Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

anticholinergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Atropine

Therapeutic uses

A

Bradycardia
Asthma/COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Solifenacin (VESIcare)

Class
Therapeutic Use
Adverse effects

A

Anticholinergic for OAB

Adverse effects:
Blurred vision
Dysrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Tolterodine (Detrol, Detrol LA)

A

Anticholinergic - nonselective muscarinic antagonist
Therapeutic use: OAB

Fewer anticholinergic side effects than Solifenacin (VESIcare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Physostigmine

A

antidote for anticholinergic toxicity
Inhibitor of acetylcholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Adrenergic agonists

Therapeutic uses

A

Congestive heart failure
Asthma
Preterm labor (beta 2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cathecholamines

A

Dopamine
Epinephrine
Norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Catecholamines cannot be given through this route of administration

A

PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Catecholamines have a ____ duration of action

A

brief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Can catecholamines cross the blood-brain barrier?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What receptors does albuterol bind to?

A

Beta 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What receptors does Isoproterenol bind to?

A

beta 1 and beta 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What receptors does epinephrine bind to?

A

Alpha 1 alpha 2
Beta 1 and beta 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

As ____ increases, some receptor selectivity is lost

A

dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

common alpha-1 adrenergic receptor agonists

A

epinephrine
norepinephrine
dopamine
phenylephrine
dobutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Alpha-1 agonists

Adverse effects

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Beta 1 Agonists

Therapeutic Uses

A

Heart Failure
Shock
Bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Beta-1 activation

Adverse effects

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Beta-2

Therapeutic uses

A

BETA 2 - TWINS - TWINS OFTEN COME EARLY

-Asthma
-Delay of preterm labor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are adverse effects of beta 2 activation?

A

-Hyperglycemia
-Tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What happens to urine output if you give a drug that activates dopamine receptors?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hypotension, bronchoconstriction, and edema of the glottis are all symptoms of _____

A

anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the treatment for anaphylaxis?

A

IM Epinephrine
Because epi has a short half-life, about 20% of patients will require a second dose 5-15 minutes later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are therapeutic uses of epinephrine (besides anaphylaxis)?

A

-Delays absorption of local anesthetic
-Elevates BP
-Mydriasis during opthalmologic procedures
-Restores cardiac function in arrest

30
Q

What are adverse effects of epinephrine?

A

Hypertensive crisis
Dysrhythmias
Angina
Necrosis following extravasation
Hyperglycemia

31
Q

Unlike epi, nor-epi does not activate _____ receptors

A

beta 1

32
Q

Does nor-epi promote hyperglycemia?

A

No, because nor-epi does not activate beta 2 receptors, it does not promote hyperglycemia like epi does.

33
Q

What is the chemical classification of isoproterenol?

A

catecholamine

34
Q

What receptors does isoproterenol bind to?

A

beta 1 and beta 2

35
Q

What is the therapeutic use of isoproterenol?

A

AV heart block
cardiac arrest

36
Q

What are the adverse effects of isoproterenol?

A

-Fewer than those of NE or epinephrine
-Tachycardia
-Angina pectoris
-Hyperglycemia (DM pts)

37
Q

What are drug interactions with isoproterenol?

A

MAOIs, TCAs, beta-adrenergic blockers

38
Q

What is the route of administration for Isoproterenol?

A

IV, IM, intracardiac

39
Q

What receptors does dopamine activate at LOW doses?

A

Dopamine only

40
Q

What receptors does dopamine activate at very high doses?

A

Alpha1, beta 1, and dopamine

41
Q

What are the therapeutic uses of dopamine?

A

-Shock (increases cardiac output, increases renal perfusion)
-Heart failure (increases force and contractability)

42
Q

What are adverse effects of dopamine?

A

Tachycardia
Dysrhythmias
Angina
Necrosis with extravasation

43
Q

Phenylephrine is a _____ agonist

A

alpha 1

44
Q

Chemical classification for phenylephrine

A

Noncatecholamine

45
Q

What is the therapeutic use of phenylephrine?

A

Reduces nasal congestion

46
Q

Albuterol

Receptor Specificity

A

Beta 2

47
Q

Albuterol

Chemical Classification

A

Noncatecholamine

48
Q

What are the therapeutic applications of alpha blockade?

A

-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
Q

Alpha blockers

Adverse effects

A

Adverse effects from alpha 2 blockers are minor.

Adverse effects of alpha 1 blocker:
Orthostatic hypotension
Reflex tachycardia
Nasal congestion
Inhibition of ejaculation

50
Q

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

A

Alpha 1 blockers

51
Q

Why are alpha 1 blockers usually prescribed along with a diuretic?

A

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
Q

Prazosin:

Receptor Specificity

Therapeutic use

A

Alpha 1 blocker

Treats hypertension

53
Q

Beta blockers

Therapeutic uses

A

Angina pectoris
Hypertension
Cardiac dysrhythmias
Myocardial infarction
Heart failure

54
Q

Beta blockers

Adverse effects

A

Bradycardia
Precipitation of heart failure
AV heart block
Rebound cardiac excitation (beta blockers need to be tapered to prevent rebound HTN and tachycardia)

55
Q

Beta 2 blockers

adverse effects

A

Bronchoconstriction
Hypoglycemia

56
Q

Beta 2 blockers should be used with caution is patients with these conditions

A

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
Q

Propranolol

Receptor Specificity

A

Propranolol is a NON-SELECTIVE beta-blocker

58
Q

Propranolol

Adverse effects

A

Bradycardia
AV heart block
Heart failure
Bronchoconstriction
Inhibition of glycogenolysis
Depression

59
Q

What education is important for a diabetic who is taking propranolol?

A

Beta 2 blockade inhibits the production of glucose. Propranolol may also mask the symptoms of hypoglycemia such as anxiety and tremors

60
Q

Propranolol

Drug interactions

A

Calcium channel blockers
Insulin

61
Q

What does it mean for a drug to have a positive inotropic effect?

A

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
Q

Atropine

Pharmacological effects

A

-Mydriasis (dilated pupils) and cycloplegia (blurry vision)
-Increases HR
-Relaxes smooth muscle (bladder and bronchi)
-CNS: Mild excitation to hallucinations and delirium

63
Q

Anticholinergics

Therapeutic uses

A

Bradycardia
Asthma/COPD
OAB

64
Q

Atropine

Drug interactions

A

Avoid combining atropine with other drugs capable of causing muscarinic blockade

65
Q

Mechanisms of Adrenergic
Receptor Activation

A

Direct receptor binding
Promotion of norepinephrine (NE) release
Inhibition of NE reuptake
Inhibition of NE inactivation

66
Q

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

A

Phentolamine

67
Q

Propranolol vs metoprolol

Receptor Specificity

A

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
Q

Why would you choose metoprolol over propranolol in a patient with Asthma/COPD or diabetes?

A

Metoprolol has a lower risk of bronchospasm and hypoglycemia compared to propranolol due to its beta-1 selectivity.

69
Q

Beta-2 agonists

Adverse effects

A

Hyperglycemia
Tremor

70
Q

Signs of anaphylactic shock

A

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
Q

How do monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) affect catecholamines and non-catecholamines differently?

A

Catecholamines are susceptible to rapid metabolism by these enzymes, non-catecholamines have structural differences that make them less prone to enzymatic degradation

72
Q

Signs / Symptoms of Heart failure

A

“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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions