Pig intestinal mucosa, pig and cow lungs

Sulfated glycosaminoglycan GAGs mixture (mucopolysaccharide sulfates)

D-glucosamine L-iduronic acid D-glucuronic acid

Large amounts of negative charges, strong acidity, and strong polarity

Not absorbed after oral administration

im, symptoms of bleeding and local irritation

intravenous administration

Liver (mononuclear-macrophage system) metabolism, renal excretion

Blood coagulation time and partial thrombin time APTT were significantly prolonged.

Weak effect on prothrombin time

The effect lasts for 3~4 hours

anticoagulant effect

Blood lipid regulating effect

anti-inflammatory effect

Inhibit platelet aggregation

Inhibit VSMC proliferation and resist vascular intimal hyperplasia

Prevent and treat the formation and expansion of blood clots (deep vein thrombosis, pulmonary embolism, peripheral arterial thromboembolism, etc.)

Prevention and treatment of myocardial infarction, cerebral infarction, cardiovascular surgery, and peripheral venous postoperative thrombosis

Sepsis, early placental dissection, malignant tumor lysis, etc.

Cardiac catheterization, extracorporeal circulation, hemodialysis, etc.

Performance

Prevention and control

reason

Allergic reactions (asthma, urticaria, conjunctivitis, fever), osteoporosis and fractures, premature birth, stillbirth

alkaline drugs

Nonsteroidal anti-inflammatory drugs, dextran, dipyridamole, etc.

GCs, ethacrynic acid

Insulin, sulfonylureas

iv, combined use of heparin and nitroglycerin

ACEI

LMWH (1.5~4), heparin (1)

Prevention and treatment of deep vein thrombosis and pulmonary embolism

Preventing thrombosis after surgery

Thrombosis in acute myocardial infarction and unstable angina pectoris

Anticoagulation for hemodialysis, extracorporeal circulation, etc.

Available for outpatient use

The anticoagulant dose is easy to control and has small individual differences.

Low toxicity and safe

Long acting time

No laboratory monitoring of anticoagulant activity required

Bleeding, thrombocytopenia, hypoVldemia with hyperkalemia, skin necrosis, allergic reactions, temporary ALT and AST↑, etc.

Determination of plasma FXa activity

Protamine Sulfate to the Rescue

LMWH is less likely to cause PF4 release and is less likely to cause type II thrombocytopenia.

Pentosaccharide synthesized based on antithrombin heparin binding site structure

Binds to the catalytic site and anionic exosite of thrombin

Can only bind to the catalytic site or anionic exosite

Potent and specific thrombin inhibitor

Not absorbed after oral administration

intravenous administration

Not easily able to penetrate the blood-brain barrier

anticoagulant effect

antithrombotic effect

Prevent postoperative thrombosis

Adjunctive treatment of post-percutaneous coronary angioplasty restenosis, unstable angina, and thrombolysis after acute myocardial infarction

DIC

Hemodialysis, extracorporeal circulation

Use with caution in patients with renal failure

Daily monitoring of APTT is required

There is no effective antidote for hirudin

Synthetic arginine derivatives

short half-life

Narrow therapeutic safety range

No effective antagonist

Can be used in combination with aspirin

Binds to the catalytic site → inhibits thrombin activity and fibrin formation

Inhibit fibrin cross-linking and promote fibrinolysis

Inhibit thrombin-induced platelet aggregation and secretion

Prevention and treatment of thrombotic diseases

Prevent graft thrombosis (topical application)

VitK——essential factor for activation of FII, VII, IX, and X

Dicoumarol, warfarin (benzyl acetone coumarin), acenocoumarol (new anticoagulant)

Oral absorption, rapid and complete

Small apparent volume of distribution and high plasma protein binding rate

Can pass through the placenta

Liver metabolism, renal excretion

Oral absorption, slow and irregular

High plasma protein binding

Mainly distributed in lungs, liver, spleen, kidneys

Liver metabolism, renal excretion

Kidney excretion

VitK antagonists

VitK (γ-carboxylase coenzyme) - affects the activation of coagulation factors and anticoagulant proteins containing glutamic acid residues

