MindMap Gallery Clinical diagnostic procedures and selected tests for bleeding
Clinical Medicine Undergraduate Internal Medicine Hematology, understand the patient’s family medical history, drug history, surgical history, past medical history, etc.
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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.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
Clinical diagnostic procedures and selected tests for bleeding
Diagnosis idea 1
Determine whether it is a bleeding disorder
Detailed medical history
Understand the patient's family medical history, drug history, surgical history, past medical history, etc. Understand whether the patient has had similar symptoms before, how they manifested, and whether they have significantly worsened or decreased.
Physical examination
Including examination of skin, mucous membranes, lymph nodes, liver, spleen and other parts. Pay attention to observe whether there are ecchymosis, bleeding spots, jaundice and other symptoms on the skin, and whether the liver and spleen are enlarged, etc.
It can be roughly differentiated into abnormalities in blood vessels and platelets, coagulation disorders or other diseases; It is judged to be a quantitative abnormality or a quality defect.
screening test
1. Initial hemostasis screening test
Platelet CountPLT
PLT<100×10⁹/L, that is, thrombocytopenia
Note: At least 2 counts are required for diagnosis, and blood smear is required to observe whether the number and shape of platelets are consistent with the PLT results.
Bleeding time BT
clinical significance
Prolonged BT indicates a defect in initial hemostasis completed by blood vessels and platelets.
reason
1||| Decreased platelet count: the most common cause of prolonged BT, ITP
2||| Platelet dysfunction: Thrombthethenia, giant platelet syndrome
3||| Von Willebrand disease (vWD), prolonged BT
4||| Perivascular connective tissue disease, Down syndrome, prolonged BT
5||| Antiplatelet drugs: aspirin, dipyridamole, clopidogrel, etc. should be stopped 7 days before BT measurement
Hereditary telangiectasia, Henoch-Schönlein purpura, and Vc deficiency may cause bleeding symptoms but generally do not cause BT prolongation.
2. coagulation screening test
Plasma prothrombin time PT
Reference interval: 11~14s, it is meaningful to extend/shorten PT in control plasma by 3s
clinical significance
Prolonged PT is seen in bleeding disorders caused by reduction of exogenous coagulation factors (Ⅰ, Ⅱ, Ⅴ, Ⅶ, Ⅹ)
Congenital reduction: rare
Reduced acquisition
Liver disease, Vk deficiency (biliary tract disease, chronic enteritis), DIC
Mid to late stage of DIC (hyperfibrinolytic stage)
Clotting factors are consumed and reduced
Hyperfibrinolysis, increased fibrin degradation products, interference with fibrin production/
Therefore, PT is clinically used as a screening test before surgery or for suspected bleeding disorders and as one of the diagnostic tests for DIC.
Activated partial thromboplastin timeAPTT
Reference interval: 26~36s, which is more meaningful than extending/shortening plasma APTT by 10s
clinical significance
Prolongation is mainly seen in
Bleeding disorders caused by decreased endogenous coagulation factors (1, 2, 5, 8, 9, 10, 11, 12)
congenital reduction
Hemophilia: Deficiency of factors 8 and 9
Von Willebrand's disease: vWF deficiency leads to reduced activity of factor 8
Therefore, APTT is an important screening test for von Willebrand disease
Reduced acquisition
liver disease
Vk deficiency: biliary tract disease, chronic enteritis, extensive long-term antibiotic use
Mid to late stage of DIC (hyperfibrinolytic stage)
Bleeding disorders due to increased heparin-like anticoagulants and lupus anticoagulants
Hyperfibrinolysis: primary and secondary hyperfibrinolysis
Therefore, APTT is clinically used as a screening test before surgery or for suspected bleeding disorders, especially hemophilia and abnormal anticoagulants, and as one of the diagnostic tests for DIC.
thrombin time TT
Reference interval: 16~18s, TT is meaningfully longer than control plasma TT by more than 3s
clinical significance
TT prolongation is seen in
Hyperfibrinolysis
Seen in primary or secondary hyperfibrinolysis (DIC)
Decreased fibrinogen
Fibrin degradation products (FDP) increase, inhibit thrombin, and interfere with fibrin production.
Abnormal or hypofibrinogenemia
Too much heparin or heparin-like anticoagulant substance
Liver disease, post-radiotherapy, malignant tumors, etc., the cause of prolonged TT can be identified through the toluidine blue correction test
3. Hyperfibrinolysis screening test
Plasma fibrin(ogen) degradation products (FDP)
Reference interval: normal <5mg/L. When >10mg/L is clinically significant
clinical significance
The increase is mainly seen in
Primary hyperfibrinolysis: FDP>40mg/L or above
DIC (secondary hyperfibrinolysis): FDP>20mg/L or above, which is one of the tests for diagnosing DIC.
