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64 Cards in this Set

  • Front
  • Back
deficiency in # of RBC, quantity of hemoglobin &/or volume of hematocrit
-not a specific disease but a manifestation of pathologic process
anemia
causes of anemia
blood loss
trauma
blood vessel rupture
menstrual flow
gastritis
hemorrhoids
causes of anemia due to impaired production of RBC
iron deficiency
Thalassemias
B12 deficiency
chemotherapy
causes of anemia due to increased destruction of RBC
sickle cell anemia
prosthetic heart valve
malaria
compensation mechanisms of anemia include:
oxygen-hemoglobin dissociation curve shifts to the right
blood taken to more vital organs
increased COP
incr RBC production
mild anemia Hb value
Hb 10-14
moderate anemia hb value
Hb 6-10
severe anemia hb values
Hb <6
nsg mgmt anemia
PMH - dialysis, hepatic disease, ulcers caused by ASA, NSAIDS, anticoagulants, PCN
physical assessment
medication use
surgery or treatments
plan rest & activity to avoid fatigue - GOAL
limit visitors, calls, noise
check H&H
teach foods hi in iron, protein, calories
small frequ meals - req less energy
check for hypoxemia
transfuse prn
breathing exercises
relaxation techniques, very anxious can't breath
Nutrition for erythropoiesis
B12-red meat, liver
folic acid-green leafy veg, fish, grains
vit B6-pork,liver,bananas
Fe-liver,eggs,dark green veg
amino acids-milk,dairy,chicken
vitC-citrus,strawberries, cantalope
anemia in the elderly
common
from chronic disease
s/s misleading-feel part of aging
-pallor
-confusion, ataxia
-fatigue
-incr angina
iron deficiency anemia
most common chronic disorder in the very young, those on poor diets, women in reprod yrs
malabsorption of iron common after GI surgeries
reasons for blood loss-2ml of whole blood has 1 mg of iron
peptic ulcer
gastritis
esophagitis
diverticuli
hemorrhoids
neoplasma
lose 45ml of blood via menstruation each month & 22 mg of iron
pregnancy due to iron to fetus, delivery, lactation
chronic renal failure due to dialysis
clinical manifestations of iron deficiency anemia
pallor
h/a
burning tongue
paresthesia
care of iron deficiency anemia
treat cause, replace iron, replace blood loss
iron supplements-don't take ER, take 50-100 mg TID or QID
take 1 hr before meals & w/OJ to enhance absorption
dilute liquid to avoid staining teeth
causes black stools
give stool softeners/laxatives prn
s/e incl heartburn, constipation, diarrhea
iron by IM
change needles to prevent staining skin
leave 0.5 ml air in syringe to clear iron
give deep IM in upper outer quadrant of buttocks with a 2-3 inch 19-20G needle
z-track
do not massage
iron by IV
don't mix or add to solutions
give undiluted over 1 ml/min
then flush with NSS
thalassemia
autosomal recessive genetic disorder of inadequate production of normal hb
mediterranean heritage
generalized anemia, jaundice, chronic bone marrow hyperplasia leading to thickening of cranium & maxillary cavity, retarded physical & menthal growth
transfusion w/IV Desteral to reduce iron overload due to chronic transfusions
keep hb @ 10 to prevent enlarging spleen
megaloblastic anemia
caused by impaired DNA synthesis & presence of large RBCs. These RBCs are easily destroyed due to:
cobalamin, folic acid def
suppression of DNA synthesis by drugs
inborn errors of cobalamin & folic acid metablism
malignant blood disorders
cobalamin deficiency
intrinsic factor (IF) a protein from gastric mucosa is not made, from lack of HCl secretion by stomach therefore cobalamin is not absorbed in distal ileum
pernicious anemia
when B12 is decr due to lack of IF
dietary def, gastrectomy, malabsorption, family hx
seen in pts w/gastrectomy, ileum resection, Crohn's Disease, diverticuli of small intestine, users of long-term H2 histamine receptor blockers (acid reflux)
symptoms of pernicious anemia
tissue hypoxia
sore tongue
anorexia, n/v
abdominal pain
paresthesias of feet & hands
impaired though
Treatment for cobalamin deficiency
-give B12 IM 1000ug QID x 2wks, then q week until Hct normal, then q month for life
-Nascobal intranasal q week
-will die in 1-3 yrs w/o replacement
care for cobalamin deficiency includes
general anemia care
safety measures due to sensation losses
screen for gastric CA
teach about need for meds
reasons for folic acid deficiency
-poor nutrition
-malabsorption of small bowel
-drugs such as methotrexate, BCP, phenobarbital, Dilantin
-alcohol abuse
-anorexia
-hemodialysis
s/s folic acid deficiency
similar to cobalamin, i.e.