It is ineffective against carboxylated factors and requires depletion of factors in the body to exert anticoagulant effect (≥12~24h)

Prevent and treat thromboembolic diseases (atrial fibrillation, valvular heart disease) orally

Hip surgery, taken after surgery (reduces the probability of venous thrombosis)

Prevent and treat venous thrombosis and pulmonary embolism

Reduce the incidence of venous thrombosis after major surgery, rheumatic heart disease, and artificial valve replacement (combined with antiplatelet drugs)

Slow onset of effect, long action time, and difficult to control

spontaneous bleeding

Fetal hemorrhagic diseases, affecting the normal development of fetal bones

Warfarin-induced skin necrosis

Determine prothrombin PT time, control it at 18~24s (normal 12s)

Slowly intravenously inject large amounts of VitK and transfuse fresh blood

Aspirin, phenylbutazone, etc.

Liver enzyme inhibitors (amiodarone, etc.)

Drugs that reduce VitK utilization and cause bile reduction

Broad-spectrum antibiotics (inhibiting Vit production)

Decreased synthesis of clotting factors

Hepatic enzyme inducing drugs (phenobarbital, phenytoin, rifampicin)

(FIIa inhibitor) dabigatran etexilate, (FIIa inhibitor) rivaroxaban

Pharmacokinetics and pharmacodynamics are predictable

Fixed-dose therapy without routine anticoagulation monitoring

Fewer interactions with food and other medications

Patients with non-valvular atrial fibrillation (alternative to warfarin)

Prodrugs of dabigatran

competitive inhibition of thrombin

(Specific Antagonist) Idarucizumab

Low bioavailability

active drug

Competitive binding to FXa

Recombinant FXa preparation Andexanet Alfa (antagonist)

High bioavailability

Block the synthesis of PGG2, PGH2, and TXA2

Non-steroidal anti-inflammatory drugs (aspirin, indomethacin, sulfinpyrazone, ibuprofen)

Performance

mechanism

Coronary arteriosclerosis, myocardial infarction, cerebral infarction, deep vein thrombosis, pulmonary infarction, etc.

Adjuvant antithrombotic therapy to thrombolytic therapy

TXA2 synthase inhibitor drugs → inhibit TXA2 synthesis → cyclic endoperoxide (PGG2, PGH2 accumulation) → promote PGI2 synthesis

This type of drug has a short half-life, and its inhibitory effect on TXA2 is not strong and lasting enough.

The increased PGG2 and PGH2 after inhibition have an equivalent platelet aggregation effect on PLT as TXA2

After the use of TXA2 synthase inhibitors, plasma PGE2 concentration ↑ (reverse anti-aggregation activity of PGI2, PGD2)

Strong TXA2 synthase inhibitor, moderate TXA2 receptor antagonism

Reduce the incidence of re-embolization, recurrent angina, ischemic stroke, etc.

Prevent new ischemic lesions

Vascular infarction rate and reperfusion rate in patients with acute myocardial infarction

Enhance the fibrinolytic effect of streptokinase

Mild gastrointestinal reaction

Lidogrel similar drugs

Intensity of action < lidogrel, mild adverse reactions

Anti-platelet aggregation and release

Relax vascular smooth muscle

Deaggregation of platelet aggregates (extracorporeal bypass)

Inhibit platelet adhesion to vascular endothelial cells

PLT→AC→cAMP↑→reuptake of cytosolic calcium into the calcium store→cytoplasmic free calcium concentration↓→quiescent state (unresponsive to stimulation)

Prevent thrombocytopenia, thrombotic thrombocytopenic purpura, micro-thrombosis, and bleeding tendencies

