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255 test 4
| Question | Answer |
|---|---|
| Genetics | study of genes and their role in inheritance |
| Genomics | – study of an individual’s genes (the genome), Includes study of complex diseases (heart disease, diabetes and cancer) |
| Genes | 30,000 genes in each person’s genome Carry the instructions for making proteins and direct activities of cell Each gene has a specific location on a chromosome (locus) |
| Allele | 1 of 2 alternating forms of a gene that occupy corresponding loci on a chromosome 1 from mother, 1 from father Each allele codes for a specific inherited characteristic |
| Chromosomes | Occur in pairs – humans have 23 pairs 22 of 23 are autosomes (same in both males and females) Sex chromosome makes up the 23rd pair Female – (2) x chromosomes Male – (1) x and (1) y chromosome |
| Genotype | actual genetic makeup of a person |
| Phenotype | physical traits expressed by a person |
| Autosomal dominant | Mutation of a single gene of a pair on a chromosome Not sex linked, a pattern of genetic inheritance where a single altered copy of a gene from one parent is enough to cause a trait or disease. |
| Autosomal recessive | Mutations of both genes of a pair on a chromosome Not sex linked, a pattern of inheritance where a genetic condition occurs when a child inherits two non-working copies of a gene |
| X-linked recessive | Mutation on the x chromosome Sex linked, severe disease mostly affects males |
| Autosomal Dominant chart info | You have it or you don’t, no carrier, Males & Females, More common, Variable expression, affected parent, affected every generation, Breast cancer (BRCA gene) Hypercholesterolemia Huntington’s disease Neurofibromatosis Marfan’s syndrome |
| Autosomal Recessive chart info | Have a carrier, both parents exhibit disease, Males & Females Carriers asymptomatic 25% affected, 50% carriers No Family history, Cystic fibrosis Phenylketonuria Sickle cell disease Thalassemia |
| X-Linked Recessive | Sex linked disorders, males affected more bc they have one X chromosome, females carriers, Usually Males affected Females carriers, Hemophilia Duchenne muscular dystrophy |
| Gene therapy | Experimental technique used to treat the underlying cause of a disease Uses Supply a missing gene Provide the missing gene’s role Enhance treatment of a disease Goal: Provide a normally functioning gene to a person with a pathogenic gene variant |
| Stem cell therapy | regeneration of lost tissue and restore function, Stem cells are unspecialized cells in the body that can Remain in an unspecialized state and divide Differentiate and develop into specialized cells, Uses-burn, bone grafts, hematologic cancers |
| Identify risk for genetic-related diseases | Disease in more than 1 relative does not usually affect a certain gender (breast cancer in a male) Disease that occurs at an age earlier than expected (MI before age 35) Combinations of diseases (breast and ovarian ca, heart disease and diabetes) |
| blood makeup | 55% is plasma 45% is blood cells Erythrocytes (RBCs) Leukocytes (WBCs) Thrombocytes (platelets) |
| RBC | cells-anemias, clotting, blood loss Hemoglobin (Hgb) Hematocrit (Hct) RBC indices |
| WBC | Total WBC count Useful in evaluating infection, inflammation, tissue injury Differential Measures the percent of each type of WBC |
| platelet count | cause clotting, high platelets means clot risk, low levels-risk for bleeding |
| HgB range | 12-18 |
| Hct range | 37-52 |
| total rbc count range | 4.2-6.1 x 10 ^6 |
| total wbc range | 5000-10000 |
| total platelet count range | 150,000-400,000 x 10^3/L |
| Total RBC Count meaning | Number of circulating RBCs per volume of blood |
| hemoglobin | Measures gas carrying capacity of blood |
| hematocrit | Percent of RBCs compared to blood volume Low: bleeding, anemia, dilution Increased: polycythemia and dehydration |
| Mean corpuscular volume (MCV) | Size of RBC High: macrocytic (large size) Normocytic (normal size) Low: microcytic (small size), High MCV: cobalamin and folic acid def anemia, poss hemolytic anemia Low MCV: chronic blood loss or disease, iron deficiency anemia, poss thalassemia |
| Mean corpuscular hemoglobin (MCH) | Amount of Hgb in RBC Normochromic (normal color) Low: hypochromic (pale color), Low MCH: iron def anemia, vit B6 deficiency, thalassemia |
| Mean corpuscular hemoglobin concentration (MCHC) | Concentration of Hgb in RBC |
| WBC count | Total count of WBCs in blood Over 10,000 µL = infection, inflammation, tissue injury or cancers (leukemia/lymphoma) Below 5,000 µL = leukopenia (bone marrow depression, illness or leukemia) |
| high and low wbc | High WBC: leukocytosis Low WBC: leukopenia |
| WBC differential | Neutrophils (bands [immature young]+ segs [more mature neutrophils]) Can indicate bacterial infection A WBC differential measures the types and percentages of white blood cells in your blood. It helps figure out infections, inflammation, allergies |
| Eosinophils | Can indicate allergic reaction, parasitic infection, asthma |
| Lymphocytes | Can indicate viral infection, leukemias |
| Monocytes | Can indicate viral infection, inflammation or malignancy |
| Basophils | Least number, can indicate inflammation/contributes to allergic reactions |
| platelets count meaning | Number of platelets per microliter of blood Below 150,000µL = thrombocytopenia Risk of bleeding Above 400,000µL= thrombocytosis risk of clotting |
| Erythropoiesis gut | Iron, Cobalamin (B12), Folate, Riboflavin, B2 and B6 |
| Erythropoiesis Functional Kidneys | Erythropoietin (EPO) |
| Functional Bone Marrow | Iron Storage Ferritin & Transferrin |
| STEM Cells-immature RBC | Erythroblast form begin to form hemoglobin Released as Reticulocytes-these mature in 48 hours |
| Erythrocytes are | new rbc |
| liver | To process RBC Waste: Amino acids and bilirubin |
| stem cells | immature RBC or in the bone marrow begin to form hemoglobin |
| Transferrin | Transporters of iron rich cells |
| Ferritin | Stored iron reserves in Long bones. a protein that stores iron |
| Negative Feedback System | When supply is low the demand for more production goes up |
| Biconcave disks | which increases surface area to allow for passage through capillaries. |
| hct values | 37-52 |
| hgb values | 12-18 |
| plt values | 150,000-400,000 |
| MCV | size, Normocytic: 80-95 Microcytic (Small): <80 Macrocytic/Megablastic (Large): >95 |
| MCH | Normochromic: 27-31 Hypochromic (Pale): <27 Oxyhemoglobin: What gives the RBC its deep red color. |
