Anemia

Question 1

Microcytic Anemia

Answer 1

Iron Deficiency 
     Increased requirements (pregnancy)
     Poor intake
     decreased absorption
     chronic blood loss
anemia of chronic disease (late)
    normoctic early, microcytic later
thalassemia
sideroblastic anemia
other hemoglobinopathies (sickle cell)

Question 2

Iron deficiency

Answer 2

blood loss
major cause of iron deficiency
occult bleeding more difficult to track down and
usually result of gi blood loss examples:
upper-pepic ulcer, esophageal varices, gastritis
lower-hemorrhoids, diverticula, colorectal caner, ibd (crohns and ulcerative colitis)

Question 3

Iron deficiency iron stores

Answer 3

normal iron content 3-4 grams
hemoglobin-2 grams
iron containing proteins (myoglobin,..) 400 mg
Iron bound to transferrin- 3-7 mg
remainder is in ferritin or hemosiderin

most iron is in hemoglobin
most ferritin is stored in liver

Question 4

iron deficiency clinical manifestations

Answer 4

usually presenting sxs in adults are primarily due to anemia include weakness, HA, irritability, and varying degrees of fatigue and exercise intolerance

however many pts are asymptomatic and present only w/ anemia

Pica- cravings for non food stuff

pagophagia-pica for ice (very specific for iron)

sxs are highly dependent on rate of blood loss..the more acute, the more sxs appear. w/ chronic loss, usually takes substantial loss before pt becomes symptomatic

Question 5

iron deficiency labs

Answer 5

serum ferritin-excellent indicator of iron stores (gold
   standard test) normal-15-200 ng/ml
serum iron (reduce)
Total iron binding capacity (increased)
transferrin saturation (low)

fe deficiency happens in stages 1. serum ferritin decreases 2. serum iron decreases. 3. TIBC increases

Question 6

RDW and iron deficiency

Answer 6

RDW measures anisocytosis so looks at variation in size of rbc
Microcytic anemia w/ a low or normal RDW= anemia of chronic disease or thalassemia
microcytic anemia w/ high RDW=iron deficiency

Question 7

tx of iron deficiency anemia

Answer 7

correct underlying cause

iron supplementation

Question 8

Anemia of Chronic disease (late)

Answer 8

KEY IS THAT ACD FERRITIN IS HIGH AND IDA FERRITIN IS LOW
SERUM IRON LOW IN BOTH ANEMIA OF CHRONIC DISEASE AND IRON DEFICIENCY ANEMIA, AND TOTAL IRON BINDING CAPACITY IS HIGH IN IDRON DEFICIENCY ANEMIA AND LOW IN ANEMIA OF CHRONIC DISEASE
EPO is low in almost all cases
anemia usually moderate Hb around 7-11

Question 9

tx of anemia of chronic disease

Answer 9

correction of underlying disorder if possible

pts w/ low epo levels can be given EPO

Question 10

common diseases associated w/ anemia of chronic disease

Answer 10

RA
lupus
hiv
tb
carcinomas
lymphomas
leukemias

Question 11

megaloblastic vs nonmegaloblastic

Answer 11

megaloblastic-presence of oval macrocytes and hypersegmented neutrophils
nonmegaloblastic-absence of neutrophil hypersegmentation along w/ the presence of round macrocytes

Question 12

macrocytic megaloblastic anemias

Answer 12

Abnormalities of dna metabolism
b12 deficiency (cobalamin)
folate deficiency
drug side effects

Question 13

what separates Folate from B12 deficiency

Answer 13

neurological sxs occur only w/ b12(cobalamin) indicating that additional mechanisms are involved in the central nervous system

Question 14

what does absorption of b12 depend on 5 factors

Answer 14

adequate dietary intake
acid pepsin in the stomach
pancreatic proteases
gastric secretion of functional IF
ileum w/ functioning cobalamin-intrinsic factor receptors

anything that interferes w/ any of these steps can lead to a deficiency in b12 w/ a subsequent anemia and potential neurological sxs

Question 15

B12 adequate dietary intake

Answer 15

meat and dairy provide b12
total body stores of cobalamin is 2-5 mg, one half which is in the liver, so it takes years to develop vitamin b12 deficiency after absorption of dietary b12 ceases

Question 16

what can interfere w/ the dietary intake of b12

Answer 16

vegan diet

Question 17

what interferes w/ acid pepsin in stomach

Answer 17

gastrectomy/bariatric surgery, gastritis

Question 18

what interferes pancreatic enzymes

Answer 18

pancreatic insufficiency

Question 19

what interferes w/ IF secretion

Answer 19

pernicious anemia

Question 20

what interferes w/ absorption in ilium

Answer 20

absorption interference: crohns or ileal resection

Question 21

pernicious anemia

Answer 21

autoimmune
parietal cells in stomach fail to secrete enough IF to ensure intestinal absorption of b12
sx- weakness, glossitis (enlarged, smooth tongue), paresthesias, gi sxs-diarrhea, N/v, and pain, severe anemia can reveal signs of cardiac failure

