anemias and blood cancer update f10 student

8/6/2019 Anemias and Blood Cancer Update F10 Student

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ALNU 4050 Care of the Older Adult

Anemia and Blood Malignancies


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Categorizing Anemias in your Text

Hypoproliferative-resulting from defective redblood cells Iron Deficiency

Vitamin B-12 Folate Deficiency

Chronic Disease causes

Erythropoietin deficiency-renal

Cancer/inflammation

Blood loss GI bleed, menorrhagia, trauma

Hemolytic-RBC being destroyed


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Anemia

Is not normal as you age

Can be caused by a chronic illness or amalignancy

Symptoms determined by severity

Remember oxygen carrying capacity is affected

Classified by cause or cell size, shape or

substance Categorized microcytic, macrocytic, and

normocytic


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Microcytic Anemia: (hypoproliferative)

Iron Deficiency Anemia

MCV is less than 80, Small, pale RBC

Depleted iron stores, have to have for HGB to function

Need to find out what is the cause

Acute blood loss, chronic blood loss, inadequate nutritional intake

Consider GI first (occult blood, GI workup)

Tests

MCV

Iron studies

Serum Ferritin reflects body stores of iron in bone marrow

Transferrin saturation

Total iron binding capacity

Bone marrow aspiration (if suspect leukemia)


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Symptoms of Iron Deficiency Anemia

Onset gradual Usually Hgb drops to 7-8g/dl and then seek medical attention

Non-specific early symptoms so difficult to diagnose

Fatigue, weakness, shortness of breath, pale earlobes, palms, and

conjunctiva

More severe symptoms such as fingernails brittle and concave,soreness and redness of tongue, corner of mouth dry and cracked

As it progresses, Gastritis, Neuromuscular changes, Irritability, Headache,

Numbness and tingling of feet and hands, Vasomotor disturbances

Elderly-mental confusion, memory loss, and disorientation


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Treatment

Dont treat anemia without knowing the cause

Then treat the underlying cause Can be reversed with 1-2 weeks of treatment

Ferrous Sulfate 325mg for 6-12 months after

bleeding stops Daily until menopausal if Gynecological cause

Patient education about Ferrous sulfate


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Normocytic Anemia:

Types:

Anemia of chronic disease(hypoproliferative),

Hemolytic anemia Aplastic anemia

Normal size cells

Decreased production and survival of RBC,premature or rapid destruction


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Anemia of Chronic Disease: Hypoproliferative

Malnutrition-missing folic acid and Vitamin C = decreasedRBC

Chronic infection/inflammation-decreased EPO production,

decreased RBC survival, impaired transport to bone marrow

Cancer-chemo side effects decreasing nutrition and

suppression of bone marrow

Renal insufficiency-decreased erythropoiesis and

decreased RBC survival

Chronic liver disease-alcohol toxic to bone marrow

results in decreased iron stores and iron bindingcapacity


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Hemolytic Anemia

Occurs at any age, More common with aging

Hemolysis or premature destruction of RBC

May be associated with autoimmune antibodies, Hodgkin's

disease and non-Hodgkin's lymphoma, trauma, heart valves,

burns, exposure to toxic chemicals, drugs, sickle cell anemia Ibuprofen, l-dopa, penicillin, cephalosporin's, tetracycline's,

acetaminophen, ASA, PCE, hydralazine, HCTZ, insulin

Hemolysis stops when drug withdrawn

Folic Acid (need increased amount to increase RBCproduction)


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Aplastic Anemia-Rare More in young

Overall mortality > 50%

Bone marrow suppressed, decreased RBC,

Low reticulocyte count

Cause unknown or radiation or chemical

substance

Bone marrow transplant in patients over 65

usually not effective


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Macrocytic Anemias (hypoproliferative)

Pernicious and folate deficiency

MCV greater than 100

Most common cause of macrocytic anemia in

older person B12 or folate deficiency Unusually large size RBC

Defective DNA synthesis causes abnormally

large and thickened cells.


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Macrocytic Anemia: B-12 Deficiency

B-12 deficiency (pernicious anemia)

Lack of intrinsic factor

Gastrectomy, small bowel disease, H-pylori infection,

prolonged antacids, strict vegetarian diet Heavy alcohol ingestion

Cigarette smoking

Autoimmune disorders-particularly those effecting endocrine

B-12 injections

Neurologic deficits do not usually reverse, halts

Lifetime treatment d/t incurable


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Signs and symptoms of Pernicious

Anemia Develops slowly over 20-30 years

By the time seek medical attention, verysevere

Early signs Infections

Mood swings

GI/Cardiac/Kidney ailments Hgb 7-8g/dl develop classic signs of anemia

Weakness, fatigue, paraesthsia of feet and fingers,

weight loss, sore mouth, beefy red tongue, difficultywalking, abdominal pain


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Macrocytic anemia: Folate Deficiency

