Exam #3 Flashcards
1
Q
hematology gerontologic considerations
A
- decreased red bone marrow in elderly leads to less reserves of blood cells, slower making of WBCs, RBCs
- very few changes
- may drop slightly, but remain in normal limits
- have diminished reserve capaciy
- have less reserve so harder to fight back after llness, esp with clotting, oxygen transport and fighting infection
- decreased red bone marrow to create new cells
- anemia is not an expected finding in elderly
- HGb is only decreased slightly: look for other causes if it is low (GI bleed)
- anemia causes in older adults: 1/3 is nutritional, 1/3 is renal insufficiency or chronic inflammation, 1/3 is unexplained
2
Q
hematology subjective assessment
A
- hemophilia, sickle cell disease, thalassemia, hemachromatosis, leukemia, pernicious anemia, clotting disorders
- medications:
~ salicylates (aspirin) - decrease platelet stickiness
~ NSAIDs - inhibit platelet aggregation
~ Herbs - many herbs affect coagulation
~ oral contraceptives - increased clotting risks
~ immunosuppressants - affect WBCs
~ chemo - affects all cells, decreased bone marrow activity - past surgical procedures
~ splenectomy - loss of 300ml of blood storage and platelets, increae number of circulating platelets
~ duodenal or ileal surgeries - interferes with iron absorption, b12 absorption
~ stomach surgery
~ partial or total gastrectomy or ilea resection: affects intrinsic factor with affects b12 absorption
~ gastric bypass surgery: interferes with iron absorption
~ ileal resection - affects intrintic factor b12 absorption - ethnic decent: aftican americans (sickle cell), norther euros (pernicious anemia/b12 issues), mediteraneans (thalassemia)
- alcohol or cigarette use: GI bleeds, vitamin deficienceis, damages to liver which affects clotting factors, hypoxia, decreased platelets, increased blood viscosity
- nutrition history: inadeuqate intake of iron, iron/cobalamin/folic acid are required to make RBCs, liver meat eggs whole grain pottateos leafy green veggies dried druits legumes citrus fruits
- joint pain: autoimmune disorder, gout from uric acid breakdown of cells (hemolytic anemia), bleeding into joints, pain from leukemia,
3
Q
Hematology objective assessment
A
- lymph nodes:
4
Q
splenomegaly
A
- spleen’s function is to filter the blood, clear microorganisms and antigens, remove abnormal and old RBCs, store paltelets and WBCs, fights the bacteria of menningitis and pneumonia
- spleen can trap all the blood cells, stores 30% of the body’s platelets and iron for later
- if spleen is removed, higher circulating platelets and potential for clotting problems
- when enlarges, it doesnt work as well and can lead to a decrease in blood cells, increased risk for rupturs – S/s = asymptomatic, abdominal pain, early satiety, anemia, thrombocytopenia, leukopenia
- spelenctomy is done to increase blood cell count or for splenic rupture
- post spelenctomy: can have immunologic deficiencies leading to a lifelong risk of infection, recommend pneumovax, influenza vaccine
5
Q
lab tests for spelnomegaly
A
- normal hematocrit = 35-45
- normal hemoglobin = 12-16
- normal total RBCs = 4-5
- CBC
- assess 3 major blood cells formed in the bone marrow (RBCs, WBCs, platelets)
- hemoglobin: decreased with anemia, hemorrhage, fluid overload; increased with polycythemia, dehydration (more concentrated)
- hematocrit: percentage of RBCs in total blood volume, affected by the same things as hgb
- total RBCs:
~ MCV = mean corpuscular volume - size (low is small)
~ MCH = mean corpuscular hemoglobin - weight (low is hypochromia
~ MCHC = mean corpuscular hemoglobin concentration - saturation with Hgb
6
Q
WBC lab tests
A
- WBCs: 4,000-11,000
- indicated infection, inflammation, leukemia
- total count and differential count which tells the percentage of each type of WBC
- if lots of bands = shift to the left = inflammation; bands are immature WBCs that increase during infection/inflammation
- can have a normal WBC but abnormal differential like with neutropenia
- CBC with differential = WBC cell type counts (neutrophils, basophils, etc), absolute neutrophil count
- (% neutrophils {segs + bands} x total WBC count) = abs neutrophil count
