Two cases of Waldenstrӧm macroglobulinemia along with brief disease pathology. Waldenstrӧm macroglobulinemia is a rare B cell lymphoma involving bone marrow with IgM monoclonal gammopathy of any concentration
Two cases of Waldenstrӧm macroglobulinemia along with brief disease pathology. Waldenstrӧm macroglobulinemia is a rare B cell lymphoma involving bone marrow with IgM monoclonal gammopathy of any concentration
acute leukemia
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AML:ACUTE MYELOID LEUKAEMIA
for medical colleges teaching faculty and students as well. it includes AML causes , histopathological slides of subclasses of Acute myeloid leukemia, classification , diagnosis, management modalities, complications .Acute leukemias are stem cell disorders characterized by malignant neoplastic proliferation and accumulation of immature and non functional hematopoietic cells in the bone marrow.
The neoplastic cells show increased proliferation and/or decreased apoptosis.
If the defect primarily affects the common myeloid progenitor (CMP) then it is called Acute myeloid leukemia.
Acute myeloid leukemia (AML) is a neoplastic disease characterized by infiltration of the blood, bone marrow, and other tissues by proliferative, clonal undifferentiated cells of the hematopoietic system.
AML is the result of a sequence of somatic mutations in a multipotential primitive hematopoietic cell or, in some cases, a more differentiated progenitor cell.
It can be slow growing or rapidly fatal.
AML is the predominant form of leukemia during the neonatal period
Incidence : 1.5/100,000/year in infants decreases to approximately 0.4 per 100,000 children ages 5 to 9 years, increases gradually to 1.0 persons per 100,000 until age 25 years, and thereafter increases exponentially until the rate reaches approximately 25/100,000 persons.
AML accounts for 15 to 20 percent of the acute leukemias in children and 80 percent of the acute leukemias in adults.
Men > Women (4.5 : 3)
HEREDITY
1) Chromosomal aneuploidy like Trisomy 21 noted in Down syndrome
2) Defective DNA repair, e.g., Fanconi anemia, Bloom syndrome, and Ataxia telangiectasia
3) Congenital neutropenia ie Kostmann syndrome
4) Germline mutations of CCAAT/enhancer-binding protein α (CEBPA), runt-related transcription factor 1 (RUNX1), and tumor protein p53 (TP53) have also been associated with a higher predisposition to AML
RADIATION
Peaks after 5 to 7 yrs of exposure.
Therapeutic radiation alone seems to add little risk of AML but can increase the risk in people also exposed to alkylating agents.
CHEMICAL AND OTHER EXPOSURES
Exposure to benzene, plastic, rubber, petroleum products, paint, ethylene oxide, herbicides and pesticides can increase the risk.
Smoking can also increase the risk
DRUGS
Anticancer drugs are the leading cause of therapy-associated AML.
Alkylating agent–associated leukemias occur on average 4–6 years after exposure, and affected individuals have aberrations in chromosomes 5 and 7.
Topoisomerase II inhibitor–associated leukemias occur 1–3 years after exposure, and affected individuals often have aberrations involving chromosome 11q23.
Other agents like Chloramphenicol, phenylbutazone, and, less commonly, chloroquine and methoxypsoralen.
SYMPTOMS :
Present with nonspecific symptoms initially.
Fatigue is the first symptom
Fever with or without infection will be present in approximately 10% patients
Bleeding, easy bruising
occasional
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.
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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
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
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
1. Myeloid Neoplasm MALIGNANT NEOPLASM OF HEMATOPOIETIC STEM CELLS ARISE PRIMARILY IN BONE MARROW ALSO SPLEEN, LIVER, LN - To a Lesser Extent FLOOD THE CIRCULATING BLOOD & OTHER ORGANS
5. Features Affects primarily Adults 15 – 39 y/o peak incidence Acute Onset of symptoms R/T Anemia Neutropenia - Infections Spontaneous mucosal & cutaneous Bleeding Bleeding diasthesis is most striking feature
6. Features Enlargement of liver, spleen LN enlargement is not pronounced If untreated, course is rapidly progressive
7.
