Resusitasi cairan dan elektrolit membahas tentang resusitasi cairan pada pasien perdarahan akut dan dehidrasi, termasuk pilihan cairan, algoritme resusitasi, dan penilaian status volume darah."
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
Resusitasi cairan dan elektrolit membahas tentang resusitasi cairan pada pasien perdarahan akut dan dehidrasi, termasuk pilihan cairan, algoritme resusitasi, dan penilaian status volume darah."
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
Este documento define y describe varios tipos de software malicioso como virus, troyanos, spyware y phishing, así como programas de seguridad como antivirus, cortafuegos y anti spyware diseñados para proteger las computadoras de este software dañino.
AZEE Securities is a securities company founded in 2003 that is headed by CEO Amir Zia. The company aims to be a trendsetter in the stock market through its trading platform and services. Contact information is provided for the company website, email, cell phone, and Twitter handle.
This document is the second edition of the book "Indian Foods: AAPI’s Guide to Nutrition, Health & Diabetes" edited by Ranjita Misra. It contains 20 chapters contributed by various authors on topics related to the epidemiology, risks, and complications of diabetes; preventing heart disease; regional Indian cuisines; low fat cooking; choosing healthy snacks; desserts; managing menus in Indian restaurants; carbohydrate counting; weight management; exchange lists; the role of Indian spices in health; and managing diabetes through diet. The book is intended to help Asian Indians, especially Indian Americans, better manage and prevent conditions like diabetes, hypertension, obesity, and hyperlipidemia.
Teoria de las relaciones internacionalesRosa Suarez
Este documento define las relaciones internacionales como el conjunto de transacciones que cruzan fronteras entre Estados u organizaciones. Explica que tradicionalmente se consideraban como relaciones entre Estados pero que también incluyen iniciativas privadas. Brevemente describe los orígenes de los estudios de relaciones internacionales desde la antigüedad hasta la Primera Guerra Mundial, enfocándose en autores como Maquiavelo y enfoques como el equilibrio de poder. Finalmente, contrasta las escuelas clásicas del utopismo/idealismo, que enfatiza cómo
The document summarizes responses from qualitative questionnaires about festivals. It discusses what festivals people have attended, how they view festivals in terms of entertainment, atmosphere and social aspects, examples of specific festivals named, reasons festivals are important, and things people would like to see at festivals. Common responses indicated Notting Hill Carnival and food as attractions, and that festivals are seen as fun occasions that bring people together.
Diez imágenes para reconocer y comentar desde la Prehistoria hasta Bizancio. Es el segundo juego de los ejercicios preparatorios para el examen de la primera evaluación, curso 2011-12.
Objective: Design projects to seek balance between technical and administrative aspects.
Implement a sub-basin approach.
Avoid decisions based on achieving a quick fix.
Be focused but also flexible.
Use environmental projects as a starting point for cooperation on other issues.
Design projects to actively involve countries.
Consider the full impacts of the project, including poverty alleviation.
This patient with newly diagnosed myeloma presented with a large gluteal hematoma one week following a bone marrow biopsy. Initial workup found decreased factor XIII antigen and activity levels. Further testing showed evidence of amyloid deposits on fat pad biopsy and cardiac MRI consistent with amyloidosis, which can cause acquired bleeding disorders through effects on coagulation factors and platelets. The differential diagnosis includes evaluating for qualitative or quantitative platelet disorders, coagulation factor deficiencies, and structural causes of bleeding in the setting of a paraproteinemia like myeloma.
Coag testing for hema fellows mskcc 10 15 2015 dr peerschkederosaMSKCC
1) Coagulation screening tests such as PT, APTT, fibrinogen and thrombin time are used to identify underlying coagulation defects, monitor anticoagulation therapy, and evaluate for disorders involving coagulation and fibrinolysis.
2) Prolonged screening test results require follow up with mixing studies and specific factor assays to determine if the cause is a factor deficiency, inhibitor, or circulating anticoagulant.
3) Lupus anticoagulant testing involves two assays based on different principles, such as a dilute Russell's viper venom time and a sensitive activated partial thromboplastin time, to diagnose the presence of antibodies against phospholipids.
