Leukemias, Lymphomas, and Misc. Flashcards
Leukocytosis
increases leukocyte count
often a normal protective response
Leukopenia
Decrease in leukocyte count
Below ____ = risk of infection
1000/mm 3
Below ____ = life threatening
500/mm 3
Hematologic Neoplasias
Cancer which originates in hematologic tissues of the body - specifically from changes in the stem cells
Metastasis to bone marrow
Ex of hematologic neoplasia
Multiple myeloma
Leukemia
Polycythemia vera
How common is leukemia
9th most common cancer in US
Avg age of diagnosis for leukemia
66
Leukemias (Weissus Blut) is what
primary neoplasm is within the bone marrow
Lympho =
involving lymphoid tissue
Myelo =
involving hematopoietic stem cells
-blastic =
acute
immature cells
-cytic =
chronic
mature cells
Acute leukemias
accumulation of immature (blast) cells
Overcrowding of bone marrow
Anemia might be first s/s
Onset is abrupt
Common clinical findings with acute leukemia
Anemia Coagulopathy DIC Infection Weight loss Bone pain Inc uric acid excretion Liver, spleen, lymph node enlargement
Acute lymphoblastic leukemia (ALL) defined as
more than 30% lymphoblasts
Acute lymphoblastic leukemia (ALL) epidemiology
Accounts for 20% of all leukemias
Most common (57%) in those under 20 yrs
Median age diagnosis is 15
Acute lymphoblastic leukemia (ALL) 5 yr survival
68%
Children 95% attain remission, 80% long term survivial
Adults 40% long term
Acute Myelogenous Leukemia (AML)
Most common (35%)
Variety of subtypes
Peak diagnosis btw 60-70 yrs
Rare to occur in less than 40 yrs
Acute Myelogenous Leukemia (AML) - survivial (5 yr)
27%
Acute Myelogenous Leukemia (AML) - s/s
Typical manifestations
About 2% have neuro s/s including disorientation and HA
Might see CN problems
Acute Myelogenous Leukemia (AML) - treatment
Significantly high WBC count which can cause vascular damage secondary to occlusion
Chemotherapy - phased with the goal of achieving remission
Acute Myelogenous Leukemia (AML) - chemotherapy phased treatment
1 = Induction therapy - eradication of neoplastic cells
2 = Post Remission - delivery of additional drugs to inc eradication effects
3 = Consolidation therapy - stem cell or bone marrow replacement
Maintenance and supportive therapy
Chronic leukemias
slow onset with vague s/s
cells are well differentiated
some functional WBCs are being produced at the same time
Chronic myelogenous leukemia - epidemiology
15% of all leukemias
Almost exclusively an adult onset (2% in children)
Chronic myelogenous leukemia - diagnosis
Philadelphia chromosome is diagnostic marker
Chronic myelogenous leukemia - survival
overall 5 yr survival is 67%
dramatic inc since 2001 with new drug
Chronic myelogenous leukemia - phases
1 chronic phase - lasts 2-3 yrs with mild symptoms (most are diagnosed in this phase)
2 accelerated phase - inc number of problems and severity of symptoms (4 yrs)
3 Blast phase - resembles the acute leukemia
Chronic myelogenous leukemia - treatment
stem cell transplantation is curative but not everyone is a candidate (secondary to multisystem issues)
Biological therapies like interferon can induce remission or supress progression
Chronic myelogenous leukemia - new drug
imatinib mesylate (gleevac) Hugely expensive
Chronic lymphocytic leukemia - epi
2nd most common type (28%)
Adults over 50
85% survivial rate
Chronic lymphocytic leukemia - primary cell involved is
B cell therefore see side effects as suppression of humeral immunity
Chronic lymphocytic leukemia - what is it
accumulation of mature but incompentent cells
Fatigue, lymphadenopathy
Opportunistic infections are often a hallmark of disease (75%)
Chronic lymphocytic leukemia - treatment
hugely resistent to drugs
Treatment is more palliative in nature
Younger have more success with bone marow transplants
Lymphoma
Cancers that develop in immune system
2 types
- Hodgkins disease
- Non-Hodgkins disease
Hodgkins disease characterized by presence of what
Reed Sternberg cell (owl eyes)
Hodgkins disease - epi
8% of all lymphomas
peak age 20-35
most common in young adult males
Hodkins disease is considered an
immunodeficient disease
can metastasize to non lymph tissue but does so infrequently!
