Learn — Oncology & haematology

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Colorectal cancer

Colorectal cancer is adenocarcinoma arising from the glandular epithelium of the colon or rectum, and in most patients it develops slowly through the adenoma-carcinoma sequence in which a normal mucosa becomes an adenomatous polyp and then an invasive cancer over 10 to 15 years. That long pre-invasive window is the whole reason screening works, and it is why a nurse who explains a faecal occult blood test or persuades a patient over 45 to accept a colonoscopy is doing more for survival than any drug given after the diagnosis.

Risk rises steeply after the age of 50 and is multiplied by familial adenomatous polyposis (an APC gene mutation with hundreds of polyps and near-certain cancer by 40, which is why prophylactic colectomy is offered in the teens or twenties), Lynch syndrome or hereditary non-polyposis colorectal cancer (mismatch-repair gene mutations, right-sided tumours at a young age), ulcerative colitis of more than eight to ten years, a diet low in fibre and high in red and processed meat, obesity, smoking and alcohol.
Side determines the presentation: a right-sided tumour sits in a wide caecum with liquid stool and presents late with iron-deficiency anaemia, fatigue, weight loss and a palpable mass, while a left-sided or sigmoid tumour narrows a smaller lumen carrying formed stool and presents with a change in bowel habit, blood mixed into the stool and eventually large-bowel obstruction.
Rectal cancer presents with bleeding, tenesmus, mucous discharge, a sense of incomplete evacuation and spurious diarrhoea, and a large proportion of rectal tumours are within reach of a digital rectal examination — the cheapest test in the department and the one most often skipped.
Screening in an average-risk adult starts at 45 to 50 years: an annual faecal immunochemical test or faecal occult blood test, or a colonoscopy every 10 years; patients with familial adenomatous polyposis, Lynch syndrome or long-standing colitis start younger and are scoped far more often.
Colonoscopy with biopsy of the whole colon is the diagnostic standard because synchronous tumours occur in a small percentage of patients; carcinoembryonic antigen is not a screening or diagnostic test but a baseline drawn before surgery whose later rise signals recurrence, and staging uses contrast CT of chest, abdomen and pelvis with MRI of the pelvis and endorectal ultrasound for rectal tumours.
Staging is TNM, but the Dukes classification is what is asked: A confined to the bowel wall, B through the muscularis into the perirectal or pericolic tissue with negative nodes, C with lymph node involvement (C1 local, C2 apical node) and D with distant metastases, most often liver; five-year survival falls from over 90 per cent in Dukes A to under 10 per cent in Dukes D.
The operation follows the blood supply: right hemicolectomy for caecal and ascending tumours, left hemicolectomy for the descending colon, sigmoid colectomy or high anterior resection for the sigmoid, low anterior resection with total mesorectal excision for the mid rectum, and abdominoperineal resection with a permanent end colostomy for a tumour within a few centimetres of the anal verge; Hartmann's procedure with an end colostomy is the answer to an obstructed or perforated left-sided cancer.
Adjuvant chemotherapy (a fluorouracil and oxaliplatin regimen) is standard for node-positive colon cancer, and locally advanced rectal cancer is given neoadjuvant chemoradiotherapy before surgery to shrink the tumour and improve the chance of a sphincter-saving resection.

Massive blood transfusion protocol

Massive transfusion is conventionally defined as the replacement of one entire blood volume within 24 hours, or 10 or more units of red cells in 24 hours, or 4 or more units in one hour with bleeding that is still going on. The massive transfusion protocol is the pre-agreed pathway that releases red cells, plasma and platelets together in a fixed ratio the moment it is activated, and it exists because patients bleeding at this rate die not of the missing red cells alone but of the lethal triad of hypothermia, acidosis and coagulopathy that transfusing them badly creates.

