This case report describes a 3-year-old female patient presenting with bleeding symptoms including rashes, nosebleeds, gum bleeding, and bloody stools. Initial investigations revealed pancytopenia. The peripheral smear and bone marrow findings were suggestive of idiopathic thrombocytopenic purpura with evidence of infection rather than acute promyelocytic leukemia due to the absence of features such as organomegaly and specific immunophenotyping or cytogenetic findings. The patient was treated with antibiotics and supportive care and diagnosed with idiopathic thrombocytopenic purpura complicated by infection based on clinical presentation, investigations, and differential diagnosis workup.
Approach to Pancytopenia with cases.pptxYogeetaTanty1
Approach to pancytopenia with case based discussion and brief details regarding each condition. Causes of pancytopenia. Details of congenital causes of aplastic anemia.
Approach to Pancytopenia with cases.pptxYogeetaTanty1
Approach to pancytopenia with case based discussion and brief details regarding each condition. Causes of pancytopenia. Details of congenital causes of aplastic anemia.
We studied the review article about How I investigate eosinophilia, which was published in the International Journal of Laboratory Hematology in August 2018. This paper has clearly and simply introduced how clinicians investigate eosinophilia. Hopefully, it can be helpful to everyone who interested in this field.
Thrombocytopenia is generally defined as platelet count <150 × 109/L. It can occur due to several reasons, like decreased platelet production (e.g., inherited bone marrow failure syndromes, acquired aplastic anemia, leukemia), ineffective platelet production (myelodysplastic syndrome, megaloblastic anemia), increased destruction (ITP, HLH), increased consumption (DIC, TTP, HUS), sequestration (hypersplenism), or may be due to combination of multiple mechanisms described above.
During evaluating a case of thrombocytopenia, the first step is getting a detailed history and doing a proper clinical examination. Then the next step would be checking the other parameters of complete blood count (CBC), especially hemoglobin (Hb) and the total WBC count, complemented by a peripheral smear (PS) examination, which will clear many doubts and will help us pinpointing our diagnostic approach.
Many a times pseudo-thrombocytopenia is encountered in a PS due to platelet clumping by EDTA and can be rectified by collecting blood samples in a citrate or heparin vials or by doing a direct finger prick smear. Any accompanying cytopenia will expand the differential diagnosis and an isolated thrombocytopenia will further narrow it down. Presence of any additional abnormalities of red cells (megaloblasts) or white cells (presence of hyper-segmented neutrophils, atypical lymphoid/myeloid cells) could be present in megaloblastic anemia/MDS, leukemia respectively, while in the presence of fragmented red cells microangiopathic hemolytic anemia should always be ruled out by doing PT and aPTT (DIC, TTP, HUS). In case of isolated thrombocytopenia, the platelet morphology is also important. In many patients in India, especially in eastern region many people have large platelets with their normal platelet count around 100 × 109/L with normal platelet function (Harris platelet syndrome). However, presence of any abnormal platelet morphology along with a low platelet count may indicate a platelet function disorder (large platelets in Bernard Soulier syndrome/ Glanzmann thrombasthenia or small platelets in Wiskott-Aldrich syndrome), especially if encountered in early part of life during evaluation for bleeding symptoms. In case of isolated thrombocytopenia, presence of additional congenital anomalies may point out towards an inherited marrow failure syndrome, e.g. amegakayocytic thrombocytopenia. Exposure to certain drugs may result in isolated low platelet count, e.g., ceftriaxone, piperacillin, heparin. Presence of toxic changes in neutrophils may indicate sepsis related thrombocytopenia. By excluding all these, immune thrombocytopenia (ITP) to be thought as no specific tests or markers are available for this entity and its diagnosis is largely clinical. A further work up complemented by bone marrow examination and in few cases a platelet function test will definitely help in reaching the final diagnosis.
So, summarizing, in the evaluation of a case of thrombocytopenia, all the
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
We studied the review article about How I investigate eosinophilia, which was published in the International Journal of Laboratory Hematology in August 2018. This paper has clearly and simply introduced how clinicians investigate eosinophilia. Hopefully, it can be helpful to everyone who interested in this field.
Thrombocytopenia is generally defined as platelet count <150 × 109/L. It can occur due to several reasons, like decreased platelet production (e.g., inherited bone marrow failure syndromes, acquired aplastic anemia, leukemia), ineffective platelet production (myelodysplastic syndrome, megaloblastic anemia), increased destruction (ITP, HLH), increased consumption (DIC, TTP, HUS), sequestration (hypersplenism), or may be due to combination of multiple mechanisms described above.
