Download MSN 277 EXAM 2 REVIEW UPDATED 2023 and more Exams Nursing in PDF only on Docsity!

MSN 277 EXAM 2 REVIEW

MODULE 7

Genetics and Genomics Quick facts: Genes – basic unit of heredity

• Controls how cells in body function
• Produce proteins that perform only 1 specific function
• Composed of sequences of DNA – found along a person’s chromosomes
• Passed from one generation to next Genome – complete set of DNA
• Contains all of organism’s gene
• Has info for organism to build and maintain itself Genetics – the study of genes and their role in inheritance
• Determines how certain traits or conditions pass from one generation to the next through genes
• A person’s genes can have profound impact on health and disease – more than 4k disease believed to be related to altered genes Genomics – the study of a person’s genes
• Determines how genes interact w/ other genes
• Determines how genes interact w/ the person’s environment
• Studies complex diseases – typically caused by combination of genetic and environmental factors rather than 1 single gene alteration
• Helps us understand why disparities exist o Ex: person A eats healthy and exercises but dies at young age and person B eats unhealthy and never exercises but lives to old age  based on person’s genes The Basics of Genetics Genes – approx. 30k genes in each person’s genome
• Has specific location on chromosome
• Controls how cells function – growth, cell division, longevity, etc.
• Correct code is essential  proteins are made correctly, functions perform properly Alleles – possible form of a gene

1. Dominant – if heterozygous for trait (possess both alleles “Bb”)  dominant is expressed
2. Recessive – not expressed if dominant allele is present Phenotype – physical traits a person expresses – height, eye/hair color, etc. Genotype – genetic make up of a person – comprised of all genes inherited from each parent Chromosomes – hangout inside cell’s nucleus – occur in pairs

• Each cell contains 23 pairs

• 1 st^22 pairs = autosomes – same in both sex
• 23 rd^ pair = sex chromosome – male determines sex of baby
• XX = female, XY = male Deoxyribonucleic acid (DNA) – molecule that contains our unique genetic code – “recipe book”
• Genes are made up of DNA – stores genetic info Genetic Mutations – permanent change or alteration in DNA sequence
• Range in size
• Can affect single DNA block up to large segment of chromosome
• Can result in development of disease in person
• Can result in  risk of disease 2 types of mutations:

1. Germline mutations – inherited from parent

• Sickle cell anemia, cystic fibrosis

2. Acquired (somatic) mutations – changes that occur in DNA at any point in life

• Cannot be passed on to next generation
• Mistake made as DNA is replicating during cell division or environment factor alters DNA o Ex: not wearing sunscreen  skin cancer o Ex: smoking  lung cancer o Ex: chemotherapy  leukemia or lymphoma Inheritance Patterns – describes how disease is transmitted in families 4 types of patterns:

1. Autosomal dominant – only 1 copy of disease allele is necessary for individual to be susceptible to expressing phenotype

• 50% chance of inheritance o Ex: breast cancer, ovarian cancer, Huntington’s disease, Marfan syndrome

2. Autosomal recessive – 2 copy of disease required to be susceptible to expressing phenotype

• Parents are gene carriers
• 25% chance of 2 alleles or none
• 50% chance of 1 allele o Ex: cystic fibrosis, sickle cell disease, Tay-Sachs disease

3. X-Linked – only 1 copy of disease allele required

• Both males and females affected
• Males more severely affected o Ex: Duchenne muscular dystrophy, hemophilia

4. Y-Linked – only on Y chromosome

• Only males affected o Ex: infertility

Genetic Screening and Testing Genetic screening – 1st^ level of detection  at risk but no symptoms or family Hx Genetic testing – focused on individuals and families for specific reason  show  risk, has symptoms or family Hx Genetic Information Nondiscrimination Act (GINA) – federal law that protects individuals’ discrimination w/ health insurance and employment

• Illegal for insurance companies to request or require or use genetic info to make decision about eligibility for health insurance Direct-to-consumer testing – genetic tests marketed directly to consumers through advertisement Genetic technology – moving at fast pace  finger print testing Pharmacogenomics and Pharmacogenetics Because everyone has different genetic make up, different people have different reactions to drugs Pharmacogenomics – the study of genetic variation associated w/ drug response in multiple genes Pharmacogenetics – the study of genetic variability drug responses related to variations in single gene Future: tailor-made drugs – development of drugs made to adapt to each individual person’s genetic make up (personalized medication) Gene Therapy – replaces faulty gene or adds new gene in attempt to cure disease or improve body’s ability to fight disease
• Experimental therapy only used in pt who have disease where there is no cure  lethal or disabling disease caused by single gene deficiency
• Does not prevent passing mutation to offspring
• In U.S., currently only available as clinical trial 3 focus areas:

1. Replacing – if gene is not doing its proper action
2. Inactivating – turn off gene so no longer promote disease
3. Introducing – making disease more evident to immune system because system does not recognize disease cells Stem Cell Therapy Stem cell – cells from which all other cells with specialized functions are generated  can divide to form more cells called daughter cells  new stem cells or specialized cells

• Function is to regenerate lost tissue and restore function
• Ability to remain unspecialized or differentiate Derived from:

