Exam #3 Flashcards
(110 cards)
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
anemia, due to blood loss
- 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
anemia, hemolytic, icnreased RBC destruction
* 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
Sickle Cell Disease, increased RBC destruction
- 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
Diagnosis and TX of sickle cell disease
* 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
hemachromatosis, iron overload
- 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
polycythemia
- 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
bleeding, clotting disorders
- 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
thrombocytopenia
- plateltes
33
thrombocytopenic precautions
- 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
immune thrombocytopenic purpura (ITP)
- most common acquired thrombocytopenia
- autoimmune disease
- platelets survive
35
thrombotic thrombocytopenic purpura (TTP)
- 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
heparin induced thrombocytopenia (HIT)
- 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
Disseminatee Intravascular Coagulation (DIC)
- 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
DIC S/S
- 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
DIC diagnosis and tx
- 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
DIC nursing care
- 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
hemophilia and von willebrand disease
- 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
hemophilia and von willebrand disease S/s
- 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
hemophilia and von willebrand disease TX
- 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
hemophilia and von willebrand disease CX
- 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
45
hemophilia and von willebrand disease nursing care and teaching
- genetic counseling
- aminister specific coagulation factor
- if joint bleeding: rest joint, pack with ice, treat pain without NSAIDs/ASA, once bleeding stops then do ROM and PT, no weight bearing until healed
- watch for life threatining complications
- no contact sports
- wear gloves when doing household chores
- wear a medic alert bracelet
46
neutropenia
- normal ANC: 1500-7000
- ANC = (% neutrohils) x WBC count
- reduction in neutrophils: absolute neutrophil count
- ANC 100.4 is an issue, growth colony stimulating factor to prevent neutropenia, handwashing, private room, avoid crowds, wear mask, dont garden or clean up after pets, no uncooked meats, no fresh flowers, bathe or shower daily
47
blood component administration
1) get VS
2) get blood
3) 2 RNs check blood
4) get VS again
5) prime line with NS
6) prime with blood
7) hook up to pt
8) 1st set slower then increase after 15 mins after no reaciton has occured
9) 150.hr the rest of the bag
- 19 gauge needle or bigger
- y tubing with filter
- NS only
- meticulous product-to-patient identification
- administer immediately, don't refrigerate
- obtain baseline, pre transfusion, 15 minutes after starting and after transfusion VS
- remain with client or first 15 minutes
- proper rate of infusion: give over 2-4 hours, platelets and FFP over 15-30 minutes
48
normal cranial values
- Intracranial pressure (ICP): 5-15mmhg
- > 15 is a concern, complications are inadequate perfusion (decreases CPP), herniation (death)
- Cerebral perfusion pressure (CPP): 60-100 mmhg
-
49
CPP/ICP
- cerebral perfusion pressure: pressure needed to ensure blood flow to the brain, this is affected by oxygentation, cerebral blood volume, BP, cerebral edema, and ICP
- usually a higher BO helps to reprorofuse cerebral tissue
- with increased ICP it makes it worse: high iCP collapses the arteries, CO2 increases, chemoreceptors are activated and the BP is increased more to open the arteries
- decreased o2 = brain arteries dilate
- increased co2 = brain arteries dilate
- increased o2 = brain arteries constrict
- decreaesd co2 = brain arteries constrict
50
compensation
- monro-kellie hypothesis says that any increase in volume, in any of the components, must be compensated for by a decrease in the olume of one of the other components
- change in CSF volume: absorption or producitnon, movement of CSF to the spinal subarachnoid space means it will get shunted somewhere else
- change in intracranial blood volume: collapse of cerebral veins/dural sinuses, cerebral vasoconstriction/dilation, change in venous outflow
- change in brain tissue volume: distention of dura, compression of brain tissue
- an increased ICP causes and Increased BP to keep the brain arteries open
51
causes of increased ICP
- space-occupying lesions: tumor, absecess
- CSF flow obstruction: hydrocephalus, CSF wont drain out of the brain
- cerebral edema: head trauama, ischeic stroke, hepatic encephalopahty, postop edema, low sodium
- menningitis or encephalitis