Folate deficiency

Malabsorption syndromes, poor nutrition, alcoholism,

malignancies

Folate essential for RBC/DNA synthesis in theerythrocyte

Humans are totally dependent on nutritional intake

Occurs more than B-12 deficiency particularly in

alcoholics Malnourished especially fad diets or diets that limits

vegetables


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Macrocytic anemia:

Folic Acid

Symptoms

Scales and fissures in mouth

Stomatitis Painful ulceration of the buccal mucosa and

tongue

Dysphagia

Flatulence

Water diarrhea


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Malignancies of the Blood


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Hematologic Malignancies

Immature lymphoid and myeloid cells are

over-produced with associated bone marrow

failure

Classified by

1. Cell of origin

2. Degree of differentiation


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Types of Leukemia

Acute Lymphocytic Leukemia-ALL

Chronic Lymphocytic Leukemia- CLL

Acute Myelogenous Leukemia-AML

Chronic Myelogenous Leukemia-CML


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Acute Myeloid Leukemia-AML

Unknown cause

Rarely occurs before age 40, peaks 67

Characterized by immature myeloblasts in thebone marrow

WBC may be low, normal or high

Prognosis depends on patient Develops as a secondary cancer,


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Symptoms of AML

What are the symptoms of AML?

Result from insufficient Blood cells

Fever and infection (neutropenia)

Fatigue and weakness (anemia)

Bleeding tendencies (thrombocytopenia)

Petechiae, bruising, massive blood loss

Painful enlarged liver or spleen (engorgement) Hyperplasia of gums

Bone pain (expansion of marrow)


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Diagnosis and Treatment

CBC

Decreased erythrocytes and plates

Leukocytes may be normal, high or low

Bone marrow aspiration-excessive immatureblast cells sitting in marrow

Classification (7 subgroups we will not cover)

Treatment-try to induce remission Aggressive-cytarabine

Elderly patients who cannot tolerate can take hydroxyurea (lower curerate/increased quality of life)

BMT use increasing (infused with donor cells to rescue marrow)


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Complications of Treatment

Tumor lysis syndrome (pg. 390 table)

Lysis of cells leads to intracellular contentsflooding the body.

Electrolyte imbalances Renal calculi

Renal failure

Prevention: pre-hydration, imbalances

Eradicating the bone marrow Complications of chemo listed in overview

powerpoint


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Nurses Role

Monitor for

Bleeding

Infection

Pain

End of Life issues


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Acute Lymphocytic Leukemia

(lymphoblastic)

Most common type

80% age 2-4

Will not cover in this class


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Chronic Leukemia

Progresses more slowly

Longer Life expectancy (depending on stage)

Cells better differentiated

25-40% of all leukemia's

Cause unknown

Link between Epstein Barr virus Predisposition in families


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Chronic Leukemia

Chronic Lymphocytic Leukemia

Chronic Myelogenous Leukemia


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Chronic Lymphoid Leukemia (CLL) disease ofthe older person (>72 usually)

Characterized by malignant transformation of

B cells

Proliferation of small abnormal lymphocytesin bone marrow, peripheral blood, and body

tissues Cells fail to develop into antibody producing

cells


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B symptoms

Fevers, night sweats, unintentional weight loss

and infections

Onset

Weak, fatigue and painful lymphadenopathy

Anemia

Thrombocytopenia (depending on stage)

Enlarged spleen

Elevated WBC 20-100, 000


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Diagnosis and Treatment of Chronic

Lymphocytic Leukemia

Bone marrow

Treatment not started until symptoms appear/severe

Treatment: Not curable only induce periods of remission

combination therapy (prolonged suppression)

Radiation to thymus, spleen or entire body

Older person have a heightened risk of second malignancy with

radiation

5 remission in 70% of patients

As progresses need nutritional support, pain control, skin care

and emotional support


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Chronic Myelogenous Leukemia

Philadelphia chromosome a good diagnostic

marker is in 95% of patients*

Overproduction of abnormal myeloid/blast Uncontrolled proliferation of granulocytes

Causes bone marrow and organs to enlarge (pain)

Risk dramatically increases with age

If in chronic stage Life expectancy > 5 yrs.

No known cause except for ionizing radiation


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Symptoms of CML

May be asymptomatic and see leukocytosis Classic chronic symptoms

Fatigue, weakness, anorexia, weight loss, and

splenomegaly (more prominent and painful) Shortness of breath/confusion with very high

leukocyte counts

Lymphadenopathy generally not present

Liver enlarged but function not effected

Fever and adenopathy in blast stage

WBC 15,000-500,000 (blast phase)*


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Symptom Phases of CML

Symptom Stable Accelerated/t

ransformatio

n

Blast Crisis

Presence of

symptoms

None to

minimal

Moderate Pronounced

Splenomegaly Mild Increased Marked

WBC Slight

elevation

Erratic Very High

Differential 25% blasts


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CML moving through stages

How do we know?

