Haematology Flashcards
Describe Amyloidosis and its types, and features,
A group of disorders characterised by extracellular deposition of a protein in abnormal fibrillar form. Can be primary (AL amyloid “L for immunoglobulin Light chain fragment”) or Secondary (AA amyloid “A for precursor serum amyloid A protein”) or familial.
AL Amyloid (primary) features: associated with waldenstroms and lymphoma. Kidneys: nephrotic syndrome Heart: restrictive cardiomyopathy (looks sparkling on echo), arrhythmias, angina Nerves: peripheral and autonomic neuropathy, carpel tunnel syndrome Gut: macroglossia, malabsoprtion, weight loss, hepatomegaly, perforation, haemorrhage, obstruction Vascular: purpura, especially perioribtal (characteristic feature)
AA Amyloid (Secondary): RA, IBD, Chronic infections e.g. TB, Bronchiectasis. Mostly affects kidneys liver and spleen presenting with nephrotic syndrome or hepatosplenomegaly, macroglossia is not seen and rarely affects the heart.
Diagnosis is made with abdominal fat or rectal biopsy and postive Congo Red staining with red-green birefringence under polarised light microscopy.
llWhat are Bence Jones proteins
Ig light chains excreted by kidney in excess in some patients with myeloma.
What are the causes of macrocytic anaemias?
Megaloblastic causes: Folate deficiency, B12 deficiency, anti-folate drugs e.g (phenytoin)
Normoblastic causes: alcohol, liver disease, hypothyroidism, pregnancy, reticulocytosis, myelodysplasia, cytotoxic drugs,
What are the causes of microcytic anaemias?
- iron deficiency anaemia (most common)
- thalassaemia
- sideroblastic anaemia (very rare)
- Hereditary Spherocytosis
What are some causes of a normocytic anaemia?
acute blood loss anaemia of chronic disease renal failure bone marrow failure hypothyroidism (may be macrocytic) Haemolysis ( may be macrocytic) pregnancy
Describe iron-deficiency anaemia, it’s causes, diagnostic tests and treatment
Commonest cause of anaemia with microcytic hypochromic RBC’s
Causes: •blood loss e.g menorrhagia or GI bleeding •poor diet •malabsorption • hookworm in tropics
Signs: conjunctival pallor, lethargy, koilonychia, atrophic glossitis, angular cheilosis
Tests: FBC shows decreased MCV, MCH and ferritin (confirms diagnosis)
Treatment: ferrous sulphate 200mg BD PO follow up FBC if no response consider sideroblastic anaemia if Hb improves but MCV still low consider thalassaemia
What are the Side effects of oral ferrous sulphate?
- nausea
- abdominal discomfort
- diarrhoea or constipation
- black stools
Describe anaemia of chronic disease (secondary anaemia)
2nd most common anaemia after IDA most common anaemia in inpatients Due to 3 problems:
- poor use of iron in erythropoiesis
- cytokine-induced shortening of RBC survival
- decreased production of and response to erythropoietin
tests: FBC shows normocytic anaemia with normal or raises ferritin.
With regards to a peripheral blood film what is anisocytosis?
Variation in RBC size e.g. Due to megaloblastic anaemia, IDA, thalassaemia
With regards to a peripheral blood film what are acanthocytes?
Acanthocytes are spiked RBCs seen in splenectomy, alcoholic liver disease, abetalipoproteinaemia, spherocytosis
With regards to a peripheral blood film, what is basophilic RBC stippling?
Speckled RBC cells due to denatured RNA fragments found in RBCs indicative of accelerated erythropoiesis or defective Hb synthesis.
Causes: lead poisoning, megaloblastic anaemia, myelodysplasia, liver disease, haemoglobinopathy e.g. Thalassaemia
With regards to a peripheral blood film, what are Burr cells?
RBC projections less prominent that acanthocytes may be indicative of renal or live failure or due to an EDTA storage artefact
What are the normal values of a FBC?
HB: Men;130-180g/L Women;115-160g/L
MCV: 77-95fL
MCH: 27-32pg
PLT: 150-400x10^9/L
RBC: Men;4.5-6.5 Women; 3.8-5.8 x10^12/L
WBC: Men;3.7-9.5 Women;3.9-11.1x10^9/L
NEUT: Men;1.7-6.1 Women;1.7-7.5x10^9/L LYMP: 1-3.2x10^9/L MONO: 0.2-0.6x10^9/L EOS: 0.03-0.06x10^9/L BASO: 0.02-0.09x10^9/L
What at some causes of neutrophilia and what’s is the normal range?
