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Learn all about anemia

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Anemia  (hr.  anemia;  ICD-10:  D50-D64) is strictly defined as a decrease in red blood cell mass (erythrocytes, RBC from red blood cell) and is the most common blood disorder.  Erythrocytes’ role is to deliver oxygen from the lungs in tissues and carbon dioxide from tissues into the lungs. This is achieved using hemoglobin (Hb), a tetrameric protein composed of heme and depth. Anemia, therefore, impairs the body’s ability to exchange these gases, reducing the number of erythrocytes that can carry oxygen and carbon dioxide.

Anemia, like fever, is only a symptom, a consequence (or clinical condition) that requires investigation of a further causal etiology.

Erythrocyte measurement methods

erythrocyte examination

Erythrocyte mass measurement methods are time-consuming, expensive, and often require transfusion of radioisotope-labeled erythrocytes. Therefore, in practice, anemia is often detected and quantified by measuring the number of erythrocytes, hemoglobin concentration, and hematocrit. However, these values should be interpreted with caution, as concentrations are affected by plasma volume changes. For example, dehydration raises these values, and increased plasma volume in pregnancy can decrease values without actually affecting erythrocyte mass.

Etiology

Basically, all causes of anemia can be grouped into three basic groups: due to anemia blood loss (hemorrhage  ), anemia due to increased destruction of erythrocytes  ), and anemia due to decreased erythrocyte production (ineffective hematopoiesis  ). These cases include several etiologies (genetic, nutritional, physical,  chronic, and malignant diseases, infectious diseases  ) that require specific and appropriate therapy.

Another clinically useful approach to anemia classifications is a change in red blood cell morphology, which often indicates a specific cause. Morphological features that indicate etiology include erythrocyte size (normocytes, microcytes, or macrocytes); the amount of hemoglobin reflected in cell color (normochromic or hypochromic); and cell shape. In general, microcytic hypochromic anemias are caused by hemoglobin synthesis disorders (most commonly iron deficiency). In contrast, macrocytic anemias most commonly originate from abnormalities that impair erythroid precursors’ maturation in the bone marrow. Normochromic normocytic anemias have different etiologies: in some of these anemias, specific erythrocyte-shaped abnormalities observed on the peripheral blood smear provide an important etiological signpost.

In emergency services, by far, the most common cause of anemia is acute bleeding.

Drug-induced anemia

Medicines or other chemicals often cause aplastic and hypoplastic group disorders. Certain types of these causative agents are dose-related, and others are idiosyncratic. Any man exposed to a sufficient dose of inorganic arsenic, benzene, radiation, or conventional chemotherapeutic agents develops bone marrow suppression with pancytopenia. In contrast, only occasionally does a reaction occur among idiosyncratic agents that result in the suppression of one or more cell lines (1 in 100 to 1 in a million). Thus chloramphenicol can cause pancytopenia, while granulocytopenia is more commonly seen with sulfonamides or antithyroid drugs.

Epidemiology

Prevention of anemia

The prevalence of anemia in population studies of healthy people (excluding pregnant women) depends on the hemoglobin concentration selected as the lower limit of normal. The World Health Organization (WHO) selects 12.5 g / dL for adult and adult women. So it is estimated that approximately  4% of men and 8% of women have values lower than this. A significantly higher prevalence is observed in the patient population.  In less developed countries, the prevalence of anemia 2-5 is higher than in developed countries, which is probably influenced by geographical diseases (sickle cell anemia, thalassemia, malaria, chronic infections), and nutritional factors iron deficiency and, to a lesser extent folic acid deficiency. Populations with little red meat in the diet have a higher incidence of anemia due to iron deficiency because iron from heme is better absorbed than inorganic iron present in vegetables.

Age and a half

Overall, anemia is twice as common in women as in men. The difference is significantly greater during the fertile years due to pregnancy and menses. Approximately 65% of all iron in the body is incorporated into circulating hemoglobin. One gram of hemoglobin contains 3.46 mg of iron (1 mL of blood with a hemoglobin concentration of 15 g / dL; therefore contains 0.5 mg of iron). Every healthy pregnancy takes the mother approximately 500 mg of iron.