During evaluating a case of thrombocytopenia, the first step is getting a detailed history and doing a proper clinical examination. Then the next step would be checking the other parameters of complete blood count (CBC), especially hemoglobin (Hb) and the total WBC count, complemented by a peripheral smear (PS) examination, which will clear many doubts and will help us pinpointing our diagnostic approach.
Many a times pseudo-thrombocytopenia is encountered in a PS due to platelet clumping by EDTA and can be rectified by collecting blood samples in a citrate or heparin vials or by doing a direct finger prick smear. Any accompanying cytopenia will expand the differential diagnosis and an isolated thrombocytopenia will further narrow it down. Presence of any additional abnormalities of red cells (megaloblasts) or white cells (presence of hyper-segmented neutrophils, atypical lymphoid/myeloid cells) could be present in megaloblastic anemia/MDS, leukemia respectively, while in the presence of fragmented red cells microangiopathic hemolytic anemia should always be ruled out by doing PT and aPTT (DIC, TTP, HUS). In case of isolated thrombocytopenia, the platelet morphology is also important. In many patients in India, especially in eastern region many people have large platelets with their normal platelet count around 100 × 109/L with normal platelet function (Harris platelet syndrome). However, presence of any abnormal platelet morphology along with a low platelet count may indicate a platelet function disorder (large platelets in Bernard Soulier syndrome/ Glanzmann thrombasthenia or small platelets in Wiskott-Aldrich syndrome), especially if encountered in early part of life during evaluation for bleeding symptoms. In case of isolated thrombocytopenia, presence of additional congenital anomalies may point out towards an inherited marrow failure syndrome, e.g. amegakayocytic thrombocytopenia. Exposure to certain drugs may result in isolated low platelet count, e.g., ceftriaxone, piperacillin, heparin. Presence of toxic changes in neutrophils may indicate sepsis related thrombocytopenia. By excluding all these, immune thrombocytopenia (ITP) to be thought as no specific tests or markers are available for this entity and its diagnosis is largely clinical. A further work up complemented by bone marrow examination and in few cases a platelet function test will definitely help in reaching the final diagnosis.
So, summarizing, in the evaluation of a case of thrombocytopenia, all the
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
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Richard's entangled aventures in wonderlandRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
THE IMPORTANCE OF MARTIAN ATMOSPHERE SAMPLE RETURN.Sérgio Sacani
The return of a sample of near-surface atmosphere from Mars would facilitate answers to several first-order science questions surrounding the formation and evolution of the planet. One of the important aspects of terrestrial planet formation in general is the role that primary atmospheres played in influencing the chemistry and structure of the planets and their antecedents. Studies of the martian atmosphere can be used to investigate the role of a primary atmosphere in its history. Atmosphere samples would also inform our understanding of the near-surface chemistry of the planet, and ultimately the prospects for life. High-precision isotopic analyses of constituent gases are needed to address these questions, requiring that the analyses are made on returned samples rather than in situ.
Multi-source connectivity as the driver of solar wind variability in the heli...Sérgio Sacani
The ambient solar wind that flls the heliosphere originates from multiple
sources in the solar corona and is highly structured. It is often described
as high-speed, relatively homogeneous, plasma streams from coronal
holes and slow-speed, highly variable, streams whose source regions are
under debate. A key goal of ESA/NASA’s Solar Orbiter mission is to identify
solar wind sources and understand what drives the complexity seen in the
heliosphere. By combining magnetic feld modelling and spectroscopic
techniques with high-resolution observations and measurements, we show
that the solar wind variability detected in situ by Solar Orbiter in March
2022 is driven by spatio-temporal changes in the magnetic connectivity to
multiple sources in the solar atmosphere. The magnetic feld footpoints
connected to the spacecraft moved from the boundaries of a coronal hole
to one active region (12961) and then across to another region (12957). This
is refected in the in situ measurements, which show the transition from fast
to highly Alfvénic then to slow solar wind that is disrupted by the arrival of
a coronal mass ejection. Our results describe solar wind variability at 0.5 au
but are applicable to near-Earth observatories.
