Immunogenic heparin-induced thrombocytopenia (HIT) is an immune response to heparin associated with significant morbidity and mortality in hospitalized patients if unidentified as soon as possible, due to thromboembolic complications involving both arterial and venous systems. Early diagnoses based on a comprehensive interpretation of clinical and laboratory information improve clinical outcomes. Management principles of strongly suspected HIT should not be delayed for laboratory result confirmation. Treatment strategies have been introduced including new, safe, and effective agents. This review summarizes the clinical therapeutic options for HIT addressing the use of parenteral direct thrombin inhibitors and indirect factor Xa inhibitors as well as the potential non-Vitamin K antagonist oral anticoagulants.
Oral Surgery in Patients on Anticoagulant TherapyVarun Mittal
Management of patients on Anticoagulant Therapy in Surgical Practice with special emphasis on Oral Surgical Procedures; along with Guidelines drawn from various Text Books and Journals
Oral Surgery in Patients on Anticoagulant TherapyVarun Mittal
Management of patients on Anticoagulant Therapy in Surgical Practice with special emphasis on Oral Surgical Procedures; along with Guidelines drawn from various Text Books and Journals
Blood transfusion is the process of transferring blood or blood-based products from one person into the circulatory system of another. Blood transfusions can be life-saving in some situations, such as massive blood loss due to trauma, or can be used to replace blood lost during surgery. Blood transfusions may also be used to treat a severe anaemia or thrombocytopenia caused by a blood disease. People suffering from hemophilia or sickle-cell disease may require frequent blood transfusions. Early transfusions used whole blood, but modern medical practice commonly uses only components of the blood.
This presentation will throw light on transfusion reactions that are commonly observed in blood bank. These transfusion reactions are minor or allergic but sometime results in sever reactions and in severe cases may eventually leads to death of patient.
Webinar Series on COVID-19 vaccine: Jointly organized by Malaysian Society of Infection Control and Infectious Diseases (MyICID) & Institute for Clinical Research (ICR), NIH
Speaker: Dr. Veena Selvaratnam is a Haematologist, Ampang Hospital, Ministry of Health Malaysia.
Convalescent Plasma and COVID-19: Ancient Therapy Re-emergedasclepiuspdfs
Convalescent plasma has again re-emerged as a therapy during coronavirus disease (COVID-19) outbreaks currently use as a prophylactic or an interventional treatment in infected patients. Convalescent plasma has been used in the 20th century confronting different infectious diseases where there was no other therapy available. Conceivably, this convalescent plasma therapy tends to be proving a game-changing treatment in some COVID-19 patients and could support treatment, in addition to the current interventions before other developed therapies are available for the population.
The Negative Clinical Consequences Due to the Lack of the Elaboration of a Sc...asclepiuspdfs
Until a few years ago, the immune system was considered as responsible for the only defense against microbial infections and other external agents. On the contrary, the immune cells have been proven to be linked not only through cell-cell contact but also by releasing proteins capable of influencing the immune-inflammatory response, the so-called cytokines or interleukins. Moreover, the cytokines have appeared to play not only immune activities but also metabolic and systemic effects influencing the overall biological systems, including the nervous, the endocrine, and the cardiovascular systems, by representing the main endogenous molecules responsible for the maintenance of the unity of the biological life. Therefore, only the systematic clinical consideration of cytokine effects may allow the generation of real future holistic medicine.
The great benefit of blood/blood constitutes therapy is the ability to provide transfusion support for patients with many unique hematologic conditions. For some patients, such as patients with sickle cell disease, thalassemia major, immune hemolytic anemia, anemia of kidney disease, and aplastic anemia may need for this consolidation extends throughout their life. By knowing the alteration mechanisms of these conditions, we can appreciate the stationary, urgency, and the value of the transfused red blood cell (RBC).
Decreasing or Increasing Role of Autologous Stem Cell Transplantation in Mult...asclepiuspdfs
During the past four decades, autologous stem cell transplantation (ASCT) has been the first choice and the standard option for the treatment of newly diagnosed patients with multiple myeloma. The introduction of new agents such as thalidomide, lenalidomide, and bortezomib has led to a clear improvement in basic approach and those agents became the standard of care in the induction phase; however, they were not able to play the role of ASCT in term of progression-free survival and overall survival. Debate continues about the best induction, consolidation, and maintenance taking into account the toxicities of these new agents. The new monoclonal antibody (anti CD38) starts to take its place in the induction setting and it seems to be a promising agent in the high-risk group. Until recently, ASCT is the standard treatment for newly diagnosed patients.
