BIBLIOGRAPHY:
Datta Parul, Textbook of Pediatric Nursing, edition 4, The medical sciences publishers, 4838/24 Ansari road, Daryaganj, New Delhi, 110002, India
INTRODUCTION
Leukemia is the most common type of childhood malignancy.
It is characterized by persistent and uncontrolled production immature and abnormal WBCs.
It is a disease of abnormal proliferation and maturation of bone marrow which interferes with the production of normal RBCs, WBCs and platelets.
Leukemia is defined as uncontrolled neoplastic proliferation of leukocyte precursors.
According to National Cancer Institute,
Leukemia is defined as a cancer that starts in blood-forming tissue, such as the bone marrow, and causes large number of abnormal cells to be produced and enter the bloodstream.
95-98% of childhood leukemia are acute type.
70-75% of acute lymphocytic leukemia.
common malignancy of children less than 15 years.
peak incidence is four years of age.
males are more affected than females.
twice more common in white then black in children.
The exact cause is unknown.
viruses like HPV ,Epstein Barr virus ,human T cell lymphoma leukemia virus (HTLV).
Radiations
exposure to chemicals and drugs like benzene and Dilantin
familial predisposition
chromosomal abnormalities like Down syndrome
Genetic like Fanconi's anemia ,bloom syndrome
ACUTE LYMPHOCYTIC LEUKEMIA
Primary disorder of bone marrow in which normal bone marrow elements are replaced by immature or undifferentiated blast cells.
develop when lymphoid cell line is affected.
characterized by anemia, thrombocytopenia, neutropenia, especially granulocytopenia.
the incidence rate is one in 2000 live birth.
the peak age of onset is 3 to 7 years and males are more affected than females
According to French American British classification on the basis of cell morphology it is classified as
L1
L2
L3
According to type of cell it is classified as
T cell
B cell
Pre-B cell
Null cell
T cell
10 to 15% ,high risk ,seen in older children especially males ,featured as mediastinal mass ,hepatosplenomegaly ,high WBC count ,CNS involvement and has poor prognosis.
B cell
1 to 2% children ,aggressive form ,poor prognosis and high-risk type.
Pre-B cell
Good prognosis and respond well to therapy.
Null cell
No cellular surface markers (80% ).
Great imitator, with vague and varied signs and symptoms, resembling almost any disease.
Peripheral blood examination which shows decrease hemoglobin, RBC, hematocrit and platelet count
bone marrow analysis in which large number of lymphoblasts and lymphocytes with hypercellular visible.
chest X-ray
CSF
Chemotherapy
radiation therapy
bone marrow transplantation
supportive and symptomatic management
Chemotherapy
Remission induction chemotherapy
Vincristine, Prednisolone, Asparaginase and Adriamycin are given for 4-6 weeks.
maintenance therapy or systemic continuation
6 MP (Mercaptopurine) and MTX (Methotrexate) are given for 2.5-3 years.
late intensification or THERAPY
Blood coagulation disorders and laboratory diagnosis
Blood coagulation disorders and laboratory diagnosis
Coagulation disorders are disruptions in the body's ability to control blood clotting. Coagulation disorders can result in either a hemorrhage (too little clotting that causes an increased risk of bleeding) or thrombosis (too much clotting that causes blood clots to obstruct blood flow).
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Pancytopenia is a reduction in the number of RBC, WBC and platelet. It's a combination of anaemia, leukopenia and thrombocytopenia. Pancytopenia caused by Decreased bone marrow function and increased peripheral destruction. diseases are diagnosed by physical examination, complete blood counting, peripheral smear examination, bone marrow examination and other special methods. Treatment to pancytopenia is treated to anaemia, thrombocytopenia and leukopenia
acute leukemia
For More Medicine Free PPT - http://playnever.blogspot.com/
For Health benefits and medicine videos Subscribe youtube channel - https://www.youtube.com/playlist?list=PLKg-H-sMh9G01zEg4YpndngXODW2bq92w
Summary - Neoplasms of infancy and childhood - Asem M. Shadid Asem Shadid
Neoplasms of infancy and childhood :
obj :
1. Describe the findings from the history and physical exam that suggest malignant disease.
2. Know the incidence rates of the major childhood neoplasms and the significance of neoplasms in childhood mortality.
3. Identify the presenting symptoms, physical findings, and diagnostic tests for the major neoplasms (leukemia, CNS tumors, lymphoma, neuroblastoma and Wilm's tumors).