Normal range: 1.7-6.1 or 7.5 (Female) x10^9/L
Causes:
- bacterial infections
- inflammation (MI, PAN, SLE, RA etc)
- myeloproliferative disorders
- drugs (steroids)
- disseminated malignancy (e.g .colonic cancer)
- stress e.g. Trauma, surgery, burns, haemorrhage, seizure
What are the causes of thrombocytosis?
Causes of increased platelets:
- bleeding
- infection
- chronic inflammation
- malignancy
- trauma
- post-surgery
- IDA
Describe myeloproliferative disorders
Causes by proliferation of a clone of haemopoetic myeloid stem cells in the marrow.
Classified depending on the cell type which is proliferating:
RBC - polycythaemia rubra Vera
WBC - chronic myeloid leukaemia
PLT - essential thrombocythaemia
Fibroblasts - myelofibrosis
What are some causes of thrombocytopenia?
May be due to decreased marrow production:
- aplastic anaemia
- megaloblastic anaemia
- marrow infiltration (e.g. Myeloma, leukaemia)
- marrow suppression (cytotoxics, radiotherapy)
Or may be due to excess destruction of platelets:
- immune causese e.g. ITP, SLE, CLL
- Non-immune causes: TTP or HUS, DIC, hypersplenism
Describe Immune/Idiopathic Thrombocytopenic Purpura (ITP), its symptoms, tests, and management.
Caused by anti-platelet antibodies, may be acute (commonly self-limiting disease in children ~2 weeks post infection) or chronic (seen mainly in young/middle-aged women).
Symptoms:
- Acute ITP presents wth bruising, purpura, petechiae. Usually history of recent gastroenteritis or URTI.
- Chronic ITP presents with varying history of bleeding, purpura, epistaxis, menhorragia.
Tests: bone marrow biopsy shows increased megakaryocytes and anti platelet antibodies
Treatment:
- none if mild, gradual resolution over 3 months.
- if symptomatic or platelets less than 20, immunosuppression to keep platelets above 30 e.g Prednisolone 1mg/kg/d
- if no response or relapse splenectomy cures
Describe Disseminated Intravascular Coagulation (DIC), it’s causes, investigations, and management.
Widespread activation of coagulation leading to consumption of clotting factors and platelets with increased risk of bleeding. Fibrin strands fill small vessels Haemolysing RBCs.
Causes: malignancy, sepsis, trauma, obstetric events, liver disease
Investigations:
- Prolonged clotting times
- Thrombocytopaenia
- Decreased fibrinogen
- Increased fibrinogen degradation products.
Treatment:
- replace platelets if less than 50, cryoprecipitate to replace fibrinogen, FFP to replace coagulation factors.
- Activated protein C reduces mortality in DIC with severe sepsis or multi-organ failure.
What do the presence of blast cells indicate?
Blasts cells are nucleated precursor cells that are not normally in peripheral blood. They may be seen in myelofibrosis, leukaemia, and malignant infiltration by carcinoma
Describe MyeloDysplastic Syndrome (MDS), its features, and management.
A heterogenous group of disorders that manifest as marrow failure with risk of life-threatening infection and bleeding.
May be primary or secondary due to chemotherapy or radiotherapy. 30% transform to acute myeloid leukaemia.
Features: Anaemia, Neutropenia, Thrombocytopaenia. Splenomegaly. Dysplastic cells in bone marrow biopsy
Management:
- Supportive - transfusions
- Azacytidine
What are the main types of Leukaemia?
Leukaemia divides into 4 main types depending on the cell line involved.
Lymphoid:
- Acute Lymphoblastic Leukaemia (ALL)
- Chronic Lymphocytic Leukaemia (CLL)
Myeloid:
- Acute Myeloid Leukaemia (AML)
- Chronic Myeloid Leukaemia (CML)
Describe tumour lysis syndrome, its risk factors and preventative measures.
Caused by a massive destruction of cells leading to release of K+, Urate, and then kidney injury.
Increased risk if levels of LDH are increased, Creatinine increased, urate increased or WCC >25
Prevention with high fluid intake and allopurinol pre-cytotoxics
Describe Acute Lymphoblastic Leukaemia, its features, and prognostic factors.
