This document discusses drugs used to treat hemophilia and other bleeding disorders. It covers factors VIII and IX replacement therapies for hemophilia A and B, as well as treatments for hemophilia C and acquired hemophilia. It also discusses management of bleeding episodes, inhibitors, and complications. A variety of factor replacement products, desmopressin, antifibrinolytics, activated prothrombin complex concentrate, recombinant factor VIIa, monoclonal antibodies, fresh frozen plasma, and fibrin sealants are described for treating different types and severities of hemophilia and controlling bleeding in patients.
Hemophilia is perhaps the most well-known inherited bleeding disorder, although it is relatively rare. It affects mostly males. Many more people are affected by von Willebrand disease, the most common inherited bleeding disorder in America caused by clotting proteins.
This document provides guidance on dental management of medically compromised children, focusing on those with bleeding disorders like hemophilia. It discusses evaluating coagulation factor levels, using local anesthetics safely, replacing deficient factors, and administering antifibrinolytic drugs to prevent bleeding complications. Minor procedures may require only local measures, while more extensive work like oral surgery demands factor replacement, antifibrinolytics, and close monitoring to safely manage bleeding risks. Prevention through oral hygiene and regular cleanings can reduce need for invasive dental work in these high-risk patients.
This document discusses coagulation, anticoagulants, and fibrinolytics. It begins by describing the coagulation cascade and fibrinolysis system, which work to stop bleeding through platelet plug formation and blood clotting. It then discusses natural anticoagulants like prostacyclin and antithrombin III that prevent inappropriate clotting. Various coagulants and anticoagulants are outlined, including heparin and low molecular weight heparins, vitamin K, and newer oral anticoagulants. Adverse effects and clinical uses of different agents are also summarized.
1) She has a partial quantitative defect of von Willebrand factor as shown by her decreased vWF activity compared to her antigen level.
2) Her multimers were normal.
3) Her bleeding was responsive to DDAVP and factor replacement initially but her levels decreased over time, consistent with type 1 VWD.
This document provides information on hemophilia, including the objectives, coagulation factors, types and severity of hemophilia, clinical manifestations, complications, labs, treatment including factor replacement therapy and management in special situations. It discusses the basic concepts of hemophilia, how to approach cases, calculate factor requirements, lifestyle modifications, and management during situations like surgery, dental procedures, delivery, and menstruation in hemophiliacs.
Hemophilia is perhaps the most well-known inherited bleeding disorder, although it is relatively rare. It affects mostly males. Many more people are affected by von Willebrand disease, the most common inherited bleeding disorder in America caused by clotting proteins.
This document provides guidance on dental management of medically compromised children, focusing on those with bleeding disorders like hemophilia. It discusses evaluating coagulation factor levels, using local anesthetics safely, replacing deficient factors, and administering antifibrinolytic drugs to prevent bleeding complications. Minor procedures may require only local measures, while more extensive work like oral surgery demands factor replacement, antifibrinolytics, and close monitoring to safely manage bleeding risks. Prevention through oral hygiene and regular cleanings can reduce need for invasive dental work in these high-risk patients.
This document discusses coagulation, anticoagulants, and fibrinolytics. It begins by describing the coagulation cascade and fibrinolysis system, which work to stop bleeding through platelet plug formation and blood clotting. It then discusses natural anticoagulants like prostacyclin and antithrombin III that prevent inappropriate clotting. Various coagulants and anticoagulants are outlined, including heparin and low molecular weight heparins, vitamin K, and newer oral anticoagulants. Adverse effects and clinical uses of different agents are also summarized.
1) She has a partial quantitative defect of von Willebrand factor as shown by her decreased vWF activity compared to her antigen level.
2) Her multimers were normal.
3) Her bleeding was responsive to DDAVP and factor replacement initially but her levels decreased over time, consistent with type 1 VWD.
This document provides information on hemophilia, including the objectives, coagulation factors, types and severity of hemophilia, clinical manifestations, complications, labs, treatment including factor replacement therapy and management in special situations. It discusses the basic concepts of hemophilia, how to approach cases, calculate factor requirements, lifestyle modifications, and management during situations like surgery, dental procedures, delivery, and menstruation in hemophiliacs.
This would give an idea of the various bleeding disorders, associated clotting factors and more specifically management in the dental office of the patients with bleeding disorders
- The document discusses anticoagulation and blood clotting. It describes how blood clots form and are broken down, as well as drugs that can regulate clotting such as heparin, warfarin, and dicoumarol. It provides details on the coagulation factors, classes of anticoagulant drugs, the blood clotting process, and coagulation disorders.
The document discusses drugs used in coagulation disorders and bleeding. It describes two major groups of drugs - those that decrease clotting like anticoagulants and thrombolytics, and those that increase clotting for deficiencies. Anticoagulants discussed include heparins, warfarin, and direct thrombin/factor Xa inhibitors. Antiplatelets to inhibit platelet aggregation are also covered. Drugs to arrest bleeding include local haemostatics applied topically and systemic agents like vitamin K and antifibrinolytics. Key points for dentists on managing patients taking these drugs emphasize safer options and monitoring coagulation levels before procedures.
