Mar22 M2-Fever Flashcards

1
Q

normal body temperature range

A

35.6 to 38.5

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2
Q

extremes of temperature at what time of the day + one thing that makes it higher

A
  • lowest at 6 am
  • highest at 4-6 pm
  • 0.6 degrees higher after ovulation
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3
Q

temp measurement methods

A
  • IDEAL = core temperature = RECTAL OR ESOPHAGEAL
  • oral = 0.6 lower
  • axillary = 1 lower
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4
Q

fever is part of what process in inflammation

A

acute phase response: neutrophilia, change in serum proteins, hormones, intermediary metabolism, sickness behavior, anorexia, lethargy

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5
Q

fever definition and max value

A

increase in core temperature due to a change of the hypothalamic set point. *rarely goes over 41.1

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6
Q

hyperpyrexia def

A

FEVER that is over 41.5

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7
Q

hyperthermia def

A

when the body temperature overrides the hypothalamic set point that is still normal. For ex, may go over 41.5

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8
Q

mechanisms we use to increase temp

A
  • vasoconstriction
  • thermogenesis in brown fat
  • shivering (striated muscle)
  • behavioral changes
  • piloerection (weak)
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9
Q

mechanisms we use to decrease temp

A
  • vasodilation
  • evaporation (insensible water loss, sweating)
  • behavioral changes
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10
Q

causes of fever

A
  • infections
  • rheumatic diseases (autoimmune for ex)
  • autoinflammatory diseases
  • immune reactions (to transfusion or drug)
  • malignancies
  • tissue damage (trauma, MI, etc.)
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11
Q

steps before ‘‘end cytokines of fever’’ are released

A
  1. macrophages see PAMPs wth their TLRs specific to LPS and other stuff.
  2. cascade of IC events leading to NF kappa beta translocating in nucleus: stim release of pro inflam cytokines
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12
Q

consequence of NF kappa beta activation

A

secretion of IL-1, TNF-a and possibly IFN-a and IFN-gamma

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13
Q

consequence of the secretion of IL-1, TNF-a and possible IFN-a and IFN-gamma

A

secretion of IL-6 end cytokine

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14
Q

3 main cytokines found in circulation during fever

A
  • TNF, IL-1 in nanogram qts

- IL-6 (FINAL CYTOKINE)** (microgram qts)

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15
Q

effect of IL-1, TNF-a and IL-6 act where (for fever) and do what

A

-anterior hypothalamus
-stim increase in PGs, PGE2**
(hypoth center ablation or PGE2 knockout or ASA, NSAIDs (blocks PG) = no febrile resp)

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16
Q

probable cause of peripheral symptoms that accompany fever (muscle aches, malaise, etc.)

A

PGE2 produced peripherally

17
Q

probable site of PGE2 production in the brain

A

vascular endothelium

18
Q

protein translocated in vascular endothelium cells nucleus as a response to IL-6

A

STAT3

19
Q

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

A

circumventricular organs (brain). (*main thing is highly vascular + fenestrated endoth, unlike rest of brain with BBB)

20
Q

consequence of PGE2 injection in mouse ventricle or anterior hypothalamus

A

fever in minutes

21
Q

COX-2 knockout mice consequence

A
  • NO fever when infection

- still regulate temperature normally

22
Q

alternate pathways leading to fever (causing fever before high cytokines in the blood)

A

PG produced peripherally lead to vagal stim of hypothalamus

23
Q

how conserve heat in fever

A
  • less blood to extremities (feel cold bc of that)
  • shivering
  • thermogenesis in brown fat
24
Q

how lose heat in fever

A
  • more blood to skin
  • more water loss (skin and lungs)
  • behavioral changes
25
Q

what’s used to raise temp in experimental animals + causes cold-blooded animals to seek hot environment if injected to them

A

LPS

26
Q

advantages of fever

A
  • 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
27
Q

bad things in fever: increases what

A
  • *increases O2 requirement** so get more
  • CO2 prod
  • water loss
  • cerebral injury
  • discomfort
  • seizure activity
28
Q

people with weakest immune system

A

newborns and elderly, immunosuppressed

29
Q

82 year old with a stroke: possible cause of fever in this individual

A

primary CNS damage due to hypoxia, ischemia, reperfusion, blood in brain, compression or damage to hypothalamus (pathogenesis poorly understood)

30
Q

consequences of fever in someone with brain injury

A

exacerbates injury

  • more toxic ntr release
  • higher O2 free radical production
  • disrupts BBB
  • increased zone of injury
31
Q

recurrent fevers in a child probable cause and treatment

A

periodic fever syndromes. treat with IL-1 blockers.

32
Q

military recruit with temp over 42 after running a lot dx

A

heat stroke. (over 42, irreversible damage to liver, brain, vascular endothelium)
*nothing wrong with his hypothalamic control
(HYPERTHERMIA)

33
Q

when is there a real necessity to treat fever and what about the rest

A
  • temp over 42 (becomes dangerous), or see it going towards such a high temp
  • below that, it just causes anxiety for nothing
34
Q

why is it thought that fever causes discomfort?

A
  • 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