4. Recognize the major therapeutic modalities for childhood neoplasms and the relative advantages and disadvantages of each (chemotherapy, surgery, irradiation, bone marrow transplants).
BIBLIOGRAPHY:
Datta Parul, Textbook of Pediatric Nursing, edition 4, The medical sciences publishers, 4838/24 Ansari road, Daryaganj, New Delhi, 110002, India
INTRODUCTION
Leukemia is the most common type of childhood malignancy.
It is characterized by persistent and uncontrolled production immature and abnormal WBCs.
It is a disease of abnormal proliferation and maturation of bone marrow which interferes with the production of normal RBCs, WBCs and platelets.
Leukemia is defined as uncontrolled neoplastic proliferation of leukocyte precursors.
According to National Cancer Institute,
Leukemia is defined as a cancer that starts in blood-forming tissue, such as the bone marrow, and causes large number of abnormal cells to be produced and enter the bloodstream.
95-98% of childhood leukemia are acute type.
70-75% of acute lymphocytic leukemia.
common malignancy of children less than 15 years.
peak incidence is four years of age.
males are more affected than females.
twice more common in white then black in children.
The exact cause is unknown.
viruses like HPV ,Epstein Barr virus ,human T cell lymphoma leukemia virus (HTLV).
Radiations
exposure to chemicals and drugs like benzene and Dilantin
familial predisposition
chromosomal abnormalities like Down syndrome
Genetic like Fanconi's anemia ,bloom syndrome
ACUTE LYMPHOCYTIC LEUKEMIA
Primary disorder of bone marrow in which normal bone marrow elements are replaced by immature or undifferentiated blast cells.
develop when lymphoid cell line is affected.
characterized by anemia, thrombocytopenia, neutropenia, especially granulocytopenia.
the incidence rate is one in 2000 live birth.
the peak age of onset is 3 to 7 years and males are more affected than females
According to French American British classification on the basis of cell morphology it is classified as
L1
L2
L3
According to type of cell it is classified as
T cell
B cell
Pre-B cell
Null cell
T cell
10 to 15% ,high risk ,seen in older children especially males ,featured as mediastinal mass ,hepatosplenomegaly ,high WBC count ,CNS involvement and has poor prognosis.
B cell
1 to 2% children ,aggressive form ,poor prognosis and high-risk type.
Pre-B cell
Good prognosis and respond well to therapy.
Null cell
No cellular surface markers (80% ).
Great imitator, with vague and varied signs and symptoms, resembling almost any disease.
Peripheral blood examination which shows decrease hemoglobin, RBC, hematocrit and platelet count
bone marrow analysis in which large number of lymphoblasts and lymphocytes with hypercellular visible.
chest X-ray
CSF
Chemotherapy
radiation therapy
bone marrow transplantation
supportive and symptomatic management
Chemotherapy
Remission induction chemotherapy
Vincristine, Prednisolone, Asparaginase and Adriamycin are given for 4-6 weeks.
maintenance therapy or systemic continuation
6 MP (Mercaptopurine) and MTX (Methotrexate) are given for 2.5-3 years.
late intensification or THERAPY
Blood coagulation disorders and laboratory diagnosis
Blood coagulation disorders and laboratory diagnosis
Coagulation disorders are disruptions in the body's ability to control blood clotting. Coagulation disorders can result in either a hemorrhage (too little clotting that causes an increased risk of bleeding) or thrombosis (too much clotting that causes blood clots to obstruct blood flow).
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Pancytopenia is a reduction in the number of RBC, WBC and platelet. It's a combination of anaemia, leukopenia and thrombocytopenia. Pancytopenia caused by Decreased bone marrow function and increased peripheral destruction. diseases are diagnosed by physical examination, complete blood counting, peripheral smear examination, bone marrow examination and other special methods. Treatment to pancytopenia is treated to anaemia, thrombocytopenia and leukopenia
acute leukemia
For More Medicine Free PPT - http://playnever.blogspot.com/
For Health benefits and medicine videos Subscribe youtube channel - https://www.youtube.com/playlist?list=PLKg-H-sMh9G01zEg4YpndngXODW2bq92w
Summary - Neoplasms of infancy and childhood - Asem M. Shadid Asem Shadid
Neoplasms of infancy and childhood :
obj :
1. Describe the findings from the history and physical exam that suggest malignant disease.
2. Know the incidence rates of the major childhood neoplasms and the significance of neoplasms in childhood mortality.
3. Identify the presenting symptoms, physical findings, and diagnostic tests for the major neoplasms (leukemia, CNS tumors, lymphoma, neuroblastoma and Wilm's tumors).
