This document provides guidelines for peripheral blood smear examination, including slide preparation, staining, and microscopic evaluation. Key points include:
- Blood smears are used to evaluate anemia, infections, and abnormal cells. Three steps are involved in making blood films: preparation, fixation, and staining.
- Under the microscope, a preliminary low and high power scan examines staining quality and cell distribution before a 100-cell differential count at oil immersion.
- RBCs, WBCs, platelets, and parasites are examined for morphologies, counts, and any abnormalities. Terms like pancytopenia and bicytopenia are defined.
- Detailed guidelines are given for examining and reporting R
I have listed out the LE cells structure and Microscopical examinaton of LE CELLS, Difference between tart cells and le cells, clinical symptoms and diagnostic procedure.
I have listed out the LE cells structure and Microscopical examinaton of LE CELLS, Difference between tart cells and le cells, clinical symptoms and diagnostic procedure.
An absolute eosinophil count is a blood test that measures the number of one type of white blood cells called eosinophils.
Eosinophils become active when you have certain allergic diseases, infections, and other medical conditions.
An absolute eosinophil count is a blood test that measures the number of one type of white blood cells called eosinophils.
Eosinophils become active when you have certain allergic diseases, infections, and other medical conditions.
A blood smear is a sample of blood that's spread on a glass slide which is treated with a special stain. In the past, all blood smears were examined under a microscope by laboratory professionals. Now automated digital systems may be used to help examine blood smears.
BODY FLUIDS EXAMINATION.pptx FOR MBBS AND PGNehaBanseria1
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Analysis of Body Cavity Fluids
Sep 08, 2014
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Analysis of Body Cavity Fluids. Lab 8. Indications and Sampling. Indications: - Identifies the type of fluid present: transudate, exudate, neoplastic or other effusion and may identify the cause of fluid accumulation Sampling: - Sterile preparation of site
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Analysis of Body Cavity Fluids Lab 8
Indications and Sampling Indications: - Identifies the type of fluid present: transudate, exudate, neoplastic or other effusion and may identify the cause of fluid accumulation Sampling: - Sterile preparation of site - Use a fine needle (21- 23 G) - Avoid movement or causing pain during sampling - Split sample into EDTA & plain sterile tubes - Process as soon as possible - Monitor the animal
Tests Applied Four basic tests are applied: • Appearance of fluid • Protein content • Nucleated cell count (NCC) • Examination of a direct and/or sediment smear to identify cell type Additional tests such as biochemistry may be used in certain clinical situations, e.g. urea or creatinine, if uroabdomen (from bladder rupture) is suspected.
Specimen Management for Smears - Mix sample well - Make a direct smear - Centrifuge & smear the deposit (sediment smears) - Air-dry rapidly & stain Special centrifuges (cytocentrifuges) yield better smears A standard centrifuge may be used at a slow speed for a short period (<1000 rpm)
Procedure to get a smear “Wedge” method Flat-slide method A drop of the fluid is placed on a cleaned glass slide A smear can be made by the “wedge” method used for making blood smears Alternatively, a 2nd slide may be superimposed on the first, and the two are drawn smoothly apart to make two thin smears.
Examination of sediment smears • Blood stains e.g. Diff-Quik or Giemsa usually used • The smear is scanned at low power, to locate cells and cell clusters • NORMAL FINDINGS: N
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
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ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
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- Prix Galien International Awards Ceremony
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.
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.
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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
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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.
1. Peripheral blood smear examination
(Slide preparation and reporting)
Caesar Abu Arra
MSc Life sciences
BSc Medical lab. Sciences
Medicare Labs
2. Aim of blood smear
Evaluation of anemia
Infections
• bacteria, malaria, microfilaria..etc.
Abnormal cells
• blasts, inclusions..etc.
Cells morphology and count
Abu Jad Caesar
3. Making blood films
Three basic steps to make blood film:
Preparation of blood smear.
Fixation of blood smear.
Staining of blood smear.
Abu Jad Caesar
4. Preparation of blood smear
Different types of blood smears:
The wedge smear slide to slide method.
The spun smear.
Two additional types of blood smears (used for specific
purposes):
o Buffy coat smear for WBCs < 1.0×109/L.
o Thick blood smears for blood parasites .
Abu Jad Caesar
5. Wedge blood smear
Smears should be made within 1 hour of blood
collection from EDTA specimens stored at
room temperature to avoid distortion of cell
morphology.
