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Pharmacology [drugs that act on the blood]
It mildly inhibits platelet cyclooxygenase and has a weak effect in reducing TXA2 production. It is generally used in combination with oral anticoagulants to treat thromboembolic diseases and irreversibly inhibits platelet aggregation and adhesion.
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Pharmacology [drugs that act on the blood]
- bacteria
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Drugs that act on the blood and hematopoietic system
1. Anticoagulant drugs
Drugs that prevent the blood clotting process by affecting clotting factors
1. Indirect thrombin inhibitor (heparin)
it acts on the blood Therefore, bleeding can be stopped both in vitro and in vivo
Anticoagulants in vivo and in vitro enhance the activity of antithrombin III and can prevent the formation and expansion of thrombus, but are ineffective against already formed thrombi.
In vivo process, oral administration is not absorbed, intravenous administration is powerful and rapid.
Pharmacological effects
1) Anticoagulation
Activates AT-III (antithrombin III), a serine protease inhibitor
2) Adjust blood lipids
Causes vascular endothelial cells to release lipoprotein esterase to hydrolyze chylomicrons and VLDL in the blood
3) Anti-inflammatory
4) Inhibit vascular smooth muscle cell proliferation and resist vascular intimal hyperplasia
5) Inhibit platelet aggregation and avoid combination with platelets
Clinical application
1) Thromboembolic diseases
2) Disseminated intravascular coagulation (DIC)
3) Prevention and treatment of myocardial infarction, cerebral infarction, vascular surgery and peripheral venous postoperative thrombosis
4) Extracorporeal anticoagulation
Adverse reactions
1) Spontaneous bleeding
2) Thrombocytopenia
3) Others
When using heparin Dosage should be strictly controlled Clotting time (PPT) should be closely monitored Stop taking the medicine immediately if the bleeding becomes hard Detoxification of overdose poisoning with protamine
Contraindications
Liver and kidney insufficiency, bleeding tendency, ulcer disease, severe hypertension, trauma and surgery, pregnant women
1,1 low molecular weight heparin (LMWH) <6.5kD
advantage
1) The anticoagulant dose is easy to control and has small individual differences.
2) Laboratory monitoring of anticoagulant activity is generally not required
3) Low toxicity and safe
4) Long acting time, subcutaneous injection 1 to 2 times a day
5) Small molecular weight, difficult to induce thrombocytopenia
Commonly used preparations enoxaparin, dideparin
Clinical application
Used to prevent blood clots after orthopedic surgery, etc.
2. Thrombin inhibitor drugs
Direct inhibitor of thrombin (hirudin)
A powerful and specific thrombin inhibitor, 1:1 molecule directly binds to thrombin and inhibits thrombin activity.
Prevent postoperative thrombosis, unstable angina, etc.
Vitamin K antagonists (dicumarin, warfarin)
Its target is the liver! Can only stop bleeding inside the body
internal processes
Warfarin is absorbed quickly and completely after oral administration and has high bioavailability, while dicoumarin is absorbed slowly and irregularly.
High plasma protein binding rate and long half-life
Pharmacological effects
Competitive antagonists of vitamin K
Mechanism: Inhibit the transformation of vitamin K and prevent its repeated use
Features
Anticoagulant in vivo, ineffective in vitro
Effective when taken orally, with slow and long-lasting anticoagulant effect
Ineffective against activated coagulation factors
Clinical application
1) Thromboembolic disease: first heparin and then coumarin maintenance
2) Prevent postoperative thrombosis: can be combined with antiplatelet drugs
Adverse reactions
1) Spontaneous bleeding: It is necessary to measure the prothrombin time (18-24s) and use vitamin K and fresh blood for rescue during medication.
2) Fetal malformations: Warfarin (can pass the placental barrier)
3) Skin necrosis
2. Antiplatelet drugs
Classification
1. Drugs that inhibit platelet metabolism: aspirin
1) Cyclooxygenase inhibitor: aspirin
mechanism:
Prevents the conversion of arachidonic acid into PGG2 and PGH2, thereby reducing platelet TXA2 synthesis.
