1. A 12-year-old girl presented with fever, lethargy, gum bleeding, and epistaxis. On examination, she had pallor, petechiae, hepatomegaly, and hyperpigmented knuckles.
2. Laboratory findings showed pancytopenia, macroovalocytes on peripheral smear, and low serum B12 and folate levels. Bone marrow aspiration showed megaloblastic erythroid precursors and giant myelocytes/metamyelocytes.
3. Based on the findings, she was diagnosed with megaloblastic anemia secondary to vitamin B12 and folate deficiency. Treatment involves vitamin B12 and folate supplementation.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Basic approach to a case of anemia. Investigations to do and to arrive at the diagnosis. (Management not discussed). Peripheral smear findings with pictures are included.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Basic approach to a case of anemia. Investigations to do and to arrive at the diagnosis. (Management not discussed). Peripheral smear findings with pictures are included.
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
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
- 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
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Approach to pancytopenia.pptx
1. Approach to a child with
pancytopenia
Moderator: Dr. Alka Yadav
Presenter: Dr. Animesh Debbarma
2. CYTOPENIA:
Reduction in either of cellular component of blood.
BICYTOPENIA:
Reduction in any of the 2 cell lines of blood-
• Anemia + thrombocytopenia (77.5%)
• Anemia + leukopenia (17.3%)
• Thrombocytopenia + leukopenia (5.2%)
Naseem S, Varma N, Das R, Ahluwalia J, Sachdeva MU, Marwaha RK. Pediatric patients with bicytopenia/pancytopenia: review of
etiologies and clinico-hematological profile at a tertiary center. İndian Journal of pathology and microbiology. 2011 Jan 1;54(1):75.
4. Presenting symptom of pancytopenia may be attributable to anemia, leucopenia
and/or thrombocytopenia.
• Anemia fatigue, breathlessness and cardiac symptoms
• Neutropenia febrile illness
• Thrombocytopenia mucocutaneous bleeding or bruising
5.
6. CLASSIFICATION OF PANCYTOPENIA
CAUSE
oBONE MARROW FAILURE
INEFFECTIVE MARROW PRODUCTION
MARROW SPACE OCCUPYING LESION
PERIPHERAL DESTRUCTION OF HEMATOPOIETIC CELLS
BM FINDING
HYPOCELLULAR BM
CELLULAR BM
BM INFILTRATION
INHERITANCE
ACQUIRED CONGENITAL
7. CAUSES OF PANCYTOPENIA
BM failure
Ineffective marrow
production
Nutritional
B12 deficiency
Folate deficiency
Non-nutritional
AA
MDS
Drugs
Viruses
Radiation
Marrow space
occupying lesion
Metastatic solid
tumors
Myelofibrosis
HLH
Osteopetrosis
Peripheral
destruction of
hematopoietic cells
Hypersplenism
Immune
Sepsis
8. Hypocellular bone marrow Cellular bone marrow Bone marrow infiltration
IBMFS with pancytopenia
• Fanconi anemia
• Dyskeratosis congenita
• Shwachmann-Diamond syndrome
• Amegakaryocytic thrombocytopenia
• Diamond-Blackfan anemia
Acquired aplastic anemia
Hypocellular variant of MDS
Paroxysmal nocturnal hemoglobinuria
Primary BM disease (acute leukemia,
myelodysplasia)
20 to autoimmune disorders (SLE)
Vit B12 or folate deficiency
Storage disorders (Gaucher, Niemann-Pick)
Overwhelming infections
Sarcoidosis
Hypersplenism
Metastatic solid tumors
Myelofibrosis
Hemophagocytic
lymphohistiocytosis (HLH)
Osteopetrosis
Acute myelogenous leukemia
Acute lymphoblastic leukemia
Classification of pancytopenia based on bone marrow findings
9. CLASSIFICATION OF PANCYTOPENIA BASED ON INHERITANCE
ACQUIRED INHERITED
Secondary
Radiation
Drugs & chemicals
• Direct toxicity- chemotherapy & benzene
• Idiosyncratic- chloramphenicol, anti-inflammatory
drugs, anti-epileptics
Viruses:
• EBV
• Hepatitis (non-A, B, C, E or G)
• HIV
• Parvovirus B-19
Immune diseases: SLE
Paroxysmal nocturnal hemoglobinuria
Myelodysplasia
Idiopathic
Fanconi anemia
Dyskeratosis congenita
Shwachmann- Diamond syndrome
Amegakaryocytic thrombocytopenia
Diamond-Blackfan anemia
10. APPROACH TO A CHILD WITH PANCYTOPENIA
HISTORY
LABORATORY
EVALUATION
PERIPHERAL BLOOD
EXAMINATION
BM
EXAMINATIONS
SPECIFIC
INVESTIGATIONS
11. POINTS TO CONSIDER IN HISTORY
• Age
• Sex
• Duration of symptoms