Small drop (10 µl)
Hold the spreader slide at a 30°- 45° angle,
and draw it back against the drop of blood.
Air dry at room temperature.
Abu Jad Caesar
7. Procedure notes
1. The smear should be made without delay.
Any delay results in an abnormal distribution
of the white blood cells, with many of the
large white cells accumulating at the thin
edge of the smear.
2. HCT↑ ↓ The angle of the spreader slide
HCT↓ ↑ The angle of the spreader slide
Abu Jad Caesar
9. Spin method
Automated method
Placeadrop of blood in thecenter of aglassslide.
Spin atahighspeed in aspecialcentrifugecytospin.
Blood spreads uniformly.
Abu Jad Caesar
10. Characteristics of a Good Smear
Thick at one end, thinning out to a smooth
rounded feather edge.
Should occupy 2/3 of the total slide area.
Should not touch any edge of the slide.
Abu Jad Caesar
12. Common causes of a poor blood smear
Drop of blood too large or too small.
Spreader slide pushed across the slide in a
jerky manner.
Failure to keep the spreader slide at a 30°
angle with the slide.
Failure to push the spreader slide completely
across the slide.
Abu Jad Caesar
13. Common causes of a poor blood smear
Holes in film: Slide contaminated with fat or
grease
Cellular degenerative changes:
delay in fixing
Inadequate fixing time
Methanol contaminated with water.
Abu Jad Caesar
14. Biologic causes of a poor smear
Cold agglutinin - RBCs will clump together.
Warm the blood at 37° C for 5 minutes.
Lipemia - holes will appear in the smear.
Nothing you can do to correct this.
Rouleaux - RBC’s will form into stacks as coins.
Nothing you can do to correct this.
Abu Jad Caesar
15. Staining of blood smear
Romanowsky stain:
Any Combination of:
Eosin Y (Acidic or anionic dye):
o Binds to cationic sites (cytoplasm & Hb)
Methylene blue (Basic, cationic or Azure B dye):
o Binds to anionic sites (nucleus and RNA)
Abu Jad Caesar
16. Staining of blood smear
Buffer:
Used to maintain an adequate pH.
0.05M Na2PO4 (pH 6.4) or dH2O (pH 6.4-6.8)
Abu Jad Caesar
17. pH of the phosphate buffer
If the pH is too acidic:
RBC :Pinker
WBC nuclei : very pale staining (very pale purple)
If the pH is too basic:
RBC :Grayish blue
WBC nuclei :very deeply purple
Abu Jad Caesar
19. Staining Troubleshooting
Too Acid Stain:
Insufficient staining time
Prolonged buffering or washing
Old stain
Correction:
Lengthen staining time
Check stain and buffer pH
Shorten buffering or wash time
Abu Jad Caesar
20. Staining Troubleshooting
Too Alkaline Stain:
Thick blood smear
Prolonged staining
Insufficient washing
Alkaline pH of stain components
Correction :
Check pH
Shorten stain time
Prolong buffering time
Abu Jad Caesar
22. Macroscopic view:
Quality of the smear
The microscopic view:
Progressing from low power to high power:
Blood film examination - preliminary
Abu Jad Caesar
24. Low-Power (10x) Scan
Determine the overall staining quality of the blood
smear.
Determine if there is a good distribution of the cells.
o Discussed later
Find an optimal area for the detailed examination and
enumeration of cells
Blood film examination - preliminary
Abu Jad Caesar
25. High-Power (40x) Scan
Determine the WBC estimate.
o WBCs are counted in 10 fields and averaged X 2000
o The estimate could be reported according to the table below:
Blood film examination - preliminary
Abu Jad Caesar
26. • High-Power (40x) Scan
Grading scale for WBC count (X103 cell/µl)
Blood film examination - preliminary
Low WBC High WBC
Mild 3-4.5 Mild 10-15
Moderate 2-3 Moderate 15-30
Severe <2 Marked 30-100
Extreme >100
Abu Jad Caesar
27. Oil Immersion (100x) Examination
Perform a 100 WBC differential count.
Correct WBC count that has greater than 10 NRBCs per
100 WBCs.
o Report as: WBC count was corrected due to presence of
NRBCs.