Plasma D-dimer (DD)
Reference interval: normal <0.5mg/L. When >0.5mg/L is clinically significant
clinical significance
Differentiate between primary and secondary hyperfibrinolysis
Primary hyperfibrinolysis: increased FDP, normal DD
Secondary hyperfibrinolysis: both FDP and DD are increased
DIC: DD>2~3mg/L
deep vein thrombosisDVT
DD<0.5mg/L, DVT can basically be eliminated
Thrombotic disease or hypercoagulable state
DD is increased and can be used as one of the screening tests.
Commonly used diagnostic tests for bleeding disorders
1. Tests related to the diagnosis of von Willebrand's disease (vWD)
Definition: vWD is a type of hereditary or acquired bleeding disorder caused by a lack of von Willebrand factor (vWF) in the plasma or abnormal molecular structure, and is inherited in an autosomal recessive manner.
vWF antigen content: vWF is mainly synthesized and secreted by vascular endothelial cells. Detection of vWF antigen content is often used as the first choice test for the diagnosis of vWD.
vWF function analysis:
Mediates the binding of platelet membrane glycoprotein Ⅰb-Ⅸ (GP Ⅰb-Ⅸ) complex to subendothelial collagen, allowing platelets to adhere to the site of vascular injury.
Binds to coagulation factor VIII and acts as a carrier to stabilize FVII
2. Tests related to diagnosis of platelet disease
Platelet autoantibody assay
Anti-platelet membrane glycoprotein autoantibodies are positive and have high specificity for the diagnosis of ITP (primary immune thrombocytopenia)
3. Tests related to the diagnosis of coagulation factor deficiencies
coagulation cross-over test
Procoagulant activity of individual coagulation factors
Plasma fibrinogen (FIB)
Reference interval: 2.0~4.0g/L
clinical significance
Decreased fibrin
Primary fibrinogenopenia: congenital low or no fibrinogenemia, dysfibrinogenemia, rare
secondary fibrinogen reduction
Reduced synthesis: seen in cirrhosis and alcoholism
Excessive consumption:
primary hyperfibrinolysis
Due to hyperfibrinolysis, FIB is degraded, thus reducing
DIC (FIB is one of the diagnostic tests for DIC)
Due to coagulation, FIB is consumed
FIB is degraded due to hyperfibrinolysis
If it is a congenital or hereditary disease, genetic and other molecular biology testing should be performed to determine the precise nature and pathogenesis of its cause.
Diagnosis idea 2
1. Ask about medical history
Age of onset, bleeding triggers, bleeding locations and characteristics, accompanying symptoms and family history, etc.
2. Physical examination
On the basis of a comprehensive physical examination, pay attention to the location and characteristics of bleeding. For bleeding in various organs, the possibility of local lesions must be ruled out.
3.Laboratory and auxiliary examinations
Diagnostic Thrombosis Program
prothrombotic state
Screening Tests Common Tests
Primary hemostatic defects: PLT & BT
Both BT and PLT are normal.
Normal or mostly caused by vascular purpura caused by a simple increase in blood vessel wall permeability and/or fragility.
BT extension
Secondary hemostatic defects: APTT & PT
APTT and PT are normal.
Normal human or hereditary and acquired factor XIII deficiency
Abnormal APTT and PT
Hyperfibrinolysis: FDPs&D-D
FDPs and D-D are normal.
Indicates that fibrinolytic activity is normal and clinical bleeding symptoms may have nothing to do with fibrosis.
FDPs elevated, D-D normal
Most of them are false positives of FDPs, which are seen in liver disease, surgical bleeding, severe DIC, early fibrinolysis, after strenuous exercise, rheumatoid arthritis, the presence of anti-Rh(D) antibodies, etc.
FDPs normal, D-D elevated
Most of them are false negatives of FDPs, which are found in DIC, venous thrombosis, arterial thrombosis and thrombolytic therapy, etc.
Both FDPs and D-D are elevated
Indicates that fibrinogen and fibrin are degraded simultaneously, seen in secondary fibrinolysis, such as DIC and after thrombolytic therapy
special test
Thrombomodulin (TM) and/or endothelin-1 (ET-1)
Increased → reflects damage to vascular endothelial cells
P-selectin and/or 11-deshydrothromaxane B2 (11-DH-TXB2)
Increased → reflects platelet activation
Prothrombin fragment 1 2 (F1 2 ) and/or fibrinopeptide A (FPA)
Increased → reflects the enhanced activity of thrombin
Thrombin antithrombin complex (TAT)
Increase →Reflects enhanced thrombin activity
Plasmin Antiplasmin Complex (PAP)
Decrease →reflects decreased plasmin activity
Thrombophilia
arterial/venous thrombosis
DIC project
clinical diagnosis
There are underlying diseases that can easily induce DIC, such as multiple bleeding that cannot be explained by the primary disease, general skin and mucosal embolism, or organ failure such as brain, kidney, and lung, and anticoagulant treatment is effective.
Points diagnosis
Diagnosis of overt (decompensated) DIC
Diagnosis of non-overt (compensated) DIC