Products are given in a balanced ratio of about 1:1:1 — one unit of packed red cells to one unit of fresh frozen plasma to one pooled platelet dose — because giving red cells alone dilutes the clotting factors and platelets and makes the bleeding worse; crystalloid is kept to a minimum for the same reason.
The lethal triad is hypothermia, acidosis and coagulopathy, and each drives the other two: cold blood slows the clotting enzymes and the platelets, poor perfusion generates lactic acidosis, and the resulting coagulopathy causes more bleeding, more cold fluid and deeper acidosis.
Tranexamic acid 1 g intravenously over 10 minutes followed by 1 g infused over 8 hours reduces death from bleeding in trauma when the first dose is given within 3 hours of injury; given later it is not beneficial, so the time of injury must be established and recorded.
Citrate in stored blood binds ionised calcium, so rapid transfusion causes hypocalcaemia with perioral tingling, tremor, a prolonged QT interval and hypotension; ionised calcium is monitored and calcium gluconate or calcium chloride is given as prescribed, and citrate metabolism later produces a metabolic alkalosis.
Potassium leaks out of red cells during storage, so rapid transfusion of older units — especially through a central line, in a neonate or in renal failure — can cause hyperkalaemia with peaked T waves and arrhythmia, while after resuscitation the potassium often swings the other way as the cells take it back up.
Every unit is warmed through an approved blood warmer and the patient is warmed with forced-air blankets and warmed fluids, aiming to keep core temperature above 35 degrees Celsius; blood is never warmed in a microwave, in hot water or on a radiator, because uncontrolled heat haemolyses the cells.
In extremis, group O red cells are given uncrossmatched — O negative for girls and women of childbearing age to avoid rhesus sensitisation — then group-specific blood, then fully crossmatched blood as soon as the laboratory can supply it; the sample for grouping must be taken before the first unit runs.
Laboratory targets guide the later units: platelets above 50 x 10^9/L (higher with head or eye injury), fibrinogen above 1.5 g/L in trauma and above 2 g/L in obstetric haemorrhage with cryoprecipitate to correct it, prothrombin time and activated partial thromboplastin time under one and a half times control, alongside ionised calcium, potassium, lactate, arterial blood gases and temperature.
Bedside safety does not relax because the situation is an emergency: two staff check the patient's identity band against the compatibility label at the bedside, each unit is started within 30 minutes of leaving the controlled refrigerator and completed within 4 hours, a 170 to 200 micron filter set is used, and only 0.9 per cent sodium chloride shares the line — never Ringer's lactate, whose calcium clots the unit, and never dextrose, which haemolyses it.

Iron deficiency anaemia

Iron deficiency anaemia is a microcytic hypochromic anaemia that develops when the body's iron stores are exhausted and the marrow can no longer make enough haemoglobin. It is the commonest anaemia in the world and by far the commonest in India, where NFHS-5 found more than half of women and children anaemic, which is why every recruitment paper carries at least one question on its indices and its treatment.

WHO 2024 defines anaemia by age, sex and pregnancy status: below 13 g/dL in men aged 15 and over, below 12 g/dL in non-pregnant women aged 15 and over, below 11 g/dL in the first trimester and below 10.5 g/dL in the second and third, below 10.5 g/dL in children aged 6 to 23 months, below 11 g/dL at 24 to 59 months, below 11.5 g/dL at 5 to 11 years and below 12 g/dL at 12 to 14 years.
The blood picture is a low MCV under 80 fL, a low MCH under 27 pg, a raised red cell distribution width, and pencil cells with target cells on the film; the reticulocyte count is low until treatment starts.
The iron studies are the discriminator: serum ferritin is LOW (under 15 microgram/L confirms empty stores and under 30 microgram/L is the practical clinical cut-off), serum iron is low, the total iron-binding capacity is HIGH and transferrin saturation is under 16%. In anaemia of chronic disease the ferritin is normal or high and the total iron-binding capacity is low.
Ferritin is an acute-phase reactant, so during infection, inflammation or malignancy a ferritin as high as about 70 microgram/L can still mean iron deficiency; check a CRP alongside it before calling the stores adequate.
Causes in India are chronic blood loss (menstrual loss, hookworm, haemorrhoids, gastrointestinal cancer), a cereal-based diet high in phytates that binds the iron, malabsorption such as coeliac disease, and the demand of repeated closely spaced pregnancies.
Oral iron: a ferrous sulphate 200 mg tablet contains 65 mg of elemental iron; give it on an empty stomach with a source of vitamin C and never with tea, coffee, milk, antacids or the calcium tablet, all of which cut absorption sharply.
Response is judged by a reticulocyte rise within 5 to 10 days and a haemoglobin rise of about 1 g/dL every 2 to 3 weeks; iron is then continued for a further 3 months after the haemoglobin normalises in order to refill the stores.
Under Anemia Mukt Bharat, pregnant and lactating women take one red IFA tablet containing 60 mg elemental iron with 500 microgram folic acid daily for 180 days in pregnancy and 180 days after delivery, and treatment of established mild or moderate anaemia doubles this to two tablets a day.
Intravenous iron such as iron sucrose or ferric carboxymaltose is used for intolerance, malabsorption, continuing losses that outrun oral iron, or when there is not enough time before delivery or surgery; blood transfusion is not a treatment for uncomplicated iron deficiency and is reserved for haemodynamic compromise or cardiac failure.
In any man, or in a woman past the menopause, iron deficiency means a gastrointestinal source until endoscopy proves otherwise — treating the number without finding the bleed is how a colonic cancer gets missed.