- normal abs neutrophil ct = 1500-7000, ~ 1000 = cautious,
7
Q
platelets lab tests
A
- normal range: 150,000-400,000
- below 100,000 = thrombocytosis
- thrombocytosis would be platelets > 400,000 and casues excessive clotting
- peripheral smear: sickle cells, indicates the presence of abnormal or immature cells, looks more closely at the types of cells, shapes of cells, maturity of cells; may be performed when a person has s/s that sugest a condition affecting blood cell or lifespan
8
Q
coagulation lab tests
A
- aPTT: activated partial thromboplastin time
~ measures clotting time
~ normal 25-35 seconds but up to 70 if on anticoagulants
~ focuses on the intrinsic pathway in the blood clotting process
~ PTT monitors affects of heparin
- PT: prothrombin time ~ measures clotting time ~normal 11-13 seconds ~ focuses on extrinsic pathways in the blood clotting process ~ monitors effects of coumadin
- INR: international normalized ratio
~ standardized way of reporting the PT
~ normal 0.9-1.1, but 2-3 if on anticoagulation
9
Q
other coag tests
A
- D-dimer:
- shows hypercoagulability, helps diagnose PE, DIC
- D-dimer is the degradation product of cross-lined fibrin
- meaning there has been a thrombosis of some sort
- shows the break down of a clot going on somewhere int he body
- FSP: fibrin split products or FDPs: fibrin degredation products
- shows bleeding risk, helps diagnose DIC
- FSP and FDP are the products of a dissolving clot
- FDP can increase if plasmin has been activated somewhere without there being a clot
- high levels of FDP suggests DIC
- Fibrinogen:
- if low suggests bleeding risk, if high suggest hypercoagulability
10
Q
anemia laboratory tests
A
- hemoglobin electophoresis
- used to identify sickle cell anemia, thalassemia
- measures the different types of hemoglobin in the blood: Hgb S = sickle cell anemia, Hgb C = hemolytic anemias, diagnos thalassemia
- reticulocyte count
- immature RBCs
- increased in bleeding, hemolytic anemia
- decreased in other types of anemia
- erythrocyte sedimentation rate ESR
- measure the settling rate of RBCs
- shows increased cell destruction
- usually indicative of inflammation
- iron tests
- TIBC: all proteins that bind or transport iron between the tissues and the bone marrow
- 2/3 of total body iron bound to heme in erethrocytes and muscle cells
- ferritin: body iron stores, bone marrow, spleen, liver, macrophages (when RBCs break down, iron gets stored)
- transferrin saturation: better indicator of iron availability than iron because this iron is already bound and ready to be used
- B12 or folate levels
- make RBCs
- schilling test (urine test)
- urine test used to determine whether the body absorbs B12/cobalamin
- client is given an oral dose of radioactive b12 and then 2-6 hours later is given a non-radioactive injeciton of b12
- urine is then collected to see how much b12 is absorbed
- several stages of this test can be given to determin if the problem is with intrinsic factor
- helps determine if it is a low b12 issue or an intrinsic factor issue
11
Q
Bone marrow examination
A
- may use conscious sedation or local anesthesia
- preferred site: posterior iliac crest
- very painful
- gives a full evaluation of hematopoiesis
- need signed consent
- pressure dressing over site
- lie on rolled towel for additional pressure for 30-60 minutes post procedure
- may be sore 3-4 days after
- monitor s/s of bleeding after
- lay laterally, sterile technique
12
Q
hematology disorders
A
- anemias: low RBCs, Hgb, Hct
- low RBC production - deficiencies, aplastic anemia, anemia of chronic disease
- blood loss
- high RBC destruction ; SCD, G6PD, external damage
- risk of fatigue and possible hypoxia
- thrombocytopenias: low platelets
- hemophillia, von willebrands
- ITP, TTP, HIT, DIC
- risk of bleeding
- neutropenia: low neutrophil/WBC count
- risk of infection
- pancytopenia: all cell types are low
- aplastic anemia
- chemotherapy
- spenlomegaly
- causes thrombocytopenia, anemia, luekopenia
- polycythemia: too many cells
- hypoxia is the primary cause
- tells body to make more RBCs but still not enough 02 in the body
- can cause a stroke - increased RBC, WBC, platelets = major risk for clotting