1. Embryo – “pluripotent stem cells”, early stage of development (3-5 days old blastocyst – made of approx. 150 cells total)

• Used to regenerate or repair tissue in damaged/diseased organs

2. Adult – found in small # in bone marrow or fat

• More limited in developing into various cells
• May not be as versatile or durable as embryonic stem cells  had more exposure to toxin/damages MODULE 8 Hematologic Problems Quick facts: Hematology – the study of blood and blood forming tissues
• Bone marrow
• Blood
• Spleen
• Lymphatic system Hematologic system:
• Helps transport O2 and CO
• Maintains intravascular volume  coagulation
• Helps fight infection 3 main hematologic problems:

1. Anemia
2. Thrombocytopenia
3. Neutropenia Anemia – tissues become hypoxic because they are not getting the O2 they need A deficiency in:

• of erythrocytes (RBC)  carries Hgb

• quantity or quality of hemoglobin (Hgb)  Fe-rich protein that attaches to lungs and carries O2 throughout body
• volume of packed RBC (hematocrit) 3 causes of Anemia:

1.  RBC production
2. Blood loss
3.  RBC destruction Diagnosis based on:
4. Complete blood count (CBC) – measures all cells that make up blood (RBC, WBC, platelets)
5. Peripheral blood smear – looks at morphology (shape and appearance of RBC)
6. Reticulocyte count – measures how fast reticulocytes (RBC) are made by bone marrow and released into blood Classified by morphology: “cytic” = size “chromic” = content (high or low)

• Normocytic, microcytic, macrocytic
• Normochromic, hypochromic, hyperchromic

Anemia Clinical Manifestations Hgb – best way to determine severity of anemia Mild:

• Hgb 10-12 g/dL
• Asymptomatic or palpitations, dyspnea, mild fatigue w/ exertion Moderate:
• Hgb 6-10 g/dL
•  cardiopulmonary symptoms, occurs at rest and w/ activity Severe:
• Hgb <6 g/dL
• Many manifestations involving many body systems Anemia: Integumentary Manifestations Anemia – most evident in people’s skin

1. Pallor – paleness caused by  Hgb R/T  BF to skin
2. Jaundice – yellowing of skin or whites of eyes caused by body not processing bilirubin properly, destroyed RBC =  bilirubin settling in skin
3. Pruritus – itching R/T  serum skin bile salt concentration Iron Deficiency Anemia Most common nutritional disorder in world Fe – essential to make RBC and is needed for Hgb synthesis Hgb – essential for transporting O2 in blood from lungs to tissues Most susceptible:

• Very young
• Poor diet
• Women in reproductive yr Iron Deficiency Anemia Etiologies
• Inadequate dietary intake – women who are menstruating or pregnant need more level of Fe
• Malabsorption – occurs after GI surgeries  malabsorption syndrome – small intestine can’t absorb nutrients or fluids
• Blood loss – major cause in adults o GI bleed (acute/chronic) ▪ Gastritis ▪ Peptic ulcer ▪ Esophagitis ▪ Hemorrhoids ▪ Tumor o GU bleed ▪ Menstrual bleeding – avg 45 mL of blood loss o Melena (dark/black stool)

▪ Avg 50-75 mL of blood loss Iron Deficiency Anemia Clinical Manifestations 3 main manifestations:

1. Pallor
2. Glossitis – inflammation of tongue
3. Cheilitis – inflammation of lips and mouth Iron Deficiency Anemia Diagnostic Studies

• Labs – any that will help indicate problem w/ RBC or Fe levels (Hgb, Hct, RBC, serum Fe, Total Iron Binding Capacity (TIBC), bilirubin, platelets
• Fecal occult blood test – smear stool on lab plate
• Endoscopy/colonoscopy – suspects GI bleed
• Bone marrow biopsy – done if other tests are inconclusive Iron Deficiency Anemia Nursing Management Goal – to treat underlying problem first! Determine what is causing the anemia  not enough Fe but WHY? (absorption, alcoholism, malnutrition?) Replace Fe:
• Nutritional therapy – incorporate foods rich in Fe
• Fe supplements – if diet already has sufficient Fe intake o Expected finding – constipation, GI upset, very dark stools
• Blood transfusion – if anemia was caused by acute blood loss Anemia of Chronic Disease – anemia that is associated w/ inflammatory process in body  underproduction of RBC 2 nd^ most common among hospitalized pt Occurs 1-2 mos after disease activity Cytokines are released   reuptake/retention of Fe by macrophages in liver  Fe taken out of circulatory system and put into storage site in liver   availability of Fe for erythropoiesis  shorter RBC life span Disease findings:
• High serum ferritin levels   Fe stores caused by macrophages in liver “kidnapping” Fe and storing them Treatment:
• Treat underlying cause
• Blood transfusion – for severe cases, not recommended long term due to Fe build up
• Epoetin-Alfa – SQ injection that acts like erythropoietin, helps body create more RBC   Hgb levels Aplastic Anemia – condition where body stops producing enough new blood cells In aplastic anemia – stem cells are damaged leaving bone marrow aplastic (empty) or containing few blood cells (hypoplastic)

