Fever Normal Axillary temperature 3637 0 C Sublingual

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 thermoregulatory center body temperature

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

¬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: the substance can cause fever

Activators of fever microbe: G- LPS, ET G+ peptidoglycan virus: enveloped virus 1. Extragenou particle: transfuse response pyrogen 2. internal production immune complexes etiocholanolone

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 LPS joint pro Toll receptor trigger NF-κB Start transcription , EP express cell of producing EP

LPS s. CD 14 LPS joint pro LPS –s. CD 14 complexes T

三、Mechanism : increase of set point 1. the pathway: EP entry temperature center

Pathways of EP signal transduction to thermoregulation center a. blood Activator brain barrier Cell of Activator Producing EP blood brain barrier T SP Thermoregulation center

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 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. PGE 2: warm sensitive neuron cold sensitive neuron SP Effective medicine: Asprin, buprofen (Fenbid) 2. CRH(corticotrophin releasing hormone) EP (IL-1β, IL-6 ) CRH media fever TNFα, IL-1 α PGE 2 media fever

3. c. AMP : SP EP hypothalamus: Na+ /Ca 2+ c. AMP SP 4. Na+ /Ca 2+ : 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 Thermogenesis brown adipose tissue(scapula , large vessle of thoracicand cervical metabolic rate

Manifestation: pale , gooseflesh, chill warm sensitive neuron (POAH) Chill center Chill cold sensitive neuron (POAH) cold stimuli Chill center Chill skin T

Chill Up Rubro nucleus Down Lateral spinothalamic tract Rubrospinal tract Reticulospinal tract anterior motor cells

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 3 9℃ 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. watereletrolyte metabolismvitamin

metabolism T 1 ℃ metabolism rate 13% acute phase response WBC

Physiological changes: 1. CNS: headach , dizzy, drowsiness, febrile convulsion: 24 h 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: salicylic mezolin 2. physics: brain 1 g water 2. 5 KJ(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 100/70 mm. Hg, 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?