8. PATHOPHYSIOLOGY 1. MOSTLY with Acquired genetic alterations INHIBITION OF TERMINAL MYELOID DIFFERENTIATION Proliferation of Relatively Undifferentiated Myeloblast REPLACED NORMAL MARROW ELEMENTS Its replication rate is LOWER than normal myeloid cells INDICATING : 1. BLOCKED MATURATION 2. INCREASED SURVIVAL
9. PATHOPHYSIOLOGY 2. Chromosomal Abnormalities- AML t(8;21) , inv(16) , t(15,17) De Novo cases Associated with Myelodysplastic syndromes Radiation therapy
10. PATHOPHYSIOLOGY Recurrent Chromosomal Aberrations Translocation Disrupt genes encoding for Factors needed for NORMAL MYELOID DIFFERENTIATION Eg. t(8,21) AND inv(16) Chimeric gene New Protein Dominant Negative activity Daughter cells exhibit partial or complete block in terminal differentiation
11. Additional Collaborative Aberration present Promyelocytic Leukemia (AML-M3) T(15,17) producing fusion gene RARaand PML Suppress the function of RARa Becomes a Repressor of Transcription Turns off genes needed for full and complete myeloid differentiation Point mutation in FLT3 constitutive activation of tyrosine kinase promote cellular proliferation & survival
12. Diagnosis: Dxrequires at least 30% of ANC are Myeloblast(ANC- all nucleated cells ) WHO criteria Been lowered to 20% With elimination of of MDS Refractory anemia w/ excess blast Blastin Transformation Helpful in the dx is (+) Auer rods in myeloblast cells
15. AUER RODS Linear or Spindle Red- Purple Inclusions In Myeloblast/myelocyte Derivatives of Azurophilic granules Stain (+) SBB, MPO, ACP Especially associated w/ M1 to M3
19. M6 Erythroleukemia Erythroid precursor predominates Blast are also Increased Dx when > 50% of BM cells are erythroid precursors and Myeloblast represent > 30% of Non-Erythroidcells M7 Megakaryoblast are identified by Ab against Platelet-associated Antigens
20.
21. TREATMENT / PROGNOSIS With ChemoTx 60% Complete remission 15-30% remain free from disease for 5 years t(8;21) , inv(16) Relative good response to chemoTx Allogenic BM therapy High risk forms AML Develop from myelodysplastic syndrome Relapse AML
22. Vit A derivative Overcome the block in differentiation r/t t(15,17) and presence of RAR PML fusion protein Ultimately relapses when used alone Fail to prevent self-renewal of neoplastic progenitor cells TREATMENT / PROGNOSIS
24. AML-M1 M1- Blast cells are minimally differentiated Express CD 34 (marker of multipotent stem cells ) Negative for CD 64 ( marker of mature myeloid cells ) (+) CD33 ( marker for immature myeloid cells Subset (+) CD 15 ( marker for more mature myeloid cell
25. Acute Myeloblastic Leukemia w/ Maturation M2 Myeloblast represent 20% (WHO) to 89% of total marrow cells > 10% of NEC are promyelocyte to neutrophils Auer rods are usually present –mulitple
26. ACUTE PROMYELOCYTIC LEUKEMIA M3(35-40y/o) Promyelocytes predominate Azurophilic granules abundant & stain intenselyHypergranularpromyelocytes Auer rods almost always (+) , multiple or clusters Hemorrhagic complications frequent due to DIC Initiated by PROCOAGULANT materials from Leukemic cell Granules
27. ACUTE MONOCYTIC LEUKEMIA M5 Promyelocytes and Blast Gum Infiltrates 2 types Poorly Differentiated M5A LARGE BLAST >80% OF MARROW MONOCYTIC CELLS Differentiated M5B FEWER MONOBLAST < 80% OF MARROW MONOCYTIC CELLS MORE PROMONOCYTES & MONOCYTES
28. ERYTHROLEUKEMIA M6 Erythroblast predominates Myeloblast are also Increased > 50% NC of BM are Erythroblast >20% (WHO) of NEC are Myeloblast