病理生理英文课件
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病理生理英文课件
PVN CRH↑
LC-NE
limbic system
Peripheral effector Physical stress response
Emotion stress response
pituitary ACTH↑
Cortex of adrenal gland
GC↑
23
Stress
(2) Basic effects of stress
Stressor
Internal factors
Homeostasis, disease, cancer.
Psychological, sociological factors
Work pressure, life rhythm, interpersonal relation
6
Stress
7
8
human
burn operation infection hypoxia Strong light noise necrosis
Definite intensity stimulate
Specific reactions
fester acidosis
non-specific reaction
Stress
anxiety dread blood reditribution HR ↑
peri-resistance↑ prolonged
blood redistribition
key organs blood supply
Heart afterload↑ hypertension unfavorable results
21
3）Respiratory system StressRR faster & deep O2 carrying ↑ tissue O2 supply↑ Respiratory alkalosis tissue lack blood & O2 unfavorable results
病理生理学课件：英文课件汇总
of brain e) Breath stop over 15 min under
resuscitation f) Brain ciVegetative state: death of cerebral cortex with alive brain stem.
Health: a normal state in soma,
psyche and social well-being
Chapter 2
二.Etiology
1. Etiological factors: the direct cause
1) Biological factor 2) Physiological factor 3) Chemical factor
Chapter 2
3. Precipitating factor
The factor that promote ,intensify the
disease attack.
Chapter 2
三.Development of Disease 1. General rules
1) Damage and Antidamage Responses The fight between etiology and body
60% (±)of body weight Intracellular fluid : 40% Interstitial fluid : 15% Transcellular fluid : 2% Plasma : 5%
defence 2) Interchange of Cause-Effect
The evolution of disease
Chapter 2
2. Basic Mechanisms
resuscitation f) Brain ciVegetative state: death of cerebral cortex with alive brain stem.
Health: a normal state in soma,
psyche and social well-being
Chapter 2
二.Etiology
1. Etiological factors: the direct cause
1) Biological factor 2) Physiological factor 3) Chemical factor
Chapter 2
3. Precipitating factor
The factor that promote ,intensify the
disease attack.
Chapter 2
三.Development of Disease 1. General rules
1) Damage and Antidamage Responses The fight between etiology and body
60% (±)of body weight Intracellular fluid : 40% Interstitial fluid : 15% Transcellular fluid : 2% Plasma : 5%
defence 2) Interchange of Cause-Effect
The evolution of disease
Chapter 2
2. Basic Mechanisms
病理生理课件
NEW WORDS
• • • • • • • • • • annulus fibrosus ['ænjʊləs] [faɪ'brəʊsɪs] 纤维环 pathophysiology ['pæθəʊfɪzɪ'ɒlədʒɪ]病理生理 biomechanical 生物力学 trapezius [trə'pi:zɪəs]斜方肌 sternocleidomastoid ['stərnɒ'klɪdmas'tɔɪd]胸锁乳突肌 scalene ['skeɪli:n]斜角肌 pectoralis minor['pektərəlɪs]胸小肌 torticollis [ˌtɔ:tɪ'kɒlɪs]斜颈 zygopophyseal joint关节突关节 discs[disks]椎间盘
pathophysiology
• 髓核退行性变
Nucleus propulsus undergoes degeneration Data show 17% of men and 12% of women in 20+ years of age had degeneration of discs that % increases linearly with age 文献显示20多岁的人群中，17%的男性和12%的女性有椎间盘退行性 改变，患病率随年龄增加呈线性改变 In those over 45 year of age ,found no gel-like nucleus propols in cervical discs 在年龄大于45岁的人群中，颈椎椎间盘凝胶样结构消失 Anterior and lateral margins of the C5/C6 nucleus propulsus had highest levels of pathology since these discs may be subject to greater stress as a result of having the greatest flexion/extension and to greater mechanical strain C5/C6髓核的前及外侧缘最可能发生病理改变，因为这些椎间盘可能 因其较大幅度屈伸活动而引致较大的机械性张力劳损
