Lymph node enlargment in regards Hodgkin's Lymphoma

painless
(per prep U)

Interventions to prevent renal complications from chemotherapy for AML

hydration
allopurinol (prevent uric acid stones)
rasburicase (decrease uric acid)
*per Prep U

Recovery from induction therapy is indicated by:

neutrophil and platelet counts have returned to normal and patient is free from infection
*Prep U

Important goals after induction therapy:

-maintain nutrition (induction can cause severe diarrhea leading F&E imbalance)
*Prep U

Myeloid stem cells

responsible for haematopoiesis of RBCs and platelets
*Prep U

only curative treatment for chronic myeloid leukemia

Allogeneic stem cell transplant
*Prep U

Leukopenia

general reduction in all WBCs
*Prep U

Classic symptoms of multiple myeloma

Bone pain usually in back or ribs
*prep u

Small shaped hemoglobin molecules is related to which deficiency

Iron
*Prep U

Major function of neutrophils

phagocytosis
*prep u

AML treatment

-Induction, Consolidation, Maintenance
-Hematopoietic stem cell transplant HSCT (aggressive treatment)
-supportive therapy

Risk Factors for Leukemia

-previous cancer treatment (chemo and radiation)
- Genetic disorder (Downs)
-chemical exposure
-Smoking (Especially AML)
-Family history
*lecture

Leukemia Pathophysiology

Bone marrow becomes overcrowded with immature NON FUNCTIONING cells
Therefore production of RBCs is greatly reduced
The immature cells do not provide protection from infection
*lecture

leukemia is classified by

-Cell type (cell they attack)
Further classified by acute or chronic

Acute Myelogenous Leukemia

-Most common form
-Acute onset
-Affects myeloid cells in body
-Can be fatel if note treated quickly
-starts in bone marrow and can progress to lymph nodes, spleen, testes, CANS, and liver

AML clinical manifestations

-Developes without warning over a few weeks
-fever
-infection
-weakness
-fatigue
-dyspnea on exertion
-pallor (dt anemia)
-petechia, ecchymosis, and bleeding tendencies (r/t⬇️ Platelets)
-Pain

AML labs/diagnostics

-⬇️ erythrocytes
-platelets (⬆️ risk for bleeding)
-leukocyte count can be L WNL or H)
- excess immature blast cells in bone marrow

Induction

1st step:
- intense chemo
-starts at Dx
Goal: complete and rapid remission

Consolidation

Maintenance

3rd step (AML Tx)
-usually an milder chemo
-can last 2-5 years
Goal: prevent reocurrance

Induction, consolidation, maintenance
S/e

- severe bone marrow suppression
(neutropenia/ risk for infection)
-alopecia
-stomatitis
-GI s/sx (diarrhea)
-kidney, liver, and cardiac toxicity

5 phases of HSCT

obtainment
conditioning
transplant
engraftment
post- transplant recovery

Autologous

self

Syngeneic

identical twin

Allogeneic

sibling, unrelated, or umbilical cord

purpose if conditioning

myeloablation: wiping out of of patients own bone marrow

Conditioning

-give higher than normal doses of chemo or radiation
( to rid body if ALL cancer cells)

S/e of HSCT

-raise BP (give antihypertensives)
-throw off fluid balance and cause fluid retention (give diuretics)

how can chemotherapy be administered

only be put through Central lines or ports

transplant stage (HSCT)