| Hemolysis | RBC DESTRUCTION Lysed by phagocytes: Spleen, Liver, Bone Marrow through Lymph System. Wastes: Iron are reabsorbed in bone as (Ferritin) Amino acids Bilirubin |
| billirubin | 1.2mg/Dl Golden skin, sclera or Jaundice Impaired Liver function can cause high levels of Bilirubin in the blood. Seen in: Alcoholic |
| Excessive Acute and Chronic Hemolysis can cause | organ congestion: Splenomegaly; Enlarged Liver; Acute Kidney Injury/Failure |
| Anemia is a | deficiency in the number of erythrocytes, the quantity or quality of hemoglobin, and volume of packed RBCs (hematocrit). It is a common condition with many diverse causes, such as impaired production of RBCs, blood loss, and increased destruction of RBCs |
| anemia signs | fatigue, confusion, parestesia, icteric sclera, spoon shaped nails, jaundice, SOB, tacypnea, tachycardia, postural hypotension, abd, anorexia, glossitis, beefy red tougue, stomatitis |
| Complete Blood Count (CBC) | WBC (white blood cells) – Usually WNL; Aplastic RBC (red blood cells) –Normal to Low of Normal to Low Hematocrit (Hct): RBCs compared to total blood volume (TBV)- normal to low of normal to low Hemoglobin (Hgb) Carriers of O2 – low of normal to low |
| MCHC | Amount of Hgb in RBCs Platelets: MPV (Mean platelet volume) – normal; |
| mild anemia numbers | (Hgb 10-12 g/dL) |
| moderate anemia numbers | (Hgb 6-10 g/dL) |
| severe anemia numbers | (Hgb < 6 g/dL) |
| amino acid foods for rbc production | eggs, meat, milk, cheese, poultry, fish, legumes, nuts , soy |
| vitamin b12 foods | meat, eggs, grain products, milk, dairy foods, fish |
| copper foods | shellfish, grains, beans, nuts, potatoes, organ meats, dark leafy greens, dried fruits |
| high folic acid foods | green leafy vegetables, breakfast cereals, orange juice, peanuts, avocado |
| high iron foods to improve hgb sythesis | lean beef, turkey, pork, chicken, fish, legumes, green leafy vegetables, beans |
| high niacin foods for rbc maturation | pb, beef, poultry, beef, fish, avocado |
| IRON DEFICIENCY ANEMIA | Red Blood Cell production problem Decreased ability to form Hemoglobin Most common nutritional disorder in the world. Very Young, Poor Diets Menstruating Women in reproductive years (20-45) |
| IRON DEFICIENCY ANEMIA causes | Inadequate intake of iron Malabsorption: GI surgery or malabsorption syndromes Blood loss: Peptic ulcers, gastritis, esophagitis, hemorrhoids, diverticula, cancer, menstrual bleeding |
| Assessment for IRON DEFICIENCY ANEMIA | HGB/HCT: low MCV/MCH : low (microcytic & hypochromic) Serum iron: low Serum ferritin: low Serum trans ferritin: Normal TIBC: high |
| Total iron-binding capacity (TIBC): | Measurement of all proteins that act to bind or transport iron between tissues and bone marrow |
| Transferrin saturation | Carriers of iron Circulating in serum. Better indicator of iron available for erythropoiesis. Iron bound to transferrin is ready for body to use. |
| Manifestations of IRON DEFICIENCY ANEMIA | Fatigue Paler pale sclera glossitis(painful swollen tongue) cheilitis(sores on sides of mouth) *brittle nails spoon nails *Pica |
| Management IRON DEFICIENCY ANEMIA | Treat underlying problem! Iron replacement |
| IRON DEFICIENCY ANEMIA Medications | Oral iron: ferrous sulfate or ferrous gluconate Absorbs best in an acidic environment and avoid iron binding with food. take with: Orange Juice, 30 minutes before a meal, Stay upright for 30 min. after Teeth Staining- drink through straw |
| IRON DEFICIENCY ANEMIA Medications continued | IM or IV iron: Dextran, sodium ferrous gluconate, iron sucrose (change needles and z-track) Caution: Constipation, stomach upset, intolerance to sulfites, black stool |
| Macrocytic/MEGALOBLASTIC ANEMIAS PRODUCTION AND DESTRUCTION Anemias | causes- Pernicious Anemia deficiency Folic acid deficiency, inefective DNA synthesis large & abnormal RBCs easily destroyed Less common causes: congenital disorders, drugs, inborn errors of metabolism, malignant blood disorders |
| Causes of pernicious anemia COBALAMIN (VIT B12) DEFICIENCY | Absence of Intrinsic Factor body unable to absorb B12 due to damaged parietal cells *GI surgery Malabsorption syndrome *Excess alcohol or hot tea consumption Smokers *long term use of H2 receptor blockers and PPIs strict Vegetarians |
| Manifestations of pernicious anemia | Middle age Soar Red, Beefy Tongue anorexia, nausea, vomiting, abdominal pain What sets this anemia apart from other anemias is *Neurological Symptoms weakness, *paresthesia of extremities, ataxia, muscle weakness, impaired thought processes |
| Diagnostic Studies for pernicious anemia | HGB/HCT: low Serum B12: low MCV: high (macrocytic) Ferritin: high Serum folate: normal |
| pernicious anemia Medications | Replace Vit B12 PO - Oral if GI system intact and IF confirmed OTC and prescription- Contained in many oral multivitamins *Encourage dietary sources of B12 Meat, eggs, enriched grain products, milk and dairy, fish (*especially salmon) |
| pernicious anemia Medications continued | Parenteral (IM) if cause is due to low IF or ileum disorder IM injections are for life. Cyanocobalamin (Vitamin B12 injectable) SQ Z-track for IM Protect from light Side effects: Flushing, diarrhea, itching/pain at injection site |
| Nursing considerations for im MEDICATIONS FOR pernicious anemia | Protect from light, Monitor K levels, food B12 (meat, eggs, enriched grain products, dairy products, fish, Monitor for s/s of B12 deficiency (*paranesthesia: numbness/tingling in extremities, , anorexia, loss of taste, diarrhea, memory loss) |
| Causes of FOLIC ACID DEFICIENCY | Necessary for Red Blood Cell membrane development *Dietary deficiency (found in green leafy veggies, fruits (Avocado), enriched grain cereals and meats) Increased Requirements in Pregnancy: Neural Tube Defects Most Common in: Chronic Alcoholism |
| Causes of FOLIC ACID DEFICIENCY pt 2 | Chronic Hemodialysis Drugs: Methotrexate, antiepileptic, certain antibiotics, chemo drugs, contraceptives Malabsorption syndrome: Crohn’s disease, Cystic Fibrosis, Lactose Intolerance |
| Manifestations of FOLIC ACID DEFICIENCY diagnosis | HGB/HCT: low MCV: high Serum folate: low Serum cobalamin: normal |
| Manifestations of FOLIC ACID DEFICIENCY manifestations | Similar to cobalamin deficiency, but *without neuro symptoms GI: Stomatitis Cheilosis Dysphagia *Flatulence *diarrhea |
| FOLIC ACID DEFICIENCY Medications | folate A vitamin needed for DNA synthesis and cell division Deficiency is associated with neural tube defects in fetus and megaloblastic macrocytic anemia Oral replacement for a deficiency or as a preventative in pregnancy OTC and inexpensive |
