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NSG 308 Adult Health
Cancers
| Question | Answer |
|---|---|
| Clinical manifestations of Laryngeal CA | - Hoarseness (2+ weeks) - Persistent cough - Sore throat/burning sensation - Lump in neck - Unilateral nasal obstruction - Unintentional weight loss |
| Diagnostics/Treatment for Laryngeal CA | Dx: Laryngoscopy w/ biopsy Tx: Surgery (laryngectomy with permanent tracheostomy) - Radiation - Chemotherapy |
| Diagnostic/Treatment for Lung CA | - CXR/CT Chest (imaging) - Bronchoscopy with biopsy (staging/IHC) - Surgery - Radiation/chemotherapy - Thoracotomy (if necessary) - Pre/post op nursing management |
| Laryngectomy | Surgical removal of the larynx (airflow change to mostly in tracheostomy opening) - Requires permanent tracheostomy - S/LP voice rehabilitation |
| Risk Factor for Laryngeal CA | - Carcinogens (smoke, EtOH, asbestos, paint fume, wood dust, industrial chemicals) - Nutritional deficiency - Genetic/Hereditary - Age (55+) - Male predisposition (5x likelihood) - African Americans + White Americans - Weakened immune system |
| Lung Cancer Classification | SCLC - 10-15% NSCLC - 80-85% |
| Lung CA risk factors | - Smoke/inhaled carcinogen exposure - Occupational/Environmental hazards - Genetic mutations |
| Clinical manifestations of Lung CA | - Cough or change in chronic cough - Dyspnea - Hemoptysis - Unintentional weight loss |
| Surgical treatment options for Lung CA | - Pneumonectomy (entire lung removal) - Lobectomy (removal of lung lobe(s)) - Segmentectomy (segmental resection) - Wedge resection (small pie shaped removal) |
| Leukemia Classifications | Unregulated proliferation of leukocytes from bone marrow characterized by persistent leukocytosis - Acute: abrupt onset w/ rapid progression and little room for normal cell production - Chronic: slower progression where majority of WBCs are mature Myeloid vs Lymphoid cell lines |
| Myeloid vs Lymphoid cells | Both are types of WBC cells developing in the bone marrow arising from HSC (hematopoietic stem cells) - Myeloid -> macrophage, monocytes, neutrophils, eosinophils etc. - Lymphoid -> B-cells, T- cells, NK-cells (lymphocytes) |
| Acute Myeloid Leukemia (AML) pathophysiology | Arise from mutation in myeloid HSC and develops abnormal blast cells Signs: Anemia, thrombocytopenia, abnormal WBC - Most common form of leukemia with median age 68 |
| Hematopoietic stem cells (HSC) | progenitor stem cells of WBC (both myeloid and lymphoid) |
| Risk factors for AML | Male gender Increasing age Chemical/radiation exposure Prior chemotherapy Smoking Genetic disorder/predisposition |
| Clinical Manifestations of AML | Neutropenia = fever/infection Anemia = pallor/fatigue/dyspnea Thrombocytopenia = Easy bruising/bleeding, petechiae |
| Diagnosis/Treatment for AML | Dx: CBC (decreased erythrocyte/platelets), >20% blast cells in bone marrow, cytogenetics, histology, morphology subtyping Tx: Chemotherapy (induction w/ cytarabine, then consolidation), allogeneic HSCT after chemo - Refractory (treatment resistant): targeted therapy and palliative care |
| Induction vs Consolidation in Chemotherapy | Induction: initial chemotherapy treatment to shrink tumor/force remission, short and intensive Consolidation: additional chemotherapy to maintain remission (kill/reduce all cancer response) |
| Allogeneic HSCT | hematopoietic stem cell transplantation (transplant healthy stem cells) |
| Complications of AML | - bleeding d/t thrombocytopenia (GI, lung, intracranial) - infection (bacterial vs fungal) - tumor lysis syndrome -> electrolyte imbalance |
| Tumor lysis syndrome | LIFE THREATENING destruction of tumor/cancer cells release toxic amount of electrolytes |
| AML nursing managements | - Administer blood product - Prompt treatment of infections - Granulocytic growth factor (for life threatening infections) - Monitor for adverse drug effect |
| Psychosocial support | - Addresses anxiety/grief with disease - Encourage verbalization and provide resources - Coordinate home care for catheter management |