• Pancytopenia -  in all blood cell types w/ no set pattern o WBC   risk of infection o RBC  fatigue, SOB, tiredness, pallor o Platelets  uncontrolled/excessive bleeding Aplastic Anemia Etiologies Rare disease – 2-5 new cases/million/yr Majority of cases are autoimmune – insufficient bone marrow is replaced w/ fat May be acquired – triggered by infection or environmental factors Aplastic Anemia Clinical Manifestations 3 main manifestations:

1. Anemia
2. Neutropenia -  WBC count
3. Thrombocytopenia -  platelet count Aplastic Anemia Diagnostic Studies

• Confirmed by labs o  WBC, RBC, platelets, Hgb, Hct o  Fe, TIBC
• Bone marrow biopsy – gold standard o  yellow marrow (fat) inside bone Aplastic Anemia Nursing Management
• Identify and remove cause
• Provide supportive care until pancytopenia reverse – transfusion support, monitor labs, pt teaching to  infection risk
• Prevent complications from infection and hemorrhage – maintain safety due to  fall risk
• Prognosis of severe untreated aplastic anemia is poor – transplant for pt younger than 55 yr Anemia caused by Acute Blood Loss – result of sudden hemorrhage, secondary to trauma, complications of surgery, or disease/conditions that disrupt total blood volume 2 main concerns:

1. Hypovolemic shock -  in total blood volume
2. Compensatory  plasma volume – helps body maintain overall blood volume but content is different due to # of RBC significantly  caused by more plasma than RBC Acute Blood Loss Anemia Clinical Manifestations

• Pain o Internal bleeding caused by tissue distention or organ displacement

o From nerve compression

• Shock Acute Blood Loss Anemia Diagnostic Studies
• Lab values may seem normal or high for 2-3 days – loss of RBC not reflected in blood draws due to blood being lost too quickly  plasma has not had a chance to regenerate
• Once plasma is replaced  low RBC, Hgb, Hct is evident Acute Blood Loss Anemia Nursing Management
• #1 priority – Replace blood volume to prevent shock – infuse IV fluids to keep fluid in vascular system to maintain blood volume
• Identify source of hemorrhage and stop blood loss – apply pressure to site, get pt to OR to surgically repair site or find where bleeding is occurring
• Blood transfusion – to  RBC levels
• Supplemental Fe Thrombocytopenia –  platelet count caused by separate disorder or disease Quick facts: Platelet count <150,000/uL – normal range 150- 450k Platelet life span 8-10 days Results in abnormal hemostasis Most cases are acquired 3 types of thrombocytopenia:

1. Immune thrombocytopenia (ITP) – most common acquired immune disorder

• Disorder that leads to easy or excessive bruising or bleeding as a result of unusual low levels of platelets
• Platelet function is normal until it reaches spleen
• Spleen attacks platelets – sees them as foreign for being antibody-coated
• Acute in children, chronic in adults

2. Thrombotic thrombocytopenia purpura (TTP)

• Blood condition that causes little blood clots to form in small vessels throughout body
• Almost always associated w/ hemolytic uremic syndrome – condition where small blood vessels in kidneys become inflamed  clot formation in kidneys
• Bleeding into skin (purpura) caused by few platelets in blood  prolonged, internal bleeding and sudden formation of small blood clots in brain and kidneys
• R/T o drug toxicity caused by chemotherapy, birth control, antivirals o pregnancy and preeclampsia o infection o autoimmune disorder

3. Heparin-induced thrombocytopenia (HIT) – associated w/ use of heparin

• Occurs when immune system identifies heparin as foreign  body develops antibodies to bind to heparin  activates platelet production  send body to hyperthrombotic state  platelets clumping and forming clots  venous thromboembolism (VTE) and PE Thrombocytopenia Clinical Manifestations 2 types:

1. Mucosal bleeding

• Blood blisters on tongue, cheeks, lips
  2. Cutaneous bleeding
• Petechiae – microhemorrhages, nonblanching lesions, small red spots caused by intradermal capillary bleeding
• Purpura – bruise from numerous petechiae
• Ecchymosis – very large bruise caused from hemorrhage Major complication is hemorrhage – weakness, fainting, dizziness, tachycardia, AB pain, hypotension Cerebral hemorrhage – can be fatal, complete a thorough neuro assessment, ensure pt safety due to  risk of falls Epistaxis – nose bleeds Prolonged bleeding after venipuncture – apply pressure to stop bleeding Thrombocytopenia Diagnostic Studies
• Medical Hx and physical assessment
• Platelet count o <150k o <50k – prolonged bleeding from trauma or injury o <20k – spontaneous, life threatening hemorrhages o <10k – platelet transfusion
• Bone marrow biopsy – gold standard o Shows how platelets are produced in bone marrow Thrombocytopenia Nursing Management
• Nursing Dx – risk for bleeding
• Treat underlying cause
• Avoid aspirin or other drugs that effect platelet function or production
• ITP o Give corticosteroids 1st^  alters how spleen sees platelets, allows platelet life span to  o Infusion on immunoglobulins o Platelet transfusion o Removal of spleen
• TTP – if not treated  irreversible kidney failure

o Plasmapheresis – removes unhealthy plasma from blood and returns healthy plasma to body (same concept as dialysis) o Plasma exchange – remove molecules that bind w/ platelets o Corticosteroids