• • • • • • • • • • annulus fibrosus ['ænjʊləs] [faɪ'brəʊsɪs] 纤维环 pathophysiology ['pæθəʊfɪzɪ'ɒlədʒɪ]病理生理 biomechanical 生物力学 trapezius [trə'pi:zɪəs]斜方肌 sternocleidomastoid ['stərnɒ'klɪdmas'tɔɪd]胸锁乳突肌 scalene ['skeɪli:n]斜角肌 pectoralis minor['pektərəlɪs]胸小肌 torticollis [ˌtɔ:tɪ'kɒlɪs]斜颈 zygopophyseal joint关节突关节 discs[disks]椎间盘
pathophysiology
• 髓核退行性变
Nucleus propulsus undergoes degeneration Data show 17% of men and 12% of women in 20+ years of age had degeneration of discs that % increases linearly with age 文献显示20多岁的人群中，17%的男性和12%的女性有椎间盘退行性 改变，患病率随年龄增加呈线性改变 In those over 45 year of age ,found no gel-like nucleus propols in cervical discs 在年龄大于45岁的人群中，颈椎椎间盘凝胶样结构消失 Anterior and lateral margins of the C5/C6 nucleus propulsus had highest levels of pathology since these discs may be subject to greater stress as a result of having the greatest flexion/extension and to greater mechanical strain C5/C6髓核的前及外侧缘最可能发生病理改变，因为这些椎间盘可能 因其较大幅度屈伸活动而引致较大的机械性张力劳损
【英文课件-病理生理学】_Inflammation-上海交通大学医学院学习
cells and macrophages
General Features of
Inflammation
Local Signs of Inflammation
redness swelling heat pain loss of function
Systemic Manifestations
Fever and leukocytosis
Vascular changes
Increased Vascular Permeability – Mechanism
– Formation of endothelial gaps in venules (endothelial contraction)
– Increased transcytosis
1, Alteration
Degeneration and necrosis
Alteration
Parenchymal cells – Cellular swelling, fatty
degeneration – Necrosis Interstitial tissues – Edema, mucoid degeneration – fibrinoid necrosis
– Endothelial injury
Increased Vascular Permeability
Exudate and Transudate
Edema denotes an excess of fluid in
the interstitial or serous cavities; it can be either an exudate or transudate
Chapter Four
General Features of
Inflammation
Local Signs of Inflammation
redness swelling heat pain loss of function
Systemic Manifestations
Fever and leukocytosis
Vascular changes
Increased Vascular Permeability – Mechanism
– Formation of endothelial gaps in venules (endothelial contraction)
– Increased transcytosis
1, Alteration
Degeneration and necrosis
Alteration
Parenchymal cells – Cellular swelling, fatty
degeneration – Necrosis Interstitial tissues – Edema, mucoid degeneration – fibrinoid necrosis
– Endothelial injury
Increased Vascular Permeability
Exudate and Transudate
Edema denotes an excess of fluid in
the interstitial or serous cavities; it can be either an exudate or transudate
Chapter Four
病理生理学Pathophysiology
皮肤粘膜：
发绀
？
2019/10/23
病理生理学 Pathophysiology
2019/10/23
病理生理学 Pathophysiology
血液性缺氧（hemic hypoxia）
由于血红蛋白数量减少或性质改变，使血氧含量 降低或血红蛋白释放氧不足，引起的供氧障碍
贫血
携带氧的数量减少
一氧化 原 碳中毒 因 高铁血
特点： 急性缺氧有效，伴有PaO2降低者明显
2019/10/23
病理生理学
呼吸功能障碍（损伤性变化）Pathophysiology
高原肺水肿
呼吸困难，咳嗽，血性泡沫痰 肺部有湿罗音，紫绀
缺氧引起血管收缩，回心血量增 加，肺血量急剧增加，肺毛细血 管压力升高
中枢性呼吸功能衰竭 呼吸抑制，通气量减少 PaO2过低
损伤性变化：RBC增多，血粘度增高，血流阻力增大， 心脏的后负荷增大，可促进心衰的发生。
2019/10/23
中枢神经系统
病理生理学 Pathophysiology
急性缺氧： 头痛，烦躁，记忆力下降，运动不协调
慢性缺氧： 疲劳，嗜睡，注意力不集中，抑郁
严重缺氧：
不安，惊厥，昏迷，死亡
机制：
发生于吸入一个大气压的氧8小时以后 症状：胸骨后疼痛、咳嗽、呼吸困难， PaO2↓，肺部炎性变。 (二）脑型氧中毒
发生于吸入2-3大气压以上的氧。 症状：视、听觉障碍、先抽搐、后昏迷。
2019/10/23
病理生理学 Pathophysiology
请预习
应激（Stress）
2019/10/23
②
2019/10/23
病理生理学 Pathophysiology
2015.3 hypoxia (双语班) 病理生理学双语课件
Mechanism : PaO2, SaO2, CO2max, CaO2 normal
CvO2? →（CaO2 － CvO2）?