| Patient education in cancer therapy | - Medication regimen compliance - Educate on side effects of medications - Teach about improved outcomes with medication/treatment adherence - Bleeding/infection precautions in non-hormonal treatments (eg. chemotherapy) |
| Chronic myeloid leukemia (CML) pathophysiology | D/t myeloid stem cell mutation - BCR-ABL gene (Philadelphia chromosome) results in excess leukocytes - marrow expands into long bones, liver, spleen - 15% of new leukemia cases S/S: Fatigue, anemia, splenomegaly, dyspnea, bone pain, fever, weight loss |
| Clinical phases of CML | Chronic: few symptoms with incidental leukocytosis Accelerated: worsening count and new chromosomal change Blast crisis: resembles AML, leukostasis |
| Leukostasis | life-threatening oncologic emergency extremely high white blood cell counts (hyperleukocytosis) cause the blood to thicken |
| Medical management for CML | - Tyrosine Kinase Inhibitors (TKI) - (eg. imatinib, dasatinib, nilotinib) - Allogeneic HSCT (potentially curative, age 65+) - Induction chemotherapy (for blast crisis) |
| Nursing management for CML | TKI side effect management - Fatigue, pruritis, rash, headache - Educate drug interactions and safe handling - Monitor for adherence - Provide psychosocial support |
| Acute Lymphocytic Leukemia (ALL) Pathophysiology | Uncontrolled proliferation of immature lymphoblasts - B-cell (75%) vs T-cell (25%) origin - BCR-ABL in 20% of blast cells S/S: hepatomegaly/splenomegaly, bone pain, cranial nerve palsies, headache, vomiting, extranodal manifestations in testes/breasts |
| Philadelphia Chromosome | BCR-ABL gene translocation, mutation for leukemias - Treatment involves tyrosine kinase inhibitors to block BCR-ABL gene - Mostly seen in CML, occasionally in ALL - Rare in other forms of leukemia |
| Extranodal | Spread of cancer cells (mostly refers to leukemia/lymphomas) that spread to other systems/sites |
| Treatment goals for ALL | Remission without excess toxicity Induction -> Consolidation -> Maintenance |
| Treatments for ALL | - intrathecal chemotherapy - chemotherapy injected into CSF (spine), bypass blood brain/barrier - Cranial irradiation for CNS - Allogeneic HSCT for high relapse risk - TKI if Philadelphia chromosome positive ALL |
| Tyrosine Kinase Inhibitors | - main treatment for BCR-ABL gene positive leukemias (most common in CML/ALL) |
| Chronic Lymphocytic Leukemia (CLL) Pathophysiology | Most common ADULT leukemia (age ~72, strong FHx link) - Malignant B-lymphocyte clone - Cells escape apoptosis and accumulate in marrow/circulation - Lymph node/spleen involvement (common) - Immunophenotyping/cytogenetics for Dx/prognosis S/S: asymptomatic, lymphocytosis, lymphadenopathy (can be severe/painful), splenomegaly |
| Treatments for CLL | - Watch/wait for asymptomatic - Immunotherapy + chemotherapy - TKI for TP53 mutation/deletion S/E: prolonged BMS (bone marrow suppression), infection risk |
| Lymphoma definition | Neoplasm of lymph - can involve spleen/GI/liver/marrow - Hodgekins (HL) vs Non-Hodgekins (NHL) |
| Lymphoma risk factors | - Viral (EBV, HIV, HHV8) - FHx - Immunosuppression - Cytotoxic agent exposure (Agent Orange - banned herbicide) |
| Hodgekin Lymphoma (HL) Pathophysiology | - Start in single lymph node and spread by extension along lymphatics - Reed-Sternberg Cell (hallmark) - Gigantic unique tumor cell of B-lymphocyte origin S/S: painless/firm cervical lymphadenopathy, mediastinal mass (dyspnea), mild anemia Advanced S/S: fever, night sweat, wt loss |
| Hodgekin Lymphoma (HL) Diagnosis | Excisional lymph node bx (Reed-Sternberg cells) - Imaging: CXR, CT, PET - BW: CBC, ESR, LFT, renal fn, HIV Ag, HBV Ag, HCV Ag |
| Hodgekin Lymphoma management | - Cure rate 90% - Early (I-II): Combo chemo w/ or w/o radiation therapy - Advanced (III-IV) + B Symptoms: ABVD w/ additional cycles, immunotherapy for refractory/relapse - NLPHL (early): radiation or observation, chemo/Immuno S/E: secondary malignancy, cardiovasc disease, hypothyroidism, infertility |