• HIT – stop using heparin Nursing interventions:
• Avoid SQ or IM – give PO or IV
• Monitor labs
• Count sanitary pads – for women who are menstruating
• No suppositories
• No rectal temps/enemas  bleeding Pt Education:
• Notify MD w/ S&S of bleeding
• Restrict activity – to avoid falls
• Prevent epistaxis – do not blow nose forcefully
• Prevent constipation – stay hydrated, use stool softener
• Avoid shaving – electric razor is okay
• Oral care – use soft bristle toothbrush
• Avoid certain meds – NSAIDs  prolong bleeding
• Avoid tampon use – damages skin and capillaries Neutropenia –  in total WBC and  in neutrophils leading to  risk of infection Quick facts: Most common cause is result of chemotherapy or immunosuppressive therapy Leukopenia -  in total WBC Neutropenia -  in neutrophils – plays role in attacking and ingesting microbes Absolute Neutrophil Count (ANC) – a measure of the number of neutrophils in blood Nadir – lowest point of neutropenia usually 10-14 days after chemo Neutropenia Clinical Manifestations
• Infection  minor can lead to sepsis or death o Classic S&S may be absent – inflammation (redness, warmth, swelling)
• Neutropenic fever – medical emergency, neutropenic protocol o Draw blood cultures o Collect urine culture o CXR o Start antibiotic in 1 hr or less Neutropenia Diagnostic Studies
• WBC count <
• Neutrophil count
• ANC count <
• Bone marrow biopsy – done if cause is unknown

Neutropenia Nursing Management

• Nursing Dx – risk of infection
• Determine cause of neutropenia – bacteria and source
• Start broad spectrum antibiotic
• Identify if organism of infection is present
• Admin growth factors SQ after chemo – to reduce fever and infections
• Implement protective practices o Handwashing o Oral hygiene o Private room for hospitalized pt – isolation o Vitals q4h o No fresh flowers
• Pt Education: o Handwashing o Notify MD – temp >100.4, new onset of sore throat, cough, runny nose o Avoid crowds and people w/ illnesses o Wear mask in public o Neutropenic diet – avoid uncooked meat, seafood, eggs o Daily hygiene and oral care o No gardening o No cleaning up after pets Myelodysplastic Syndrome – ineffective RBC production due to dysplastic cells in bone marrow Quick facts: Unknown etiology Disease progression is usually slow Precursor to Acute Myeloid Leukemia (AML) – 1/3 of pt with MDS progress to AML MDS Clinical Manifestation
• Bleeding – gums, nose, stool
• Infection due to  WBC and platelets MDS Diagnostic Studies
• Bone marrow biopsy – gold standard o Gives specific classification of MDS MDS Nursing Management
• Nursing Dx: risk of infection, risk for bleeding, risk for falls
• Treatment based on aggressiveness of disease
• Epoetin and growth factors – for low risk/less aggressive disease pt o Supplements blood cell #
• Chemotherapy injections/infusions – for high risk/aggressive disease pt

o Given qmonth to restore normal cell growth and differentiation of hemopoietic cells

• Stem cell transplant – reserved for younger pt that can handle effects of transplant Leukemia – cancer of the blood, bone marrow, lymph system, and spleen Quick facts: Affects WBC – occurs when young, abnormal WBC (blasts) begin to fill up bone marrow  prevents normal cell production and slows RBC and platelet production Blasts outnumber normal cells – blasts count also indicate relapse of leukemia Accounts for 29% of all childhood cancers – fatal if untreated □ risk of bleeding due to  platelets □ risk of infection due to  mature WBC Leukemia Etiologies
• Combination of genetic and environmental influences
• Oncogenes – abnormal genes that can cause many types of cancer
• Chemical agents – more prone to developing leukemia if exposed
• Chemotherapeutic agents – pt who has had chemo in past can develop leukemia later on
• Viruses – triggers leukemia response
• Radiation – exposure to any type  risk Types of Leukemia 4 types of leukemia:

1. Acute lymphocytic leukemia (ALL) – most common in children, 20% in adults

• Abrupt onset of S&S o Fever o Acute onset of bleeding or bruising
• Insidious onset of S&S o Progressive weakness o Fatigue o Joint pain/bone pain o Bleeding or bruising tendencies

2. Acute myelogenous leukemia (AML) – 25% of all leukemia, 80% in adults

• Abrupt dramatic onset of S&S o Acute onset of fever or infection and/or abnormal bleeding – characterized as uncontrolled proliferation of myeloblasts and hyperplasia of bone marrow

3. Chronic myelogenous leukemia (CML) – excessive development of neoplastic to peripheral blood in huge #

• Takes over liver and spleen o Present w/ enlarged liver or spleen

• Philadelphia chromosome – genetic marker of 90% of pt
• Stays as chronic phase for many years
• Blastic phase = more aggressive phase – proliferates and overtakes body o Treat as acute leukemia

