This document discusses myeloproliferative disorders (MPDs), which are clonal stem cell diseases that result in increased and abnormal blood cell production. It describes the main MPDs: polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis (MF). PV is characterized by elevated red blood cell counts. ET results in sustained elevated platelet counts. MF involves clonal stem cell changes that cause fibrosis of the bone marrow and enlargement of the spleen and liver. The document provides details on clinical features, diagnostic criteria, genetic mutations, outcomes, and treatment options for each condition.
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
ACUTE MYELOID LEUKEMIA is a neoplastic disease characterized by
infiltration of the blood,
bone marrow, and
proliferative, clonal undifferentiated cells of the hematopoietic system.
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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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.
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!
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. MYELOPROLIFERATIVE
DISORDERS (MPD)
MPD are clonal diseases originating in
pluripotential haematopoietic stem cell.
The clonal expansion results in increased and
abnormal haematopoiesis and produces a
group of interrelated syndromes, classified
according to the predominant phenotypic
expression of the myeloproliferative clone.
3. CHRONIC MYELOPROLIFERATIVE
DISORDERS (MPD)
Neoplastic (clonal) disorders of hemopoietic
stem cells
Over-production of all cell lines, with usually
one line in particular
Fibrosis is a secondary event
Acute Myeloid Leukemia may occur
4. Rationale for classification
Classification is based on the lineage of the
predominant proliferation
Level of marrow fibrosis
Clinical and laboratory data (BPF, BM,
cytogenetic & molecular genetic)
5. Myeloproliferative disorders
WHO Classification of CMPD
Ch Myeloid leukemia
Ch Neutrophillic leukemia
Ch Eosinophillic leukemia / Hyper Eo Synd
Polycythemia Vera
Essential Thrombocythemia
Myelofibrosis
CMPD unclassifiable
6. Myeloproliferative disorders
Ch Myeloid leukemia (BCR-ABL positive)
Polycythemia Vera
Essential Thrombocythemia
Myelofibrosis
– Specific clincopathologic criteria for diagnosis
and distinct diseases, have common features
– Increased number of one or more myeloid cells
– Hepatosplenomegaly
– Hypercatabolism
– Clonal marrow hyperplasia without dysplasia
– Predisposition to evolve
7. Bone marrow stem cell
Clonal abnormality
Granulocyte
precursors
Red cell
precursors
Megakaryocytes Reactive
fibrosis
Essential
thrombocytosis
(ET)
Polycythaemia
rubra vera
(PRV)
Myelofibrosis
AML
Chronic myeloid
leukemia
70%
10% 10%
30%
9. POLYCYTHEMIA VERA
Chronic, clonal myeloproliferative disorder
characterized by an absolute increase in
number of RBCs
2-3 / 100000
Median age at presentation: 55-60
M/F: 0.8:1.2
10. POLYCYTHEMIA VERA (PV)
(Polycythaemia rubra vera)
Definition of polycythemia
Raised packed cell volume (PCV / HCT)
Male > 0.52 (52%)
Female > 0.48 (48%)
Classification
Absolute
Primary proliferative polycythaemia (polycythaemia vera)
Secondary polycythaemia
Idiopathic erythrocytosis
Apparent
Plasma volume reduced but no red cell mass changes
11. 11
ERYTHROCYTOSIS (Classification)
I. Absolute erythrocytosis (Polycythemia):
A. Secondary erythrocytosis (abnormal increase of serum
erythropoietin level)
1. Erythrocytosis secondary to decreased tissue oxygenation:
a) chronic lung diseases
b) cyanotic congenital heart diseases
c) high-altitude erythrocytosis
d) hypoventilation syndromes
- carboxyhemoglobin in „smoker’s polycythemia”
12. POLYCYTHEMIA VERA (PV)
Clinical features
Age
– 55-60 years
– May occur in young adults and rare in childhood
Symptoms common to all erythrocytosis
– Headache, mental acuity, weakness
Symptoms more specific to P vera and myeloproliferative
diseases.
– Pruritis after bathing
– Erythromelalgia
– Hypermetabolic symptoms
– Thrombosis (arterial or venous)
– Hemorrhage
13. POLYCYTHEMIA VERA
physical examination
1. Splenomegaly – is present in 75% of patients at the
time of diagnosis.
2. Hepatomegaly - is present in approximately 30% of
patients at the time of diagnosis.
3. Hypertension
4. On examination of the eye grounds, the vessels may be
engorged, tortuous, and irregular in diameter; the veins
may be dark purple.