Blood film examination - preliminary
Abu Jad Caesar
28. Oil Immersion (100x) Examination
to correct a WBC count (/µl):
Uncorrected WBC (/ ) X l
Blood film examination - preliminary
Abu Jad Caesar
29. Oil Immersion (100x) Examination
Evaluate the RBCs for:
o Anisocytosis
o Poikilocytosis
o Inclusions
o Hypochromasia
o Polychromasia.
Blood film examination - preliminary
Abu Jad Caesar
30. Oil Immersion (100x) Examination
Perform a platelet estimate and evaluate platelet
morphology:
o Platelets are counted in 10 fields and averaged:
• X 15 Automated smear.
• X 20 Wedge smear is used.
Blood film examination - preliminary
Abu Jad Caesar
31. Oil Immersion (100x) Examination
Grading scale for platelets count (X103 cell/µl)
Blood film examination - preliminary
Abu Jad Caesar
Low Platelets High Platelets
Mild 100-150 Mild 500-700
Moderate 50-100 Moderate 700-900
Severe <50 Severe 900-1000
Extreme >1000
32. Oil Immersion (100x) Examination
The absolute WBC count (/µl) may be determined:
Relative count (%) X Total WBC count (/µl)
Blood film examination - preliminary
Abu Jad Caesar
33. Relative vs. Absolute value:
Relative value:
o Measures the percentage of corresponding WBC type in
peripheral blood.
Blood film examination - preliminary
Abu Jad Caesar
34. Relative vs. Absolute value:
Absolute value:
o Measures the total count of corresponding WBC type /µl
in peripheral blood.
o Gives more meaningful information than the percentage.
o It is the preferred reporting method for the WBC
differential.
• Reported as absolute cytosis or absolute cytopenia.
Blood film examination - preliminary
Abu Jad Caesar
35. Relative vs. Absolute value:
Example: leukopenic patient and increased susceptibility
to infection and sepsis:
WBC=5000 Relative Neutrophils=50%
o Absolute= 2500 cell/µl Normal
WBC=2000 Relative Neutrophils=85%
o Absolute= 1700 cell/µl Low
Blood film examination - preliminary
Abu Jad Caesar
37. Examination of blood films should include:
RBC
Size, Shape, color
Hemoglobin distribution
Arrangement and distribution
Inclusions
nucleated RBCs
Examination of blood films
Abu Jad Caesar
38. Examination of blood films should include:
WBC
Total counts
Differential counts
Abnormal and immature WBC
Examination of blood films
Abu Jad Caesar
39. Examination of blood films should include:
Platelets
Counts should be verified by estimation
Size
Clumping
Examination of blood films
Abu Jad Caesar
40. Examination of blood films should include:
Parasites
Examination of blood films
Abu Jad Caesar
41. Pancytopenia
Deficiency in all the three cell lines RBC, WBC, and platelets.
Aplastic anemia
When report, recommend bone marrow assessment.
Bicytopenia
Deficiency in two of the three cell lines
Viruses and drugs
Terms
Abu Jad Caesar
42. PARASITES
Abu Jad Caesar
Thick film When parasites are scanty
Thin film Identification of species
45. 1 to 4 μm in diameter and vary in shape.
Reddish-purple granules
Life span 9-12 days
One megakaryocyte can release several thousand platelets
(4000).
Report as platelets are adequate with normal-sized ones
OR platelets are normal
Abu Jad Caesar
Platelets
46. Large and Giant platelets
Large platelets (4-7 µm)
oITP
Abu Jad Caesar
Platelets
47. Large and Giant platelets
Giant platelet (7-20 µm)
oPlatelets seems to be size of RBC.
oBernard Soulier syndrome
Abu Jad Caesar
Platelets
48. Large and Giant platelets
NOTE:
o When estimate, Large platelets and platelet aggregates
NOT counted.
Report as Occasional, Few, Many
Abu Jad Caesar
Platelets
49. Platelet anisocytosis:
Small large giant platelets will be seen
Report as: Platelets anisocytosis ranging in size from
tiny to large giant platelets were seen.
Abu Jad Caesar
Platelets
50. Thrombocytosis
Post infection and Inflammation
Report as:
o Thrombocytosis (with grading).
o Platelets were estimated and approved to be about ( /µl)
In case of microcytosis (RBC and PLT diameters are
similar) report as :
o Thrombocytosis due severe microcytosis.