A malignancy of lymphoid cells, affecting B or T lymphocyte cell lines. Commonest cancer of childhood (80%) peak age 2-5yrs, rare in adults.
Features: arise from marrow failure and organ infiltration with organomegaly, Anaemia, infection, and bleeding.
Good prognostic factors:
- French-American-British (FAB) L1 type
- Common ALL
- Pre-B phenotype
- Low initial WBC
- Del(9p)
Poor prognostic factors:
- FAB L3 type
- T or B cell surface markers
- Philadelphia translocation t(9:22)
- Age less than 2 or over 10
- Male sex
- CNS involvement
- High initial WBC over 100
- non-caucasian
Describe Acute Myeloid Leukeamia, its features, prognostic features, and investigations.
May occur as primary disease or following secondary transformation of a myelodysplastic or myeloproliferative disorders. Most frequently occurs in 65-75yrs but occurs at all ages.
Features: Fatigue, SOB, Bruising, Bleeding, Increased risk of infections. Weight loss.
Good prognostic features:
- T(15;17) (Acute Promyelocytic leukaemia)
- T(8;21)
Poor Prognostic features:
- Over 60yrs
- over 20% blasts after first course of chemo
- Cytogenetics deletions of chromosome 5 or 7
- pre-exsiting myelodysplastic or myeloproliferative disorder
- Treatment-related AML.
Investigations:
- May have leukocytosis with blast cells, also can present with isolated thrombocytopenia, or anaemia or even leukopenia (if extensive bone marrow infiltration)
- blast cells may be few in peripheral blood and so diagnosis depends on bone marrow biopsy. Microscopy can allow differentiation from ALL.
- Blood film may show Auer Rods
Describe Chronic Myeloid Leukaemia, its features, investigations, and management.
Characterised by an uncontrolled clonal proliferation of myeloid cells. It accounts for 15% of leukaemias. It is a myeloproliferative disorder. Occurs most often between 40-60yrs.
Features: Massive splenomegaly, weight loss, night sweats, malaise, infections, anaemia.
Tests: Often WBC >100 with whole spectrum of myeloid cells affected i.e. neutrophilsm myelocytes, basophils, eosinophils.
Philadelphia chromosome in 95% (a reciprocal translocation of long arms of 9 + 22, which forms BCR-ABL fusion gene on chromosome 22 which has excess tyrosine kinase activity)
Management:
- Imatinib inhibits the BCR-ABL tyrosine kinase protein and induces apoptosis in Philadelphia chromosome +ve patients.
- interferon-alpha, hydroxyurea
- Allogenic bone marrow transplant
Describe Chronic Lymphocytic Leukaemia, its features, prognostic factors, indications for treatment, management and complications.
Accumulation of mature B cells that have escaped programmed cell death, it is the commonest leukaemia.
Features:
- Asymptomatic
- constitutional e.g. anorexia, weight loss
- bleeding and infections
- lymphadenopathy more marked than CML.
Poor Prognostic Factors:
- male sex
- age over 70
- lymphocyte count over 50
- Prolymphocytes comprising more than 10% of WBCs
- lymphocyte doubling time less than 12 months
- Raised LDH
- CD38 expression +ve
- deletions of part of the short arm of chromosome 17 (seen in around 5-10%)
Good prognostic factor:
-deletion of the long arm of chromosome 13 is the most common genetic abnormality, being seen in around 50% of patients.
Indications for treatment:
- Progressive marrow failure i.e the development or worsening of anaemia and or thrombocytopaenia
- Massive (over 10cm) or progressive lymphadenopathy
- Massive (over 6 cm) or progressive splenomegaly
- Progressive lymphocyctosis i.e. increase of 50% over 2 months or lymphocyte doubling time of less than 6 months
- Systemic symptoms e.g. weight loss over 10%BW in previous 6 months, pyrexia for over 2 weeks, extreme fatigue, night sweats.
Management:
- Patients who have no indications for treatment are monitored with regular blood counts
- Fludarabine, Cyclophosphamide and rituximab (FCR) has now emerged as the initial treatment of choice for the majority of patients.