Hemophilia fellow talk2015 dr parameswaranderosaMSKCC
This document provides an overview of hemophilia, including its history, genetics, clinical presentation, complications, treatment, and future directions. It discusses the case of Alexis Nicolaievich, the hemophilic heir to the Russian throne in 1904. It then reviews factor replacement therapy, prophylaxis, complications like inhibitors, and emerging therapies like gene therapy. The document is intended to define hemophilia, review its treatment over time from 1904 to the present, and discuss ongoing research directions.
Drug induced hemolytic anemia cc 10 8-15 - dr mehta-shahderosaMSKCC
A 59-year-old woman presented with new-onset jaundice and anemia 10 days after undergoing surgery for uterine cancer. Laboratory workup found evidence of hemolysis including a positive direct Coombs test. Further testing revealed the patient's red blood cells were sensitizied to the antibiotic cefotetan, indicating drug-induced immune hemolytic anemia. She was treated with transfusions and the hemolysis resolved after discontinuing the offending drug. Drug-induced immune hemolytic anemia is a rare but serious complication that can be triggered by certain antibiotics like cefotetan through non-immune or immune mediated mechanisms.
This patient case involves a 56-year-old man with a history of JAK2 V617F+ essential thrombocythemia who developed severe anemia and was found to have myelodysplastic syndrome/myelofibrosis. He presented with transfusion-dependent anemia and was found to have concurrent warm autoantibody-mediated hemolytic anemia and delayed hemolytic transfusion reaction due to alloimmunization to the Kell blood group antigen. He required intensive care for management of his conditions.
This document discusses work-life balance, burnout, and wellness among physicians. It begins by defining key terms like burnout, work-life balance, and wellness. It then discusses the high prevalence of burnout and work-life dissatisfaction among physicians compared to the general population. Some consequences of physician distress include medical errors, poorer patient outcomes, and reduced workforce. The document considers tensions between a culture that values productivity and the need for self-care. It provides strategies for building resilience through stress management, prioritizing wellness, developing social support, and creating a culture that supports physician well-being.
This document provides guidance on the management of acute gastrointestinal bleeding. It discusses:
1) Performing a thorough history and physical exam to assess bleeding severity, risk factors, and stability. Guaiac testing has limited utility for inpatients.
2) Initial stabilization including IV access, fluid resuscitation, PPI administration, and consideration of ICU care for unstable patients.
3) Etiologies of upper and lower GI bleeding and their typical clinical presentations. Endoscopic therapies are usually first-line but angiography or surgery may be needed for active or refractory bleeding.
This document provides guidance on evaluating a patient presenting with anemia. It recommends:
1. Calculating the reticulocyte index to determine if the cause is blood loss, red blood cell destruction, or impaired red blood cell production.
2. If production is impaired, check the mean corpuscular volume to identify microcytic, macrocytic, or normocytic anemia.
3. Order targeted labs depending on the mean corpuscular volume to identify causes like iron deficiency anemia, vitamin B12 or folate deficiency, or bone marrow disorders.
This document provides an overview of abnormal liver function tests (LFTs), biliary tract disease, and ascites. It discusses the common causes and patterns of abnormal LFTs, including hepatocellular and cholestatic patterns. Specific diseases that can cause these patterns like acute viral hepatitis, autoimmune hepatitis, and primary biliary cholangitis are outlined. Procedures for evaluating biliary tract disease like ultrasound, MRCP, and ERCP are mentioned. The document also reviews when and how to perform paracentesis for ascites, how to analyze the fluid for spontaneous bacterial peritonitis, and guidelines for albumin replacement after large volume paracentesis.
This document provides guidance on evaluating abdominal pain and summarizes 7 clinical cases presenting with abdominal pain. It outlines an approach to the initial assessment of abdominal pain, including differentiating between serious or surgical causes versus non-surgical causes and priorities for pain control. It also reviews high-risk features of abdominal pain and provides a template for the history, physical exam, differential diagnosis, appropriate labs and imaging to evaluate abdominal pain. The 7 cases serve as examples to demonstrate the application of this approach.
This document provides an overview of immunotherapy and how it works to treat cancer. It discusses the roles of T cells, antigen presenting cells, and cytokines in the immune response. It describes how tumors evade immune surveillance and strategies used in immunotherapy to overcome tumor resistance, such as blocking inhibitory receptors like CTLA-4 and PD-1 to reactivate T cells. Several studies are summarized that show improved survival outcomes for cancers like melanoma when treated with immunotherapies like nivolumab compared to chemotherapy. Combination approaches blocking multiple pathways are also discussed.
