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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
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Normal Axillary temperature 36~37 .0 C Sublingual temperature 36.7~37.7 C rectal temperature36.9~37.9 C
一、Concept pyrogen set point of the thermoregulatory center body temperature
sport • physiological Tpregnancy • 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
LPS LPS joint pro Toll receptor Start transcription ,EP express cellof producingEP Producing and releasing of EP trigger NF-κB
LPS LPS joint pro sCD14 LPS –sCD14 complexes T
三、Mechanism : increase of set point 1.the pathway: EP entry temperature center
Thermoregulation center Pathways of EP signal transduction to the thermoregulation center a. blood brain barrier Cell of Producing EP Activator EP Activator Activator Activator blood brain barrier T SP
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 center 1. The positive regulation preoptic anterior hypothalamus, POAH 2. The negative regulation medial amygdaloid nucleus,MAN ventral 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 : SP EP hypothalamus: Na+ /Ca2+ cAMP SP 4. Na+ /Ca2+ : 5. NO: a. Activate metabolism Brown fat b. Inhibit Negative regulation mediators c. 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
Up Chill Rubro nucleus Lateral spinothalamic tract Rubrospinal tract Reticulospinal tract anterior motor cells 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
fervescencepersistentdefervescence set pointperiodperiodperiod 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 treatment 1.medicine Inhibit production of pyrogen: glucocorticoid: inhibit IL-6 and TNF Inhibit production of PGs: salicylicmezolin 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 byheadach ,dizzy,aching pain and fever. Check: T 39℃,P100/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 T41.3℃, P120/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?