Mar22 M2-Fever Flashcards
normal body temperature range
35.6 to 38.5
extremes of temperature at what time of the day + one thing that makes it higher
- lowest at 6 am
- highest at 4-6 pm
- 0.6 degrees higher after ovulation
temp measurement methods
- IDEAL = core temperature = RECTAL OR ESOPHAGEAL
- oral = 0.6 lower
- axillary = 1 lower
fever is part of what process in inflammation
acute phase response: neutrophilia, change in serum proteins, hormones, intermediary metabolism, sickness behavior, anorexia, lethargy
fever definition and max value
increase in core temperature due to a change of the hypothalamic set point. *rarely goes over 41.1
hyperpyrexia def
FEVER that is over 41.5
hyperthermia def
when the body temperature overrides the hypothalamic set point that is still normal. For ex, may go over 41.5
mechanisms we use to increase temp
- vasoconstriction
- thermogenesis in brown fat
- shivering (striated muscle)
- behavioral changes
- piloerection (weak)
mechanisms we use to decrease temp
- vasodilation
- evaporation (insensible water loss, sweating)
- behavioral changes
causes of fever
- infections
- rheumatic diseases (autoimmune for ex)
- autoinflammatory diseases
- immune reactions (to transfusion or drug)
- malignancies
- tissue damage (trauma, MI, etc.)
steps before ‘‘end cytokines of fever’’ are released
- macrophages see PAMPs wth their TLRs specific to LPS and other stuff.
- cascade of IC events leading to NF kappa beta translocating in nucleus: stim release of pro inflam cytokines
consequence of NF kappa beta activation
secretion of IL-1, TNF-a and possibly IFN-a and IFN-gamma
consequence of the secretion of IL-1, TNF-a and possible IFN-a and IFN-gamma
secretion of IL-6 end cytokine
3 main cytokines found in circulation during fever
- TNF, IL-1 in nanogram qts
- IL-6 (FINAL CYTOKINE)** (microgram qts)
effect of IL-1, TNF-a and IL-6 act where (for fever) and do what
-anterior hypothalamus
-stim increase in PGs, PGE2**
(hypoth center ablation or PGE2 knockout or ASA, NSAIDs (blocks PG) = no febrile resp)
probable cause of peripheral symptoms that accompany fever (muscle aches, malaise, etc.)
PGE2 produced peripherally
probable site of PGE2 production in the brain
vascular endothelium
protein translocated in vascular endothelium cells nucleus as a response to IL-6
STAT3
name of brain regions activated in fever that are highly vascularized, fenestrated endoth, activated by injection of LPS and that have microglia with TLRs that can resp to LPS directly
circumventricular organs (brain). (*main thing is highly vascular + fenestrated endoth, unlike rest of brain with BBB)
consequence of PGE2 injection in mouse ventricle or anterior hypothalamus
fever in minutes
COX-2 knockout mice consequence
- NO fever when infection
- still regulate temperature normally
alternate pathways leading to fever (causing fever before high cytokines in the blood)
PG produced peripherally lead to vagal stim of hypothalamus
how conserve heat in fever
- less blood to extremities (feel cold bc of that)
- shivering
- thermogenesis in brown fat
how lose heat in fever
- more blood to skin
- more water loss (skin and lungs)
- behavioral changes
what’s used to raise temp in experimental animals + causes cold-blooded animals to seek hot environment if injected to them
LPS
advantages of fever
- some bacteria grow more slowly
- less availability of Fe to bacteria
- PMNs fight bacteria better
- activated dendritic cells reach regional lymph node more rapidly
- sickness behavior limits spread of infection
bad things in fever: increases what
- *increases O2 requirement** so get more
- CO2 prod
- water loss
- cerebral injury
- discomfort
- seizure activity
people with weakest immune system
newborns and elderly, immunosuppressed
82 year old with a stroke: possible cause of fever in this individual
primary CNS damage due to hypoxia, ischemia, reperfusion, blood in brain, compression or damage to hypothalamus (pathogenesis poorly understood)
consequences of fever in someone with brain injury
exacerbates injury
- more toxic ntr release
- higher O2 free radical production
- disrupts BBB
- increased zone of injury
recurrent fevers in a child probable cause and treatment
periodic fever syndromes. treat with IL-1 blockers.
military recruit with temp over 42 after running a lot dx
heat stroke. (over 42, irreversible damage to liver, brain, vascular endothelium)
*nothing wrong with his hypothalamic control
(HYPERTHERMIA)
when is there a real necessity to treat fever and what about the rest
- temp over 42 (becomes dangerous), or see it going towards such a high temp
- below that, it just causes anxiety for nothing
why is it thought that fever causes discomfort?
- hard to know if fever or the disease causes discomfort so think it’s fever
- some antipyretics are good analgesics too so discomfort relief associated with drop in temp