Aspirin can partially antagonize platelet activation caused by fibrinolysis and also inhibit the release of t-PA.
Small doses can prevent and treat thrombotic diseases
2) TXA2 synthase inhibitors and TXA2 receptor blockers: lidogrel
Strong effect on platelets and coronary thrombosis
2. Drugs that increase cAMP in platelets: dipyridamole
epoprostenol
Synthetic PGI2 antagonizes TXA2, has strong anti-platelet aggregation and relaxes vascular smooth muscle effects
Mechanism: Activating platelet adenosine cyclase increases cAMP concentration, reduces intracellular free Ca2 concentration, and keeps platelets in a resting state
Inhibits platelet aggregation, adhesion to vascular endothelium, and promotes depolymerization.
Dipyridamole (Dipyridamole)
Inhibits phosphodiesterase and increases cAMP
Activation of platelet adenosine cyclase increases cAMP concentration
Enhance PGI2 activity or promote PGI2 production
Mildly inhibits platelet cyclooxygenase and has a weak effect in reducing TXA2 production. It is generally used in combination with oral anticoagulants to treat thromboembolic diseases.
3. Drugs that hinder ADP-mediated platelet activation: Ticlopidine
Irreversibly inhibit platelet aggregation and adhesion
Prevention of acute myocardial reinfarction, cerebrovascular and coronary embolic disease
4. GP IIb/IIIa receptor blocking drug: abciximab
GPIIb/IIIa-R: specific recognition and binding site of adhesion protein for platelet aggregation
Strong inhibitory effect on platelet aggregation
3. Fibrinolytic drugs
fibrinolytic system
Plasminogen (plasminogen)
plasmin
plasminogen activator or inhibitor
1. Streptokinase (SK)
Mechanism
Combines with plasminogen to form sk-plasminogen complex, which indirectly promotes the conversion of plasminogen into plasmin and dissolves thrombus.
Clinical application
1Acute thromboembolic disease
2Acute myocardial infarction
Adverse reactions
1. Spontaneous bleeding: aminotribenzoic acid
2. Allergic reaction: antigenicity
Contraindications: Bleeding diseases, peptic ulcers, severe hypertension, maternal use before and after childbirth
2. Urokinase (UK)
Mechanism of action: Directly activates plasminogen into plasmin
Features: Non-antigenic, does not cause allergic reactions, can be used for those allergic to streptokinase
3. Tissue plasminogen activator (t-PA)
Features: Selective to thrombus site
4. Procoagulant drugs
1. Dimension K
basic structure
1) Natural form: Vitamins K1 and K2, fat-soluble, requiring bile to assist absorption (fast action, long duration, generally administered by intramuscular injection)
2) Artificial synthesis: Vitamins K3 and K4, water-soluble, do not require bile to assist absorption (can be taken orally)
Pharmacological effects
As a coenzyme of carboxylase, it participates in the activation of IIa, VIIa, IXa, anticoagulant protein C, anticoagulant protein S, etc.
When antibiotics are used to destroy intestinal flora, Vk decreases and coagulation dysfunction leads to bleeding.
Has a certain analgesic effect
Clinical application
1) For bleeding caused by Vk deficiency
Absorption disorders: obstructive jaundice, biliary fistula, chronic diarrhea (reduced bile, poor absorption)
Synthetic disorders: premature infants, newborns (less intestinal bacteria)
2) Bleeding due to low prothrombin
3. Prevent vitamin K deficiency secondary to long-term use of broad-spectrum antibiotics
4. Bleeding caused by overdose of oral anticoagulants after extensive intestinal resection
Adverse reactions
1. Excessive vein speed: causing facial flushing, sweating, and decreased blood pressure (must be injected intramuscularly)
2. Gastrointestinal reactions
3. Larger doses of premature infants and neonatal hemolytic anemia
2. Thrombin
Features
Promote the conversion of fibrinogen into fibrin to stop bleeding
Commonly used for bleeding from small blood vessels and solid organs, and can also be used for local hemostasis
3. Fibrinolysis inhibitor drugs
Aminomethylbenzoic acid (PAMBA)
Mechanism
Competitively inhibits plasminogen activating factor, preventing plasminogen from converting into plasmin, thus inhibiting the dissolution of fibrinoprotein and producing hemostasis.
