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Leukemia Case > questions > Flashcards

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1
Q

What is mucositis in neutropenic patients?

A

Chemotherapy-induced damage to mucosal barrier causing ulceration and inflammation.

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2
Q

How does mucositis present clinically?

A

Pain, swelling, difficulty eating, swallowing, diarrhoea, changes in mucus production.

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3
Q

What are the additional risks of infection in neutropenic patients with mucositis?

A

Increased morbidity, complications, especially infections due to gut translocation.

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4
Q

Explain the role of adaptive immunity in neutropenic patients.

A

Acts as the third line of defense involving both humoral and cellular mechanisms.

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5
Q

What factors determine infections in immunocompromised hosts?

A

Type of immune deficit, severity, and duration of immune defect.

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6
Q

List examples of immunocompromised hosts.

A

Extremes of ages, pregnant women, patients on immunosuppressive therapy, HIV/AIDS patients, stem cell transplant recipients.

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7
Q

How does immunosuppression affect infection risk?

A

Increases susceptibility to severe, rapidly developing infections, reactivation of latent infections, and opportunistic pathogen infections.

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8
Q

Define virulence and primary pathogen.

A

Virulence is microorganism’s disease-causing ability, primary pathogen causes disease regardless of host’s immune system.

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9
Q

What is an opportunistic pathogen? Give examples.

A

Organism causing disease when host’s defenses are compromised. Examples include Pseudomonas, Mycobacteria, Herpes viruses.

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10
Q

Describe the characteristics of Pseudomonas aeruginosa infections.

A

Nosocomial, severe, life-threatening infections, especially in neutropenic patients with persistence in hospital environments.

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11
Q

Explain the significance of Mycobacteria in immunocompromised hosts.

A

Mycobacteria like M. tuberculosis can cause latent or reactivated disease, especially in those with reduced immunity.

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12
Q

What are the key points about Aspergillus infections?

A

Opportunistic fungal disease from inhalation with a risk of pneumonia, especially in immunocompromised individuals.

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13
Q

Discuss the impact of immunosuppression on herpes viruses.

A

Immunosuppression can lead to reactivation or acquisition of latent herpes virus infections.

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14
Q

What is Pneumocystis jirovecii, and how is it transmitted?

A

It’s an airborne fungus with a poorly understood life cycle transmitted through exposure to infected individuals.

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15
Q

Define necessary and sufficient causes in disease.

A

A necessary cause is required for a disease to occur; a sufficient cause alone can cause disease.

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16
Q

Explain why most causes of non-communicable diseases are not necessary causes.

A

Non-communicable diseases often have multiple component causes that together are sufficient for the disease.

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17
Q

List some factors at multiple levels that can be causes of certain effects.

A

Racism, genetic factors, violence, sex, social factors, and more are cited as influencing factors.

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18
Q

Discuss the concept of evidence-based practice regarding pertussis vaccine and brain damage.

A

Evidence-based practice involves accessing and appraising the evidence, then applying it to the patient’s case.

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19
Q

What are some key factors to consider in causal interference?

A

One must question if an association is real and critically appraise study methods before results.

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20
Q

Explain the importance of bias and confounding in research studies.

A

Bias and confounding can skew results through selection bias, measurement bias, and unadjusted significant differences.

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21
Q

Why is sample size important in research studies?

A

Sample size affects the ability to detect real associations and evaluate statistical significance.

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22
Q

Discuss the Bradford Hill causal association criteria and its relevance in epidemiology.

A

The criteria include temporality, strength of effect, dose-response effect, biological plausibility, and consistency.

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23
Q

Why is temporality considered an absolute requirement in causal inference?

A

Temporality ensures that the cause precedes the effect, essential for establishing causality.

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24
Q

What are some key considerations in making clinical judgments based on evidence?

A

Factors include the best evidence available, disease epidemiology, and patient applicability and acceptance.

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25
Q

Define ‘evidence’ in the context of epidemiology and research.

A

Evidence refers to the best available data used to make informed clinical decisions.

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26
Q

What is the strong association of nodal enlargement with in endemic Burkitt lymphoma?

A

Strong association with EBV infection.

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27
Q

Describe the common sites of intestinal involvement in sporadic/non-endemic Burkitt lymphoma.

A

Most common in the ileum with mesenteric nodes.

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28
Q

What is the histological characteristic of Burkitt lymphoma with respect to cellular infiltration?

A

Diffuse infiltration of monomorphic, medium-sized cells.

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29
Q

Explain the ‘starry sky’ pattern seen in Burkitt lymphoma histology.

A

‘Stars’ are tingible body macrophages taking up apoptotic tumor cells.

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30
Q

What is the significance of a positive EBV stain (EBER) in Burkitt lymphoma?

A

Positive in endemic African cases and immunodeficiency cases.

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31
Q

What is the characteristic feature of Anaplastic large cell lymphoma histology?

A

Large lymphoid cells with abundant amphophilic cytoplasm.

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32
Q

Explain the presence of ALK gene translocation in Anaplastic large cell lymphoma.