3rd stage
stem cells infused

engraftment HCST

4th stage
-successful take of transplant
-may take 8 to 28 days

assessment of successful engraftment
HCST

-rbc's wbc's and platelets start to rise

recovery phase HCST

5th stage
goal: so we can prevent complications including infection bleeding failure to engraft and graft-versus-host disease

failure to engraft

stem cells don't take hold
-another transplant can be done otherwise patient will die

graft-versus-host disease

-donated sell sees patient transplant as foreign cells and attacks
-usually occurs with allergenic transplants

medications given to prevent transplant rejection

methotrexate
cyclosporine
corticosteroids

nursing goals for AML

minimize injury
conserve energy
prevent infection
prevent bleeding

hydroxyurea

controls increased number of blast cells

hemorrhage

increased risk when patient platelet level drops below 10,000

chronic myeloid leukemia

-mutation in the myeloid stem cell
-uncommon and people younger than 20 years
-risk increases with age

three stages of chronic myeloid leukemia

-chronic
-transformation
- accelerated or blast crisis

chronic myeloid leukemia
clinical manifestations

-usually asymptomatic (may not be found until seen by provider for other reasons)

-leukocyte count greater than 100,000

-may also have sob, confusion, enlarged or tender spleen, enlarged or tender liver, malaise, anorexia and weight loss

CML treatment

Gleevac (imatinib)
hsct if less than 65 years of age

(higher rate of cure if given together during chronic phase)

Gleevac

-Target's abnormal tyrosine kinase proteins
useful in the chronic phase

-avoid grapefruit or grapefruit juice (effects absorption)

-can potentially cure

acute lymphocytic leukemia

-most common form and children
-ages 2 to 10 years
-poor prognosis with relapse
-effects lymphocytes

acute lymphocytic leukemia ALL
clinical manifestations

-pain secondary to enlarged spleen/liver
-bone pain
CNS disturbances (vomiting, headache, seizures, coma, vision alterations, cranial nerve palsies)

ALL
treatment

-chemotherapy
goal: complete remission
HSCT: relapses or less responsive ALL

chronic lymphocytic leukemia

-older adults

-slow-growth and asymptomatic

-can invade other body parts: lymph nodes, liver, and spleen

-can lead to autoimmune complications including idiopathic thrombocytopenia purpura

-increased risk for other cancers including bone lung and skin

chronic lymphocytic leukemia (CLL)
clinical manifestations

usually asymptomatic but may have:

-lymphocytosis
(increased lymphocyte counts however erythrocyte and platelets may be normal but as disease progresses they may decrease)

-enlarged lymph nodes
-splenomegaly
-frequent infections
- fever
- increased sweat
-unintentional weight loss

CLL
treatment

-watchful waiting (patients without symptoms)
-chemotherapy (fludarabine and cylophosphamide)
-monoclonal antibodies (alemtuzumab and rituximab)
-unclear if HSCT is helpful

lymphoma

-cancer of lymphoid tissue
-overgrowth of 1 type of leukocyte lymphocyte
-attacks mature cells
-two types:
Hodgkin's lymphoma and Non-Hodgkin's lymphoma

Lymphoma with high cure rate

Hodgkin's

10-15% of all childhood cancers

Hodgkin's lymphoma

Hodgkin's lymphoma
pathophysiology

Hodgkin's lymphoma
Stats

Hodgkin's lymphoma
clinical manifestations

Hodgkin's lymphoma
early sign

large painless lymph node especially in neck

Hodgkin's lymphoma
diagnosis

Hodgkin's lymphoma
labs

-Mild anemia (most common finding)
-elevated or decreased lymphocytes
-platelets WNL
-Elevated ESR
-Elevated serum copper

Hodgkin's lymphoma
stage 1

Hodgkin's lymphoma
stage 2

Hodgkin's lymphoma
stage 3

Hodgkin's lymphoma
stage 4

lymphangiography
teaching points

lymphangiography

inherited blood disorder (factor VIII, classic, type A)
No cure
causes bleeding

All ethnic groups

usually males

hemophilia teaching

avoid injury (contact sports, use electric razors, avoidance of meds/supplements that increase bleeding)
importantance of good nutrition
importance of good dental hygiene
s/sx of bleeding including GI

hemophilia treatment

Sickle Cell Crisis:

obstruction of vessels by clumped cells

- RBC destruction

- Acute chest pain

- fever

- cough

- increase RR

- hypoxia

Sickle Cell Crisis:

Vasoocclusive Crisis

- Pain (acute abdominal, hand/foot syndrome)

- Splenomegaly (congested with blood, infarction)

- Hemolytic crisis (anemia, jaundice)

- Stroke

- Kidney

-Ischemia

Sickle cell crisis

Nursing interventions

HOP

Hydration (and electrolytes)

Oxygen (including bed rest to decrease O2 needs)

Pain relief

Stage 1 and 2: short course of chemo and then targeted radiation

Stage 3 and 4:

Combination chemotherapy (ABVD)

adriamycin (doxorubicin)

blenoxane (bleomycin)

Velban (vinblastine)

DTIC (dacarbazine)

Non-Hodgkins Lymphoma

-Single lymph node, group, or organ such as spleen

-can spread to almost any part of body

-can start anywhere in body

-Does not have Reed-Sternberg cells

-usually older adults

Non-Hodgkins Lymphoma

Clinical manifestations

Swollen lymph nodes

fever

night sweats

extreme fatigue

unexplained weight loss

abdominal/back pain

Non Hodgkins Lymphoma

Diagnostics

Similar to Hodgkins

may examine CSF

Ann Arbor staging system

- more complex than hodgkins

looks for specific genetic markers

Treatment based on staging and patients ability to tolerate

chemo and radiation

WBC cancer involving plasma cells

Secrete cytokines

Rare under age 40

No Cure

Multiple Myeloma

Manifestations

-Bone pain (back and ribs)

-Hypercalcemia (breakdown of bone which releases Ca into blood)

- pathological fractures d/t weakened bones

-Renal Failure

-Weakness and fatigue

-Weight loss

Multiple Myeloma

Diagnosis-

-Serum protein electrophoresis (monoclonal proteins or M proteins AKA Bence Jones proteins)

- increased serum calcium

- uric acid

- creatinine

-X ray

-Bone marrow biopsy

Multiple myeloma

Teaching

S/sx of hypercalcemia

prevention of injury

Multiple myeloma

treatment

varies depending on disease process

monitoring (no cure - make comfortable)

Chemotherapy

Easier to control bleeding with pressure

- petechiae

- decreased production

- increased destruction

- increased consumption

Platelets <50,000

s/sx

-petechiae

-gingival bleeding

- bleeding after surgery

- excessive menstrual bleeding

Platelets <5,000

s/sx

-large risk for spontaneous bleeding and death

**immediate platelet transfusion, usually in ICU**

Hemophilia

Clinical manifestations

-Bleeding in joints - hemarthrosis (pain with movement, swelling, and limited movement)

- Children may be late to crawl/walk or stop

- hematuria

- GI bleeding

-mucous membrane bleeding

-intracranial bleeds

Hemophilia

Nursing

- risk for bleeding

- risk for injury (life style modifications - no contact sports etc...)

- Where ID bracelets

- Pad elbows and knees in children learning to crawl/walk

-protective equipment (i.e. when riding bike)

Disseminated Intravascular Coagulation

DIC

Not a disease but a sign of underlying disorder

may be life threatening

Altered hemostasis mechanism

causes massive clotting in microcirculation --> which leads to depletion of clotting factors --> which leads to bleeding

-sepsis

-trauma

-Cancer

-abrupto placenta

- toxins

-allergic reactions

related to tissue ischemia and bleeding

- oozing from IVs catheters and old incisions

- treat underlying cause

-correct tissue ischemia

- replace fluids

- maintain BP

- replace coag factors

-heparin (helps keep body from depleting coag factors)

risk DIC

nursing

-Be aware of patients at risk for DIC

-assess for s/sx and progression of thrombi and bleeding

-assess for progression to multiple organ dysfunction

-avoid things that increase risk for bleeding and risk for increased bleeding

- improve O2

Replace fluids

Platelets (D)

PT (I)

aPTT (I)

Fibrinogen (D)

D-dimer (I)