- metabolic disorders: hyponatremia (neuro issues, fluid shifts into cell
- increase in abdominal, cehst pressure, valsalva, suctioning or coughing, posture (decreases o2 and increases ICP)
- vasodilation: acidosis, low PH and high co2 are vasodilators
- increase in metabolic demand: fever, decreases o2 available in body
52
symptoms of increased ICP
- change in LOC (the only early symptom)
- most sensitive and reliable indicator of neuro status
- happens b/c of hypoxia, increased co2
- any patient who becomes acutely unconscious should be suspected of having increased ICP
- 40 ICP will cause a change in LOC
- changes in VS: temp may vary widely, cushing's triad (widended pulse pressure, low HR, altered resp pattern) emergency! late sign of increased ICP
- very rare to have shock even with a bleed
- hypothalamus controls temp
- medical emergency with impending death from brainstem compression
- lack of autoregulation
- cushing's triad (late sign): decreased HR with full/bounding pulse, systolic HTN with widening pulse pressure, altered respiratory pattern
- change in pupils: ipsilateral (same side as injury), one fixed pupil and one dilated, can mean a herniation, emergency, blurred vision, diplopia, pailledema (optic disc swelling)
- change in motor function (contralateral): opposite side of injury, hemiparesis/hemipalegia
53
decorticate, decerebrate
- decorticate: flexor, adduction of limbs/hands (issue with cerebral cortex)
- decerebrate: extensor, arms extended, more serious issue with brainstem and midbrain
54
diagnostic testing for increased ICP
- CT/MRI: looks for causes
- ICP monitoring and LICOX: brain oxygenation
- EEG, evoked potentials: look at permanent damage and seizures, evokes potentials to look for brain activity
- PET: radioactive tracer to see how the brain tissues are working, showing blood flow and oxygen and glucose metabolism in the brain
- do not do lumbar pucnture! it can quickly drop the ICP and cause a brain herniation
55
ICP monitoring
- ventriculostomy: monitors ICP, give meds, drains CSF
- keep open to drain and stay within ordered pressure
- then close to get an accurate reading of the true ICP
- Tranducer must be at the tragus of the ear, close clamp for 5-20 minutes before reading the pressure
- big risk of infection, put a sign above the bed
* ICP 5-15 mmhg
- P1: percussion wave: represents arterial pulsations, highest wave of the three; blood hitting arteries during heart beat, arterial pulsations
- P2: rebound wave: reflects intracranial compliance, higher than P1 when intercranial compliance is compromised; ability for cranial arteries to comply with blood flow
- P3: dicrotic notch: represents venous pulsations, lowest wave form; venous draning of the brain
- if high ICP, then P2 > P1
* * P2 tells us about ICP issues
56
Licox
- brain tissue oxygenation catheter: placed in healthy white brain matter, measures brain oxygenation and temperature; used a lot in severe ischemic stokes to measure extent of damage
- placed into the healthy white matter of the brain
- normal range for PbtO2 is 20-40mmhg = proper o2 to brain tissue
- cooler brain temperature is better: vasoconstricts and decreases ICP
- jugular vein oxygenation saturation SJV02 = 55-75% - tells us how much 02 the brain is using, returned 02 from the brain to the heart through the JV
57
treatment for increased ICP
- CSF drain, ICP monitoring
- ET tube, trach to keep pa02 at 100, paCO2 30-35
- surgical removal of mass
- decompressive hemicarniectomy to decrease ICP/prevent herniation
- only light sedation, be careful with drugs that alter the neuro state: rapid opioids (moriphine) have calming effect; , propolfol is good, it can work quickly and then fade quickly; avoid long lasting benzos
58
cranial surgery
- burr hole: opening into the cranium with a drill, removes fluid and blood beneath the dura
- cariotomy: opening into the cranium with temporary removal of bone flat and opening of the dura; removeslesions, repairs damage, drains blood, relieves ICP
- cariectomy: removal of a bone flap
- cranioplasty: repair of a cranial defect, can use artifical material to replace bone
- stereotactic: uses frame and 3 dimensional coordinates to precisely locate an area of the brain, and do biopsy radiosurgery, dissection
- shunt: redirects CSF from one ares to another - fluid can drain from brain to periotoneal cavity or other ares of the body
59
Drugs to decreased ICP in brain
1) mannitol/osmitrol
- osmotic diuretic given IV
- plasma expansion reduces the hematocrit and blood viscosity increasing cerebral blood flow and thus oxygen delivery to the brain
- osmotic effect helps move fluid from tissues into blood vessels therefore decreasing total brain fluid content
- give when ICP is around 20! (norm 5-15)
2) hypertonic saline 3%
- can be as effective as mannitol or used concurrently
- raises the osmolality of the ECF in the brain
- give when ICP is around 20!
