Leukaemia (5-mark answer)

Definition Leukaemia is a group of clonal malignant disorders of haematopoietic stem cells. Neoplastic white cell precursors proliferate in the bone marrow, spill into the peripheral blood, and infiltrate organs such as the spleen, liver, lymph nodes and CNS. Normal marrow output falls as a result.

Classification

	Acute	Chronic
Lymphoid	ALL (mostly children, 2-10 years)	CLL (elderly, over 50)
Myeloid	AML (adults)	CML (30-50 years)

Acute leukaemia has more than 20% blasts in the marrow (WHO). Chronic leukaemia has mature or maturing cells.

Aetiology and risk factors

Ionising radiation, and benzene (benzol) exposure. Park's Textbook of Preventive and Social Medicine, p. 912 notes that leukaemia may appear long after exposure has ceased.
Alkylating agents and topoisomerase II inhibitors.
Down syndrome, Fanconi anaemia, and HTLV-1 (adult T-cell leukaemia).
Genetic lesions, including t(9;22) BCR-ABL (Philadelphia chromosome) in CML, and t(15;17) PML-RARA in acute promyelocytic leukaemia (APL).

Clinical features

Marrow failure:
- Anaemia: pallor, fatigue, dyspnoea.
- Neutropenia: fever and infections.
- Thrombocytopenia: bleeding, purpura, petechiae.
Infiltration:
- Hepatosplenomegaly and lymphadenopathy.
- Bone pain.
- Gum hypertrophy in monocytic AML.
- CNS and testicular involvement in ALL.
Other:
- CML is often asymptomatic or presents with massive splenomegaly.
- CLL is often found incidentally as lymphocytosis.
- APL is associated with DIC.

Investigations

CBC and peripheral smear:
- Anaemia and thrombocytopenia.
- Leucocytosis, or sometimes leucopenia.
- Blasts in acute leukaemia. Auer rods indicate AML.
- CML shows a full spectrum of granulocyte maturation.
- CLL shows smudge cells.
Bone marrow aspiration and biopsy: confirms the diagnosis (blasts above 20%).
Cytochemistry and immunophenotyping (flow cytometry):
- Myeloperoxidase positive in AML.
- TdT positive in ALL.
Cytogenetics and molecular tests: karyotype, FISH, and PCR for BCR-ABL.
Other:
- Lumbar puncture in ALL.
- Uric acid and LDH.
- Coagulation profile (APL).

Management

Supportive care: blood and platelet transfusion, antibiotics, and allopurinol or rasburicase with hydration to prevent tumour lysis syndrome.
ALL: multi-agent chemotherapy in phases (induction, consolidation, maintenance) with CNS prophylaxis.
AML: "7+3" induction (cytarabine plus an anthracycline), then consolidation. Stem cell transplant is used for high-risk disease.
APL: ATRA plus arsenic trioxide.
CML: tyrosine kinase inhibitors (imatinib, dasatinib, nilotinib). Allogeneic transplant is used if the disease progresses or resistance develops.
CLL: observe if asymptomatic. Treat with BTK inhibitors (ibrutinib), venetoclax, or chemoimmunotherapy.

Prognosis

Childhood ALL has a cure rate of about 80-90%.
CML is now a largely chronic, controlled disease.
Adult AML has a poorer outlook, especially in the elderly.

Notes on sources: The library only covered leukaemia incidentally (cause and splenectomy), so the rest of this answer comes from my own knowledge. A search for recent systematic reviews found nothing that changes this standard outline.

For a 5-mark answer, the usual scoring points are the classification table, the clinical features, the blood and marrow findings, and the main treatment. I can also write a full 10-mark note on a specific type, such as ALL, AML, CML or CLL.

