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53 Cards in this Set

  • Front
  • Back

Leukopenia

decreased white blood cells

Neutropenia (granulocytopenia)

a drop in the absolute count of neutrophils

Agranulocytosis

severe granulocytopenia

Pancytopenia

decreases in all components (RBCs,WBCs, platelets)

Thrombocytopenia

decrease in platelets to less than 20,000 (150,000-400,000 normal)

Leukostasis

# of circulating blasts is elevated

Remission

absence of any detectable leukemic cells in the bone marrow

Leukemia

malignant neoplasm of bone marrow and cells originally derived from hematopoietic stem cells

Leukemia Basic Pathology

rapidly multiplying cells invade organs and tissues suppress normal cells

Leukemia Type of Cell

Lymphocytic (lymphoblastic) - B, T, & NK


Myelocytic (myeloblastic) - all others

Basic Categories of Leukemias

Acute Lymphocytic Leukemia (ALL)


Chronic Lymphocytic Leukemia (CLL)


Acute Myelogenous Leukemia (AML)


Chronic Myelogenous Leukemia (CML)

Leukemia General Manifestations

Pale (anemic)


SOB


Fatigue


susceptible to infection


Bleeding due to lack of platelets

Acute Lymphocytic Leukemia (ALL)

Aburpt onset, primarily children (80-85%), 1-7 yrs of age, white, well developed countries

ALL Etiology and Patho

Unknown. ? virus or exposure to chemicals inutero



Pahto - B cells (85%)

Clinical Manifestations ALL

increased blast cells, decreased WBCs, enlarged spleen and liver, CNS invasions (headaches and seizures)

ALL Prognosis

Children 95% remission (5 yrs - 90%)


Adults 80% remission (5 yrs - 75%)

AML Incidence and Onset

Incidence - increases with age, primarily adults


Onset - abrupt, 60 -65 yrs old median

AML Etiology and Pathi

Etiology - unknown, ? high doses of radiation, smoking



Patho - neutrophils

AML Clinical Manifestations

anemia, bleeding, infections, decreased platelets & RBCs, pain in bone & joints, increased WBCs

AML Prognosis

w/o treatment 3 months


1/4 alive after 5 yrs

CLL Incidence and onset

Incidence - older adults median age 60, 72 average, M:F - 2:1



Onset - slow

CLL Risk Factors and Patho

Risk Factors - agent orange (vietnam)



Patho - 95% malignant B cell precursor, aquired change to DNA, T or NK involved, very aggressive

CLL Clinical Manifestations

hypermetabolic state, found on routine blood work, rarely goes to CNS, prone to infections

CLL Prognosis

variable 70% survive 5 yrs with treatment

CML Incidence and Onset

Incidence - older adults



Onset - gradual


CML Etiology and Patho

Etiology - unknown, ? acquired injury to DNA



Patho - unique chromosomal abnormality (Philadelphia chromosome 9 & 22)

CML Clinical Manifestations

pain on left side (spleen), hypermetabolic state, chronic, accelerated,

Prognosis CML

poor, doesn't respond well to chemo

Chemotherapy Phases

1. Induction - hit hard, a lot quickly


2. CNS prophylaxis


3. Consolidation (intensification) - reduce amt of cells.


4. Maintenance - oral chemo

Complications of Chemotherapy

uric acid in blood stream 24 - 72 hours after initial chemo. Increased potassium.

Bone Marrow Transplant Autologous

from self during remission

Bone Marrow Transplant Allografts

from a close resembalence to patient

Bone Marrow Procedure

1. Chemo


2. Infusion of bone marrow


3. Wait

Peripheral Stem Cell Treatment

receive stem cells from donor

Bone Marrow Transplant Syngenic

from identical twin

Lymphoma

malignant tumor that arises from the malignant transformation of a lymphocyte in the lymphatic system

Hodgkin Lymphoma Incidence

increased in young population & again in the elderly, slightly increased in males

Hodgkin Lymphoma Etiology

unknown, Epstein Barr 50% of cases

Hodgkin Lymphoma Patho

Reed-Sternberg cell, 3 nuclei, acquired damage to DNA in lymphocyte

Hodgkin Lymphoma Clinical Manifestations

increased size of lymph nodes (cervical and diaphragm), increased WBCs, asymptomatic, dry cough, splenomegaly, increased temp, night sweats

Hodgkin Lymphoma Treatment and Prognosis

Treatment - radiation



Prognosis - 86% cured

Non Hodgkin Lymphoma Incidence

increases with age, male more than female, increase with AIDS

Non Hodgkin Lymphoma Etiology

unknown, Epstein-Barr, side effect of leukemia

Non Hodgkin Patho

acquired damage to DNA of lymphocyte (B cells)

Non Hodgkin Clinical Manifestations

enlarged lymph nodes, weight loss, GI symptoms, fatigue

Non Hodgkin Prognosis

Stage I or II - favorable



Stage III or IV - poor (5th most common for death)

Multiple Myeloma

bone marrow / plasma cells, mass formation within bone

Multiple Myeloma Incidence and Onset

Incidence - rare (1%), increased with age, males more than females, 22,000 new cases / yr, African Americans 2 x's as often.



Onset - very slow

Multiple Myeloma Risk Factors

chronic exposure to chemicals and radiation, increased in HIV patients

Multiple Myeloma Etiology

acquired injury to DNA of one cell in the sequence destined to be a plasma cell

Multiple Myeloma Patho

B cell, usually IgG (after mature) IgA

Clinical Manifestations Multiple Myeloma

C - increased calcium


R - renal insufficiency


A - anemia


B - bone lesions



Bence Jones protein or M protein in urine, infections (urinary & bronchial), pathological fractures



Multiple Myeloma Prognosis

long term survival decreased, 30% alive within 5 yrs, die within a year without treatment