Question 22

eval of pernicious anemia

Answer 22

review pts drug list
measure of serum b12 and folate
smear to look for megaloblasts (macroovalocytes) and hypersegmented neutorphils

Question 23

how to tell from labs folate vs b12

Answer 23

specific metabolites (methylmalonae and homocysteine)
serum conc of homocysteine as well as serum and urinary conc of methylmalonic acid are elevated in b12 deficiency due to a decreased rate of metabolism

only Homocysteine is elevated in folate deficiency since folate does not participate in methylmalonic acid metabolism

antibodies to IF

Question 24

Tx of B12 deficiency

Answer 24

parenteral or sublingual b12
vegans can take oral therapy cause they don’t have absorption problem 25-100 micrograms
IMPORTANT- a person treated w/ folate who has a b12 deficiency may have their sxs masked…which is bad news cause neurological damage form b12 deficiency can be irreversible so have to make sure you find the underlying problem

Question 25

folate deficiency

Answer 25

comes form animal products and leafy vegetables folate stores are low can develop megablastosis within 4-5 months MOST COMMON CAUSE OF of folate deficiency is nutritional due to poor diet and/or alcoholism other causes include increased requirements in pregnancy and w/ pts w/ hemolytic anemia drugs also interfere w/ folate metabolism (trimethoprim, methotrexate, phenytoin)

Question 26

nonmegaloblastic macrocytic anemias

Answer 26

``` alcoholism liver disease aplastic anemia drug induced myelodysplastic syndrome pregnancy myeloma hypothyroidism ```

Question 27

cells characteristic of liver disease

Answer 27

target cells-area of central density surrounded by a halo of pallor.

Question 28

Diff Diagnosis for normocytic anemia

Answer 28

``` N=normal preg o=over hydration r-renal disease (lack of epo) m=marrow problems, mixed anemia a=acute blood loss l=liver disease (can be macrocytic) si=systemic inflammation (anemia of chronic disease (early) z=zero prod (aplastic anemia (can be macrocytic)) e=endocrine disorder hemolytic anemias ```

Question 29

anemia of chronic renal failure

Answer 29

don't confuse w/ anemia of chronic disease | tx- Human recombinant EPO (procrit)

Question 30

Mixed Anemia

Answer 30

very important to order a smear cause MCV will be normal if have microcytic cells from iron deficiency and macrocytic cells from a b12 deficiency the MCV may be normal RDW would be increased

Question 31

Reticulocytes

Answer 31

young immature RBC that contain residual RNA, which explains their tendency to stain w/ certain dyes make up 1% of rbc circulate 1 day before maturing to rbc

Question 32

what does reticulocyte count represent

Answer 32

ability of bone marrow to produce mature rbc normal 1-2% In an anemic pt an increase in the reticulocyte count provides evidence that the bone marrow is adequately responding to the anemia (in an effort to maintain the hemoglobin level) have blue stains on smear

Question 33

Reticulocyte count

Answer 33

very useful in context of a normocytic anemia 3 situations acute blood loss hemolytic anemia response to iron, folate, or b12 replacement

Question 34

Anemia of acute blood loss

Answer 34

initially hemoglobin is normal but after time hemoglobin will fall Retic count will be normal for the first few days but will increase shortly after

Question 35

Hemolytic anemias

Answer 35

``` RBC destruction marrow prod can't compensate for rbc destruction extravascular (spleen, liver, marrow) intravascular (rare) intrinsic abnormalities of rbc contents (Hb, enzymes) membranes extrinsic to rbc serum antibodies traumas in the circulation infectious agents ```

Question 36

Extravascular destruction of rbc- Intrinsic defects

Answer 36

Enzyme deficiencies (G6PD or pyruvate kinase) Hemoglobinopathies (sickle cell, thalassemia, unstable hemoglobin Membrane defects (hereditary spherocytosis, elliptocytosis)

Question 37

extravascular destruction of rbc-extrinsic defects

Answer 37

``` Liver disease hypersplenism infections oxidant agents other agents (snake bites, lead, etc) microangiopathic (DIC, TTP) Autoimmune hemolytic anemia intravenous immune globulin infusion large granular lymphocyte leukemia ```

Question 38

what is main sx of hemolytic anemia

Answer 38

jaundice

Question 39

tests for hereditary spherocytosis

Answer 39

``` Reticulocyte count elevated MCHC (mean corpuscular HgB conc)-most helpful osmotic fragility testing ektacytometery acidified glycerol lysis test cryohemolysis test eosin 5 maleimide binding test ```