4. Recognize the major therapeutic modalities for childhood neoplasms and the relative advantages and disadvantages of each (chemotherapy, surgery, irradiation, bone marrow transplants).
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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.
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
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.
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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.
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.
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
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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leucemias 2.pptx
1. son aquellas que afectan la producción de los elementos formes de la
sangre como: los glóbulos rojos, glóbulos blancos, la hemoglobina,
las proteínas plasmáticas, el mecanismo de coagulación
(hemostasia), causando serios problemas a nivel sistémico.
TRASTORNOS HEMATOLOGICOS EN NIÑOS
2. EPISTAXIS
salida de sangre al exterior por vía anterior
o posterior, de origen endonasal, retronasal
o extranasal, causada por la ruptura de los
elementos vasculares que garantizan la
irrigación de las fosas nasales, senos
paranasales y la nasofaringe.
Trastornos de la Coagulación
Déficit de coagulación o trastornos de la
misma incluyen la Enfermedad de Von
Willebrand, púrpura trombocitopénica
idiopática (PTI), trombocitopenia, hemofilia,
deficiencias de factores, las deficiencias de
vitaminas (A, D, C, E, o K), leucemia y otras
coagulopatías congénitas y adquiridas.
3. la enfermedad de Von Willebrand, se manifiesta por sangrado espontáneo de
las mucosas. Se caracteriza por un tiempo de sangrado prolongado, una
deficiencia de factor VIII y un deterioro de adhesividad de las plaquetas con un
recuento normal de las mismas.
Las enfermedades vasculares en los niños incluyen la Telangiectasia
Hemorrágica Hereditaria (THH), alteraciones del colágeno y otros tipos de
vasculitis. Aquí se excluyen los hemangiomas y las malformaciones
vasculares como aneurismas.
La hemofilia presentan hemorragias tisulares (p. ej., hemartrosis, hematomas musculares,
hemorragia retroperitoneal). La hemorragia puede ser inmediata o producirse lentamente, lo que
depende del grado de traumatismo y de la concentración plasmática de factor VIII o IX.
.
4. LEUCEMIAS
Es la proliferacion neoplasica de celulas
hematopoyeticas en una estirpe celular con
posterior proliferacion y expansion.
.
se origina en las células que
normalmente madurarían hacia
los diferentes tipos de células
sanguíneas.
la leucemia se origina en formas tempranas
de glóbulos blancos, pero algunas leucemias
comienzan en otros tipos de células
sanguíneas
6. Leucemia linfocítica (linfoblástica)
aguda (LLA).
Este es el tipo de leucemia más común en los
niños Se inicia a partir de los linfoblastos, las
células que forman los linfocitos en la médula
ósea.
Se inicia a partir de los mieloblastos o células
mieloides que forman muchos glóbulos blancos,
además de glóbulos rojos y plaquetas.
las células de la línea mieloide (mieloblastos) proliferan
de forma anormal invadiendo progresivamente la
médula ósea e interfiriendo la producción de células
normales de la sangre, lo que origina insuficiencia
medular e infiltra tejidos extramedulares.
las células cancerosas desplazan las células
sanguíneas sanas, lo cual puede causar
fiebre, fatiga, formación de moretones con
facilidad, sangrado, infecciones y otros
problemas
Leucemia mielógena (mieloide, mielocítica,
no linfocítica) aguda (LMA).
tienen demasiados glóbulos blancos inmaduros
(blastos) en su médula ósea. Estas células no
funcionan con normalidad. Ellas desplazan a los
glóbulos blancos, los glóbulos rojos y las plaquetas
normales.
el cuerpo tiene mayor dificultad para combatir
infecciones, la piel se vuelve pálida y el paciente
desarrolla problemas de sangrado.
7. Leucemia mielógena
crónica (LMC).
la progresión es insidiosa, con un estadio "benigno"
asintomático (malestar general, anorexia, descenso de
peso) que finalmente da lugar a estadios acelerados o
blásticos con signos más ominosos.
.