While a man must absorb about 1mg of iron to maintain balance, premenopausal women must absorb an average of 2mg of iron per day. Further, since women eat less food than men, they must have twice as effective iron absorption to avoid deficiency.

Women have a significantly lower incidence of X-linked anemias, such as G-6-PD deficiency and sex-linked sideroblastic anemias, than men. Additionally, in younger age groups, men have a higher incidence of acute anemia due to traumatic causes.

Previously, severe, genetically acquired anemias (e.g., sickle cell anemia, thalassemia, Fanconi syndrome) were more common in children because they did not survive adulthood. However, with advances in medical care and advances in transfusion and chelation, along with fetal hemoglobin modifiers, life expectancy in people with these diseases has been significantly prolonged.

Acute anemia has a bimodal frequency distribution, affecting mainly younger adults and people in their late fifties. Causes among young adults include trauma, menstrual and ectopic bleeding, and acute hemolysis problems.

In people between the ages of 50 and 65, acute anemia is usually the result of acute blood loss with a chronic anemic condition. This is the case with uterine and gastrointestinal bleeding.

Anemia and ethnic groups

blacks anemia

The prevalence of neoplasms increases with each decade of life. It can cause anemia through bleeding, invasion of the bone marrow by a tumor (where the bone marrow is replaced by a tumor, or for example, granuloma -[podtiip] myelophthisical anemia[/podtip] ), or the development of anemia associated with chronic disorders. The use of aspirin, nonsteroidal antirheumatic drugs, and warfarin also increases with age and can create gastrointestinal bleeding.

As mentioned earlier, certain ethnic groups have an increased prevalence of genetic factors associated with certain types of anemia. Diseases such as hemoglobinopathies, thalassemia, and G-6-PD deficiency have different mortality in different populations due to differences in the genetic abnormalities that create the disorder. For example, G-6-PD deficiency and thalassemia have lower morbidity in African Americans than in the Mediterranean due to genetic differences. Conversely, sickle cell disease has higher morbidity and mortality in African Americans than in Saudis.

Ethnicity is also a factor in nutritional anemias and anemias associated with untreated chronic diseases. Socioeconomic benefits that positively affect diet and access to health care lead to a reduction in the prevalence of these types of anemias. Thus, iron deficiency anemia is more prevalent in developing countries (which have less meat in their diet) than in developed countries. Similarly, chronic disease anemia is common in populations with a high incidence of chronic infectious diseases (e.g., malaria, tuberculosis, AIDS). This is partially exacerbated by these populations’ socioeconomic status and their limited access to adequate health care.

Pathophysiology

Physiological responses to anemia vary with acuteness and type of stroke.

The gradual onset of the disease may allow the activation of compensatory mechanisms. Except for anemia due to chronic renal failure, in which the cells produce erythropoietin, a decrease in tissue oxygenation that accompanies anemia usually triggers increased erythropoietin production. Erythropoietin stimulates compensatory hyperplasia of erythroid precursors in the bone marrow, and in severe anemia, the appearance of extramedullary hematopoiesis in secondary hematopoietic organs (spleen, liver, and lymph nodes).

In well-nourished individuals who become anemic due to acute bleeding or hemolysis, the compensatory response may also increase red blood cell regeneration five to eight-fold. The main feature of increased erythrocyte production in the bone marrow is reticulocytosis, i.e., the characteristic appearance of an increased number of newly formed cells (reticulocytes) in the peripheral blood. In contrast, disorders with decreased erythrocyte production (regenerative anemia) are characterized by reticulocytopenia.

Anemia due to acute blood loss

In anemia due to acute blood loss, a decrease in oxygen transfer capacity occurs along with a decrease in intravascular volume, with resultant hypoxia and hypovolemia. Hypovolemia leads to hypotension, which is detected by baroreceptors in the carotid bulb, aortic arch, heart, and lungs. These receptors transmit impulses to the vagus’s afferent fibers and glossopharyngeal nerves in the medulla oblongata, cerebral cortex, and pituitary gland.