Create a comparison table of ALL vs AML vs CML vs CLL

Reading File

Finding Sources

Reading File

Comparison of ALL, AML, CML and CLL

Feature	ALL	AML	CML	CLL
Cell lineage	Lymphoid precursors (B or T lymphoblasts)	Myeloid precursors (myeloblasts)	Myeloid stem cell, with maturing granulocytes	Mature-appearing B lymphocytes
Course	Acute	Acute	Chronic, triphasic (chronic, accelerated, blast crisis)	Chronic, often indolent
Typical age	Peak 2-10 years, second smaller peak in the elderly	Adults, median about 65 years	25-60 years, peak in the 4th-5th decades	Over 50 years, mostly elderly
Marrow or blood picture	Over 20% lymphoblasts	Over 20% myeloblasts	Leucocytosis, often over 100,000/µL, with granulocytes at all stages of maturation, basophilia and thrombocytosis	Sustained lymphocytosis, smudge cells
Characteristic cytogenetics	t(12;21) is favourable. t(9;22) is poor risk. Hyperdiploidy is favourable.	t(8;21) and inv(16) are favourable. t(15;17) defines APL. Complex karyotype is adverse.	t(9;22) BCR-ABL1 (Philadelphia chromosome) in about 95%	del(13q) is favourable. del(17p)/TP53 and del(11q) are adverse. Trisomy 12 is intermediate.
Cytochemistry and markers	TdT+, CD10, CD19, CD20 (B-ALL), CD3 (T-ALL), MPO negative	MPO+, Sudan black+, CD13, CD33, CD117, Auer rods	Low leucocyte alkaline phosphatase (LAP) score	CD5+, CD19+, CD20 (weak), CD23+, sIg (weak)
Main clinical features	Marrow failure, bone pain, lymphadenopathy, hepatosplenomegaly, CNS and testicular involvement, mediastinal mass in T-ALL	Marrow failure, gum hypertrophy and skin infiltration (monocytic types), DIC in APL, moderate splenomegaly	Insidious onset, fatigue, weight loss, massive splenomegaly	Often an incidental finding. Lymphadenopathy, mild splenomegaly, autoimmune haemolytic anaemia or ITP, hypogammaglobulinaemia and infections.
Splenomegaly	Mild to moderate	Mild	Massive	Mild to moderate
Transformation	Not applicable	Not applicable	Blast crisis (myeloid in about 70%, lymphoid in about 30%)	Richter transformation to DLBCL
Treatment	Multi-agent chemotherapy with CNS prophylaxis. Add TKIs for Ph+ ALL. Blinatumomab, inotuzumab and CAR-T for relapse.	"7+3" (cytarabine plus anthracycline), midostaurin (FLT3), allogeneic stem cell transplant. APL is treated with ATRA plus arsenic trioxide.	TKIs (imatinib, dasatinib, nilotinib, bosutinib, ponatinib)	Watch and wait if early and asymptomatic. BTK inhibitors, venetoclax, anti-CD20 antibodies.
Prognosis	Children about 80-90% cure. Adults poorer.	Poor in the elderly. Good in APL.	Near-normal life expectancy with TKIs	Variable. About one third never need treatment.

Mnemonics

ALL: children, TdT+, CNS involvement.
AML: Auer rods, MPO+.
CML: Philadelphia chromosome, massive splenomegaly, low LAP.
CLL: smudge cells, elderly, CD5+/CD23+.

Textbook support

CML is defined by the BCR-ABL fusion gene, present in about 95% of cases as a (9;22) translocation. The peak incidence is in the 4th-5th decades, and the white cell count is often over 100,000/µL. - Robbins & Kumar Basic Pathology
CLL is an accumulation of mature-appearing B lymphocytes. It is often indolent, and as many as one third of patients never need therapy. It is associated with autoimmune cytopenias, herpes zoster and hypogammaglobulinaemia. - Textbook of Family Medicine 9e, p. 1170
p190 BCR-ABL1 is found in about two-thirds of Ph-positive ALL. p210 is the usual form in CML. - Harrison's Principles of Internal Medicine 22E

Cytogenetic risk groups, immunophenotype markers and treatment regimens in the table come from my own knowledge, not the retrieved passages. Check them against your syllabus textbook before an exam.

I can also turn this into a Word or PDF handout, or add the peripheral smear images for each type.

Snake poisoning in tabular format along with treatment

Reading File

Finding Sources

Searching PubMed

"snake bites"[MeSH Terms] AND "antivenoms"[MeSH Terms]

Reading File

Snake poisoning (envenomation): tabular summary with treatment

1. Venom types and clinical features

Feature	Neurotoxic (Elapids)	Haemotoxic / Vasculotoxic (Vipers)	Myotoxic (Sea snakes)
Snakes	Cobra, common krait	Russell's viper, saw-scaled viper (Echis), hump-nosed viper	Enhydrina and other sea snakes
Main venom action	Blocks the neuromuscular junction (post-synaptic in cobra, pre-synaptic in krait)	Procoagulants cause consumptive coagulopathy (defibrination). Haemorrhagins damage vessel walls. Direct cytotoxicity.	Rhabdomyolysis
Local signs	Cobra: pain, swelling and necrosis. Krait: little or no local swelling or pain.	Severe pain, swelling, blistering, bleeding from the bite site, necrosis, compartment syndrome	Little or no local reaction
Systemic features	Ptosis (earliest), then ophthalmoplegia, bulbar palsy, limb weakness, respiratory paralysis. Drowsiness, salivation, vomiting.	Incoagulable blood, gum, nose and GI bleeding, haematuria, shock, acute kidney injury (especially Russell's viper), intracranial haemorrhage	Muscle pain, stiffness, trismus, myoglobinuria, hyperkalaemia, flaccid paralysis, renal failure
Time of onset	Cobra: local signs in 6-8 minutes, systemic in about 30 minutes. Paralysis is complete in about 2 hours.	Pain within about 8 minutes. Bleeding over hours.	0.5-1 hour
Cause of death	Respiratory failure	Shock, haemorrhage, renal failure	Respiratory or cardiac arrest, hyperkalaemia
Key test	Single breath count, ability to lift the head	20-minute whole blood clotting test (20WBCT): unclotted blood means viper envenomation	CK, K+, urine myoglobin

Source for clinical features: The Essentials of Forensic Medicine and Toxicology, 36th ed., pp. 564-566.