-tissue hypoxia, sore tongue, anorexia, n/v, abdominal pain, -dyspepsia
-smooth, beefy red tongue
-ABSENCE OF NEUROLOGIC PROBLEMS
lab test results for low serum folate level reveal
normal 3-25 mg/ml
serum cobalamin level normal
HCL present in gastrict acid
treatment for folic acid deficiency
1-5 mg PO of folic acid QD & folid acid containing foods (green leafy veggies, legumes, whole grains)
type of anemia that is caused by an underproduction of RBCs & shortening of their survival
anemia of chronic disease
causes of anemia of chronic disease
-ESRD (end stage renal)
-chronic liver disease
-chronic infection
-heavy metals & chemo
-alcohol abuse
-HIV
-chronic endocrine diseases (DM, thryoid)
how to treat anemia of chronic disease
-correct underlying cause
-give erythropoietin therapy (Epogen, Procrit)
type of anemia that is caused by peripheral blood pancytopenia & hypocellular bone marrow
aplastic anemia
origin of aplastic anemia
congenital or acquired
ways aplastic anemia is acquired
ionizing radiation
chemical agents (benzene, insecticides, aresenic, alcohol)
viral & bacterial infections
medications
70% are idiopathic
s/s of aplastic anemia
-slow progression with
-fatigue
-dyspnea
-neutropenia
-thrombocytopenia
-ALL CELL COUNTS ARE LOW
-BLEEDING TIME PROLONGED
-ELEVATED SERUM IRON & TIBC
-BONE MARROW IS HYPOCELLULAR W/YELLOW MARROW (FAT CONTENT) CALLED "DRY TAP"
care of aplastic anemia
based on id & removal of causative agent
-untx have 75% fatality rate
-bone marrow transplant <45 yrs old w/o prev blood transfusion matched w/human leukocyte antigen matched donor
->45 yr old w/o HLA matched donor then immunosuppression w/ATG or cyclosporine
biggest reasons for acute blood loss
trauma
complications of OR
what occurs w/sudden loss of blood volume
hypovolemic shock (incr HR, RR incr then decr, decr BP & LOC
-sudden loss can occur postpartum or w/esophageal varices
what should you assess for in addition to VS with acute blood loss
pain -- potential for internal hemorrhage -- cramping
% of blood loss s/s
10% loss - no s/s
20% loss - nothing at rest, incr HR w/exercise
30% loss - okay supine BP
40% loss - problems w/BP, CP, CVP
types of anemia caused by increased erythrocyte destruction include
hemolytic anemia
Sickle Cell Disease
causes of hemolytic anemia
-defects in RBCs caused by abnormal hbg
-enzyme def altering glycolysis or RBC membrane abnormalities (IF)
-extrinsic factors such as trapping cells in sinuses of liver or spleen, toxins, mechanical injury (prosthetic heart valve)
s/s of hemolytic anemia
jaundice
enlarged liver/spleen
treatment of hemolytic anemia
-Fluids (LR, albumin) - vol expanders
-PRBC
-platelets PRN
-replace Fe PO or IM
inherited, autosomal recessive disorders by presence of abnormal form of hgb in the RBC. Hbg S causes the RBC to stiffen, elongate, taking on a sickle shape due to low O2 levels
Sickle Cell Disease
found in infancy or childhood
incurable, fatal by middle age due to renal & pulmonary complications
Sickle Cell Disease
most severe type of anemia
Sickle Cell Disease
carrier state of sickle cell disease & is mild type of SCD (1 in 10 african amer has this trait)
Sickle Cell trait