Characteristic alterations of blood O2
PaO2 CO2max CaO2 SaO2
CO2 (a-v)
Hypotonic-
Hemic-
Circulatory-
Classification, etiology and pathogenesis
External respiration
tissue
blood circulation
hypotonic
histogenous
hemic circulatory
Supply↓ hypoxia utilization↓
Treatment and prevention
1. Etiological treatment 2. Oxygen therapy
Oxygen therapy
Most effective: in hypotonic hypoxia CO intoxication
Lower O2 concentration (25-30%) for hypoxia with hypercapnia
1. Hypotonic hypoxia — PaO2↓
Causes : 1) PiO2 (PO2 in the inspired air) ↓
Altitude Atmospheric pressure
(m)
(mmHg)
Sea level
760
1000
680
2000
600
3000
530
5000
CvO2? →（CaO2 － CvO2）?
Characteristic alterations of blood O2
PaO2 CO2max CaO2 SaO2
CO2 (a-v)
Hypotonic-
Hemic-
Circulatory-
Classification, etiology and pathogenesis
External respiration
tissue
blood circulation
hypotonic
histogenous
hemic circulatory
Supply↓ hypoxia utilization↓
Treatment and prevention
1. Etiological treatment 2. Oxygen therapy
Oxygen therapy
Most effective: in hypotonic hypoxia CO intoxication
Lower O2 concentration (25-30%) for hypoxia with hypercapnia
1. Hypotonic hypoxia — PaO2↓
Causes : 1) PiO2 (PO2 in the inspired air) ↓
Altitude Atmospheric pressure
(m)
(mmHg)
Sea level
760
1000
680
2000
600
3000
530
5000
case discusion-2 病理生理学双语课件
MODS 病例讨论
(13日)主诉：左上肢断裂，全身多处刀伤，伴流 血疼痛7小时。
现病史：入院前晚全身多处刀伤，左上肢断裂， 大量流血后出现昏迷，在当地医院作伤口处理与 输血、输液治疗。
入院查体：T：37℃，R：22次/分，P：130次/ 分，BP：75/50mmHg。一般情况：神清，烦躁， 脸色苍白，大汗淋漓，左手无感觉，挠动脉搏动 消失。
D-二聚体（+），
肾功：Cr：283umol/L， 查体： T： 37.7 ℃，HR：145次/分，BP：
96/48mmHg，SPO2:98%.
处理：行断臂再植术。
病情发展
（15日）：患者持续镇静，双侧睑结膜充 血水肿，头面部及胸廓肿胀，胸部饱满，皮 下软组织水肿积液。胸腔少量引流液 （100ml/24小时），液面未见明显波动， 胸部抠诊音浊，心音微弱。
实验检查：WBC:12.0 ×109/L, RBC:2.91 ×1012/L, HGB:110g/L, PT:28s,
(13日)主诉：左上肢断裂，全身多处刀伤，伴流 血疼痛7小时。
现病史：入院前晚全身多处刀伤，左上肢断裂， 大量流血后出现昏迷，在当地医院作伤口处理与 输血、输液治疗。
入院查体：T：37℃，R：22次/分，P：130次/ 分，BP：75/50mmHg。一般情况：神清，烦躁， 脸色苍白，大汗淋漓，左手无感觉，挠动脉搏动 消失。
D-二聚体（+），
肾功：Cr：283umol/L， 查体： T： 37.7 ℃，HR：145次/分，BP：
96/48mmHg，SPO2:98%.
处理：行断臂再植术。
病情发展
（15日）：患者持续镇静，双侧睑结膜充 血水肿，头面部及胸廓肿胀，胸部饱满，皮 下软组织水肿积液。胸腔少量引流液 （100ml/24小时），液面未见明显波动， 胸部抠诊音浊，心音微弱。
实验检查：WBC:12.0 ×109/L, RBC:2.91 ×1012/L, HGB:110g/L, PT:28s,
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General introduction
Definition of DIC “A dynamic pathologic process triggered by activation of the clotting cascade with resultant generation of excess thrombin within the vascular system that leads to further activation of the coagulation system, shortened survival of certain hemostatic elements, deposition of fibrin in the micro-circulation and activation of the fibrinolytic system.” DIC is not a primary disorder but it is a secondary expression of an underlying process.