Hodgkins disease - stages - stage 1
signle node region or a single extra lymphatic site
survivial is 90%
Hodgkins disease - stages - stage 2
Two or more nodes on one side of the diaphragm
Hodgkins disease - stages - stage 3
involved tissue both sides of diaphragm
Hodkins disease - stages - stage 4
Multifocal involvement including extra lymphatic involvement
Hodskins disease - lymphadenopathy =
firm, rubbery, usually not tender or painful
more than 1cm in diameter
Hodgkins disease s/s
Night sweats - severe Intermittent fever Weight loss of more than 10% in 6 months Pruritis Pain and/or neuro s/s in extremities CNS s/s and symtpoms are NOT common
Hodgkins prognosis
Highly curable
5 yr survival is 85% (avg)
stages 1 and 2 have 93%
Age is a factor
Hodgkins treatment
Stage 1 and 2 radiation with supplemental chemo
Satge 3 aggressive chemo
Stage 4 Multiagent drug regimen
Non hodgkins lymphoma is what
hetergenous group of lymphoproliferative malignancies
7th most common cancer in US
significant inc since 1970 - secondary to increase in HIV
Non hodgkins lymphoma - epi
95% occur after age 45
M more than F
Typically diagnosed 65-74 yrs
Survival rate 71%
Non hdgkins lymphoma - course
Bx and spread not as predicitive as hodgkins
tends to spread to extranodal sites (spleen, GI, bone)
Clinical course varies depending on subtype
Subtypes of Nonhodgkins lymphoma
Low grade (follicular) lymphoma AKA indolent Intermediate grade (indolent) High grade (aggresive)
Non hodgkins lymphoma - s/s
painless lymphadenopathy fever fatigue, night sweats spread to extranodal areas visceral and structural obstruction or impingement s/s
Non hodgkins lymphoma - tx
Chemo Biological/immunotherapy - hormonal, interferon Radiation Plasmapheresis Stem cell transplant
Disseminated Intravascular Coagulation (DIC) is what? and what is it commonly seen with?
Hyper or over activation of the coagulation system
Acquired platelet malfunction
Sepsis, trauma, ob/gyn complication, leukemia complication
Disseminated Intravascular Coagulation (DIC) - pathology
Coagulation leads to thrombosis formation
Deposits of fibrin due to activation of fibrolytic system
Fibrinolysis impaired
Because there is clotting widespread, clotting factors within both intrinsic and extrinsic pathways are used up
Hemorrhage occurs
Thrombi develop as clotting factors are depleted
Disseminated Intravascular Coagulation (DIC) - clinical features
Unexpected bleeding from all body openings Hematomas, petechieae Swelling Mottled/cold hands and feet Resp distress Neuro issues Hypotension, tachycardia Renal issues
Disseminated Intravascular Coagulation (DIC) - diagnosis
clinical diagnosis confirmed with lab tests
Disseminated Intravascular Coagulation (DIC) - treatment
directed at the cause
Heparin may be used to get rid of clots
Blood product replacement therapy can be used (transufion)
Can be fatal!
Monito lab test frequently with PT - generally seen bedisde
Hematopoietic stem cell transplant
blood (or bone marrow) source
Umbiical cord
Allogenic vs. Autologous
Hematopoietic stem cell transplant - who
Pt about to undergo aggressive chemo or high dose radiation
Certain hematological neoplasias
Hematopoietic stem cell transplant - s/s
Severe immunosuppression weakness fatigue cardiac and liver toxicity (from the drugs) hemorrhage myopathy and osteoporosis risk for integumentary breakdown
Hematopoietic stem cell transplant - beforehand
Pre-transplant assessment and education is recommended
Hematopoietic stem cell transplant - PT
Typically they will be deconditioned (we wont see them until long time after transplantation) pulmonary sys dec Energy conservation Pt education on safety Regular and close monitor of labs Infection control procedures
