What is Lymphoma?
Malignant lymphoma is a term given to tumors of the lymphoid system and specifically of lymphocytes and their precursor cells
i.e.
Cancer of the lymphatic system.
Many lymphomas are known to be due to specific genetic mutations.
chronic myeloid leukemia, CML, epidemiology, BCR ABL1 gene, philadelphia chromosome, t(9;22), CML incidence, etiology of CML, pathophysiology of CML, phases of CML, treatment of CML, Allogenic stem cell transplant, TKI therapy for CML, Sokal index for CML,
Invasive Squamous Cell Carcinoma (SCC)
SCC of the skin is a malignant tumor of keratinocytes, arising in the epidermis.
SCC usually arises in epidermal precancerous lesions and, depending on etiology and level of differentiation, varies in its aggressiveness.
The lesion is a plaque or a nodule with varying degrees of keratinization in the nodule and/or on the surface.
Thumb rule:
Undifferentiated SCC: is soft and has no hyperkeratosis;
Differentiated SCC: is hard on palpation and has hyperkeratosis.
Exposure:
Sunlight. Phototherapy, PUVA (oral psoralen + UVA). Excessive photochemotherapy can lead to promotion of SCC, particularly in patients with skin phototypes I and II or in patients with history of previous exposure to ionizing radiation or methotrexate treatment for psoriasis.
Lesions :
Indurated papule, plaque, or nodule ; adherent thick keratotic scale or hyperkeratosis ; when eroded or ulcerated, the lesion may have a crust in the center and a firm, hyperkeratotic, elevated margin
Clark levels
level I, intra-epidermal;
level II, invades papillary dermis;
level III fills papillary dermis;
level IV, invades reticular dermis;
level V, invades subcutaneous fat.
Aplastic anemia is one of the stem cell disorder which leads to pancytopenia in the peripheral blood and decrease production of all cell line in bone marrow. it require bone marrow transplantation to cure the patient.
chronic myeloid leukemia, CML, epidemiology, BCR ABL1 gene, philadelphia chromosome, t(9;22), CML incidence, etiology of CML, pathophysiology of CML, phases of CML, treatment of CML, Allogenic stem cell transplant, TKI therapy for CML, Sokal index for CML,
Invasive Squamous Cell Carcinoma (SCC)
SCC of the skin is a malignant tumor of keratinocytes, arising in the epidermis.
SCC usually arises in epidermal precancerous lesions and, depending on etiology and level of differentiation, varies in its aggressiveness.
The lesion is a plaque or a nodule with varying degrees of keratinization in the nodule and/or on the surface.
Thumb rule:
Undifferentiated SCC: is soft and has no hyperkeratosis;
Differentiated SCC: is hard on palpation and has hyperkeratosis.
Exposure:
Sunlight. Phototherapy, PUVA (oral psoralen + UVA). Excessive photochemotherapy can lead to promotion of SCC, particularly in patients with skin phototypes I and II or in patients with history of previous exposure to ionizing radiation or methotrexate treatment for psoriasis.
Lesions :
Indurated papule, plaque, or nodule ; adherent thick keratotic scale or hyperkeratosis ; when eroded or ulcerated, the lesion may have a crust in the center and a firm, hyperkeratotic, elevated margin
Clark levels
level I, intra-epidermal;
level II, invades papillary dermis;
level III fills papillary dermis;
level IV, invades reticular dermis;
level V, invades subcutaneous fat.
Aplastic anemia is one of the stem cell disorder which leads to pancytopenia in the peripheral blood and decrease production of all cell line in bone marrow. it require bone marrow transplantation to cure the patient.
Lymphoma is a cancer of lymphocytes. The most common place for abnormal lymphocytes is in lymph nodes (glands) particularly
under the arms, in the neck and in the groin.
Lymphoma is solid tumors of the immune system arising from cells of lymphoid tissues; lymphocytes, histiocytes, and reticulum cells. It can happen anywhere in the immune system, but usually in lymph nodes, spleen, marrow, and tonsils. Location and the behavior of lymphomas separate them from leukemia.The malignancy starts and restricted to lymphoid tissues and progress to involve the BM and appears in PB, at this stage it may be named, “lymphosarcoma cell leukemia.