Complications:
- Hypogammaglobulinaemia leading to recurrent infections
- Warm autoimmune haemolytic anaemic seen in 10-15% of patients
- Transformation to high-grade lymphoma (Richter’s transformation)
Describe Sepsis (+/-Neutropenia), the sepsis six, and severe sepsis signs.
is a potentially fatal complication of anti-cancer treatment (particularly chemotherapy). Identify with Quick Sepsis Related Organ Failure Assessment (qSOFA) with 2 or more of the following.
- SBP less than 100mmHg
- RR >22
- new altered mental state.
Do the sepsis six:
- high-flow oxygen
- IV antibiotics
- IV Fluid challange (hartmann’s)
- Catheter and UO monitoring
- Serum lactate
- Blood cultures
Regularly screen for signs of severe sepsis:
- SBP less than 90mmHg
- SpO2 less than 90% despite high flow oxygen
- INR >1.5 or APTT >60s
- Plt less than 100
- UO less than 0.5ml/kg/hr
- lactate >2.0mmol/L
What is GCSF?
Granulocyte-colony stimulating factor is a protein that stimulats the bone marrow to make WBCs
Describe lymphoma
Disorders caused by malignant proliferation of lymphocytes , which accumulate in the lymph nodes causing lymphadenopathy, but may also be found in peripheral blood or infiltrate organs. They are histologically classified into Hodgkins and Non-hodgkins depending on the presence of characteristic cells with mirror-image nuclei called Reed-Sternberg cells.
What is the management of a high INR, in the context of a patient on warfarin with major bleeding?
- Stop Warfarin
- IV Vitamin K 5mg
- Prothrombin complex concentrate (FFP if unavailable)
What is the management of a high INR, in the context of a patient on warfarin with minor bleeding and INR > 8.0?
- Stop warfarin
- Give intravenous vitamin K 1-3mg
- Repeat dose of vitamin K if INR still too high after 24 hours
- Restart warfarin when INR less than 5
What is the management of a high INR, in the context of a patient on warfarin with no bleeding and INR > 8.0?
- Stop warfarin
- Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
- Repeat dose of vitamin K if INR still too high after 24 hours
- Restart when INR less than 5
What is the management of a high INR, in the context of a patient on warfarin with minor bleeding and INR 5.0-8.0?
- Stop warfarin
- Give intravenous vitamin K 1-3mg
- Restart when INR less than 5
What is the management of a high INR, in the context of a patient on warfarin with no bleeding and INR 5.0-8.0?
- Withhold 1 or 2 doses of warfarin
- Reduce subsequent maintenance dose
Describe Haemophilia A its presentation and tests, and management
Factor VIII defiency (x linked recessive) though high rate of new mutations so may be no family history.
Presentation depends on severity but is often early in life or after surgery/trauma with bleeds into joints leading arthropathy and bleeding into muscles causing haematomas (increased pressure can lead to nerve palsies and compartment syndrome)
Tests: increased APTT, decreased factor VII
Management:
- Factor VIII replacement
- 10% develop Factor VIII inhibitors
Describe Haemophilia B
Factor IX deficiency also know as Christmas disease, inherited x-linked recessive behaves clinically like haemophilia A
Describe Von Willebrand disease, the types, investigation, and management
The most common inherited bleeding disorder. Mostly in autosomal dominant fashion due mutations in vWF gene on chromosome 12. Behaves like platelet disorder i.e. epistaxis, and menorrhagia. Von Willebrand factor (vWF) has 3 roles in clotting:
- To bring platelets into contact with exposed subendothelium
- to make platelets bind to each other
- to bind to factor VIII, protecting it from destruction in the circulation
Types: (Over 20 types)
- Type 1: Partial reduction in vWF (80% of patients)
- Type 2: Abnormal form of vWF
- Type 3: Total lack of vWF (Autosomal recessive)
Investigations:
- Prolonged bleeding time
- APTT prolonged
- Reduced Factor VIII levels
- Defective platelet aggregation with ristocetin
Management:
- Tranexamic acid for mild bleeding
- Desmopression raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells.
- Factor VIII concentrate.
What are the causes of thrombophilia?
Thrombophilia is an inherited or acquired coagulopathy predisposing to thrombosis usually venous: DVT, PE
Inherited causes:
- factor V Leiden increase
- prothrombin increase
- protein C and S deficiency
- anti-thrombin deficiency
Acquired causes:
- Pill/HRT
- antiphospholipid syndrome
Describe Glucose-6-phosphate dehydrogenase (G6PD) deficiency and it’s presentation.
