Pharm questions

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Just started CRNA school this week and feeling extremely overwhelmed. Can someone explain to me in simple terms how Etomidate blocks the adrenocortical response to stress?? Also explain the increase in the sympathetic outflow one sees with the administration of desflurane and isoflurane?? The program I am in starts us in a pharmacology class with M2 students that have already been in this class for a semester...trying to keep from drowning.

Specializes in Nurse Practitioner/CRNA Pain Mgmt.

In answer to your first question (others may have differing opinions): The body responds to stress by releasing CORTISOL (among other things). It can increase HR, vasoconstrict vessels, etc. Etomidate transiently inhibits an enzyme that normally converts cholesterol to cortisol. So, if you block cortisol, your body cannot adjust to a stressful situation such as intubation or anesthesia or surgery. This can be bad for sick pts who have sepsis or hemorrhage problems who might need an intact cortisol response. BUT, it can also be advantageous to pts who are otherwise healthy and can withstand a stress-free anesthesia/surgical procedure. Does that help you understand it better? :)

etomidate:

a single dose of etomidate will not block the adrenocortical response to stress .... however repeated exposure to etomidate will lead to the following

1) inhibition of P450c11 hydroxylase - which plays a role in steroidogenesis

2) leads to reduced expression of ACTH receptors

3) decreased cell proliferation in the adrenals.

So exposure to etomidate over time will lead to adrenal dysfunction. In fact, etomidate is sometimes used to suppress adrenocortical cancers.

Therefore the implication is that a patient undergoing stress (surgery/sepsis) who has been exposed to multiple doses of etomidate will have a weak adrenocortical response.

Isoflurane:

Kotrly KJ, Ebert TH, Vucins E, et al: Baroreflex reflex control of heart rate during isoflurane anesthesia in humans. Anesthesiology 1984; 60: 173

That is one of the better studies that demonstrates that the Sinus Tachycardia that can be seen with higher doses of Isoflurane is a reflex response to the vasodilatory and myocardial depressant properties of isoflurane.

Thanks for the reponse. We started lectures today that will be an extensive coverage of all antibiotics...did your program focus a great deal on this topic and if so what are some hints on how to LEARN not rememarize this large amount of material?? I LOVE THIS BOARD.

Thanks for the reponse. We started lectures today that will be an extensive coverage of all antibiotics...did your program focus a great deal on this topic and if so what are some hints on how to LEARN not rememarize this large amount of material?? I LOVE THIS BOARD.

I've learned that mapping the reflexes in a type of box plot really helps me remember what goes where and in order. For instance (with the RAAS pathway):

Angiotensinogen

l

l (renin converts to)

l

ANG I in the plasma

l

l (ACE converts to)

l

ANG II in the plasma

l

l (results in)

l

Systemic response

(Arterioles - vasoconstrict ... CV control center in the M.O. increases CV response ... Hypothal. releases ADH and increases thirst ... Adrenal cortex releases Aldosterone)

l

l (results in)

l

Increased BP and Increased volume

It's kind of hard to show in this forum, but each underlined part is the primary response, and the line that connects each section is usually a verb. I do this with a lot of my classes when applicable [pharm drugs, physiology (esp. cellular responses), chem/physics] ... hope this didn't confuse you! Good luck with your classes this semester :).

-Kat

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