12
What is the essences of DIC? blood clotting dysfunction ！ Blood coagulability turn to heighten ---- change into lower
13
General introduction
Clinical Manifestations of DIC
11
General introduction
Features of DIC • Rapid & massive activation of coagulation sequence • Normal body defenses overwhelmed • Consumption of circulating platelets • Depletion of clotting factors • Generation of anticoagulants - FDP • Results in severe hemorrhagic disorder • Not a specific disease - triggered by a number of factors
■
Tissue damage
clotting cascade
Ⅲ VIIa Ca2+
IXa VIIIa Ca2+ PF3 X
■
组织因子Tissue factor (Ⅲ)
Xa Va Ca2+ PF3 (凝血酶原激活物)
XIII 凝血酶 Thrombin
■ ■
凝血酶 Thrombin 纤溶酶原 plasminogen 纤溶酶 plasmin
21
The activity of tissue factor
8
reviews
HEMOPHILIA
Clinical Severity - Correlates with Factor Level
Mild – > 5% factor level – Bleeding only with significant trauma or surgery; only occasional hemarthroses (骨关节病), with trauma Moderate – 1–5% factor level – Bleeding with mild trauma; hemarthroses with trauma; occasionally spontaneous hemarthroses Severe – < 1% factor level – Spontaneous hemarthroses and soft tissue bleeding Within each kindred, similar severity of disease Multiple genetic defects
Stable Hemostatic Plug
Hemostasis Homeastasis
6
reviews
CONGENITAL CLOTTING DISORDERS
Von Willebrand disease
• Incidence 0.6-2% of population
Hemophilia
• • • • • Incidence 20/100,000 males 85% Hemophilia A (factor Ⅷ) 15% Hemophilia B (factor Ⅸ) Hemophilia C (factor Ⅺ) Most serious bleeding disorder
Excess Thrombin formation
DIC
19
tissue damage TF Ca2+ TF VIIa VII Ca2+ Traditional pathway thrombokinase Va Xa Ca2+ X
PL
II I IIa Ia monomer
XIIIa Ca2+
Ia multimer
凝血酶原 Prothrombin
Ca2+, XIIIa
■
XIIIa
纤维蛋白降解 产物FDP
■: inhibiting sites of AT-Ⅲ
Stable Fibrin clot
纤维蛋白单体 Fibrinmonomer
纤维蛋白原 Fibrinogen
5
reviews
Physiologic Hemostasis
Blood Vessle injury
Nerve
Tissue Factor
vasoconstriction
Aggregation of PLT priபைடு நூலகம்ary hemostatic plug
Coagulation cascade Fibrin formation
Blood flow↓
PLT
activation
Trauma & major operations
multi-fracture, burns, brain, liver, pancreas trauma, organ transplatation shock, snake, bee venom, wasp venom
Severe allergic/toxic reactions Severe immunologic reactions
DIC
1
OUTLINE
Reviews Concept of DIC Causes and pathogenesis
Factors influencing DIC development
Stages and classification
Function and metabolism changes
Prot. S
Prot. C TFPI
Fibrinolytic System
AT-III
Procoagulant
Anticoagulant
4
内源性途径 Intrinsic pathway
外源性途径 Extrinsic pathway
reviews
surface contact XII XI XIIa XIa PF3 Ca2+ -PL IX
20
extrinsic coagulation pathway
Tissue factor,TF
Character: (thromboplastin, CD142), (促凝血酶原激酶 ) 263 AA, transmembrane glycoprotein Expression: express in extravascular cells. no express in normal intravascular cells, but express in infection. Role: activate factor VII
Pathogenesis
(1)Severe tissue trauma---tissue factor and systemic activation of coagulation
Severe trauma Burns Major operation Malignant necrosis Obstetric accident endothelium injury
9
reviews
ACQUIRED CLOTTING DISORDERS
Inhibitors of factor Ⅷ-die old 50%: idiopathic 50%: autoimmune disease
(rheumatoid arthritis, SLE)
Acquired Von Willebrand disease :Autoimmune disorders Acquired platelet dysfunction drug-induced, renal failure
fibrinolytic system F IXa, XIIa, t-PA u-PA Kallikrein, FDP
Tissue type, urokinase
3 plasminogen activator-酶原激活物
reviews
Hemostatic Balance
PAI-1 Antiplasmin Tissue factor* Clotting Factors
Management and prevention