X-linked RBC enzyme defect. Mostly affecting males in the Mediterranean, Africa and Middle/Far East. Mostly asymptomatic, but may get oxidative crises due to decreased glutathione production.
Presentation: Rapid anaemia and jaundice, precipitated by drugs (primaquine, aspirin, sulphonamides, quinolones, nitrofurantoin, NSAIDs), broad beans, or illness.
Describe B-Thalassemia and its treatment.
Usually caused by point mutations in the B-globin genes on chromosome 11 leading to decreased production or its absence. Can be split into Thalassemia minor/trait, intermedia and major.
Minor and intermedia do not require transfusions but may be anaemic. healthy diet fitness and folate supplements help.
Thalassemia Major require regular blood transfusions and usually presents in 1st year of life. with extramedullary haemopoiesis causing characteristic skull bossing. Also require iron-chelators to prevent iron overload.
What are the available anti-coagulants and which are used therapeutically and prophylactically
Prophylactic: Most commonly used is LMWH e.g. dalteparin, enoxaparin, tinzaparin. It inactivates Factor Xa It has longer half-life than heparin and response is more predictable meaning it needs only be taken once or twice daily and no monitoring is usually required.
Therapeutic: First line is LMWH and depending on cause warfarin is given in combination. LMWH is continued until INR >2.2 and until day 5 as warfarin has an initial prothrombotic effect.
Describe paraproteinaemia and the different types
Presence in the circulation of immunoglobulins produced by a single clone of plasma cells. There are six major categories:
- Multiple myeloma
- Waldenstroms macroglobulinaemia
- Primary Amyloidosis
- Monoclonal gammopathy of uncertain significance
- paraproteinemia in lymphoma or leukaemia (seen in 5% CLL)
- Heavy chain disease
Describe Sickle-cell anaemia, it’s crises’ and management
Autosomal recessive disorder causing production of abnormal beta-globin chains due to an amino acid substitution of glutamate to valine. Heterozygotes have sickle cell trait which is protective against malaria as cells sickle when deoxygenated and only presents an issue in severe hypoxia
Features:
-Haemolysis and chronic anaemia is usually well tolerated
-Vaso-occluive ‘painful’ crises common due to microvascular occlusion. Often affects marrow causing severe pain but can happen in gut (mesenteric ischaemia) CNS (stroke, seizures) or limbs (ulcers, avascular necrosis, dactylitis)
-aplastic crisis, this is due to parvovirus B19 with sudden reduction in marrow production, usually self-limiting.
-sequestration crises, mainly affects chilren as the spleen has not yet undergone atrophy. There is pooling of blood in the spleen +/- liver with organomegaly severe anaemia and shock
-Acute chest syndrome, Pulmonary infiltrates involving complete lung segments causing pain, fever, tachypnoea, wheeze and cough. A sickle crises. Prodromal painful crises occur 2.5days before any abnormalities on CXR. Chief Causes are fat embolism or infection e.g with chlamydia or mycoplasma or viruses
Management:
- oxygen if desaturating
- analgesia e.g. Morphine
- rehydration with IV fluids
- transfusion for severe anaemia
- hydroxycarbamide for anaemia ( Increase foetal haemoglobin)
Describe myeloma, its symptoms, tests and diagnosis.
Myeloma is a type of plasma cell dyscrasia (PCD). Plasma cell dyscrasias are due to an abnormal proliferation foa signl clone of plasma or lymphoplasmacytic cells leading to secretion of immunglobulin ultimately leading to dysfunction of many organs. Bence-Jones proteins present in 2/3 of urine. Most commonly occurs over 60 average age at diagnosis is 70
Symptoms + Signs:
- Osteolytic bone lesions (backache)
- Hypercalcaemia
- Anaemia, Neutropenia or thrombocytopenia (marrow infiltration)
- recurrent bacterial infections
- renal impairment (due to light chain deposition)
Tests:
FBC, U+E, serum and urine electrophoresis. Xrays in case of bony pain shows punched out lesions, vertebral collapse. osteoporosis. Marrow biopsy.
Diagnosis depends on:
- monoclononal protein band in serum or urine electrophoresis
- increased plasma cells on marrow biopsy
- evidence of end organ damage e.g. hypercalcaemia, renal insufficiency, anaemia.
- bony lesions.
What are the causes of pancytopenia?
