Pancytopenia is a reduction in red blood cells, white blood cells, and platelets. The document outlines an approach to evaluating a case of pancytopenia, including considering decreased bone marrow production, increased cell destruction, a thorough history and physical exam, and diagnostic tests like complete blood count, peripheral smear, and bone marrow aspiration and biopsy to determine the underlying cause. The causes of pancytopenia are grouped based on mechanism and include conditions like aplastic anemia, megaloblastic anemia, myelodysplastic syndrome, liver disease, and others.
Dr Abdullah Ansari
MBBS, MD Medicine
Aligarh Muslim University
Clinical case
Hemolytic Anemia
Intravascular vs extravascular hemolysis
Classification of hemolytic anemia
Approach to hemolysis
Patient history
Clinical features
Peripheral blood smear
Investigation
Treatment
Stroke in people under 45 years of age is less frequent than in older populations but has a major impact on the individual and society. In this article we provide an overview of the epidemiology and etiology of young stroke.
download link : https://www.dropbox.com/s/xc0fpdul47g1gu8/IgA%20Nephropathy.ppt?m
Join us on our facebook group: NephroTube...............Follow our blog: www.nephrotube.blogspot.com
lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
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
Dr Abdullah Ansari
MBBS, MD Medicine
Aligarh Muslim University
Clinical case
Hemolytic Anemia
Intravascular vs extravascular hemolysis
Classification of hemolytic anemia
Approach to hemolysis
Patient history
Clinical features
Peripheral blood smear
Investigation
Treatment
Stroke in people under 45 years of age is less frequent than in older populations but has a major impact on the individual and society. In this article we provide an overview of the epidemiology and etiology of young stroke.
download link : https://www.dropbox.com/s/xc0fpdul47g1gu8/IgA%20Nephropathy.ppt?m
Join us on our facebook group: NephroTube...............Follow our blog: www.nephrotube.blogspot.com
lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
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
A presentation made by Dr Gauhar Mahmood Azeem on the interpretations of a simple CBC and the information it can give us, Various conditions which may cause derangement are mentioned,
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.
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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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
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
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
3. Pancytopenia is a
reduction in the number of
RBCs,
WBCs and,
platelets
in the peripheral blood
below the lower limits of the age-adjusted normal
range for healthy people.
4. Therefore it is the combination of anemia,
leukopenia, and thrombocytopenia :-
Hb < 13.5 in males & 11.5 in females
Leucocyte count < 4x109
/l
Platelet count < 150x109
/l
5. It may result from
decreased production of blood cells or bone
marrow failure,
Defective stem cells,
from their immune-mediated destruction or
non-immune-mediated sequestration in the
periphery,
Deficiency of factors stimulating haematopoiesis
6. • The diagnosis is made from the results of CBC,
preferably automated and a P/S
7.
8. With Hypocellular marrow Cellular marrow with deficiency &
systemic disease
Cellular marrow with primary bone
marrow disease
Acquired aplastic anemia Vitamin B12 & Folic Acid Deficiency Aleukemic Leukemia
Inherited Bone Marrow Failure syndromes Hypersplenism Myelodysplastic syndrome
Hypocellular myelodysplastic syndrome Kala Azar Myelofibrosis
Hypocellular acute leukemia SLE, Sjogrens Syndrome, Sarcoidosis PNH
Paroxysmal Nocturnal Haemoglobinuria TB, Brucellosis Marrow Necrosis
GVHD Metastatic Solid Tumor
Lymphoma Alcoholism
Myelofibrosis Storage Disease
Infections : Mycobacterial Infections
Gelatinous transformation of bone
marrow
Chemotherapy & Drugs
Aplastic crisis in hemolytic anemia
16. History
Clinical Examination
CBC
Peripheral smear examination
Bone Marrow Aspiration
Bone Marrow Biopsy
Other specific investigations
17. Mild pancytopenia is often symptomless and detected incidentally when a full blood count/CBC
is performed for another reason.
Duration of symptoms
H/o Transfusions
H/o Haemoglobinuria
Dietary history
Socio economic status
Exposure to –
Drugs
Anti cancer, Antibiotic, Anti epileptics, Anti thyroid (Aplastic)
Barbiturates, Phenytoin, OCP ( B12 & FA)
Chemicals (Aplastic)
Radiation (Aplastic)
Infections (Aplastic)
Weight loss, fever – malignancy & inflammatory
Jaundice – Hep B & C
Infections – TB, Malaria
Joint Pain – SLE
Blood Loss
18. • A thorough physical exam is required, preferably by a hematologist.
• Weight loss and/or anorexia are harbingers of underlying infection (either
precedent to the pancytopenia or as a result of it) and malignancy.
• Spontaneous mucosal bleeding (gums, GI tract), petechiae, and purpura
with easy bruising secondary to thrombocytopenia are usually the first signs
to develop directly related to more severe pancytopenia.