Abu Jad Caesar
Platelets
51. Thrombocytopenia:
Could be due to:
o Decreased production Aplastic anemia
o Increased destruction ITP
Abu Jad Caesar
Platelets
52. Thrombocytopenia:
In case of no aggregates report as:
o Thrombocytopenia (with grading).
o No platelet clumps are noted OR Negative for
microaggregates.
o Platelets were estimated and approved to be about ( /µl)
Abu Jad Caesar
Platelets
54. Pseudothrombocytopenia:
In vitro EDTA dependent phenomena
oPlatelet satellitism
• Platelets adhere to neutrophil surface
Abu Jad Caesar
Platelets
55. Pseudothrombocytopenia:
Repeat on new samples (EDTA and sodium citrated)
Scan for platelet clumping in thin and thick portion of
smear
Abu Jad Caesar
Platelets
56. Pseudothrombocytopenia:
Reporting criteria:
Two samples were drawn to rule out EDTA- induced
pseudothrombocytopenia:
o EDTA smear revealed platelet clumps / Platelet
satellitism
o Na+ citrated smear revealed normal platelets count and
distribution.
Conclusion: Platelets are adequate
Abu Jad Caesar
Platelets
57. Morphology of Normal RBC
Biconcave disc
Diameter 7 ~ 8 μm
Central pallor occupy 3rd of total size
Approx same as nucleus of mature lymphocyte
Stained with eosin component of Romanowsky dyes
Abu Jad Caesar
RBC
59. RBC Abnormality
Examination of blood films for RBC’s should
include:
Anisocytosis
Poikilocytosis
Hemoglobin distribution
Arrangement and Distribution
Inclusions
NRBCs
Abu Jad Caesar
61. Arrangement and Distribution
Normal arrangement and distribution:
The thin portion of the smear where RBC’s are slightly
separated from one another or at most, barely touching,
with no overlap.
The thin area should represent at least 3rd of the entire
film.
Abu Jad Caesar
62. Arrangement and Distribution
Normal arrangement and distribution:
The reviewer should avoid the thicker portion of the
slide where cells are overlapping and the edges of smear
where cells may be distorted in size, shape, and color.
o An exception is to be made when scanning for platelet
clumping
Abu Jad Caesar
63. Arrangement and Distribution
Rouleaux
RBC’s appear as stacks of coins (linear)
Due to ↑ Globulins or fibrinogens
seen in:
o Multiple myeloma
o Macroglobulinemia
Abu Jad Caesar
64. Arrangement and Distribution
Agglutination
More irregular and round clumping than linear rouleaux
Seen in:
o Cold agglutinin
o Anti RBC antibodies
o Autoimmune HA
o Macroglobulinemia
Abu Jad Caesar
65. Inclusions
Basophilic stippling (Punctate basophilia)
Aggregates of Ribrosomes.
Multiple blue black inclusions (coarse or punctate )
Seen in:
o Lead and arsenic poisoning
o Thalassemias
o Alcoholism
o Megaloblastic anemias
Abu Jad Caesar
66. Inclusions
Howell Jolly bodies
Large round inclusions which are remnant of nuclear
chromatin
Appear singly or doubly in an eccentric position on the
cell periphery
Deep purple
Abu Jad Caesar
67. Inclusions
Howell Jolly bodies
Seen in:
o Postsplenectomy
o Megalobalstic anaemia
o Haemolytic anaemia
Abu Jad Caesar
69. Inclusions
Pappenheimer Bodies
Unlike basophilic stippling:
o Basophilic stippling appears homogeneously over the cell
whereas Pappenheimers tend to appear as single or clusters
in the cells periphery.
Unlike Howell–Jolly bodies:
o Howell–Jolly bodies appear to be
larger
Abu Jad Caesar
70. Inclusions
Pappenheimer Bodies
Seen in:
o Sideroblastic erythropoiesis
o Postsplenectomy
o Hemolytic anemia
o Thalassemia
Abu Jad Caesar
71. Inclusions
Heinz bodies
Result of denatured or precipitated hemoglobin
Purple, blue, large, single or multiple inclusions
attached to the inner surface of the red blood cell.
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72. Inclusions
Heinz bodies
Stained by supravital stains
Not Stained by Romanowsky stain.
Seen in:
o Postsplenectomy
o oxidant stress of drugs and
chemicals
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73. Inclusions
Cabot rings
Represent a part of the mitotic spindle, remnants of
microtubules, or a fragment of the nuclear membrane.