Pancytopenia is a reduction in all the major cell lines: red cells, white cells and platelets. Causes are due to:
- Decreased marrow production i.e aplastic anaemia, infiltration (e.g. acute leukaemia, myelodysplasia, myeloma, lymphoma, solid tumours, TB) megaloblastic anaemia, paroxysmal nocturnal haemoglobinuria, myelofibrosis, SLE
- peripheral destruction: hypersplenisn.
Describe Aplastic anaemia, its symptoms, causes and management.
it is a rare stem cell disorder leading to pancytopenia and hypoplastic marrow.
Symptoms:Presents with features of anaemia, infection or bleeding.
Causes:Most cases are due to autoimmune, triggered by drugs or radiotherapy.
Management:
- Bone marrow biopsy needed for diagnosis,
- treatment is supportive in milder cases otherwise bone marrow transplant may be needed.
Describe heavy chain disease in the context of paraproteinaemia
This is where neoplastic cells produce free Ig heavy chains. alpha chain disease is the most important, causing malabsorption from infiltration of small bowel wall. It may progress to lymphoma.
Describe Protein C+S deficiency and its features.
A type of thrombophilia. These vitamin K-dependent factors act together to cleave and so neutralise factors V + VIII.
Features:
- Heterozygotes deficient for either protein risk thrombosis. Skin necrosis also occurs.
- Homozygous deficiency for either protein causes neonatal purpura fulminans, fatal if untreated.
- Testing for protein C is done using snake venom to activate the protein C, which is then quantified by clotting methods.
Describe Antithrombin deficiency
Antithrombin is a co-factor of heparin, and inhibits thrombin. heterozygotes risk is greater than protein C or S deficiency by ~4-fold. Homozygosity is incompatible with life.
What are some causes of polycythaemia
May be absolute (increased RBC mass) or Relative (Normal RBC mass and decreased plasma volume)
Relative may be acute and due to dehydation (e.g. alcohol or diuretics)
Absolute causes may be primary (polycythaemia Rubra vera) or secondary due to hypoxia (e.g. high altitudes, chronic lung disease, cyanotic congenital heart disease, heavy smoking) or inappropriate erythropoietin secretion (e.g. renal carcinoma, hepatocellular carcinoma. Testosterone replacement can cause polycythaemia
Describe agranulocytosis and some common drug causes
Granulocytes (neutrophils, basophils, eosinophils) stop being made. It may present as a sore throat before a fatal infection so warn all patients to report any fever when starting a risk drug. If presents stop drug, and GCSF may have a role.
Important drugs to note are:
- Clozapine
- anti-thyroid e.g. Carbimazole
- anti-epileptics
- cytotoxics
What are some causes of a lymphocytosis?
- Acute viral infection
- Chronic infection e.g. TB, Brucella, Hepatitis, Syphilis
- Leukaemias and lymphomas, especially chronic lymphcytic leukaemia (often presents as incidental finding on FBC)
Describe Hodgkin’s Lymphoma, its symptoms, tests, classification, and management.
Malignant proliferation of lymphocyte with characteristic mirror-image nuclei called Reed-Sternberg Cells. Peak incidence in young adults and elderly. It is the leading cause of malignancy if aged 15-24yrs.
Symptoms: Often presents with enlarged, painless, non-tender, rubbery superficial lymph nodes, typically cervical (60-70%), also axillary or inguinal. Node size may increase and decrease spontaneously and nodes can become matted. 25% have B symptoms e.g. Fever, weight loss, night sweats, pruritis, and lethargy. There may be alcohol induced lymph node pain.
Tests: Bloods, FBC (anaemia, lymphocytosis), film, ESR (raised), LFT, LDH (raised in increased cell turnover), Urate, Ca2+/Image guided needle biopsy + CT/MRI for staging
Grading:
I = one area involved
II = two or more areas involved
III = areas above and below diaphragm involved
IV = bone marrow involvement or other organ
A/B = Absence/presence of B symptoms
Classification:
- Nodular Sclerosing (70%)- most common good prognosis more common in women associated with lacunar cells
- Mixed cellulalrity (20%) - good prognosis associated with a large number of Reed-Sternberg cells.
- Lymphocyte predominant (5%) - best prognosis
- lymphocyte depleted - rare worst prognosis.
Treatment:
-Chemoradiotherapy, increases risk of secondary malignancy Common course is ABVD Adriamycin, Bleomycin, Vinblastine, Dacarbazine.
