Fever

Normal

Axillary temperature 36~37 .0 C

Sublingual temperature 36.7~37.7 C

rectal temperature 36.9~37.9 C

一、  Concept

pyrogen set point of the thermoregulatory center body temperature

sport physiological T pregnancy luteal phase hyperthermia pathological T （ set point ± ） fever

T

Hyperthermia :

thermogenesis

thermolysis

dysfunction of thermoregulatory center

二、 Causes and pathogenesis of fever

Pyrogen and activator of fever

Activator : the substance can activate the cells that can produce the pyrogen.

pyrogen: the substance can cause fever

Activators of fever

microbe: G- LPS, ET G+ peptidoglycan virus: enveloped virus particle:transfuse response 2. internal production immune complexes etiocholanolone

1. Extragenou

pyrogen

Endogenou pyrogen(EP)

interleukin-1(IL-1) :MC,fibroblast

IL-6:T,B lymphocyte,tumor cell

TNF :

TNFα Mφ

TNFβ (lymphotoxin) active T

interferon ( IFN ): T lymphocyte

Producing and releasing of EP

cell of producing EP

Toll receptor

LPSLPS joint

pro trigger NF-κB

Start transcription ,EP express

LPSLPS joint

pro

sCD14

LPS –sCD14

complexes

T

三、Mechanism : increase of set point

1.the pathway: EP entry temperature

center

Pathways of EP signal transduction

to the thermoregulation center

a. blood brain barrier

Activator ActivatorActivatorActivatorCell of Producing EP

EP

blood brain barrier

Thermoregulation center

Thermoregulation center

SPSPTT

a.OVLT(organum vasculosum laminace terminalis ）

O V L T MC capillary POAH EP neuron

third ventricles of brain optic chiasma

c. vago:

2.The mechanism: increase of set point

a. Warm sensitive neuron: thermolysis

b. Cold sensitive neuron: thermogenesis

Imbalance:

Normal:

warm sensitive neuron

cold sensitive neuron

Thermoregulation mechanism of fever

一 . Thermoregulation center1. The positive regulationpreoptic anterior hypothalamus, POAH

2. The negative regulationmedial amygdaloid nucleus,MANventral septal area,VSA

Positive regulation mediators

1.PGE2: warm sensitive neuron

cold sensitive neuron

Effective medicine:Asprin,buprofen (Fenbid)

2.CRH(corticotrophin releasing hormone) EP (IL-1β, IL-6 ) CRH media fever

TNFα, IL-1 α PGE2 media fever

SP

3. cAMP : SPEP hypothalamus: Na+ /Ca2+ cAMP

SP

4. Na+ /Ca2+ :5. NO:a. Activate metabolism Brown fatb. Inhibit Negative regulation mediatorsc. OVLT POAH T

Negative regulation mediators

Negative feedback: Febrile ceiling: < 42℃ endogenous cryogens AVP

α-MSH

T center T

四、 period and metabolism of fever

The period of febrile: 1.the fervescence period characteristic: thermogenesis>thermolysis chill brown adipose tissue(scapula

,large vessle of thoracicand

cervical metabolic rate

Thermogenesis

Manifestation:

pale , gooseflesh, chill

warm sensitive neuron (POAH) Chill center

Chill cold sensitive neuron (POAH) cold stimuli Chill center

Chill skin T

Chill

Rubro nucleus

Lateral spinothalamic tract

Rubrospinal tract Reticulospinal tract

anterior motor cells

Up

Down

2.the persistent febrile period

The temperature reaches the new set point

★ Thermogenesis = thermolysis :

SP on higher level

★Manifestation:

febrile , headache

metabolic rate and pulse rate anorexia( 厌食 )

3.The defervescence period

★ characteristic:

Thermogenesis < thermolysis

SP is reset to the normal level

★ Manifestation:

the skin is warm and flush, sweat

fervescence persistent defervescence set point period period period

39 ℃

38 ℃ T

37℃ time

metabolism change of fever

1. Glycometabolism

Glycogenolysis Glycogen storage

2. Fat metabolism

lipodieresis Fat storage

Ketosis 酮症 magersucht

3. proteometabolism

Protein catatabolism, negative nitrogen

4. water\eletrolyte metabolism\vitamin

metabolism

T 1 metabolism rate 13%℃

acute phase response

WBC

Physiological changes:

1.CNS: headach , dizzy,drowsiness,

febrile convulsion: 24h

inheritance

hypoxia

discharge

2.immunity system

IL-1: activator of lymphocyte

IL-6 ： differentiation factor

IFN: humoral factor

TNF: anti-tumor

3.Digestion system

Sympathetic digestive juice

EP hypothalamus

nauseated,vomit

abdorminal distention

constipation

4. circulation system

HR 1 HR 18℃ /min

CO

induce heart failure

5. Respiratory system

四、 principal of treatment1.medicine Inhibit production of pyrogen:

glucocorticoid: inhibit IL-6 and TNFInhibit production of PGs: salicylic mezolin

2. physics: brain 1g water 2.5KJ(lose)

50%1~2%

Advantage and disadvantage

1.disadvantage

2. Advantage

Signal:

malaria

Case

A 36-year-old man, One day prior to admission he was made worse by headach ,dizzy,aching pain and fever.

Check: T 39 ,℃ Ｐ 100/min,R 20/min,Bp

100/70mmHg,congestion of throat,swelling of tonsil,respitatory rudeness,no bubbling sound

Lab findings: WBC ： 13.3×109/L,lymphocyte 16%, neutrophil 83% 。 Treatment: He was given antibiotic. During transfusion, the patient suffer

from chilly, shake, dysphoria and tempreture rose to Ｔ 41.3 ,℃

Ｐ 120/min, R 24/min, Dexamethasone intravenous injection

Questions

1.What pathogenic mechanism account for this patient`s fever?

2.Why the patient shown chilly , shake, dysphoria and tempreture rose more?

3.How to treat and give medical order of nursing?