Have no internal structure
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74. Inclusions
Cabot rings
Red or reddish purple
Could be appear in a figure-of-eight conformation
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77. Poikilocytosis
Spherocytes
Loss of biconcavity
o ↓ Surface-to-volume ratio
o ↑ Osmotic fragility
Smaller diameter
Dense-staining
o No central pallor area
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79. Poikilocytosis
Target cell
Codocytes
↑ membrane cholesterol and phospholipid and ↓ cellular
hemoglobin.
↑ surface-to-volume ratio
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80. Poikilocytosis
Target cell
Seen in:
o Obstructive liver disease
o Iron deficiency anemia
o Thalassemia
o Post-transfusion
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83. Poikilocytosis
Elliptocyte and ovalocyte
Elliptocytes
o Pencil, rod, or cigar shaped
o Hb appears to be concentrated on both ends of the cell
o Seen in IDA
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84. Poikilocytosis
Elliptocyte and ovalocyte
Ovalocyte
o More egg-shaped
o Have a greater tendency to vary in their Hb content
o Seen in megaloblastic anemia
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86. Poikilocytosis
Teardrop cell
Dacrocytes
Physiologic mechanism is unknown
Seen in:
o IDA
o Pernicious anemia
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87. Poikilocytosis
Stomatocyte
RBC with narrow slit-like area of central pallor
Normal size, but are not biconcave
Seen in:
o Acute alcoholism
o Hemolytic anemia
o Malignancies
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90. Poikilocytosis
Echinocyte
Burr Cells, crenated cells
10 to 30 regular spicules, evenly placed over the surface
of RBC
Considered pathologic and should be reported.
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92. Poikilocytosis
Fragmented cells
Several types
o Schistocytes
o Helmet Cells (bite cell) usually 2 projections
o Keratocytes
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93. Poikilocytosis
Fragmented cells
All fragmented RBC reported as schistocytes
Sometimes counted as platelets
o Estimate platelets and report thrombocytosis due to
presence of RBC fragments
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98. Anisocytosis
Microcytes
MCV <80 fl
Diameter <7 μm
Results from a defect in hemoglobin formation
Seen in:
o IDA
o Thalassemia
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99. Anisocytosis
Macrocytes
MCV >100 fl
Diameter >9 μm
Result from impaired DNA synthesis.
Seen in:
Megaloblastic anemia (↓ B12 and folic acid).
Aplastic anaemia
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100. Anisocytosis
Anisocytosis is a feature of most anemias.
o Report as anisocytosis (with Qual. or Quan. Grading):
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RDW: 16-18 Slight
RDW: 18-22 Moderate
RDW: >22 Marked or severe
101. Anisocytosis
Mixture of large and small with normal MCV and high
RDW usually due:
Recent blood transfusion
Anemia or recovery stages of anemia.
o Report as Anisocytosis with dimorphic RBC population
(with grading):
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RDW: 16-18 Slight
RDW: 18-22 Moderate
RDW: >22 Marked or severe
102. Hemoglobin Distribution
MCHC used in conjunction with MCV used
do describe anemias
Normochromia
Hypochromia
Hyperchromia
Polychromasia
Anisochromia
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104. Hemoglobin Distribution
Hypochromia : MCHC < 32%
Unusually palely RBC (↓Hb content)
The central pallor > 3µm (>1/3 rd of total size)
Seen in:
o IDA
o Thalassemia
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106. Hemoglobin Distribution
Hyperchromia : MCHC > 36%
Decreased or absent central pallor
Seen in:
o Sperocytosis (↓surface-to-volume ratio)
o hemolytic anemias (hemolysis caused by burns)
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107. Hemoglobin Distribution
Hyperchromia : MCHC > 36%
Even though true hyperchromia does exist it is not
reported as such:
o It is reported in terms of the cell abnormalities resulting
from the increased volume of hemoglobin and the
decreased surface area (e.g spherocytes).
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108. Hemoglobin Distribution
Polychromasia
Premature RBC in circulation called Polychromatophilic
cells actually reticulocytes.
Gray-blue in color and usually larger than normal RBC
o Result of the residual RNA involved in Hb synthesis.