triggered by low O2 in blood from infection, high altitude, stress, surgery, blood loss, dehydration
initially sickling is reversible w/reoxygenation but becomes irreversible due to cell damage
Sickling Episodes
severe, painful acute exacerbation of RBC causing vasocclusive crisis, hypoxia, thrombi formation, tissue ischemia, infarction, necrosis
sickle cell crisis
s/s of Sickle Cell Disease
pallor of mucus membranes
fatigue
decr exercise tolerance
gray cast to skin
jaundice common
prone to gallstones
pain of hands, joints "Hand-foot syndrome" c/o deep gnawing & throbbing, edema of hands/feet, due to bone infacrction
complications of Sickle Cell Disease
CHF
CV complications, spleen becomes small due to scarring "autosplenectomy"
osteoporosis
leg ulcers-ankles
pneumonia-pneumococcal
pulmonary hypertension
renal failure
heart failure/MI
retinal detachment
infection major cause of morbidity
care of Sickle Cell Disease
avoid high altitudes
good fluid intake
treat infection promptly
rest
pain mgmt
O2 therapy
antisickling agents - Droxia (beneficial for some)
bone marrow transplant
education how to prevent crisis
Pneumovac, H Influenza
check for hepatitis
teaching for Sickle Cell Disease
about disease (parents/child)
avoidance of dehydration
avoidance of altitudes
tx resp infections immediately
pain control
tx anxiety & depression
reasons for acquired hemolytic anemia
-physical destruction of RBC (hemodialysis, heart-lung bypass, prosthetic heart valves)
-antigen-antibody response (blood transfusion reaction or autoimmune response (lupus, leukemia)
-infectious agents/toxins (malaria, clostridium)
tx for for acquired hemolytic anemia
remove cause
supportive care
corticosteroids
splenectomy
transfusions
production & presence of incr # of RBCs - impairs circulation causing hyperviscosity & hypervolemia
polycythemia
info re: polycythemia vera (primary)
chromosomal mutation
incr in all blood cells
insidious in those >50 yrs
not preventable
avoid smoking
avoid high altitudes
s/s of polycythemia
h/a
vertigo
tinnitis
visual disturbances
CHF, chest pain
intermittent claudication
thrombophlebitis
pruritis
hemorrhage
plethora
mgmt of polycythemia
monitor I&O
avoid fluid overload but hydrate
active or passive leg exercises to prevent thrombosis
phlebotomy - daily until Hct normal then q 2-3 months removing 500cc/time
death due to CVA
decrease in platelet < 150,000 due to hereditary, acquired (malignant disorders, myelosuppressive drugs, alcoholism, viral infections)
thrombocytopenia
most common in women between 20-40
autoimmune disease, platelets covered with antibody that spleen recognizes as foreign & destroys them, unable to survive the normal 8-10 days, last 1-3 days
immune thrombocytopenic purpura
s/s thrombocytopenia
bleeding
epitaxis
gingival
petechiae
purpura
ecchymosis
fainting
vertigo
tachycardia
abdominal pain
hypotension
acute nsg mgmt for thrombocytopenia
control hemorrhage
use small gauge needles w/ 5-10 min of direct pressure after
count menstrual pads (50cc blood soaks a pad)
give platelets
teach to avoid-suppress or cause abnormal platelet production or aggregation
thiazide diuretics, alcohol, estrogen, chemo drugs, ASA, NSAIDS, tylenol, lasix, estrogen, PCN
watch ginger, cumin, tumeric, cloves, Vit C&E