This presentation provides information about chronic myeloid leukemia (CML). It begins by outlining 8 learning objectives about CML, including defining it, describing its subtypes and epidemiology, explaining its pathophysiology and genetic alterations, comparing its clinical signs in different phases, and more. It then covers CML's introduction, pathogenesis involving the Philadelphia chromosome and BCR-ABL fusion gene, epidemiology and risk factors, clinical features in chronic and advanced phases, diagnosis methods including cytogenetics, and reference books for further information. The goal is for students to understand CML and be able to answer questions about classifying, detecting, diagnosing, and comparing its various aspects.
Chronic myelogenous leukemia (CML) - pluripotential stem cell disease
A malignancy the treatment of which has been revolutionised over the last decade.
Here is a comprehensive discussion on the disease
Chronic myelogenous leukemia (CML) - pluripotential stem cell disease
A malignancy the treatment of which has been revolutionised over the last decade.
Here is a comprehensive discussion on the disease
Learning Objectives:
Introduction
Definition of CML
Philadelphia Chromosome
Normal Granulopoiesis
Pathogenesis of CML
Aetiology
Incidence
Clinical Features
Phases of CML
Lab Diagnosis of CML
Course & Prognosis
Differential Diagnosis
Brief Overview of Treatment
Chronic Lypmhocytic leukemia/SLL/B-PLL/T-PLL/ATLL By SOLOMON SUasb by SOLOMON SUASB
the following presenation include
Introduction/Background
• Etiology of CLL
• Symptoms
• Test and Diagnosis
• Staging
• Prognosis
• Treatment
• B Cell diseases BPLL
• T cell diseases
T-PLL
ATLL
LGLL
acute leukemia
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Learning Objectives:
Introduction
Definition of CML
Philadelphia Chromosome
Normal Granulopoiesis
Pathogenesis of CML
Aetiology
Incidence
Clinical Features
Phases of CML
Lab Diagnosis of CML
Course & Prognosis
Differential Diagnosis
Brief Overview of Treatment
Chronic Lypmhocytic leukemia/SLL/B-PLL/T-PLL/ATLL By SOLOMON SUasb by SOLOMON SUASB
the following presenation include
Introduction/Background
• Etiology of CLL
• Symptoms
• Test and Diagnosis
• Staging
• Prognosis
• Treatment
• B Cell diseases BPLL
• T cell diseases
T-PLL
ATLL
LGLL
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
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
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.
4. After reading this presentation students will be
able to solve the followings questions…………..
. 1. Define and Classify the chronic myloid leukemia?
2.Name the subtypes of chronic myelogenous leukemia (CML)?
3.Describe the epidemiology of CML ?
4.Explain the pathophysiology of this leukemia?
5.Delineate the usefulness of detection of genetic alterations in CML?
6.Compare the clinical signs and symptoms of this leukemia in the three
phases of chronic myelogenous leukemia?
7.Describe the cellular aspects of CML?
8.Explain the application of cytochemistry in the diagnosis of CML compared
to a leukemoid reaction?
5. INTRODUCTION;
It is one of the myeloproliferative neoplasm (MPN) of
pluripotent hematopoietic stem cell characterized
by overproduction of cells of the myeloid series
which results in marked splenomegaly and
leukocytosis.
It have presence of Philadelphia chromosome
and/or BCR/ABL fusion gene in all the
neoplastic cells.
It constitutes 15% of all leukemia.
6.
7.
8. It occure mostly in Adults .
It is Insidious in nature.
It take Months to years.
It occure with predominance of mature
granulo-cytes and their precursors accumu-
lating in excess in the marrow and blood.’
It have Mild anemia.
It have Mild thrombocytopenia.
9.
10.
11.
12. It account 15% of all Leukemia,
In 2015 approximately 6500 cases were noted of CML in
US.
Highest rate;
Approximately 1.5 per 100,000 persons account is the
highest rate of CML occurring in US and Switzerland,
Lowest rate;
Its lowest rate is .7 per 100,000 persons occurring in china
and Sweden,
13.
14. 2.3 per 100,000 persons for man is the age
adjusted incidence of CML in US.
1.2 per 100.000 persons for woman is the age
adjustment rate of CML in US.