Oral consideration and laboratory investigations of bleeding and clotting dis...kashmira483
This document provides information on bleeding and clotting disorders. It discusses the pathophysiology of hemostasis including the vascular, platelet, coagulation, and fibrinolytic phases. It describes different types of bleeding disorders like vessel wall disorders, platelet disorders, and coagulation disorders. Laboratory tests for identifying bleeding disorders are outlined. Oral manifestations and dental considerations for management are summarized. Local hemostatic agents and systemic agents for different bleeding disorders are also mentioned.
The document discusses various coagulation disorders including:
1. Congenital coagulation disorders such as hemophilia A and B which are caused by deficiencies in coagulation factors VIII and IX.
2. Acquired coagulation disorders including disseminated intravascular coagulation (DIC), vitamin K deficiency, liver disease, and antibodies against coagulation factors.
3. The pathogenesis, clinical features, laboratory findings, and treatment of various coagulation disorders are explained.
This document summarizes several coagulation disorders including haemophilia A, haemophilia B, von Willebrand disease, other hereditary coagulation factor deficiencies, and disseminated intravascular coagulation. It describes the clinical features, inheritance, laboratory findings, treatment, and management of each condition. Key points include that haemophilia A is the most common clotting factor deficiency, von Willebrand disease is the most common inherited bleeding disorder, and disseminated intravascular coagulation can be triggered by trauma, infection, cancer and other conditions.
This document summarizes anticoagulants and their uses. It discusses the coagulation cascade and how anticoagulants work to prevent unwanted clotting. Several classes of anticoagulants are covered, including unfractionated and low molecular weight heparins, vitamin K antagonists like warfarin, and direct acting anticoagulants. Indications, dosages, monitoring, and adverse effects are provided for many of the discussed anticoagulants. The document also addresses perioperative management of anticoagulation and treatments for bleeding or over-anticoagulation.
The document discusses anti-coagulants and fibrinolytic drugs. It covers the normal coagulation cascade and hemostasis. It then discusses various anti-coagulant drugs including heparin and low molecular weight heparins, which work by potentiating antithrombin. Oral vitamin K antagonists like warfarin are also covered. Fibrinolytic drugs discussed include tissue plasminogen activator, streptokinase and urokinase, which work by converting plasminogen to plasmin to lyse clots. The risks of bleeding are also summarized for anti-coagulant and fibrinolytic therapies.
Heparin is a powerful anticoagulant that acts indirectly by binding to antithrombin III and inactivating clotting factors. It can be given intravenously or subcutaneously. Heparin is used to treat and prevent conditions involving blood clots such as deep vein thrombosis, pulmonary embolism, and arterial thromboembolism. Adverse effects include bleeding and heparin-induced thrombocytopenia. Warfarin is an oral anticoagulant that works by interfering with vitamin K dependent clotting factor synthesis in the liver. It is used long-term for conditions requiring anticoagulation like atrial fibrillation. Risks include bleeding and fetal harms
Anticoagulants are used to treat and prevent blood clots that may occur in your blood vessels. Blood clots can block blood vessels (an artery or a vein). A blocked artery stops blood and oxygen from getting to a part of your body (for example, to a part of the heart, brain or lungs).
This document provides an overview of hemostasis and drugs that affect coagulation and act as anticoagulants. It describes the coagulation cascade and how tests like aPTT and PT are used to evaluate it. Local hemostatic agents, transfusional agents, and non-transfusional agents are discussed. Specific agents are explained including their sources, uses, dosages, and potential side effects. The roles of vitamins K and C, rutin, aprotinin, and conjugated estrogens are summarized.
This document discusses different classes of antithrombotic drugs including anticoagulants, antiplatelet drugs, and fibrinolytic drugs. It describes the major classes of anticoagulant drugs which include unfractionated heparin, low molecular weight heparins, fondaparinux, direct thrombin inhibitors, and factor Xa inhibitors. It discusses their mechanisms of action, therapeutic indications, pharmacokinetics, side effects and how to treat bleeding caused by different anticoagulants.
This document summarizes the toxicity of oral anticoagulants and related drugs. It discusses how oral anticoagulants like warfarin work by inhibiting vitamin K, which is necessary for blood clotting. It outlines the narrow therapeutic window and need for monitoring with drugs like warfarin. It describes potential toxic effects like bleeding, skin necrosis, and birth defects if taken during pregnancy. Treatment involves investigating coagulation factors, stabilizing the patient, giving vitamin K as an antidote, and supporting bleeding patients with blood products or fresh frozen plasma.