PLT→Inhibit PDE activity→cAMP content↑

PLT→inhibits adenosine reuptake and activates AC→cAMP synthesis↑

PLT→mildly inhibits COX→TXA2 synthesis↓

Vascular endothelial cells→PGI2 synthesis↑

Inhibit platelet aggregation

Anti-thrombotic

Prolongs shortened platelet survival time

Patients with angina pectoris, use with caution

antiplatelet

dilate blood vessels

Anti-vascular proliferation

PLT→Inhibit PDE-III→cAMP content↑

Irreversible inhibition of platelet aggregation and adhesion

Selectively and specifically interferes with ADP-mediated platelet activation

Inhibit ADP-induced α-granule secretion → Inhibit adhesion response to vascular wall injury

Inhibit ADP-induced exposure of platelet membrane GPIIb/IIIa receptor complex and fibrinogen binding site → inhibit platelet aggregation

Antagonizes the inhibitory effect of ADP on AC

Efficacy>Aspirin

GPIIb/IIIa receptor monoclonal antibody

Significantly inhibits platelet aggregation

Prevent and treat thrombosis

Thrombolytic therapy to prevent blood vessel re-occlusion

Lamifiban, tirofiban, jemirofiban (oral), frafiban (oral), xilafiban (oral)

Strong inhibitory effect on platelet aggregation

Easy to apply, fewer adverse reactions

Acute myocardial infarction, thrombolytic therapy, unstable angina, reinfarction after angioplasty

Mixed preparations of FII, FVII, FIX, FX, etc.

Treatment of hemophilia B (congenital FIX deficiency), severe liver disease, overdose of coumarin anticoagulants, and bleeding caused by VitK-dependent coagulation factor deficiency

FVIII, small amounts of fibrinogen

Treatment of hemophilia A (congenital factor FVIII deficiency)

Treatment of severe bleeding caused by hemolytic hemophilia and anti-factor VIIIc antibodies

Headache, fever, urticaria, etc. (ivgtt too fast)

Rapidly increase blood fibrinogen concentration → promote blood coagulation and hemostasis

Treatment of primary hypofibrinogenemia

Treatment of secondary fibrinogen deficiency

Promote fibrinogen activation and hemostatic effect

Promote epithelial cell mitosis and accelerate wound healing

Hemostasis of bleeding from small blood vessels, capillaries, and solid organs that are difficult to stop

Hemostasis of wounds, oral cavity, urinary tract, digestive tract and other parts of the body

Hemostasis of puncture site bleeding

Local hemostasis (spray or wound dressing)

It has no hemostatic effect on cancer bleeding, trauma bleeding, and bleeding caused by non-fibrinolysis.

Bleeding caused by surgery on the lungs, liver, pancreas, prostate, thyroid, adrenal glands, etc.

Postpartum hemorrhage, prostatic hypertrophy bleeding, upper gastrointestinal bleeding, etc.

Chronic blood loss, malnutrition, pregnancy, child growth and development

Children, if taken by mistake >1g

Gastric lavage with phosphate or carbonate solution, detoxification with special antidote deferoxamine

Folic acid → dihydrofolate reductase → tetrahydrofolate → combined one-carbon unit → tetrahydrofolate coenzymes

transfer one carbon unit

Nutritional megaloblastic anemia (malnutrition, folic acid requirement↑) - mainly folic acid, supplemented by VitB12

Megaloblastic anemia caused by folic acid-resistant drugs (methotrexate, pyrimethamine) - treatment of tetrahydrofolate preparation leucovorin (calcium leucovorin)

It can only correct abnormal blood images but cannot improve symptoms of neurological damage. It is used as auxiliary treatment.

invalid

Necessary for cell division and maintaining the integrity of myelin sheath in nervous tissue

VitB12 (methylcobalamin)

VitB12 (5'-deoxyadenosylcobalamin)

anemia, hypoxia

Kidney disease, bone marrow damage, insufficient iron supply, etc.

Best indication - anemia due to chronic renal failure and end-stage renal disease

Anemia caused by low bone marrow hematopoietic function, tumor chemotherapy, AIDS drug treatment, and connective tissue diseases

Stimulate proliferation and differentiation of hematopoietic precursor cells

Stimulate the growth of neutrophils, monocytes and T lymphocytes and induce colony formation

Promote the lysis of tumor cells by macrophages and monocytes

Indirectly affects erythrocyte proliferation