4. Chronic lymphocytic leukemia (CLL) – most common in adults, introduction and accumulation of functionally inactive but long-lived and mature lymphocytes

• Inflammation of lymph nodes throughout body
• Complications are rare in early stage but could develop as disease advances
• Pain and paralysis caused by pressure of enlarged lymph nodes
• Mediastinal node enlargement  pulmonary symptoms o Cough o Change in breathing pattern
• Early stage may not need treatment Leukemia Clinical Manifestations
• Splenomegaly
• Hepatomegaly
• Lymphadenopathy
• Bone pain/ joint pain
• Meningeal irritation – HA, nausea/vomiting caused by  ICP
• Oral lesions
• Solid mass (chloroma) – lumps of WBC that accumulate outside of bone marrow o Seen in AML
• Leukostasis – seen in acute leukemia o Life-threatening o Very high WBC due to circulating blasts o WBC >100, o Blasts overtaking bone marrow and blood o Blood becomes very thick due to  circulation Leukemia Diagnostic Studies
• CBC w/ differential blasts count
• Bone marrow biopsy – gold standard o Identifies cell type, stage, cell color/shape o CML pt – (+) for Philadelphia chromosome
• Lumbar puncture – determines if WBC accumulate outside bone marrow in the CSF
• PET/CT scan Leukemia Interprofessional Care Goal – to attain remission = no evidence of disease 4 stages of remission:

1. Complete – no evidence of disease (NED)
2. Minimal residual disease – small # of leukemic cells that remain during or after treatment, no S&S of disease
3. Partial – cancer is still there but less of it
4. Molecular – complete remission w/ NED 3 phases of chemotherapy treatment to achieve remission: Except CLL
5. Induction – aggressive treatment designed to kill leukemic cells in blood and bone marrow

• Remains for 4 weeks in hospital
  2. Post-induction/consolidation – designed to kill any remaining leukemic cells that might be inactive but could grow again
• 1-2 mos after induction, given after disease is considered to be in remission
• Ongoing for several months
  3. Maintenance – designed to kill any remaining leukemic cell that could cause recurrence
• Doses are lowered over time
• 2-3 yr process Leukemia Hematopoietic Stem Cell Transplant – procedure that replaces damaged stem cells w/ healthy stem cells Conditioning chemotherapy – pt receives high doses of chemo before transplant to prepare body for transplant  wipes bone marrow clean Goal of HSCT – eliminate all leukemic cells Replace with HLA-match:
• Relative (allogenic)
• Volunteer donor or matched unrelated donor (MUD) (allogenic)
• Identical twin (syngeneic) Engraftment – when stem cells start dividing/proliferating in bone marrow Autologous transplant – when pt own stem cells are infused back into themselves Reduced intensity stem cell transplant – stem cells come from healthy donor and conditioning chemo is less intensive Leukemia Assessment Data Subjective data:
• Past health Hx o Exposure to toxins, chromosome abnormalities, frequent infections
• Medications o Previous chemo
• Sx or radiation treatments Objective data:
• Fever
• Lymphadenopathy
• Lethargy
• Skin - pallor, jaundice, petechiae, ecchymosis

• CV – tachycardia, systolic murmurs
• GI – oral lesions or bleeding, herpes or infection, hepatomegaly, splenomegaly
• CNS – seizures, disorientation, confusion
• Muscle wasting, bone/joint pain Leukemia Nursing Diagnosis Acute care:
• Emotional support for pt and family
• Manage side effects of treatment – pancytopenia, oncologic emergencies
• Pt education – medications, pt involvement Ambulatory care:
• Monitor S&S of disease control or relapse
• Pt education o Self care – ADLs o When to call MD – fever, new onset of bleeding o Importance of follow-up apt – pneumococcal vaccine, influenza vaccine
• Support
• Follow-up care Lymphoma – cancer that affects lymphatic system – proliferation of lymphocytes Quick facts: Originates in the lymph system – lymph nodes, spleen, bone marrow, thymus gland 2 types:

1. Hodgkin’s lymphoma
2. Non-Hodgkin’s lymphoma Hodgkin’s Lymphoma Most curable form of cancer Epstein-Barr virus – causes mononucleosis associated w/ development of Hodgkin’s Originates in single lymph node – forms masses Spreads by extension along the lymph system Metastasis to lungs, spleen, liver Cervical lymph node often 1 st^ to be affected Hodgkin’s cells – larger than normal lymphocytes but smaller than Reed-Sternberg cells Hodgkin’s Lymphoma Clinical Manifestations

• Enlargement of lymph nodes – movable, non-tender, not painful unless pressure on nerves o 2 nd^ most common node enlargement – mediastinum node  cough, dyspnea, stridor, dysphagia
• Weight loss
• Fatigue and weakness
• Fever and chills
• Tachycardia

