Hypothalamus controlling temperature set point is briefly mentioned in Pathoma 2018 edition page 13, Chapter 2 III Cardinal signs of inflammation D. Fever
Pyogenes -> macrophage release IL-1 and TNF -> increased cyclooxygenase activity in hypothalamus perivascular cells -> increased hypothalamus PGE2 -> raised temperature set point
Can someone explain why when you transect the spinal cord superior to the level of sympathetic outflow -- and you get a systemic infection -- the response is alteration of the thermostatic set point?
i got this question wrong, but i think what this question is really asking is what happens in a systemic infection: which is fever
in systemic infection, the most obvious sign to look for is a fever, not necessarily shivering, sweating, heat production by brown fat, etc.
and how does fever occur? like someone already mentioned: pyogenes --> macrophages releasing IL1 and TNF which increases COX activity in hypothalamus perivascular cells, increase production of PGE2 in hypothalamus and reset the temperature set point.
i think the whole phrase "complete transection of the spinal cord superior to the level of sympathetic..." is a distraction. it just tells you that development of a fever has nothing to do with it
So, how do you explain the actual fever by just changing the thermostat?? Fever 'effect' IS under Sympathetic control, just the changing the temperature (like thermostat) is mediated by cytokines and hypothalamus
Okay boys and girls this question is easier than you think.
Hypothalamus relays via the sympathetic nervous system to control the body when a new set point as been reached in lets say...fever...cause by....infection.
If the connection between the hypothalamus and spinal cord (mainly the sympathetic outflow) is cut, the thalamus cannot relay the body reaction of a fever, but the hypothalamus itself can still change the set point.
Boom
Within the brain, the autonomic nervous system is regulated by the hypothalamus. Autonomic functions include control of respiration, cardiac regulation (the cardiac control center), vasomotor activity (the vasomotor center), and certain reflex actions such as coughing, sneezing, swallowing and vomiting.
B-E occur as a result of a change in set point.
A happens to cause the B-E when a new set point is reached.
In systemic infection, wouldn't you get cutaneous vasoDILATION (i.e. distributive shock)? This was my reasoning for choosing B) in this wacky question.
From ShoryukenHadooken on reddit:
What the question is getting at is the sympathetic chain was spared. It was a terrible way of wording it.
Your anterior hypothalamus is responsible for cooling features and is under parasympathetic control. A lesion would cause hyperthermia.
Your posterior hypothalamus is responsible for heating when you're cold and to generate the Fever response and is under sympathetic control. A lesion would cause hypothermia.
In this question it is simply asking a person gets sick, hypothalamus was spared, what happens.
Answer: hypothalamus will still be able to elevate set body temperature to battle infection.
Hint: IF they give a question similar to this but reworded to include a lesion of the sympathetic fibers or of the hypothalamus, you would in turn NOT be able to generate a fever response to infection. The hypothalamus would be entirely under parasympathetic control
This adds more context to the fact the Q states that the sympathetics was spared
submitted by โkeycompany(351)
Alteration of the thermostatic set point is a hypothalamic process mediated by prostaglandins and is independent of the sympathetic nervous system.
B, C, D, and E all require sympathetic nerves to ellicit a response.