This document provides an overview of immunotherapy and how it works to treat cancer. It discusses the different types of T cells like CD4+ helper T cells and CD8+ cytotoxic T cells. It describes antigen presenting cells and their role in activating T cells. It explains how tumors evade immune surveillance and the factors that allow this. It discusses different immunotherapy approaches like blocking the CTLA-4 and PD-1 pathways with drugs like ipilimumab and nivolumab. Clinical trial results are summarized that show improved survival with these immunotherapies compared to chemotherapy in cancers like melanoma. Combination approaches are also discussed.
A 69-year-old man with metastatic pancreatic cancer presented with coagulopathy, hypotension, and melena. He had been receiving enoxaparin for DVT but now had markedly elevated PT and aPTT due to accumulation of enoxaparin from renal impairment, vitamin K deficiency from poor nutrition, and possible DIC. Hematology recommended administering protamine to reverse the effects of enoxaparin, 4-factor prothrombin complex concentrate to correct the coagulopathy, and continued vitamin K to address the deficiency. The patient's coagulopathy improved after these interventions but his renal function did not.
This document discusses the treatment of anemia and the need for red blood cell substitutes. It begins by outlining the reasons to treat anemia and discusses the mortality risk of anemia versus the morbidity of red blood cell transfusions. Current possibilities for red blood cell substitutes are then summarized, including hemoglobin-based oxygen carriers (HBOCs) such as Hemopure, Polyheme, and Sanguinate. Toxicities of HBOCs like vasoconstriction and nitric oxide depletion are also noted. The document concludes by discussing protocols for managing severe anemia in the interim before fully developed red blood cell substitutes, and the potential of in vitro production of red blood cells as a future option.
This document discusses three cases of von Willebrand disease (VWD) and provides details on evaluating and diagnosing the condition.
Case 1 is an 18-year-old woman with easy bruising and heavy menses, who has type 1 VWD. Case 2 is a 32-year-old pregnant woman with a family history of bleeding, who has type IIN (VWD Normandy). Case 3 is a 55-year-old woman with life-long severe bleeding who has type 3 VWD.
The document then provides in-depth information on VWD classification, laboratory evaluation, clinical presentation, treatment options including DDAVP and Humate-P, and modifiers like blood type and comor
This document provides an overview of evaluating and managing chest pain. It discusses the many potential causes of chest pain including cardiac, pulmonary, gastrointestinal and psychiatric conditions. Key points include that up to 30% of cardiac catheterizations for suspected coronary artery disease are negative. The diagnostic workup involves considering the patient's history, symptoms, physical exam, ECG, cardiac biomarkers, imaging and ruling out life-threatening causes like aortic dissection and pulmonary embolism. For suspected acute coronary syndrome, treatment involves antiplatelet agents, anticoagulants, nitroglycerin, beta-blockers, oxygen and considering cardiac catheterization if within 90 minutes of symptoms.
1. Neutropenic fever and tumor lysis syndrome are hematologic oncologic emergencies that require prompt assessment and treatment to prevent complications and death.
2. Patients at high risk for complications from neutropenic fever should receive inpatient empiric antibiotics targeting pseudomonas such as an antipseudomonal beta-lactam with vancomycin.
3. For persistent fevers, the treatment regimen should be modified based on cultures and the patient should be reassessed for new infections, including invasive fungal infections if fevers persist for more than 4 days. Catheter-related bloodstream infections also require prompt management.
Empiric antibiotic management for major infectionsderosaMSKCC
This document provides guidance from an infectious diseases physician on various infectious disease topics. It addresses appropriate workups, empiric antibiotic choices, and treatment durations for common infections seen at MSKCC including bloodstream infections, pneumonia, intra-abdominal infections, C. difficile colitis, skin and soft tissue infections, and febrile neutropenia. Emphasis is placed on obtaining appropriate cultures prior to antibiotics and tailoring treatment based on culture results and patient risk factors.
This document discusses various types and classifications of pneumonia, including community acquired pneumonia (CAP), hospital acquired pneumonia (HAP), healthcare associated pneumonia (HCAP), and ventilator-associated pneumonia (VAP). It then presents four clinical case studies of patients presenting with pneumonia and discusses the likely pathogens involved, appropriate testing, and treatment recommendations for each case. Key considerations included distinguishing between various pneumonia types and selecting initial empiric antibiotic therapy based on likely pathogens and patient risk factors or comorbidities.