• These signs are often accompanied by lymphadenopathy (underlying
infection, mononucleosis, lymphoproliferative disorder, and malignancy).
• Abdominal discomfort is a common presentation of splenomegaly and
associated conditions.
• Widespread bone pain and loss of height suggest myeloma, joint pain
systemic lupus erythematosus (SLE), and sore throat mononucleosis.
19. The following reference points to specific organ systems and associated conditions and is helpful to guide
the examination.
• Eye examination
▫ Retinal hemorrhage (thrombocytopenia)
▫ Leukemic infiltrates (acute leukemia)
▫ Jaundiced sclera (paroxysmal nocturnal hemoglobinuria, hepatitis, cirrhosis)
▫ Epiphora (dyskeratosis congenita)
• Oral examination
▫ Oral petechiae or hemorrhage (thrombocytopenia)
▫ Stomatitis or cheilitis (neutropenia, vitamin B12 deficiency)
▫ Gingival hyperplasia (leukemia)
▫ Oral candidiasis or pharyngeal exudate (neutropenia, herpes family virus infections)
• Cardiovascular examination
▫ Tachycardia, edema, congestive cardiac failure (all signs of symptomatic anemia)
▫ Evidence of prior cardiac surgery (cardiac disease associated with congenital syndromes)
▫ Respiratory examination
▫ Clubbing (lung cancer)
▫ Tachypnea (sign of symptomatic anemia)
• Abdominal examination
▫ Right upper quadrant tenderness (hepatitis)
▫ Lymphadenopathy (infection, lymphoproliferative disorder, HIV disease)
20. • Signs of chronic liver disease
▫ Splenomegaly (infection, myeloproliferative and lymphoproliferative disorders)
▫ Skin examination
▫ Malar rash (SLE)
▫ Purpura/bruising (thrombocytopenia)
▫ Reticular pigmentation, dysplastic nails (dyskeratosis congenita)
▫ Hypopigmented areas
• Hyperpigmentation, café au lait (Fanconi anemia)
• Musculoskeletal examination
▫ Short stature (Fanconi anemia, other congenital syndromes)
▫ Swelling/synovitis (SLE)
▫ Abnormal thumbs (e.g., Fanconi anemia)
• Signs associated with HIV disease
▫ Morbilliform rash early
▫ Kaposi sarcoma, ulcerating nodules later
21. • A CBC and examination of peripheral blood film by
a hematologist are essential. A standard battery of
evaluative tests may include:
▫ Serum reticulocyte count
▫ Serum LFTs
▫ Hepatic serology
▫ Serum coagulation profile, bleeding time, fibrinogen,
and D-dimer
▫ Serum direct antiglobulin test
▫ Serum B12 and folate
▫ Serum HIV and nucleic acid testing.
22. Red Cell Morphology
Normocytic normochromic with no anisopoikilocytosis, few macrocytes, no nRBCs,
reticulocytopenia – Aplastic anemia
Macro ovalocytes with Howell Jolly Bodies – Megaloblastic anemias
Tear drop cells, HJ bodies & Basophilic stippling – MDS
nRBCs, Sickle cells – Aplastic crisis in Hemolytic anemia
WBCs
Leucopenia (mostly mature ~80%) – Aplastic anemia
Neutrophils present in increased number with toxic granules, shift to left – Infections
Basophilic stippling, hypersegmented neutrophils – Megaloblastic anemia
Blasts – subleukemic leukemia
Hypogranular neutrophils, pseudo Pelger Heut Anomaly – MDS
Platelets
Normal count – rules out aplastic anemia
Giant platelets – MDS/ Hypersplenism
23. • Examination of bone marrow is almost always indicated in cases of
pancytopenia unless the cause is otherwise apparent (e.g., established liver
disease with portal hypertension).
• The bone marrow exam consists of both an aspirate and a trephine biopsy,
• The differential diagnosis of pancytopenia may be broadly classified based
on the
▫ bone marrow cellularity (reduced cellularity indicates decreased production of blood cells,
▫ whereas normal/increased cellularity indicates ineffective production or increased
destruction or sequestration of blood cells).
• Specifically, bone marrow aspirate permits examination of:
• Cytology (megaloblastic change, dysplastic changes, abnormal cell
infiltrates, hemophagocytosis, and infection [e.g., Leishman-Donovan
bodies])
• Immunophenotyping (acute and chronic leukemias, lymphoproliferative
disorders)
• Cytogenetics (myelodysplasia, acute and chronic leukemias,
lymphoproliferative disorders).