May not

Bone pain, fevers (no signs of infection), weight

loss


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Treatment

Goal is to control the proliferation of

WBC/induce remission

Chemotherapy to suppress-in early stages Hydroxyurea

Busulfan

Imatinib(gleevac)

Blast Phase-aggressive

Prognosis 2-4 months

Anthracyclines

Cytosine Arabinoside


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CML treatment continued

Bone marrow transplants-sibling donor

successful if early is disease, under 50, and in

good health

Can potentially be cured with BMT

Decreasing leukocytes in blast phase

Leukophoresis: for Leukocytes > 300,000 can be lifethreatening. (temporary)

Anthracycline chemotherapy when non-emergent


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Nursing Care of Patients with

Leukemia

Know potential effects of leukemia and of

treatments and assess

Manage mucositis (chapter 16) Control pain and discomfort

Risk of dehydration

Weakness and fatigue Rest between activities

Assist with self-care

Anxiety/Grief


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Lymphomas

Neoplastic tumor affecting lymphoid tissue

Hodgkins

Non-Hodgkins


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Hodgkins Lymphoma

Peaks 20s and over the age of 50

More common in immunosuppressed patients

Agent Orange

Possible link to EBV

5 subgroups we will not cover each

Characterized by:

Progression from one group of lymph nodes to another*

Development of systemic symptoms

Presence of the Reed-Stenberg cell(malignant lymph cell)*


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Symptoms of Hodgkins lymphoma First sign often enlarged cervical node

The lymphadenopathy moves to axillary, inguinal, retroperitoneal Presents with one or more enlarged, painless lymph nodes

Symptoms from pressure of lymph nodes

Asymptomatic, painless mediastinal mass on chest x-ray

Organ symptoms from compression by tumor

B symptoms: fever (without chills), Night sweats, weight loss Fatigue

Pruiritus

Early mild Anemia, then worsen and if accompanied by weight loss, poor

prognosis

Increased sedimentation rate, leukocytosis, eosinophilia, leukopenia(advanced), platelet count normal

Impaired cellular immunity so decreased response to skin testing


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Diagnosis of Hodgkins lymphoma

Because painless can go many years without

diagnosis

Lymph node biopsy PET*

CT

CXR Classification


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Treatment of Hodgkins lymphoma

`Depends on staging

`Stage I Radiotherapy

Cure Rate of 80%

`Stage II Radiotherapy

`Stage III-IV Combination Chemotherapy

Radiotherapy

80% can be put in remission

High rate of toxicity


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Non-Hodgkins Lymphoma`

Rate has doubled since 1970 possibly d/t immune deficiencies (5

th

mostcommon type of cancer)

` Median age 67

` Begin with one node and spread throughout body, to bone, CNS, and GI tract

` Lymphoid tissue replaced with disease cells resulting in infection and immunedeficiency

` Prognosis for older adult poorer than with Hodgkins lymphoma` Success of Treatment depends on stage, with aggressive treatment can

achieve remission

` Cause links to

Impaired immune system (immunosuppression)

Phenytoin use

Prior treatment for cancer

EBV/HIV

Chemical exposure


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Non-Hodgkins Lymphoma

Diagnosed through lymph node biopsy

PET scans*

Staged based on nodular or diffuse cytology Stage does not necessarily predict prognosis

See text for prognosis classification


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Non-Hodgkins Lymphoma-symptoms

B complex symptoms

Non-tender peripheral lymphadenopathy

May have moderately enlarged liver andspleen


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Non-Hodgkins Lymphoma

Treatment (can be cured)

Incidence of secondary cancer high

Depends on staging

Radiotherapy/chemotherapy

Treat when symptoms appear

BMT can be used in those under the age of 60.


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Multiple Myeloma

5 year survival for newly diagnosed patients

33%


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Presentation of Multiple Myeloma

Infiltrates bone marrow and aggregates into

tumor masses in skeletal system

Most common presentation is bone pain

Bone lesions

Caused by destruction of bone tissue

Increased calcium from re-absorption of bone by

osteoclasts

Renal failure secondary to hypercalcemia

Anemia d/t inhibited erythropoiesis


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Symptoms of Multiple Myeloma

Pathological fractures

Back pain/ribs* usually presenting symptom

Vertebrae

Skull

Pelvis Femur

Clavicle

scapula

10% have spinal cord compression

Repeated infection from suppressed humoral response

(pneumonia/pyelonephritis)

Fever

Weight loss

Night sweats

Breakdown of bone can lead to renal failure


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Diagnosis of Multiple Myeloma

Diagnosis by blood test

Sudden spike in protein (blood/urine)

End organ damage

C: elevated calcium

R: renal insufficiency

A: anemia

B: Bone lesion

Bone marrow aspiration

x-ray

Nuclear bone scan


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Treatment of Multiple Myeloma

Prognosis is poor (no cure)

Treatment

Chemo used to treat intermediate and high grade Radiation

Plasmapheresis-when blood viscosity high


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Treatment of Multiple Myeloma

Difficult with older adult with comorbidities

6-8 months of aggressive treatment

May need help with Pain control

ADL

Nutrition

Symptom control

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