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Patient Chapter 14 Disseminated Intravascular Coagulation
Patient Chapter 14 The main clinical manifestations of disseminated intravascular coagulation are bleeding, shock, organ dysfunction and microangiopathic hemolytic anemia.
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Patient Chapter 14 Disseminated Intravascular Coagulation
- bacteria
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
- Plant asexual reproduction
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- Reproductive development of animals
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- Outline
disseminated intravascular coagulation
concept
Disseminated intravascular coagulation (DIC): refers to the fact that under the action of certain pathogenic factors, a large amount of procoagulant substances enter the blood, coagulation factors and platelets are activated, causing the thrombin to increase, forming extensive microthrombi in the microcirculation, and then Due to the massive consumption of coagulation factors and platelets, the secondary fibrinolysis function is enhanced, and the body develops a pathophysiological process characterized by hemostasis and coagulation dysfunction.
Main clinical manifestations
Hemorrhage, shock, organ dysfunction, microangiopathic hemolytic anemia, etc.
Causes and mechanisms
Cause
31-43% infectious diseases (bacterial infection, sepsis, viral myocarditis, etc.)
24-34% neoplastic diseases (pancreatic cancer, colon cancer, leukemia, cervical cancer, etc.)
4-12% Obstetric and gynecological diseases (miscarriage, amniotic fluid embolism, stillbirth, etc.)
1-5% trauma and surgery (severe soft tissue trauma, extensive burns, organ transplantation, etc.)
Pathogenesis
Tissue factor is released, the exogenous coagulation system is activated, and the coagulation process is initiated.
Damage to vascular endothelial cells, disorders of coagulation and anticoagulation regulation
Massive destruction of blood cells and activation of platelets
Massive destruction of red blood cells (abnormal blood transfusion, malaria, paroxysmal nocturnal hemoglobin, etc.)
Destruction or activation of white blood cells
activation of platelets
Procoagulant substances enter the blood
In acute pancreatitis, a large amount of trypsin enters the blood, activates prothrombin, and promotes thrombin generation.
The procoagulant component of snake venom activates FX and promotes the occurrence of DIC.
Factors affecting the occurrence and development of DIC
Impaired function of the monocyte-phagocytic system
Severe liver dysfunction
Closely related to coagulation (the main anticoagulant substances are synthesized in the liver, and coagulation factors are also inactivated in the liver)
hypercoagulable state
Starting from the third week of pregnancy, platelets and coagulation factors increase in the blood of pregnant women.
microcirculation disorder
Clinical pathophysiological basis
Bleeding (initial symptom, may be bleeding from multiple locations)
Blood clotting substances are consumed and reduced
fibrinolytic system activation
Fibrin(ogen) degradation product formation
Microvascular damage
organ dysfunction
A large number of microthrombi cause microcirculation disorders and lead to ischemic organ dysfunction.
Involvement of the adrenal glands causes hemorrhagic necrosis of the adrenal cortex, leading to Wolff syndrome.
Involvement of the pituitary gland leads to necrosis, leading to Shearen syndrome.
Shock (occurs in 2/3 acute DIC)
DIC and shock are cause and effect of each other, forming a vicious cycle. (DIC reduces effective blood volume and causes shock)
anemia
Patients with DIC develop microangiopathic hemolytic anemia.
mechanism
Fibrin filaments form a fine mesh within the lumen of microvessels
Red blood cells are stuck, trapped, or hung on fibrin filaments
Red blood cells rupture under the impact of blood flow
The pathophysiological basis of prevention
Prevent and treat primary disease
Improve microcirculation
Establish a new dynamic balance between coagulation, anticoagulation and fibrinolysis
Maintain and protect organ function