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Ms Finals

ms finals

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jessie marietan
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0% found this document useful (0 votes)
35 views9 pages

Ms Finals

ms finals

Uploaded by

jessie marietan
Copyright
© © All Rights Reserved
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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 hntpsdocs. google.com/documentio!1H48n.Noh47N-kFKGTaFewéZeqVnPBH2Flot 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 ane Note: 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 hntpsdocs. google.com/documentio!1H48n.Noh47N-kFKGTaFewéZeqVnPBH2Flot ‘© 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 hntpsdocs. google.com/documentio!1H48n.Noh47N-kFKGTaFewéZeqVnPBH2Flot 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

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