Comparison of the Hypocalcemic Effects of Erythropoietin and U-74389Gasclepiuspdfs
Aim: This study calculated the effects on serum calcium (Ca) levels, after treatment with either of two drugs: The erythropoietin (Epo) and the antioxidant lazaroid (L) drug U-74389G. The calculation was based on the results of two preliminary studies, each one of which estimated the certain influence, after the respective drug usage in an induced ischemia-reperfusion animal experiment. Materials and Methods: The two main experimental endpoints at which the serum Ca levels were evaluated were the 60th reperfusion min (for the Groups A, C, and E) and the 120th reperfusion min (for the Groups B, D, and F). Especially, the Groups A and B were processed without drugs, Groups C and D after Epo administration, whereas Groups E and F after the L administration. Results: The first preliminary study of Epo presented a non-significant hypocalcemic effect by 0.34% ± 0.68% (P = 0.6095). However, the second preliminary study of U-74389G presented a non-significant hypercalcemic effect by 0.14% ± 0.66% (P = 0.8245). These two studies were coevaluated since they came from the same experimental setting. The outcome of the coevaluation was that L is 2.3623042-fold (2.3482723–2.3764196) more hypercalcemic than Epo (P = 0.0000). Conclusions: The antioxidant capacities of U-74389G ascribe 2.3623042-fold more hypercalcemic effects than Epo (P = 0.0000).
The term refractory anemia (RA) may be confusing to those who are not hematologists. RA should be well defined because it means more than what it says. RA is defined as anemia that is not responsive to therapy except transfusion.[1] The term RA is used to rule out those types of anemia with a known cause such as anemia of systemic diseases (liver and kidney) and anemia of inflammation even though they are considered refractory to therapy.[2] RA with cellular or hypercellular bone marrow was formerly used to exclude aplastic anemia.
73-year-old woman without any pertinent history was admitted to the hospital due to remittent fever with erythema. She showed itching and linearly arranged erythema on the chest, back, and abdomen [Figure 1a and b]. As she had been taking daily cefditoren pivoxil for the 4 days before her admission, she was diagnosed as having drug-related scratch dermatitis, and the antibiotic treatment was stopped. Her fever remained. Laboratory data showed elevated levels of white blood cells (14,800/μl, normal range 4000–7000) and liver enzymes such as aspartate aminotransferase (AST) 138 IU/L (normal range 5–40), alanine aminotransferase 97 IU/L (normal range 5–35), and ferritin (17469.5 ng/mL, normal range 5–152).
Bone Marrow Histology is a Pathognomonic Clue to Each of the JAK2V617F, MPL,5...asclepiuspdfs
According to the World Health Organization and Clinical Laboratory Molecular and Pathological criteria bone marrow pathology in JAK2V617F mutated trilinear myeloproliferative neoplasm (MPN) patients essential thrombocythemia (ET) and polycythemia vera are indistinguishably featured by clustered medium to large pleomorphic megakaryocytes and increased cellularity (60–90%) due to increased erythropoiesis and megakaryopoiesis. MPL515 mutated ET is the second distinct clonal MPN characterized by thrombocythemia in a normocellular bone marrow showing clustered increased large to giant mature megakaryocytes with staghorn-like hyperlobulated nuclei. Calreticulin (CALR) mutated hypercellular thrombocythemia associated with prefibrotic megakaryocytic, granulocytic myeloproliferation (MGM) recently became the third distinct MPN featured by dense clusters of immature megakaryocytes with cloud-like nuclei. Bone marrow pathology in newly diagnosed MPN patients appears to be a pathognomonic clue for diagnostic differentiation between JAK2V617F mutated trilinear MPN, MPL515 normocellular thrombocythemia, and CALR thrombocythemia with MGM characteristics followed by secondary reticulin fibrosis. Their natural histories clearly differ featured by an increase of erythro/granulopoiesis and cellularity in JAK2V617F, decrease of erythropoiesis and cellularity in MPL515 and increase of dual megakaryo/granulopoiesis and cellularity in CALR mutated MPN.