Clinical application
Bleeding due to fibrinolysis
5. Anti-anemia drugs and blood cell growth factors
Common clinical ischemic diseases and therapeutic drugs
Iron deficiency anemia (iron treatment)
Megaloblastic anemia (treated with folic acid and vitamin B12)
Aplastic anemia (low hematopoietic function of bone marrow, treatment with hematopoietic cell growth factors)
anti-anemia drugs
1. Iron supplement
Commonly used preparations: ferrous sulfate, ferric citrate, iron dextran
Factors affecting iron absorption
Promote absorption
Gastric acid or dilute hydrochloric acid, Vc, fructose, cysteine, glutathione, etc.
hinder absorption
Achlorhydria, antacids, tannic acid, high calcium and phosphorus foods, strong tea, tetracycline, etc.
Pharmacological effects
It is an essential substance for the synthesis of heme during the mature stage of red blood cells and promotes the synthesis of hemoglobin and other substances.
Clinical application
For iron deficiency anemia caused by excessive blood loss, increased iron demand and malabsorption
Adverse reactions
gastrointestinal reactions
Take after meals (orally, not by injection)
acute poisoning
Gastric lavage, deferoxamine
2. Folic acid
Clinical application
1) Megaloblastic anemia
Nutritional megaloblastic anemia: folic acid plus VB12
Megaloblastic anemia caused by the use of methotrexate and trimethoprim: calcium leucovorin
2) Adjuvant treatment of pernicious anemia
Used with VB12
3) Prevent neural tube defects
3. Vitamin B12
internal processes
VB12 is absorbed into the blood with the participation of intrinsic factors. When the gastric mucosa atrophies, the synthesis of intrinsic factors decreases and the absorption of VB12 decreases (pernicious anemia)
Pharmacological effects
1) Participate in folic acid recycling
2) Maintain myelinated nerve fiber function
Clinical application
1) Treatment of pernicious anemia: VB12 mainly combined with folic acid
2) Adjuvant treatment of megaloblastic anemia: combined with folic acid
3) Adjuvant treatment for neuritis, nerve atrophy, and liver disease
hematopoietic cell growth factor
1. Erythropoietin/erythropoietin (EPO)
Pharmacological effects
Stimulate the production of erythroid stem cells and promote the maturation of red blood cells
Clinical application: The best indication is anemia caused by chronic renal failure
Effective for anemia caused by low bone marrow hematopoietic function, tumor chemotherapy, and AIDS drug treatment
6. Blood volume expansion drugs
Dextran
Expansion effect
Medium molecule>Low molecule>Small molecule
Treating DIC
Small molecules>Low molecules
Pharmacological effects
1. Increase plasma osmotic pressure and expand blood volume
2. Inhibit platelet and red blood cell aggregation and improve microcirculation
3. Osmotic diuresis
Clinical application
1. Prevention and treatment of hypovolemic shock (medium)
2. Prevention and treatment of thromboembolic diseases (low, small)
3. Prevent and treat acute renal failure (low, small)
Adverse reactions
1. Allergic reaction
2. Coagulation disorders and bleeding
medicine interactions
enhance drug efficacy
1. The lack of vitamin K in food or the use of broad-spectrum antibiotics to inhibit intestinal bacteria will reduce the content of vitamin K in the body.
2. Combined use of aspirin, phenylbutazone and other antiplatelet drugs
3. Combined use of hepatic enzyme inhibitors such as imipramine
weaken the effect
Combined use of hepatic enzyme inducers such as barbiturates