ANEMIA DUE TO INCREASED

DESTRUCTION (HEMOLYTIC ANEMIA)

 HEMOLYTIC ANEMIA
HEMOLYTIC ANEMIA
CAUSES

INTRINSIC FACTOR EXTRINSIC FACTOR

(INTRACORPUSCULAR) (EXTRACORPUSCULAR)

INHERITED ACQUIRED

MEMBRANE DEFECT PNH

ENZYME DEFECT

HGB DEFECT
 HEMOLYTIC ANEMIA
HEMOLYTIC ANEMIA
CAUSES

INTRINSIC FACTOR EXTRINSIC FACTOR

(INTRACORPUSCULAR) (EXTRACORPUSCULAR)

NON IMMUNE
IMMUNE MEDIATED
MEDIATED

SPLENOMEGALY/
INFECTION CHEMICAL MECHANICAL CAUSES
SPLENIC
SEQUESTRATION

MAHA(Macroangiopathic
MALARIA LEAD EBV Hemolytic Anemia)

MAHA(Microangiopathic
CLOSTRIIDIUM CMV Hemolytic Anemia)
 MACROANGIOPATHIC HEMOLYTIC
ANEMIA (MAHA)

ILL FITTING
TRAUMATIC CALCIFIC AORTIC
PROSTHETIC
DAMAGE VALVE STENOSIS
CARDIAC VALVE

CONGENITAL
CARDIOVASCULAR MARCH
ATHLETES
ANOMALIES eg HEMOGLOBINURIA
coarctation of aorta
 MICROANGIOPATHIC HEMOLYTIC
ANEMIA (MAHA)
DIC (Disseminated
TRAUMATIC
Intravascular
DAMAGE
Hemolysis)

TTP
(Thrombocytopenic HUS (Uremic
Thrombotic Syndrome)
Purpura)
 HEMOLYTIC ANEMIA
HEMOLYTIC ANEMIA CAUSES

INTRINSIC FACTOR EXTRINSIC FACTOR

(INTRACORPUSCULAR) (EXTRACORPUSCULAR)

NON IMMUNE MEDIATED IMMUNE MEDIATED

AUTO ANTIBODY

ISO ANTIBODY
IMMUNE MEDIATED HEMOLYSIS

AUTO
ANTIBODY
1. WARM ANTIBODY HEMOLYTIC
ANEMIA
2. COLD ANTIBODY HEMOLYTIC
ANEMIA
3. COLD ANTIBODY AGGLUTINS
 NURSING CONSIDERATIONS

MONITOR FOR
EDUCATE THE
SIGNS AND BLOOD
PATIENT ABT THE
SYMPTOMS OF TRANSFUSION
DISEASE
ANEMIA

INSTRUCT ABT
MEDICATION PREPARE PT FOR
(STEROIDS, SPLENECTOMY
CHEMOTHERAPY)
IMMUNE MEDIATED HEMOLYSIS

ISO ANTIBODY
1. ABO
INCOMPATIBILITY
2. RH INCOMPATIBILITY
• 28 weeks AOG
• Within 72 hours post partum
COOMB’S TEST
WBC DISORDERS
 PROLIFERATIVE DISORDER OF WBC

1. REACTIVE PROLIFERATION
– SIMPLE LEUKOCYTOSIS
– LEUKEMOID REACTION

1. NEOPLASTIC PROLIFERATION
– LEUKEMIA
– LYMPHOMA
 RISK FACTORS
• Aging
• Cellular Mutations (Environment & Lifestyle agents)
• Exposure to Cancer-causing agents
• Hormone exposure (i.e. breast cancer)
• Occupation and Environment Factors
• Social and Psychological Factors
• Chemicals in Food
• Viral (i.e. herpes, HPV, mononucleosis) create an
opportunistic environment
• Medical Factors
 PATHOPHYSIOLOGY
SELF SUFFICIENT INSENSITIVE TO DYSFUNCTIONAL
IN GROWTH INHIBITORY DNA REPAIR
SIGNAL SIGNAL SYSTEM

LIMITLESS
EVASION OF SUSTAINED
REPLICATING
APOPTOSI ANGIOGENESIS
CAPACITY

CAPACITY FOR
ESCAPE FROM
INVASION AND
IMMUNITY
METASTASIS
LEUKEMIA VS LYMPHOMA
ACUTE LEUKEMIA/LYMPHOMA

MORE
FAST PACED AGGRESSIVE
PROLIFERATIVE

LARGE CELLS UNDIFFERENTIATED IMMATURE

NON FUNCTIONAL
CHRONIC LEUKEMIA/LYMPHOMA

LESS
SLOW PACED LESS AGGRESIVE
PROLIFERATIVE

SMALL CELLS DIFFERENTIATED MATURE

MINIMAL
FUNCTION
 DIAGNOSTICS

GENOTYPING PHENOTYPING MORPHOLOGY

BONE
CLINICAL
MARROW MARKERS
FEATURES
ASPIRATE
 TREATMENT

CHEMOTHERAPHY RADIATION

BM/SC
TRANSPLANT
TRADITIONAL CHEMOTX SIDE EFFECTS

1. Bone marrow suppression

– Neutropenia
– Thrombocytopenia
– anemia
2. Nausea/vomiting
3. Alopecia
4. Mucositis
5. Fatigue
 MYELOBLASTIC

MONOBLASTIC

MYELOID

ERYTHROBLASTIC

ACUTE
MEGAKARYOBLASTIC

LYMPHOID LYMPHOBLASTIC

LEUKEMIA

CHRONIC
MYELOCYTIC

MYELOID

POLYCYTHEMIA VERA
CHRONIC

CHRONIC
LYMPHOID
LYMPHOCYTIC
LYMPHOMA
HODGKIN’S LYMPHOMA NON HODGKIN’S LYMPHOMA
Good prognosis Poor prognosis
Predictable Unpredictable
Almost always starts in the LN Starts in different tissues in the body
Originates from: cervical, axillary, inguinal LN Affects deep LN like mesenteric LN
which is very accessible and observable

Spreads in decent, predictable and orderly Jumps from different areas

fashion

Diagnosed at 1st – 2nd stage of the disease Diagnosed at late stage

Has predictable response to treatment Unpredictable response to treatment
Presence of Reed sternberg cells which is Reed sternberg cells almost always absent
surrounded by inflammatory reactive cells.
Causing “B” symptoms
Fever SYMPTOMS ON AFFECTED AREA
Unexplained weight loss CHEST– coughing
Night sweats BRAIN - seizure
Anorexia COLON - constipation
 TREATMENT

CHEMOTHERAPHY RADIATION

BM/SC
TRANSPLANT
PLASMA CELL DYSCRASIAS

MULTIPLE MYELOMA
 MULTIPLE MYELOMA

• More common in males, >60 years old, african

descent
• Proliferative disorder of B cells which are
terminally differentiated
 SIGNS & SYMPTOMS

ANEMIA INFECTION BLEEDING

SPINAL CORD PATHOLOGIC

BONE PAIN
COMPRESSION FRACTURE

HYPERCALCEMIA RENAL FAILURE

DIAGNOSTICS
 TREATMENT

CHEMOTHERAPHY RADIATION

BM/SC
TRANSPLANT