| folate side effects | Yellow discoloration of urine *Nausea *Altered sleep *Depression Rash Bronchospasm Nursing considerations Educate patient that alcohol consumption decreases folic acid levels |
| folate dietary sources | green leafy veggies grain products and cereal orange juice Peanuts avocado |
| APLASTIC ANEMIA Destruction of/and production of Cells | WBC, RBC: HGB/HCT, Platelets: low (Pancytopenia) cell size, shape WNL Causes: cytotoxic T cells-suppression of bone marrow: Chemotherapy/Radiation genetics stem cell defect |
| APLASTIC ANEMIA s/s | Can occur abruptly or over weeks Decrease in WBC, RBC, and Platelets varies from mild to severe S/S of anemia (fatigue, dyspnea), fever, bruising Risk: INFECTION AND BLEEDING |
| APLASTIC ANEMIA Treatment goals | Restore bone marrow function Prevent and manage infection and bleeding Treat the underlying cause when identified Support oxygen delivery and tissue perfusion |
| APLASTIC ANEMIA Treatment | Hematopoietic Stem Cell Transplant (HSCT): *Treatment of choice for eligible patients Best outcomes in: Younger patients (under age 40) Patients with matched sibling donors Can be curative Risks:(GVHD) Infection Transplant-related complication |
| 4. Supportive Care (Essential for All Patients) aplastic anemia | Blood Product Transfusions Administer blood products as ordered: Fresh frozen plasma, Cryoprecipitate Packed red blood cells (PRBCs) for anemia Platelet transfusions for thrombocytopenia Use cautiously to prevent iron overload and alloimmunization |
| Neutropenic Precautions | Hand Hygiene: Perform hand hygiene before and after all patient contact Use soap and water or alcohol-based hand sanitizer Teach patient and visitors proper hand hygiene, private room |
| Neutropenic Precautions pt 2 | no raw or udercooked meals, avoid deli meats, daily bathing, oral care every 4 hrs |
| emergency rule Neutropenic Precautions | A fever in a neutropenic patient is a MEDICAL EMERGENCY.Start broad-spectrum IV antibiotics |
| Anemia from BLOOD LOSS: ACUTE | Sudden Signs & symptoms are more important than lab values CBC: HGB/HCT: low Major complication is shock: Average person has 5 L blood volume Loss of 1,000 ml (20% TBV): tachycardia with exercise Loss of 2,500 ml- shock, lactic acidosis, death |
| Anemia from BLOOD LOSS: ACUTE treat | Support vital signs with fluid replacement: NS or LR Stop blood loss Replace blood volume Body needs 2-5 days to make more RBCs Monitor labs: CBC, Electrolytes |
| Anemia from Chronic Blood Loss | GI Bleeding: Peptic ulcer Hemorrhoids Gynecological: Menstrual cycle Postmenopausal blood loss Diagnosis: CBC HGB/HCT: low MCV, Serum iron, TIBC: all low Treatment: Identify the source control and/or stop the bleeding Supplemental iron |
| Hemolytic Anemias RBC Destruction | Extrinsic (Acquired): Antibodies against RBCs Infectious agents (e.g., malaria) and toxins (Chemotherapy) Physical destruction Extracorporeal circulation Prosthetic heart valves |
| Hemolytic Anemias RBC Destruction intrinsic | (Hereditary): Abnormal hemoglobin (sickle cell disease) Enzyme deficiency (glucose-6-phosphate dehydrogenase [G6PD]) Membrane abnormalities (paroxysmal nocturnal hemoglobinuria, hereditary spherocytosis) |
| SICKLE CELL DISEASE INCREASED ERYTHROCYTE DESTRUCTION: hEMOLYSIS | Most common inherited blood disorder in the US Can affect Hispanic Americans, Mediterranean, Caribbean, Arabian and East Indians 1 in 13 African American babies born with sickle cell trait *Inherited, autosomal recessive disorder |
| SICKLE CELL TRAIT VERSUS DISEASE | Sickle Cell trait Inherits Hgb S from one parent and a normal gene: Heterozygous Symptoms are mild to asymptomatic (carrier state) Sickle Cell Anemia Most severe of Sickle cell syndromes Inherits Hgb S from both parents: Homozygous |
| SICKLE CELL DISEASE | Sickling Episodes Triggered by: *Respiratory Infection - most common cause *Assess low O2 levels in the blood stress, surgery, blood loss, high altitude |
| Sickle Cell Crisis | Acute exacerbation of sickling causing: Vasoconstriction and Vaso-occlusive crisis Severe and painful |
| Manifestations of SICKLE CELL DISEASE | Usually anemic and asymptomatic except during sickling episodes Subjective: Heart Racing, SOB, pain, n/v, fatigue Objective: Grayish skin color, jaundice, low oxygen saturation |
| Manifestations of SICKLE CELL DISEASE diagnostics | HGB/HCT: low Iron: low or normal Bilirubin: high |
| SICKLE CELL DISEASE complications | Repeated sickling episodes cause organ damage (spleen, lungs, kidneys, brain) |
| SICKLE CELL DISEASE treat | Sickling episodes are triggered by low blood O2 Oxygen, pain meds, IV fluids, DVT prophylaxis *Chelation therapy for removal of RBC waste: Hydroxyurea Transfusions |
| Hydroxyurea | Oral Antineoplastic agent Used in sickle cell (decreases number of sickled cells and reduces hemolysis) Contraindicated in Pregnancy Pregnancy category D Side effects Bone marrow suppression, stomatitis, rash |
| POLYCYTHEMIA INCREASED PRODUCTION OF BLOOD COMPONENTS | Production increases blood viscosity and volume RBC, WBC, Platelets high *Serum Erythropoietin (EPO)will be high Primary Polycythemia (Polycythemia vera) Involves RBCs, WBCs, and platelets (increased numbers of all) Splenomegaly and hepatomegaly |
| Secondary Polycythemia (most common) | Hypoxia driven: hypoxia stimulates erythropoietin (EPO) production in the kidneys which increases RBCs (high altitude, lung disease, smokers) Hypoxia independent: Cancer or benign tumor tissues makes EPO Splenomegaly does not occur |
| Manifestations of POLYCYTHEMIA | HA, vertigo, tinnitus, nose bleeds, visual changes, paresthesia, itching, plethora, petechiae, bruising, htn, *Major cause of death is: Thrombosis and Stroke |
| Treatment of POLYCYTHEMIA | Reduce blood volume and viscosity Phlebotomy (reduce hct by removing 300-500ml of blood) every 2-3 months Assess I&O Suppress bone marrow activity Myelosuppressive agents (hydroxyurea) a-Interferon (a-IFN) (PREGNANT WOMEN) Prevent clotting |
| PLATELETS (THROMBOCYTES) | Originate from stem cells in the bone marrow; 1/3 are stored in the: Spleen Primary function: Start the Clotting Process Produces a “platelet plug” at the site of injury Responds to immune activation |
| CLOTTING CASCADE | V-P-F-H Vessel constriction Platelet plug Factors activate Hard (fibrin) clot Why This Matters in Nursing Too little clotting → bleeding (hemophilia, thrombocytopenia) Too much clotting → thrombosis (DIC, stroke, PE) |