This document discusses drugs used to treat disorders of blood clotting and bleeding. It describes three classes of anticoagulant drugs that reduce clotting: oral anticoagulants like warfarin that inhibit vitamin K-dependent clotting factors; injectable anticoagulants like heparin and hirudin that inhibit thrombin; and antiplatelet drugs like aspirin and clopidogrel that decrease platelet aggregation. It also discusses fibrinolytic drugs like tissue plasminogen activator that dissolve blood clots, and hematopoietic drugs used to treat anemia, such as iron supplements, folic acid, and vitamin B12.
This document discusses bleeding and thrombotic disorders. It provides information on hemostasis, mechanisms of bleeding, key aspects of diagnosis such as history and clinical characteristics. It covers laboratory testing including platelet count, bleeding time, platelet function assay, prothrombin time, activated partial thromboplastin time, thrombin time and tests for fibrinolysis. It also discusses hereditary and acquired causes of bleeding disorders and provides details on specific conditions like hemophilia, von Willebrand disease and treatments.
Hemophilia is a bleeding disorder caused by deficiencies in clotting factors VIII or IX. It can range from mild to severe depending on factor levels. The knees, elbows, and ankles are most prone to recurrent bleeding in joints (hemarthrosis) leading to hemophilic arthropathy. Treatment involves replacing the missing clotting factor, though some develop inhibitors requiring bypassing agents. For mild cases, desmopressin can stimulate factor release instead of replacement. Surgery and radiation synovectomy may help joints with persistent bleeding. Von Willebrand disease also involves a platelet dysfunction protein.
This seminar includes hemostasis,mechanism of blood clotting and associated blood dyscrasias commonly seen in children and their treatments with a note on antifibrinolytics
The document provides an overview of anticoagulants and their clinical use. It discusses hemostasis and the mechanisms of coagulation. It then classifies anticoagulants as oral, parenteral or antiplatelets. The document focuses on warfarin and heparin, describing their mechanisms of action, dosing, and perioperative management considerations for patients receiving these anticoagulants. It emphasizes balancing the risks of bleeding and thromboembolism during the perioperative period.
This document provides information about haemophilia. It begins with an introduction defining haemophilia as a genetic bleeding disorder caused by deficiencies in coagulation factors VIII or IX. It then discusses the causes, clinical manifestations, diagnostic evaluation, and management of haemophilia. For diagnostic evaluation, it describes tests such as CBC, platelet function tests, and chromogenic assays. For management, it outlines replacing the deficient coagulation factor medically as well as nursing care involving pain management and injury prevention. The document concludes with a practice quiz on haemophilia.
Tranexamic acid is an antifibrinolytic drug that inhibits fibrinolysis by reversibly binding to plasminogen. It is effective at reducing surgical bleeding across many procedures like cardiac, orthopedic, and cranial surgery. It also reduces bleeding in gynecological conditions like heavy menstrual bleeding and postpartum hemorrhage. Tranexamic acid is generally well tolerated with side effects including headache, nausea, and diarrhea. It is given orally, intravenously, or topically depending on the condition being treated.
This would give an idea of the various bleeding disorders, associated clotting factors and more specifically management in the dental office of the patients with bleeding disorders
- The document discusses anticoagulation and blood clotting. It describes how blood clots form and are broken down, as well as drugs that can regulate clotting such as heparin, warfarin, and dicoumarol. It provides details on the coagulation factors, classes of anticoagulant drugs, the blood clotting process, and coagulation disorders.
The document discusses drugs used in coagulation disorders and bleeding. It describes two major groups of drugs - those that decrease clotting like anticoagulants and thrombolytics, and those that increase clotting for deficiencies. Anticoagulants discussed include heparins, warfarin, and direct thrombin/factor Xa inhibitors. Antiplatelets to inhibit platelet aggregation are also covered. Drugs to arrest bleeding include local haemostatics applied topically and systemic agents like vitamin K and antifibrinolytics. Key points for dentists on managing patients taking these drugs emphasize safer options and monitoring coagulation levels before procedures.
Oral consideration and laboratory investigations of bleeding and clotting dis...kashmira483
This document provides information on bleeding and clotting disorders. It discusses the pathophysiology of hemostasis including the vascular, platelet, coagulation, and fibrinolytic phases. It describes different types of bleeding disorders like vessel wall disorders, platelet disorders, and coagulation disorders. Laboratory tests for identifying bleeding disorders are outlined. Oral manifestations and dental considerations for management are summarized. Local hemostatic agents and systemic agents for different bleeding disorders are also mentioned.
The document discusses various coagulation disorders including:
1. Congenital coagulation disorders such as hemophilia A and B which are caused by deficiencies in coagulation factors VIII and IX.
2. Acquired coagulation disorders including disseminated intravascular coagulation (DIC), vitamin K deficiency, liver disease, and antibodies against coagulation factors.
3. The pathogenesis, clinical features, laboratory findings, and treatment of various coagulation disorders are explained.
