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‘© An acute or malignant disorder ofthe blood and bone
‘marrow This resulls i accumulations of dysfunctional
immature cells that ate the caused by loss of regulation of
coll divisions
‘© The uncontrolled replication ofthe hematofogic progenitor
cxlls involved inthe development of white blood cells, red
‘blood cells, and platelets
‘© May originate in any ofthe blood-forming organs,
including the bone marrow, lymphatie system, and spleen
© Ahtterogenous disease with various biologie and clinical
presentations that influence a persons response to therepy
© Atype of cancer that affects the blood and bone marzov,
Teading too the production of abnormal white blood cell
‘These sbaormal cells crowd out the healthy blood calls,
alfeting the body's ability to funetion properly.
‘© The clasifcation depends on which progenitor cel it
originated (Iymphoid or myeloid) and i further classified
as being cute o chronic on the bass of clinical
presentation and cell maturity
‘© Inthe acute phase, the malignancy oceurs during early cell
Aierentiation, resulting in rapid replication with blasts
‘© Inthe chronic phase, unregulated replication of
Aiterentiated cals occurs
‘© The four major classifications of leukemis:
(© Acute iymphocytic leukemia (ALL)
© Chronic lymphocytic leukemia (CLL)
© Acute myelogenous leukemia (AML)
(© Chronic myelogenous leukemia (CML)
2004 ~ estimated 33,440 new cases diagnosed
10x likelier to occur on adulthood than in childhood
(Overall ineidence: MF
More often in the older adult, with more than half the cases
‘occuring in the 6th decade
“Most common leukemias among adults: AML and CML.
‘© CML: seen more frequently in adults and accounting fora
small proportion of the overall leukemias
© ALL: makes up the smallest proportion of leukemias, and is
‘most frequently seen among pediatric patents
Genetics
Environmental exposures
Viral infections
Immunodeficiency
Children with Trisomy 21 are approximately 20x likelier to
develop leukemia than the general population
Children younger than 3 years of age likeliest to develop
rmegakaryoblastic subset of AML
Older children are likeliest 9 develop ALL
Siblings ate to- to fourfold greater tisk of AML
igh risk among ideotiea wins
Diagnostic and ionizing radiation
Cigarette smoke
lectromagnetc fields or high power lines
Alkylating agents is associated with secondary AMI.
Viruses ~T and B eal Iyraphoma
Immunodeficiency ~ high risk for lymphoma
TPoge
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Broom pe
‘The patient experiences symptoms within weeks to mouths
of the beginning of the acute malignant process
‘The most common symptoms and physical findings at
diagnosis
‘Anemia
Fever
‘Thrombocytopenia
Neutropenia
Pallor
Fatigue
Anorexia
Potechiae Bleedingiash
Infection
In addition, the patient may have extramedullary disease
and present with generalized or local lymphadenopathy ,
‘bone pain, bone fracture
Excamedullary disease:
CNS involvement vertigo, nausea, vomiting, papilledeme,
and blurted vision
Parotid gland infiltration
Hepatomegaly
‘Testicular Infiltration
Splenomegaly
‘Clinical manifestations st
an insidious onset
Fatigue
Exercise
Intolerance
Night sweats
‘Abnormal fullness secondary to splenomegaly
Infection secondary to hypogammaglobulinemia
to acute leukemia but have
Tae
came Pace
tine rane
oe ieee
ence ave
‘Sa
cos Sone ber
cron
seer
RATIONALE:
Systemic: due tothe decrease in WBC
Shortness of breath because of anemia (decrease of RBC
‘that caries 02 to the diferent pars ofthe body)
Easy bleeding and bruising because of thrombocytopenia
purplish patches or spots called petechial bleeding
‘Complete PE and history
‘CBC with platelets and differential count - peripheral
‘Chemistry panel
Bone marrow aspiration
Cytogenetic*molecular features
Flow cytometry
Immunophenotype
LAP (leukocyte alkaline phosphatase) scoring
‘Myelodysplastic syndrome
‘Acute myoloid leukamiaWHO
‘Chronic myeloproliferative diseases
‘Myelodysplastic/myelopeoliferatve diseases
‘Myelodysplastic syndromes
‘Aeute myeloid leokemias
aneNote: The WHO classification system puts afew diseases that show
characteristics of both mycloproliferative and myclodysplastic
conditions into a new, separate group
(amyeloprolifeativeimyelodysplastic diseases).
FAB
Chronic myclogenous leukemia (CML)
‘Agnogenie myeloid metaplasia with
rnyeloibrosis (MF)
{iopathic myelofibrosis)
Polyeythemia vera (PV)
sential thrombocythemia (ET)
wi
3
(CML Pht: #(9;22)(q934:g11), BCR/ABL
CChronie neutrophilic leacemia
CCronie eosinophilic leukeria/hypercosinaphili syndrome
Chronie idiopatie myelofibrosis,
Polyeythemia vera
Essential thrombocythemia
(AML) FAB.