• Night sweats
• Alcohol-induced pain
• Generalized itching w/o lesions or rash
• B symptoms – 40% experiences o Fever >100. o Drenching night sweats o Weight loss exceeding 10% in 6 mos Hodgkin’s Lymphoma Diagnostic Studies
• Excisional lymph node biopsy – determines if Reed-Sternberg cells are present
• Radiological evaluation – XR, CT, CAT, MRI
• Peripheral blood analysis – evaluate liver and kidney function
• Bone marrow biopsy – thin needle inserted in hip bone, pulls bone marrow out
• Pulmonary function test – determines how well the lungs are working Stages of Hodgkin’s Lymphoma Stage I – involvement of 1-2 cervical lymph nodes Stage II – involvement of 2 or more lymph nodes on one side of diaphragm Stage III – involvement above and below diaphragm Stage IV – involvement outside of diaphragm – liver, bone marrow, lungs Hodgkin’s Lymphoma Treatment Goal – cure! Treatment is based on staging
• Chemotherapy
• Radiation therapy
• Stem cell transplant Risk for development of secondary cancer – occurs usually 10 yr after solid tumor cancer develops Hodgkin’s Lymphoma Nursing Management
• Manage the problems related to the disease and treatment of the disease
• Reduce risk factors for development of secondary cancers
• Psychosocial
• Spiritual
• Cultural
• Fertility concerns – most common w/ young adults, making sperm or harvesting eggs for future reproductive use Non-Hodgkin’s Lymphoma Quick facts: Does not have Reed-Sternberg cells Affects all ages Most common types:

• Diffused large B-cell lymphoma
• Follicular lymphoma
• Mantle cell lymphoma
• Peripheral T-cell lymphoma Non-Hodgkin’s Lymphoma Etiologies
• Unknown cause
• May results from o Chromosomal translocations o Infections – H. Pylori, HPV, HepB, HepC o Environmental factors o Immunodeficiency states o Involve lymphocytes that are in various stages Non-Hodgkin’s Lymphoma Clinical Manifestations
• Diagnosis usually occurs after disease has widely spread
• Painless lymph node enlargement – primary clinical manifestation
• Lymphadenopathy can wax and wane
• High grade lymphoma and B symptoms – fevers, night sweat, weight loss Non-Hodgkin’s Lymphoma Diagnostic Studies
• Resemble those used for Hodgkin’s
• Lymph node biopsy
• MRI – to rule out CNS disease
• Lumbar puncture – to rule out CNS disease
• Bone marrow biopsy
• Barium enema or upper endoscopy – to rule out GI involvement Non-Hodgkin’s Lymphoma Treatment Goal – improvement in symptoms
• Chemotherapy
• Biotherapy
• Radiation therapy
• Phototherapy – exposing skin to UV light
• Stem cell transplant
• CAR-T cell therapy – still in clinical trial but looks promising Non-Hodgkin’s Lymphoma Nursing Management
• Similar to Hodgkin’s nursing care
• Management of problems related to disease and treatment – pancytopenia, side effects from chemo, assess lung function
• Psychosocial
• Spiritual
• Cultural

• Fertility concerns
• Nursing presence Blood Component Therapy Quick facts: Care given to pt receiving a blood transfusion to:

1. Correct blood loss
2. Treat shock
3.  blood volume Blood Products

• Packed RBC (PRBCs) – used in pt who need  O2 transporting blood cells o Most commonly given o Blood w/o plasma
• Platelets – used for pt who have platelet deficiency, platelet dysfunction, or serious bleeding disorder
• Fresh frozen plasma (FFP) – used for pt who need clotting factors, need  in blood volume o Does not need to be a match in blood type because does not contain RBC
• Albumin – used for pt who need expanded blood volume or plasma proteins
• Clotting factors and cryoprecipitate – used for pt who have clotting disorder and lack fibrinogen o Used in OR and oncology setting
• Whole blood – used for pt w/ severe case of hemorrhage o Contains all components of blood – clotting factors, WBC, RBC, plasma, platelets, and plasma proteins Supplies Needed for Transfusion
• Transfusion order – special instructions that indicates blood product to be infused and # of units
• Type and crossmatch – draw blood, send to lab for type, blood bank crossmatch to donor blood available to avoid reactions
• Informed consent – allows team to assess allergies, pt understanding of transfusion, S&S to report, if they had a blood transfusion before – any reactions? o Job of physician or NP
• IV access – blood can be infused through central line o 18-22 gauge IV o RBC start to lyse if gauge is too small o Do not mix medication in w/ blood transfusion
• Y-tubing
• Bag of 0.9% NS – no other fluid should be given w/ blood

Process for Transfusion

• Pt education prior
• Baseline vitals 15 min prior to transfusion and physical assessment – any abnormality before transfusion need to be noted to physician
• Dual check w/ licensed caregivers
• Start infusion within 30 min of receipt
• Remain w/ pt for 1 st^15 min – check for any reactions o Fevers o Chills o Flank pain o Nausea o HA o Itching o Dyspnea o Bronchospasm o Cough
• Recheck vitals at 15 min
• Infuse over 4 hr max – applies to RBC, usually 2 hr/unit
• Monitor for transfusion reactions
• Check vitals at end of transfusion
• Documentation Transfusion Reactions Acute reactions:
• Acute hemolytic – RBC given were destroyed by pt immune system – ABO incompatibility
• Febrile non-hemolytic – presents w/ fevers, chills, flushing, nausea o Most common
• Mild allergy – flushing, itching, hives but afebrile
• Anaphylactic and severe allergy – itching, dyspnea, chest tightness, hypotension, □ O
• Circulatory overload – occurs when too much fluid is transfused or too quickly  PE and acute respiratory failure
• Sepsis
• Transfusion-related acute lung injury (TRALI) – acute respiratory distress due to donor plasma containing antibodies against pt leukocytes o Presents w/ dry cough, hypoxia, breathlessness, frothy sputum, fever, rigors
• Massive blood transfusion Delayed reactions: could be undetected for days or weeks, generally >48 hr after transfusion
• Delayed hemolytic – pt has antibody that was not detected in previous blood screening