• Fever, night sweats, malaise, wt loss
• Bleeding from any site
• Jaundice
• Joint pain, rash, photosensitivity
• Any radiation exposure
• Exposure to potentially toxic chemicals
• Treatment history including herbals & drug intake , blood transfusions
• Dietary history
12. CLINICAL EXAMINATION
• Anthropometry including stature (Fanconi anemia, other congenital syndromes)
• Dysmorphic features: abnormal thumb (Fanconi anemia)
• Pallor, jaundice (PNH, Hepatitis, Cirrhosis), lymphadenopathy (infection,
lymphoproliferative disorder, HIV disease)
• Signs of congestive heart failure
• Stomatitis, cheilitis (neutropenia, vit B12 deficiency)
• Nail dystrophy (dyskeratosis congenita), leukoplakia, skin pigmentation
• Oral candidiasis, pharyngeal exudates (neutropenia, herpes family virus infections)
13. • Gum hypertrophy
• Patechiae, purpura, hyperpigmentation, café au lait (Fanconi anemia)
• Hepatosplenomegaly
• Weight loss or anorexia (underlying infections & malignancy)
• Widespread bone pain and loss of weight suggest malignancy.
14. 3 Y old boy with Fanconi anemia who
exhibit classic phenotypic features:
A. short stature, dislocated hips;
B. microcephaly, broad nasal base,
epicanthal folds, micrognathia;
C. thumb attached by a thread;
D. cafe au lait spots with hypopigmented
areas beneath
15. Physical findings in patient
with dyskeratoiss congenita:
A & B: dystrophic nails in 2
different patients
C: lacy reticular pigmentation
D: Leukoplakia of tongue
22. Other peripheral smear findings:
Anisocytosis & poikilocytosis:
Moderate degree is common
Very marked poikilocytosis: Myelofibrosis
Less degree: Aplastic anemia, marrow infiltration by lymphoma/multiple myeloma
Invariably absent: Acute leukemia
23. RETICULOCYTE COUNT
• Absolute reticulocyte count (ARC) is a marker of red cell production by bone marrow
• ARC = reticulocyte count % X RBC count
• It helps in distinguishing hypoproliferative vs hyperproliferative anemias
• Normal range of ARC: 50,000-100,000/cumm
• All cases of pancytopenia with very low ARC (< 25,000/ cmm) should be examined by bone marrow
aspiration for aplastic anaemia
• All cases of pancytopenia with high ARC (> 100,000/cmm) should also be evaluated by bone
marrow aspiration unless there is a history suggestive of sepsis or malaria.
• Pancytopenia with ARC 25,000-50,000/cmm should initially be evaluated with serum B12 , folate
and ferritin assays and if any one of these is found to be low, bone marrow aspiration is not
needed.
25. BONE MARROW EXAMINATION
Almost always indicated in cases of pancytopenia unless cause is apparent
Both aspiration and biopsy are indicated
Differential diagnosis is based on BM cellularity.
26. Hypocellular bone marrow Cellular bone marrow Bone marrow infiltration
IBMFS with pancytopenia
• Fanconi anemia
• Dyskeratosis congenita
• Shwachmann-Diamond syndrome
• Amegakaryocytic thrombocytopenia
• Diamond-Blackfan anemia
Acquired aplastic anemia
Hypocellular variant of MDS
Paroxysmal nocturnal hemoglobinuria
Primary BM disease (acute leukemia,
myelodysplasia)
20 to autoimmune disorders (SLE)
Vit B12 or folate deficiency
Storage disorders (Gaucher, Niemann-Pick)
Overwhelming infections
Sarcoidosis
Hypersplenism
Metastatic solid tumors
Myelofibrosis
Hemophagocytic
lymphohistiocytosis (HLH)
Osteopetrosis
Acute myelogenous leukemia
Acute lymphoblastic leukemia
Classification of pancytopenia based on bone marrow findings
27. Cellularity of bone marrow
• Hypocellular: excessive amount of fat cells
• Normocellular: 50-70% hematopoietic cells & 30-50% fat
• Hypercellular: 80-100% cells with little fat
NORMOCELLULAR HYPOCELLULAR
32. Other bone marrow fingings
• Erythroid hyperplasia with megaloblastosis megaloblastic anemia
• Trilineage dysplasia with ring sideroblasts on Pearl’s stain MDS
• Infiltration by malignant cells metastasis
• Empty particles, markedly hypocellular, only scattered mature lymphocytes & sometimes
excess plasma cells aplastic anemia
• Pockets of cellularity with widespread hypocellularity evolving aplastic anemia
Note:
In PNH & Fanconi anemia: early stage will show hypercellular normal appearing marrow.