Earliest Galaxies in the JADES Origins Field: Luminosity Function and Cosmic ...Sérgio Sacani
We characterize the earliest galaxy population in the JADES Origins Field (JOF), the deepest
imaging field observed with JWST. We make use of the ancillary Hubble optical images (5 filters
spanning 0.4−0.9µm) and novel JWST images with 14 filters spanning 0.8−5µm, including 7 mediumband filters, and reaching total exposure times of up to 46 hours per filter. We combine all our data
at > 2.3µm to construct an ultradeep image, reaching as deep as ≈ 31.4 AB mag in the stack and
30.3-31.0 AB mag (5σ, r = 0.1” circular aperture) in individual filters. We measure photometric
redshifts and use robust selection criteria to identify a sample of eight galaxy candidates at redshifts
z = 11.5 − 15. These objects show compact half-light radii of R1/2 ∼ 50 − 200pc, stellar masses of
M⋆ ∼ 107−108M⊙, and star-formation rates of SFR ∼ 0.1−1 M⊙ yr−1
. Our search finds no candidates
at 15 < z < 20, placing upper limits at these redshifts. We develop a forward modeling approach to
infer the properties of the evolving luminosity function without binning in redshift or luminosity that
marginalizes over the photometric redshift uncertainty of our candidate galaxies and incorporates the
impact of non-detections. We find a z = 12 luminosity function in good agreement with prior results,
and that the luminosity function normalization and UV luminosity density decline by a factor of ∼ 2.5
from z = 12 to z = 14. We discuss the possible implications of our results in the context of theoretical
models for evolution of the dark matter halo mass function.
A brief information about the SCOP protein database used in bioinformatics.
The Structural Classification of Proteins (SCOP) database is a comprehensive and authoritative resource for the structural and evolutionary relationships of proteins. It provides a detailed and curated classification of protein structures, grouping them into families, superfamilies, and folds based on their structural and sequence similarities.
Seminar of U.V. Spectroscopy by SAMIR PANDASAMIR PANDA
Spectroscopy is a branch of science dealing the study of interaction of electromagnetic radiation with matter.
Ultraviolet-visible spectroscopy refers to absorption spectroscopy or reflect spectroscopy in the UV-VIS spectral region.
Ultraviolet-visible spectroscopy is an analytical method that can measure the amount of light received by the analyte.
1. D R . P R I YA N K A YA D AV
D R . V A I B H AV M O D I
CASE REPORT
MIMICKING APML
A DIAGNOSTIC CONFUSION
2. LAYOUT
• Case report
• Investigations
• Peripheral smear
• Bone marrow
• Differential Diagnosis
• Further Approach
3. CASE REPORT
• 3 year old female patient
• Complaints :
Bluish red rashes over body
Bleeding from nose and gums
Subconjunctival bleed on minor trauma
Reddish brown stools
since 2 days
No family history of bleeding
4. CASE REPORT…
• On examination:
Pallor
Ecchymoses & purpuric rashes all over body
No oraganomegaly/ lymphadenopathy
• CBP Platelets –
Hemoglobin – 9.3 g/dl
Total WBC - 22,600 cells/cumm
Differential - N 36 L60 E02 M02 B00
Platelets - 13,000 /cumm
7. PS COMMENT
WBC series:
• Total WBC -
22,600 cells/cu mm
• Differential - N
36 L60 E02 M02 B00
• Shift to left seen in myeloid
series
• Occassional Blast cells
seen
8. PS COMMENT
BLAST CELLS ?
myeloblast
• Some had coarse
azurophilic granules
• At places, auer rod like
structures in cytoplasm
? Artifact
? Toxic granules
? Promyelocytes
10. PS COMMENT- IMPRESSION
• Clinical picture ; age, bleeding **
• Anemia
• Leukocytosis with shift to the left**
• Thrombocytopenia
? Acute Promyelocytic Leukemia
? Infection
Important to rule out Acute Promyelocytic Leukemia
- Hematological emergency
Our Diagnosis: Infection
Follow up was advised.
11. FURTHER CLINICAL COURSE
• Antibiotics (Cephalosporins) and supportive treatment
• 6 transfusions (2 PRCs and 4 RDP)
• In one week, no improvement
• Platelet count still low
Patient was sent for review and for Bone Marrow Examination
13. REPEAT PERIPHERAL BLOOD/ SMEAR
1st PS REPEAT PS
Hemoglobin 9.3gm/dl 8.9 g/dl
RBC Series Normocytic
hypochromic
Normocytic
hypochromic
Total WBC 22,600 cells/cumm 17,600 cells/cumm
Differential N 36 L60 E02 M02 B00 N 65 L30 E02 M03 B00
Blasts +
Promyelocytes
11% 4%
Toxic granulation in
neutrophils
Few Large number
Platelets Markedly reduced Markedly reduced
14. BONE MARROW ASPIRATION
• Marrow- normocellular
• M:E ratio – 2:1
• Eryhthroid series:
Reaction pred.