Helicobacter pylori Frequency in Polycythemia Vera Patients without Dyspeptic...asclepiuspdfs
Introduction: In polycythemia vera (PV) patients, peptic ulcer and gastroduodenal erosions are more common than the general population, but there are insufficient data on the frequency of Helicobacter pylori (HP) and its role in etiopathogenesis. In this study, we aimed to compare the prevalence of HP infection in PV patients without dyspeptic complaints with a healthy control group without dyspeptic complaints. Materials and Methods: Fifty patients with PV without dyspeptic complaints and 50 controls without dyspeptic complaints were enrolled in this study after informed consent obtained. Stool samples of selected patients were analyzed using HP stool antigen test (True Line®). Results: There was surprisingly striking difference between HP prevalence in PV patients without dyspeptic complaints and asymptomatic healthy controls (64% vs. 2%) (P < 0.05). There was no significant relationship found between HP presence and age, gender, treatment modalities, complete blood count, positivity of JAK2 V617F, serum erythropoietin level, and splenomegaly in PV patients (P > 0.05). Conclusion: As the susceptibility of HP infections in PV patients are higher, it is recommended to have close surveillance of these patients by screening HP presence. In addition, when HP positivity is determined, the eradication of HP is essential to prevent possible future gastrointestinal lesions in patients with PV.
Lymphoma of the Tonsil in a Developing Communityasclepiuspdfs
The lymphoma of the tonsil is a rarity. Single case reports have appeared in countries as disparate as China, Greece, India, Japan, and Turkey. Therefore, this paper presents cases found in Nigeria among the Ibo ethnic group. The epidemiological comparisons are deemed to be worthy of documentation such as age ranges and sides of involvement.
Should Metformin Be Continued after Hospital Admission in Patients with Coron...asclepiuspdfs
Background: In most patients with diabetes, guidelines recommend discontinuation of oral anti-diabetic agents. Preliminary data suggest that pre-admission metformin use may have a mortality benefit in patients with coronavirus disease (COVID)-19 admitted to the hospital. Objective: The objective of the study was to review the impact of metformin on morbidity and mortality among hospitalized patients with COVID-19. Methods: Review of English literature by PUBMED search until November 10, 2020. Search terms included diabetes, COVID-19, metformin, retrospective studies, meta-analyses, pertinent reviews, pre-print articles, and consensus guidelines are reviewed.
Clinical Significance of Hypocalcemia in COVID-19asclepiuspdfs
Background: Preliminary data suggest that hypocalcemia is common among patients with COVID-19 admitted to the hospital. Objective: The objective of the study was to examine the clinical significance of hypocalcemia in the setting of COVID-19. Methods: Literature search (PubMed) until August 5, 2020. Search terms include hypocalcemia, COVID-19, mortality, and complications. Retrospective studies are reviewed due to a lack of randomized trials. Results: Prevalence of hypocalcemia among hospitalized patients with COVID-19 ranges from 62% to 78%, depending on the definition of hypocalcemia and patients’ characteristics. In most cases, hypocalcemia is mild to moderate biochemically. Hypocalcemia is a risk factor for hospitalization of patients with COVID-19. In already hospitalized patients, hypocalcemia is significantly associated with increase severity of COVID-19 and its complications, including multiorgan failure, acute respiratory distress syndrome, and death. Hypocalcemia is significantly correlated with inflammatory markers of COVID-19. Causes of hypocalcemia in COVID-19 patients are unclear, but Vitamin D deficiency may be a contributing factor. Conclusion: Hypocalcemia is common in hospitalized patients with COVID-19 and carries unfavorable outcomes. Further studies are needed to examine the causes of hypocalcemia in COVID-19 and to see whether normalization of circulating calcium levels improves prognosis.
Excess of Maternal Transmission of Type 2 Diabetes: Is there a Role of Bioche...asclepiuspdfs
Objective: An excess of maternal transmission of Type 2 diabetes (T2D) has been reported in some populations but not confirmed in other studies. Mitochondrial inheritance has been proposed to explain such excess. In the present paper, we have considered the presence of T2D in the mother and/or in the father in relation to the risk of T2D and to age at onset of the disease in the offspring. The distribution of two genetic polymorphisms involved in glucose metabolism in relation to the presence of T2D in the mother has been also considered. Materials and Methods: Two hundred and seventy-nine participants with T2D were studied in the population of Penne, a small rural town in the eastern side of central Italy. Adenosine deaminase locus 1 (ADA1) and phosphoglucomutase locus 1 (PGM1) phenotypes were determined by starch gel electrophoresis. Statistical analyses were carried out using commercial software (SPSS). Results: The proportion of patients from T2D mothers is much greater as compared to the proportion of the patients from T2D fathers (P < 0.0001). Age at onset of the disease in patients in whom one or both parents are T2D is lower as compared to other patients. The distribution of ADA1 and PGM1 phenotypes in participants with T2D depends on the presence of diabetes in the mother. Conclusions: About the transmission of T2D, our data confirm the high proportion of maternal T2D and show the role of two common biochemical polymorphisms involved in glucose metabolism.
