UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Thrombocytopenia is generally defined as platelet count <150 × 109/L. It can occur due to several reasons, like decreased platelet production (e.g., inherited bone marrow failure syndromes, acquired aplastic anemia, leukemia), ineffective platelet production (myelodysplastic syndrome, megaloblastic anemia), increased destruction (ITP, HLH), increased consumption (DIC, TTP, HUS), sequestration (hypersplenism), or may be due to combination of multiple mechanisms described above.
During evaluating a case of thrombocytopenia, the first step is getting a detailed history and doing a proper clinical examination. Then the next step would be checking the other parameters of complete blood count (CBC), especially hemoglobin (Hb) and the total WBC count, complemented by a peripheral smear (PS) examination, which will clear many doubts and will help us pinpointing our diagnostic approach.
Many a times pseudo-thrombocytopenia is encountered in a PS due to platelet clumping by EDTA and can be rectified by collecting blood samples in a citrate or heparin vials or by doing a direct finger prick smear. Any accompanying cytopenia will expand the differential diagnosis and an isolated thrombocytopenia will further narrow it down. Presence of any additional abnormalities of red cells (megaloblasts) or white cells (presence of hyper-segmented neutrophils, atypical lymphoid/myeloid cells) could be present in megaloblastic anemia/MDS, leukemia respectively, while in the presence of fragmented red cells microangiopathic hemolytic anemia should always be ruled out by doing PT and aPTT (DIC, TTP, HUS). In case of isolated thrombocytopenia, the platelet morphology is also important. In many patients in India, especially in eastern region many people have large platelets with their normal platelet count around 100 × 109/L with normal platelet function (Harris platelet syndrome). However, presence of any abnormal platelet morphology along with a low platelet count may indicate a platelet function disorder (large platelets in Bernard Soulier syndrome/ Glanzmann thrombasthenia or small platelets in Wiskott-Aldrich syndrome), especially if encountered in early part of life during evaluation for bleeding symptoms. In case of isolated thrombocytopenia, presence of additional congenital anomalies may point out towards an inherited marrow failure syndrome, e.g. amegakayocytic thrombocytopenia. Exposure to certain drugs may result in isolated low platelet count, e.g., ceftriaxone, piperacillin, heparin. Presence of toxic changes in neutrophils may indicate sepsis related thrombocytopenia. By excluding all these, immune thrombocytopenia (ITP) to be thought as no specific tests or markers are available for this entity and its diagnosis is largely clinical. A further work up complemented by bone marrow examination and in few cases a platelet function test will definitely help in reaching the final diagnosis.
So, summarizing, in the evaluation of a case of thrombocytopenia, all the
This presentation describes the technique of bone marrow aspiration and biopsy and shows the maturation of elements in sequence and finally adds a note on how to report a bone marrow slide
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Thrombocytopenia is generally defined as platelet count <150 × 109/L. It can occur due to several reasons, like decreased platelet production (e.g., inherited bone marrow failure syndromes, acquired aplastic anemia, leukemia), ineffective platelet production (myelodysplastic syndrome, megaloblastic anemia), increased destruction (ITP, HLH), increased consumption (DIC, TTP, HUS), sequestration (hypersplenism), or may be due to combination of multiple mechanisms described above.
During evaluating a case of thrombocytopenia, the first step is getting a detailed history and doing a proper clinical examination. Then the next step would be checking the other parameters of complete blood count (CBC), especially hemoglobin (Hb) and the total WBC count, complemented by a peripheral smear (PS) examination, which will clear many doubts and will help us pinpointing our diagnostic approach.
Many a times pseudo-thrombocytopenia is encountered in a PS due to platelet clumping by EDTA and can be rectified by collecting blood samples in a citrate or heparin vials or by doing a direct finger prick smear. Any accompanying cytopenia will expand the differential diagnosis and an isolated thrombocytopenia will further narrow it down. Presence of any additional abnormalities of red cells (megaloblasts) or white cells (presence of hyper-segmented neutrophils, atypical lymphoid/myeloid cells) could be present in megaloblastic anemia/MDS, leukemia respectively, while in the presence of fragmented red cells microangiopathic hemolytic anemia should always be ruled out by doing PT and aPTT (DIC, TTP, HUS). In case of isolated thrombocytopenia, the platelet morphology is also important. In many patients in India, especially in eastern region many people have large platelets with their normal platelet count around 100 × 109/L with normal platelet function (Harris platelet syndrome). However, presence of any abnormal platelet morphology along with a low platelet count may indicate a platelet function disorder (large platelets in Bernard Soulier syndrome/ Glanzmann thrombasthenia or small platelets in Wiskott-Aldrich syndrome), especially if encountered in early part of life during evaluation for bleeding symptoms. In case of isolated thrombocytopenia, presence of additional congenital anomalies may point out towards an inherited marrow failure syndrome, e.g. amegakayocytic thrombocytopenia. Exposure to certain drugs may result in isolated low platelet count, e.g., ceftriaxone, piperacillin, heparin. Presence of toxic changes in neutrophils may indicate sepsis related thrombocytopenia. By excluding all these, immune thrombocytopenia (ITP) to be thought as no specific tests or markers are available for this entity and its diagnosis is largely clinical. A further work up complemented by bone marrow examination and in few cases a platelet function test will definitely help in reaching the final diagnosis.
