xerostomia (dry mouth)
CAN’T PEE - urinary retention
CAN’T SHIT - constipation

Can’t sweat - anhidrosis - can therefore overheat

Tachycardia
CNS effects: hallucinations, delirium

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5
Q

Solifenacin (VESIcare)

Class
Therapeutic Use
Adverse effects

A

Anticholinergic for OAB

Adverse effects:
Blurred vision
Dysrhythmia

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6
Q

Tolterodine (Detrol, Detrol LA)

A

Anticholinergic - nonselective muscarinic antagonist
Therapeutic use: OAB

Fewer anticholinergic side effects than Solifenacin (VESIcare)

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7
Q

What are the signs and symptoms of anticholinergic toxicity?

A

Blurred vision
Photophobia
Mydriasis (dilated pupils)
Dry mouth
Hot, dry, and flushed skin
Hyperthermia
CNS effects (delirium, hallucinations)

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8
Q

Physostigmine

A

antidote for anticholinergic toxicity
Inhibitor of acetylcholinesterase

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9
Q

Adrenergic agonists

Therapeutic uses

A

Congestive heart failure
Asthma
Preterm labor (beta 2)

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10
Q

Cathecholamines

A

Dopamine
Epinephrine
Norepinephrine

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11
Q

Catecholamines cannot be given through this route of administration

A

PO

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12
Q

Catecholamines have a ____ duration of action

A

brief

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13
Q

Can catecholamines cross the blood-brain barrier?

A

No

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14
Q

What advantages do non-catecholamines have over catecholamines?

A

-Can be given orally
-Metabolized slowly by MAO - longer half-life
-More able to cross the BBB

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15
Q

What receptors does albuterol bind to?

A

Beta 2

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16
Q

What receptors does Isoproterenol bind to?

A

beta 1 and beta 2

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17
Q

What receptors does epinephrine bind to?

A

Alpha 1 alpha 2
Beta 1 and beta 2

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18
Q

As ____ increases, some receptor selectivity is lost

A

dose

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19
Q

common alpha-1 adrenergic receptor agonists

A

epinephrine
norepinephrine
dopamine
phenylephrine
dobutamine

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20
Q

Alpha-1 agonists

Therapeutic uses

A

-Hemostasis (stops bleeding)
-Nasal decongestion
-Adjunct to local anesthesia
-Elevation of blood pressure (vasoconstriction)
-Mydriasis (dilation of pupils)

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21
Q

Alpha-1 agonists

Adverse effects

A

Hypertension (widespread vasoconstriction)
Necrosis (with extravasation from IV)

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22
Q

Beta 1 Agonists

Therapeutic Uses

A

Heart Failure
Shock
Bradycardia

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23
Q

Beta-1 activation

Adverse effects

A

-Tachycardia
-Dysrhythmia
-Angina pectoris (due to increased cardiac oxygen demand)