Development 1

In the medulla oblongata, sympathetic tone increases as a reflex response, while parasympathetic activity decreases. Increased sympathetic tone leads to the release of norepinephrine from the sympathetic nerve endings and adrenaline release and noradrenaline from the adrenal medulla. Sympathetic association with hypothalamic nuclei increases the secretion of antidiuretic hormone (ADH) from the pituitary gland. ADH increases the reabsorption of water from the distal collecting tubules of the kidney. The response is reduced renal perfusion, juxtaglomerular cells in afferent arterioles releasing renin into the renal circulation, leading to elevated angiotensin I, which angiotensin-converting enzyme (ACE) converts to angiotensin II.

Development 2

Angiotensin II has a potent pressor effect on arteriolar smooth muscle. Angiotensin II also stimulates the adrenal cortex’s glomerular zone to produce aldosterone. Aldosterone increases the reabsorption of sodium from the kidney’s proximal tubules, thus increasing the intravascular volume. The sympathetic nervous system’s primary effect is to maintain tissue perfusion by increasing systemic vascular resistance. Increased venous tone increases preload and final diastolic volume, increasing stroke volume. Therefore, stroke volume, heart rate, and systemic vascular resistance are maximized by the sympathetic nervous system. Improving oxygen delivery is made possible by increased blood flow.

Hypovolemic hypoxia

In hypovolemic hypoxia conditions, increased venous flow due to increased sympathetic tone is likely to dominate the vasodilatory effects of hypoxia. Counterregulatory hormones (e.g., glucagon, adrenaline, cortisol) are likely to move intracellular water into the intravascular space, possibly due to the resulting hyperglycemia. This contribution to intravascular volume has not yet been fully elucidated.

Patient prognosis

The prognosis usually depends on the underlying cause of the anemia. However, the severity of the anemia, its etiology, and the rate at which it develops may play an important role in the prognosis. Similarly, the patient’s age and the existence of other comorbid conditions affect the outcome of the disease.

Liver cirrhosis

Approximately 30% of patients with cirrhosis of the liver die from bleeding. The prognosis for traumatic aortic rupture is also poor, where approximately 80% of patients die before reaching the hospital, and most patients who do not receive adequate care die within 2 weeks. Non-traumatic aneurysm rupture also has a poor prognosis and is essentially fatal if left untreated. In patients with sickle cell anemia, homozygotes (Hgb SS) have the worst prognosis because they are more likely to have crises. In contrast, heterozygotes (Hgb AS) have crises only in extreme conditions.

Thalassemia

In thalassemia, homozygotes (Cooley’s anemia or thalassemia major) have a worse prognosis than patients with any other thalassemia. The chances of survival are worse for patients with idiosyncratic aplasia caused by chloramphenicol and viral hepatitis and better when paroxysmal nocturnal hemoglobinuria or antisepticizes are probable causes. The prognosis for idiopathic aplasia lies between these two extremes, where the mortality rate for untreated cases is approximately 60-70% within two years of diagnosis.

Hyperplastic bone marrow

Among patients with hyperplastic bone marrow and decreased erythrocyte production, one group has an excellent prognosis, and the other does not respond to therapy and has a relatively poor prognosis. The first group includes patients with relative bone marrow failure disorders due to nutritional deficiency where appropriate treatment with vitamin B12, folic acid, or iron leads to the correction of anemia once the appropriate etiology is established. The second group includes patients with idiopathic hyperplasia who may partially respond to pyridoxine therapy but more often do not respond. These patients have annular sideroblasts in the bone marrow, suggesting inappropriate use of iron in mitochondria for heme synthesis.

Other cases of anemia

As for other conditions, such as ectopic pregnancy, the prognosis with prompt care is excellent, with a mortality rate of only 1-2%. In patients with hemophilia, about 15% of them eventually develop factor VIII inhibitors and may die from bleeding complications. Patients with idiopathic platelet purpura usually respond to immunosuppression or splenectomy and have an excellent prognosis. Approximately 80-90% of patients with TTP who receive plasmapheresis fully recover. Hemolytic-uremic syndrome carries significant morbidity and mortality if left untreated. Up to 40% of patients may die, and almost 80% develop renal failure.