A

Lymphoma cells exhibit ALK gene translocation and expression of ALK protein.

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33
Q

Define Mycosis fungoides and Sezary syndrome in terms of presentation.

A

These are cutaneous lymphomas presenting on the skin.

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34
Q

What is the role of the spleen as a lymphoid organ?

A

Function as a lymphoid organ (white pulp).

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35
Q

Explain the function of the spleen in phagocytosing particulate matter and culling red cells.

A

Capacity for phagocytosing particulate matter and culling senescent red cells.

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36
Q

Describe the circulation pathways within the spleen.

A

Closed circulation via splenic artery and vein, open circulation through cords of Billroth.

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37
Q

What are the clinical implications of primary hypersplenism?

A

Marked massive splenomegaly and pancytopenia, usually requiring splenectomy.

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38
Q

Explain the term ‘hypersplenism’ and its association with pancytopenia.

A

Association between peripheral blood pancytopenia and splenic enlargement.

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39
Q

How is splenomegaly classified in terms of enlargement?

A

Grossly enlarged, moderately enlarged, mildly enlarged.

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40
Q

What are the causes of congestive splenomegaly?

A

Causes include chronic myeloid leukemia, myelofibrosis, amyloidosis, infections, autoimmune diseases.

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41
Q

Describe the characteristics of spleen in congestive splenomegaly.

A

Variably enlarged, thickened and fibrotic capsule, beefy-red color with firm brown nodules.

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42
Q

How is congenital asplenia or polysplenia characterized?

A

May present with accessory spleens or absence/multiple additional spleens.

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43
Q

Explain the relationship between splenic congestion and systemic infections.

A

Systemic infections cause moderate splenomegaly characterized by congestion.

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44
Q

What are the metabolic abnormalities required for Howard’s definition of Laboratory TLS?

A

Hyperkalaemia, hyperuricaemia, hyperphosphataemia, hypocalcaemia

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45
Q

What defines the Modified Howard definition of Clinical TLS?

A

Same as laboratory TLS with elevated creatinine level, seizures, cardiac dysrhythmia, or death

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46
Q

How does cancer cell lysis lead to metabolic abnormalities in TLS?

A

Cells release potassium, phosphorus, uric acid overflow in blood

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47
Q

What can hyperuricaemia induce in TLS?

A

Acute kidney injury by crystallization and pro-inflammatory effects

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48
Q

Why is hyperkalaemia in TLS particularly dangerous?

A

It may cause serious and sometimes fatal cardiac dysrhythmias

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49
Q

How can hyperphosphataemia affect the body in TLS?

A

Can cause secondary hypocalcaemia, calcification in kidney and soft tissues

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50
Q

What complications can arise due to hypocalcaemia in TLS?

A

Neuromuscular irritability (tetany), dysrhythmia, seizures

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51
Q

What is a way to prevent TLS during treatment?

A

Adequate IV hydration to maintain high urine output

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52
Q

Which medications can be used to reduce uric acid load prophylactically in TLS?

A

Allopurinol, Rasburicase (recombinant urate oxidase)

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53
Q

What is the recommended course of treatment for TLS?

A

Watch renal function, hydration, uric acid reduction, electrolyte correction

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54
Q

What is the characteristic feature of gout in clinical presentation?

A

Acute painful arthritis in a single joint

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55
Q

What are gouty tophi and how do they impact the body?

A

Depositions of urate crystals causing local destruction, lack of function

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56
Q

How is gout diagnosed?

A

Clinical features, uric acid crystals in joint fluid, elevated serum uric acid levels

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57
Q

What is the treatment for gout?

A

Colchicine for pain, Allopurinol to reduce uric acid, Uricosurics

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58
Q

What is Multiple Myeloma characterized by?

A

Malignant proliferation of plasma cells in bone marrow

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59
Q

Which immunoglobulins do plasma cells produce in Multiple Myeloma?

A

Pairs of identical heavy and light chains; IgG, IgA, IgM, IgD, IgE

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60
Q

What is the significance of the extremely variable N-terminal end of each antibody?

A

Allows for millions of antibodies with different antigen binding sites.

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61
Q

Define polyclonal antibodies in the context of antibodies production.

A

Antibodies from different ‘clones’ of plasma cells, each with unique binding sites.

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62
Q

What does MM stand for in the context of antibody production?

A

Multiple Myeloma.

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63
Q

Explain the process leading to the production of a monoclonal antibody in Multiple Myeloma.

A

Uncontrolled proliferation leads to over-production of a single antibody.

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64
Q

What are some clinical presentations of Multiple Myeloma?

A

Includes bone pain, fatigue, pathological fractures, weight loss, and more.

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65
Q

What are the diagnostic criteria for Multiple Myeloma?

A

Clonal bone marrow plasma cells >10% or presence of CRAB or MDE features.

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66
Q

How are plasma proteins separated in protein electrophoresis?

A

Proteins move based on charge towards anode or cathode in a buffer.

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67
Q

What can be determined by visually inspecting proteins separated by electrophoresis?