• HepB
• HepC
• Fe overload
• Other Transfusion Reaction Clinical Manifestation
• Pain
• Anxiety
• Hematuria
• Fever
• HA
• Pruritus
• Rash/hives
• Nausea
• Respiratory difficulty
• Bleeding
• Hypotension
• Oliguria Transfusion Nursing Management
• Stop transfusion! – 1 st^ priority
• Maintain IV w/ saline
• Notify blood bank and MD
• Recheck identifying tags and numbers – confirm right product
• Monitor vitals signs and urine output
• Treat symptoms per MD orders
• Send blood bag and tubing back to blood bank – for examination and determination of type of reaction occurs
• Draw labs and collect urine sample – evaluate for hemolysis
• Document! – action that was taken

MODULE 10

Pre-Operative Care Lasts from the decision to have Sx until the beginning of Sx Nursing assessment – identify risk factors and plan of care to ensure pt safety Identify Risk Factors

• Psychological/emotional status – pt Hx and pt fears
• Physiological status – complete head to toe, focused assessment on area of Sx
• Allergies – to drugs, food, environment
• Establish baseline data – head to toe and vitals to identify any changes during Sx
• Identification of surgical site – where and what is pt getting Sx for
• Medication usage – OTC, herbals, recreational, prescriptions can impact perception of pain, experience of pain, and response to anesthesia

• Pre-op lab work assessment – CBC, bleeding time, electrolytes, blood sugar, CXR/EKG
• Cultural/ethnic factors – any practice that could influence/impact procedure and recovery time
• Adequate knowledge for informed consent
• Food restrictions before Sx Informed Consent Prior to any Sx – shared decision between pt and HCP, signed before any pre-op meds are given
• Surgeon’s responsibility – adequate disclosure to what the procedure entails o Risk vs benefit o Alternatives – “if you don’t have this procedure, then XYZ can occur” o Possible complications o Procedure and recovery period – how long it takes, what is happening during recovery?
• Valid consent o Voluntary o At least 18 y/o o Witnessed by professional staff o Competent pt – able to make own decisions ▪ Pt who are not autonomous – mentally ill, neurological incapacitation, cognitively impaired o Comprehendible – in language that pt can read
• Nurse’s role o Answering general q’s about Sx o Specific q’s must be notified to MD o Ensure consent is signed prior to any pre-op meds given o Ensure pt is not under any influence of any psychoactive meds that can influence decision making Review of Systems – to compare postop findings to pre-op findings
• Baseline – alerts possibility of potential postop complications or factors that may delay recovery
• Neurological – able to follow commands, responds to q’s, past medical neuro Hx
• Respiratory – Sx postponed (non-emergent case) if pt has respiratory infection o  risk of bronchospasm o  O2 saturation o If smoker – stop 6 wk prior to Sx ▪  pack/yr =  risk for pulmonary complications ▪  risk for wound healing complications ▪  risk for Sx site infection ▪  risk for DVT ▪  risk for pneumonia

o lungs help eliminate anesthesia from body ▪ impaired lung functioning = anesthesia retained in body longer

• Cardiovascular – needs O2 to support fluid/nutritional needs o Impaired CV = 12 lead EKG and cardiac clearance ▪ Cardiologists assesses pt to ensure they are able to withstand stress of Sx o HTN need to be controlled prior to Sx
• Hepatic-renal o Liver disease = problems w/ clotting abnormalities o Renal impairment = unpredictable drug elimination
• Musculoskeletal – especially if pt is older adult o  risk of impaired mobility postop
• Immune function o Immunosuppression = delayed wound healing and  risk for infection o Steroid therapy =  risk for renal insufficiency o Corticosteroids needs to be tapered off o Uncontrolled thyroid disorders =  risk for complications ▪ Hyperthyroidism  thyrotoxicosis ▪ Hypothyroidism  respiratory failure
• Nutrition – needed for effective healing and infection prevention o Adequate protein stores to repair tissues o Assess malnutrition/protein stores ▪ Serum albumin levels ▪ Total protein levels o Obese/underweight =  risk for impaired wound healing/infection o If malnourished prior to Sx  need peripheral, parenteral, or TPN o Adequate hydration important to prevent fluid imbalances
• Integumentary – assess Sx site for rashes or skin breakdown prior to Sx
• Endocrine - DM o Hypoglycemia can occur during surgery or postop R/T inadequate CHO intake or excessive insulin admin o Hyperglycemia R/T stress response ▪  risk of wound infection ▪ BG 80-110 yields better outcomes ▪ Monitor BG before, during, and after Sx ▪ Verify w/ MD if usual dose of insulin should be admin morning of Sx
• Fluid and electrolyte o Bowel preps =  risk of fluid volume deficit o Diuretics or NPO =  risk for fluid volume deficit and electrolyte imbalance o Assess pre-op to ensure no postop complications occur