REFERENCES
cancer.org | 1.800.227.2345
Advances in the diagnosis and management
of lymphoma
Zachary H Word1
Matthew J Matasar1,2
1
Lymphoma Service, Department of
Medicine, Memorial Sloan–Kettering
Cancer Center, 2
Department of
Medicine, New York Presbyterian
Hospital, New York, NY, USA
Correspondence: Matthew J Matasar
Memorial Sloan–Kettering Cancer Center,
1275 York Avenue, New York,
NY 10065, USA
Tel +1 212 639 8889
Fax +1 646 422 2291
Email matasarm@mskcc.org
Lymphoma and CLL Forms
Parameswaran Hari, MD, MS
CLymphoma 101: The Basics
Neha Mehta-Shah, MD, MSCI
Assistant Professor
Department of Medicine
Division of Oncology
IBMTR , Milwaukee
Antibody mediated rejection of solid organ allograftstashagarwal
Objectives:
Introduction of Antibody mediated rejection AMR
Role of C4d in transplant rejection
Donor specific antibodies DSA
Presentation of AMR in kidney, liver, lung and heart.
Cutaneous manifestations of hiv infectiontashagarwal
Dermatological problems occur in more than 90% of patients with human immunodeficiency virus (HIV) infection. In some patients, skin is the first organ affected. Skin diseases have proved to be sensitive and useful measures by which HIV progression can be monitored.
Fluid cytology in serous cavity effusionstashagarwal
The intrathoracic and intraperitoneal organs are covered by a single layer of mesothelial cells, which is continuous with the lining of the thoracic and peritoneal cavities. The potential space between the two layers of epithelium contains a small amount of lubricating fluid.
Serous fluid lies between the membranes lining the body cavities(parietal) and those covering the organs within the cavities(visceral).
Production and reabsorption are normally at a constant rate. They are influenced by
Changes in osmotic and hydrostatic pressure in the blood.
Concentration of chemical constituents in the plasma
Permeability of blood vessels and membranes.
An accumulation of fluid, called an effusion, results from an imbalance of fluid production and reabsorption. This fluid accumulation in the pleural, pericardial, and peritoneal cavities is known as serous effusion.
CSF:
Derived through ultrafilteration and secretion through choroid plexus, produced at the rate of 500 ml/day.
Provides physical support, collects wastes, circulates nutrients and lubricates the CNS.
Normal CSF volumes:
In Adults: 90 - 150 ml
In Neonates: 10 - 60 ml
Total CSF volume is replaced every 5-7 hours.
COLLECTION
Lumbar puncture, Cisternal puncture, Lateral cervical puncture, Shunts and cannulas
Opening pressure – 90-180 mm H2O
Approximately 15-20 cc fluid collected
LAB
REQUIRED
Opening CSF pressure
Total cell count
Differential cell count
Glucose
Total protein
OPTIONAL
Cultures, Gram stain, AFB, Fungal and bacterial
antigens, Enzymes, PCR, Cytology, Electrophoresis,
VDRL, D-Dimers
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.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
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.
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
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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.
2. Hematopoietic Malignancies
Lymphoma is a general term used for proliferations that
arise as discrete tissue masses.
Leukemia is used for neoplasms that present with
widespread involvement of the bone marrow and
the peripheral blood(usually).
2
3. What is Lymphoma
Malignant lymphoma is a term given to tumors of the
lymphoid system and specifically of lymphocytes and
their precursor cells
i.e.
Cancer of the lymphatic system.
• Many lymphomas are known to be due to specific
genetic mutations.
3
5. Hodgkin disease
Hodgkin lymphoma
Type of malignant lymphoma in which Reed-Sternberg cells are present in
a characterstic background of reactive inflammatory cells of various types,
accompanied by fibrosis of variable degree.
( except NLPHL)
5
7. Introduction
• Are group of cancers which originate from lymphatic systems.
• It was named after Thomas Hodgkin who first described it in 1832.
• Dorothy Reed and Carl Sternberg first described the malignant cells of
Hodgkin lymphoma call Reed Sternberg cells.
• Hodgkin lymphoma was the first cancer which could be successfully
treated by radiation therapy and also by combination chemotherapy.
7
9. Risk Factors
• No clear risk factors, several implicated
• EBV (pathogen or passenger)
• HIV
• woodworking, farming
• rare familial aggregations
• First degree relatives have five fold increase in risk for Hodgkin lymphoma.
• Associated with EBV infection mainly with mixed cellularity type.
• High socio economic status.
• Prolonged use of of human growth hormone.