- hemochromatosis: too much iron
- can be deadly
- genetic or from chronic blood transfusions
- toxic levels of iron in body deposits in organs, liver, heart, kidneys
- cancers
- leukemia, hodkin’s lymphoma
- non-hodgkin’s lymphoma
- multiple myeloma
13
Q
Anemia
A
- too few RBCs or not enough hemoglobin
- can be grouped by cell type (morphology) or by cause (etiology)
- normocytic, normochromic = normal size, normal color
- microcytic, hypochromic = small size, pale color
- macrolytic, normochromic = large size, normal color
- pathophys = blood loss, impaired produciton of RBCs, increased destruction of RBCs, can be a primary problem or a result of a chornic condition
- results from chronic disease, poor diet, defects in RBCs
14
Q
Anemia S/S
A
- mild: hgb 10-12 – no symptoms, may have few symptoms with exercise
- moderate: hgb 6-10 – palpiations, dyspnea, mild fatigue with activity and at rest
- severe: hgb
15
Q
anemia treatment/nursing care
A
- goals: be able to do ADLs, maintain nutrition, have no complications
- give volume replacement and oxygen only if needed and treat the cause: blood loss (give blood products and find the source of the blood loss); chronic disease (treat the disease, give epogen); deficiencies (give vitamins, supplements, change diet or improve absorption
- help with fatigue: alternate rest and activity periods, prioritze activities
16
Q
anemia caused by decreased RBC production
A
- iron deficiency anemia: dietary or blood loss
- cobalamin (vit b12) deficiency: dietary issue or lack of intrinsic factor
- folic acid deficiency: dietary
- thalassemia: genetic, decreaesd RBC production
- aplastic anemia: genetic or aquired
- anemia of chronic disease: kidney, liver, immune, endocrine
17
Q
Iron deficiency anemia, decreased RBC prodcution
A
- causes: inadequate dietary intake, malabsorption or GI/intestinal issues, blood loss/chronic GI and GU losses
- s/s: pallor, glossitis (inflamm of tongue), chelitis (inflamm of lips), headache, parasthesias, burning sensation of the tongue (lack of iron in tissues)
- DX testing: iron studies, RBC indices (shows shape of RBCs), testing to determine where bleeding is coming from, may need endoscopy or colonoscopy to determine cause of the anemia
- TX: treat underlying problem, increased iron intake (Meats, green leady veggies, beans, tofu, iron-fortified breads and cereals), oral iron supplements
- identify those at risk: premenopausal and pregnant women, persons from low socioeconomic backgrounds, older adults, those experiencing blood loss
18
Q
Iron Supplementation
A
- ferrous sulfate is the best
- no enteric-coated or sustained-release iron
- liquid stains the teeth if not diluted, give via straw
- take with vitamin c or OJ (acid increases iron absorption)
- take iron one hour before meals
- GI side effects: black stools, constipation
- IV or IM needs to be given Z track, separate needlse for withdrawing and administering to prevent staining of the skin
19
Q
Cobalamin (vit B12) dficiency, decreased RBC production
A
- cause: Intrinsic factor is normally secreted by the cells of the gastric mucosa and cobalamin cant be absorbed without IF; pernicious anemia: issue with parietal cells and b12 absorption; nutritional deficiencies after GI surgery/problems; long term users of stomach acid blockers; strict vegetarians; herediary enzyme deficiencies
- S/S: insidious onset/no warning signs, megaloblastic anemia (RBCs are large, abnormal and fragile), sore, red, beefy tongue, shiny; GI Problems, neuromuscular problems (difference between folic acid issues and IF issues_
- DX testing: schilling test (if lots of B12 in urine, it means the body isnt absorbing it correctly
- TX: IM or intranasal cobalamin - bypasses the GI tract to help body absorb B12
20
Q
Types of: Cobalamin (vit B12) dficiency, decreased RBC production
A
- pernicious anemia
- megaloblastic anemia: RBCs are large, abnornal, fragile
- gastric mucosal atrophy/immune destruction: body cant make enough RBCs, doesnt have enough B12 (RBCs cant divide norally and are to big, get stuck in bone marrow, nervous system dysfunction
- S/S: usually begins after age 40, more common in northern europeans and african americans – sore tongue, n/v, abdominal pain, weakness, paresthesias, confusion, dementia
