Are you ladies with pale face, without strength, with white lips? In the morning you can not get out of bed, while it torments you the thought of having to face a day with the head office, the children, the partner, the house ... Do to go up the stairs with the shopping bag, but there is it short of breath? Have you checked your blood count? It could be an anemia. How do we understand it?
We talk about "anemia" whenever the amount of hemoglobin is reduced in blood below 13 grams% in humans and 12 grams% in women, regardless of whether the number of red blood cells can fall below 4.5- 5 million red blood cells per mm3 (oligocitemia): if a patient, for example It is thalassaemic, it may have 6,000,000 Red Blood Cells, but a content in grams per deciliter of 7.
So is it anemic or not?
In clinical practice, we are concerned if a patient has a
hemoglobin value in g / dl below 8 which represents the threshold below which it
is imperative not to fall. Even if the blood cells have to be transfused, due to
the need to save the resource of the blood cells to be transfused, the
hemoglobin values must be strictly below 8 g / dl. It is clear that even an
anemia of 9 g / dl or 10, in a subject that previously had 13 g / dl must worry
us and allow to start the diagnostic-therapeutic process to solve the case.
Normally, due to clinical experience, anemia depends on an acute or chronic
blood loss, sometimes macroscopically evident (melena, rectorrhagia, hematemesis)
or a chronic loss (in this case the value of ferritin will be low and the value
of MCV below 75, see below).
Furthermore, in an inveterate drinker, for chronic
gastritis, we can have secondary anemias that are deficient with folic acid and
vitamin B12, with MCV greater than 95, in general. Attention, also to
myelodysplastic anemias, to the old preleuuclear forms that often occur with
macrocythemia and simulate the deficiency anemias etc.
Be that as it may, anemia is a symptom not a diagnosis or disease that you want,
and it is one of the most difficult symptoms to investigate if you are not an
expert. Treatment is subject to the definition of the underlying disease.
Why do we have anemia?
Because we can have either a failure to produce red blood cells,
or an accelerated destruction, or an occult or obvious loss (eg tumor of the
digestive tract, NSAID gastritis with melena, prostate adenoma, tumor of the
female genital tract, menstrual cycle , tumor and lesions of the kidney and
urinary tract, lung cancer, etc.). The relationship between plasma (liquid
component of blood) and the corpuscular part is the hematocrit or Htc.
The hematocrit must normally be:
- men: 40-45%
- women 37-47%
- newborn child: 44-62%
- children from the 1st year up to 12 years: 36-44%.
Normal erythrocytes or red blood cells (g.r.) have a biconcave lens shape (in
the shape of a "italian pavesino cookie" ), with a diameter ranging between 6.7-7.7 microns and
a thickness of 2 microns. They contain a corpuscular hemoglobin concentration of
27-32 pg (picograms); this is reduced, for example in thalassemia and in
hypos-iodemic microcytic anemias (i.e. small and with poor Hb). The corpuscular
hemoglobin is calculated from the Hb% / g ratio in millions / mm3. Hemoglobin (Hb)
consists of a protein part (globin) consisting of alpha, beta, delta and gamma
chains, and the prosthetic group of heme, which contains tetrapyrrolic nuclei
with the iron at the center of the structure, which covers the task to "oxidize"
and transport oxygen and transfer it to tissues.
We distinguish a normal hemoglobin consisting of 2 + 2 chains, thus divided:
-HbA1 or adult, with alpha 2 and beta 2 chains;
-HbA2 also of the adult, with alpha2 and delta2 chains;
-Hb F or fetal, with alpha2 and gamma2 chains
However, due to genetic anomalies, we can have hemoglobinopathies, that is the
synthesis of abnormal hemoglobin chains that ultimately give the name to
hemoglobinopathy; in the case, instead, of beta-thalassemia and
alpha-thalassemia, the defect consists in the lack or reduced synthesis of
chains of the beta and alpha type, that are replaced with chains of other type.