This document summarizes several coagulation disorders including haemophilia A, haemophilia B, von Willebrand disease, other hereditary coagulation factor deficiencies, and disseminated intravascular coagulation. It describes the clinical features, inheritance, laboratory findings, treatment, and management of each condition. Key points include that haemophilia A is the most common clotting factor deficiency, von Willebrand disease is the most common inherited bleeding disorder, and disseminated intravascular coagulation can be triggered by trauma, infection, cancer and other conditions.
This document summarizes anticoagulants and their uses. It discusses the coagulation cascade and how anticoagulants work to prevent unwanted clotting. Several classes of anticoagulants are covered, including unfractionated and low molecular weight heparins, vitamin K antagonists like warfarin, and direct acting anticoagulants. Indications, dosages, monitoring, and adverse effects are provided for many of the discussed anticoagulants. The document also addresses perioperative management of anticoagulation and treatments for bleeding or over-anticoagulation.
The document discusses anti-coagulants and fibrinolytic drugs. It covers the normal coagulation cascade and hemostasis. It then discusses various anti-coagulant drugs including heparin and low molecular weight heparins, which work by potentiating antithrombin. Oral vitamin K antagonists like warfarin are also covered. Fibrinolytic drugs discussed include tissue plasminogen activator, streptokinase and urokinase, which work by converting plasminogen to plasmin to lyse clots. The risks of bleeding are also summarized for anti-coagulant and fibrinolytic therapies.
Heparin is a powerful anticoagulant that acts indirectly by binding to antithrombin III and inactivating clotting factors. It can be given intravenously or subcutaneously. Heparin is used to treat and prevent conditions involving blood clots such as deep vein thrombosis, pulmonary embolism, and arterial thromboembolism. Adverse effects include bleeding and heparin-induced thrombocytopenia. Warfarin is an oral anticoagulant that works by interfering with vitamin K dependent clotting factor synthesis in the liver. It is used long-term for conditions requiring anticoagulation like atrial fibrillation. Risks include bleeding and fetal harms
Anticoagulants are used to treat and prevent blood clots that may occur in your blood vessels. Blood clots can block blood vessels (an artery or a vein). A blocked artery stops blood and oxygen from getting to a part of your body (for example, to a part of the heart, brain or lungs).
This document provides an overview of hemostasis and drugs that affect coagulation and act as anticoagulants. It describes the coagulation cascade and how tests like aPTT and PT are used to evaluate it. Local hemostatic agents, transfusional agents, and non-transfusional agents are discussed. Specific agents are explained including their sources, uses, dosages, and potential side effects. The roles of vitamins K and C, rutin, aprotinin, and conjugated estrogens are summarized.
This document discusses different classes of antithrombotic drugs including anticoagulants, antiplatelet drugs, and fibrinolytic drugs. It describes the major classes of anticoagulant drugs which include unfractionated heparin, low molecular weight heparins, fondaparinux, direct thrombin inhibitors, and factor Xa inhibitors. It discusses their mechanisms of action, therapeutic indications, pharmacokinetics, side effects and how to treat bleeding caused by different anticoagulants.
This document summarizes the toxicity of oral anticoagulants and related drugs. It discusses how oral anticoagulants like warfarin work by inhibiting vitamin K, which is necessary for blood clotting. It outlines the narrow therapeutic window and need for monitoring with drugs like warfarin. It describes potential toxic effects like bleeding, skin necrosis, and birth defects if taken during pregnancy. Treatment involves investigating coagulation factors, stabilizing the patient, giving vitamin K as an antidote, and supporting bleeding patients with blood products or fresh frozen plasma.
This document discusses drugs used to treat disorders of blood clotting and bleeding. It describes three classes of anticoagulant drugs that reduce clotting: oral anticoagulants like warfarin that inhibit vitamin K-dependent clotting factors; injectable anticoagulants like heparin and hirudin that inhibit thrombin; and antiplatelet drugs like aspirin and clopidogrel that decrease platelet aggregation. It also discusses fibrinolytic drugs like tissue plasminogen activator that dissolve blood clots, and hematopoietic drugs used to treat anemia, such as iron supplements, folic acid, and vitamin B12.
This document discusses bleeding and thrombotic disorders. It provides information on hemostasis, mechanisms of bleeding, key aspects of diagnosis such as history and clinical characteristics. It covers laboratory testing including platelet count, bleeding time, platelet function assay, prothrombin time, activated partial thromboplastin time, thrombin time and tests for fibrinolysis. It also discusses hereditary and acquired causes of bleeding disorders and provides details on specific conditions like hemophilia, von Willebrand disease and treatments.