- schilling test: shows how much b12 gets absorbed or not
- TX: increasing dietary cobalamin will no help since it cant be absorbed without IF, must take IM or intranasal cobalamin or they will die within 1-3 years and then must take it for life
- pernicious anemia increases the risk of gastric cancer so need frequent/careful screenings
21
Q
Folic Acid Deficiency, decreaesd RBC production
A
- folic acid is required for DNA synthesis leading to RBC formation and maturation
- cause: dietary deficiency, malabsorption syndromes, drugs (methotrexate, dilantin), alcohol abuse, hemodialysis
- S/S: megaloblastic anemia, smooth/beefy/red tounge, no neurologic impairment, lack of neurologic involement helps distinguish between this and cobalamin deficiency
22
Q
Thalassemia, decreased RBC production
A
- autosomal recessive genetic disorder
- some of the genes needed to make hgb are missing: cuauses the RBCs to form incorrectly or not carry enough O2, hemolysis also ocurs but decreased production is primary problem
- causes: genetic disease, mediteranean descent
- S/S: minor - not many symptoms, major - severe physical and mental retardation, pallor, pronounced spenomegalry and hepatomegaly, jaundice, cranial problems
- TX: DO NOT GIVE IRON (body is already breaing down RBCs and so th body has an overload of iron), blood transfusions q 2-4 weeks to help them get normal RBCs with hemoglobin, iron chelation therapy (strips excess iron), spenectomy (300ml blood loss), human stem cell tx increase good RBC production
23
Q
anemia of chronic disease, decreased RBC production
A
- cause: end stage renal disease, chornic liver disease, immune disorders, endocrine disorders
- S/S: usually mild anemia with mild syptoms
- DX test: normocytic RBCs, normochromic RBCs, decreaesd RBCs
- TX: correction of underlying disorder, epogen, procrit, rarely transfusions, IV iron
24
Q
aplastic anemia, decreased RBC production
A
- decrease of all blood cell types and hypocellular bone marrow
- Cause: congenital (fanconi syndrome), acquired (chemica agents, drugs, idopathic, pregnancy, radiation, infection), 75% is idopathic and thought to have autoimmune basis
- S/S: usually develops gradually bu can be acute, pancytopenia, hypocelluarl bone marrow, general manifestion of anemia, gatigue, dyspnea, as well CV, neuro responses, neutropenia (infections, shock), thrombocytopenia (bleeding)
- DX tests: pancytopenia, bone marrow aspiration - finds hypocellular bone marrow and increased yellow marrow
- TX: supportive care, remove causitive agent, prognosis is poor if untreated, BMT or immunosuppression
25
Q
anemia, due to blood loss
A
- CAUSE: acute hemorrhage, chornic blood loss (GI, GU)
- S/S: look at clinical symptoms more than lab values, clinical symptoms are much more import, may take a while for the HGB/HCT to decrease
- DX results: RBC, Hgb, Hct wont drop for 2-3 days
- TX: prevent shock, identify source of hemorrhage, blood transfusions and iron may be needed, plasma expander, LR, albumin, dextran, may need supplemental iron, blood transfusions may be neded for a few days while the body produces more if its own RBCs
26
Q
anemia, hemolytic, icnreased RBC destruction
A
- intrinsic, genetic defects in RBCs
- abnormal hemoglobin (sickle cell), enzyme deficiency (G6PD - makes proper size and shape of RBCs)
- Extrinsic: external damage to RBCs
- physical trauama: hemodialysis, prosthetic heart valves, narrowed vessels
- antibodies: blood transfusion reactions, SLE, leukemia, certain meds
- infectious agents and toxins: malaria, clostridium, arsenic lead, copper, snake venom
- S/S: jaundice is common, hepatomegaly and splenomegaly is common, increase in reticulocytes (immature RBCs) as the body tries to compensate
- tx: maintain kidney function and prevent acute tubular necrosis
- iron and heme can clog kidneys when relseased during RBC destruction
27
Q
Sickle Cell Disease, increased RBC destruction
A
- abnormal form of Hgb (Hgb S) in the RBC
- when there is hypoxia, the RBCs sickle
- primarily affects african americans
- Types: sicke cell anemia (from both parents), sickle cell thalassemia, sickle cell Hgb C, sickle cell trait