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110. Hemoglobin Distribution
Polychromasia
Grading excellent indicator of therapeutic effectiveness
when patient is given iron or vitamin therapy as treatment
of anemia
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111. Hemoglobin Distribution
Anisochromia
Hypochromic cells and normochromic cells in the
same film
Seen in:
o Development or recovering from anemias
o Post-transfusion
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113. White blood cells
WBC categories:
Granulocytes (PMN):
o Neutrophils, Eosinophils and basophiles
o Granules in their cell cytoplasm.
o Multilobed nucleus
Agranulocytes (MNC):
o Lymphocytes and monocytes.
o Do not have granules (contain non specific azurophilic
granules)
o Nonlobular nuclei.
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115. Neutrophil
Terms
Shift to the left
o Release of younger granulocytes (specifically bands and
metamyelocytes from the bone marrow).
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116. Neutrophil
Terms
Shift to the right
o An abnormal cell maturation situation that occurs when
hypersegmented cells are seen.
• It is indicative of vitamin B12 and/or folate deficiency.
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118. Neutrophil
Report as:
o Mature/normal appearing neutrophils.
o In case of leukocytosis neutrophilic leukocytosis
o Absolute / relative neutrophilia or neutropenia
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119. Neutrophil
Neutrophilia
o Acute bacterial infection.
o Many inflammatory processes.
Neutropenia
o Typhoid fever
o Brucellosis
o Viral diseases.
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120. Abnormal neutrophil
Abnormal neutrophil morphology:
Band or stab forms
Hypersegmentation (≥ 6 lobes)
Vacuolization
Toxic granulation
Dohle bodies
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121. Band or Stab
Cytoplasm
o Pink
Nucleus
o U shaped nucleus of uniform thickness.
o Purplish red
o Dense chromatin
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122. Band or Stab
Normally form 5-10% of WBC’s
Increased bands:
o Acute infection (usually bacterial)
o Non infectious inflammatory disease
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123. Band or Stab
Include it when calculate absolute neutrophil
Report as:
o Many/Few neutrophilc bands OR with shift to the
left
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125. Hypersegmentation
Report as:
o Few/many hypersegmented neutrophils OR with shift to
the right.
o Further hematological examinations are recommended
(B12 & folic acid).
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126. Vacuolization
Vacuoles in neutrophil contain ingested microorganisms.
Seen in:
o Severe infection (leukemoid reaction)
o Non infectious inflammation
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127. Toxic granulation
↑ staining density and number of granules
Seen in:
o Bacterial infection and leukemoid reaction
o Other inflammation
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128. Döhle bodies
Pale blue inclusions at the periphery of the cytoplasm
Strands of RER that have aggregated
o Bacterial infection and leukemoid reaction
o Inflammation
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130. Eosinophil
Cytoplasm
o Full of orange-red granules
Nucleus
o Blue purple
o Coarsely granular chromatin
o 2 Lobes (like a pair of glass)
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136. Monocyte
Cytoplasm
o Pale gray-blue
o Vacuoles and granules may be observed
Nucleus
o Blue-purple
o large irregularly, folded, kidney shaped, ….etc
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141. Lymphocyte
Report as:
o Mature-appearing lymphocytes with homogenous chromatin
pattern (Resting lymphocytes).
o In case of leukocytosis Lymphocytic leukocytosis
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144. Abnormal lymphocyte
Abnormal lymphocyte morphology:
Reactive lymphocytes
Smudge cells (Basket cell)
Turk cell (Transformed lymphocyte or immunoblast)
Atypical Lymphocytes (Malignant-appearing cell)
All should be reported
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145. Reactive lymphocyte
Normally < 10% of the total lymphocytes
Nucleus:
o Slightly large with more open chromatin
Cytoplasm:
o Abundant and irregular (↓N:C)
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146. Reactive lymphocyte
Seen in:
o Infectious mononucleosis
o Viral infections
The term atypical should not be used interchangeably with
reactive lymphocyte.
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147. Smudge cell
Normally < 1%
Remnants of cells that lack:
o Identifiable cytoplasmic membrane and Nuclear structure.
Associated with abnormally fragile lymphocytes (mostly
CLL)
Should be reported.
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148. Turk cell
Reactive lymphocyte with large nucleolus, abundant and
deeply basophilic cytoplasm
Seen in bacterial and viral infection
Round nucleus
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150. Leukemia
Two major types according to cell maturity:
Acute
o The malignant cells are immature (stem cells, blasts, or other
immature precursors.
Chronic
o The cells are predominantly mature.