27. CCllaassssiiffiiccaattiioonn ooff vvoonn WWiilllleebbrraanndd
DDiisseeaassee
Type Description
1 Partial quantitative deficiency of VWF
2 Qualitative deficiency of VWF
2A
Decreased platelet-dependent VWF function with
selective deficiency of high-molecular-weight
multimers
2B Increased affinity for platelet GPIb
2M
Decreased platelet-dependent VWF function with
high-molecular-weight multimers present
2N Markedly decreased binding of factor VIII to VWF
3 Complete deficiency of VWF
von Willebrand disease (VWD) is a coagulation disorder of the blood. It is considered the most commonly inherited bleeding disorder, manifesting as an increased tendency for spontaneous or trauma-related bleeding in 1%-3% of the general population.1,2 The spectrum of clinical symptom-atology is great, ranging from a very mild bleeding disorder in some persons to a severe disorder similar to hemophilia in others. The disease is caused by the inheritance of a mutated von Willebrand factor (VWF) gene, resulting in a quantitative or qualitative abnormality of VWF, an adhesive glycoprotein involved in both primary and secondary hemostasis.3
Tomogram sections and images showing VWF tubules. (A) Section of tomogram (after 18° rotation of tomogram about an axis along the granule) shows a VWF tubule closely following the membrane and buckling at the granule end. (B) A 100-Å thick projected tomogram section from Body B showing VWF tubules and a microtubule (MT). (C) Structural model for VWF tubules. Tubules running full-length of the granule in yellow (one bending at the granule end is orange), shorter tubules in blue, hinges indicated. (D) VWF tubule from the edge of an irregular WPB recorded at 300 keV in Fig. S4B before and (E) after Fourier filtering to include only the equator and layer lines 1 and 3 in the Fourier transform (F) of the tubule in (D). [Scale bar, 250 Å in (D and E).]
There are 3 general categories of VWD that are characterized by their gene mutations. Type 1 VWD is the most common form – 75%-80% of VWD patients have type 1 disease12 – characterized by relatively normal-appearing VWF expressed in diminished amounts. Generally mild to moderate in severity, type 1 disease is characterized by prolonged bleeding times, proportionately reduced levels of FVIII, VWF:RCo, and VWF:Ag, and functionally and structurally normal VWF. The mutations observed consist mainly of deletions, frameshifts, and nonsense mutations.9 Type 1 VWD can be further subclassified into 3 categories based on the platelet VWF content: a) “platelet normal,” with a normal content of functionally normal VWF; b) “platelet low,” with a low concentration of functionally normal VWF; and c) “platelet discordant,” with normal concentrations of dysfunctional VWF.8 Whether these variations in platelet VWF have clinical relevance in patients with type 1 disease is unclear.
Type 2 mutations are associated with qualitative defects of the protein. The hallmark of the more common type 2 defects is loss of the high and intermediate molecular weight multimers (2A) or loss of only the high molecular weight multimers (2B), which are the most hemostatically effective.3 Type 2 accounts for approximately 15%-21% of all VWD patients. Patients with type 2 disease exhibit mild to severe bleeding symptoms.13-15
Type 2A can be further subclassified based on platelet and plasma VWF discrepancies that reflect either defective intracellular processing or increased sensitivity to proteolysis of the circulating multimer forms.4,8
The type 2B mutation occurs in a region of the gene encoding the binding site to platelet GPIb in exon 28, in the A1 loop of the protein.9 This mutation results in a gain-of-function phenotype characterized by increased binding of VWF to platelet GPIb with subsequent clearing of these large complexes and, oftentimes, accompanying thrombocytopenia.4
Two more recently described subtypes include 2N and 2M. Decreased binding of VWF to FVIII is characteristic of type 2N disease wherein the mutation is located in the binding site of VWF to FVIII.5 The clinical phenotype of 2N disease is that of “autosomal hemophilia” with a disproportionately low FVIII activity level compared with the VWF because of accelerated clearance of FVIII. The prevalence of 2N VWD is not fully characterized because it is often misdiagnosed as mild hemophilia A. Coinheritance of the type 2N allele with type 1 has been noted and may account for some of the clinical variability associated with type 1 disease.9