- S/S: varies greatly, often have chronic health problems, anemic but asymptomatic except during crisis, jaundice and gallstones are commone
- Sickle Cell Crisis: severe, painful, acute exacerbaton with vaso-occlusion, pain, fever, tachypnea, HTN, n/v
- pathophys: sickling of the RBCs triggered by low o2 level of the blood caused by infection, high altitiude, stress, surgery, blood loss, dehycration, acidosis, low body temp, siclled cells get stuck worsening the symptoms; occurs when o2 is low
- clumped cells caused increaesd risk for cots, increasd potassium and uric acid
- complications: clotting, kidney issues, heart issues, immune issues, tissue necrosis from being blocked from blod flow, stasis and ulcers
28
Q
Diagnosis and TX of sickle cell disease
A
- lab tests:
- Hgb electrophoresis: determines the amount of Hgb S (specific to sickle cells)
- peripheral blood smear: reveals sicled cells, abnormal reticulocytes
- sicking test: agent is added to RBCs to see if they will sickle
- bilirubin: released from hemolysis
- prevention of SCC: teach pts to avoid high altitudes, get good fluid intake, treat infecitons promptly, flu/pneumonia/hepatitis vaccines
- TX of SCC
- fluids: helps increased perfusion to tissues
- oxygen: help prevent further cells from sickling
- aggressive opioid pain mamangement
- close monitoring of respiratory status: PEs, acute chest syndrome
- rest and DVT prevention: decreased amt of O2 needed
- transfusion
- iron chelation therapy
- hydroxyurea increases the production of hemoglobin F seems to help by decreasing hemolysis and sickled cells
- stem cells are only possible cure
29
Q
hemachromatosis, iron overload
A
- usually genetic but can be from thalassemia, liver disease, or frequent blood transfusions
- present at birth but often dont get symptoms until age 50-60
- less common with females because they lose blood during regularly montly menses
- S/S: fatigue, arthralgia, impotence, abd pain, weight loss, liver problems, bronze skin, cardiac changes
- labs: increased iron, increased TIBC, increased ferritin
- TBI: normal 2-6, hem 50
- TX: remove excess iron, remove 500ml weekly for 2-3 yrs, manage organ involvemtn, dietary changes
- most common cause of death if not monitored are cirrhosis, liver failure, liver cancer, heart failure
30
Q
polycythemia
A
- increased production of RBCs leading to increased blood viscosity and volume
- polycythemia vera: chromosomal mutation, insidius, chronic, increased production of RBCs, WBCs and platelets
- S/S: HTN, headache, vertigo, dizziness, pruritis, paresthesias, painful burning/redness of hands and feet, angina, heart failure, intermittent caludication, thrombophlemtitis, hemorrhage, hepatomegaly, splenomegaly, ruddy complextion, gout; increased risk for DVT
- all lags are elevated, spenomegaly in 90% of pts with polycythemia vera; hgb 20+, hct 50%, s/s are often due to increased blood thickness and clotting
- tx: phlebotomy, no iron, hydration, hydroxurea, low dose ASA
31
Q
bleeding, clotting disorders
A
- vascular endothelium, platelts, coagulation factors, which normally function together to stop hemorrhage and repair vascular injury. disruption in any of these compinents may result in beldding or thrombotic disorders
- Thrombocytopenias: ITP, TTP, HIT, DIC, hemophilia, von willebrand’s
32
Q
thrombocytopenia
A
- plateltes
33
Q
thrombocytopenic precautions
A
- discourage use of OTC meds that can caused thrombocytopenia = ASA, NSAIDs
- teach pt to notify dr even for minor nosebleed, gums bleeding, new petechiae
- aboid injections if possible
- if needed, us small gauge needels and hold pressure for 5-10 minutes after
- supress menses
- soft toothbrushes, no flossing, use electric razor, avoid high impact activities
- blow nose gently, prevent constipation, do not tweeze body hair
- no tattoos or piercings
- call dr if BMs black, black vomit or urine, bruising, petechiiae, bleeding, heacahce, change in vision, stroke symptoms
34
Q
immune thrombocytopenic purpura (ITP)
A
- most common acquired thrombocytopenia
- autoimmune disease
- platelets survive
35
Q
thrombotic thrombocytopenic purpura (TTP)
A
- medical emergency!