A

Concentrations and relative increases or decreases of proteins.

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68
Q

What lab features are associated with Multiple Myeloma?

A

Increased total protein, monoclonal antibodies, immunoparesis, and Bence Jones proteinuria.

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69
Q

List the human herpes viruses discussed in the notes.

A

Herpes simplex 1 & 2, Varicella-Zoster, Epstein Barr Virus, Human Cytomegalovirus, HHV 6 & 7, HHV 8.

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70
Q

Explain the characteristics of successful human parasites according to the notes.

A

High prevalence, minimal clinical disease, milder disease with early life infection.

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71
Q

Describe the virology of human herpes viruses discussed in the notes.

A

dsDNA, large, enveloped, complex genome, primary infection leads to latency and reactivation.

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72
Q

What are the characteristics of Herpes Simplex 1 and 2 infections?

A

Cause painful blisters at site of inoculation, can infect oral or genital sites.

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73
Q

Define Monoclonal Gammopathy of Undetermined Significance (MGUS).

A

Low level paraprotein (<30g/L), asymptomatic patient, without diagnostic features of plasma cell myeloma.

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74
Q

What is the progression rate of MGUS to overt disease per year?

A

1% per year.

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75
Q

List the CRAB criteria used for diagnosing symptomatic plasma cell myeloma.

A

Hypercalcaemia, Renal insufficiency, Anaemia, Bone lesions.

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76
Q

Explain the bone disease in plasma cell myeloma.

A

Osteoclast activation results in lytic lesions, osteoblast inhibition leads to bone resorption.

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77
Q

What are the common clinical problems associated with plasma cell myeloma?

A

Recurrent infections, abnormal antibody production, neutropenia, bleeding, amyloidosis, hyperviscosity.

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78
Q

How is plasma cell myeloma diagnosed?

A

M protein (>30g/L in serum), clonal plasma cells in BM, end organ damage, genetic changes.

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79
Q

Outline the management strategies for plasma cell myeloma.

A

Pain control, renal impairment management, hypercalcaemia treatment, bone disease care, anaemia treatment, infection control.

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80
Q

What are the specific aims of plasma cell myeloma management?

A

Control disease, improve quality of life, prolong survival.

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81
Q

Describe the management approach for patients eligible for stem cell transplant (SCT).

A

Combination chemotherapy cycles, stem cell collection, autograft; allograft has cure potential but high mortality risk.

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82
Q

What are the characteristics of aggressive B cell lymphomas?

A

Rapid progression, nodal/extra-nodal disease, risk of tumour lysis syndrome.

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83
Q

What are the common extranodal sites affected by aggressive B cell lymphomas?

A

Gastrointestinal tract (GIT), skin, CNS, other areas.

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84
Q

Describe the staging system utilized for Burkitt lymphoma.

A

Anne Arbour system.

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85
Q

What are common clinical presentations of T cell lymphoproliferative disorders?

A

Skin lesions (prominent pruritis), lymphadenopathy, hepatosplenomegaly, effusions, constitutional symptoms, bone lesions, and hypercalcaemia.

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86
Q

How is Chronic Myeloid Leukemia (CML) characterized at a genetic level?

A

Characterized by t(9:22), resulting in the BCR-ABL1 fusion gene on chromosome 22.

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87
Q

What are the symptoms associated with the cytokine clustering in myeloproliferative neoplasms?

A

Constitutional symptoms and fatigue.

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88
Q

What are the symptoms associated with hyperviscosity clustering in myeloproliferative neoplasms?

A

Headache, hypertension, visual disturbance, tinnitus, gout, vertigo, plethora, peripheral neuropathy.

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89
Q

What are the symptoms associated with splenomegaly clustering in myeloproliferative neoplasms?

A

Abdominal discomfort, early satiety.

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90
Q

What is the significance of JAK2 V617F mutation in myeloproliferative neoplasms?

A

Increases the risk of thrombosis.

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91
Q

How can Chronic Myeloid Leukemia (CML) be diagnosed?

A

Triade of splenomegaly, Philadelphia Chromosome BCR-ABL1, and ↑ granulocytes in peripheral blood and bone marrow.

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92
Q

What are the common morphological findings in the peripheral blood in Chronic Myeloid Leukemia (CML)?

A

Raised WCC, usually > 50 x 109/L, neutrophil predominance, basophilia, eosinophilia, normocytic normochromic anemia.

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93
Q

Describe the phases of Chronic Myeloid Leukaemia (CML).

A

Initial chronic stable phase, chronic phase with high-risk features, blast phase.

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94
Q

What are the defining features of the initial chronic stable phase in CML?

A

Granulocytic population expansion, retains ability to differentiate, <10% blasts, basophils <20%.

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95
Q

What differentiates the chronic phase with high-risk features in CML?

A

Increasing blast count 10-19%, basophil count ≥20%, platelet count extremes, spleen enlargement, additional cytogenetic abnormalities.

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96
Q

How does tyrosine kinase inhibitors (TKIs) prevent progression in CML?