- both hypetonic saline 3% and mannitol cause hypernatremia, dries out the brain
- draws fluid out of brain tissue and makes body urinate it out
3) corticosteroids/Decadrom
- used for vasogenic edema around tumors and abscesses but not for head-injury patients
4) barbituates/nembutal
- reduce metabolic rate decreasing cerebral brain flow and ICP
60
Assessment for increased ICP
* glascow coma scale:
- higher number is better, lower number is worse
- 15 is alert,
61
internventions for ICP issues
- decrease fevers, shivering, agitation, seizures, pain: decreased cell metabolism, promote oxygenation, give tylenol, cooling blanket, benzos, antiseizure meds
- no valsalva, coughing, sneezing, vomiting: avoid suctioning when you can
- avoid restraints unless absolutely necessary
- have family at bedside
- seizure precautions
- quiet, non-stimulating environment
- use light touch and talk even if in coma
- respiratory: patent airway, watch breathing patterns, watch for snoring/obstruciton, careful use of suctioning (decreases pa02 and increases ICP which lowers CPP)
- monitor ABGs
- nutrition: increase glucose, body will break down fat for fuel if it doesnt have enough glucose and may increase ketones and acidity in pt
- F&Es: monitor closely, watch for DI and SIADH
- body positioning: HOB at 30 degrees, no neck flexion (affects jugular veins), avoid hip flexion (increases abdominal pressure), turn gently and slowly (no pain or agitaiton), prevent pain!
62
head injuries
- death can occur at 3 different times: immedaitely (from bleeding), within 2 hours (from bleeding), 3 weeks after injury (multisystem failure or prolonged bleeding)
- more likely to occur: with hematoma, increased age, abnormal motor or pupil response, early low BP, low 02, high co2, high ICP, glascow scale
63
skull fractures
- linear: break in the bone, doesnt move the bone, usually need no internvetions except close observation, heals on its own
- depressed: part of skill sinks in, may need surgery, usually frontoparital, open (split open), closed (skull just sinks in), basilar skull fracture is the most serious (at base of skull)
64
basilar skull fracture
- most serious
- break in bone at the base of the skull (behind the nose, anything around the eyes, ears, nose, near the base of the spine)
- usually heals on its own but needs close observation because usually a dura tear (increases risk of CSF leaks and infection risk)
- battle's sign (brusing behind the ear), bruising under the eyes, headache, tinnitius, rhinorrhea, racoon eyes, bulging of the tympanic membrane
- big risk of menningitis! - determine if there is a CSF leak, dextrostix, halo ring wign
- DO NOT use NG tubes or oral tubes
- DX tests: CT, MRI, dextrose stick (sugar = CSF), halo sign (drainage from nose taken and blood stays in middle and yellow CSF goes around the blood)
65
diffuse injuries, head trauma
- diffuse aconal injury DAI
- rapid acceleration and deceleration thought to be caused by sheared axons from a traumatic force
- due to sweelin that occurs 12-24 hours after a hit
- usually leads to coma and a vegetative state
- massive heard injury, brain shakes and rips axons, swelling shears axons more and leads to death
66
concussion, head injury
- may or may not loose consciousness
- retrograde amnesia
- headache
- can go home if LOC less than 5 minutes
- post-concussion syndrome: 2 weeks to 2 months later with headache, lethargy, personality changes, shortened attention span and memory, changes in intellectual ability
- no drivint
- return to hosp is dizzy or nauseated
- tylenol only for pain: nothing stronger due to sedative effects
67
focal injury, head injury
- local area of damage
| - lacerations, contusions, hematomas, cranial nerve injuries
68
epidural hematoma
- neurosurgical emergency
- bleeding between the dura and the skull
- arerial or venous
- intial LOC, brief lucid interval, decrease in LOC
- headache, nausea, vomiting
- may pass out, then wake up, then pass out again = common sign
69
subdural hematoma
- bleeding between the dura mater and the arachnoid layer
- usually venous
- slower bleed