• men > women
• whites > blacks > Asians
9
10. Natural history
• Hodgkin lymphoma arises in a single node or chain of nodes and spreads
first to anatomically contiguous lymphoid tissue.
• Visceral involvement by hodgkin lymphoma may be secondary to
extension from adjacent lymph nodes.
• Hematogenous spread occurs to liver or multiple bony sites.
• Mechanism of spleen involvement is unclear but all patients with hepatic
and bone involvement are associated with splenic involvement.
10
11. Clinical features
• Most common presentation is asymptomatic lymphnode enlargement,
typically in the neck.
• Cervical lymphnodes are involved in 80% cases.
• Mediastinal involvement is seen in about 50% cases. They produce
symptoms like chest pain, cough and dyspnoea.
• Infradiaphrgamatic involvement is seen in 5% cases and usually seen with
older patients.
• Other less common symptoms are :
Pruritis, alcohol induced pain over involved lymphnodes, nephrotic syndrome,
erythema nodosum, cerebellar degeneration, immune hemolytic
anaemia, thrombocytopenia, hypercalcemia.
11
12. B symptoms
• About 33 % present with B symptoms overall
• Only 15-20% of stage I-III have B symptoms like
1. Fever(>38^C)
• May first present as fever of unknown origin
• Fever persists for days to weeks followed by afebrile intervals and then
recurrence.
• This pattern is called Pel Ebstein fever.
2. Drenching night sweats
3. Weight loss (>10% in 6 months)
12
18. Relative frequencies of different
lymphomas
Hodgkin
lymphoma
NHL
Diffuse large B-cell
Follicular
Other NHL
Non-Hodgkin Lymphomas
~85% of NHL are B-lineage
18
19. Hodgkin lymphoma
• Cell of origin: Germinal centre B-cell
• Reed-Sternberg cells (or RS variants) in the affected
tissues.
• Most cells in affected lymph node are polyclonal
reactive lymphoid cells, not neoplastic cells.
19
20. JACKSON AND PARKER
(1947)
SMETANA AND
COHEN’S ADDITION
(1956)
LUKES
(1963)
PARAGRANULOMA PARAGRANULOMA LYMPHOCYTIC AND
HISTIOCYTIC, NODULAR
LYMPHOCYTIC AND
HISTIOCYTIC, DIFFUSE
GRANULOMA GRANULOMA
NODULAR SCLEROSIS
MIXED CELLULARITY
NODULAR SCLEROSIS
SARCOMA SARCOMA DIFFUSE FIBROSIS
RETICULAR
Early Classifications
20
21. Later Classifications
• The Lukes-Butler classification of HL, modified at the Rye Conference in
1966, described the criteria for the four familiar subtypes of HL:
lymphocyte-predominant, nodular sclerosing, mixed cellularity, and
lymphocyte-depleted.
• The REAL classification separated the nodular lymphocyte-predominant
(NLP) subtype from so-called classic HL based on the immunophenotypic
and genotypic differences
• The REAL classification of HL was carried forward to the 2001 WHO
classification of HL and the 2008 WHO classification.
21
23. Reed Sternberg cell
Common feature of ALL Hodgkin Lymphomas.
• Large cells ( >45um in diameter) with classically binucleate or bilobed
central nucleus each with a large acidophilic central nucleoli surrounded
by a clear halo. “owl’s eye appearance”
• Variants: mononuclear (Hodgkin’s cell), mummified cell, lacunar cell, L/H
cell.
• Requirement of Reed-Sternberg cell for initial diagnosis is “absolute”(less
strict for LPHL or recurrent disease)
• Classic Reed-Sternberg cell:
+ CD15, CD30, CD25
– CD45, pan-B, S-100, keratin, EMA
• Most current studies indicate the RS cells of HL are lymphocytic in nature
and, in the great majority of cases, are of B-cell origin.
23
26. Lymph node, nodular-sclerosing Hodgkin lymphoma. (A) Clusters of Reed-Sternberg
cells and variants react with anti-CD15. (B) Reed-Sternberg cells in the same case show
negative results for CD45 (leukocyte common antigen), in contrast to positive
surrounding small lymphocytes.
A
B
26
27. A possible model of pathogenesis
germinal
centre
B cell
transforming
event(s)
loss of apoptosis
RS cell
inflammatory
response
EBV?
cytokines
27
28. Cytokines (such as IL-5, IL-10, IL-13, and
TGF-β) and chemokines (such as TARC, MDC,
IP-10, and CCL28) are secreted by Reed-
Sternberg cells.