The Effect of Demographic Data and Hemoglobin A 1c on Treatment Outcomes in P...asclepiuspdfs
Objective: Diabetes mellitus, the most common cause of non-traumatic foot amputations, is a life-threatening condition due to its high mortality and morbidity. In our study, we retrospectively evaluated our patients with diabetic foot syndrome in our clinic. Materials and Methods: The demographic data, duration of diabetes, Wagner classification, haemoglobin A 1c (HbA1c) levels, white blood cell, C-reactive protein sedimentation levels, hospital stay, and treatment results were evaluated retrospectively in 14 patients with diabetic foot between January 2017 and December 2018. Results: The mean age of the patients was 62.43 ± 7.7 years. Of the 14 patients, 3 were females and 11 were males. All 14 patients were type 2 diabetes mellitus. When diabetic foot Wagner classification was performed, 6 patients were evaluated as Wagner 2, five patients were Wagner 3, and three patients were evaluated as Wagner 4. Nine patients had complete amputation and 3 had vascular surgery. Conclusion: Although the level of HbA1c is below the target level, the risk of diabetic foot is increased when there is no adequate diabetes mellitus foot training. Inadequate diabetic patient education and hospitalization of patients after infection progress the amputation rate.
Self-efficacy Impact Adherence in Diabetes Mellitusasclepiuspdfs
The aim of the paper is to explore how self-efficacy (SE) is associated with adherence among adults with diabetes mellitus (DM). Methods: The search of electronic databases identified 564 records from 2007 to 2017 on SE and adherence from different perspectives and its effect on adults with DM. Discussions: SE increases the confidence in adults in their self-care behaviors. Non-adherence continues to be a significant barrier to SE. SE and adherence should be informed by an understanding of theoretical frameworks and the individual characteristics. Conclusion: Adherence is likely among adults with better SE to empower them to make valid decisions about their health. Interventions to improve SE should be tailored based on different types of non-adherence such as intentional and unintentional non-adherence. Implications: An intercollaborative professional practice approach is crucial to improve SE and adherence for sound judgment and valid decision-making.
Uncoiling the Tightening Obesity Spiralasclepiuspdfs
While an underweight prevalence was once more than twice that of obesity, now more people are obese than underweight. Obesity is one of the leading causes of preventable death in the world. There are an estimated 2,100,000,000 obese people worldwide and that number is forecast to grow to 51% of the world’s population by 2030. Escalating obesity-related disease costs threaten to bankrupt the world’s health-care systems.
Prevalence of Chronic Kidney disease in Patients with Metabolic Syndrome in S...asclepiuspdfs
Background and Objective: Chronic kidney disease (CKD) which is an increasingly important clinical and public health issue is associated with cardiovascular disease. Epidemiologic studies have also linked metabolic syndrome (MetS) with an increased risk of incident CKD. Therefore, the present study was designed retrospectively to find the prevalence and potential risk factors of CKD in patients with MetS in Saudi Arabia.
Management Of Hypoglycemia In Patients With Type 2 Diabetesasclepiuspdfs
Hypoglycemia is the rate-limiting step of intensive management in patients with diabetes. Lowering one’s A1C to a prescribed target is expected to mitigate one’s risk of developing long- and short-term diabetes-related complications. Several of the less expensive and commonly prescribed glucose lowering agents favored by practitioners result in weight gain, hypoglycemia, and even an increased risk of cardiovascular (CV) mortality. Although achieving a targeted A1C of <7 % is the standard of care, clinicians often fail to evaluate patients for glycemic variability which can increase oxidative stress driving long-term diabetes-related complications including CV death. The use of concentrated insulins and glucagon-like peptide-1 receptor agonists separately or in combination with each other reduces glycemic variability and one’s risk of hypoglycemia. Pharmaceutical agents which allow patients to safely achieve their targeted A1C without weight gain and hypoglycemia should be preferred in patients with type 2 diabetes.