Pre-op Medications Assessment Can interact w/ anesthesia and  desired effects of anesthetic If med is critical  switch to IV

• Aspirin/anticoagulants – inhibits platelet aggregation
• Herbals – risk of bleeding, can lead to excessive sedation, and  BP o DC 2-3 wk before Sx
• Corticosteroids – can cause CV collapse if DC abruptly o Bolus IV before and after Sx
• Diuretics – can cause electrolyte imbalance especially K – loss w/ loop diuretics o K imbalance = impaired cardiac functioning
• Opioids – alters response to analgesics postop
• Antihypertensive – predisposes pt to hypovolemic shock if taken prior to Sx o Drug interaction w/ anesthesia
• Tranquilizers – can cause seizures if DC
• Insulin – dose adjustments
• Anticonvulsants – change to IV route during Sx and postop to prevent seizures
• Thyroid meds – given IV to maintain therapeutic level to ensure adequate thyroid functioning
• Antidepressants – drug interactions w/ anesthesia
• Reactional drug/alcohol use – weakens immune system Pre-op Allergies Assessment How do you react? Intolerance – unpleasant side effect to med – not allergy
• Nausea
• Constipation
• Diarrhea Allergy – immune response
• Hives
• SOB
• Anaphylaxis – hypotension, tachycardia, bronchospasm Pt Education to Prevent Complications Goal – improve circulation, prevent venous stasis, promote optimal respiratory function
• Use multiple teaching strategies o Discussion o Written instructions o Demonstration/return demonstration
• Leg exercises – simulate bike riding, tracing circles o SCD – needs to stay in place while in bed
• Early ambulation – most significant intervention o  muscle tone o stimulates circulation to prevent venous stasis

o maintains normal respiratory function

• Diaphragmatic breathing – to fully expand lungs
• Coughing – facilitates lung expansion and mobilize secretions
• Turning
• IBE/ Spirometer – inhalation expands lungs
• Splinting – holding pillow against incision when deep breathing, coughing, or turning to prevent pain/discomfort Venous Thromboembolism (VTE) Venous thrombosis – formation of thrombus in association w/ inflammation of vein
• Superficial vein thrombosis
• Deep vein thrombosis VTE – represents spectrum of pathology from DVT to PE R/T immobility and positioning VTE Etiologies Virchow’s triad:
• Venous stasis – occurs when valves and veins are dysfunctional or muscles in extremities are inactive o More frequent in older adults, obese pt who have varicose veins, pt undergoing prolonged Sx procedure, or pt who are immobile for long period of time
• Endothelial damage – results from direct injury to vein, during Sx or trauma o Indirect damage occurs from agents that are caustic to veins – chemo o DM predisposition o Sepsis – endotoxins are being released ▪ Stimulates platelet aggregation and clotting cascade to be activated
• Hypercoagulability o Anemia o Malignancy o Nephrotic syndrome o Protein deficiency o Use of tobacco, corticosteroids, and estrogen (oral contraceptives) o Women who smoke and use oral contraceptive – 2x risk of developing VTE If thrombus forms in vein  at risk for becoming detached  embolus (clot that travels) can travel to heart and pulmonary vessels and lodge  PE
• S&S of PE o  RR o  HR o SOB o Chest pain o Agitation

o Cough up blood o Dysrhythmias VTE Clinical Manifestations Always compare bilaterally Most common in lower extremities Can be seen in upper extremities if thrombus in SVC or jugular vein

• Unilateral leg edema
• Pain
• Tenderness
• Sense of fullness
• Paresthesia
• Erythema
• Warm skin
• Temp >100.4°F VTE Diagnostic Studies
• Labs o aPTT – activated partial thromboplastin time – screening test that helps evaluate a person’s ability to appropriately form blood clots o bleeding time o activated clotting time (ACT) o Hgb/Hct for blood dyscrasias o Platelets – elevation
• D-dimer o (-) – rules out thrombosis o (+) – indicates thrombosis but does not rule out other potential causes
• Duplex ultrasound – noninvasive, uses colorful Doppler to determine where clot is and how big it is o Gold standard for diagnosing VTE
• Venography – invasive, use w/ CT, MRI, contrast injection o Identifies location of thrombus but MRI distinguishes it from being acute or chronic VTE Management
• Prophylaxis – wear Ted-hose (thromboembolic deterrent hose – prevents thrombophlebitis by shunting blood through the deep veins of calves and thighs
• SCD (sequential compression device – DVT prevention that improves blood flow in legs) o Do not put SCD on pt w/ VTE  potential dislodge in lower extremity  embolus  PE
• Activity – early ambulation 4-6x/day o Turn, cough, deep breath q2h