nutritional anemia Flashcards
macrocytic anemia
Vitamin B12 and Folate
Deficiencies in either of these nutrients effect the development of rbc in the bone marrow
rbc increases before dividing resulting in macrocytic rbs
hypersegmented neutrophils
vitamin B12 deficiency
meat and dairy products only dietary source of B12
Adequate absorption depends on: dietary intake, acid-pesin in stomach to B12 from binding to proteins, pancreatic proteases to free B12 from R factor, secretion of IF by parietal cells, and an intact ileum
etiologies of b12 deficiency
Pernicious anemia-usually seen in older adults, seen primarily in blacks and whites (not mexicans or asians), autoimmune that attack IF
Chronic Atrophic gastritis-leads to decrease in IF prod., associated w/ autoantibodies directed against gastric parietal cells, results in less acidic pH in stomach, increase in gastric caner
Factors that contribute to B12 malabsorption
Chronic alcoholism-BIggest gastrectomy/gastritis-big too H plori long term ingestion of metformin, H2, ppi, antacids crohns hiv
clinical presentation of b12 anemia
mcv>100
often elevated Fe levels, indirect bilirubin and LDH (indicating increased RBC breakdown due to both peripheral destruction and ineffective erythropoiesis)
peripheral smear- megaoblasts, hypersegmented neutrophils and macrocytosis
when anemia is severe there may be thrombocytopenia and neutropenia called pancytopenia
clinical presentation b12 cont…
hyperhomcysteinemia-
both b12 and folate required for the metabolism of homocysteine to methionine
deficiencies in theses vitamins result in elevated homocysteine levels, which are a risk factor for atherosclerosis and venous thromboembolism
Neurologic changes-(only in b12)
due to defect in myelin formation
peripheral neuropathy sxs parathesias, numbness, if severe gait becomes ataxia
memory loss, dementia, irritability
increased risk of osteoporosis
due to suppression of osteoblast activity
increased risk of hip and spine fractures
Folate deficiency etiologies
Poor nutrition (folate found in great leafy vegetables, nuts and fruit)
alcoholism-biggest cause
infants who are fed goats milk
when there are increased requirements (pregnancy and pts w/ chronic hemolytic anemia)
drugs that interfere w/ folate metabolism (trimethroprim (antibiotic), methotrexate (immunosuppresion), phentoin (anti seizure)
folate defeciency presentation
macrocytic anemia and hyperhomocysteinema
NO neurologic findings
folate deficiency can occur w/in 4-5 months (b12 deficiency takes years because there are stores of b12 but not folate)
hypersegmented nucleus
diagnosing b12/folate deficiency
presence of hypersegmented neutrophils/pt who has neurologic sxs even if NOT anemic
oval macroctic rbs on smear
panctyopenia of uncertain disease
unexplained neurologic signs: dementia, sensory ataxia, and parestheisias
special populations (older adults, alcoholics, pts w/ malnutrition, vegans, bariatric surgery and not compliant w/ vitamins)
laboratory eval
serum B12 level: <2ng/mL= deficiency
RBC folate levels
metabolite testing-for those w/ borderline vitamin values-measures intermediates methymalonic acid and homocysteine
If see macrocytic anemia want to check both B12 and folate
diagnosing pernicious anemia
measure antibodies to IF-specificity 100%
elevated gastrin/low pepsinogen- highl sensitive if antibodies negative
schilling test-not used anymore
tx of folate disease
Folic acid 1-5 mg po daily for 1-4 months or until complete recovery
usually 1 mg a day is sufficient
taking folic acid can partially reverse some of the hematologic effects of b2 deficiency (important to rule out b12 deficiency before administering folic acid)( if tx w/ folic acid is urgent-draw blood prior to tx to test for b12 deficiency and then treat w/ both folic acid and b12 until test results are known)
tx for b12 disease
usually treated w/ IM or deep SQ injection of b12
1000 mcg every day for a wekk
1 mg every week for 4 seeks
if underlying disorder persists then 1 mg every month
other preparations: oral b12 1-2 mg/ day
also sublingual and nasal spray preparations
response to tx
elevated serum iron, indirect bili and ldh fall w/in 1-2 days following tx w/ parenteral b12
bone marrow changes from megaloblastic to normoblastic
hypokalemia is common during this early response due to marked increase in K+ utilization in prod of new hematopoetic cells, pts should be monitored
Iron deficiency anemia (absolute and etiologies)
iron stores in bone marrow and liver/spleen ABSENT
serum ferritin is LOW
etiologies-poor dietary intake, reduced iron absorption, increased blood loss (usually the cause), intravascular hemolysis, congenital iron deficiency
iron deficiency anemia
functional iron deficiency
insufficient availability of iron in face of normal or increased iron stores
enough iron but not available
anemia of inflammation (anemia of chronic disease)
hepcidin-induced block in the release of iron from macrophage back into circulatoin
this makes iron less available for rbc prod
seen in pts w/ infection, inflammation, or malignancy
erythropoiesis stimulating agents
available body iron stores may be unable to release iron rapidly enough to satisfy the increase brought about by the stimulating agent (making so much rbc due to epo so using tons of Fe and looks like Fe deficient but actually not)
clinical manifestations of Fe defeciency
asymptomatic exercise intolerance pica restless leg syndrome weakness fatigue HA irritability
Diff diagnosis for iron defeciency
thalassemia
serum Fe are normal to igh
HgB A2 level increased
RBC count is high
Anemia of chronic inflammation
serum Fe and TIBC low
normal or increaed ferritin
critical to look at the clinical setting and do thorough eval for chronic inflammation
sideroblastic anemias
diagnosis made by demonstrating ringed sideroblasts on prussian blue stain of the bone marrow
most commonly drug induced or may be due to a myelodysplastic disorder
Tx of Iron deficiency anemia
oral iron therapy is 1st line
There are conditions when oral iron is either poorly tolerated or ineffective:
GI side effects are VERY common and compliance is bad
malabsorption states
tx w/ oral iron can take 6-8 wks to resolve anemia and 6 months to replenish iron stores
in pts w/ inflammatory bowel disease
in conditons w/ heavy bleeding
dialysis pts
what should oral iron salts not be given with
food
antacids, H2 blockers, ppi
Calcium containg foods, cereals, coffee, milk
certain antibiotics (tetracyclines, quinalones
oral iron therapy
iron should be given 2 hrs before or 4 hrs after antacids
iron is best absorbed in mildly acidic medium so adding vitamin c or oj is good
GI sxs are directly related to amt of ELEMENTAL iron so can decrease that and get rid of GI side effects
side effects of iron
recommended tx is 150-200 mg of ELEMENTAL Fe daily
50% nausea, constipation, diarrhea, epigatric pain, vomiting
Tx options if get side effects
switch to a preparation w/ lower dose of elemental iron
slowly increase from 1 pill a day to 3 over 6 weeks
iron may be taken w/ meals but it will decrease absorption
use liquid preparation especially in older adults
try iv iron
Parenteral Iron
good for pts intolerant to oral iron preparations
max amt of ELEMENTAL iron absorbed orally is 25 mg/day w/ parenteral infusion the max is as high as 1000 mg
IV iron is effective for those unresponsive or intolerant to oral iron
Iv iron is required when the amt of iron loss through daily blood loss exceeds the capacity of GI tract to absorb oral iron
what iron prep causes anaphylaxis
High molecular weight iron -dextran