Age specific rate;
It increase logarithmically with age,
less than 10 percent of all cases occur in
persons between 1 and 20 years old.
15.
16. Its rate of incidence is from .2 per 100,000 to 10 per
100,000 in people younger than 20 years,
CML represents approximately 3 percent of all childhood
leukemia's
No familial predisposition,
Its incidence is increased with obesity and weight.
17. Exposure to ionizing radiation and benzene is the risk
factor for CML.
In humans, each cell normally contains 23 pairs
of chromosomes, for a total of 46. Twenty-two of these
pairs, called autosomes, look the same in both males and
females. The 23rd pair, the sex chromosomes, differ
between males and females.
18.
19. Is chromosomes have some genes which play
a key role In the activity of cells like division
and differentiation so whenever these
become mutated there is abnormal division
occurs and also there is lake of
differentiation i.e. CML ……Ex
20.
21. Philadelphia (Ph) Chromosome ;
Acquired chromosomal abnormality in all proliferating
hematopoietic stem cells (erythroid, myeloid, monocytic
and megakaryocytic precursors).
Balanced reciprocal translocation between long arm of
chromosome 9 and 22, i.e.t (q9; q22)(q34;q11) .It
increases the length of chromosome 9 and shortening of
22. This shortened chromosome 22 is known as
Philadelphia chromosome .
22.
23. BCR-ABL Fusion Gene ;
ABLproto-oncogene from chromosome 9
joins the BCR on chromosome 22.
It produces a new chimeric (fusion) gene
called BCR-ABL, thus converting ABL proto-
oncogene into oncogene. The product of the
fusion gene plays a central role in
development of chronic myloid leukemia.
The product of this oncogene i.e.,
oncoprotein(e.g. p210) causes cell division
and inhibition of apoptosis.
24. This oncoprotien (tyrosine kinas ) stimulates
uncontrolled production of abnormal blood
cells by B/M.
Oncogenic role of p210 (tyrosine kinas)is
found in association with increased G-CSF
and platelet-derived growth factor.
So due to this process a large number of
myeloid cells produced and released into the
blood and When immature are unable to
work properly, known as blasts.
25.
26. • Age: usually occurs between 40 to 60 years
of age.
• Sex: males slightly more affected than
females.
• Onset: insidious.
Symptoms:
• Nonspecific symptoms: fatigue, weakness,
weight loss, anorexia.
27.
28. Fullness of abdomen due to splenomegaly
(caused by leukemic infiltration and extra-
medullary hematopoiesis). Splenomegaly is
moderate to severe and is characteristic
feature in majority (80–90%) of patients.
Hepatomegaly: mild or moderate seen in 60–
70% of cases.
29.
30. Gout like symptoms
Anaemia
Hyperurecemia
Bruising
Epistaxis
Menorrhagia
Hemorrhages from other sites
Visual disturbance
31. On the basis of Prognostic features at the time of
diagnosis include age, splenomegaly, platelet count,
number of blasts or metaphases in the marrow, extent
of basophilia and eosinophilia, and chromosomal
abnormalities ,progression ,duration of the disease CML is
classified into following phase……
32.
33. In this phase granulocyte and platelets count is
close to normal,
Leukemic cell have there capacity to
differentiation and maturation,
Patient is asymptomatic ,
Less then 10% blast ,
The disease is responsive to chemotherapy and
remains stable for variable period. The
duration of this stage is 3 to 5 years.
There is no anemia,in this phase,
It can be progress to accelrated phase.
34.
35. In 70% of patients, chronic phase gradually evolves
into accelerated phase.
In this phase, leukemic cells show increasing loss
differentiation and maturation, increased
proliferation, and resistance to chemotherapy that
controlled the chronic phase.
Patient’s disease becomes more aggressive and signs
and symptoms of disease progression appear;
majority of patients in this phase eventually progress
to blast crisis within a span of few months.
36. More aggressive and lasts for few months.
Myeloblasts: 10–19%in the blood or bone marrow.
Striking basophilia(20% or more).
Persistent thrombocytopenia(less than 100 ×10 9/L) or
(<100,000 ) unrelated to therapy or persistent
thrombocytosis (more than 1000 ×109/L) or
(>1,000,000) uncontrolled by therapy.
Megakaryocytic proliferation in sheets or clusters in
association with fibrosis.