Los signos y los síntomas pueden estar ausentes o
pueden observarse adenopatías, esplenomegalia,
hepatomegalia, fatiga, fiebre, sudoración nocturna,
pérdida de peso no intencional y saciedad temprana
.
a LMC es una leucemia crónica. Esto significa que se
desarrolla lentamente con el paso del tiempo. Por eso, pueden
pasar semanas o meses hasta que los niños desarrollen
síntomas
Al igual que la LMA, se inicia a partir de los mieloblastos
o células mieloides que forman muchos glóbulos
blancos, además de glóbulos rojos y plaquetas.
acumulación progresiva de linfocitos B malignos
fenotípicamente maduros. Los sitios primarios de la
enfermedad incluyen la sangre periférica, la médula
ósea, el bazo y los ganglios linfáticos.
La leucemia linfocítica crónica ocurre cuando hay cambios
en el material genético (ADN) de las células de la médula
ósea. No se conoce la causa de estos cambios genéticos.
Leucemia linfocítica
crónica (LLC).
8. CAUSAS SINTOMAS
Se han encontrado cambios
(mutaciones) en los genes de las
células de la médula ósea. Estos
cambios pueden ocurrir temprano en
la vida de un niño o incluso antes del
nacimiento
Los síntomas pueden ser levemente distintos en cada niño. Estos
pueden incluir:
9. La púrpura es producida por la extravasación de células sanguíneas a la piel
y/o mucosas, dando origen a lesiones de coloración purpúrea que no
desaparecen a la vitropresión.
Se clasifican de acuerdo con su localización.
PURPURAS
Púrpuras superficiales: se denominan petequias
las lesiones menores de 2 mm y equimosis las
de mayor de 1 cm. . Las de tamaño intermedio
constituyen la púrpura propiamente dicha.
Púrpuras profundas o hematomas: cuando
invade los distintos estratos cutáneos
10. Etiopatogenia
Puede producirse por alteración de alguno de los tres
componentes de la hemostasia: plaquetas, factores de la
coagulación o lesiones de la pared vascular (vasculitis).
púrpuras trombopénicas o
plaquetopenias
se produce una disminución aislada
del recuento plaquetario a valores
<100-150.000/ μl
Producidas por descenso de
la producción plaquetaria,
que puede ser de origen
congénito o adquirido.
Por un aumento de la
destrucción de plaquetas
de causa inmunitaria o no
inmunitario
Por alteración de la
distribución plaquetar con
secuestro de plaquetas en
un bazo aumentado de
tamaño o en otros órganos
Las púrpuras trombopáticas o
plaquetopatía
son cuadros más infrecuentes,
debidos a alteraciones de la
función plaquetaria
es un tiempo de hemorragia/tiempo de obturación
(TO) alargado, con un número de plaquetas
normal o discretamente disminuido
11. La púrpura de Schönlein-
Henoch (PSH).
es una enfermedad en la
que los vasos sanguíneos
pequeños se hinchan e
irritan, a esta afección se le
llama vasculitis.
dolor en las articulaciones,
dolor abdominal o
problemas renales.
sarpullido llamado púrpura
palpable que se presenta
como manchas rojizas
oscuras en los pies, las
piernas y las nalgas.
Se aconseja reposo en
cama los primeros días. Los
AINE se emplean para
aliviar las molestias
articulares.
Púrpura trombocitopénica inmune (idiopática) en
niños
es un trastorno de la sangre que provoca una disminución
en el número de plaquetas en la sangre.
La PTI puede ser aguda o
crónica:
Púrpura trombocitopénica aguda. Es la más común en
niños pequeños (de entre 2 y 6 años de edad).
Púrpura trombocitopénica crónica. Este trastorno puede
comenzar a cualquier edad. Los síntomas duran por lo
menos 12 meses
12. Blood
Donation
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33. Next Week
•Here you can enter a subtitle if you
need it
•Here you can enter a subtitle if you
need it
•Here you can enter a subtitle if you
need it
•Here you can enter a subtitle if you
need it
34. Análisis de sistema
Conclusiones
There are many variations of passages of
Lorem Ipsum available, but the majority have
suffered
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Lorem Ipsum available, but the majority have
suffered
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Lorem Ipsum available, but the majority have
suffered
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suffered
35. Mobile Web
•You can replace the image on the
screen with your own work. Just
delete this one and add yours
You can replace the image on the
screen with your own work. Just
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STRENGTHS
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44. Análisis
It is a long established fact that a reader will be
distracted by the readable content of a page when
looking at its layout. The point of using Lorem Ipsum is
that it has a more-or-less normal distribution of letters,
as opposed to using 'Content here.
Análisis de datos
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