Anemia treatment

Question 1

Hematopoiesis

Answer 1

the process of blood cells formation in the bone marrow, requires iron, vitamin B12 and folic acid, as well as hematopoietic growth factors

Question 2

Anemia

Answer 2

a is a decrease in the number of red blood cells and the amount of hemoglobin (Hb) in the blood below the accepted normal values

Question 3

The most common cause is the ____

Answer 3

iron deficiency that causes hypochromic and

microcytic anemia - iron deficiency anemia.

Question 4

Deficiency of vitamin B12

Answer 4

or folic acid produces megaloblastic erythropoiesis, with asynchronous maturation between nucleus and cytoplasm - megaloblastic anemia.

Question 5

Iron is found in the body :

Answer 5

extracellularly and intracellularly, in the hem group of
hemoglobin, myoglobin, or in deposit form of transferrin, ferritin or hemosiderin, in the amount of about 4 grams.
- 70% in hemoglobin
- 10% in myoglobin
- 10-20% in deposits (ferritin and hemosiderin) and in plasma transferrin

Question 6

Iron is absorbed into

Answer 6

deposits (ferritin and hemosiderin) and in plasma transferrin.
Iron is absorbed into the proximal duodenum and jejunum. Daily absorption is 5-10%
of ingested iron, ie 0.5-1 mg / day but can increase up to 30% depending on the body’s needs.
Iron from products with animal origin is direct absorbed in hem form, which is taken
up by a transporter - HCP1 (hem carrier protein 1) from the luminal surface of intestinal cells and released at the erythrocyte level

Iron from vegetable products is absorbed very hard.

Question 7

Iron deposits are found especially

Answer 7

in the liver, spleen and hematopoietic marrow in
the form of ferritin and hemosiderin, where iron is released according to the needs of the body.
There are no specific iron removal mechanisms.

Question 8

The iron requirement in iron deficiency anemia can be calculated according to

Answer 8

the hemoglobin value. For the recovery of each gram of missing hemoglobin, 150 mg of iron is required, to which 400 - 1000 mg of iron will be added to restore the deposits.

Treatment is done with oral or injectable iron compounds along with the treatment of the cause (bleeding, malabsorption syndromes).
Iron compounds are also administered
prophylactically during pregnancy, in children during the growing period

Question 9

Within 5-10 days after the onset of iron treatment,

Answer 9

the reticulocyte crisis appears,

hemoglobin and serum iron begin to increase and deposits are gradually restored

Question 10

Oral iron preparations are most often used in the treatment of iron-deficiency anemia,
in the form of the most easily absorbed ferrous salts -

Answer 10

ferrous sulphate, ferrous gluconate,

administered before meals. Vitamin C promotes intestinal absorption of iron.

Question 11

The most common adverse reactions during oral iron preparations administration are

Answer 11

gastrointestinal adverse reactions: gastric irritation, nausea, epigastric pain, intestinal transit disorders - constipation by fixation of hydrogen sulphide at low doses or diarrhea by gastrointestinal irritation at doses and coloring of faeces in black.

Question 12

Iron injectable compounds are used only when

Answer 12

oral administration is not possible
(absorption deficiency, inflammatory bowel disease, gastric ulcer).
Iron can be administered intravenously or intramuscular.

Question 13

Specific adverse reactions for injectable administration of iron are

Answer 13

allergic reactions - rash, bronchospasm, anaphylactic shock.

Question 14

Acute iron intoxication is very severe;

Answer 14

nausea, vomiting, abdominal pain, bloody
diarrhea, dyspnea and shock with severe metabolic acidosis, coma are specific for acute iron
overdose.

Question 15

Deferoxamine (iron chelator)

Answer 15

is used to treat the overdose

Question 16

Chronic iron intoxication

Answer 16

hemochromatosis occurs as a result of excessive iron

deposition in the myocardium, liver and pancreas causing insufficiency of these organs.