* acute: 24-48 hours, decreased LOC, headache, ipsilateral pupil fixed and dialted
* subacute: 2-14 days, slowly leaks out to increase ICP
* chronic: weeks to months, more common in older adults and alcoholics, often looks like TIA/stroke/dimentia (older adults have brain atrophy so there is more space to fill and takes longer before symptoms occur)
70
diagnostic studies for head injuries
- CT: do this first, shows bleeds
- MRI: smaller lesions can be seen
- cervical spine xrays: always treat c-spine with head injuries
- most imporant to diagnose timely and get them to surgery (if needed) and keep ICP from increasing
- carniectomy: remove bone flap
- caniotomy with surgical evacuation: open to repair
- hemicraniectomy: one side of the head
71
head trauma interventions
- prevention: helmets, seatbelts, car seat
- monitor for changes in neuro status: may deteriorate rapidly
- encourage family members to stay with pt
- prevent increased ICP: cooling blankets, decrease pain, decrease movement, no shivering or fever, monitor position changes
- seizure precautions: tend to develop seizures about 1 week after injury so we can give prophylactic seizure drugs (dilantin)
- watch for ottorhea/rhinorhea: HOB up, collection pad, no NG tubes, no sneezing or blowing nose, no NT suction
72
brain tumors
* symptoms depend on location:
- right frontal lobe: judgement problems
- parietal lobe: speech problems
- brainstem: breathing and swallowing problems
- weakness and hemaplegia on contrallateral side of tumor (opposite side)
- headache at night that awaken the pt are common, seiuzures, n/v, cognitive problems, personality changes
- DX studies: CT, MRI, no LP
- TX: surgical removal, shunt, radiation therapy, chemo
- nursing care: help with behavioral problems, anti-seizure drugs, self care, establish a communication system, encourage pt to eat
73
bacterial meningitis
- usually step pneumonia, nesseria mennigntiidi
- medical emergency! mucous, pus, increased ICP
- s/s: fever, headache, n/v, nuchal rigidity (stiff neck), photophobia, decreased LOC, increased ICP, skin rash, seizures, kernig's sign (flex hip and pt cannot extend leg straight), brudzinski's sign (flex eck and causes hips and knees to flex)
- CX: neuro deficits, chornic headache, DIC, shock
- DX: blood, CSF, nasopharyngeal cultures, CT, LP, collect arobic and anarobic cultures
- TX: immediate abx therapy, may give decadron to decrease inflamm
74
bacterial meningitis interventions
- prevention with immunizations
- vigorous tx of ear and resp infections
- respiratory isolation
- seizure precautions
- coedine for pain (dont sedate too much)
- dark room, cool cloth, quiet, decreased stimuli, keep fever controlled
- avoid restraints
- family at bedside
75
viral meningitis
- also called aspetic meningitis
- caused by a variety of viruses (enterovirus), sometimes through personal contact by insects, fecal contamination, respiratory secretions
- most people ave the viruses but dont develo meningitis
- usually mild and self-limiting
- give abx until you confirm that it is viral
- only tx symptoms
76
encephalitis
- acute inflammation of the brain: affects the brain itself with more flu-like symotoms than meningitis
- can be fatal
- usually caused by a virus (west nile, HSV)
- see as a complication of AIDS
- sx: fever, headache, n/v, CNS abnormalities
- tx: may need ICU, antivirals
- nrsg care: mosquito control, acyclovir if HSV
77
MAP
[(2 x dia) + sys] / 3
78
CPP
MAP - ICP
79
trigeminal neuralgia (tic douloureux)
- cranial nerve V
- found in pts with hypertension
- excruciating severe pain, brief (2-3 minutes), unilateral
- may cause twitching, grimacing, blinking
- attacks triggered by light touch, chewing, yawning, face washing
- monitor for suicide
- cx: malnourished, dehydration, psychosocial issues, drug abuse
* DX/TX
- Ct or MRI: r/o tumors or other issues that may be causing the pain
- tegretol (carbamazepine) or Nuerontin (gabapentin): slow down electrical impulses that may be causing the pain
- nerve blocks, glycerol rhizotomy, microvascular decompression, gamma knife -- scar the site to stop the pain from transfering