Thalassaemia

Thalassaemia is an inherited quantitative defect of globin chain synthesis — too few alpha chains in alpha-thalassaemia, too few beta chains in beta-thalassaemia — so the unpaired chains precipitate, the red cells are destroyed in the marrow and in the spleen, and the child is left with a severe microcytic anaemia. India carries one of the largest burdens in the world, with a beta-thalassaemia carrier rate of roughly 3 to 4% overall and considerably higher in some communities, which is why carrier screening and prenatal diagnosis are national priorities.

Beta-thalassaemia major presents at 4 to 6 months of age, when the switch from fetal to adult haemoglobin is complete: severe anaemia, failure to thrive, hepatosplenomegaly, and the frontal bossing, maxillary overgrowth and hair-on-end skull of marrow expansion.
Haemoglobin electrophoresis or HPLC is diagnostic — HbF is greatly raised in beta-thalassaemia major, and an HbA2 above 3.5% identifies the beta-thalassaemia trait.
Thalassaemia trait is confused with iron deficiency in every examination: both are microcytic, but in trait the red cell COUNT is normal or high with a disproportionately low MCV and a normal or high ferritin, while iron deficiency has a low red cell count and a low ferritin. The Mentzer index (MCV divided by the red cell count) is under 13 in thalassaemia trait and over 13 in iron deficiency.
Regular transfusion aims to keep the PRE-transfusion haemoglobin at 9 to 10.5 g/dL, usually with leucodepleted packed cells every 2 to 5 weeks; this suppresses the ineffective marrow, prevents the bone deformity and allows normal growth.
Iron overload is the price of transfusion and the usual cause of death from cardiac failure — chelation is started after about 10 to 20 transfusions or when the serum ferritin passes 1000 ng/mL, and is monitored by ferritin together with cardiac and hepatic T2-star MRI.
The three chelators are deferasirox (oral, once daily, monitor creatinine and liver enzymes), deferoxamine (subcutaneous infusion over 8 to 12 hours on 5 to 7 nights a week, monitor hearing and vision) and deferiprone (oral, three times a day, best for cardiac iron but needs a weekly neutrophil count because of agranulocytosis).
Iron supplements are contraindicated in thalassaemia because the patient is iron overloaded and not iron deficient, but folic acid is given because the hyperplastic marrow consumes it.
Haematopoietic stem cell transplantation from a matched sibling is the only established cure and works best when done young, before iron has damaged the organs; splenectomy is now avoided where possible and, when unavoidable, needs pneumococcal, meningococcal and Hib vaccination beforehand and penicillin prophylaxis afterwards.
Prevention is the national strategy: carrier screening of the extended family and of couples before or early in pregnancy, genetic counselling, and prenatal diagnosis by chorionic villus sampling at 10 to 12 weeks when both partners are carriers, since two carriers face a 25% risk in every pregnancy.

Leukaemia — AML, ALL, CML, CLL

Leukaemia is the clonal malignant proliferation of white cell precursors in the bone marrow, which crowds out normal haematopoiesis and produces the triad of anaemia, infection from neutropenia and bleeding from thrombocytopenia. The four classical types are separated by cell line (lymphoid or myeloid) and by speed (acute with blasts, chronic with maturing cells), and the examination almost always tests the single marker that identifies each one.