They lead to florid accumulation of reactive
cells in tissues involved by classical HL.
These reactive cells produce factors that
support the growth and survival of the
tumor cells and further modify the reactive
cell response.
28
30. Lymphocyte predominant Hodgkin
lymphoma
• <5% of Hodgkin lymphoma
• Mainly involves cervical, axillary or mediastinal
• L&H cells or Popcorn cells are seen
• Positive for CD20, 45, CD79a, Bcl-6, J-chain, and PAX-5. EMA positive
in 50% cases.
• Negative for CD15, 30.
• Differential Diagnosis: Well differentiated lymphocytic lymphoma,
mononucleosis, malignant melanoma,, progressive transformation of
germinal centers
30
31. • LPHL is divided into two histopathologic subtypes:
1. Lymphocytic and histiocytic (L&H) nodular
2. L&H diffuse
• Currently the WHO classification recognizes only the nodular type and
requires at least a partially nodular growth pattern for diagnosis . Whether
the diffuse type is a distinct entity is controversial.
• Small lymphocytes predominate in the reactive component in both types
and are intermixed with varying numbers of histiocytes. Eosinophils,
neutrophils, and “diagnostic” or “classic” RS cells are rare. In fact, the
diagnosis of LPHL is doubtful if diagnostic RS cells are found easily; the
number of such cells should be fewer than one per histologic section.
31
32. • In LPHL, L&H variants of RS cells are conspicuous with folded, multilobed
nucleus and smaller nucleoli(“popcorn nuclei”).
• In the nodular subtype of LPHL, there is almost total obliteration of the
nodal architecture by a vaguely nodular process. LPHL nodules are
composed of small, round lymphocytes with varying numbers of
epithelioid histiocytes which gives them a mottled appearance. L&H
variants of RS cells may be numerous and are principally seen in the
nodules.
• “Diagnostic” or “classic” RS cells are rare or nonexistent and are not
required for the diagnosis of NLPHL.
32
34. • An attenuated rim of residual normal node (top) is often present in
nodular NLPHL. The vaguely nodular growth pattern and compressed
adjacent normal node seen at low magnification are features highly
suggestive of Nodular NLPHL.
34
36. 1. Nodular Sclerosis
• Most common type diagnosed
• About 70%
• Lacunar cells seen
• CD15, 30 positive
• EBV negative
• Only subtype without a male predominance
• Seen in younger patients with stage I-II disease.
• Differential diagnosis: Large cell Non Hodgkin lymphoma, carcinoma,
germ cell tumour and thymoma.
36
37. The classic histopathologic criteria for NSHL are
(a) prominent nodularity
(b) presence of lacunar RS cell variants, and
(c) birefringent broad collagen bands
• Nodal architecture is obliterated by relatively large nodules of tumor
partly or totally encircled by dense connective tissue bands that are
birefringent when viewed under polarized light.
37
38. LACUNAR VARIANT RS CELL : These variants possess large, multilobated, or
irregular nuclei with finely dispersed chromatin; nucleoli are usually small.
The cytoplasm of lacunar cells retracts when fixed in formalin, so the
nuclei gives the appearance of cells that lie with empty spaces between
them. (lacunae)
This retraction in absent in tissues fixed in Zenker and B5.
38
39. • Hodgkin lymphoma, nodular sclerosis type. A low-power view shows well-
defined bands of pink, acellular collagen that subdivide the tumor into
nodules 39
40. 2. Mixed Cellularity
• Constitutes about 20%
• More than 50% present as stage III or IV disease
• Biphasic incidence, peaking in young adults and again in adults
older than 55
• CD15, 30, EBV positive
• Presents in advanced stages
• Tendency to involve spleen, bone marrow.
• Differential diagnosis: Some cases of MCHL display an interfollicular
growth pattern. Such cases may be difficult to distinguish from peripheral
T-cell lymphomas. Lennert’s lymphoma (diffuse mixed T-cell ML with
excessive histiocytes). Diffuse follicular lymphoma.