A

Displace ATP from BCR ABL1 kinase pocket. Imatinib is first line in stable phase.

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97
Q

What molecular testing is used in CML to monitor treatment efficacy?

A

Quantitative PCR for BCR ABL1 on peripheral blood.

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98
Q

Name the three types of Philadelphia-negative MPN disorders.

A

Essential Thrombocythaemia (ET), Polycythaemia Vera (PV), Primary Myelofibrosis (PMF).

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99
Q

What are the main causes of morbidity and mortality in Philadelphia-negative MPNs?

A

Arterial and venous thrombosis.

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100
Q

What is the key characteristic of Essential Thrombocythaemia (ET) on a molecular level?

A

Clonal haematopoietic stem cell disorder with active Jak-Stat signalling.

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101
Q

How is clonality assessed in Essential Thrombocythaemia?

A

Via mutation analysis: JAK2 V617F, CALR, MPL mutations or triple negative status.

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102
Q

What is the main pathological finding in Polycythaemia Vera (PV)?

A

Increase in red blood cell production independent of regulatory mechanisms.

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103
Q

What are the serum markers used to diagnose Polycythaemia Vera (PV)?

A

Elevated hemoglobin or hematocrit, often with increased white cell and platelet counts.

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104
Q

In ET, how is thrombosis managed based on platelet count?

A

Low dose aspirin unless count >1500 x 10^9/L or actively bleeding.

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105
Q

Why does EBV transform naive B cells during primary infection?

A

To evade immune recognition and persist since naive B cells are not normally long-lived.

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106
Q

Which latency gene of EBV is expressed after the specific immune response develops during primary infection?

A

EBNA 1 is expressed as the other 9 latency genes are driven down.

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107
Q

What percentage of B cells in a healthy seropositive person are infected with EBV?

A

Approximately 1 in 10,000 B cells in a healthy seropositive person are infected.

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108
Q

What is the treatment approach for EBV-associated diseases?

A

Reduction in immunosuppression, rituximab (CD20 monoclonal antibody), and no benefit from antivirals.

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109
Q

What are the key oncogenes associated with EBV lymphoproliferative diseases?

A

LMP-1 and LMP-2A are key oncogenes associated with EBV lymphoproliferative diseases.

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110
Q

What is the primary disease associated with HHV6 in babies?

A

Primary infection in babies presents as roseola Infantum with febrile illness, rash, and febrile convulsions.

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111
Q

What percentage of humans have germline HHV6 with high blood viral load and DNA in all body cells?

A

About 0.8-1.5% of humans have germline HHV6 with high blood viral load and DNA in all body cells.

112
Q

What are the possible ways HHV8 can be transmitted?

A

High prevalence: mother to child, close contact in families. Low prevalence: sexual transmission in adulthood.

113
Q

Which diseases are associated with HHV8 due to poor immune control of virus-infected cells?

A

Kaposi sarcoma, Multicentric Castleman’s disease, Primary effusion lymphoma, Plasmablastic lymphoma.

114
Q

What are the key diseases caused by HHV8 with oncogenes derived from altered cellular genes?

A

Diseases include Kaposi sarcoma, Multicentric Castleman’s disease, Primary effusion lymphoma, Plasmablastic lymphoma.

115
Q

What is the main route of excretion for uric acid?

A

Mainly excreted by the kidney (75%) and rest via the intestine.

116
Q

Why do humans have higher blood uric acid levels compared to other animals?

A

Humans lack uricase which degrades uric acid to non-toxic allantoin.

117
Q

Explain the uric acid paradox in humans.

A

Humans evolved strategies to retain uric acid due to its antioxidant and immune enhancing properties.

118
Q

What base pairs with thymine in DNA?

A

Adenine (A) pairs with thymine (T) in DNA.

119
Q

What are the characteristics of purine nucleotides metabolism?

A

Managed by de novo synthesis, catabolism, salvage, and eventually degradation to uric acid.

120
Q

What are the causes of hyperuricaemia related to overproduction?

A

Include malignancy, myeloproliferative disorders, and increased de novo synthesis.

121
Q

How is Tumour Lysis Syndrome characterized?

A

Characterized by hyperkalaemia, hyperuricaemia, hyperphosphataemia, and hypocalcaemia.

122
Q

What are common tumours associated with Tumour Lysis Syndrome?

A

Hematological malignancies such as ALL, AML, and NHL.

123
Q

When can Tumour Lysis Syndrome occur?

A

Usually 48-72 hours after the start of chemotherapy, radiotherapy, or steroid treatment.

124
Q

Why is Tumour Lysis Syndrome considered a life-threatening emergency?

A

Due to high morbidity and risk of mortality associated with metabolic complications.

125
Q

What is the gold standard for detecting HSV in cerebrospinal fluid?

A

PCR

126
Q

What is the primary cause of chickenpox in children?

A

Varicella

127
Q

What is the main reason for the adult manifestation of chickenpox known as shingles?

A

Latency in ganglia

128
Q

How is EBV primarily transmitted in adults?

A

Saliva

129
Q

What is the % of lymphocytes in adults with infectious mononucleosis?