Predictive and Preventive Care: Metabolic Diseasesasclepiuspdfs
South Asians have a very high incidence of ischemic heart disease and stroke. In addition, they also have a very high incidence of metabolic diseases such as prehypertension, hypertension, visceral obesity, metabolic syndrome, prediabetes, type-2 diabetes, and its clinical complications. Currently, there are over 75 million diabetic subjects in India and an equal number of prediabetics. Republic of China has taken over India as the diabetes capital of the world, with over 115 million diabetics. Modern medicine is disease focused and has failed to address the prevention of these chronic diseases. According to the reports from the United Nations (Millennium Development Goals [MDGs], the World Health Organization, Global Health Initiatives, and the non-communicable disease risk task force), obesity has increased by 2-fold and type-2 diabetes by 4-fold worldwide. Experts in this field predict that chances of meeting the MDGs set by the UN members of reducing the incidence of these diseases at 2025 to the level of 2020 are very little. Western medicine has failed to reduce or reverse the trend in the incidence of these diseases. We feel that an integrated approach to health care may be a better option, to reduce the disease burden in developing and resource-poor countries. Having said that, one cannot prevent something that one is not aware of, as such it is the need of the hour for us, to develop a robust predictive and preventive health-care platform. In an earlier article, we presented our views on reducing or reversing cardiometabolic diseases. There is great enthusiasm among the health-care providers and professional bodies that integration of emerging technologies will help develop personalized, precision medicine, as well as reduce the cost of health-care worldwide.
It is known that the cancer development process is multifactorial nowadays. The relationship between insulin and cancer has recently been gaining in importance. The number of studies between insulin resistance and thyroid cancer is very small, although the association between obesity, type 2 diabetes, and insulin resistance, particularly breast, colon, and pancreatic cancer development, is long. There are studies advocating increased growth factors with insulin resistance as well as triode cancer after thyroid angiogenesis. Insulin and insulin-like growth factors may be the primary causes of pathophysiology in many cancers, especially thyroid cancer, with mitogenic activity.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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2. Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia
13 Clinical Research in Hematology • Vol 2 • Issue 1 • 2019
RISK FACTORS
Exposure to heparin is the main risk factor and a critical step
in the development of HIT [Table 1]. A heparin source such
as bovine lung is more immunogenic than those produced
from porcine intestine,[15]
and the risk of HIT rises with the
length and volume of exposure to heparin as well as the route
of administration[16]
and more likely with intravenous heparin
than subcutaneous administration.[17-19]
Nevertheless, HIT
can develop from any heparin exposure, including incidental
amounts from heparin flushes or heparin-coated devices.[20,21]
Although HIT is more common in patients receiving UFH
than in those treated with LMWH.
LABORATORY AND CLINICAL
ASSESSMENT
HIT may occur rapidly or with a delayed onset, depending
on the presence of heparin-PF4 antibodies from a previous
administration and sensitization of heparin and related
molecules may induce rapid-onset HIT.[22]
In patients exposed
toheparinforthe1st
time,theonsetofHITmayoccur5–10 days
after receiving heparin.[4,5,12,23]
The thrombocytopenia in HIT is
usuallymoderateinseverity,withamedianplateletcountbeing
between 50 and 80 109
/L, although the nadir platelet count
can remain at a level considered normal (i.e., 150 109
/L) but
having dropped by 50%. The immunoassays (enzyme-linked
immunosorbent assay) are very sensitive to detect the HIT
antibody that binds to the PF4/heparin complex. However,
not all antibodies detected (immunoglobulin [Ig] G, IgM, and
IgA) are capable to induce clinical HIT Immunoassays are
both technically easier to perform and more sensitive than
functional assays. On the other hand, functional assays are
more specific and better in the diagnosis of clinical HIT.[1,24]
PLATELET MONITORING
Platelet count monitoring should be started as baseline
measurement before heparin administration, whereas routine
monitoring is recommended for most patients receiving
heparin formulation based on stratified incidence of HIT
according to patient’s population and type of heparin exposure
[Table 2].[3,4]
MANAGEMENT OF IMMUNOGENIC
HIT
Initially, a clinician should apply the 4Ts (thrombocytopenia,
timing of platelet count fall, thrombosis, and other cause of
thrombocytopenia) scoring system to identify patients who
are at high, intermediate, or low risk of developing HIT
[Table 3].
