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Cancer and Clinical Genetics > Hematological Malignancy > Flashcards

Hematological Malignancy Flashcards

1
Q

How can the stage of haemopoiesis affect the cancer’s aggression

Name of cancers based on each cell in haemopoiesis

  • blasts
  • mature RBC, platelets, granulocytes
  • plasma
  • mature lymphocytes
A

Precursor cells - acute (more aggressive)
Mature cells - chronic (less aggressive

Blasts - acute leukemia
Mature RBC, platelets, granulocytes - MPNs
Plasma - myeloma
Maturę lymphocytes - B, T, NK lymphomas

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2
Q

What is the main defining feature of acute leukemias

2 main types of acute leukemia and their main characteristics

  • acute lymphoblastic leukemia
  • acute myeloid leukemia
A

20%+ blasts in blood or BM

Acute lymphoblastic leukemia

  • childhood cancer but incidence increases with age
  • curable in children but less in adults

Acute myeloid leukemia

  • elderly cancer
  • prognosis depends on genetic abnormalities
  • an umbrella term that covers leukemic changes at any point in hematopoiesis
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3
Q

Presentation of acute leukemias

  • pathophysiology
  • past medical history
A

Dysfunctional leukoblasts are made in the BM, not released => affects other cell lines and leukemia cells leak out

Abrupt onset
Loss of BM function - pancytopenia
-anemia, fatigue
-fever, infection
-bruising, easy bleeding

Organ infiltration - hepatomegaly, splenomegaly
-lymphadenopathy in ALL

CNS - headache, nausea, nerve palsy

AML can have strong FHx
MPN, MDS can develop into AML

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4
Q

Investigations to diagnose acute leukemia (ALL, AML)

A

Blood and BM morphology
Immunophenotyping - identify antigens present
Karyotyping - chromosomal abnormalities
Genetic analysis - assess for mutations

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5
Q

Management of acute leukemias

A

Combination chemotherapy with repeated courses

Allogenic hemopoietic stem cell transplant if

  • relapse
  • poor prognosis

Treatment guided by flow cytometry, PCR, sequencing

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6
Q

Pathophysiology of tumour lysis syndrome

A

Rapid release of cellular components into circulation after rapid destruction of rapidly proliferating malignant cells

Release of DNA => increased uric acid
Release of Ca, PO4 => arrythmias
Both can lead to AKI

Hydration
Allopurinol (xanthine oxidase) => prevent uric acid formation
Monitor K, manage if needed
Dialysis is an option

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7
Q

Acute promyelocytic leukemia

  • pathophysiology
  • management
A

Aggressive form of AML

MEDICAL EMERGENCY

  • promyelocytes release cytokines => DIC
  • platelet production low => bleed risk

Can manage with vitamin A analogues and arsenic trioxide

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8
Q

What are lymphoid neoplasms

A

Clonal tumours of B, T, NK cells

-malignancy can form at any stage of development and maturation

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9
Q

Myeloma

  • epidemiology
  • pathophysiology
  • presentation
A

BM plasma cell neoplasm => excess IgG, IgA released into serum, urine

  • can arise from MGUS
  • 60-70 years

Bone pain, lesions, osteoporosis => high Ca
Fatigue, infection
Renal failure from high Ca, dehydration, amyloid

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10
Q

Myeloma

  • investigations
  • diagnosis
A

IgG, IgA monoclonal proteins in serum, urine
Increased plasma cells in BM

Whole body MRI - bone lesions

BM aspirate - identify myeloma cells

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11
Q

Presentation of myeloma in kidneys

A

Light chains block tubules => form cast nephropathy

Light chain accummulate in glomerulus => nephrotic syndrome
-can accumulate in other areas => macroglossia, peripheral neuropathy, HF, GI, liver

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12
Q

Describe the impact myeloma can have on the spinal cord

-management

A

SC compression - sensory loss, paraesthesia, limb weakness, difficulty walking, sphincter changes

Management
Supportive - bed rest, backbrace

Imaging - urgent MRI

Medical - high dose steroids to reduce plasma cell burden

If soft tissue lesion - local radio
If bony compression/SC unstable - surgery

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13
Q

What is hyperviscosity syndrome

  • presentation
  • management
A

High levels of paraprotein => increase viscosity => reduces O2 delivery => end organ dysfunction

Bleeding into skin, retina
CNS - headache, blurred vision, poor conc, low GCS, tinnitus, seizures
CV - HF, intermittent claudication
Resp - pulmonary congestion, SOB