Question 17

Vitamin B12 (cobalamin) is a co-factor in 2 biological reactions:

Answer 17

• homocysteine - methionine synthesis.

- transformation of methyl malonyl-CoA into succinyl-CoA

Question 18

Synthesis of methionine.

Answer 18

Vitamin B12 transfers the methyl group from N-methyl
tetrahydrofolate to homocysteine which is converted to methionine; N-methyltetrahydrofolate is converted to tetrahydrofolate (the active form of folic acid).
Tetrahydrofolate is the precursor of some important co-factors in the synthesis of DNA.
In the absence of vitamin B12, tetrahydrofolate cannot be formed and DNA synthesis will be
disturbed.

Question 19

The absence of vitamin B12 blocks the

Answer 19

conversion of N-methyl-tetrahydrofolate into
tetrahydrofolate, the precursor of some very important co-factors in DNA synthesis.
Deficiency of tetrahydrofolate blocks the conversion of uridylate into thymidylate required
for DNA synthesis.
N-methyl-tetrahydrofolate accumulates, the formation of tetrahydrofolate - the “folate trap” decreases, and desynchronization of nucleus-cytoplasmic maturation, typical for megaloblastic anemia, occurs.

Question 20

The metabolism of vitamin B12 interferes with

Answer 20

the metabolism of folic acid at this level, explaining why megaloblastic anemia can be partially corrected also with high doses of folic acid.

Question 21

Transformation of methyl malonyl-CoA into succinyl-CoA

Answer 21

This reaction is important for the synthesis of myelin sheath. Deficiency of vitamin B12 leads to accumulation of methyl malonyl-CoA and methylmalonic acid.

Plasma and urinary dosage of methylmalonic
acid is useful for diagnostic of megaloblastic anemia through vitamin B12 deficiency.

Deficiency of myelin sheath formation will also cause significant neurological damage, which can be corrected only by vitamin B12 administration

Question 22

Vitamin B12 comes from animal sources;

Answer 22

daily absorption is 1-5 mcg and is conditioned by the presence of the intrinsic factor (Castle) produced by the gastric parietal cells.
The complex vitamin B12 - intrinsic factor is absorbed in the ileum.
Vitamin B12 is stored in the liver - 3000 - 5000 mcg. The daily requirement of vitamin B12 is 2 mcg,
megaloblastic anemia occurring after approximately 5 years of deficiency.

Question 23

Causes of megaloblastic anemia due to vitamin B12 deficiency are:

Answer 23

• inadequate intrinsic factor secretion (Biermer anemia, gastrectomy, congenital absence of intrinsic factor)
• malabsorption syndrome (Crohn’s disease, intestinal resections)
• particular diets (vegetarianism).

Question 24

Vitamin B12 deficiency can cause

Answer 24

megaloblastic anemia and neurological lesions -
peripheral neuritis type with paresthesia, muscle weakness, severe neurological disorders.
Vitamin B12 administered intramuscularly or subcutaneously rapidly corrects megaloblastic
anemia.
The reticulocyte crisis occurs 5-10 days after the start of treatment and recent neurological lesions are corrected within a few weeks; old neurological lesions are irreversible.

Question 25

Folic acid is found in

Answer 25

vegetables (but is destroyed by boiling), meat and eggs;
it is completely absorbed at the level of the proximal junction in the form of N-methyl-tetrahydrofolate which will be transformed into tetrahydrofolate at the cellular level.

Question 26

Tetrahydrofolate

Answer 26

is involved in the synthesis of thymidylate, used in DNA formation.
The enzymes involved in the synthesis of thymidylate are destroyed by drugs such as methotrexate, trimethoprim, 5-fluorouracil; therefore, folic acid is recommended during treatment with these drugs to prevent megaloblastic anemia.

Question 27

The folate deficiency is manifested by

Answer 27

megaloblastic anemia without neurological lesions and

is corrected quickly after folic acid administration - oral preparations