- avoid strong opioids
- careful with dental care
- foods high in protein and calories, easy to chew, lukewarm
- avoid light touch and palpation
- watch for dehydration
- encourage social interaction
80
Bells' Palsy
- cranial nerve VII
- viral issues, normally HSV
- virus triggers immune response to HSV and attachs CN 7
- causes ischemia and demyelination of nerves, paralysis of half the face, twitching, weakness, drooping of mouth corners, impaired taste
- first r/o stroke with a CT/MRI and get medical history
* TX:
- start corticosteroids immediately: two weeks then titrate down
- may give antivirals if linked to HSV or virus
- moist heat and gentle massage
- mild analgesics (tylenol)
- facial exercises, electrical never stimulation
- protect the face from cold and drafts
- good nutrition, meticulous oral hygeine
- wear dark glasses, artificial tears, tapin eyelid closed to protect
81
Guillain-Barre Syndrome
- caused by virus, trauma, inflammation, enterovirus
- damages myelin sheath
- starts at feet then goes up to brain
- ascending, symmetric paralysis
- preceded by viral infection or trauma
- can caused ANS symptoms (decreased BP, bradycardia)
- complications: respiratory failure, dysphagia
* TX:
- plasmapheresis or IV high-dose immunoglobin (sandoglobulin) begun w/in first 2 weeks, no corticosteroids
- carefully assess respiratory status, prepare for intubation if vital capacity
82
botulism
- most serious type of food poisoning: spore found in soils, releases neurotoxin that blocks ach from working
- causes: decreased muscle movements, everything slowly becomes paralyzed, from head to foot
- sx: n/v, diarrhea, abdominal cramping, afebrile, no mental deficits, descending paralysis with cranial nerve deficits
- death can occur from circulatory failure, resp paralysis, resp complications
- TX: IV botulinum, purge of GI tract with non-magnesium containing laxatives (can exacerbate ach)
- prevention is key
- nursing care is like guillain-barre
83
tetanus (lockjaw)
- from an anarobic spore
- from rusty nails, IV drug use -- goes into anarobic site and grows
- S/S: jaw stiffness, fever, generalized tonic spasms, opisthotonus, laryngeal/respiratory spasms, sweating, HTN, tachy, hyperthermia, dysrhythmias, seizures
- TX: prevent by immunizing, thoroughly clean wounds, antitoxin, deep sedation, opioid analgesics, trach, ventilator, tdap q 10 years
84
spinal cord injury
- primary injury: initial disruption of the axons, initial blow, inflammation response
- secondary injury: ongoing, progressive damage, further damage due to massive inflamm response
- can not determine the extent of damage until at least 72 hours after injury, injury ogten rises 1-2 spinal
- flexion: ruptured posterior ligaments, forward dislocation, damage to spinal cord
- hyperextension: ruptured anterior ligament, compressed ligament in back
- compression: compression of spinal cord, fractured vertebrae
- flexion/rotation: displacement of vertebrae, turn neck
85
shock, spinal injury
* spinal shock:
- 50% experience this
- lasts hours to days
- decreased reflexes
- loss of sensation
- flaccid paralysis
- all below the level of the injury
- can last days to months
- still start active rehabilitation
* neurologic shock (most common in injuries above T6)
- lasts 1-3 weeks
- occurs due to loss of vasomotor tone
- hypotension
- bradycardia
- peripheral vasodilation (warm, dry skin)
- venous pooling
- hypothermia (except extremities where blood pools)
- usually assocaited with cervical or high thoracic injury
- loss of vasomotor tone, affects SNS
86
degree of paralysis
- c4 injury: tetraplegia, complete paralysis below the neck
- c6: results in partial paralysis of hands and arms as well as lower body
- T6: paraplegia, results in paralysis below the chest
- L1: paraplegia, results in paralysis below the waist
87
DX/TX for spinal cord injury
- CT: shows where the injury is and if the brain was affected
- treat systemic and neurogenic shock
- if cervical injury, must maintain all body systems (airway, breathing, respiratory)