NON-HEPARIN ANTICOAGULANT
Direct thrombin inhibitors and indirect factor Xa inhibitors
are two anticoagulant classes that were used in the treatment
of HIT with or without thrombosis [Table 4]. The clinical
presentation of the patient, availability of the drugs, and
clinician experience should dictate the choice of therapy.
CONCLUSION AND RELEVANCE
The diagnosis of HIT requires clinical evaluation and
laboratory confirmation. Platelet count monitoring should
perform every 2 or 3 days in patient population with a risk
of HIT 1%. When HIT is strongly suspected, management
should include immediate discontinuation of all heparin
formulations and the start of alternative, non-heparin
anticoagulants. Vitamin K antagonist (VKA) should not
be given. Instead, if VKA was given, reverse elevated
international normalized ratio by administering Vitamin K
and avoid platelet transfusions. A serotonin release assay
may be performed for HIT antibody detection; however, if
such a test was not available, enzyme-linked immunosorbent
assay would be sufficient to confirm the diagnosis. Doppler
ultrasonography of the upper and lower limbs and computed
tomography of the chest should be performed when clinically
Table 1: Factors contributing to the development of heparin‑induced thrombocytopenia
Risk category Immunogenicity value (immunogenic effects)
Heparin source Bovine higher than porcine
Heparin type UFH more than LMWH
Volume of heparin dose Therapeutic dose prophylactic flush or heparin‑coated
devices
Heparin exposure
First exposure Platelet fall day 5–10 after heparin initiation
Previous exposure (within 90 days) Platelet fall within 1 day after heparin initiation
Patient population Post‑operative more than medical more than obstetric
Patient gender Female more than male
LMWH: Low‑molecular‑weight heparin, UFH: Unfractionated heparin
3. Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia
Clinical Research in Hematology • Vol 2 • Issue 1 • 2019 14
Table 2: Platelet count monitoring guideline for HIT
Population Scenario Monitoring of platelet count
Recent heparin exposure Patient starting UFH and LMWH and who received
UFH within the previous 100 days; patients whose
heparin exposure history is unknown
Obtain baseline platelet count and repeat
platelet count within 24 h of starting
heparin
Acute, systematic
reactions after
intravenous UFH bolus
Patients with acute inflammatory,
cardiorespiratory, neurologic, or other unusual
symptoms and signs within 30 min after an
intravenous UFH bolus.
Obtain platelet count immediately to
compare with recent prior platelet counts
Risk* of HIT 1% Patients receiving UFH and LMWH at therapeutic
doses
Post‑operative patient receiving UFH/LMWH
antithrombotic prophylaxis
Obtain baseline then at least every 2 or
3 days until day 14 of treatment or until
heparin is stopped, whichever occurs first
Baseline then at least every 2 or 3 days
between post‑operative days 4 and 14 or
until heparin is stopped, whichever occurs
first
Risk of HIT 1% Medical/obstetric patients receiving prophylactic
dose UFH, or LMWH after receiving UFH,
post‑operative patients receiving prophylactic dose
LMWH, or intravascular catheter UFH flushes
As clinically indicated (no routine
monitoring)
LMWH: Low‑molecular ‑weight heparin, UFH: Unfractionated heparin, *Risk stratification is based on the overall incidence of HIT in different
patient population
Table 3: The pretest probability of HIT: 4Ts scoring system*
Clinical feature Score=2 Score=1 Score=0
Thrombocytopenia: Compare
the highest platelet count
within the sequence of
(declining platelet counts with
the lowest count to determine
the percentage of platelet fall
(select only one option)
50% platelet fall and
nadir of ≥20 and no
surgery within preceding
3 days
50% platelet fall but surgery
within preceding 3 days; any
combination of platelet fall and
nadir that does not fit criteria for
score of 2 or 0 (e.g., 30%–50%
platelet fall or nadir 10–19)
30% platelet fall; Any
platelet fall with nadir 10
Timing (of platelet count fall
or thrombosis*): Day 0=first
day of most recent heparin
exposure (select only one
option)
