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Pharmacology Final > Lecture 20 > Flashcards

Lecture 20 Flashcards

1
Q

What are SNS effects on eyes, heart, bronchi, GI tract, adrenal medulla, sweat glands?

A

Eyes: mydriasis and increase ocular fluid formation
Heart: Increase heart rate and force of contraction. Increase blood flow to coronary arteries. Overall increase in blood pressure.
Bronchi: Dilation of bronchi
GI tract: relaxation of GI tract, bladder. Constriction of urinary sphincter
Adrenal medulla: release of epinephrine
Sweat glands: increase sweating (although this is not an adrenergic receptor. It’s mAChR).

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2
Q

Which are the three main norepinephrine (NE) receptors?

A

Alpha 1, Alpha 2, and Beta 1.

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3
Q

What is the main ligand at the B2 receptor?

A

Epinephrine

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4
Q

What are the norepinephrine effects on the a1, a2, and b1 receptors? Where are these receptors located?

A

Alpha 2: decrease cAMP, GI relaxation, CNS effects (sedation, pain analgesia)

Alpha 1: GLASS-S (GI relaxation. Liver gluconeogenesis and glygenoysis. Arterial constriction to skin and viscera. Smooth muscle constriction of vas deferens, pupils, uterus, sphincters. Skin piloerector muscle contraction. Salivation.)

Beta 1: Heart- increased rate and force of contraction. Kidneys- renin release to increase BP. Fat- lipolysis.

Alpha 2 is located on the presynaptic cell and Alpha 1 and Beta 1 are located on post-synaptic cells.

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5
Q

In what respect is the a2 receptor different from the others?

A

It is on the presynaptic cell and it provides negative feedback to the release of norepinephrine. Activating it suppresses sympathetic tone.

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6
Q

How is norepinephrine action in the cleft terminated?

A

It is taken up by either the pre or post synaptic cell and metabolized by MAO or COMT.

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7
Q

What are catecholamines? Name 3 examples. What is their deitary precursor?

A

Catecholamines are molecules used as neurotransmitters by the sympathetic nervous system that all have catecholamines as their backbones.

Examples: dopamine, norepinephrine, and epinephrine.

Their common dietary precursor is Tyrosine.

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8
Q

How is norepinephrine broken down in the presynaptic versus the postsynaptic cell (2 enzymes)?

A

Presynaptic metabolism uses MAO and post synaptic metabolism uses COMT.

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9
Q

Which receptors will epinephrine mostly activate as an agonist and which less so?

A

Epinephrine is non-selective adrenergic agonist but it has a higher affinty for beta receptors than alpha receptors.

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10
Q

Why does epinephrine have a short half-life?

A

Because it is metabolized so quickly. The body breaks it down quickly because it has drastic effects on the cardiovascular system.

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11
Q

What are cardiovascular effects of epinephrine (by receptor)?

A
  1. B1 actionontheheartincreasesheartrateandforceofcontraction
  2. B2 actiononbloodvesselscausesvasodilationanddecreasesperipheralresistance
  3. A1 actiononbloodvesselscausesvasoconstrictionandincreasesperipheralresistance(bloodpressure). This A1 actioniswhatmakesepinephrinesuchapotentvasoconstrictionlocally.
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12
Q

What are dose-dependent affects of epinephrine on BP (low versus high concentrations)?

A

At low dose, epinephrine will activate beta receptors causing vasodilation to the skeletal muscle, coronary arteries, and renal arteries. This causes a decrease in BP.

At higher doses, alpha receptors are activated which cause perihperal constriction of blood vessels, leading to an increase in blood pressure.

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13
Q

What are 5 epinephrine effects on different smooth muscle tissues?

A

Relaxation of: bronchi, uterus, urinary bladder, GI tract.

Constriction of sphincters, pupils.

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14
Q

What are the effects of epinephrine on metabolism (think “flight and fight”)?

A

They increase lipolysis, glycogenolysis and gluconeogenesis. Also inhibits secretion of insulin and increases secretion of glucagon.

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15
Q

4 clinical applications for epinephrine

A

Increase heart rate and force of contraction in cardiac arrest.

Reduce bronchospasm

Treat allergic reactions (hypersensitivity reaction, anaphylactic shock)

Local vasoconstriction (w/local anesthetic, control hemorrhage, glaucoma)

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16
Q

What are possible adverse effects of epinephrine?

A

Potential for arrhythmia;
Excess vasoconstriction will cause hypertension;
Problems in circulation w/local anesthetics due to excessive vasoconstriction (tissue necrosis)

17
Q

How does NE act on alpha and beta receptors to change BP and heart rate?

A

A1- constriction of perihperal blood vessels —>Increased blood pressure

B1 - accelerated heart but baroreceptor reflex slows heart (vagal activation) —> slows heart rate

18
Q

Explain how the baroreceptor reflex regulates BP. Start out with BP being too high.

A

Increased BP—> activated stretch receptors (carotid sinus/aortic arch)—> increased afferent discharge to CNS —> decreased SNS, increased PNS output —> activation of M2 receptor —> decreased heart rate/peripheral resistance —> decreased BP

19
Q

What are therapeutic uses of NE?

A

None

20
Q

Dopamine acts on __ receptors, in high doses also on __ receptors and very high doses on __ receptors as well.