- assess muscle groups, sensory status, brain injury, musculoskeletal injuries, internal injuries
- logroll during transfers
- stabilization of injury: traction, realignment, surgery
- Drugs: vasopressors (neurogenic shock), all drugs may be metabolized differently with spinal cord injuries
88
acute interventions, spinal cord injuries
- immobilization
- stabilize neck to prevent lateral rotation
- keep body correctly aligned
- logroll when turning
- if traction is used, it must be maintained at all times
- kinetic thearpy bed: pulmonary edema from blood shunting, rotates person around to move fluids and prevent skin breakdown
89
halo fixation
- perform pin site care 2 x shift
- skin care under vest, be able to insert 1 finger under vest
- do not hold onto halo to move
- weights must hand freely
- dont release traction, only per drs orders
- keep a set of wrenches close, for CPR
- wear sheepskin pad under vest, wash weekly
90
spinal cord injury and respiratory
- s/s: above c4 have total loss of resp muscle function, below c4 can have problems with phrenic nreve (diaphragm), cervical thoracic injuries cause paralysis ob abdominal and intercostal msucles, may need trach, neurogenic pulmonary edema (shunts blood to lungs)
- acute interventions: critical to assess during first 48 hours, above c4 requires mechanical vent, assess carefully, chest PT, assisted coughing or incentive spirometry
91
spinal cord injury and cardiovascular
- S/S: above T6 decreases the activity of the SNS (bradcardia, hypotension), DVT and PE risk (pooling blood)
- acute interventions: limit vagal stimulation (can cause card arrest), asses VS frequently, give anticholinergics (atropine) for bradycardia
- give vasopressors (dopamine) for hypotension
- ROm adn stretching exercises, prophylactic heparin
92
spinal cord injury, fluids and nutriton
- test stool and gastric contents for blood
- give steroids with anatacids or foood
- histamine receptor blockers (zantac, pepcid) or PPIs
- NG tube, prone to Gi bleeds due to fight or fight reponse
- high priotein high calorie diet
- start on foods when bowl sounds are heart of flatus
- dietary supplements as needed
93
spinal cord injury and bowel and bladder
- S/S: urinary retention, neurogenic bladder (bewlo t 12)
- interventions: catheter, lots of fluid intake, watch for UTIs, begin intermittent cath as soon as possible, rectal stimulation as needed, trigger every morning with breakfast
94
spinal cord injury and temperatre
- S/S: poikilothermism (below injury you lose the ability to control temperature), decreased ability to sweat/shiver below level of injury, worse with high cervical injuries
- interventions: maintain environmental temp, dont everload with covers or expose too long in baths, cooling banket for fevers
95
spinal cord injury acute interventions
- sensory deprivation: stimulate patietn above the level of injury; prism glasses to see things when laying down, conversation, music, smells, flavors
- reflexes: explain that this is not always a return to function, antispasmodic drugs
- skin: potential for skin breakdown
96
autonomic dysreflexia
- life threatening emergency
- massive uncompensated cardiovascular reaction caused by the SNS
- occurs in response to visceral stimulation (can be bladder issues, etc)
- SX: HTN (up to 300), throbbin headahces, sweating above the level of the lesion, bradycardia, piloerection, flushing of skin above the level of the lesion, blurred vision/spots, nasal congestion, anxiety, nausea
- TX: check BP, elevate HOB to 45 degrees or situpright, call Dr. assesss for cause, cath, ensure cath is not kinked, digital rectal exa, remove constrictive clothing, monitor BP cloesly, give procardia, teach the pt
- really high bp and low HR, red face, sweating
- have to ride noxious stimuli to treat this
97
home care for spinal cord injury
- respiratory: if ventilator-dependent can still be mobile, assisted coughing, incentive spirometry
- neurogenic bladder: identify appropariate drainage method, surgical options, anticholinergic drugs, adrenerguc blockers
98
bronchodilators