Pernicious anemia

Chronic illness/anemia resulting from insufficient absorption of vitamin B 12. 

 

It occurs in adults due to gastric atrophy (you cannot absorb vitamin B12). Parietal cells in the stomach that produce an intrinsic factor required to absorb vitamin B12 and their destruction lead to a deficiency of this essential vitamin.

The name pernicious anemia has remained since this type of anemia was fatal, which is no longer the case, but the name has been retained for historical reasons. 

To lack vitamin B12 it can lead to several diseases and conditions. Still, pernicious anemia is understood only due to atrophic gastritis and loss of parietal cell function.

Dr. Addison was the first to describe this disease, and until 1920, people died from it a year to 3 years after diagnosis. Three physicians in their thirties treated this anemia so that patients consumed raw liver juice in large quantities. That is why they deservedly won the Nobel Prize in 1934, curing a hitherto incurable disease !!

We are very grateful for the progress and the fact that we do not have to drink raw liver, but we elegantly solve the lack of this vitamin with tablets or injections!

Vitamin B12 and anemia

Vitamin B12 cannot be created/synthesized in the human or animal body, so we must ingest it through food. It is essential for the brain and nervous system; it participates in every cell’s metabolism in the body.

We get the most vitamin B12 from meat (especially liver), fish, shellfish, and dairy products.

The genetic variant of pernicious anemia is an autoimmune disease with a definite genetic predisposition. Antibodies (anti parietal) occur in 90% of people with pernicious anemia, while they are present in only 5% of people in the general population.

Classical pernicious anemia occurs due to the lack of intrinsic factors synthesized in the stomach’s parietal cells. There is no absorption of vitamin B12, the result: megaloblastic anemia.

Any disease or malabsorption condition can lead to vitamin B12 deficiency and macrocytic/megaloblastic anemia accompanied (though not always) by neurological outbursts.

Causes of vitamin B12 deficiency

  • Insufficient consumption (strict vegetarian diet: vegans)
  • Atrophy or severe disorder of the gastric mucosa
  • Deficiency or impaired function of intrinsic factor
  • Pancreatic enzyme deficiency
  • Inflammation of the small intestine, ileitis, celiac disease, intestinal amyloidosis, intestinal resection, Crohn’s disease
  • Infection with the parasite Diphyllobothrium latum: this parasite interferes with the absorption of vitamin B12

Frequency:

It most often occurs in the northern European population: English, Scandinavians, Irish, Scots, aged 40 to 70.

Symptoms:

  • Weight loss, subfebrile fever
  • Anemia: paradoxically anemia is well tolerated, even when hemoglobin is extremely low (40-50), MCV (mean corpuscular volume) is high: angle over 100
  • About 50% of patients have a very smooth tongue, without papillae (glossitis)
  • Changes in character and personality
  • Thyroid dysfunction
  • Diarrhea
  • Paresthesias: tingling in the arms/legs
  • The most severe: neurological outbursts: balance problems, unsteady gait, muscle weakness. In the elderly, people with symptoms of dementia must exclude vitamin B12 deficiency as memory problems, hallucinations. Irritability may occur.

Diagnosis:

Laboratory tests: complete blood count, peripheral blood smear, levels of vitamin B12, folate, methylmalonic acid, and homocysteine in the blood

 Schilling test: the patient’s ability to absorb vitamin B12 is checked.

The presence of antibodies to intrinsic factors in the blood.

Therapy:

As you have probably guessed so far, the therapy is: to replace vitamin B12. The synthesized vitamin B12 is called cyanocobalamin. It does not exist in nature but is synthesized and administered to patients orally, transdermally, intranasally, or by injection (intramuscularly, subcutaneously).
Today, some tablets contain high doses of vitamin B12: 500-1000 mcg, so there is quite enough vitamin to keep the cells in the body functioning well.

If in doubt, it is certainly advisable to give replacement therapy in the form of an injection! 

Famous people with this disease:

Alexander Graham Bell
Annie Oakley: 1925. died from the effects of pernicious anemia in 65 g of life

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