A

DA

B1

A1

21
Q

What are dopamine effects on heart rate and (coronary heart) blood vessels?

A

Increases heart rate (positive ionotropic and chronotropic effects on heart via b-action)

Better perfusion of systems during shock (dilation of coronary arteries)

22
Q

What are very high doses dopamine effects on BP and which receptors cause that?

A

Increase in blood pressure (a1 receptors activation (still activating DA receptors as well) —> increased perfusion of kidney, mesentey and heart —> useful in shock)

23
Q

What are therapeutic uses of dopamine and what are its potential adverse effects?

A

Therapeutic uses: acute heart failure (cardiogenic and septic shock) ; stimulate heart (b1 effect) while dilating renal and coronary arteries

Adverse effects: possible tachycardia and ventricular arrhythmias ; BP effects potentially dangerous ; leakage of dopamine from vein can cause tissue necrosis

24
Q

What is dobutatmine and how does it act on the heart and BP?

A

Dobutatmine is a synthetic compound that has mostly beta 1 effects.

Cardiovascular effects: stimulation of heart (increase HR) and SMALL changes in peripheral resistance (BP)
*Greater effect to increase contractility vs. heart rate compared to dopamine or epinephrine

25
Q

What are clinical uses of dobutamine? Why are these short-term?

A

Heart failure (short term)- myocardial failure due to dilated cardiomyopathy (emergency situation)

Short term effect due to rapid uptake and metabolism

26
Q

What are adverse effects of dobutamine?

A

Increased potential fro arrhythmias - but less of a problem than with epinephrine

Tachycardia and increase O2 demand in heart muscle

27
Q

What are examples, effects and adverse effects of long-acting b agonists?

A

Terbutaline, (Clenbuterol)
-selective for beta (2 >1)

Therapeutic effects: bronchial dilation, short term decrease in BP, heart disease, hyperthyroidism, hypertension

Adverse effects: tachycardia, BP changes, refractoriness possible (receptor down regulation)

28
Q

Which drug is an example of a selective a1 agonist and how is it used clinically?

A 
Phenylephine
Effects: constricts smooth muscle: arteries, radial muscles of the eye, possible effects on bladder, uterus, GI
Therapeutic uses: 
-treat hypotension
-decrease bleeding
-eye exam/surgery
-nasal congestion
29
Q

What are adverse reactions of selective a1-agonist?

A

Vasoconstriction
Hypertenstion
Reflex bradycardia

30
Q

In contrast to a1-agonists, what effects do a2-agonsits have?

A

Ex: Xylazine

Effects: CNS effects- sedation, decrease pain sensation, decrease arousal

Therapeutic uses: sedation and analgesia

31
Q

How does ephedrine exert its effects? What are side effects of ephedrine?

A

Phenylpropanolamine

Effects: Indirect acting- NE release from terminals ; increase BP (b1 receptor for cardia, a1 peripherally); bronchodilation (B2 effect, release of EPI) ; constriction of sphincters, notably bladder sphincter

Therapeutic uses: urinary bladder sphincter incompetence

Adverse effects: hypertension, tachycardia, cardiac stimulation (insomnia, nervousness, agitation), tachyphylaxis (loss of NE from terminals)

32
Q

What are examples of non-selective beta blockers and how are they used clinically?

A

Ex: Sotalol, propranolol, timolol

  1. Antiarrhythmic : control dysrhythmias due to overstimulation of SNS; decrease AV conduction in patients with atrial fibrillation or flutter; control atrial and ventricular arrhythmias
  2. Reduce cardiac work effort in cardiomyopathies
  3. Control hypertension
  4. Timolol can be used to treat glaucoma
33
Q

Beta blocker effects are broad- try to recapitulate and group by affected organs.

A
  • Cardica effects: reduce SNS tone; decrease propensity for arrhythmias
  • Vascular effects: transient small increase in BP (B2); prolonged decrease in blood pressure (b1-renin)
  • Pulmonary effects: little effect; can be fatal in asthmatics due to B2 block
  • Metabolic effect: reduce hepatic and HR response to hypoglycemia —> fatal in diabetics (?)
  • Eye effects: B2 block reduced fluid formation
34
Q

What is the main difference between effects of non-selective b versus selective b1 antagonists ?

A

Selective b1-adrenergic antagonists have all the same cardiovascular effects of non-selective b clockers without effects on the lungs.

35
Q

What are a-adrenergic antagonist drug effects, including on the heart, BP?

A

Heart: reflex tachycardia

Blood pressure: decrease peripheral resistance

Smooth muscle: relax- including urethral, eye

36
Q

How are a-adrenergic antagonist drugs used therapeutically? What are their adverse effects?

A

Therapeutic uses:

  1. Reduce vasoconstriction (alleviate laminitis, hypertension associated with pheochromocytoma, peripheral vasospasm, visceral ischemia)
  2. Hypertonus of the urethral sphincter

Adverse effects:

  1. Vasodilation and hypotension
  2. Reflex tachycardia
  3. Nasal congestion, increase intraocular pressure, diarrrhea, inhibit ejaculation.
37
Q

What is Yohimbine and what is it used for?

A

Used to reverse a2-agonist anesthetics (ex. Xylazine)

Pharmacology Final (5 decks)

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