| NCLEX Tip clotting | Platelets start the clot Fibrin stabilizes the clot Clotting factors connect the two |
| Thrombocytopenia Platelet count of < 150,000 | Abnormal hemostasis and prolonged bleeding Impaired platelet production: Cancers & ITP Increased platelet destruction: Cardiopulmonary bypass hemodialysis |
| Thrombocytopenia Platelet count of < 150,000 pt 2 | HELLP Syndrome- associated with pregnancy Hemolysis high liver enzymes low platelets Abnormal platelet distribution DIC- Disseminated Intravascular Coagulation HIT- Heparin-Induced Thrombocytopenia |
| MANIFESTATIONS: THROMBOCYTOPENIA | Asymptomatic Excessive bruising and bleeding most common Skin: Petechiae: small, flat, red microhemorrhages Purpura: many petechiae, non-blanching Ecchymosis: purplish lesions Mucosal: gums/gingiva/nosebleeds; soft bristle toothbrush |
| DIAGNOSTIC STUDIES: THROMBOCYTOPENIA | CBC: Platelets: <150,000 Clotting studies: Thrombin Time, PT/INR, PTT Prothrombin Time (PT) Normal PT = 10-13 seconds |
| Warfarin “WEPT” | Warfarin Extrinsic PT Three letters → Targets Vitamin K dependent factors - Factor VII |
| INR: International Normalized Ratio | Normal INR = < 1.1 if not on oral blood thinner INR is a standardized blood test that tells you how fast blood clots. It’s mainly used to monitor patients taking anticoagulants like Warfarin. 2.0 -3.0 therapeutic range for taking oral blood thinners |
| Prothrombin Time (PT) | How long does blood take to clot in the clotting cascade via Extrinsic pathway (Factor VII) |
| Aptt DIAGNOSTIC STUDIES: THROMBOCYTOPENIA | Partial Thromboplastin Time (aPTT) How long does blood take to clot in the intrinsic pathway (clotting FACTORS) of the clotting cascade Normal PTT - 25-35 seconds Testing used for Heparin therapy Therapeutic Range anticoagulant = 60-70 seconds |
| THROMBOCYTOPENIA OTHER DIAGNOSTICS | Bone Marrow Aspiration/biopsy Functioning of the bone marrow to produce platelets To rule out: myeloproliferative disorders (blood cancers) cancers (Leukemias) aplastic anemia Treatments: Based on the cause AND diagnosis |
| Immune Thrombocytopenic Purpura (ITP) | COMMON low platelet problem Production can not keep up Present with: bleeding gums, nose petechiae, purpura, autoimmune disorder where body destroys its own platelet Autoimmune response to infection Helicobacter Pylori- stomach bacterial infectio |
| ITP Treatment | Corticosteroids >6 weeks - Prednisone hypertension, hyperglycemia, mood disturbances, ulcer formation, glaucoma, osteoporosis *IV Immunoglobulin if steroids contraindicated *Immunosuppressant – Rituximab Splenectomy *Avoid Contact Sports! |
| Disseminated intravascular Coagulation | DIC Most common cause: Sepsis A trigger (like infection or trauma) activates clotting everywhere Tiny clots form throughout blood vessels Platelets & clotting factors get used up Body can’t clot properly anymore → severe bleeding |
| Disseminated intravascular Coagulation thrombosis | Cyanosis Ischemic extremity; Necrotic skin Trouble Breathing: tachypnea, dyspnea, pulmonary emboli, respiratory distress ECG changes: Chest Pain Abdominal pain/ileus Kidney damage and oliguria |
| Disseminated intravascular Coagulation bleeding | Pallor, petechiae, purpura, oozing Hematomas - joint swelling GI bleeding -hemoptysis Hematuria CV collapse: tachycardia, hypotension |
| Abnormal response to clotting cascade | Accelerates fibrinogen to fibrin and enhances platelet aggregation and adhesion= Thrombus Microscopic clotting in vessels Lactic acid indicates sepsis |
| Lab studies OF DIC | Thrombin time PT, PTT *D-dimer: (increased)- protein in blood that indicates if a clot is in the body Treatment: Diagnose quickly, stabilize and treat underlying cause! *Antibiotics if Sepsis |
| Heparin-Induced Thrombocytopenia (HIT) | Venous and/or arterial thrombus due to immune response to the heparin in the body (clotting factor 4 and heparin molecule combine causing more clotting, the body produces antibodies against these molecules increasing the fibrin molecules = thrombus) |
| Heparin-Induced Thrombocytopenia (HIT) causes | Heparin therapy 5% of pts HIT Develops 5-10 days after onset of heparin therapy Suspect: platelet count drops by 50% or below 150,000/µL (Hold or Stop Heparin Therapy) |
| HIT TREATMENT | Notify MD, Hold or Stop Heparin! These complexes will continue to form Administer Antidote: Protamine sulfate Pt should NEVER receive heparin or LMWH again This must be documented in the medical record |
| Thrombotic thrombocytopenic purpura | RARE: associated with a deficiency in ADAMTS13 enzyme Microscopic thrombi: excessive clotting in the blood Clots deposit in arterioles and capillaries (collagen and vWF) BIND TO PLATELETS Multi Organ Failure |
| Thrombotic Thrombocytopenic Purpura (TTP) | CBC – hemolytic anemia & low platelets Too much clotting in small vessels But also low platelets (thrombocytopenia) → bleeding risk Lactic Acid – elevated s/t Hemolysis Blood Type and Cross match – for transfusions Troponin, EKG - Heart BUN, Crea |
| Manifestations of TTP | pancreatitis, AKI, CNS injury, heart injury, macrothrombosis |
| TTP TREATMENT | *Plasmapheresis (plasma exchange) within 4-8 hours of diagnosis with Fresh Frozen Plasma IV Corticosteroids – Methylprednisolone Oral Corticosteroids – Prednisone Rituximab RBC transfusion - Anemia Low-Dose ASA NEVER GIVE PLATELETS |
| TTP if not treated | **If NOT treated Kidney Failure and DEALTH usually from STROKE!** |
| HEMOPHILIA | X-linked recessive (female carriers, almost always male disorder) Punnett Squares of Probability Deficient/defective coagulation factor Hemophilia A (classic; Factor VIII (8) deficiency) Hemophilia B (Christmas disease; Factor IX (9) deficiency) |
| HEMOPHILIA diagnostics | Factor assays (VIII, IX, vWF) Determine type of hemophilia PT, PTT, Platelet count, Thrombin time |
| HEMOPHILIA treat | Hemophilia A: replace Factor VIII (8), desmopressin acetate (DDAVP) Hemophilia B: replace Factor IX (9) Topical thrombin and fibrin *Replace clotting factors before procedures/surgery |
| CLINICAL MANIFESTATIONS & COMPLICATIONS: HEMOPHILIA | Bleeding & life threatening hemorrhage Slow, persistent, delayed bleeding Uncontrollable hemorrhage from dental work GI bleeding Splenic rupture Hemarthrosis Joint bleeding Use “RICE” protocol (rest, ice, compress, elevate) |
| Penia versus cytosis | Leukopenia Decrease in total WBCs: Bone marrow depression, severe/chronic illness Sepsis especially alarming in older adults WBC count of < 5,000/µL |
