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Staying organized can be a challenge, and people living with ADHD might need more help than others. We rounded up our favorite products to help you…. Health Conditions Discover Plan Connect. Warnings About Side effects Interactions Other warnings Dosage Take as directed Considerations Alternatives Highlights for clonidine Clonidine is available as both a generic and brand-name drug. Brand name s : Kapvay. Clonidine extended-release tablets are used to treat attention deficit hyperactivity disorder ADHD.
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This site complies with the HONcode standard for trustworthy health information: verify here. This content does not have an English version. I know pheochromocytoma is a catecholamine secreting tumor of the adrenal gland, so wouldn't a strong beta-blocker help to neutralize this? Answer: The main problem with pheochromocytoma is the high BP not the tachycardia.
If a beta-blocker alone is given then you allow the alpha1-activity of the catecholamines to act unopposed. This would increase the BP still further. Beta-blockers can safely be given after the BP has been stabilized with an alpha-blocker. Labetalol beta- and alpha-blocker can be given alone to treat the crisis. Question: I have 2 questions: 1. When Isoproterenol is administered in the presence of Atropine, why isn't HR elevated slightly more than the control due to removal of any vagal tone?
Why is pulse pressure increased in high doses of Epi. You are absolutely correct. Atropine would remove the vagal tone to the heart leading to a slight increase in heart rate that would be additive to the effect of ISO. This was academic and I wanted to avoid complicating a difficult area. Changes in pulse pressure will reflect changes in cardiac contractility. EPI has increased this through actions on the beta1-receptors. Question: Why do antimuscurinic agents cause hypotension in high concentrations?
Answer: The muscarinic and nicotinic receptors although different recognize the same transmitter ie. Therefore the receptive site for Ach is different but close. Atropine will block muscarinic receptors, and at high toxic doses can block ganglionic nicotinic receptors to cause a fall in BP. The muscarinic receptors in the vasculature do not receive any activity, hence blocking these has no effect. Atropine does have a direct vasodilator effect at high toxic doses Red as a beet.
The other terms for atropine toxicity are 'Hot as hell' referring to decreased sweat secretion and CNS changes in thermoregulation; 'Mad as a hatter': CNS delium; 'Dry as a bone': decreased saliva and 'Blind as a bat': cycloplegia blurred vision. Is this a completely different reflex controlling HR and if so, what's the pathway? Answer: The baroreceptor reflex is concerned with changes in BP either up or down , and not by changes in HR or pulse pressure.
The strength of the reflex depends on the rate of change in BP. High EPI will cause an increase in BP as the alpha1-mediated constriction dominates over the beta2-mediated vasodilation. Because of the significant increase in BP the baroreflex has been activated.
It will try to lower BP by decreasing HR. Therefore we still see the tachycardia although it has been reduced by the reflex. In the case of NE, the reflex evoked is stronger than the direct effect of NE on the heart so we see an increase in BP with reflex bradycardia. Question: 1. Question: Why is the heart rate unchanged from the control situation to atropine and high dose isoproterenol? In the control the increase in heart rate is direct and reflex mediated. If atropine eliminates the reflex wouldn't the heart rate increase less than in the control?
However in this example the reflex will increase the HR to attempt to counteract the fall in BP ie. Since this involves activation of the SNS to the heart atropine has no effect.
Question: I can't quite understand how operational alpha-2 receptors will prevent a reflex tachycardia. Answer: Because of the fall of BP due to alpha1-receptor blockade the baroreceptor has been activated to increase the BP. One way to do this is to increase HR to increase CO. In the case of prazosin alpha1-selective the alpha2-receptors are still operational and can exert their inhibition of release to prevent the reflex tachycardia.
Whereas phentolamine non-selective blocks both the alpha1- and the alpha2-receptors thus preventing the action of the alpha2-receptors ie. Question: Can you explain the reflex response and the role of HR? The strength of the reflex is determined by the rate of change increase or decrease. The role of the reflex is to oppose BP changes.