Hemophilia is a bleeding disorder caused by deficiencies in clotting factors VIII or IX. It can range from mild to severe depending on factor levels. The knees, elbows, and ankles are most prone to recurrent bleeding in joints (hemarthrosis) leading to hemophilic arthropathy. Treatment involves replacing the missing clotting factor, though some develop inhibitors requiring bypassing agents. For mild cases, desmopressin can stimulate factor release instead of replacement. Surgery and radiation synovectomy may help joints with persistent bleeding. Von Willebrand disease also involves a platelet dysfunction protein.
This seminar includes hemostasis,mechanism of blood clotting and associated blood dyscrasias commonly seen in children and their treatments with a note on antifibrinolytics
The document provides an overview of anticoagulants and their clinical use. It discusses hemostasis and the mechanisms of coagulation. It then classifies anticoagulants as oral, parenteral or antiplatelets. The document focuses on warfarin and heparin, describing their mechanisms of action, dosing, and perioperative management considerations for patients receiving these anticoagulants. It emphasizes balancing the risks of bleeding and thromboembolism during the perioperative period.
This document provides information about haemophilia. It begins with an introduction defining haemophilia as a genetic bleeding disorder caused by deficiencies in coagulation factors VIII or IX. It then discusses the causes, clinical manifestations, diagnostic evaluation, and management of haemophilia. For diagnostic evaluation, it describes tests such as CBC, platelet function tests, and chromogenic assays. For management, it outlines replacing the deficient coagulation factor medically as well as nursing care involving pain management and injury prevention. The document concludes with a practice quiz on haemophilia.
Tranexamic acid is an antifibrinolytic drug that inhibits fibrinolysis by reversibly binding to plasminogen. It is effective at reducing surgical bleeding across many procedures like cardiac, orthopedic, and cranial surgery. It also reduces bleeding in gynecological conditions like heavy menstrual bleeding and postpartum hemorrhage. Tranexamic acid is generally well tolerated with side effects including headache, nausea, and diarrhea. It is given orally, intravenously, or topically depending on the condition being treated.
Similar to Hematoligical System Pharmacology.pptx (20)
GLAUCOMA of human eye for certificate nursesokumuatanas1
This document provides information about glaucoma, including:
1. Glaucoma is a group of eye conditions marked by increased pressure in the eye that can damage the optic nerve and lead to vision loss.
2. The two main types are open-angle glaucoma, the most common type caused by blocked drainage canals, and angle-closure glaucoma caused by a narrowed drainage angle.
3. Risk factors include age over 40, family history, and other medical conditions. Treatment involves medications, laser treatments, or surgeries to lower pressure and improve drainage in the eye.
Trachoma of human eye for certificate nursesokumuatanas1
Trachoma is a contagious eye disease caused by the bacterium Chlamydia trachomatis that can lead to blindness. It spreads through direct contact with eye or nose secretions from infected individuals or indirect contact via fomites. Repeated infections cause scarring of the inner eyelid and distortion of the eyelashes which can scrape the cornea. The SAFE strategy aims to eliminate trachoma through surgery, antibiotics, facial cleanliness, and environmental improvements.
CONJUCTIVITIS of the human eye for certificate nursesokumuatanas1
The conjunctiva is the thin membrane that lines the eyelids and covers the white part of the eye. Conjunctivitis is inflammation of the conjunctiva that can be caused by allergens, irritants, viruses, bacteria, fungi, trauma, or neoplasms. Common symptoms include eye redness, discharge, itching, and tearing. Diagnosis is usually based on symptoms and signs. Treatment depends on the underlying cause but may include antibiotics, antivirals, or anti-allergens.
CATARACTS NEW of the human eye and its management.okumuatanas1
A corneal ulcer is an open sore on the cornea caused by a break in the corneal epithelium that allows bacteria or other pathogens to enter. Common causes include bacterial or viral infections, especially in contact lens wearers, or due to eye injuries or dry eyes. Symptoms include eye redness, pain, blurred vision, and photophobia. Diagnosis involves fluorescein dye staining and tissue biopsy. Treatment consists of antibiotic, antifungal or antiviral eye drops depending on the cause, along with pain medications and eye patching. Complications can include vision loss if left untreated.
Qualitative and Quantitative Research Approaches.pptxokumuatanas1
Qualitative and quantitative research approaches are the two main paradigms used in nursing research. Qualitative research explores phenomena through interviews and observations to understand experiences, while quantitative research tests hypotheses through statistical analysis of numerical data to quantify relationships. Mixed methods research incorporates both approaches. The choice of approach depends on the research question and objectives. Both help nurses determine best practices for patient care.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
3. Hemophilia A
• Hemophilia A is an X-linked, recessive disorder caused by deficiency
of functional plasma clotting factor VIII (FVIII), which may be inherited
or arise from spontaneous mutation.
• The development of inhibitory alloantibodies to FVIII can severely
complicate the treatment of genetic cases.
• Rarely, development of autoantibodies to FVIII results in acquired
hemophilia A.