| Penia versus cytosis pt 2 | Leukocytosis Increase in total WBCs: infection, leukemias, lymphomas, stress/trauma WBC count > 10,000/µL |
| LEUKOCYTES (WBCS) | WBCs originate from stem cells in the bone marrow Normal WBC count: 5,000-10,000/µL Granulocytes (have granules in the cytoplasm) Primary function is phagocytosis (digesting unwanted organisms = Bacterial) |
| Agranulocytes | (do not have granules in the cytoplasm = Viral) (LMN) -Lymphocytes, Monocytes, Natural killer cells |
| neutropenia | WBC = 2,000 cells Normal neutrophil count 2200-7700 cells/µL: To calculate Total Neutrophil count: Add percentages from: 14% + 6% = 20% Segs = 14% Bands = 6 |
| neutropenia pt 2 | Absolute neutrophil count (ANC): Multiply the total WBC count by percent of neutrophils, divide by 100 2000 x 20 = 40,000 / 100 = 400 Bone marrow aspiration and biopsy Neutropenia: Absolute neutrophil count (ANC) < 1000 cells/µL |
| NEUTROPENIA: Causes, MANIFESTATIONS, Management | Causes: Autoimmune disorders, drugs (chemo), hematologic disorders, infections, sepsis Manifestations: Depend on the cause Fever requires immediate attention Minor infections can lead to sepsis and death Sore throat and dysphagia, mouth ulcers |
| NEUTROPENIA management | Monitor for S/S of infection and septic shock Broad spectrum antibiotics IV *Protective isolation: Contact/Neutropenic Screen visitors and foods (sick; no fresh flowers or vegetables) Teach strict hand washing and oral hygiene |
| autosomal | NOT sex inherited |
| With the autosomal dominant Huntington’s disease, if the result is positive | the patient will develop the disease manifestations and can plan accordingly for their future. There is a 50% chance for each child to be affected |
| Genetic carrier screening should be done in families with a history of | sickle cell |
| sickle cell disease destroys | RBC |
| As part of standard procedure, the nurse remains with the patient for the first | 15 min after transfusion |
| blood test to test for HIT | Platelet count |
| anemia numbers | Microcytic → think iron problems Normocytic → think chronic disease or blood loss Macrocytic → think B12/folate |
| The aPTT level is increased (prolonged) in | heparin administration. aPTT is used to monitor whether heparin is at a therapeutic level (needs to be greater than the normal range of 30 to 40 |
| normal aPTT | between 25 and 35 seconds. |
| The complete blood count (CBC) indicates that a patient is thrombocytopenic. Which action would the nurse include in the plan of care? | avoid IM injections |
| shock | Clinical syndrome characterized by a decreased tissue perfusion and impaired cellular metabolism, or an imbalance between supply and demand for O2 and nutrients Imbalance results in a state of inadequate blood flow to body organs and tissues |
| Pathophysiology of Shock | Sustained drop in MAP (mean arterial pressure) Decrease in CO Decrease in circulating blood volume Increase of the vascular bed (vasodilatation) |
| Initial Stage of Shock: Cellular changes | Not clinically apparent Switch from aerobic to anaerobic metabolism Lactic acid builds up Liver needs oxygen to remove lactic acid |
| Compensatory Stage shock | Body activates neural, hormonal and biochemical compensatory mechanisms to overcome the anaerobic metabolism to maintain homeostasis Clinical symptoms begin Classic sign: Drop in BP (due to decrease in CO) |
| Progressive Stage shock | Mental changes, CO drops =profound decrease in tissue perfusion Pulmonary system Movement of fluid from pulmonary vasculature into interstitial space= pulmonary edema Renal Hypoperfusion = acute kidney injury = decreased UOP GI tract ischemia |
| Refractory Stage shock | Accumulation of lactic acid = increased capillary permeability and dilation Loss of intravascular volume Decreased coronary blood flow = decline in CO Decreased cerebral blood flow = cerebral ischemia Profound hypotension and hypoxemia |
| Cardiogenic Shock | This shock is different in the fact that the heart is failing. You do not treat this patient with large volume of fluids, instead you give Oxygen, treat source, give meds such as positive ionotropes |
| Cardiogenic Shock part 2 | either systolic or diastolic dysfunction of the heart’s pumping action results in reduced cardiac output MI, Cardiomyopathy, cardiac tamponade, dysrhythmias, valve stenosis (tachycardia, hypotension, tachypnea, and pulmonary edema) |
| Hypovolemic Shock | Loss of intravascular fluid volume Can be absolute loss (hemorrhage, vomiting diarrhea) or relative loss (third spacing, moving out of vascular space; burns) Manifestations: Anxious, tachycardia, tachypnea, cool and clammy skin. RAPID FLUID REPLACEMENT |
| Obstructive Shock | Physiological obstruction to blood flow with decreased CO Cardiac tamponade, tension pneumothorax, abdominal compartment syndrome, PE, RV thrombus Manifestations: JVD and pulses parodoxus Tx: maintain airway patency, supplemental O2 |
| Septic Shock | persistent hypotension despite fluid resuscitation; a syndrome in response to an infection (dysregulated patient response with new organ dysfunction) Manifestations: Abnl temp, hyperventilation, hypoxemia, warm and flushed and cool and mottled |
| Septic Shock treat | supplemental O2, aggressive fluid resuscitation, IV antibiotics, vasopressors |
| Neurogenic Shock | Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury; can last up to 6 weeks Usually associated with cervical and high thoracic injury Manifestations: Hypotension, bradycardia, unable to regulate body temperature |
| Neurogenic Shock treat | Maintain patent airway, Supplemental O2, cautious admin of IV fluids, spinal cord stabilization, atropine (for bradycardia) |
| Anaphylactic Shock | Acute, life threatening hypersensitivity to a sensitizing substance (drug, chemical, vaccine, food, insect venom) Massive vasodilation from an allergic/hypersensitivity reaction to some substance with acute laryngeal edema |
| Anaphylactic Shock manifestations and treat | dizziness, chest pain, incontinence, swelling, wheezing, stridor, anxious, confusion, hives, flushing, cramping, nausea, vomiting, sudden onset Maintain airway, fluids, Epinephrine immediately.Epinephrine, antihistamines (diphenhydramine,Bronchodilators |
| shock nursing care | Measure and record I & O hourly using a urometer Monitor bowel sounds, abdominal distention, and abdominal pain Maintain bedrest and provide a calm, quiet environment vitals q5-15min |
| Arteries | Thick-walled, elastic High pressure system Aorta 1” in diameter |