Platelet fall 5–10 days
after start of heparin
Platelet fall within 1 day
of start of heparin and
exposure of heparin with
the past 5–30 days
Consistent with platelet fall days
5–10 but not clear (e.g., missing
counts)
Platelet fall within 1 day of start
of heparin and exposure to
heparin in the past 31–100 days
platelet fall after day 10
Platelet fall ≥day 4 without
exposure to heparin in the
past 100 days
Thrombosis (or other clinical
sequelae; Select only one
option)
Confirmed new thrombosis
(venous or arterial)
Skin necrosis at
injection site
Anaphylactoid reaction to
IV heparin bolus
Adrenal hemorrhage
Recurrent venous
Thrombosis in a patient receiving
therapeutic anticoagulants
Suspected thrombosis (awaiting
confirmation with imaging)
Erythematous skin lesions at
heparin injection sites
Thrombosis suspected
Other causes of
thrombocytopenia (select
only one option)
No alternative explanation
for platelet fall is evident
Possible another cause is
evident:
Sepsis without proven microbial
source
Thrombocytopenia associated
with initiation of ventilator
Other
Probable another cause
present:
Within 72 h of surgery
Confirmed bacteremia/
fungemia
Chemotherapy or radiation
within the past 20 days
DIC due to non‑HIT cause
other
DIC: Disseminated intravascular coagulation, HIT: Heparin‑induced thrombocytopenia, IV: Intravenous, *Upon adding the score, the patient is
stratified into low (0–3 points), intermediate (4–5 points), or high (6–8 points) risk for having HIT. Table adapted with permission from Linkins et al.[4]
4. Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia
15 Clinical Research in Hematology • Vol 2 • Issue 1 • 2019
indicated. At present, two parenteral therapeutic approaches
areavailabletotreatHITwithorwithoutthrombosis: (a) Direct
thrombin inhibitors or (b) indirect Xa inhibitors. The third
potential option for the treatment of HIT is using NOACs.
Unfortunately, all of the available anticoagulation agents
used to treat HIT are associated with hemorrhage and none
of these drugs has an antidote for rapid reversal. Adequate
hydration and early mobilization are supportive measures
may utilized in the prevention of thrombotic complication.
It is our recommendation and conviction that research should
continue to identify new therapeutic agents offering effective
and safe non-heparin alternatives for the management of
patients with HIT.
REFERENCES
1. Warketin TE. Heparin-Induced Thrombocytopenia:
Pathogenesis And Management. Br J Haematol 2003;121:
535-55.
2. Warketin TE. Heparin-induced thrombocytopenia. Diagnosis
and management. Circulation 2004;110:e454-8.
3. Cines DB, Bussel JB, McMillan RB, Zehnder JL. Congenital
and acquired thrombocytopenia. Hematol Am Soc Hematol
Educ Program 2004;2004:390-406.
4. Linkins LA, Dans AL, Moores LK, Bona R, Davidson BL,
Schulman S, et al. Treatment and prevention of heparin
induced thrombocytopenia: Antithrombotic therapy and
prevention of thrombosis, 9th
ed: American college of chest
physicians evidence-based clinical practice guidelines. Chest
2012;141 Suppl 2:e495S-530.
5. Watson H, Davidson S, Keeling D, Haemostasis and
Thrombosis Task Force of the British Committee for Standards
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of heparin-induced thrombocytopenia: Second edition. Br J
Haematol 2012;159:528-40.
6. Warketin TE. An overview of the heparin-induced
thrombocytopenia syndrome. Semin Thromb Hemost 2004;30:
273-83.
7. Franchini M. Heparin induced thrombocytopenia: An update.
Thrombosis J 2005;3:14-20.
8. Rice L. Heparin-induced thrombocytopenia: Myths and
misconceptions. Arch Intern Med 2004;164:1961-4.
9. Kelton JG, Sheridan D, Santos A, Smith J, Steeves K, Smith C,
et al. Heparin induced thrombocytopenia: Laboratory studies.
Blood 1988;72:925-30.
10. Greinacher A, Potzch B, Amiral J, Dummel V, Eichner A,
Mueller-Eckhardt CM. Heparin-associated thrombocytopenia:
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11. Amiral J, Bridey F, Dreyfus M, Vissoc AM, Fressinaud E,
Wolf M,et al.Plateletfactor4complexedtoheparinisthetarget
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Thromb Haemost 1992;68:95-6.