Acute lymphoblastic leukaemia is the commonest cancer of childhood, peaking at 2 to 5 years: lymphadenopathy, hepatosplenomegaly, and bone pain that makes a child refuse to walk, with 20% or more lymphoblasts in the marrow. It has the best cure rate of the four and needs central nervous system prophylaxis with intrathecal methotrexate because the meninges are a sanctuary site.
Acute myeloid leukaemia is a disease of adults, with Auer rods in the blast cytoplasm and myeloperoxidase positivity; the diagnostic threshold is 20% marrow blasts, except when a defining genetic abnormality such as t(8;21), inv(16) or PML-RARA is present, when the blast count no longer matters.
Acute promyelocytic leukaemia, the M3 subtype, carries t(15;17) with the PML-RARA fusion and presents with disseminated intravascular coagulation and catastrophic bleeding — it is the one leukaemia that is an emergency on day one, and it is treated with all-trans retinoic acid and arsenic trioxide rather than with standard chemotherapy.
Chronic myeloid leukaemia is defined by the Philadelphia chromosome t(9;22) producing the BCR-ABL1 fusion: a very high white count containing the full range of maturing myeloid cells, massive splenomegaly and a low leucocyte alkaline phosphatase; imatinib and the other tyrosine kinase inhibitors have turned it into a chronic disease.
Chronic lymphocytic leukaemia is a disease of people over 60 and is usually found by chance on a blood count: a sustained monoclonal B lymphocytosis, smudge or basket cells on the film, and CD5 with CD19 and CD23 on flow cytometry; early-stage disease is watched rather than treated.
Diagnosis rests on the peripheral smear, bone marrow aspiration and biopsy, flow cytometric immunophenotyping and cytogenetics with molecular studies — it is the immunophenotype and not the microscope that assigns the lineage.
Tumour lysis syndrome follows the first chemotherapy of a bulky fast-dividing leukaemia: a high potassium, high phosphate and high uric acid with a LOW calcium and acute kidney injury. It is prevented with generous intravenous hydration and allopurinol or rasburicase, and the nursing task is strict hourly intake-output measurement with daily electrolytes.
Febrile neutropenia — a single temperature of 38.3 degrees Celsius, or 38.0 degrees sustained for an hour, with an absolute neutrophil count under 500 per cubic millimetre — needs blood cultures and broad-spectrum intravenous antibiotics within one hour, because there are too few neutrophils to make pus and fever may be the only sign of overwhelming infection.

Sickle cell disease

Sickle cell disease is caused by a single point mutation that substitutes valine for glutamic acid at position 6 of the beta globin chain, producing haemoglobin S, which polymerises when deoxygenated and deforms the red cell into a rigid sickle. The sickled cells block small vessels and haemolyse, so the disease is a lifetime of painful vaso-occlusive crises on a background of chronic haemolytic anaemia; in India it is concentrated in the central and western tribal belts, and the National Sickle Cell Anaemia Elimination Mission now screens for it.

Inheritance is autosomal recessive: two carriers have a 25% chance of an affected child in each pregnancy, and the trait protects against falciparum malaria, which is why the gene has persisted in malarial belts.
Symptoms begin after about 6 months of age as HbF falls; diagnosis is by haemoglobin electrophoresis or HPLC showing HbS, and the solubility or sickling test only screens because it cannot separate trait from disease.
The vaso-occlusive crisis is the commonest presentation — severe bone, back, chest or abdominal pain triggered by cold, dehydration, infection, hypoxia, exertion or stress — and it is treated with warmth, generous oral or intravenous fluids and prompt analgesia stepped up to opioids without delay.
Acute chest syndrome, a new pulmonary infiltrate with fever, chest pain, cough or hypoxia, is the leading cause of death: give oxygen, antibiotics that cover atypical organisms, carefully controlled fluids, incentive spirometry and analgesia good enough to allow deep breathing, and arrange exchange transfusion if it is severe.
Other crises are aplastic crisis from parvovirus B19 with a reticulocyte count near zero, splenic sequestration in young children with a rapidly enlarging spleen, falling haemoglobin and shock, and hyperhaemolytic crisis; long-term complications include stroke, avascular necrosis of the femoral head, priapism, leg ulcers, retinopathy, pigment gallstones and renal papillary necrosis.
The spleen infarcts itself by early childhood, so these patients are functionally asplenic and need pneumococcal, Haemophilus influenzae type b, meningococcal and influenza vaccination, with penicillin prophylaxis in childhood.
Hydroxyurea raises HbF and reduces the frequency of crises, acute chest syndrome and transfusion need; folic acid is given for the chronic haemolysis, and transcranial Doppler in children identifies those at stroke risk who need a transfusion programme.
Oxygen is given only when the patient is actually hypoxic, and fluids are run at about 1 to 1.5 times maintenance, because flooding a patient in crisis is itself a cause of acute chest syndrome.

Lymphoma — NHL vs HL

Lymphomas are malignancies of lymphocytes that arise in lymph nodes and lymphoid tissue and present as painless, rubbery, progressive lymphadenopathy. They divide into Hodgkin lymphoma, defined by the Reed-Sternberg cell in a background of reactive inflammatory cells, and the much larger and more varied group of non-Hodgkin lymphomas; the distinction matters because their pattern of spread, their staging, their treatment and their prognosis all differ.