| artery layers | Intima: Inner layer, including the endothelial layer Media: middle layer of smooth elastic tissue, gives strength & ability to constrict & dilate Adventitia: outer layer of connective tissue |
| artery structures | Able to withstand pressure demands. Contain elastic fibers which allow their walls to stretch with systole and recoil with diastole. Contain smooth muscle to control the amt of blood delivered to the tissues. The |
| veins | Thinner-walled, distensible Low pressure system Less muscular Capable of great distension Holds 75% of TBV, do not have a pump to generate their blood flow. Skeletal muscle around the veins contract to push blood towards the heart |
| valves | Help blood flow against gravity back to heart |
| Capillaries | Referred to as the microcirculation Place where the exchange of gasses, nutrients and metabolites takes place between the tissue and the circulating blood. |
| Capillaries pt 2 | no elastic or muscle tissue. The capillaries connect the arterioles and venules. This is where the exchange of cellular nutrients and metabolic end products takes place |
| Atherosclerosis | form of arteriosclerosis where deposits of fat and fibrin obstruct and harden arteries, gradual thickening of the intima and media These changes cause impaired blood flow which is known as Peripheral Arterial Disease (PAD) |
| Peripheral arterial disease (PAD) | Thickening of artery walls = progressive narrowing Increases w/ age, 50-70 years, African Americans highest Risk factors Tobacco use (#1), CAD, Diabetes, Hypercholesterolemia, HTN, age over 60 |
| PAD Manifestations | Intermittent Claudication aching pain in calves, thighs, butt wt activity; relieved with rest heaviness, weakness to extremity Decreased or absent pulses, cap refill > 3 sec Rubor (dependent position), pallor (elevation) Skin thin, shiny, & hairless |
| PAD progression | As blood flow decreases, symptoms become more severe Rest Pain Usu in foot or toes; increases with elevation Critical Limb Ischemia Chronic rest pain lasting more than 2 weeks Includes non-healing arterial ulcers or gangrene |
| PAD complications | Ulcers (arterial) tips of toes, foot or lateral malleolus Gangrene Black eschar Amputation if blood flow is not restored Infection/sepsis |
| pad diagnosis | Ankle-brachial index (ABI) 0.90-0.71 – mild PAD 0.70-0.41 – moderate PAD <0.40 – severe PAD, Doppler ultrasound Angiography-invasive, needle in artery/dye |
| how to calculate ABI | ankle/brachial, check pt bp in branchial and leg(calf), worry abt systolic, leg bp- systolic 90, brachial-130 syst., 90 divided by 130= .69 |
| PAD meds | ACE inhibitors , Low dose ASA clopidogrel both (in high-risk pts) “Dual antiplatelet therapy” |
| meds to treat intermittent claudication | Cilostazol (Pletal) (inhibits platelet aggregation and inc vasodilation) Pentoxifylline (Trental) –dec blood viscosity |
| PAD antiplatlets | critical for reducing cardiovascular events and death in pad patients Controlling diabetes Not treating blockage, just helps blood flow better Walk 45 min a day 3x a week |
| PAD nursing care | Walk 30-45 min/day, 3x/week Risk factor modification Aggressive lipid management, tobacco cessation, control diabetes Nutritional therapy Maintain BMI < 25 kg/m² Waist circumference < 40 (men) and < 35 (women) Proper foot care |
| Treatment of PAD | Revascularization Percutaneous transluminal angioplasty, stent placement |
| Nursing care- Pre angiography | NPO, informed consent Assess patient for allergies (especially IV dye) and Metformin use IV fluids (if not contraindicated) Premedication (depends on facility) Preop labs (BMP, coags, CBC, poss type and screen, UPT) |
| Nursing care- Post angiography | Vitals q15 mins initially, then q30, then hourly Arterial Puncture site checks Usually groin, radial, brachial artery Assess for swelling, bleeding, hematoma Assess perfusion to affected extremities |
| Acute Arterial ischemia | Sudden interruption in arterial blood supply Ischemia—results in tissue death Embolization of thrombus from heart Risk factors: Afib, prosthetic heart valves, infective endocarditis, valve disease |
| Manifestations & Diagnosis Acute Arterial ischemia | 6 P’s Pain, pallor, pulselessness, paresthesia, paralysis (late sign), and poikilothermia (adaptation of limb to environmental temp) Will progress to tissue necrosis and gangrene within a few hours Diagnosis |
| Poikilothermia is the | adaptation of the limb to the environmental temperature, most often cool |
| Acute Arterial ischemia treat | IV Heparin, followed by long-term anticoagulation Catheter directed Thrombolytics : alteplase or urokinase Infused over a period of 24-48 hr Surgery Thrombectomy Surgical bypass PTA/Stent (percutaneous) Amputation |
| Thromboangiitis Obliterans (Buerger’s Disease) | Occlusive vascular disease—small peripheral arteries inflame and spasm—clots form Affects upper or lower extremity Risk factors: Male, <45 years old, long hx of smoking cigarettes or marijuana |
| Thromboangiitis Obliterans manifestations | Pain (claudication & rest pain), ischemic ulcers Color and temp changes of limbs Paresthesia Superficial vein thrombosis Cold sensitivity |
| Thromboangiitis Obliterans dgx and treat | Based on S&S and history Management: COMPLETE cessation of smoking (nicotine replacement products are contraindicated) Avoid exposure to cold Walking program Medications: IV iloprost (prostaglandin that promotes vasodilation) |
| Raynaud’s Phenomenon | Intense vasospasm in small arteries of fingers and toes Imbalance between vasodilation and vasoconstriction Usually women ages 15-40 |
| Raynaud’s Phenomenon manifestations | Intermittent spasms—digits turn white, then blue, then very red Coldness and numbness, followed by throbbing, aching pain, tingling and swelling Fingertips thicken & nails brittle Ulcerations, gangrene |
| Raynaud’s Phenomenon dgx and treat | symptoms persist for 2 years, Keep hands warm, avoid temp extremes, stop tobacco, avoid caffeine Sustained Release Ca Channel blocker (nifedipine) Vasodilators: phosphodiesterase-5 inhibitors(sildenafil) or topical NTG (do not use together) |
| Aneurysm | Abnormal dilation of a blood vessel Occurs in aorta/ peripheral arteries Form due to weakness of arterial wall. Hypertension is a major contributing cause. Complications: Dissection possible if a tear in tunica intima and meda alow invasion of blood |
| An aneurysm is permanent | permanent outpouching or dilation of the vessel wall. ¾ involve abdominal aorta Larger the aneurysm greater risk for rupture High bp |