Persistent or increasing splenomegaly unresponsive to
therapy
In addition to the Philadelphia chromosome other
chromosomal abnormalities may be present
37.
38. This occurs when there is transformation to acute leukemia
and the disease becomes extremely resistant to chemotherapy.
Median survival is 2 to 6 months.
About 30% of patients progress to blastic phase without
intervening accelerated phase.
Blood picture resembles acute leukemia and has poor
prognosis.
Peripheral smear – Blasts 20% or more.
May be either myeloblast (70% cases) or lymphoblast (30%
cases).
Myeloblast does not contain Auer rods.
Thrombocytopenia causes bleeding episodes.
39.
40. A benign condition in which the high number
of white blood cells found in a blood test
resembles the numbers seen in leukemia. For
example, infectious mononucleosis can
return blood-test results with a leukemoid
reaction
Leukaemoid reaction can occur in infections,
inflammation, and malignancy. In leukaemoid
reactions due to infections or haemolysis,
leucocytosis is usually modest and shift to
left is usually up to metamyelocyte or
myelocyte stage; however occasional blast
may be seen.
41. Other features favouring leukaemoid
reaction are absence of splenomegaly
orbasophilia,presence of toxic granules
in neutrophils (in infections), normal or
increased NAP score, and absence of Ph’
chromosome.
42. Characteristics Lekemoid Reaction CML
total WBC count 60 to 100 10 9/L 50 to 500 10 9/L
left shift myelocyte 5 to 15% usually numerous
blasts 5% more than 30% blasts
toxic granulation marked especially in mild or absent
infective case
anaemia slight or absent present & progressive
NRC frequent in LEBP less frequent
due to marrow
infiltration
eosinophils & decreased increased
basophils
platelets normal or increased increased
decreased in LEBP
bone marrow hyperplasia of WBC marked hyperplasia
but to a mild extent with increased
proportion of immature
cells
clinical features C/F of causitive splenomegaly
disorders & obvious lymphadenopathy
hemorrhage
NAP score increased decreased
autopsy infiltration of organs leukemic infiltration
& tissues absent of organ & tissue
45. Peripheral blood;
Hemoglobin: usually less than 11 g/dL
Peripheral smear;
RBCs: normocytic normochromic anemia
WBCs: Marked leukocytosis(12–600 × 109/L) total leukocyte
count usually exceeds 100 × 109/ L (1,00,000/cu mm).
46. Shift to left (shift to immaturity);—
granulocytes at all stages of development
(neutrophils, metamyelocytes, myelocytes,
promyelocytes and an occasional
myeloblasts).
Predominant cells are neutrophils and
myelocytes.
Blasts are usually less than 10% of the
circulating WBCs Basophilia and eosinophilia
Platelets: platelets range from normal (150–
450 × 109/L) to greater than 1000 × 109/L.
Up to 50% have thrombocytosis.
47. Eosinophils normal or some time increased
NRBCs are seen
Absolute Basophilia
Macrocytosis
Hypogranulated myeloid cells
48. Cellularity: markedly hypercellular due to myeloid
hyperplasia.
M: E ratio: often exceeds10:1.
Erythropoiesis: diminished erythropoiesis as disease
progresses.
Myelopoiesis: marked hyperplasia. Blast cells usually less
than 10%.Basophils, eosinophils and their precursors are
usually found.
49.
50. Megakaryopoiesis;
megakaryocytic are either normal or increased.
Dwarf megakaryocytic.
Sea-blue histiocytes;
(Gaucher-like cells/pseudo Gaucher cells)
are seen.
Eosinophilic and basophilic granules are abnormal
Nuclear to cytoplasmic asynchrony
51. In Serum Uric acid
increased
Serum iron
Increased
Serum B12 and B12 binding capacity
Increased
NAP score
Decreased
Serum LDH
Elevated
Ca++ increase
53. Cytogenetic analysis in CML serves to
confirm the diagnosis.
It also has prognostic importance.
Cytogenetic analysis of bone marrow and
peripheral blood shows a characteristic
abnormality, the Philadelphia
chromosome and BCR-ABL fusion gene:
demonstrated either by chromosomal
analysis or fluorescent in situ hybridization
(FISH)or PCR based tests.