To do this it can increase or decrease HR or increase or decrease peripheral vasoconstriction. Thus it can change the HR when activated but it is not triggered by the HR.
Atenolol beta1-selective blocker in this instance would block the reflex response on the heart. Propranolol non-selective blocker would block all actions of ISO. Question: What is the role of diastolic and systolic BP on the reflex?
Answer: The net effect on mean BP is more important as this determines the action of the barorelex response. In most cases the changes in systolic and diastolic BP are in the same direction whereas in other instances they may differ ie. Therefore it helps to have an understanding of them. It can also provide a clue that multiple receptors are involved such as in the eg.
Question: Why does vasoconstriction lead to nasal decongestion? Fluid is leaking from the nasal vascular vessels. PE or other vasoconstrictors will decrease this and are commonly found as the active ingredient in nasal decongestions. Usually the forms are pseudoephedrine or pseudophenylephrine. Pseudoephedrine should not be used by someone taking MAOI agents, as this can cause a hypertensive crisis similar to tyramine response. Question : Why is it important to maintain renal blood flow during septic shock by administering Dopamine vs.
Wouldn't you want to activate the renin-angiotensinogin system by decreasing renal blood flow? Answer: During shock there is a fall in BP, decreasing tissue perfusion and cerebral blood flow. We need to maintain BP to maintain adequate blood flow to the various organs and brain.
NE has potent alpha1-actions, causing vasoconstriction to increase BP. But it also causes vasoconstriction of the renal vasculature, this would restrict the blood flow to the kidneys and decrease renal function.
Whereas dopamine can activate alpha1-receptors to maintain BP and activate the D1-receptors in the kidney to dilate them and hence increase renal blood flow and urination good thing. The renin-angiotension system has already been activated because of the fall in BP.
Question: How does guanethidine alone cause heart rate to increase? I understand that the baroreceptor reflex would try to increase HR in response to drop in MAP, but wouldn't that effect be blocked by guanethidine? Answer: Guanethidine inhibits the release of NE from the nerve terminal.
In the heart this removes the sympathetic tone ie. This triggers the reflex response which attempts to dampen the fall in BP 4. The reflex response turns off the vagus parasympathetic NS inhibition of HR - 10bpm 5.
The net effect is HR increases by 5 bpm ie. Question: Why do we see cardiovascular side effects as a result of using selective beta2 agonists and selective alpha1 agonists? And what is the side effect? Is it reflexive tachycardia in the case of beta2 agonists and reflexive bradycardia in the case of alpha1 agonists?
Answer : Although I state that an agent is alpha1-selective ie. Prazosin or beta2-selective ie. Terbutaline , this does not mean that they act solely on alpha1- or beta2-receptors. At higher concentration they can act on the other receptors. When they do this, it is considered a side-effect. For example, Terbutaline given for asthma beta2-action may cause some tachycardia beta1-action. The tachycardia is considered a side-effect.
This may be minimized by inhalation vs oral administration. The term 'reflex' is used to describe heart rate changes that are not the direct action of the agent but baroreflex mediated.
For example NE causes an increase in BP with reflex bradycardia. In this case the tachycardia is partially direct and partially reflex mediated. Upon stimulation however the upside 70 to bpm is greater than the downside 70 to zero bpm. There is a limit to the inhibition of HR. Therefore the sympathetics wins upon ganglionic stimulation. Question : I'm confused with regard to the syllabus and my own notes on pgs. On page 96 I have a moderate understanding of the reflex involving the baroreceptors with the carotid sinus and aortic arch which control BP, but not HR nor Pulse Pressure.
On pg. Is this a completely different reflex controling HR and if so, what's the pathway? Question: Why would propranolol be contraindicated for a Pheochromocytoma patient about to undergo tumor removal surgery, suffering from severe headaches and palpitations? Should we associate palpitations with heart failure? Remember question 6 from my review yesterday about the woman stung by a bee.