| Aneurysm risk | HTN, CAD, tobacco use, high cholesterol Male gender Advancing age Strong genetic component Familial tendency related to congenital anomalies |
| Thoracic Aortic Aneurysm | often asymptomatic Manifestations based on location, size, growth rate Deep, diffuse chest pain extending to interscapular/shoulder area Ascending Aorta and aortic arch Angina, TIA, coughing, SOB, hoarseness, |
| Abdominal Aortic Aneurysm | Associated with arteriosclerosis and hypertension Mostly found in adult >65 Smoking is a contributing factor The larger the aneurysm, prevent rupture |
| Abdominal Aortic Aneurysm signs | Often asymptomatic Patient can present with a pulsatile abdominal mass/pain in midabdominal region or back. Bruit may be heard Pain may be mild to severe Diagnostic tests: CT Scan, MRI, x-ray, angiography |
| Abdominal Aortic Aneurysm complications | Rupture > hemorrhage > hypovolemic shock > death Severe pain in area of rupture Back or flank ecchymosis (Grey Turner sign) if lower abd rupture |
| Abdominal Aortic Aneurysm treat | Primary goal is to prevent rupture! Risk factor modification Stop tobacco Decreasing BP Long term Beta blockers Surgical repair if 5.5cm or larger AAA repair |
| Aortic Dissections | Life-threatening condition A tear in artery allows blood to dissect or split the vessel wall, forming a blood filled channel between its layers. |
| Aortic Dissections pt 2 | Males higher risk Hypertension is most important risk factor Other risk factors: Aortic diseases, atherosclerosis, blunt trauma, tobacco, cocaine/meth use, congenital heart dz, |
| Aortic Dissections manifestations | Diagnosis Chest xray, CT scan, MRI, or TEE Manifestations Severe, sudden pain over area of dissection “Worst ever”, “tearing”, “Ripping” Syncope/weakness Dyspnea Absence of peripheral pulses |
| Aortic Dissections complications | Cardiac tamponade (ascending aorta) Obstruction of vital organs near dissection Infarction of myocardium, kidney, or bowel Rupture, Hemorrhage and death |
| Aortic Dissections Medications & Treatments | IV beta-blockers (esmolol, metoprolol) IV Calcium channel blockers Hemodynamic monitoring, bedrest, pain relief Blood transfusion (if needed) Surgical or Endovascular Repair |
| Surgical Repair AAA and Dissection | Open Surgical Repair (large wound) Endovascular repair (small arterial puncture sites) |
| Surgical Repair AAA and Dissection preop care | What to expect after surgery (lines, ventilation, catheters), critical care Follow up with scheduled MRIs / CTs Long term use of BBs and ACE inh for BP control Routine preoperative care (NPO, abx, labs, consent) Medications to control bp and pain |
| Surgical Repair AAA and Dissection Postoperative Care | Open repair: Monitor incision site (abdomen or groin) Endovascular repair: Monitor groin puncture site Vital signs performed q15 min x 4, q30 min x2 then hourly Maintain fluid replacement– PROMPTLY report changes in VS, urine output |
| Surgical Repair AAA and Dissection Postoperative Care pt 2 | Report symptoms of lower extremity embolism (pain, numbness), bowel ischemia, impaired renal function, spinal cord ischemia Maintain adequate blood pressure (avoid hypo and hypertension) – GRAFT PATENCY, Adequate BP is very important to keep patency |
| Phlebitis | inflammation of the walls of small cannulated veins of the hand or arm From IV sites, usually in areas of flexion Manifestations: pain, tenderness, swelling, palpable cord Tx: Remove IV, warm, moist heat, elevate, NSAIDs |
| Venous Thrombosis | Formation of a thrombus (blood clot) with vein inflammation Can be Superficial or Deep. formation of a blood clot, or thrombus, associated with inflammation of the vein |
| Virchow Triad | Venous stasis Age, Afib, CHF, obesity, long trips, Ortho sx, immobility Endothelial Damage-puncture Indwelling catheter IV drug abuse, trauma, atherosclerosis Hypercoagulability of Blood Anemias, malignancies, polycythemia, medicines |
| Hypercoagulability | some drugs like estrogen or corticosteroids predispose a pt to thrombus |
| Superficial Venous Thrombosis | Formation of thrombus in a superficial vein, usually the saphenous vein Risk factors: venous catheters & infusions May develop in conjunction with thromboangiitis obliterans, varicose veins, DVT Spontaneously in Pregnancy Pain & tenderness at site |
| Venous Thromboembolism (VTE) | Includes process from DVT to PE Deep veins of arms, legs, pelvis (axillary, subclavian, iliac, femoral veins) Risk factors: Surgery, immobilization, orthopedic surgeries, cancers, pregnancy, oral contraceptives |
| VTE Manifestations & Complications | Unilateral leg edema Pain, tenderness, sense of fullness in calf/thigh Paresthesias, warm skin, erythema, temp 100.4 or more Deep reddish color to skin PE |
| VTE Diagnosis & Prophylaxis | Duplex venous US MRI/CT Scan Elevated D-dimer (above 250mcg/L), Early mobilization Low-molecular weight heparins Elevating foot of bed with knees slightly flexed |
| VTE Treatment | Thrombi prevention and reducing inflammation Anticoagulants Monitor for bleeding Coag studies (PT/PTT/INR) Bedrest initially Encourage ambulation |
| Superficial DVT we are relieving | inflammation, promoting rest Deep: Bedrest, anticoags, elevate legs, sometimes TED hose to reduce swelling |
| Pulmonary embolism | Blockage of 1 or more pulmonary arteries by thrombus, fat or air embolus, or tumor tissue Lower lobes most often affected Most arise from DVT in the legs Fat emboli from fractured bones Air emboli from IV therapy (improper use) |
| Pulmonary embolism – risk factors | Immobility or reduced mobility Surgery within 3 months (esp pelvic and lower extremity) History of VTE Cancer Obesity Oral contraceptives Hormone therapy pregnancy, HF |
| Pulmonary embolism manifestations & complications | Dyspnea most common Mild/mod hypoxemia Tachypnea, cough, CP, hemoptysis, crackles, wheezing infarction, HTN |
| massive pe manifestations | sudden change in LOC, hypotension, impending doom, cardiopulm arrest |
| Pulmonary embolism - diagnostics | Spiral CT scan (most common/best diagnostic test) D-dimer (not specific) CXR Ventilation/perfusion scan (VQ scan) Done for pts who cannot have contrast media |
| Pulmonary embolism interprofessional care | Immediate anticoagulation SQ LMWH (enoxaparin) is tx of choice Transition to oral anticoagulants Thrombolytics Surgical tx Pulmonary embolectomy Used in hemodynamically unstable patients IVC filter If anticoags are contraindicated |
| Heparin | Works on thrombin; prevents fibrinogen to fibrin SQ for VTE prevention IV for VTE tx (requires q6-8h PTT monitoring) Protamine Sulfate: antidote Prolongs activated Partial Thromboplastin Time (PTT) |