40
41. Lymph node, mixed-cellularity Hodgkin lymphoma disease. Diagnostic Reed-
Sternberg cells are usually found without difficulty in mixed-cellularity
Hodgkin lymphoma. The reactive component consists of small, round
lymphocytes, histiocytes, plasma cells, and eosinophils,
41
42. 3. Lymphocyte Depleted
• Constitutes <5%
• Worst prognosis of all subtypes
• Older males, rare in children
• Present as febrile illness with
pancytopenia, hepatomegaly, and no
peripheral lymphadenopathy
• Advanced stage, Stage IV
• The biologic hallmark of LDHL is a
collapse of cell-mediated immunity,
HIV infection
• RS cells CD15+, CD30+; most EBV+
• Differential Diagnosis: Large cell Non-
Hodgkin’s lymphoma. Nodular
sclerosis HL
42
43. • Two subtypes of LDHL—diffuse fibrosis and reticular. The WHO
classification does not subdivide the LDHL. Although the morphologic
appearance of LDHL is varied, a unifying feature is the relative
predominance of RS cells compared with the depletion of background
lymphocytes.
• In some cases there is a diffuse fibrosis background. Sections show a
hypocellular background and abundant disorderly connective tissue
admixed with a PAS-positive fibrinoid material that is not birefringent.
Nodal architecture is completely obliterated. RS cells may be rare and
difficult to identify. multiple sections may be required to find RS cells.
• Other cases of LDHL have little in the way of a reactive component but are
distinguished by the presence of numerous large RS cells with bizarre
cytologic features. The sheetlike growth of bizarre RS cells is responsible
for the older term Hodgkin sarcoma.
43
44. 4. Lymphocyte-Rich
• RS cells CD15+, CD30+; 40% EBV+
• Uncommon
• M > F
• Tends to be seen in older adults
• This is an uncommon form of classical HL
• Reactive lymphocytes make up the vast majority of the cellular infiltrate.
In most cases, involved lymph nodes are diffusely effaced, but vague
nodularity due to the presence of residual B-cell follicles is sometimes
seen.
• Differential Diagnosis: This entity is distinguished from the lymphocyte
predominance type by the presence of frequent mononuclear variants and
diagnostic Reed-Sternberg cells with a “classical” immunophenotypic
profile.
• Very good to excellent prognosis.
44
47. Spread
• Generally a well behaved spread of disease through contiguous LN groups,
(especially NS and LP); <5% show non-contiguous spread
• May have direct extension into perinodal tissue.
• 85% of Stage I/II disease are above diaphragm.
• Spleen: if >400g, almost always positive.
• Liver: if positive, spleen and retroperitoneal LN’s are also positive.
47
48. Ann Arbor Staging System
• Stage I: Single lymph node region (I) or single extralymphatic organ or
site (IE)
• Stage II: > 2 lymph node regions on same side of diaphragm (II) or with
limited, contiguous extra lymphatic tissue involvement (IIE)
• Stage III: both sides of diaphragm involved, may include spleen (IIIS) or
local tissue involvement (IIIE)
• Stage IV: multiple/disseminated foci involved with > 1 extralymphatic
organs (i.e. bone marrow)
(A) or (B) designates absence/presence of “B” symptoms
*(E) Localized, solitary involvement of extralymphatic tissue, excluding liver
and bone marrow 48
50. Stage I Stage II Stage III Stage IV
Staging of lymphoma
A: absence of B symptoms
B: fever, night sweats, weight loss
50
51. PROGNOSIS
• Clinical stage
• Extranodal involvement bad (especially if distant rather than by direct
spread)
• Degree of splenic involvement: ≥5 nodules poor prognosis
• Age: >50 yrs unfavorable
• Sex and race: Black males worse than white females
• Microscopic type: LP and NS best, MC intermediate, LD worst (less
important with current treatment protocols)
• Laboratory findings: decreased hematocrit, elevated LDH, raised ESR,
elevated serum levels of CD30, soluble CD25 have negative prognosis.
• CD15- lack of expression is a negative prognostic factor.
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54. Radiotherapy
• Radiation therapy is the most effective single thrapeutic agent for treating
Hodgkin lymphoma.
• The main objective of radiation in Hodgkin lymphoma is to treat involved
and contiguous field.
• Radiotherapy can be given by
1. 2D planning
2. 3D planning
3. IFRT
• Involved field radiotherapy is the most commonly used technique at
present. It targets a smaller area rather than a classical extended field.
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55. Complications
• Autologous bone marrow transplantation can cure half of patients who fail
effective chemotherapy regimens.
• Because of the very high cure rate in patients with Hodgkin's disease,
long-term complications have become a major focus for clinical research.
The most serious late side effects include secondary malignancies, cardiac
injury, infertility and Lhermitte's syndrome.
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