Diseases Exam 3 Flashcards
(38 cards)
Leukemia vs. Lymphoma
Leukemia:
- Malignancy of hematopoetic cells
- Starts in bone marrow (can spread to blood, nodes)
- Myeloid or lymphoid
- Acute or chronic
Lymphoma:
- Malignancy of hematopoetic cells
- Starts in lymph nodes (can spread to blood, marrow)
- lymphoid only
- Hodgkin or non-hodgkin
Acute vs. Chronic Leukemia
Acute:
- Sudden onset
- Can occur in either adults or children
- Rapidly fatal w/o treatment
- Composed of immature cells (blasts)
- Patient will present w/ bleeding problems, infx probs, anemia etc.
Chronic leukemia:
- Slow onset
- ONLY in adults (
Acute Leukemia
Definition: Malignant proliferation of immature myeloid or lymphoid cells in the bone marrow
Cause: clonal expansion, maturation failure
Problems caused:
- Crowd out normal cells
- Inhibit normal cell funcitons
- Infiltrate other organs (i.e. brain) - not very common
Clinical findings:
- Sudden onset (days)
- Symptoms of bone marrow failure (fatigue, infx, bleeding)
- Bone pain (expanding marrow
- Organ infiltration (liver, spleen, brain)
Labs:
- Blasts/immature cells in blood
- Leukocytosis
- Anemia
- Thrombocytopenia
Acute Myeloid Leukemia
Things you must know:
- Malignant proliferation of myeloid blasts in blood, bone marrow
- 20% blast cells is cutoff for dx
- many subtypes
- bad prognosis
Old classification:
M0,1,2,3 - Involve neutrophilic series (myeloblasts, promyelocytes, etc.)
M4,5- involve monocytic series (monoblasts etc.)
M6 - involves erythroid series (erythroblasts)
M7 - involves megakaryocytic series (megakaryoblasts)
New clasification: AML w/:
- genetic abnormalities
- FLT-3 mutation
- w/ multilineasge dysplasia
- therapy related
- not otherwise classified
Treatment:
- Chemo
- Bone marrow transplant
Prognosis:
- Dismal
- t(8;21), inv(16), t(15;17) better
- FLT-3, therapy-related worse
AML - M0
Things you must know:
- large increase in myeloblasts
- Bland
- Myeloperoxidase negative
- Need markers (to run flow cytometry)
So early it’s hard to even tell they are myeloblasts.
AML - M1
Things you must know:
- large increase in myeloblasts
- no maturation
- auer rods
- Myeloperoxidase positive
AML-M2
Things you must know:
- Increase in myeloblasts
- Maturing neutrophils
- t(8:21) in some cases
AML - M3
Things you must know:
- Large increase in promyelocytes
- Faggot cells (lots of auer rods)
- DIC
- t(15;17) in all cases
Mutated retinoic acid receptor –> treat with ATRA (all trans retinoic acid). This has high cure rate and prevents DIC
AML-M4
- Significant increase in myeloblasts
- Significant increase in monocytic cells
- Extremedullary tumor masses
- inv (16) in some cases
AML- M5
Significant increase of monocytic cells
NSE (non specific esterase) positive
M5A and M5B
Extramedullary tumor masses
AML - M6
Significant increase in erythroblasts and myeloblasts
Dyserythropoiesis
AML-M7
Significant megakaryoblasts
Bland blasts
MPO negative
Need markers (to run flow cytometry)
AML w/ genetic abnormalities
t(8;21) –> M2 = good prognosis
inv(16) –> M4 = good prognosis
t(15;17) –> M3 = good prognosis
11q23 –> therapy related often = bad
AML w/ FLT-3 mutation
- Mutation of FLT-3 (a tyrosine kinase)
- Present in 1/3 of cases of AML!
- Monocytic cells
- Poor prognosis
AML w/ multilineage dysplasia
- ≥ 20% blasts + dysplasia in ≥ 2 cell lines
- Elderly
- Severe pancytopenia
- Chromosome abnormalities (5, 7)
- Poor prognosis
AML, Therapy-Related
- Previous chemotherapy
- Alkylating agents (Busulfan) or topoisomerase II inhibitors (Etoposide) (others too)
- 2-5 years to onset
- Chromosomal abnormalities sometimes (5, 7, 11q23)
- Very hard to treat
Meyelodysplastic Syndrome (MDS)
- Problem: abnormal stem cells
- Dysmyelopoiesis
- Maybe increased blasts
- May evolve into acute leukemia
Clinical and Lab findings:
- older patients
- Asymptomatic, or BM failure
- Macrocytic anemia
Treatment:
- Low grade: support, follow
- High-grade: be aggressive –> treat like leukemia
Red cell dysplasia looks like ?
megaloblastic nuclei, fragmentation
Neutrophilic dysplasia looks like ?
hypogranulation, hyposegmentation
Magakaryoctyic dysplasia looks like
small, non-lobulated cells
Acute Lymphoblastic Leukemia
Things you must know:
- Malignant proliferation of lymphoid blasts in blood, bone marrow
- Classified by immunophenotypes (B vs. T)
- More common in children
- Prognosis is often good
T-lymphoblastic leukemia has worse prognosis
Prognosis:
- Immunophenotype (T is bad)
- Age (1-10 good)
- WBC (
T-Lymphoblastic Leukemia
= T-lymphoblastic lymphoma
-Teenage male with mediastinal mass
-WBC usually very high
Bad prognosis
B lymphoblastic Leukemia
= B-cell lymphoblastic lymphoma
- Several sub- and sub-subtypes
- TdT +
- Rarely, Philedelphia chromosome + ! (if so = bad)
Malaria
1 child killer (1 per minute)
Epidemiology:
- Most prevalent in Africa, Asia, Latin America
- 216 million affected, 655,000 die each year (90% in SSA)
Vector: Anopheles Mosquito
Causative agent: Plasmodium vivax (common; more benign), P. falciparum (common ; most lethal), P. ovale, P. malariae
Life cycle: sporozoites transmitted from mosquito –> hepatic schizonts –> Merozoites –> ring form –> trophozoite –> schizont
Organ findings:
- Splenomegaly (parasites in RBCs, super-active macrophages, if chronic: fibrosis, grayish color)
- Hepatomegaly and liver becomes pigmented (gray)
- Brain vessels get plugged (rosettes and binding of endothelium) causes hypoxia and eventual ischemia
- Heart, lungs may also be involved.
Clinical presentation:
-Incubation = 1-2 weeks
-Prodrome: flu-like illness
-Paroxysms! Fever/chills, sweating, myalgia
Quotidian (daily) - P. falciparum
Tertian (every 48 hours) - P. vivax or ovale
Quartan (every 72 hours) P. malaria
Host resistance:
- Inherited RBC alterations: Hemoglobinopathies (i.e. sickle cell), Thalassemias, G6PD, RBC antigens (ABO - O is best, Duffy)
- Partial immune-mediated resistance: develops over time in patients in endemic areas, reduces severity of disease, and P. falciparum uses antigenic variation
Dx: Clinical sx + hx; identification of plasmodia in RBCs on regularly-stained blood smear (gold standard); and rapid immunochromatographic tests (quicker but less accurate)\
Rx: Depends on resistance, previous treatment, and area where they were infected (which species, and on sickness of person. 1.) protection/nets, 2.) prophylaxis, and 3.) treat malaria, and 4.) radical cure (primaquine) for latent forms? (debated)