A

90-100%

130
Q

What is the gold standard for diagnosing CMV in immunocompromised individuals?

A

PCR

131
Q

What is the typical presentation of CMV in adult patients?

A

IM-like illness, fever, sore throat, lymphadenopathy

132
Q

How is HHV8 mainly transmitted?

A

Early life - cell transform, proliferation, angiogenesis

133
Q

What is the characteristic feature of the transmission of HHV8 in adults?

A

Sexual transmission less common

134
Q

What is the primary defense mechanism in the body that prevents entry of pathogens?

A

Physical and biochemical barriers

135
Q

What type of response does adaptive immunity provide against pathogens?

A

Specific response to particular pathogen with memory

136
Q

What component of innate immunity is responsible for damaging the cell walls of Gram+ bacteria?

A

Lysozyme in tears, nasal secretions

137
Q

What is the mechanism through which neutrophils kill bacteria?

A

Phagocytosis and killing bacteria

138
Q

What are the cells responsible for phagocytosis in innate immunity?

A

Neutrophils and macrophages

139
Q

What is the primary risk associated with neutropenia?

A

Increased risk of infection, dissemination, severe sepsis

140
Q

Which bacteria is commonly associated with infections in neutropenic patients?

A

Pseudomonas aeruginosa

141
Q

Name a gram-positive cocci commonly causing infection in neutropenic patients.

A

Viridans Streptococci

142
Q

What are some fungi species that can cause infections in immunocompromised individuals?

A

Candida albicans and Aspergillus fumigatus

143
Q

Which virus is associated with infections in HIV/AIDS patients?

A

Herpes simplex

144
Q

What pathogen causes diseases normally controlled by T cell immunity in immunocompromised individuals?

A

Mycobacterium tuberculosis

145
Q

How does diabetes mellitus affect neutrophils’ immune response?

A

Decreases chemotaxis, adherence, phagocytosis, opsonisation, increases apoptosis.

146
Q

What vascular complication in diabetes promotes anaerobic organism growth?

A

Local tissue ischaemia

147
Q

Which organisms commonly colonize the skin and mucosa of diabetics?

A

S. aureus and Candida species

148
Q

What increases adhesion of Candida to epithelium in diabetics?

A

High glucose levels

149
Q

What is the epidemiological definition of a determinant?

A

Any factor that brings about change in a health condition.

150
Q

Define a necessary cause in epidemiology.

A

A factor that must be present before a disease occurs.

151
Q

What are component causes in epidemiology?

A

Individual factors working with necessary causes to produce disease.

152
Q

Explain a sufficient cause in epidemiology.

A

A combination of factors sufficient to produce disease in some cases.

153
Q

What are the common sites of involvement for mature lymphoid neoplasms?

A

Lymph nodes, organs, skin, other soft tissue, and bone.

154
Q

What are the two primary growth patterns of mature lymphoid neoplasms?

A

Lymphomatous (growing in tissues) and leukaemic/lymphoproliferative (circulating in blood).

155
Q

Which are the key types of mature lymphoid neoplasms with leukaemic tendencies mentioned?

A

Chronic Lymphocytic Leukaemia (CLL), Follicular Lymphoma, Diffuse Large B-cell Lymphoma (DLBCL), Mantle Cell Lymphoma, Splenic Marginal Zone Lymphoma.

156
Q

What are some of the basic lab tests mentioned for investigating mature lymphoid neoplasms?

A

Complete Blood Count (CBC), white cell differential count, blood film, ESR, LDH, CMP, uric acid, liver function, renal function, HIV testing.

157
Q

What are the possible causes of lymphocytosis mentioned in the course notes?

A

Infection (viral, certain bacteria), stress, smoking, drug allergies, post-splenectomy changes, endocrine disorders, lymphoid neoplasms.

158
Q

What are some special investigations used in the diagnosis of lymphoid neoplasms?

A

Biopsy/histology, bone marrow biopsy, flow cytometry, immunohistochemistry, cytogenetics.

159
Q

What are the presenting symptoms of Chronic Lymphocytic Leukaemia (CLL) as per the course notes?

A

Fatigue, infections, autoimmune conditions like AIHA, ITP, cytopenias, lymphocytosis, organ involvement.

160
Q

What are some adverse prognostic factors mentioned in the course notes for CLL?

A

Unmutated biological factors, ZAP-70 and CD38 expression, cytogenetic abnormalities like del11q, del17p, etc.

161
Q

What are some indications for treatment of CLL according to the course notes?

A

Constitutional symptoms, bone marrow failure, AIHA/ITP not responsive to steroids, progressive lymphadenopathy, splenomegaly.

162
Q

What are the possible management options for CLL discussed in the course notes?

A

Observation, palliation with alkylator e.g., chlorambucil, aggressive combination chemotherapy, new biological treatments.

163
Q

Describe the histological spectrum of early stage Kaposi’s sarcoma.

A

Florid reactive hyperplasia with invagination of mantle zone lymphocytes, follicular lysis, moth-eaten appearance.