- uncommon syndrome with clumping of platelets, leading to microthrombi in small vessels
- as the platelts clump up, less are available to the rest of the body causing bleeding
- almost always associated with hemolytic uremic syndrome (increased uric acid)
- causes: idiopathic, drug toxicity, pregnancy/preeclampsia, infxn, autoimmune disorders
- S/S: hemolytic anemia, thrombocytipenia, neuro problems, fever with no infection, renal problems
- tx: stop underlying disorder, remove causitive agent, plasmapheresis daily (removes antibodies that bind with platelts), corticosteroids, splenectomy, no platelet transfusions (causes more clumping and clotting)
- adam 13 enzyme issue
36
Q
heparin induced thrombocytopenia (HIT)
A
- patho: formation of abnormal antibodies that activate platelets
- major complication is venous thrombosis, DVT, PE
- other complications: stroke, kidney damage, MI
- S/S: rarely have bleeding, new or worsening thrombosis, decreased paltelt count
- TX: have to protect from thrombosis and not reduce the platelet count further (no warfrin, no platelet transfusion); stop heparin, maintain anticoagulation with direct rhombin inhibitors, for severe clotting do plasmapheresis or surgery to remove clots, no platelts, never give heparing o them again
37
Q
Disseminatee Intravascular Coagulation (DIC)
A
- complex systemic thrombo-hemorrhagic disorder
- clotting is abnorally initiated and accelerated using up all of the clotting factors and platelets leading to uncontrolable bleeding
- not a disease, but a complication - always secondary to an underlying disorder (septic shock, trauama)
- almost always causes organ failure
- can also have chornic DIC in which the body compensates (malignancies, autoimmune disease)
38
Q
DIC S/S
A
- no well-defined sequence of events
- unexplained bleeding: pallor, petechiae, pupura, oozing blood, hematomas
- weakness
- malaise
- fever
- respiratory: tachy, hemoptysis, orthopnea
- GI bleeding, abd distention, bloody stools
- urinary hematuria
- neuro, vision changes, dizziness, headache, changein LOC, irritability
- bone and joint pain
- thrombotic s/s: cyanosis, necrosis, PE, ARDS, ECG changes, paralytic ileus, oliguria
39
Q
DIC diagnosis and tx
A
- D-dimer assay: increaesd
- Fibrin Split products: increased
- Fibrin degredation products: increased
- schistocytes on blood smear
- treatment is controversial: if chornic and no bleeding, leave it alone; if bleeding then provide support with blood products and treat the primary disorder; only use platelts if life threatening; if signs of thrombosis, use heparin
40
Q
DIC nursing care
A
- identify and call the doc ASAP
- early detction of bleeding and microthrombi
- administer blood and blood products correctly
- same care as those with thrombocytopenia
41
Q
hemophilia and von willebrand disease
A
- x-lined recessive genetic disorder caused by defective or deficiecy coagulation factor
- hemophilia A: classic or factor VIII deficiency
- Hemophilia B: christmas disease, factor IX deficiency
- von willebrand disease: deficiency of von willebrand coagulation protein
- hemophilia is transmitted by female carriers but displayed almost exclusively in men, von Willenbrand is seen in both genders
42
Q
hemophilia and von willebrand disease S/s
A
- slow, persistent, prolonged bleeding in minor trauma
- delayed bleeding after minor injuries
- gi bleeding from ulcers and gastritis
- SQ hematomoas that can lead to nerve compression
- hemarthrosis leading to joint injury/deformit
43
Q
hemophilia and von willebrand disease TX
A
- preventative care
- reolacement of deficient cloting favtors with active bleeding and before surgery
- gelfoam for minor bleeding
- DDAVP for minor bleeding and dental procedures
- antifibrinolytics with oral bleeding, nosebleeds, menses
- gene therapy
44
Q
hemophilia and von willebrand disease CX
A
- development of antibodies to factors VIII or IX
- transfusion-transmitted infectious diseases (HIV, Hep B, Hep C)
- allergic reactions
- thrombotic complications with factor IX
- with con willebrands, can develop antibodies
- starting factor replacement too late or stopping too soon