These Hb have reduced electrophoretic mobility and are divided:
- hemoglobin S, with alteration of the beta chain, with mutation in position 6
of valine with glutamic acid, so called from English sickle or "sickle"; this
form is present in the African continent, but we have endemic areas in Calabria
and Sicily; even in Calabria there is a form of double heterozygosis,
microdrepanocytic anemia, with a double mutation for the S gene and for the tare
microcitemic gene, transmitted individually by the two parents.
- hemoglobin D, altered on the alpha chain; in the case of alpha thalassemia
there is an inadequate synthesis of alpha chains, to which correspond the excess
of beta chains which give rise to the HHH, which is a tetramer of beta chains;
in the newborn, where the synthesis of gamma chains is still possible, we will
find Bart's hemoglobin; however, alpha thalassemia is incompatible with
intrauterine life and the fetus dies at 32 weeks for fetoplacental hydrops; the
loci that imply the production of alpha chains are 4 and therefore there is the
possibility of an alpha thalassemia in the homozygous incomplete state, whose
clinical severity is between the t.major and the t.minor.
- hemoglobin Lepore
- hemoglobin B2
-Bart's hemoglobin (variant of HbF)
There are numerous classifications used to catalog the anemia; one of these takes into account the VCM or mean corpuscular volume which is = hematocrit / g.r in millions x mm3 and of the globular value = Hb% / number of red blood cells X 20, and is among the most followed:
We will therefore have:
- normochromic anemia, with a globular value equal to 1
- hyperchromic anemia, with a globular value> 1
- hypochromic anemia with globular value <1
Furthermore, another criterion classifies the anemias according to the VCM and
CECM (mean corpuscular hemoglobin concentration = Hbg% / Hct (hematocrit)
- hypochromic microcytic anemia (ie low Hb content for g.r. + g.r of reduced
size, eg thalassemia and iposideremica anemia);
- normochromic normocytic anemia (ie normal content in Hb for g.r. + normal size,
therefore post-haemorrhagic anemia);
- hyperchromic macrocytic anemia (ie g.r. of larger size + higher Hb content, eg
in B12 and folate deficiencies, because g.r. fails to have a normal
erythropoiesis due to vitamin deficiency)
On a pathogenic basis:
- production deficit anemia
- anemia from excess consumption
On an anatomical-functional basis:
- normogenerative anemia (with normoreticolocytosis)
- iporigenerative anemia (with hyporeticolocytosis)
- hyperrigenerative anemia (with hypereticolocytosis)
Based on the signs of hyperemolysis:
- hemolytic anemias
- anemolyic anemias.
- hypo-sideremic anemias (true ferrocarentials, and ferrocarential anemias due to
congenital iron mobilization defect)
- hypersideremic anemias (from lack of utilization of iron (sideroacrestiche),
aplastic, from excessive destruction of red blood cells (thalassemia,
ahemolytics in general).
- normocytic anemias (ie normal volume)
- macrocytic anemias (i.e., rBCs of increased volume, with Medium Corpuscular
Volume (MCV) => 95 micron3
- microcytic anemias (ie red blood cells of MCV volume <76 microns3
and therefore for the concentration of hemoglobin (Hb) in each red blood cell:
- normochromic anemias (ie with normal hemoglobin concentration per globule of
27 picograms)
- hyperchromic anemias (therefore with increased concentration of Hb)
-
hypochromic anemias (therefore with a reduced concentration of Hb).
1) Anemias secondary to endocrine diseases, for example in hypophyseal
insufficiency, hypothyroidism, M. of Addison, excess estrogen.
2) Anemia in renal failure; in this case iron deficiency should be excluded,
because these patients may have occult blood loss from the gastrointestinal
tract, or a folate deficiency that is removed by hemodialysis, an inadequate
dialysis that can worsen anemia.
3) Anemia of decreased production of red blood cells due to nutritional factors: iron, vit. B12, folate, Vit. B6.
4) from medullary insufficiency or aplastic anemias
Hematology index
related link: Anemias
Le anemie introduzione
Le anemie microcitiche
sideropeniche
Le anemie microcitiche non sideropeniche, le talassemie
o anemie mediterranee
Le anemie macrocitiche e megaloblastiche
Le anemie mielodisplasiche
Le anemie emolitiche
Eritropoietina ed anemia
Talassemie