164
Q

What are the histopathological findings in late-stage HIV lymphadenitis?

A

Lymphocyte depletion, fibrosis, vascular proliferation; not specific but often characteristic.

165
Q

Which viral capsid is shown on staining with p24 antigen in HIV lymphadenitis?

A

Viral capsid of HIV.

166
Q

What occurs in the later stages of HIV lymphadenitis?

A

Profound loss of B-cells in germinal centers, depletion of T-cells, presence of other opportunistic infections/malignancies.

167
Q

List neoplastic causes of lymphadenopathy.

A

Primary neoplasms (Hodgkin lymphoma, Non-Hodgkin lymphoma), Secondary neoplasms (Metastases).

168
Q

What is the distinguishing feature of Hodgkin Lymphoma?

A

Presence of large neoplastic Reed-Sternberg cells in a background of reactive cells.

169
Q

Differentiate between Nodular lymphocyte predominant HL and Classical HL.

A

NLPHL: B-cell neoplasm, good prognosis; Classical HL: Large Reed-Sternberg cells, reactive cell background.

170
Q

Identify the variants of Classical Hodgkin lymphoma based on histology.

A

Nodular lymphocyte predominant, Lymphocyte rich, Nodular sclerosis, Mixed cellularity.

171
Q

What determines blood viscosity?

A

Blood viscosity is determined by water content, protein, and blood cells.

172
Q

What can cause hyperviscosity?

A

Hyperviscosity can be caused by decreased water content, increased protein (e.g., paraprotein), and an increase in blood cells (WBC, RBC, platelets).

173
Q

What classification criteria are used for acute leukemia?

A

Acute leukemia classification is based on morphology and staining, immunophenotyping, cytogenetics, and molecular genetics.

174
Q

What is the aim of acute leukemia treatment?

A

The aim of treatment is to destroy the leukemic clone without harming the residual stem cell compartment.

175
Q

What supportive care is provided in leukemia management?

A

Supportive care includes transfusions, treating infections aggressively, and managing metabolic complications.

176
Q

What is neutropenic fever?

A

Neutropenic fever is a serious complication of chemotherapy characterized by fever and low neutrophil count.

177
Q

How should neutropenic fever be managed?

A

Management includes taking cultures, starting broad-spectrum antibiotics promptly, and avoiding rectal examination in neutropenic patients.

178
Q

What is the prognosis of acute leukemia without treatment?

A

Without treatment, acute leukemia has a median survival of around 5 weeks.

179
Q

What factors contribute to the etiology of hematological malignancies?

A

Factors include genetic and environmental influences with some cases linked to inherited factors and environmental exposures.

180
Q

How do hematopoietic growth factors regulate cell differentiation?

A

Hematopoietic growth factors interact at different levels in the marrow, regulating proliferation and differentiation of progenitors.

181
Q

What are the main stages of the interphase in the cell cycle?

A

The interphase consists of G1 phase, S phase (DNA replication), and G2 phase (organelle duplication).

182
Q

What are the functions of cell cycle checkpoints?

A

Checkpoints control cell cycle, coordinate divisions, and check the integrity of DNA for repair before proceeding.

183
Q

What is the commonest viral cause of congenital abnormalities?

A

Cytomegalovirus (CMV)

184
Q

What are the delayed onset symptoms of congenital CMV infection?

A

Mental retardation and deafness

185
Q

What is the main clinical feature of CMV disease in immunosuppressed patients?

A

Persistent virus controlled by cell mediated immunity

186
Q

Which organs can be affected by end organ disease in CMV infection?

A

Lung, eye, GIT, and brain

187
Q

What is the significance of IgG in CMV serology?

A

Indicates past exposure

188
Q

What is the drug of choice for life-threatening CMV infection?

A

Ganciclovir/valganciclovir (GCV)

189
Q

How do Foscarnet and cidofovir compare to Ganciclovir in treating CMV?

A

They have modest anti-CMV activity and significant toxicity

190
Q

What is the transmission route for Epstein Barr Virus (EBV)?

A

Saliva, kissing

191
Q

What antibodies are detected in the Monospot test for EBV?

A

Antibodies that bind and agglutinate sheep RBCs

192
Q

What viral component do patients make antibodies to during primary EBV infection?

A

Viral capsid antigen (VCA)

193
Q

What test results confirm acute infectious mononucleosis?

A

Positive VCA IgM and IgG; negative EBNA IgG

194
Q

What percentage of adults have antibodies to HSV1/2?

A

Almost 100% of adults.

195
Q

What percentage of children have antibodies to HSV1/2?

A

20-40% of children.

196
Q

Where does HSV establish latent infection in the host?

A

In sensory ganglion cells.

197
Q

Which nerve innervates the skin for orofacial herpes?

A

Trigeminal ganglion.

198
Q

Which nerve innervates the skin for genital herpes?

A

Sacral ganglia.

199
Q

What triggers can cause reactivation of HSV1 and 2 from latent state?

A

Sunlight, stress, febrile illness, menstruation, immuno-suppression.