4. Management
• Management of hemostasis
• Management of bleeding episodes including hemostatic support and
pain mangagement
• Use of factor replacement products and adjuvant medications
• Treatment of patients with factor inhibitors
• Treatment and rehabilitation of patients with hemophilia synovitis
5. Pharmacotherapy
• FVIII concentrates
• Desmopressin vasopressin analog, or 1-deamino-8-D-arginine
vasopressin (DDAVP). Not effective in the treatment of severe
hemophilia. Given by intravenously. Peak effect is observed in 30-60
minutes. DDAVP leads to free water retention, which can lead to
hyponatremia. A concentrated DDAVP intranasal spray is available for
outpatient use.
• Antifibrinolytics used for oral mucosal hemorrhage and prophylaxis.
Examples Epsilon aminocaproic acid and Tranexamic acid
6. Pharmacotherapy cont.
Treatments used in patients with inhibitors of FVII
• High doses of FVIII for low-titer inhibitors
• Activated prothrombin complex concentrate (aPCC)Activated
recombinant FVII (rFVIIa)
• Monoclonal antibodies directed toward restoring FVIII function (eg,
emicizumab, rituximab)
• Porcine FVIII, which has low cross-reactivity with human FVIII
antibody
7. Hemophilia B
• Hemophilia B, or Christmas disease, is an inherited, recessive disorder
that involves deficiency of functional coagulation factor IX (FIX) in
plasma.
• Hemophilia B is caused by a variety of defects in the F9 gene.[1]As
this gene is carried on the X chromosome, the disease usually
manifests in males and is transmitted by females who carry the
causative mutation on one of their X chromosomes.
8. Management
• Control of hemostasis
• Treatment of bleeding episodes
• Administration of factor replacement products and medications
• Use of factor inhibitors
• Rehabilitation of patients with hemophilia synovitis
• Primary and/or secondary prophylaxis
9. Pharmacotherapy
• Factor IX-containing products (eg, factor IX, recombinant factor IX, factor
IX complex).
• Recombinant coagulation factor VIIa
• Recombinant coagulation factor IX
• Antifibrinolytics (eg, epsilon aminocaproic acid, tranexamic acid)
• Antihemophilic agents (eg, desmopressin, anti-inhibitor coagulant
complex, human antihemophilic factor, recombinant human antihemophilic
factor, plasma-derived prothrombin complex concentrates/factor IX
complex concentrates, plasma-derived coagulation factor IX concentrate)
• Monoclonal antibodies (eg, rituximab)
• Analgesics (eg, narcotic agents, NSAIDS, acetaminophen with codeine or
synthetic codeine analogs)
• Gene therapy (ie, etranacogene dezaparvovec [Hemgenix])
10. Hemophilia c
• deficiency of factor XI
• ometimes called Rosenthal syndrome
• Unlike the bleeding tendency in hemophilia A or hemophilia B,
which is clearly related to the factor level, some patients with
severe deficiency of factor XI do not have a bleeding tendency.
• On the other hand, some patients with mild deficiency of factor
XI bleed excessively, and this unpredictability, which is not fully
understood, makes hemophilia C more difficult to manage
11. Management of hemophilia C
• In patients with hemophilia C undergoing a surgical procedure,
replacement with plasma products may be needed in the preoperative,
intraoperative, and postoperative periods, depending on the procedure,
the patient's history with other surgical procedures, and the person's
bleeding tendency, if any.
• antifibrinolytics;
• fresh-frozen plasma (FFP),
• ideally pathogen-inactivated (eg, solvent-detergent treated FFP);
• factor XI concentrates.
• Adjunctive measures include the use of fibrin glue and desmopressin
(DDAVP)
12. Acquired hemophilia
• Acquired hemophilia is a rare but potentially life-threatening
bleeding disorder caused by the development of autoantibodies
(inhibitors) directed against plasma coagulation factors, most
frequently factor VIII (FVIII).
13. Management
• Treatment of the underlying disorder or discontinuation of an
offending drug
• Recombinant FVIII porcine sequence (rpFVIII), if the baseline anti-
porcine FVIII inhibitor titer is ≤ 20 BU; recombinant activated factor
VII (rFVIIa); or activated prothrombin complex concentrate (APCC).
• Human FVIII concentrates may be used to control bleeding
• Hemostatic prophylaxis can be with rpFVIII, rFVIIa, APCC, or
emicizumab
• Eradication of the inhibitor with immunosuppression with
corticosteroids alone (first line) or combined with rituximab or
cyclophosphamide.
• Salvage therapy with cyclosporine is particularly effective in patients
with underlying systemic lupus erythematosus.