So, summarizing, in the evaluation of a case of thrombocytopenia, all the
This presentation describes the technique of bone marrow aspiration and biopsy and shows the maturation of elements in sequence and finally adds a note on how to report a bone marrow slide
Slideshow is from the University of Michigan Medical
School's M2 Hematology / Oncology sequence
View additional course materials on Open.Michigan: openmi.ch/med-M2Hematology
WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues : 2016 U...Ankit Raiyani
This is a complilation of expected changes in the myeloid neoplasms in the upcoming 2016 update of the "WHO classification of tumours of haematopoietic and lymphoid tissues".
Some of the changes may not be incorporated in the actual published book.
This compilation has been prepared from presentations from persons actually concerned with revision of the book. All credits goes to them.
this is powerpoint presentation comprising of latest updates and theory of lymphoma and plasma cell dyscrasias WHO 2016. restricted to all lymphomaniacs.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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!
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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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.
5. Mutated genes Produce Negative protein Interfere with its normal function/ or Inapropriate increase in some normal activity ( MALTomas ) Translocation of either MALT1 or BCL10 protein Upregulation of NF-kB Normally Bind to form complex regulate NF-kB NF-kB has important pro-survival function in normal lymphocytes Oncoprotein created by genomic abberations Often Block normal maturation Affect rapidly proliferating cells Acute Leukemias Proto-Oncogenes Often activated in lymphocytes by errors that occur during attempted antibody diversification 5 Chromosomal Translocation & Other Acquired Mutations
13. Lymphoid neoplasm Widespread Bone Marrow Involvement Usually (+) Large Numbers of Tumor cells in Peripheral smear 13 Lymphocytic leukemia
14. Proliferations arising as Discrete tissue masses 2 Types 1. Non-HodgkinsLmphoma 2. HodgkinsLymhoma Many types present with Leukemia Term used – Tissue distribution of the disease at time of clinical presentation 14 lymphoma
15. Most commonly arise in Bone Marrow Rarely present as Leukemia R/T Secretion of Antibodies by tumor cells 15 Plasma cell Neoplasm
16. Vast majority are B cell in origin Markers recognized by Antibodies help in characterization into 5 categories Often disrupt normal architecture & function of Immune system Susceptibility to infection Autoimmune 16 FEATURES- Lymphoid Neoplasm
17. Inherited or acquired Immunedeficiency High risk certain lymphoid neoplasm Particularly caused by oncogenic virus eg. EBV 17 FEATURES- Lymphoid Neoplasm
18. Tend to home to a particular tissue sites Follicular Lymphoma – Germinal center T-cell Lymphomas – Skin Some recirculate through the lymphatics & peripheral blood Distant sites Except Hodgkins, Marginal zone lymphoma ( MALToma ) 18 FEATURES- Lymphoid Neoplasm
19. Determined by Anatomic distribuation of disease 2/3 NHL and 100% of Hodgkin Lymphomas Enlarged Nontender LN Often > 2 cm Remaining 1/3 NHL Symptoms r/t to involvement of Extranodal sites Skin, Stomach, Brain 19 Clinical PresentationLymphoma
20. Abrupt stormy onset Present w/in days to few weeks S/S related to Suppression of normal Hematopoiesis by tumor cells in BM Characteristic is Infiltrate in Spleen & Liver 20 LYMPHOCYTICLEUKEMIA
21. Involve the skeleton Local bone destruction Pain Pathologic Fractures Addendum Secretion of whole Ab or Ig fragments 21 PLASMA CELL NEOPLASM
22. Precursor B cell Neoplasm Immature B cells Peripheral B cell Neoplasms Mature B cells Percursor T-cell Neoplasm Immature T cells Peripheral T-cell & NK cell Neoplasm Mature T cell & NK cells Hodgkin Lymphoma 22 WHO 5 CATEGORIES
23. Precursor B and T –Cell Neoplasms - Neoplasm of Immature B cells Acute Lymphoblastic Leukemia/Lymphoma 23
24. Group of Neoplasm composed of Immature pre-B or Pre-T LYMPHOBLASTS Most common cancer of Children Slightly higher in boys 2 Types: 1. Pre-B cell 2. Pre-T cell Both tumors types are morphologically indistinguishable Features : 24
25. 85% are B-ALLs Manifest as Childhood Acute Leukemia Peak age is 3 y/o Extensive BM involvement Variable Peripheral involvement Uncommonly present as Lymphoma Less common is T-ALLs Adolescent males As Thymic Lymphoma Many evolve to Leukemia Features : 25