200
Q

What is the characteristic appearance of dendritic ulcers in corneal HSV infection?

A

Branching appearance.

201
Q

What can cause aseptic meningitis during primary genital herpes infection?

A

HSV2.

202
Q

In what part of the body does HSV switch to a lytic cycle during reactivation?

A

In the cell body of the neuron.

203
Q

Where do the virus particles travel during reactivation of HSV?

A

Down the axon to reinfect the skin or mucous membrane at the original site.

204
Q

What are some triggers that can cause recurrent reactivation of HSV?

A

Sunlight, stress, febrile illness, menstruation, immuno-suppression.

205
Q

What is a rare life-threatening complication of HSV infection in neonates?

A

Neonatal HSV.

206
Q

What is the gold standard for diagnosing lymphadenopathy?

A

Excision of lymph node

207
Q

What type of response is associated with Paracortical Lymphoid Hyperplasia?

A

Predominantly T-cell response

208
Q

What is a common cause of granulomatous lymphadenitis?

A

TB and atypical mycobacteria

209
Q

In which type of lymphadenitis is a neutrophilic infiltrate seen with pyogenic organisms?

A

Acute nonspecific lymphadenitis

210
Q

What can cause granulomatous lymphadenitis besides infections?

A

Foreign bodies or secondary response to malignancy

211
Q

What triad is seen in histology of Toxoplasmosis-related lymphadenopathy?

A

Follicular hyperplasia, adjacent granulomas, marginal zone B-cell hyperplasia

212
Q

What stain is used to detect acid-fast bacilli in TB lymphadenitis?

A

Ziehl-Neelsen stain

213
Q

What features are found in sarcoidosis histology resembling tuberculosis?

A

Giant cells at the periphery and asteroid bodies

214
Q

What is noted in ~60% of sarcoidosis cases histology?

A

Schaumann bodies

215
Q

What surrounds histiocytes in sarcoidosis histology, compared with tuberculosis?

A

Inconspicuous cuff of lymphocytes

216
Q

What does IgG HSV1/2 antibodies indicate?

A

Exposure (past infection)

217
Q

What is the preferred method for testing HSV1 and 2?

A

PCR Assays

218
Q

How is Varicella transmitted?

A

Highly infectious, droplet spread

219
Q

What are the symptoms of Varicella primary infection?

A

Mild febrile illness, generalised vesicular rash

220
Q

What is Varicella zoster virus reactivation known as?

A

Zoster

221
Q

What is the incubation period of Varicella?

A

21 days

222
Q

What is the main cause of stroke in children associated with Varicella?

A

Vasculitis (due to replication in CNS blood vessels)

223
Q

What is the recommended treatment for severe HSV and VZV infections?

A

Aciclovir

224
Q

How is Varicella post-exposure prophylaxis managed for a healthy adult?

A

Varicella vaccine (or acyclovir)

225
Q

What is the primary mode of transmission of human cytomegalovirus?

A

Close contact

226
Q

Define acute leukaemia.

A

Acute leukaemia implies rapid cell proliferation at an early stage, leading to death within weeks or months.

227
Q

How does chronic leukaemia differ from acute leukaemia?

A

Chronic leukaemia involves cells that are able to mature and may not require intensive chemotherapy, with slower onset and death in months to years.

228
Q

What are the clinical effects of leukaemia?

A

Infiltration and disruption of normal tissue function, leading to bone marrow failure, bleeding, infections, anaemia, and bone pain.

229
Q

List the diagnostic classification systems for leukaemia.

A

French American British (old), WHO classification (2001-present), based on morphology, cell surface markers, cytogenetics, and molecular genetics.

230
Q

What are the clinical characteristics of mature lymphoid neoplasms?

A

May present as low or high grade, with growing lumps, destructive lesions, cytopenias, infections, constitutional symptoms, lymphadenopathy, hepatosplenomegaly, and B symptoms.

231
Q

Explain Burkitt lymphoma, Myeloma, and Chronic lymphocytic leukaemia.

A

They are important types of mature B cell neoplasms.

232
Q

What are the typical presentation syndromes of lymphoma?

A

B symptoms, significant lymphadenopathy, cytopenias, lymphocytosis, and growth of tumor masses in body cavities causing disturbance of function.

233
Q

What is the primary cause of mediastinal mass in the young and an important differential diagnosis of lung cancer?

A

Lymphoma.

234
Q

What are myeloproliferative neoplasms characterized by?

A

Proliferation of granulocytic, megakaryocytic, and/or erythroid lineages.

235
Q

What is seen in chronic myeloid leukemia (CML)?

A

Philadelphia chromosome (BCR-ABL1 fusion on Chromosome 22).

236
Q

What are the driver mutations implicated in Ph-negative myeloproliferative neoplasms?

A

Mutations resulting in increased JAK-STAT signaling.

237
Q

What organs are considered primary lymphoid organs?

A

Bone marrow and thymus.

238
Q

What is the purpose of lymph nodes in the body?

A

Detect and inactivate foreign antigens present in lymph fluid.