24. Aspiration
Empty particles, markedly hypocellular, only scattered mature
lymphocytes & sometimes excess plasma cells – aplastic
anemias
Pockets of cellularity with widespread hypocellularity – evolving
aplastic anemia
Hypocellular with BM Blasts (>20%) – hypoplastic leulemia
Hypocellular BM with dysplastic megakaryocytes – hypoplastic
MDS
Scattered proerythroblasts with large nuclear inclusions in
hypocellular BM - Parvovirus
25. Biopsy
Erythroid hyperplasia with megablastosis –
megaloblastic anemia
Trilineage dysplasis with ringed sideroblasts on pearl’s
stain – MDS
Infiltration by RS Cells – HL
Infiltration with malignant cells – metastasis
In PNH & Fanconi’s anemia – early stage will show
hypercellular normal appearing marrow
26. • Specific testing pinpoints diagnosis in the following conditions:
▫ Fanconi anemia: diepoxybutane (DEB) test for chromosomal breakage in
peripheral blood lymphocytes
▫ Lymphoproliferative disorders: immunophenotyping, cytogenetics, lymph
node biopsy
▫ Multiple myeloma: immunoelectrophoresis
▫ Paroxysmal nocturnal hemoglobinuria (PNH): peripheral blood
immunophenotyping for deficiency of phosphatidylinositol-glycan-linked
molecules on peripheral blood cells (e.g., CD55, CD59)
▫ CMV infection: serum IgM and IgG
▫ Epstein-Barr: serum monospot, viral capsid antigen (VCA), and Epstein-
Barr nuclear antibody (EBNA)
▫ Leishmaniasis and other rare infections: blood and bone marrow culture,
serum ELISA
▫ Rare genetic and metabolic disease: leukocyte glucocerebrosides
▫ Serum PSA in suspect cases of prostatic malignancy.
27. Pancytopenia
History, Examination, CBC, P/s, Retic count,
Iron / TIBC
Palpable spleen
With inc
retic
Sepsis/Bleeding
Blasts / Hypogranular
PMN Unexplained
splenomegaly,
M Band,
Metastasis
No specific
finding
Hyper segmented
neutrophils, Marked
anisopoikilocytosis
B12 & Folic
Acid LevelsHyper splenism, Malaria,
Leishmania
Bone Marrow Aspiration & Biopsy
HIV Antibody
Normal
Low
Trial of therapy
No response
28. Chemotherapy &
Radiotherapy
Vit B12 & Folic Deficiency Marrow Metastasis
Peripheral Blood Anisocytosis,
Poikilocytosis,
Basophilic Stippling
Oval macrocytic RBCs,
Irregular size & shape of
RBCs, hypersegmented
neutrophils (>5 lobes)
Leuko erythroblastic cell
forms
Reticulocyte Count Usually low Clumps of tumor cells
Bone Marrow Aspiration Variable hypoplasia Hypercellular, megaloblastic
erythoblasts, giant
metamyelocytes
Bone Marrow Biopsy Hypoplasia,
Magaloblastosis
Vit B12 & FA Depend on dietary
status, usually normal
VB12 and FA low in
respective deficiencies
LDH Normal Moderately raised
LFT Normal Bil (I) Raised Raised ALT & AST
Other Investigations Prolonged PT, PTT & D
Dimer, Low fibrinogen
X Ray, CT, PSA, Thyroid
USG, Mammography
29. NHL CLL Myelodysplasia
Peripheral Blood Variable, Circulating
lymphoma cells
Circulating leukemia cells Irregular or macrocytic
RBCs, dysplastic
granules,
megakaryocytes
Bone Marrow Aspiration Increased proportion of
lymphoid cells
Increased proportion of
lymphoid cells
Hypercellular, rarely
hypocellular, dysplastic
changes
Immunophenotyping Clonal population of
lymphoid cells
Clonal population of
lymphoid cells
LN Biopsy Lymphoproliferative
disorder
Lymphoproliferative disorder
Reticulocytes Usually Low, May be N
or Inc
30. Cirrhosis Hep B Hep C AIH
Peripheral Blood Macrocytes, target
cells,
stomatocytes,
acanthocytes
Macrocytes, target
cells, stomatocytes,
acanthocytes
Macrocytes, target
cells,
stomatocytes,
acanthocytes
Macrocytes, target
cells,
stomatocytes,
acanthocytes
Reticulocytes Inc or N Inc or N Inc or N Inc or N
LFT Elevated – AST,
ALT, GGT
Elevated – AST, ALT,
GGT
Elevated – AST,
ALT, GGT
Elevated – AST,
ALT, GGT
Viral Serology HCV +ve in HCV
cirrhosis
HBsAg+VE HCV +ve in HCV
cirrhosis
ANA, LKM, ASMA
+ve
Bone Marrow
Aspiration
Hypercellular,
erythroid
hyperplasia
Hypercellular,
erythroid hyperplasia
Hypercellular,
erythroid
hyperplasia
Hypercellular,
erythroid
hyperplasia