Until recently all beta-blockers were contraindicated for heart failure because they decreased cardiac performance. However they positive actions to decrease the cardiac post-load and decrease oxygen demand. Previously it was felt that the bad out-weighted the positive actions.
Now they know that the good out-weighs the bad. This benefical effect of beta-blockers was shown for metoprolol and not propranolol. Non-selective beta-blockers can cause problems for individuals with asthma will increase bronchial resistance , diabetes mask low glucose state and inhibit recovery from low glucose state and Raynaud D.
It can decrease their intensity and frequency. The mechanism of this action is not known. Question: Why there is no reflex bradycardia when you administer guanethidine? Answer: Guanethidine will prevent the release of NE from the nerve terminal, this will cause a fall in BP. The reflex will attempt to increase the BP by activating the alpha1-receptors to cause vasoconstriction and the beta1-receptors to increase HR. However these actions are prevented by the adrenergic neuron blocking effect of guanethidine inhibition of NE release.
Thus the overall effect with guanethidine is a fall in BP and a slight increase in HR removal of vagal tone. Question: I was wondering why high doses of Epinephrine don't produce a reflex bradycardia? Answer: High EPI will cause an increase in BP as the alpha1-mediated constriction dominates over the beta2-mediated vasodilation. Question: When high dose epi is given in conjunction with a-blocker phentolamine, then aren't the b-1 and b-2 receptors equally responsible for the result?
Here is what I thought: b-1 would give us an increase in systolic BP, b-2 would give us a decrease in diastolic BP greater then the systolic raise , rendering slight downward change in MAP--also an increase attributed to b-1 would be seen in HR. High dose EPI in the presence of phentolamine can only act on the beta-receptors.
It is a good agonist on both the B1- and B2-receptors. Question : From my understanding of things thus far, to a rise in cardiac output CO leads to an increase is systolic BP while an increase in TPR leads to an increase in diastolic BP and vice versa for both examples. If the preceding is correct which it may very well not be then how does, for example, NE in the presence of a beta-blocker such as propranolol increase both systolic and diastolic blood pressures?
CO is decreased. Question: With Prazosin and Terazosin, how come there is no reflex tachycardiac? Answer: Phentolamine non-selective, alpha1- and alpha2-blocker causes a fall in BP with refex tachycardia. Whereas Prazosin and Terazosin are selective alpha1-blockers.
It is thought that since they leave the presynaptic alpha2-receptors operational, this prevents the reflex tachycardia.
Question: Could you explain why toxicity of acetylcholinesterase inhibitors includes both Hypotension and hypertension? Answer: In the presence of AchE inhibitors the action of Ach is prolonged at all sites ie. The increased ganglionic stimulation leads to an increased sympathetic stimulation to the vascular smooth muscle leading to vasconstriction via alpha1-receptors hypertension.
However if the Ach concentration becomes too high then Ach begins to act like succinylcholine, resulting in a depolarizing blockade in the ganglia ie. This then causes the BP to fall hypotension. Question: What role does atropine have in phenylephrine and NE action. Isn't atropine blocking muscarinic receptors? Answer: Yes atropine is a muscarinic antagonist. It will prevent the reflex bradycardia seen with NE and expose the direct cardiac stimulation of NE ie.
Question: Why is there no reflexive bradycardia when phentolamine acts on NE action? Answer : In the presence of phentolamine alpha-blocker , NE can only act on the beta-receptors. It is not as powerful on beta-receptors as EPI.
It also acts on beta2-receptors to cause vasodilatation and hence decrease BP. The overall effect is no major change in BP and hence no reflex mechanism. This just represents that. This is not a major point. Question : Why is there a systolic BP increase in the control case with low doses of Epi? Answer: At low dose EPI is acting mainly at beta-receptors with a little alpha-receptor activity.
These two actions are the cause of the increase in systolic BP. The overall effect on peripheral resistance at low dose is a fall in TPR beta2-effect is greater than alpha1-effect. Answer: See above. The logic is the same as low dose EPI without the alpha1-action.
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