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24
Q

Beta-2

Therapeutic uses

A

BETA 2 - TWINS - TWINS OFTEN COME EARLY

-Asthma
-Delay of preterm labor

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25
What are adverse effects of beta 2 activation?
-Hyperglycemia -Tremor
26
What happens to urine output if you give a drug that activates dopamine receptors?
Dopamine receptors cause dilation of the vasculature of the kidneys, which increases renal blood flow and urine output. There is NO effect on the bladder though.
27
Hypotension, bronchoconstriction, and edema of the glottis are all symptoms of _____
anaphylaxis
28
What is the treatment for anaphylaxis?
IM Epinephrine Because epi has a short half-life, about 20% of patients will require a second dose 5-15 minutes later
29
What are therapeutic uses of epinephrine (besides anaphylaxis)?
-Delays absorption of local anesthetic -Elevates BP -Mydriasis during opthalmologic procedures -Restores cardiac function in arrest
30
What are adverse effects of epinephrine?
Hypertensive crisis Dysrhythmias Angina Necrosis following extravasation Hyperglycemia
31
Unlike epi, nor-epi does not activate _____ receptors
beta 1
32
Does nor-epi promote hyperglycemia?
No, because nor-epi does not activate beta 2 receptors, it does not promote hyperglycemia like epi does.
33
What is the chemical classification of isoproterenol?
catecholamine
34
What receptors does isoproterenol bind to?
beta 1 and beta 2
35
What is the therapeutic use of isoproterenol?
AV heart block cardiac arrest
36
What are the adverse effects of isoproterenol?
-Fewer than those of NE or epinephrine -Tachycardia -Angina pectoris -Hyperglycemia (DM pts)
37
What are drug interactions with isoproterenol?
MAOIs, TCAs, beta-adrenergic blockers
38
What is the route of administration for Isoproterenol?
IV, IM, intracardiac
39
What receptors does dopamine activate at LOW doses?
Dopamine only
40
What receptors does dopamine activate at very high doses?
Alpha1, beta 1, and dopamine
41
What are the therapeutic uses of dopamine?
-Shock (increases cardiac output, increases renal perfusion) -Heart failure (increases force and contractability)
42
What are adverse effects of dopamine?
Tachycardia Dysrhythmias Angina Necrosis with extravasation
43
Phenylephrine is a _____ agonist
alpha 1
44
Chemical classification for phenylephrine
Noncatecholamine
45
What is the therapeutic use of phenylephrine?
Reduces nasal congestion
46
Albuterol Receptor Specificity
Beta 2
47
Albuterol Chemical Classification
Noncatecholamine
48
What are the therapeutic applications of alpha blockade?
-Hypertension (lowers blood pressure by blocking alpha 1 receptors on blood vessels, causing vasodilation) -Reversal of toxicity of alpha 1 agonists -PROSTATE PROBLEMS: Benign prostatic hyperplasia (reduced contraction of smooth muscle in the bladder neck and prostatic capsule)
49
Alpha blockers Adverse effects
Adverse effects from alpha 2 blockers are minor. Adverse effects of alpha 1 blocker: Orthostatic hypotension Reflex tachycardia Nasal congestion Inhibition of ejaculation
50
Blockade of these receptors may cause orthostatic hypotension as follows: reduced muscle tone in the venous wall --> upon standing blood pools in the veins --> the return of blood to the heart is reduced --> cardiac output is reduced --> the blood pressure drops
Alpha 1 blockers
51
Why are alpha 1 blockers usually prescribed along with a diuretic?
Alpha 1 blockers may cause a dramatic drop in BP. The kidneys respond to reduced blood flow by retaining sodium and water, so there is an increase in blood volume.
52
Prazosin: Receptor Specificity Therapeutic use
Alpha 1 blocker Treats hypertension
53
Beta blockers Therapeutic uses
Angina pectoris Hypertension Cardiac dysrhythmias Myocardial infarction Heart failure
54
Beta blockers Adverse effects
Bradycardia Precipitation of heart failure AV heart block Rebound cardiac excitation (beta blockers need to be tapered to prevent rebound HTN and tachycardia)
55
Beta 2 blockers adverse effects
Bronchoconstriction Hypoglycemia
56
Beta 2 blockers should be used with caution is patients with these conditions
Asthma/COPD - Beta 2 blockers can cause bronchoconstriction, which can lead to dyspnea Diabetes - Beta 2 receptors on the liver and skeletal muscles regulate glycogenolysis --> so beta 2 blockers can lead to reduced glucose in the bloodstream
57
Propranolol Receptor Specificity
Propranolol is a NON-SELECTIVE beta-blocker
58
Propranolol Adverse effects
Bradycardia AV heart block Heart failure Bronchoconstriction Inhibition of glycogenolysis Depression
59
What education is important for a diabetic who is taking propranolol?
Beta 2 blockade inhibits the production of glucose. Propranolol may also mask the symptoms of hypoglycemia such as anxiety and tremors
60
Propranolol Drug interactions
Calcium channel blockers Insulin
61
What does it mean for a drug to have a positive inotropic effect?
When a drug has a positive inotropic effect, it enhances the heart's ability to contract more forcefully, leading to an increase in cardiac output
62
Atropine Pharmacological effects
-Mydriasis (dilated pupils) and cycloplegia (blurry vision) -Increases HR -Relaxes smooth muscle (bladder and bronchi) -CNS: Mild excitation to hallucinations and delirium
63
Anticholinergics Therapeutic uses
Bradycardia Asthma/COPD OAB
64
Atropine Drug interactions
Avoid combining atropine with other drugs capable of causing muscarinic blockade
65
Mechanisms of Adrenergic Receptor Activation
Direct receptor binding Promotion of norepinephrine (NE) release Inhibition of NE reuptake Inhibition of NE inactivation
66
This drug treats necrosis caused by extravasation from IV by blocking alpha-1 adrenergic receptors and reversing the vasoconstrictive effects, restoring blood flow and preventing further tissue damage
Phentolamine
67
Propranolol vs metoprolol Receptor Specificity
Propranolol is a non-selective beta-adrenergic antagonist, meaning it blocks both beta-1 and beta-2 adrenergic receptors Metoprolol is a selective beta-1 adrenergic antagonist. It primarily blocks beta-1 adrenergic receptors with a higher affinity, while having less effect on beta-2 receptors.
68
Why would you choose metoprolol over propranolol in a patient with Asthma/COPD or diabetes?
Metoprolol has a lower risk of bronchospasm and hypoglycemia compared to propranolol due to its beta-1 selectivity.
69
Beta-2 agonists Adverse effects
Hyperglycemia Tremor
70
Signs of anaphylactic shock
Skin reactions: itching, hives, redness, swelling. Respiratory symptoms: wheezing, shortness of breath, difficulty breathing. Cardiovascular symptoms: rapid or weak pulse, low blood pressure, lightheadedness. Gastrointestinal symptoms: nausea, vomiting, abdominal pain, diarrhea. Swelling of throat and tongue. Anxiety, feeling of impending doom.
71
How do monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) affect catecholamines and non-catecholamines differently?
Catecholamines are susceptible to rapid metabolism by these enzymes, non-catecholamines have structural differences that make them less prone to enzymatic degradation
72
Signs / Symptoms of Heart failure
"Crackles" may be heard when listening over the lungs with a stethoscope. When pressure backs up in the vasculature of the lungs, fluid "transudes" into the spaces surrounding the air sacs, causing them to collapse. As the patient breathes in deeply, the air sacs are forced open and this sounds like "crackle." Given the above, it makes sense that someone with heart failure would have some shortness of breath, and perhaps low oxygen levels noted when we place a pulse oximeter on their finger. It also makes some sense that they might have an elevated respiratory rate. Pedal edema (swelling of the feet) occurs in heart failure. It is a result of the release of renin --> angiotensin --> aldosterone. This happens in response to poor perfusion of the kidneys by the failing heart. Aldosterone causes the kidneys to hold on to excess water and sodium. The extra water can accumulate in gravity-dependent areas.

Pharmacology (21 decks)

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