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151. Leukemia
Two major types according to cell lineage:
Myeloid (Myelogenous)
o Granulocytic leukemia
o Monocytic leukemia
o Megakaryocytic leukemia
o Erythrocytic leukemia
Lymphoid (Lymphocytic)
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152. Leukemia
So, four major types of leukemias:
Acute myeloid leukemia (AML)
Chronic myeloid leukemia (CML)
Acute lymphoblastic leukemia (ALL)
Chronic lymphocytic leukemia (CLL)
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154. WBC Reporting
WBC Reporting should includes:
Leukocytosis/Leukocytopenia.
Maturation stage
Absolute value of major cell.
Chromatin (fine, coarse, clumped)
Nucleolus ??
Amount of cytoplasm ??.
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155. WBC Reporting
WBC Reporting should includes:
For Leukemia, recommend flow cytometry for
immunological markers
For CML Recommend Philadelphia chromosome
(BCR–ABL fusion genepositive >95%)
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164. CML
CML is characterized by three phases
Chronic phase
Accelerated phase
Blast phase
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165. CML
Chronic phase
Neutrophilic leukocytosis
o From segmented neutrophils to occasional blasts (≤10%)
But mainly mature
Basophilia/eosinophilia
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166. CML
Chronic phase
Thrombocytosis (~50% of cases).
Normocytic anemia
↑ uric acid , LDH, Vitamin B12
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167. CML
Accelerated phase
Worsening of anemia
Basophils (>20%).
Shift to the more immature myeloid forms (blasts 10-19%).
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168. CML
Accelerated phase
Persistent thrombocytopenia ( 100 X 109/L)
Persistent thrombocytosis ( 1000 X 109/L)
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169. CML
Blast phase
Blast crisis (≥20%)
Conversion of CML to AML
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171. Leukemoid reaction
Moderate or marked leukocytosis
Usually
o >30000 cell/µl
Absolute neutrophilia
Shift to the left
o Mostly neutrophilic metamyelocytes and band forms.
o Immaturity is similarly observed in the early stages of
CML
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172. Leukemoid reaction
Not a result of a leukemic disease
Infectious disease
o Bacterial (most common)
o Toxoplasma and viral (less common)
Other inflammatory process
o Uremia, acute gout and burns
Drug and chemical intoxication
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173. Leukemoid reaction
Reactive changes of neutrophils
Usually appear as follow arrangement
1- Toxic granulation
o Nonspecific reactive changes
2- Döhle bodies
o Nonspecific reactive changes
3- Cytoplasmic vacuolization
o Strongly indicates a serious bacterial infection
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174. Leukemoid reaction
Reactive changes of neutrophils
Usually appear as follow arrangement
1- Toxic granulation
o Nonspecific reactive changes
2- Döhle bodies
o Nonspecific reactive changes
3- Cytoplasmic vacuolization
o Strongly indicates a serious bacterial infection
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176. Report as:
WBC immaturity.
Neutrophils reactive changes
Features in keeping with marked response to infectious
or inflammatory processes (Leukemoid reaction).
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Leukemoid reaction
177. Slight leukocytosis with neutrophilia
With or without the shift to the left.
Toxic granulation
Report as:
Features in keeping with mild response to infection
or inflammatory process.
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Mild infection
178. Mild to severe normocytic normochromic anemia
↓ platelet counts
WBC count is variable (↓ to ↑↑↑)
Auer rods in blasts cytoplasm (for AML)
The blood smear usually reveals blasts or other immature
cells
Circulating NRBC are occasionally seen
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AML & ALL
194. Normochromic normocytic anemia
↑ Indirect serum bilirubin level
Thrombocytopenia is not common.
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CLL
195. Lymphocytic leukocytosis From mature appearing
lymphocytes to prolymphocytes (10%)
o Small lymphocytes or slightly larger than a normal
lymphocyte and have a hypercondensed nuclear
chromatin pattern
Smudge cells are common
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CLL
197. WBC Reporting
o Leukocytosis/Leukocytopenia.
o Maturation stage
o Smudge cell
o Chromatin (fine, coarse, clumped)
o Nucleolus ?? (for prolymphocyte)
o Amount of cytoplasm ??.
o For definitive diagnosis, recommend flow cytometry for
immunological markers.
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WBC Reporting for CLL
198. WBC Reporting
o Mostly reported as: Mature-appearing lymphocyte with
hypercondensed nuclear chromatin pattern and few/many
prolymphocytes
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WBC Reporting for CLL