wno
(MO: minimally differentiated
Mi: myeloblastic leukemia without maturation
M2: myeloblastic leukemia with maturation
MB: hypergranular promyelocytic leukemia
Mz myelomonocytic leukemia
“MAE: varlant, increase in marrow eosinophils
MS: monocytic leukemia
M6: erythroleukemia (Di Gugliclmo's disease)
AML with recurrent cytogenetic translocations
‘AML with multilineage dysplasia
AML with myelodysplastic syndrome, therapy elated
‘AML not otherwise categorized AML minimally
differentiated
AML without maturation
© AML with maturation
Acta myelomooncti ene
Acute mnocytinlukein
Acute erythroid leukemia
Acute megakaryocyte leukemia
Acute basophilic leukemia Acute panmyeloss with myelofibrosis
WHO classification:
1 Non-Hodgkin lymphoma
© Beell lymphoma
© Teell lymphoma
2. Hodgkin Iymphoma
‘© Nodular lymphoeyte-predominant
Hodgkins disease
Classical Tlodgkins disease
‘Nodular selerosis Hodgkins disease
Lymphocyte-rich classical Hodgkins disease
Mixed-cellularity Hodgkins disease
Lymphoeyte-depletion Hodgkins disease
Goat
|. Bradicate the malignaat clone
2, Allowing growth of normal hematopoiete cells
© ALL— treatment i divided into stages:
TPoge
| Induction
2. Consolidation
3, Maintenance
‘Based on the patient's prognostic factors, the
remission induction chemotherapy program
‘generally includes some if nat all ofthe following
drugs:
1. Cyclophosphamide
2. Vincristine
43. Dexamethasone or prednisone
4. Leasparaginase
5. Doxorubicin
‘© Some programs include high doses of methotrexate and
» It is measured by enzyme immunoassay .
‘© Typical treatment: unilateral oophorectomy or
salphingoophorectomy
TPoge
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‘© Debulking removes chemotherapy-resitant cells thus
increasing chemotherapy penetation
‘© Nodal metastases to pelvie and para-tortic nodes are
‘common if enlarged and should be resected if possible
‘© Malignant germ cell tumors (BEP) chemotherapy
© bleomycin
© etoposide
© cisplatin
‘Chemotherapy
paclitaxel (neuropathy alopecia, myelosuppression,
hypersensitivity, and bradyeardia)
Carboplatin (NIV, myelosuppression, constipation)
elton tar toy
Germ
‘Ovarian carcinoma Narsiag Management 0
‘© Sexual relations
© educate the patient about sexual relations
© explain that depression and heightened emotional
sonsitvity ae exposted because of upset
hormonal balances
‘© Exhibit interes, concems and willingness to listen to fears
‘+ Improving body image assesses how the patient feels about
undergoing a hysterectomy related to the nature of the
diagnosis
significant others’ religions belief, and prognosis
'* _Acknovledge pations concerns about the ability to have
hilren lose feminty and impact on
rosie NCR
'* Adenocarcinoma ofthe prostate isthe most common form
‘of eancer in men
‘# The increasing sizeof prostate and eancer compress the
‘urethra which eause decreased in UO or there's a dribbling
of urine
‘Accounts for 29% of cancer in the US
‘Typically a disease of men over age 50
Sereening is recommended to begin at age 40,
‘Uncommon in Asia
Age related
‘mostly on black than white
195% are adenocarcinoma
‘© Genetis, diet and lifestyle (till not clea)
‘© Diet: fatty foods has been implicated, those vich in
lycopene are suspected of preventing or delaying the
development
‘¢ Androgens play an important ole inthe development
‘¢ Most men who underwent TURP have incidental findings
‘of focal eancer and do not progress when followed up after
10 years
156© Oger men ate typically followed up
‘© Younger men with longer life expectancy may undergo
needle biopsy to look for additional cancer
Manifestation
‘© Rel. to urinary flow obstruction
© Urinary frequency, ec in caliber of ste of stream,
“diminished force, hesitaney, dribbling, nocturia and
overflow incontinence
© dysuria
© back orhip pain
PROSTATE CANCER
@ sx. Drs
Gis Cbusc.
oa
DRE
© PSA more thee 10 ngint
© Biopsy transrectal prostate biopsy under
sonography(TRUS)
Prostatic Specific Antigen
‘© PSA levels (most important test cutft point is dng/m,
‘transrectal needle biopsy imaging studies (to check for
imtasiatie osteoblastic carcinoma to the vertebrae)
1, 40:1049 years ~2.5 ngim!
2. 50:0 59 years—3.5 ngimt
3.60 10 69 years — 45 ng/ml
4. 70:0 79 years —6.5 ng/ml
—z
Note:
1, numbers 2 S shows the upper age-specific PSA reference ranges
b. For the test to be valid, there must be a least three PSA.
measurements available over a period of 1.5 to 2 years
«A man who has a significant rise, even though the latest serum
level may be below the normal cutoff (<4ng/ml) should undergo
additional work-up
TREATMENT) MANAGEMENT =
‘Surgery~ radical prostatectomy
‘© Antibiotic prophylaxis—quinolones and those that cover
anaerobic bacteria (during biopsy)
‘© Radiation like brachytherapy (both associated with
impotence)
© Cryotherapy:
© Chemotherapy for palliation
© Androgen deprivation- for those w/ metastatic disea
(leuporide, lutamide) hotflashes
RADICAL PROSTATECTOMY
After
TIT
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Postoperative effects of surgery:
[Risks of anesthesia
2. Postop bleeding
3. Impotence — teat with sildenafil (Viagra) tablets, alprostadil
(Caverject) injections into the penis, and devices lke penile
prosthesis
4. Incontinence
‘Nursing assessment
‘© History collection
‘© Physical examination egarding presenting urinary
problems, voiding functions, UTI, urinary retention,
© Dysuria
© Obsain family history
‘© Nutritional assessment and iestyle
166