26. B-ALL Leukemic Presentation Marrow Hyperplasia and packed with Lymphoblast T-ALL Mediastinalthymic mass Often with LNadenopathy & Splenomegaly 26 Morphology
27. Lymphoblast in PBS DefinitveDx based on Lymphocyte –specific markers with Antibodies Histochemical stain Negative for myeloperoxidase Often (+) PAS in cytoplasmic aggregates Immunophenotype (+) TdT in > 95% of cases DNA polymerase Expressed only in pre-B and pre-T lymphoblast Morphology : 27
29. B-ALL lymphoblast (+) CD19, CD10, CD19, CD20 T-ALL lymphoblast (+) CD1, CD2, CD5, CD7 Arrest in normal Maturation of Lymphoblast Dysregulation in epxression and function of transcription factors 29
30. About 90% ALL have numerical or structural chromosomal changes Most commonly – Hyperploidy > 50 chromosomes Hypoploidy Translocation Hyperploidy & Hypoploidy are seen only in B-ALL B & T ALL are associated wuth completely different sets of translocation 30 Molecular Pathogenesis
31. 70% of T-ALL Have gain-of-function mutations in NOTCH1 NOTCH1 is essential for T-cell development High Fraction of B-ALL Have loss-of-function mutations in genes for B cell development NET EFFECT: 1. Disturb differentiation of Lymphoid precursor 2. Promote Maturation arrest Single mutations are not sufficient to produce ALL Must Acquire additional mutation before ALL develop 31 Molecular Pathogenesis
32. Abrupt stormy onset Present w/in days to few weeks Symptoms r/t bone marrow suppression Anemia , Infection, Bleeding episodes Clinical Features : 32
33. Mass Effects Bone pain & tenderness Generalized Lymphadenopathy, Splenomegaly, Hepatomegaly T-ALL Complications R/T complression of large vessels and Airways in mediastinum Both may have CNS manifestation Due to meningeal spread Headache, Vomiting, Nerve palsies Clinical Features : 33
35. Aggressive ChemoTx often w/ prophylactic CNS treatment > 95% of children achieve complete remission 75-85% of choldren are Cured Still the leading cause of cancer death in children Treatment & Prognosis : 35
36. Unfavorable Prognostic Factors < 2y/o Presentation in adolescence or childhood Peripheral blast count > 100,000 Presence of Ph’ chromosome T(9;22) Commonly seen in adult patients ALLOGENIC BM TRANSPLANT – POOR PROGNOSTIC CATEGORIES 36
37. Age 2-10 y/o Low WBC count Early pre-B phenotype Hyperploidy or t(12;21) Favorable Prognostic Factor 37
38. Peripheral B cell Neoplasm- Neoplasm of Mature B cells 38 Chronic Lymphocytic Leukemia & Small Lymphocytic Lymphoma 2. Follicular Lymphoma 3. Diffuse Large Cell Lymphoma 4. Extranodal marginal zone Lymphoma 5. Burkitts Lymphoma
40. Features Similar - Morphological, Phenotype, Genotype Differ only in degree of peripheral blood Lymphocytosis 40
41. Features CLL – Chronic Lymphocytic Leukemia Most common leukemia of Adults in Western countries Median age 60 y/o 2:1 male preponderance Diagnostic Criteria Absolute Lymphocytosis > 4000 per mm3 PERIPHERAL BLOOD WBC counts is High Increased numbers of Small Lymphocytes Smudge cell 41
43. Features SLL – Small Lymphocytic Lymphoma. Represent 4% of Non-Hodgkin Lymphoma Total WBC count is Variable If w/ Bone Marrow Involvement can present as Leukopenia LYMPH NODE Diffusely Effaced , Predominant Small Lymphocytes Variable large Prolymphocytes CREATE PROLIFERATION CENTERS PATHOGNOMONIC FOR CLL/SLL 43
45. Immunophenotype/ Molecular Genetics CD5 – present in tumor cells T-cell marker Expressed by small subset of normal B lymphos Chromosomal translocation is rare Most are Deletions 13q14 11q 17p 45
46. Clinical Features Mostly over 50 y/o Male > Female 2:1 Often Asymptomatic Nonspecific symptoms when manifest BONE MARROW INVOLVEMENT All cases of CLL Most cases of SLL 46
47. Clinical Features 50-60% show Generalized Lymphadenopathy Hepatosplenomegaly VARIABLE INVOLVEMENT OF SPLEEN & HEPATIC PORTAL TRATS 47
48. Clinical Features Disrupts Immune function Hypogammaglobulinemia – Susceptible to INFXN Autoimmune Auto-Antibodies produced by non-neoplastic B cells 10-15% develop Hemolytic anemia /Thrombocytopenia 48
49. Prognosis Extremely Variable Depend mostly on Stage Overall Median is 4-6 years Minimal Tumor burden 10 years 49
50. Poor Prognostic Factors Presence of Deletions 11q & 17p Usually higher stage Transformation to higher grades Prolymphocytic 15%-30% Worsening cytopenias Increasing Splenomegaly Diffuse Large cell 5%-10% Rapidly enlarging mass w/in LN or spleen Richter syndrome Survival < 1 year 50