239
Q

What is the function of germinal centers in lymph nodes?

A

To generate immune responses with a predominance of B cells.

240
Q

Why are tingible body macrophages important in germinal centers?

A

They process antigen to pass to lymphocytes for immune responses.

241
Q

What clinical features are common in myeloproliferative neoplasms?

A

Increased risk of thrombosis and bleeding.

242
Q

What are the causes of lymph node enlargement?

A

Infection, autoimmune disorders, neoplasms (primary or metastatic).

243
Q

When is allogeneic hematopoietic stem cell transplant considered in PMF?

A

Used in intermediate or high-risk PMF to reduce spleen size.

244
Q

What are cytokines and their role in the immune system?

A

Cytokines are small proteins important in cell signaling, mediating immunity, inflammation, and hematopoiesis.

245
Q

How do growth factors regulate cells in the hematopoietic system?

A

Growth factors regulate growth, differentiation, and function of hematopoietic and immune cells.

246
Q

Explain the production and function of Erythropoietin.

A

Erythropoietin stimulates red blood cell production, especially when oxygen levels are low.

247
Q

What are the characteristics of acute leukemia?

A

Acute leukemia involves uncontrolled proliferation of primitive hematopoietic blasts primarily in the bone marrow.

248
Q

Describe chronic leukemias and their characteristics.

A

Chronic leukemias involve the proliferation of mature/differentiated cells with a low growth fraction.

249
Q

List signs of acute leukemia pathogenesis through infiltration of blasts.

A

Signs include lymphadenopathy, hepatosplenomegaly, gum hypertrophy, and less commonly hyperviscosity among others.

250
Q

What are the key classes of molecules controlling cell cycle checkpoints?

A

Cyclins and Cdk (cyclin dependent kinases)

251
Q

Which molecule plays a central role in the G1-S checkpoint?

A

p53

252
Q

Describe the role of p53 when damaged DNA is sensed.

A

p53 prevents activation of Cyclins, allowing time for potential repair.

253
Q

Explain the role of apoptosis in maintaining tissue homeostasis.

A

Apoptosis ensures disposal of defective cells, preventing transmission of faulty DNA.

254
Q

What genetic change leads to reduced apoptosis in Follicular Lymphoma?

A

t(14;18) translocation of the BCL2 gene.

255
Q

How do BAX proteins contribute to apoptosis?

A

BAX increases mitochondrial membrane permeability, leading to cytochrome C release.

256
Q

What determines a cell’s susceptibility to apoptosis?

A

The ratio of BAX to Bcl-2 proteins.

257
Q

What is the role of oncogenes in cancer development?

A

Oncogenes result from gain of function mutations in proto-oncogenes.

258
Q

Explain the mechanism of action for tumour suppressor genes.

A

Tumour suppressor genes protect against malignancy by regulating the cell cycle.

259
Q

What genetic alterations are visible at a microscopic level?

A

Translocations leading to abnormal karyotypes.

260
Q

Why are neoplastic cells genetically unstable?

A

Genetic instability allows for further mutations in neoplastic cells.

261
Q

What is clonal evolution in the context of genetic mutations?

A

Mutations in progeny cells provide a survival advantage, leading to clonal evolution.

262
Q

What are the two types of bone marrow mentioned in the notes?

A

Red bone marrow and yellow bone marrow.

263
Q

Which cells are made in the bone marrow according to the notes?

A

Erythrocytes, neutrophils, and platelets.

264
Q

What forms an open network of trabeculae in bone marrow?

A

The matrix.

265
Q

What are the components of blood mentioned in the notes?

A

Plasma, erythrocytes, neutrophils, platelets, and lymphocytes.

266
Q

What cell can ultimately reconstitute the entire bone marrow according to the notes?

A

Haematopoietic stem cell.

267
Q

How do megakaryocytes contribute to blood production?

A

They break into small fragments (platelets) that enter the blood.

268
Q

What is the function of stem cells in the bone marrow?

A

To differentiate into various functional mature cells.

269
Q

What is the role of red bone marrow in blood cell production?

A

Supplies nutrients to cells, forms erythrocytes, leukocytes, platelets.

270
Q

What are clues to the diagnosis of Hodgkin lymphoma?

A

Eosinophilic or basophilic nuclei, and focal necrosis or granulomas.

271
Q

What is characteristic of Hodgkin lymphoma (HL)?

A

Up to 40% of cases are associated with the Epstein-Barr virus (EBV).

272
Q

Describe the spread of Hodgkin lymphoma.

A

Begins in lymph nodes, then spreads to other groups or extra nodal sites.

273
Q

What are complications associated with Hodgkin lymphoma?

A

Infection, cachexia, organ infiltration, and treatment-related complications.

274
Q

What are the risk factors for non-Hodgkin lymphoma?

A

Factors include viruses (EBV, HTLV-1, HIV, HHV-8) and immunodeficiency.

275
Q

What are the types of Burkitt lymphoma?

A

Endemic, sporadic, and immunodeficiency-associated types.

Leukemia Case (1 decks)

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