| B-Symptoms (Lymphoma) | End stage lymphoma symptoms, remember early stage = asymptomatic but can find abnormal WBC in blood |
| Multiple Myeloma Definition | cancer of plasma cells (mature B-lymphocytes) |
| Multiple Myeloma Pathophysiology | - incurable, slowly progressing disease - cancerous plasma cells have nonfunctional M-protein - Bone destruction via osteoclast activation - MGUS precancerous - CRAB features |
| CRAB features | - multiple myeloma - hyperCalcemia | Renal dysfunction | Anemia | Bone destruction |
| Multiple Myeloma Diagnosis | - BW: CBC, BUN/Cr, Ca2+, albumin, LDH - serum protein electrophoresis (M protein) - Bone marrow bx - Skeletal imaging: CT, MRI, PET - B-2 microglobulin (indicate progression) |
| Multiple Myeloma Complications | - infection (low Ig) - hyperviscosity syndrome - Spinal cord compression - peripheral neuropathy (75%) - VTE risk (d/t corticosteroid) |
| Multiple Myeloma treatment | - Uncurable = symptom reduction - Smoldering MM = surveillance - Autologous (from self) HSCT - immunotherapy (Bortezomib/daratumumab) - Advanced = CAR-T, BCMA targeted therapy |
| Smoldering Multiple Myeloma | - Asymptomatic multiple myeloma - Surveillance Q3-6 months |
| BCMA/CAR-T | - B-Cell Maturation Ag, tells own immune system to target malignant plasma cells - Chimeric Antigen Receptor T-Cell therapy, similarly alters immune function to hunt down cancerous cells |
| Multiple Myeloma Nursing Management | - NSAIDs and opioids - monitor for hypercalcemia/renal function - Educate infection prevention - Fracture precautions and mobility maintenance |
| Colorectal CA Risk factors | - FHx - Sedentary lifestyle, obesity, poor diet - Lynch Syndrome - Familial adenomatous polyposis (FAP) - Male/older individuals |
| Colorectal CA pathophysiology | - APC gene mutation -> polyp formation -> invasive cancer - Common metastatic sites: Liver, peritoneum, lungs S/S: alter BMs, melena/rectal bleed, anemia, wt loss, fatigue S/S (R sided): dull pain, melena S/S (L sided): obstruction symptom, hematochezia S/S (Rectal): Tenesmus, incomplete evacuation |
| Colorectal CA modifiable factors | - Smoking/EtOH cessation - Maintain healthy weight/increase activity - Dietary modification (increased fiber, less red meat/processed foods) |
| Colorectal CA Screening/Diagnosis | - ASC recommend start at 45, USPSTF at 50 - Colonoscopy (Gold standard) - Labs: CBC, CEA, LFTs - CT Abd/Pelvis/Chest for staging |
| Colorectal CA complications | - Bowel obstruction/Perforation risk - Hemorrhage => surgical resection/ostomy |
| Colorectal CA Surgical Treatment | Goal: tumor removal w/ clean margin - Lap excision - Segmental resection w/ anastamosis - Abdominoperineal resection (perma colostomy) - J-pouch construction |
| ERAS pathway | protocol for surgeries to optimize patient outcome and shorten length of stay |
| Colorectal CA Treatment | Adjuvant therapy determined by stage Stage 0/I: no chemo/radiation Stage II: capecitabine if MMR-P mutation Stage III: FOLFOX Stage IV: individualized w/ or w/o targeted therapy F/U with CEA/CT/Colonoscopy |
| Bladder CA Risk Factor | - Smoking - Occupational exposure to aromatic amine (dyes/rubber) - Chronic UTI/Recurrent stone or Hx pelvic radiation - FHx - Advanced age, males |
| Bladder CA pathophysiology | - Common metastatic site: liver, bone, lungs - Often urothelial (transitional cell carcinoma) S/S: painless gross hematuria (hallmark), urinary frequency/urgency, recurrent UTI symptom, dysuria, altered urine color/odor, - S/S (advanced): Pelvic/back pain (suggest metastasis), weight loss, fatigue |
| Bladder CA diagnosis | - Cystoscopy w/ bx (Gold Standard) - Urine cytology + tumor market - Imaging: CT/MRI/US for staging/metastasis - Cystography/excretory urography - Bimanual exam |
| Bladder CA complications | - hydronephrosis d/t ureteral obstruction - bleeding = anemia |
| Bladder CA screening | - no routine screening indicated in gen pop - Annual urinalysis for high risk population (eg. occupational exposure) - Lifelong cystoscopy after curative tx |