15. Antihemophilic factor recombinant (Advate,
Adynovate, Afstyla, Eloctate, Helixate FS, Jivi,
Kogenate FS, Kovaltry, NovoEight, Nuwiq, Obizur,
Recombinate, Xyntha)
• Mechanism of Action
• Temporarily replaces missing clotting factor VIII which corrects
&/or prevents bleeding
• Adverse Effects
• Factor VIII inhibitor disorder (31.7%)
• Pyrexia (5.9%)
• Nausea (1-4.4%)
• Dizziness (3.5%)
• Headache (3.5%)
• Taste disorder (2.7%)
• Contraindications
• Hypersensitivity to mouse or hamster protein
16. Factor VIII, human plasma derived
(Monoclate-P, Hemofil M, Koate DVI)
• Mechanism of Action
• Factor VIII derived from pooled human
plasma, temporarily replaces missing clotting
factor VIII which corrects and/or prevents
bleeding in patients with hemophilia A
• Adverse Effects
• Headache, Somnolence, Lethargy, Fever,
Blurred vision
• Contraindications
• Hypersensitivity
17. Anti-inhibitor coagulant complex (Feiba NF,
Feiba VH Immuno)
• Mechanism of Action
• Provides activated blood coagulation factors II,
VII, IX and X from pooled human plasma
• May shorten the activated partial
thromboplastin time of plasma containing
factor VIII inhibitors
• Adverse Effects: Headache, Lethargy,
Nausea, Chest discomfort, Chills, Rash,
Urticaria
• Contraindications
• Treatment of bleeding occurrences resulting
from deficiencies in coagulation factors VIII or
IX
18. Antihemophilic factor/von Willebrand
factor complex (Alphanate, Humate P,
Wilate)
• Mechanism of Action
• Temporarily increases the plasma level of FVIII, thus
minimizing the hazard of hemorrhage in patients with
hemophilia A; FVIII is an essential cofactor in
activation of factor X leading to formation of thrombin
and fibrin
• VWF promotes platelet aggregation and platelet
adhesion on damaged vascular endothelium; it also
serves as a stabilizing carrier protein for the
procoagulant protein FVIII
• Adverse Effects: Pain, Respiratory distress, Pruritus,
Rash, Urticaria, Face edema, Paresthesia, Pain.
• Contraindications: Hypersensitivity
19. Factor VIIa, recombinant (NovoSeven
RT)
• Recombinant activated factor VII (rFVIIa) is
indicated to treat bleeding episodes in patients with
hemophilia A or B and inhibitors.
• It promotes hemostasis by activating the extrinsic
pathway of the coagulation cascade, forming
complexes with tissue factor, and promoting
activation of FX to factor Xa, FIX to factor IXa, and
factor II (FII) to factor IIa. rFVIIa is indicated for
treatment of bleeding episodes and for prevention
of bleeding in surgical interventions or invasive
procedures in patients with acquired hemophilia.
20. Fresh frozen plasma
Mechanism of Action
• Each unit provides all plasma proteins and clotting factors to
support adequate hemostasis to treat or prevent bleeding or to
treat other protein deficiencies that cannot be replaced with
protein specific concentrates.
Adverse Effects
• Nervous system: Headache, paresthesia
• Gastrointestinal: Nausea
• Skin and subcutaneous tissue disorders: Pruritus, urticaria
Contraindications
• IgA deficiency
• Severe protein S deficiency
• History of hypersensitivity to FFPs or Octaplas
21. Human coagulation factor Xl
• Factor XI concentrates provide the best source
for factor XI replacement.
• Advantages of factor XI concentrates include
selective delivery of the deficient factor, a
reduced volume of infusion, and viral safety.
• Issuess: Hemoleven (LFB) and factor XI
concentrate (BPL), are activation of the
coagulation system and some thrombotic
events, especially in patients with preexisting
vascular disease.
22. Fibrin sealant (Tisseel, Artiss, Evicel)
Mechanism of Action
• Forms fibrin clot from fibrinogen to achieve hemostasis
• fibrinogen (sealer protein) as the main active ingredient and fibrinolysis inhibitor
(aprotinin)
• Used in dental extractions without blood product replacement.
Contraindications
• Hypersensitivity to product or other components
• Massive or brisk arterial bleeding
• Intravascular use - risk of life-threatening thromboembolic events
• Do not spray product where the minimum recommended distance from the applicator
tip to the target site cannot be assured
Administration
• The glue is applied with a pair of syringes, one containing calcium and thrombin and
one containing fibrinogen, factor XIII, and aprotinin.