12. Cuker A, Cines DB. How I treat heparin-induced
thrombocytopenia. Blood 2012;119:2209-18.
13. Lee GM,Arepally GM. Diagnosis and management of heparin-
induced thrombocytopenia. Hematol Oncol Clin North Am
2013;27:541-63.
Table 4:
Dosing
and
monitoring
guidelines
for
the
parenteral
treatment
options
of
HIT
Agent
Mode
of
action
Normal
dose
Dose
adjustment
Monitoring
FDA/ACCP
Approval/
Recommendation
for
HIF
Argatroban
Direct
thrombin
inhibition
2
µg/kg/min
IV
CKD:
No
change
HF:
0.5
µg/kg/min
aPTT
1.5–3×baseline (not
to
exceed
100
s)
DA:
Yes
ACCP:
2C
Desirudin
Direct
thrombin
inhibitor
15–30
mg
SC
every)
12
h
CKD:
CL
CR
60
mL/min:
Adjustment
needed
HF:
No
change
None
needed
FDA:
No
ACCP:
2C
Bivalirudin
Direct
thrombin
inhibitor
0.15–0.20
mg/kg/h
IV
CKD:
CL
CR
10–29
mL/min:
0.06
mL/kg/h
IV:
CL
CR
10
Ml/min:
0.015
mg/kg/h
IV
aPTT
1.5−2.5×baseline
FDA:
Yes
ACCP:
C
Danaparoid
Indirect
factor
Xa
inhibitor
400 U/h
IV×h
then
300
U/h
IV×4
h
then
200
U/h
IV
Not
studied
in
patients
with
severe
renal
failure
Antifactor
Xa
level
0.5−0.8 U/mL
FDA:
Yes
ACCP:
2C
Fondaparinux
Indirect
factor
Xa
inhibitor
50
kg:
5mg
SQ:
50–100
kg:
7.5
mg
SQ:
100
kg:
10 mg
SQ
CKD:
CL
CR
30–50
mg/min:
Use
caution:
CL
CR
30
mL
min:
contraindicated
None
needed
FDA:
Yes
ACCP:
2C
ACCP:
American
college
of
chest
physician,
aPTT:
Activated
partial
thromboplastin
time,
CKD:
Chronic
kidney
disease,
CL
CR
:
Creatinine
clearance,
FDA:
Food
and
drug
administration,
HIT:
Heparin‑induced
thrombocytopenia,
HF:
Hepatic
failure
5. Aleidan and Alzahrani: Immunogenic heparin-induced thrombocytopenia
Clinical Research in Hematology • Vol 2 • Issue 1 • 2019 16
14. Bhatt VR, Aryal MR, Armitage JO. Nonheparin anticoagulants
for heparin-induced thrombocytopenia. N Engl J Med
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, Moroose R, DrexlerA.A comparison
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et al. Heparin-induced thrombocytopenia with thrombosis:
Incidence, analysis of risk factors, and clinical outcomes in
108 consecutive patients treated as a single institution. Am J
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17. Lubenow N, Hinz P, Thomaschewski S, Lietz T, Vogler M,
Ladwig A. The severity of trauma determines the immune
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thrombocytopenia. Blood 2010;115:1797-803.
18. Ban-Heofan M, Francis C. Heparin induced thrombocytopenia
and thrombosis in a tertiary care hospital. Thromb Res
2009;124:189-92.
19. Prechel M, Walenga JM. Heparin-induced thrombocytopenia:
An update. Semin Thromb Hemost 2012;38:483-96.
20. Kadidal VV, Mayo DJ, Horne MK. Heparin-induced
thrombocytopenia (HIT) due to heparin flushes: A report of
three cases. J Intern Med 1999;246:325-9.
21. Jang IK, Hursting MJ. When heparins promote thrombosis:
Review of heparin-induced thrombocytopenia. Circulation
2005;111:2671-83.
22. Warketin TE, Kelton JG. Temporal aspects of heparininduced
thrombocytopenia. N Engl J Med 2001;334:1286-92.
23. Warketin TE, Kelton JG. Delayed-onset heparin-induced
thrombocytopenia and thrombosis. Ann Intern Med 2001;
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How to cite this article: Aleidan FAS, Alzahrani LAK.
Management of Immunogenic Heparin-induced
Thrombocytopenia. Clin Res Hematol 2019;2(1):12-16.