Treat underlying disease
DO NOT TRANFUSE RED CELLS
-plasmapheresis
-isovolemic venesection with saline replacement

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14
Q

Myeloma management

A

Chronic disease - only treat supportively if symptomatic

  • bisphosphonates - bone protection
  • radio - pain, palliation
  • repeated chemo/steroids/meds
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15
Q

What are the main 2 types of lymphoma

-risk factors

A

Replacement of normal lymphoid structures with malignant cells

Can be nodal/extranodal
Hodgkin - 20s and increased incidence with age
Non Hodgkin - mainly associated with age
-B cell most common

Risk factors

  • increasing age
  • viruses (EBV, HIV, HepB, C)
  • chronic inflammation (Hpylori, AI)
  • IC (organ transplant, meds)
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16
Q

Presentation of lymphoma

A

Fever, night sweats, weight loss, fatigue
Lympadenopathy
Hepatosplenomegaly
Symptoms in extranodal sites

Hodgkin

  • itch or alcohol induced pain
  • mediastinal mass => SVC obstruction, SOB
  • cyclical changes in fever (PelEbstein)
17
Q

Diagnosis and staging of lymphoma

A

LN biopsy
Stage
-CT/PET
-BM aspirate - assess liquid, can be used to immunophenotyping, cytogenetics
-BM trephine - assess solid section of bone for immunohistochemistry

Also can assess for genetic abnormalities that will guide diagnosis and treatment

18
Q

Treatment of lymphomas in general

Treatment of Hodgkin lymphoma

A

High grade - urgent with curative intent
Early low grade - radio with curative intent

Symptomatic low grade - treat
Asymptomatic low grade - wait

Gastric MALT (caused by HPylori) can be cured => HPylori eradication

Hodgkin lymphoma treatment depends on staging

  • cycles of chemo and radio
  • monoclonal AB
  • stem cell rescue can be used for relapse
19
Q

What is autologous stem cell transplant

Why is this used in chemotherapy

A

For myeloma, Hodgkin and high grade lymphoma
Remove and freeze patient’s own stem cells
Chemo destroys the patient’s normal hemopoetic tissue => pancytopenia

Thawed stem cells are reinfused to aid recovery of BM

20
Q

What are the side effects of chemotherapy

A 
N+V+D
Hair loss
Myelosuppression, neutropenic sepsis
Fatigue
Lung, nerve damage, cardiomyopathy
Infertility
Secondary cancer
Steroid related side effects
21
Q

What is neutropenic sepsis

-what is the general management

A

ONCOLOGICAL EMERGENCY
Fever and neutrophil count U0.5x10^9
Broad spec ABx with G-ve coverage
-tazocin

22
Q

What is diffuse large B cell lymphoma

What is follicular lymphoma

A

Most common lymphoma
High grade CD20+ tumour
Common in older adults, males

Most common low grade lymphoma
CD20+
Only treated when symptomatic or early
-chemo + rituiximab
Common in older adults, females
23
Q

Characteristics of chronic lymphocytic leukemia

A

Proliferation of mature B cells in BM, LN and spill out into blood
Often accidentally found

Risk factors
-increased age, male

Presentation

  • cancer red flags
  • recurrent infection
  • AI hemolytic anemia, thrombocytopenia
  • BM failure
  • lymphadenopathy
  • splenomegaly
24
Q

MPN pathophysiology

Polycythemia vera presentation

A 
BM making too many blood cells
PV - too many RBCs, neutrophils, platelets
-JAK2 common
-hyperviscosity
-splenomegaly
-easy bleeds
-plethoric
25
Q

MPN - essential thrombocytopenia

  • presentation
  • pathophysiology
A

Megakaryocyte proliferation => too many platelets
-JAK2 common

  • burning feeling in hands
  • high platelets
  • thrombosis and haemorrhage
26
Q

MPN - myelofibrosis

  • pathophysiology
  • presentation
A

Hyperplasia of abnormal megakaryocytes => BM fibrosis => dysfunctional blood cells made in BM => haematopoiesis occurs in liver and spleen but cannot make enough RBCs to keep up with demand

Anemia, fatigue
Massive splenomegaly
Weight loss, night sweats

27
Q

MDS pathophysiology

A

Abnormal growth of blood cells that accumulate in BM => spill out into blood

  • pancytopenia
  • splenomegaly

Cancer and Clinical Genetics (51 decks)

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