38. Case 1
12 Y old girl presents to her local doctor with
• Fever
• Lethargy
• Gum bleeding and epistaxis x 2-3 days
Examination:
• Weight/height- 50% of age
• Pallor & petechiae present
• Liver: 2 cm BCM
• Hyperpigmented knuckles
• No dysmorphic features
5 months
42. MANAGEMENT OF MEGALOBLASTIC ANEMIA
Treatment depends on the underlying cause:
Folate deficiency:
•Folate deficiency d/t dietary insufficiency or increased demand is best treated with
supplements.
•1-5 mg daily x 3-4 wks.
Vit B12 deficiency:
•250-1000 µg by intramuscular route, daily for 1-2 wks & then wkly until hematocrit is normal.
•Patients with Pernicious anemia & malabsorption: monthly supplementation for life.
•Patients with neurological complications: 1000 µg daily for 2 wks every 2 wks for 6 months
monthly for life.
43. Case 2
9 year old boy presents to his pediatrician with c/o not gaining height
Dietary history, obstetric history and past history: nothing remarkable
Family is middle class, have an older son and daughter who are on 90% height and weight
General examination:
• Darker pigmentation from parents and other siblings.
• Pallor +
• No hepatosplenomegaly
44. CBC:
Hb: 6.8 g/dl
WBC: 1500/cumm
PC: 60,000/cumm
MCV: raised
PBS: few macrocytes seen, no abnormal cells
Reticulocyte count: low
Vit B12 & serum folate: Normal
47. INHERITED APLASTIC ANEMIA
FANCONI ANEMIA DYSKERATOSIS CONGENITA SHWACHMAN-DIAMOND SYNDROME
Clinical effects Microcephaly,
Thumb abnormalities,
Hypogonadism,
Skin changes (generalized
hyperpigmentation, café-au-lait spots,
hypopigmented areas)
Triad of:
Nail dystrophy
Lacy reticular pigmentation of skin
Mucosal leukoplakia
Exocrine pancreatic deficiency,
Short stature
Skeletal abnormalities,
Skin changes
Genes inactivated • FANCA, FANCB, FANCC, FANCD, FANCE,
FANCE, FANCF, FANCG, FANCI, FANCJ,
FANCL, FANCM, FANCN
• These genes encodes proteins known to
protect genome from excessive damage
induced by chemical cross linking agents.
• DKC1, TERC, TERT, TINF2, NOLA2, NOLA3
• These genes encodes proteins known to
participate in maintenance of telomeres.
SDBS
Screening &
diagnostic test
• Chromsomal breakage test
• Complementation analysis
• Gene sequencing
• Quantitative analysis of telomere length
(flow fish)
• Gene sequencing
• CT demonstrates fatty infiltration of
pancreas
• Gene sequencing
48. Above mentioned patient have no h/o drug or radiation exposure
Following other test are done:
• Viral serology: normal
• ANA: negative
• Immunophenotyping: negative for CD55, CD59
• Chromosomal breakage study to peripheral lymphocytes by
adding DEB or MMC: +ve
Final diagnosis ?
FANCONI ANEMIA
49. Diagnostic scheme
CBC
Platelets-
decreased
Hb - decreased
WBC count-
decreased
Peripheral smear
Few macrocytes
No abnormal cells
Bone marrow examination-
markedly reduced cellularity
Chromosomal breakage study +
Fanconi anemia
Reticulocyte
count- decreased
50. MANAGEMENT OF FANCONI ANEMIA
• Supportive treatment: PCV for severe anemia, platelets for severe
thrombocytopenia, & antibiotics for management of infections.
• Hematopoietic stem cell transplantation: only curative therapy for hematologic
abnormalities. Patients <10 yr old with FA who undergo transplantation using an
human leukocyte antigen (HLA)–identical sibling donor have a survival rate >80%.
• Androgens produce a response in 50% of patients, heralded by reticulocytosis and a
rise in hemoglobin within 1-2 mo. White blood cell counts may increase next,
followed by platelet counts, but it may take many months to achieve the maximum
response.
