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?
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