Hodgkin lymphoma has a bimodal age distribution with a peak in the twenties and another after 55, starts in the cervical or supraclavicular nodes, and spreads CONTIGUOUSLY from one nodal group to the next, so it is usually localised when found and is highly curable.
Non-Hodgkin lymphoma is commoner, occurs in older adults, spreads non-contiguously and unpredictably, and involves extranodal sites such as the stomach, bowel, skin, central nervous system and Waldeyer ring as well as the bone marrow far more often, so it is usually advanced at diagnosis.
B symptoms are defined precisely as unexplained fever above 38 degrees Celsius, drenching night sweats and loss of more than 10% of body weight in the preceding 6 months; they add the suffix B to the stage and worsen the prognosis, while pruritus and alcohol-induced nodal pain point to Hodgkin lymphoma.
Diagnosis requires an EXCISION biopsy of a whole node, because the pathologist reads the architecture of the node; fine-needle aspiration is inadequate and this is a favourite examination point.
Staging uses the Ann Arbor system in its Lugano modification: stage I is one nodal region, stage II is two or more regions on the same side of the diaphragm, stage III is regions on both sides and stage IV is diffuse extranodal or marrow disease, with A for no B symptoms, B for their presence and E for localised extranodal extension. PET-CT is the staging tool.
Hodgkin lymphoma is treated with ABVD chemotherapy — doxorubicin, bleomycin, vinblastine and dacarbazine — with or without radiotherapy, while the common B-cell non-Hodgkin lymphomas are treated with R-CHOP, which is rituximab with cyclophosphamide, doxorubicin, vincristine and prednisolone.
The drug toxicities the nurse watches for are pulmonary fibrosis from bleomycin (a dry cough with falling exercise tolerance), cardiomyopathy from doxorubicin (check the ejection fraction before and during treatment), peripheral neuropathy and constipation from vincristine, and haemorrhagic cystitis from cyclophosphamide, which is prevented with hydration and mesna.
Vincristine is fatal if given intrathecally: it is dispensed in a minibag, labelled for intravenous use only, and is never carried to the ward at the same time as an intrathecal drug.
Non-Hodgkin lymphomas with a high proliferation rate such as Burkitt and lymphoblastic lymphoma carry a high risk of tumour lysis syndrome with the first treatment, and a raised LDH is the marker of bulk and turnover.

Hodgkin lymphoma — Reed-Sternberg

Hodgkin lymphoma is a B-cell malignancy in which the tumour cells form only a small minority of the mass and the bulk of the node is made of the reactive lymphocytes, eosinophils and plasma cells that they recruit. Its diagnostic cell is the Reed-Sternberg cell, a large binucleate cell with two mirror-image nuclei each carrying a prominent eosinophilic nucleolus, giving the owl-eye appearance, and finding it in the right background is what makes the diagnosis.

The Reed-Sternberg cell is derived from a germinal-centre B cell, and its immunophenotype is CD15 positive and CD30 positive with CD45 negative and CD20 usually negative — the reverse of a normal B cell, which is CD45 and CD20 positive.
Classical Hodgkin lymphoma has four subtypes: nodular sclerosis is the commonest at about two-thirds of cases and typically affects young women with a mediastinal mass and lacunar cells, mixed cellularity is next and is associated with Epstein-Barr virus and HIV, lymphocyte-rich has the best prognosis and lymphocyte-depleted the worst.
Nodular lymphocyte-predominant Hodgkin lymphoma is a separate entity whose cell is the popcorn or LP cell, which is CD20 and CD45 POSITIVE and CD15 and CD30 negative; it runs an indolent course and can transform into a diffuse large B-cell lymphoma.
Presentation is painless cervical or supraclavicular lymphadenopathy in a young adult with a mediastinal mass on the chest film; B symptoms (fever above 38 degrees Celsius, drenching night sweats and loss of more than 10% of body weight in 6 months), pruritus and pain in the nodes after drinking alcohol are the classic extras.
Pel-Ebstein fever, in which days of fever alternate with days of normal temperature over weeks, is the described but uncommon pattern and is a favourite single-line question.
Staging is by the Ann Arbor system in its Lugano modification using PET-CT, and the diagnosis is made on an excision biopsy of a whole node and never on fine-needle aspiration.
Treatment is ABVD chemotherapy — doxorubicin (adriamycin), bleomycin, vinblastine and dacarbazine — with or without involved-site radiotherapy, and cure rates exceed 80% in early-stage disease.
The late costs of cure shape the nursing conversation: bleomycin lung fibrosis, doxorubicin cardiomyopathy, infertility, hypothyroidism after neck irradiation and second malignancies including breast cancer after chest irradiation, which is why fertility preservation is discussed before the first cycle rather than after treatment.

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