Facial plethora
15. PRV - DIAGNOSIS
exclude secondary polycythemia
look for features of primary polycythemia
measure erythropoietin
JAK-2 mutation analysis
16. POLYCYTHEMIA VERA
Lab Findings
CBC
– Hgb/Hct
– WBC in 45%
– Plts in 65%
– Basophilia (seen in all MPDs)
Uric acid (can lead to gout)
Positive JAK2 V617F mutation in about 97 percent of
patient
17. JAK2 Mutation
JAK2 :is gene in short arm of chromosome 9
that encoded cytoplasmic tyrosine kinase
activity which increase cellular proliferation
and cell survival
Abnormal signalling in PV through JAK2 was
first proposed in 2004
a single nucleotide JAK2 somatic mutation
(JAK2V617F mutation) in the majority of PV
patients
23. THROMBOCYTOSIS
Etiology of Thrombocytosis
Primary - if the thrombocytosis is caused by a
myeloproliferative neoplasm, the platelets are frequently
abnormal and the patient may be prone to both bleeding and
clotting events.
Secondary - if thrombocytosis is secondary to another disorder
(reactive), even patients with extremely high platelet counts
(e.g., > 1,000,000 cells/μl) are usually asymptomatic.
Definition: thrombocytosis is defined as a platelet count > 450,000 cells/μL
24.
25. 25
ESSENTIAL THROMBOCYTHEMIA
(ET)
ET is a clonal myeloproliferative disorder
characterized by bone marrow hyperplasia
with excessive proliferation of
megakaryocytes and sustained elevation of
the platelet count.
26. ESSENTIAL
THROMBOCYTHEMIA (ET)
Neoplastic stem cell disorder causing
dysregulated production of large numbers of
abnormal platelets
Abnormal platelets aggregate, causing
thrombosis
Abnormal platelets also cause bleeding
27. 27
ESSENTIAL THROMBOCYTHEMIA
clinical picture
1. Thrombotic complications (intermittent or permanent occlusion of small
blood vessels)
transient cerebral ischemic episodes that may progress to
infarction
peripheral arterial occlusive disease associated with erythromelalgia”
2. Hemorrhagic complications - bleeding after surgery and spontaneus upper
gastrointestinal bleeding
3. Splenomegaly - 20-50% patients
4. Hepatomegaly - rarely
28. 28
ESSENTIAL THROMBOCYTHEMIA
laboratory findings
Thrombocytosis (in most patients patients>1000 G/l)
Numerous thrombocyte aggregates in peripheral blood
smear
Leukocytosis, usually less than 20
Neutrophilia and a mild shift to the left(usually to
metamyelocyte)
Slight eosinophilia and basophilia
Marked hyperplasia of the megakaryocytes in the BM
JAC 2 mutain in about 50 of patient
29.
30. ET - OUTCOMES
Most patients with ET enjoy a normal life expectancy
Like PV, the major risks are secondary to thrombosis and disease
transformation:
▪ 15-year cumulative risks:
▪ thrombosis - 17% risk
▪ clonal evolution into either myelofibrosis (4%) or AML (2%)
High risk for thrombosis:
▪ age ≥ 60
▪ prior thrombosis
▪ long-term exposure to a plt count of > 1,000,000
32. MYELOFIBROSIS
Clonal stem cell disorder affecting megakaryocytes
predominantly
All myeloproliferative disorders can result in a spent phase
which can be difficult to distinguish from primary MF
33. MYELOFIBROSIS
Myelofibrosis is a chronic myeloproliferative disease with
clonal hematopoesis and secondary(non-clonal)
hyperproliferation of fibroblasts (stimulated by PDGF, TGF-
released from myeloid cells, mainly from neoplastic
megakaryocytes) with increased collagen synthesis. It
produces bone marrow fibrosis and to extramedullary
hematopoesis in the spleen or in multiple organs
34. MYELOFIBROSIS
Insidious onset in older people
– asymptomatic (15% - 30%)
– severe fatigue
Splenomegaly- massive
Hepatomegaly
Hypermetabolic symptoms
– Loss of weight, fever and night
sweats
Bleeding problems
Bone pain
Gout
Can transform to acute
leukaemia in 10-20% of cases
35. MYELOFIBROSIS
Anaemia
High WBC at presentation
Later leucopenia and
thrombocytopenia
Leucoerythroblastic blood film
Tear drops red cells
Bone marrow aspiration- Failed
due to fibrosis
Trephine biopsy- fibrotic
hypercellular marrow
JAK2+ (V617F) in
approximately 50% of cases
36. Pathological Features of Peripheral Blood and Bone
Marrow in Patients with Myelofibrosis with Myeloid
Metaplasia
37. MF - OUTCOME
As fibrosis progresses, cytopenias worsen leading to a
transfusion dependency
▪ symptoms related to extrmedullary hematopoiesis increase
(worsening splenomegaly) also frequently identified
38. 38
MYELOFIBROSIS
- prognosis
- a median survival of 3,5 to 5,5 years
- the principal causes of death are infections,
thrombohemorrhagic events, heart failure, and
leukemic transformation
- leukemic transformation occurs in
approximately 20% of patients during first 10
years