The type 2M mutation is characterized by decreased functional binding of VWF to GPIb and a normal multimer pattern.5 Laboratory testing for this subtype reveals disproportionately low VWF functional activity compared with antigenic levels.3
Type 3 VWD is rare and is characterized as a severe bleeding disorder. Type 3 VWD is characterized by the virtual absence of VWF protein, both the circulating and stored pools, and low levels of FVIII as a result of increased clearance. Type 3 disease is considered a recessive disorder, although many patients are found to be compound heterozygotes.4 Because these patients’ resulting FVIII levels are generally about 4%, they may experience hemarthroses much like patients with hemophilia.16 Patients with type 3 disease suffer from severe, spontaneous bleeds. Type 3 patients may develop inhibitors to VWF following replacement therapy.9
Because of the variable clinical expression of this disorder, a detailed personal and family history is critical in identifying persons who should be screened for VWD. The prothrombin time (PT), activated partial thromboplastin time (aPTT), and platelet count are routinely performed in patients being evaluated for a bleeding disorder. The aPTT may be prolonged in VWD if the residual FVIII coagulant activity (FVIII:C) is decreased to an appreciable extent (eg, < 30%). A decreased platelet count may be encountered in patients with subtype 2B VWD, but is normal in the other disease types.3
The template bleeding time (BT) has been shown to have a moderately low sensitivity and specificity for screening patients with suspected VWD. This test is also associated with low efficacy for predicting surgical bleeding, is “operator dependent,” and results in cutaneous scarring of the tested individual.3
The condition classically ascribed to VWD is caused by a mutation in the gene that encodes VWF. However, other genetic and nongenetically determined modifiers affect VWF protein levels as well. High estrogen states such as pregnancy and supplemental estrogens increase VWF levels, as does stress (epinephrine), hyperthyroidism, and several other medical conditions.1,9 In contrast, blood type O is associated with 25%-30% lower levels of VWF.10 The “deficiency” of VWF associated with blood type O is not due to a mutation in the VWF gene per se; instead, clearance of the VWF protein may be enhanced in people with this specific blood type.3 Additional modifiers of the VWD clinical phenotype include platelet receptor polymorphisms. VWD patients with high-density expression of the surface platelet receptor for collagen (21) exhibit less platelet dysfunction under high shear conditions than their counterparts who are homozygous for the 807C allele in the 2 gene, which results in lower density collagen receptor expression.11
The mechanism by which DDAVP works is by stimulating the release of VWF from vascular endothelial cells, which is accompanied by an increase in FVIII activity level. Treatment with DDAVP is effective in about 80% of patients with VWD, the majority of whom have type 1 mutations and some with types 2A, 2B (controversial), 2M, and 2N. Patients with a dysfunctional VWF protein will not benefit from the increased level of endogenous VWF achieved by the use of DDAVP. In fact, the bleeding diathesis and thrombocytopenia associated with subtype 2B disease may worsen with this therapy. For patients with severe type 3 VWD deficiency, DDAVP therapy is ineffective.3
DDAVP is indicated for patients with mild to moderate VWD with FVIII levels 5%. DDAVP may be useful for the treatment of bleeding in mild to moderate VWD patients with episodes of spontaneous or trauma-induced injuries such as mucosal bleeding or menorrhagia. DDAVP is contraindicated in individuals with known hypersensitivity to DDAVP.
Patients with mild disease experiencing severe hemorrhaging should receive a loading dose of 40-60 IU VWF:RCo/kg body weight of Humate-P® followed by 40-50 IU VWF:RCo/kg body weight every 8-12 hours for 3 days. Subsequently, 40-50 IU VWF:RCo/kg body weight daily for up to 7 days should be administered.
Minor bleeds in patients with moderate to severe VWD should receive 40-50 IU VWF:RCo/kg body weight of Humate-P®. A second dose may be administered as needed.24
Acquired VWD can occur as an autoimmune disease as a result of autoantibodies to VWF. Fewer than 100 well-documented cases have been reported in the English-language literature. Persons with acquired VWD may suffer from additional autoimmune disorders, lympho-proliferative disease, or congenital heart disease. Treatment must target the underlying cause of the condition as well as the acute symptoms.20,21