normoblastic with
megaloblastoid
changes
Marrow - easy to aspirate
15. BONE MARROW ASPIRATION
Myeloid series-
• Shift to left – (myelocytes
and metamyelocytes –
38%)
• Myelocytes and
metamyelocytes showing
heavy toxic granulations
• Percentage of blasts and
promyelocytes– 08%
• No Auer rods seen in blasts
20. INFECTION/ LEUKEMOID
REACTION
Points FOR:
• PS:
Leukocytosis
Shift to left
Toxic granulations
Reactive lymphocytes
• Bone Marrow:
Shift to left
Toxic granulations
Cytophagocytosis
Increased megakaryocytes
BM iron increased
Points AGAINST:
• Platelet count – variable
• Absence of fever/sepsis
21. APML/AML
Points FOR:
• Clinical presentation
• Leukocytosis
• Morphological
• Blasts, promyelocyts along
with other myeloid
precursors seen in PS
Points AGAINST:
• Age of presentation
• Hepatosplenomegaly of
various degree
• Blasts >20% of bone marrow
non-erythroid cells
• Suppression of erythroid and
megakaryocytic series
22. ALL
Points FOR:
• Age
• Clinical presentation
Points AGAINST:
• No Hepatosplenomegaly
• No Lymphadenopathy
• PS: Pancytopenia
• BM: Suppression of erythroid
megakaryocytic and myeloid
series
• Blasts >20% of bone marrow
non-erythroid cells
• Morphology of blast cells
L1 L2 L3
23. LYMPHOBLASTS VS MYELOBLASTS
LYMPHOBLAST MYELOBLAST
MORPHO-
LOGY
CYTO-
CHEMISTRY
PAS + (block)
Acid phosphatse + (T-cell)
PAS –
diffuse fine +ve in
M6,M7, M3*
MPO, Sudan Black, NSE +
I MMUNO-
PHENOTYPIN
G
B-cell - Strong CD19 and atleast 1 of the
following strongly expressed: CD79a,
cyCD22, CD10
T-cell - Cytoplamic CD3 or Surface CD3
MPO or
Monocytic differentiation (at least 2 of
the following NSE,
CD11C, CD14, CD64)
Only immunophenotyping permits a positive diagnosis of ALL
28. SUMMARY
• Not every bleeding is APML
• Bleeding complaints
Age,
Family history
Site of bleeding
Preceding infection
Lymphadenopathy and organomegaly
Careful examination of PS
BM Examination if indicated
Editor's Notes
Usually pancytopenia in AML/ALL pts..here bicytopenia
Family history
Bleeding disorder – m.c hemophilia – but this is girl
Then ALL – pancytopenia with blasts –
Marrow – difficulty to aspirate in cases of ALL
AML – Anemia, bleeding manifestations and infection
APML -
T(8:21); 15:17; 16:16; inv 16; myeloid sarcoma
Morphologically hematogones are distinct lymphoid cells with condensed and homogeneous chromatin, and scant cytoplasm. These cells can be observed in large numbers in the bone marrow of children with a variety of hematologic and nonhematologic disorders. They varied from 10 to 20 µ in diameter, with smaller cells predominating. The nucleus is round or oval and can exhibit one or more indentations or shallow clefts. Nucleoli were absent or small and indistinct. There is generally scant or no discernible cytoplasm; when present, cytoplasm is moderately to deeply basophilic and devoid of granules, inclusions, or vacuoles. There is often a variety of size and cytologic features that blends with those of mature lymphocytes. Frequently a portion of the hematogones exhibited features indistinguishable from lymphoblasts of ALL.
Haema-
togones tend to express TdT strongly and CD10 and
CD19 weakly, whereas the reverse pattern of reac-
tivity is seen with ALL blast cells [42].
The detection of persisting cells with an
aberrant combination of antigens is more reliable,
as is polymerase chain reaction (PCR) analysis for
rearranged immunoglobulin heavy chain (IGH) or
T-cell receptor (TCR) genes (see below).
Aplastic anemia is characterized by bone marrow hypoplasia with failure to form all 3 lineages resulting in peripheral cytopenia
MDS: Morphologcally shows impairment of proliferation and differentiation
Hb<10; ANC < 1800/cumm; Platelet < 1 lakhs