3.18.14* Microcytic and Macrocytic Anemias

Question 1

where is iron absorbed from the GI tract?

Answer 1

duodenum

Question 2

Ferrous iron in GI tract is absorbed where and by what molecule?

Answer 2

ileum; DMT-1

Question 3

When hepcidin is ________, it decreases ferroportin for decreased absorption from the gut. When iron is low, transport is needed, hepcidin secretion is ___________.

Answer 3

elevated; reduced

Question 4

High iron levels turn on or off the iron regulatory proteins. Which function to stop translation of iron absorption proteins (TFR) and allow translation of iron storage proteins (ferritin)?

Answer 4

off

Question 5

Q. At the regulatory level, a post-partum woman with iron deficiency:

a. Has decreased iron regulatory protein binding to mRNA
b. has increased iron regulatory protein binding to mRNA
c. Has elevated hepcidin levels
d. Has decreased ferriportin

Answer 5

A

Question 6

Hemosiderosis is primarily seen in ________, hemochromatosis is primarily seen in ___________.

Answer 6

macrophages; hepatocytes

Question 7

iron regulatory proteins block or promote translation of iron absorption proteins?

Answer 7

block

Question 8

Clinical manifestations of iron deficiency?

Answer 8

angular chelosis
nail spooning
glossitis (no papillae)

Question 9

What is seen in PBS with iron deficiency?

Answer 9

microcytic, hypochromic RBCS.

poikilocytosis and anisocytosis

Question 10

Q. What finding would suggest iron deficiency

a. Transferrin decreased with iron saturation decreased
b. Transferrin saturation of 45%
c. ringed sideroblasts in his bone marrow
d. Increased transferrin with 5% saturation
e. Elevated ferritin

Answer 10

D

Question 11

Normal saturation of transferrin

Answer 11

30%

Question 12

Genetic defect in Type 1 hemochromatosis

Answer 12

Homozygous recessive mutation in HFE gene leads to defect in C282Y.

Question 13

What is the mechanism of hemochromatosis?

Answer 13

C282Y mutation leads to body unable to produce hepcidin. Thus iron is continually stored leading to iron overload/ hemochromatosis.

Question 14

What medical issues are related to hemochromatosis

Answer 14

heart failure, liver and endocrine organs (pituitary, sexual) and joints

Question 15

What is the normal treatment for hemochromatosis

Answer 15

phlebotomy (bleeding the patient) will deplete the body of iron so it is mobilized out of the liver.

Question 16

Q. What approach is not likely to help with hemochromatosis

a. Leech therapy
b. Weekly phlebotomy
c. deferasirox
d. Vitamin c
e. Hepcidin infusions

Answer 16

D. Vitamin C does not help hemochromatosis because it increases iron absorption from the gut

Question 17

what are the components of heme?

Answer 17

protoporphyrin and iron (heme is made in the mitochrondria.

Question 18

what causes sideroblastic anemia

Answer 18

defect in ferritin donating iron to heme, leads to iron deposition in the microchrondria, giving the appearance of a ringed sideroblast.

Question 19

Patient has ringed sideroblasts in bone marrow. What is not the cause?
a. Hemachromatosis 
b. Lead poisoning
c. Defect in ALA synthase
D. Myelodysplasia
E. Tuberculosis

Answer 19

A.

Question 20

what can cause basophilic stipling

Answer 20

lead posioning. Caused by precepitates of undegraded RNA.

also thalassemia

Question 21

What can lead to macrocytosis?

Answer 21

megaloblastic anemia (folate/B12)
alcoholism
liver disease
hypothyroidism
increased reticulocytes
myelodysplasia
sideroblastic anemia

Question 22

what is megaloblastic anemia?

Answer 22

dis-synchrony between development of nucleus and cytoplasm. Delayed development of nucleus

Question 23

pernicious anemia

Answer 23

a. autoimmune disorder cause by antibodies to parietal cells or intrinsic factor, leading to B12 deficiency.
b. associated with other autoimmune disorders
c. happens mostly over 60
d. increased incidence of gastric cancer

Question 24

How does pernicious anemia lead to jaundice?

Answer 24

ineffective erythropoiesis leads to lots of RBC turnover/death in bone marrow releasing bilirubin.

Question 25

clinical manifestations of megaloblastic anemia

Answer 25

a. jaundice

b. bumpy, red, swollen tongue

Question 26

lab value seen in megaloblastic anemia

Answer 26

a. macrocytosis
b. hypersegmented PMNs
c. megaloblastic cells with disseminated chromatin

Question 27

B12 deficiency neuropathy

Answer 27

a. parathesia in hands
b. dementia
c. decreased vibratory and proprioception (balance)
d. spastic paralysis from demyelination of dorsal column

Question 28

Pernicious anemia patient has low folate and was given 4mg/day as sole therapy. What is the most likely outcome?

a. She gained energy quickly
b. Anemia did not improve
c. Her balance improved
d. Her balance markedly worsened
e. She craved turnip greens

Answer 28

D. When given folate to patient with B12 deficiency, folate is sucked into DNA pathway and taken out of the methionine pathway, which worsens neuropathy.

Question 29

What needs to be watched with initiation of B12 therapy?

Answer 29

potassium levels. B12 can cause rapid RBC production that depletes body of potassium, leading to severe hypokalemia.