Treatment of aquired aplastic anemia: antithymocyte globulin (ATG), Cyclosporin (CsA), Androgen
51. 5 y old boy came with c/o
• Fever x 15 days (not responding to antibiotics)
• Wt loss (5 kg) since last 1 month
• Fatigue
• Generalized body ache x 10 days
• Mucocutaneous bleeding
On examination:
• Pallor +
• Purpuric spots over the whole body
• Spleen 2 cm BCM
• Liver 3 cm BCM
CASE 3
52. CBC:
Hb: 5.1 g/dl
WBC: 3,900/cumm
Platelets: 20,000/cumm
PBS: atypical cells, blast cells +
Bone marrow aspiration:
Hypercellular
>25% blasts.
Blast cells in peripheral blood Blast cells in bone marrow
What is your diagnosis ?
ACUTE LEUKEMIA
53. Other tests:
Cytochemistry:
• MPO, Sudan black B, non-specific esterase: negative
• Large block positivity with Periodic acid Schiff (PAS)
Immunophenotyping:
Positive for CD19 & CD20.
Large block positivity with periodic acid Schiff
B-cell ALL
Final diagnosis ?
54. Diagnostic scheme
CBC
Hb - decreased WBC count-
decreased
BM findings:
>25 % blasts cells
Cytochemistry
Large block positivity with PAS
Immunophenotyping
CD19+, CD20+
B-cell ALL
Platelets-
decreased
Peripheral smear
Atypical cells
Blasts cells
55. 10 Y Old male child k/c/o thalassemia major on regular blood transfusion since 6 M
of age now came with c/o
• Pain abdomen
• Abdomen distension
• Increasing transfusion requirement since last 1 year
On examination:
• Pallor +
• Icterus +
• P/A: massive splenomegaly crossing umbilicus, tender
Case 4
15 days
56. CBC:
Hb: 5.6 g/dl
WBC: 3,900/ cumm
PC: 40,000/ cumm
MCV, MCH & MCHC: normal
Reticulocyte count: increased
PBS: schistocytes, polychromasia, nucleated red cells, giant platelets
Bone marrow:
Cellular bone marrow
No blast or any abnormal cells
Schistocytes
Polychromasia
Nucleated red cells
57. Other investigations:
Serum ferritin: markedly raised
Serum bilirubin: raised
DCT: negative
B12 & folate: normal HYPERSPLENISM
What is your diagnosis ?
59. A 10 year old child came with c/o:
• High grade fever for 1 wk, associated with chills & rigor, 1-2 spike/ day
• In between fever child is well
• Headache x 1 wk
• Vomiting: 2-3 times/day
• h/o 2 times convulsion
On examination:
• Pallor +
• Icterus +
• Splenomegaly +
Case 4
60. Lab findings:
CBC:
Hb: 6.8 g/dl
WBC: 2,100/cumm
PC: 40,000/ cumm
PBS: multiple ring form inside RBCs
Other test:
Malaria card test
• P. vivax: -ve
• P. Falciparum: +ve
Multiple ring form inside RBCs
P. FALCIPARUM MALARIA
What is your diagnosis ?
61. Diagnostic scheme
CBC
Platelets- decreased Hb - decreased WBC count- decreased
Peripheral smear
Multiple
ring froms +
Malaria rapid card test
P. vivax: -ve
P. falciparum: +ve
P. falciparum malaria
High grade
fever
62. Case 6
8 year old girl came with c/o
• Intermittent fever for 6 month duration
• Severe fatigue
• Unable to walk d/t joint pain
On examination:
• Malar rash +
• Hepatomegaly +
• Bruises and petechiae +
Malar rash
63. Laboratory findings
CBC:
Hb: 6.8 g/dl
WBC: 2,100/cumm
PC: 40,000/ cumm
PBS: Schistocytes+, nucleated RBC +
Reticulocyte count: increased
Specific test:
Coomb’s test: positive
ANA: positive
BM aspiration: Hypercellular marrow
SYSTEMIC LUPUS ERYTHEMATOSUS
What is your diagnosis ?
65. REFERENCE:
• Nelson text book of pediatrics, 21st edition.
• Nathan & Oski’s Hematology and oncology of infancy & childhood
• OP Ghai, 9th edition.
• Anderson’s hematology
• Naseem S, Varma N, Das R, Ahluwalia J, Sachdeva MU, Marwaha RK. Pediatric patients with
bicytopenia/pancytopenia: review of etiologies and clinico-hematological profile at a tertiary center. İndian
Journal of pathology and microbiology. 2011 Jan 1;54(1):75.
• Garg AK, Agarwal AK, Sharma GD. Pancytopenia: Clinical approach.
• Kamal M. Approach to Pancytopenia.
• Mishra DE, Kohli AS, Yadav R, Chandra SU. Pancytopenia in Indian children: a clinico-hematological analysis. Indian
J Clin Pract. 2018;28:759-62.
• Slide share
• Google