2. Treatment (stepwise)

Step	Management
First aid (at the scene)	Reassure the patient, keep the bitten limb still and below heart level, and remove rings and tight items. Apply a pressure immobilisation bandage for neurotoxic bites (elapids, sea snakes). Transport rapidly to hospital. Do not cut, suck, apply a tourniquet, apply ice or give herbal remedies.
Hospital assessment	Check airway, breathing and circulation, and mark the extent of swelling. Do the 20WBCT, CBC, PT/INR, creatinine, electrolytes, CK, urinalysis and ECG. Give tetanus toxoid. Observe for 24 hours. A patient with mild local swelling and no systemic signs can be observed for 24 hours, given tetanus toxoid and discharged.
Indications for ASV	Systemic envenomation: neurotoxic signs, coagulopathy (unclotted 20WBCT or spontaneous bleeding), cardiovascular abnormalities, or rapidly progressive local swelling. For local swelling, ASV is indicated if swelling involves at least half of the bitten limb or crosses a joint within 1-2 hours.
Antisnake venom (polyvalent)	Raised in horses against cobra, common krait, Russell's viper and saw-scaled viper. ASV works best within 4 hours of the bite, has less value if delayed to 8 hours, and is of doubtful value after 24 hours. No test dose, because it is a poor predictor of anaphylactoid reactions.
ASV dose (textbook)	Minimal symptoms: 5 vials. Moderate: 10 vials. Severe: 10-15 vials. The dose is the same for children. Dilute in 500 mL of saline or distilled water and infuse over 1 hour.
Repeat dosing	Neurotoxic: a second dose of 10 vials after 1 hour if there is no improvement. Haemotoxic: repeat the 20WBCT every 6 hours and repeat ASV if blood is still unclotted. Normal clotting is the end point. Then test every 12 hours for at least 48 hours to detect recurrent envenomation.
Neurotoxic support	Neostigmine with atropine (trial for reversal). Airway protection, intubation and mechanical ventilation if the patient cannot lift the head or has respiratory failure.
Haemotoxic support	Fresh frozen plasma, cryoprecipitate or platelets only after ASV, if bleeding persists. Avoid IM injections. Fluids for shock. Dialysis for renal failure. Fasciotomy only if compartment syndrome is proven.
Myotoxic (sea snake)	Sea snake antivenom. Treat hyperkalaemia, give fluids and alkalinise the urine for myoglobinuria.
Wound care	Clean the wound, give tetanus prophylaxis, elevate the limb, and give antibiotics only if there are signs of infection or necrosis. Debride necrotic tissue later.

3. Management of ASV reaction

Step	Action
1	At the first sign of urticaria, itching, chills, vomiting, hypotension, bronchospasm or angioedema, stop the ASV infusion.
2	Give adrenaline 0.5 mg of 1:1000 IM (adult) or 0.01 mg/kg (child). Repeat after 10-15 minutes if there is no improvement.
3	Give an antihistamine and hydrocortisone for longer protection.
4	Restart ASV slowly once the patient is stable.

4. Complications and monitoring

Complications: AKI, secondary infection, tissue necrosis, compartment syndrome, hypopituitarism (late, after Russell's viper), respiratory failure.
Monitoring: vital signs, urine output, neurological signs, repeat 20WBCT, creatinine and potassium.

Notes on sources and recent evidence

The ASV doses above are from the forensic medicine textbook. Current Indian national snakebite guidelines (my knowledge, not retrieved here) use a different regimen. They recommend an initial dose of 10 vials for any systemic envenomation, then repeat doses (also 10 vials) based on the 20WBCT or clinical progress. Neostigmine is given as a test dose of 0.5 mg with atropine. Check the local protocol before using any dose clinically.
Recent systematic reviews do not overturn this approach. Two reviews are a 2024 meta-analysis of Indian polyvalent antivenom (PMID 38153416) and a 2025 review of antimicrobial prophylaxis in snakebite (PMID 41287797). I only read their titles, not the full text.
Venom composition and ASV supply vary by region, so use the polyvalent product available locally.

I can also build a one-page exam revision chart or a flowchart for ASV decision-making.

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