23. Aminocaproic acid (Amicar)
MOA: Inhibits fibrinolysis through inhibition of plasminogen binding to
fibrin and subsequent conversion to plasmin, which in turn inhibits
fibrinolysis
• Exhibits antiplasmin activity
• Adverse Effects: Confusion, Vision decrease, Vomiting, Headache,
Convulsions, Malaise,etc
Contraindications
• In presence of DIC without concomitant heparin
• Evidence of active intravascular clotting process
IV Administration
• Initial 5 g in 250 mL over 1 hr, each subsequent gram in 50-100 mL at 1
g/hr
• Rapid injection undiluted into a vein is not recommended
• Continue for about 8 hr or until bleeding has been controlled
24. Tranexamic acid (Cyklokapron, Lysteda)
• Mechanism of Action
• Inhibits fibrinolysis by displacing plasminogen from fibrin
• Reduces plasmin activity, which in turn reduces activation of
complement and consumption of C1 esterase inhibitor (C1-
NH) and subsequently decreases inflammation associated
with hereditary angioedema
• Adverse Effects
• Visual abnormalities, Hypotension (with rapid injection)
• Nausea, Vomiting, Diarrhea, Anaphylaxis
• Contraindications
• Hypersensitivity, Acquired defective color vision
• Subarachnoid hemorrhage, Active intravascular clotting
25. Desmopressin (DDAVP, Stimate)
• Increase in von Willebrand factor VIII
and t-PA levels; this shortens activated
partial thromboplastin time (aPTT), as
well as bleeding time.
• Adverse Effects: Dry mouth,
Headache, Hyponatremia, Dizziness.
• Contraindications: Hypersensitivity,
Hyponatremia or history of
hyponatremia, Moderate to severe
renal impairment (CrCl <50 mL/min).
26. Anti-inhibitor coagulant complex (Feiba
VH)
• Mechanism of Action
• Provides activated blood coagulation factors II, VII, IX
and X from pooled human plasma
• May shorten the activated partial thromboplastin time
of plasma containing factor VIII inhibitors
• Adverse Effects: Headache, Lethargy, Nausea, Chest
discomfort, Chills, Rash
• Contraindications
• Treatment of bleeding occurrences resulting from
deficiencies in coagulation factors VIII or IX
• DIC
• Normal coagulation mechanisms present
27. Factor IX, recombinant (BeneFIX,
Rixubis, Alprolix, Ixinity, Rebinyn)
Mechanism of Action
• Temporarily replaces missing clotting factor IX which corrects and/or
prevents bleeding.
Adverse Effects
• Headache (10.8%)
• Dizziness (7.7%)
• Injection site reaction (7.7%)
• Injection site pain (6.2%)
• Nausea (6.2%)
• Rash (6.2%)
• Taste perversion
Contraindications
Hypersensitivity to product or its
excipients including hamster protein
Disseminated intravascular coagulation
(DIC)
Signs of fibrinolysis
28. Prednisolone
• Mechanism of Action
• Glucocorticosteroid; elicits mild mineralocorticoid
activity and moderate anti-inflammatory effects;
controls or prevents inflammation by controlling rate of
protein synthesis, suppressing migration of
polymorphonuclear leukocytes (PMNs) and
fibroblasts, reversing capillary permeability, and
stabilizing lysosomes at cellular level
• Adverse Effects: Acne, Adrenal suppression,
Delayed wound healing, Diabetes mellitus, GI
perforation, Glucose intolerance.
• Contraindications: Documented hypersensitivity,
Systemic fungal infection, varicella, superficial herpes
simplex keratitis, Receipt of live or attenuated live
vaccine
29. Cyclophosphamide (Neosar, Cytoxan)
• Mechanism of Action
• Metabolites interfere with malignant cell growth by cross-
linking tumor cell DNA; drug does not have specificity for
any phase of the cell cycle; also has potent
immunosuppressive activity
• Adverse Effects: NVD, Hemorrhagic colitis, Oral mucosal
ulceration, Jaundice, Alopecia, Skin rash
• Contraindications
• Severe myelosuppression
• Hypersensitivity
• Urinary outflow obstruction
31. Emicizumab (Hemlibra, emicizumab-
kxwh)
• Mechanism of Action
• Bispecific factor IXa- and factor X-directed antibody
that bridges activated factor IX and factor X in order to
restore the function of missing activated factor VIII
necessary for effective hemostasis
• Adverse Effects
• Injection site reaction (22%)
• Headache (15%)
• Arthralgia (15%)
• Injection site erythema (11%)
• Contraindications: None
32. Rituximab (Rituxan)
• Mechanism of Action
• Humanized monoclonal antibody, binds to CD20
antigen on surface of normal and malignant B
lymphocytes, inducing complement- or antibody-
mediated cytolysis. This results in reduced
autoantibody production.
• Adverse Effects
• Angioedema (11%)
• Asthenia (26%), chills (33%), dizziness (10%), fever
(53%), headache (19%)
• Pruritus (14%), rash (15%)
• Abdominal pain (14%), diarrhea (10%), nausea
(23%), vomiting (10%)
• Contraindications: None
Editor's Notes
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Antihemophilic Factor (FVIII) and von Willebrand Factor (VWF) are constituents of normal plasma, which are required for clotting
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This is the product of choice when factor XI concentrates are not available. FFP is easily available. It can be infused over a short period. Disadvantages include large infusion volumes to achieve appropriate control of bleeding, a potential for transmitting infective agents, and the possibility of allergic reactions.