- relax broncial smooth muscle, which causes dilation of the bronchi and bronchioles that are narrowed as a result of the disease process
99
examples: bronchodilators, beta-adrenergic agonists
- Short acting bet agonists (SABA): albuterol (ventolin), levalbuterol (Xopenex), pirbuterol (maxair), terbutaline (bethine), metaproterenol (alupent)
- Long acting beta agoinst (LABA): aformoterol (brovana), formoterol (foradil, perforomist), salmeterol (servent)
100
about bronchodilators, bet adrenergic agonists
- used during acute phase of asthma attacks
- quickly reduce airway constriction and restore normal airflow
- agonists, or stimulators, of the adrenegeric receptors in the sympatheric nervous system (sympathomimetics)
* three types:
1) nonselective adrenergics: stimulate alpha, beta1 (Cardiac), beta 2 (respiratory) receoptrs. Exp = epinephrine
2) nonselective beta-adrenergics: stimulate both beta1 and beta 2 receptors. Exp = metaproterenol (alupent)
3) selective beta 2 drugs: stimulate only beta 2 receptors. Exp = albuterol (proventil)
101
bet adrenergic agonists, indications
- relief of bronchospasms related to asthma, bronchitis, and other pulmonary diseases
- tx of prevention of acute attacks
- hypotension and shock
- produce uterine relaxation to prevent premature labor
102
bet adrenergic agonists, adverse effects
* alpha and beta (epinephrine)
- insomnia, restlessness, anorexia, vascular headache (Vasoconstriction), hyperglycemia (prompts glycogenolysis), tremor, cardiac stimulation
* beta1 and beta 2 (metaproterenol)
- cardiac stimulation, tremor, anginal pain, vascular headache, hypotension
* beta 2 (albuterol)
- hypotension or hypertension, vascular headache, tremor
103
anticholinergics
- ipratropium bromide (atrovent) and tiotropium (spiriva)
- slow and prolonged action
- used to prevent bronchoconstriction
- not used for acute asthma exacerbations
- decrease congestion and decrease bronchoconstriction from occuring
104
anticholinergics, adverse effects
- dry mouth or throat (decreased saliva)
- nasal congestion (vasoconstriction)
- heart palpitations (increased HR if blocked)
- gastrointestinal distress (blocking bowels)
- headache
- coughing
- anxiety
105
corticosteroids
- antiinflammatory properties
- used for chronic asthma
- do not relieve symptoms of acute asthmatic attacks
- oral or inhaled forms (inhaled forms reduce systemic effects)
- may take several weeks before full effects are seen
106
inhaled corticosteroids
* indications: persistent asthma: often used concurrently with beta-adrenergic agonists (albuterol)
- beclomethasone dipropionate (beclovent)
- budesonide (pulmicort turtuhaler)
- dexamethasone sodium phosphate (decadron phosphate respihaler)
- flunisolide (aeroBid)
- fluticasone (flonase)
- triamcinolone acetonide (azmacort)
- ciclesonide (omnaris)
107
inhaled corticosteroids, adverse effects
- pharyngeal irritation
- dry mouth
- oral fungal infections
- systemic effects are rare because low doses are used for inhalation therapy
108
nursing implications for bronchodilators
- take measure to promote a generally good state of health to prevent symptoms of COPD
- avoid exposure to things that increase bronchospasms
- adequate fluid intake
- compliance with medical tx
- avoid excessive fatigue, heat, extremes in temperature, caffeine
- get prompt tx for flu or other illnesses; vaccinate for pneumonia and flu
- always check with MD before taking other meds
- perform thoughrough assessment before beginning therapy: skin color, baseline VS
109
nursing implications for bet adrenergic agonists
- albuterol: if used too frequently it loses its beta2 specific actions at larger doses; can cause nausea, anxiety, palpitations, tremors, increased HR
- take meds exactly as prescribed, no double doses or omissions
- report insomnia, jitteriness, restlessness, palpitations, chest pain or any change
110
nursing implications for inhaled corticosteroids
- - teach pts to gargle and rinse the mouth with lukewarm water after to prevent fungal infections
- use bronchodilator first then wait sevral minutes and use corticosteroid
- encourage use of spacer device
