Anemias:
I.Defeciency
of substrates which are necessary for RBC or Hb production like:
1. Iron deficiency
anaemia(increaseloss, or decrease intake)
2.folic acid deficiency anaemia(low
intake) folic a. is necessary for DNA formation and maturation of RBCs.
3 B12 defeciency anaemia. B12 is
necessary for DNA formation of RBCs.defeciency due to low intake as in
vegetarians or intrinsic factor deficiency (pernicious anaemia).
II.
membrane defects as in hereditary
spherocytosis or elliptocytosis.
Haemolytic
anaemia eg:autoimmune Haemolytic anaemia,erythroblastosis fetalis.
III.Hemoglobinopathies.Thalassaemiaand
sickle cell anaemia.
IV .
bone morrow infiltration like aplastic anaemia and different forms of
leukaemias.
V.
Anaemia of chronic disease.like chronic renal failure.
Effect
of anemia on circulation:
1. Decrease
the viscosity of blood.
2. increase
work load on the heart (PALPITATION & TIREDNESS)
3. In exercise there will be tissue hypoxia that leads
to heart failure.
Treatment toward the cause.
Polycythemia:
Increase
production of RBCs (count 6-8 milio/mm3)its of 2 types:
1.primarypolycythemia
vera(count7-8 milio/mm3)
2.Secondary
due to tissue hypoxialike in high altitude or chronic smokers.
Effect
of polycythemia on circulation increases the viscisity of blood leads to sluggish
circulation this leads to thrombosis. Blood
pressure increases increase work load on the heart leads to heart failure.
Tretment
by venesection
Iron
In adults, the amount of iron lost from the body is relatively small. The losses are generally unregulated, and total body stores of iron are regulated by changes in the rate at which it is absorbed from the intestine. Men lose about 0.6 mg/d, largely in the stools. Women have a variable, larger loss averaging about twice this value because of the additional iron lost in the blood shed during menstruation.
In adults, the amount of iron lost from the body is relatively small. The losses are generally unregulated, and total body stores of iron are regulated by changes in the rate at which it is absorbed from the intestine. Men lose about 0.6 mg/d, largely in the stools. Women have a variable, larger loss averaging about twice this value because of the additional iron lost in the blood shed during menstruation.
The average daily iron intake in the United
States and Europe is about 20 mg, but the amount absorbed is equal only to the
losses. Thus, the amount of iron absorbed ranges normally from about 3 to 6% of
the amount ingested. Various dietary factors affect the availability of iron
for absorption; for example, the phytic acid found in cereals reacts with iron
to form insoluble compounds in the intestine. So do phosphates and oxalates.
Most of the iron in the diet is in the ferric (Fe3+) form, whereas it is the ferrous (Fe2+) form that is absorbed. There is Fe3+ reductase activity associated with the iron transporter in the brush borders of the enterocytes .
Most of the iron in the diet is in the ferric (Fe3+) form, whereas it is the ferrous (Fe2+) form that is absorbed. There is Fe3+ reductase activity associated with the iron transporter in the brush borders of the enterocytes .
No more than a trace
of iron is absorbed in the stomach, but the gastric secretions dissolve the
iron and permit it to form soluble complexes with ascorbic acid and other
substances that aid its reduction to the Fe2+ form. The importance
of this function in humans is indicated by the fact that iron deficiency anemia
is a troublesome and relatively frequent complication of partial gastrectomy.
Almost all iron
absorption occurs in the duodenum. Fe2+ is Transported into the enterocytes . Some is
stored in ferritin,
In the plasma, Fe2+
is converted to Fe3+ and bound to the iron transport protein transferrin.
This protein has two iron-binding sites. Normally, transferrin is about 35%
saturated with iron, and the normal plasma iron level is about 130 ug/dL (23
umol/L) in men and 110 ug/dL (19 umol/L) in women.
70% of the iron in
the body is in hemoglobin, 3% in myoglobin, and the rest in ferritin, which is
present not only in enterocytes but also in many other cells. Apoferritin is a
globular protein made up of 24 subunits. Iron forms a micelle of ferric
hydroxyphosphate, and in ferritin, the subunits surround this micelle. The
ferritin micelle can contain as many as 4500 atoms of iron.
Ferritin molecules in lysosomal membranes may
aggregate in deposits that contain as much as 50% iron. These deposits are
called hemosiderin.
Intestinal
absorption of iron is regulated by three factors:
1. Recent
dietary intake of iron.
2. The
state of the iron stores in the body.
3. The state of
erythropoiesis in the bone marrow. Iron overload causes hemosiderin to accumulate in the tissues, producing hemosiderosis. Large amounts of hemosiderin can damage tissues, causing hemochromatosis.This syndrome is characterized by pigmentation of the skin, pancreatic damage with diabetes ("bronze diabetes"), cirrhosis of the liver, a high incidence of hepatic carcinoma, and gonadal atrophy
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