| Bladder CA Treatment | - Transurethral resection (TURBT - first line) of papillomas - fulguration (cauterization) of papillomas - radical cystectomy (for invasive disease) - Pelvic lymph node dissection - Ileal conduit (urostomy - common) - continent reservoir/orthotopic bladder |
| Bladder CA Post op Nursing Care | - Stoma care/skin integrity - I/O - sexuality counseling/emotional support |
| MVAC | - methotrexate - vinblastine - Doxorubicin - Cisplatin Standard regimen to shrink/kill tumors SE: Nausea, neutropenia, nephrotoxicity |
| Intravesical Therapy | Bladder CA tx - Instillation to bladder via catheter Agents: BCG, thiotepa, mitomycin, doxorubicin |
| Bladder CA chemotherapy | - MVAC - 5-FU - IV chemo + radiation combo |
| Bladder CA radiation therapy | - indicated with spread and advance disease in inoperable tumors - relieve pain/bleeding in palliative care |
| Cervical CA Types | - Squamous cell carcinoma (most common) - Adenocarcinoma (HPV related) - Mixed adenosquamous carcinoma |
| Cervical CA prevention | - Pelvic exam/Pap smear - HPV vaccination - Smoking cessation - Safe sex practice |
| Ovarian CA pathophysiology | - increase incidence w/ age - S/S: bloating, pelvic pressure, urinary urgency |
| Ovarian CA risk factors | - FHx (most significant) - increase age |
| Uterine CA Risk factors | - Obesity - Estrogen exposure - Nulliparity (not having given birth/failed birth) - Diabetes |
| Gynecological CA Surgical treatment | - Hysterectomy/Oophorectomy (TAH+BSO) - Subtotal/supracervical (uterus only) - Radical = uterus + surrounding tissue + lymph nodes Post op risk: infection, bleeding, voiding issue |
| Gynecological CA radiation therapy | - EBRT - Intraoperative radiation (IORT) - intracavitary brachytherapy |
| Breast CA risk factors | - BRCA 1/2 mutations - Obesity/Sedentary - EtOH/Smoking - Late life weight gain |
| Tanner stages (for breast development) | Stage 1: Prepuberty Stage 2: breast budding (First sign) Stage 3: Tissue/areola enlargement Stage 4: nipple/areola form secondary mound Stage 5: Adult contour |
| Breast CA High risk prevention | - Long term surveillance - Chemoprevention (eg. Anastrazole) - Prophylactic mastectomy |
| Breast CA manifestations | - upper outer quadrant most common - Signs: Nontender, fixed, hard lesion w/ irregular border - Advanced Signs: Skin dimpling, nipple retraction, ulceration |
| Breast CA diagnosis | - Mammogram/US - CXR, CT, MRI, PET, bone scans - Staging w/ TNM |
| Breast CA treatment | - Surgical: Mastectomy (total vs modified radical) w/ SLNB - Radiation therapy after surgical tx for 5 days x 5-6 weeks S/E: erythema, edema, fatigue - Chemo - Hormone therapy (eg. tamoxifen) - Targeted therapy |
| Breast CA nursing management | - drain management - Arm exercise + lymphedema monitoring - Psychosocial support/body image - Infection/seroma monitoring |
| Seroma | pocket of clear fluid that forms under skin commonly after surgery |
| Male Breast CA pathophysiology | - Risk factor: BRCA mutation, Klinefelter syndrome (XXY male), radiation, high estrogen - Tx: Total mastectomy + SNLB, Tamoxifen |
| Prostate CA pathophysiology | - DHT = hormone mediating prostate growth S/S: early BPH symptoms, azotemia (high urine nitrogen -> cause renal failure), hydroureter, hydronephrosis, UTI |
| Prostate CA Diagnosis | - Digital rectal exam (enlarged prostate) - Labs: U/A, PSA - Pelvic US w/ postvoid residual - Bone imaging, MRI, pelvic CT |
| Actinic Keratosis | - Precursor to squamous cell carcinoma (more aggressive skin CA) |
| Mohs Surgery | conserve normal tissue for skin CA - shave tumor layer by layer until clear margins - high cure rate |
| Basal cell carcinoma | - Most common skin CA - small waxy nodule with rolled translucent borders - Recurrence common (face, neck, scalp) - Tx with Mohs surgery |
| Squamous cell carcinoma | - more aggressive than basal cell carcinoma - Can metastasize - rough thickened scaly tumor - Actinic keratosis precursor |
| Skin CA treatment | - Mohs surgery - Radiation, topical 5-FU - F/U exam Q3 months for 1 year |
Created by:
sleepingbear