| Low-molecular-weight Heparin—Enoxaparin (Lovenox) | SQ Prevents Prothrombin to thrombin Risk for HIT lower, unless previously on heparin |
| Vitamin K antagonists - Warfarin (Coumadin) | Interferes with synthesis of Vit-K dependent clotting factors Does not effect existing clotting factors Vitamin K: antidote Monitor PT & INR Give same time everyday, |
| Selective factor Xa inhibitors | Fondaparinux (Arixtra) SQ Rivaroxaban (Xarelto) and apixaban (Eliquis) PO VTE prevention and treatment Coag monitoring not required |
| Anticoagulant therapy nursing considerations | signs of bleeding: hypotension, tachycardia, hematuria, melena, hematemesis, petechiae, bruising, oozing, or visible bleeding report black or bloody stool, bleeding gums Avoid ASA, NSAIDs, fish oil, garlic, ginkgo biloba, certain abx |
| Anticoagulant therapy nursing considerations pt 2 | Monitor H&H, RBC, platelets, coag studies Avoid IM injections, minimize venipuncture Humidify O2 Use electric razor Soft toothbrushes |
| Activated clotting time (ACT) Heparin, bivalrudin | Normal value-70-120 sec theraputic->300 sec |
| Activated partial thromboplastin time (aPTT) Heparin | normal-30-40 sec theraputic-46-70 sec |
| International Normalized Ratio (INR) Warfarin | normal-0.75-1.25 theraputic-2-3 |
| Thrombolytic treatment | Catheter directed tPA Urokinase, tPA Select patients with low bleeding risk Acute, extensive VTE Dissolves the clot Used with systemic anticoagulation |
| Chronic Venous Insufficiency and Venous Leg Ulcers | Inadequate venous return Large veins occluded, increased pressure distends other veins, damage valve leaflets Venous stasis leads to chronic skin changes, edema & leg ulcers |
| Chronic Venous Insufficiency and Venous Leg Ulcers manifestations and complications | Lower leg edema, dull aching pain Itching, eczema Brown, leathery skin pigmentation-pooling of rbc Venous ulcer (located above medial malleolus - ankle) Infection |
| Treatment – Venous Insufficiency & Venous Leg Ulcers | Compression stockings daily Essential for healing and preventing recurrence Avoid prolonged standing or sitting Elevate legs Daily walking Proper foot and leg care Moist environment dressings, Eat foods high in protein, vitamin C and Zinc |
| Varicose Veins | Irregular, tortuous veins Increased pressure > increased stretching > increased blood pooling > increased valve incompetency |
| Varicose Veins risks | Female Family hx Tobacco use Age, obesity, multiparity Venous problems Occupations that require long standing or sitting |
| Varicose Veins manifestations | Asymptomatic Heavy, achy feeling or pain after prolonged sitting or standing Leg fatigue Itching or burning Complications: Venous insufficiency Venous Leg Ulcer Superficial venous thrombosis |
| Varicose Veins treat | Graduated compression stockings Frequent leg elevation Daily walking Sclerotherapy Laser ablation Surgery (removal of vein) Postoperative: compression stockings, elevation |
| Sclerotherapy is | injecting a liquid or foam sclerosing substance that destroys the vein Surgical tx involves ligation of the vein (removal) Wear stocking s long term post |
| DIC can happen in | sepsis, pregnancy, cancer pts, burn pts, heat stroke, snake bites |
| heparin prolongs | PTT |
| Difficulty swallowing may occur with a | thoracic aneurysm because of pressure on the esophagus. |
| A patient in the outpatient clinic has a new diagnosis of peripheral artery disease (PAD). Which group of drugs will the nurse plan to include when teaching about PAD management? | statins |
| An older patient with chronic atrial fibrillation develops sudden severe pain, pulselessness, pallor, and coolness in the right leg. The nurse should notify the health care provider and immediately | keep the patient in bed in the supine position.The patient's history and clinical manifestations are consistent with acute arterial occlusion |
| A patient at the clinic says, "I always walk after dinner, but lately my leg cramps and hurts after just a few minutes of starting. The pain goes away after I stop walking, though." The nurse should | palpate for the presence of dorsalis pedis and posterior tibial pulses. |
| patient admitted to the hospital with venous thromboembolism. Which action by the nurse to elevate the patient's feet is best? | One pillow is placed under the thighs and two pillows are placed under the lower legs. |
| Enoxaparin will work | right away, but warfarin takes several days to begin preventing clots." |
| Compression of the leg is essential to | healing of venous stasis ulcers. |
| Which patient statement to the nurse is most consistent with the diagnosis of venous insufficiency? | Because the edema associated with venous insufficiency increases when the patient has been standing, shoes will feel tighter at the end of the day |
| which assessment finding for a patient who has been admitted with a right calf venous thromboembolism (VTE) requires immediate action by the nurse? | New onset shortness of breath |
| key difference DIC and TTP | Key differences include DIC’s abnormal coagulation studies (high INR/PTT) and lower fibrinogen, versus TTP’s normal coagulation |
| Which Hemophilia is known as deficiency in Factor VIIII? | Christmas Disease |
| What are Agranulocytes? | Do not contain granules in cytoplasm and consist of Lymphocytes, Monocytes and Natural Killer Cells like B & T Cells of Immunity |
| What is the level of Absolute Neutrophil Count to be considered as Severe Neutropenia and very high risk of Sepsis? | Absolute Neutrophil Count of <500 can be caused by chemotherapy treatment |
| Methylmalonic Acid (MMA) and Homocysteine Levels | When B12 levels are low, these two substances increase in the blood. An elevated MMA level is a more specific indicator of B12 deficiency than just the B12 level alone |
| Intrinsic Factor (IF) Blocking Antibody | most specific test for pernicious anemia. The test looks for antibodies that block the intrinsic factor protein, preventing it from binding to vitamin B12. A positive result confirms the autoimmune nature of the disease. |
| Without intrinsic factor, Vitamin B12 cannot be | absorbed in the small intestine. This is the leading cause of B12 deficiency |
| Red Blood Cell Indices | The red blood cell indices are crucial for diagnosing the type of anemia. They measure the size and color of the red blood cells. |
| iron range | 60-170 |
| TIBC range | 250-450 |
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