Tag: anemia

Iron is responsible for manufacturing red blood cells, which are integral for the optimal functioning of our immunity and muscles and help maintain proper mental function and energy levels.

The human body is incapable of iron production, and not obtaining optimal iron levels through diet and nutrition can result in anemia. This article covers details about iron deficiency anemia and how to recognize and treat it. 

Symptoms and Signs of Iron Deficiency You Shouldn’t Ignore

Low iron levels have various symptoms, ranging from headaches, shortness of breath, fatigue, and dizziness to restless legs syndrome and difficulty focusing. 

Signs that could indicate low iron levels have caused anemia include:

• Brittle nails
• Cold hands and feet
• Pale skin
• Pain within the mouth and tongue

Main Causes of Iron Deficiency Anemia

The top reasons behind this anemia type include the following:

• Blood loss. Either internal to menstrual bleeding or significant blood loss due to an injury or trauma.
• Insufficient iron intake. Inadequate nutrition with low iron ingestion is another cause of this anemia type.
• Problems with iron absorption. Infection, bacteria, or various diseases or conditions.

Iron depletion can occur within any age group. A higher risk exists for children under two, teenagers with growth spurts, adults over 65, and those with chronic disorders and medical conditions.

Potential Treatments of Iron Deficiency Anemia

According to the American Society of Hematology, iron deficiency anemia is a nutritional anemia. Treatment begins with a medical professional confirming the condition and recommending the best action.

Potential therapies are listed below, and you can combine specific options to achieve the desired results.

An Iron IV Infusion To Restore Iron Levels Quickly

Intravenous therapy is an excellent way to boost iron levels rapidly. Thanks to mobile services, you can get anemia IV therapy while relaxing in the comfort of your own home. 

Choosing the location for your treatment allows you to watch TV or read a book while receiving the IV. Administering iron via an infusion ensures the mineral combo is absorbed directly into your bloodstream, eliminating the risk of stomach upset.

Adjust Your Diet to Ingest More Iron and Vitamin C

The human body can only ingest iron from food, so adjusting your nutrition is essential when dealing with anemia. 

Foods rich in iron include:

• Veggies: Be on the lookout for broccoli, spinach, cabbage, or other leafy greens.
• Legumes: Tofu, beans, and peas are excellent iron sources.
• Protein: Eggs, poultry, beef, fish, and liver are all great options for ingesting iron.
• Fruits: Raisins, dates, and figs are some ideal choices.

Vitamin C interacts well with iron and helps its absorption, which has been verified through scientific research. The nutrient enhances iron absorption, so consider adding foods rich in vitamin C to your diet. These include citrus fruit, strawberries, bell peppers, and cruciferous veggies.

Treat any Underlying Conditions

Blood loss is the prevalent culprit of iron deficiency anemia. Treating the underlying injuries or internal issues can help prevent the problem from worsening or reappearing. 

Final Thoughts

It may be difficult to immediately notice the symptoms of iron deficiency anemia, especially during the initial phases. Regular checkups can help observe and maintain iron levels and general health.

Depending on your health condition, lab tests might be necessary every few months or each year. Contact a medical professional if you have iron deficiency, and never attempt to diagnose or treat a severe medical condition without medical supervision.

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Pathophysiology of Sickle cell anemia

In the pathophysiology of Sickle cell anemia or Sickle cell disease (SCD), we learn that it is a systemic disorder caused by a mutation in the gene encoding the β chain of hemoglobin.

This mutation leads to the production of sickle hemoglobin HbS. Sickled red blood cells were first observed in 1910 by JB Herrick in a Black West Indian student.

Introduction to pathophysiology of sickle cell anemia

Sickle cell anemia or Sickle cell disease is the result of a single base-pair change, thymine for adenine, at the sixth codon of the beta gene.

in which the change encodes Valine instead of glutamine in the sixth position on the beta-globin molecule.

Beta globin haplotypes are the different DNA structures associated with the sickle gene are identified by a pattern of restriction enzyme sites.

Therefore, it is important to note that the HbS gene is prevalent in malaria-endemic regions, distribution is however worldwide, with the greatest incidence in tropical Africa.

It occurs in the USA, Middle East, India, the Caribbean, South and Central America, Turkey, and throughout the Mediterranean region.

A 2009 study carried out in Nigeria showed that 2-3% of Nigerian newborns are homozygous.

Incidence in the general Nigerian population is 1:300 with Frequency of the S gene in Nigeria is about 25% Mode of inheritance= autosomal recessive.

Pathogenesis and pathophysiology of sickle cell anemia

The hemoglobin molecule (alpha and beta-globin subunits) picks up oxygen in the lungs and releases it when the red cells reach peripheral tissues, such as the muscles in Sickle cell anemia or Sickle cell disease.

And also, normal red cells maintain a basic disc shape, whether they are transporting oxygen or not but the case is different with sickled hemoglobin.

Sickle hemoglobin exists as isolated units in the red cells.

when they have oxygen bound, Whereas sickle hemoglobin releases oxygen in the peripheral tissues, however, the molecules tend to stick together and form long chains or polymers (polymerization).

These rigid polymers interact with the cell and cause it to bend out of shape Polymerized sickle hemoglobin does not form single strands.

But the molecules group in long bundles of 14 strands each that twist in a regular fashion, much like a braid.

In Sickle cell anemia or Sickle cell disease, most distorted cells are simply shaped irregularly, a few have a cresent-like appearance under the microscope.

These cresent-like or “sickle-shaped” red cells gave the disorder its name. A single red cell may traverse the circulation four times in one minute. Sickle hemoglobin undergoes repeated episodes of polymerization and depolymerization (sickle-unsickle cycle).

This cyclic alteration in the state of the molecules damages the hemoglobin and ultimately the red cell itself.
 Diameter of RBC =7microns
 Diameter of capillaries =3microns

Summary on the sickle cell anemia,

In Sickle cell anemia or Sickle cell disease Polymers tend to grow from a single start site (nucleation site) and often grow in multiple directions. Star-shaped clusters of hemoglobin S polymers develop commonly.

Sickling occurs at the venous end of capillaries whereas unsickling occurs at the arterial end.

Two essential pathological processes arise from sickling: Haemolysis and vaso-occlusion

The pathological features of SCD relate to the shortened life span of the sickled blood cells, (16-20 days rather than a lifespan of 120 days in normal red cells) which leads to hemolytic anemia

The mechanism is likely to be responsible for complications such as pulmonary hypertension and stroke.

Sickled cells directly cause Small vessel occlusion

Vaso-occlusion is the major cause of morbidity and mortality in sickle cell anemia, accompanied by occlusion of blood vessels followed by ischemia or infarction in various tissues, leading ultimately to progressive end-organ damage.

The process of vaso-occlusion

It was first thought that hemoglobin S polymerization resulted in the entrapment of sickled, poorly deformable erythrocytes that mechanically blocked small-caliber vessels.

Damage similar to that seen in patients with the atherosclerotic vascular disease has been seen in the large cerebral vessels of patients with Sickle cell anemia or Sickle cell disease, including intimal hyperplasia, and fibroblast and smooth muscle proliferation.

It will be of great importance to consider these terms [CRISES]; Vaso-occlusive, Haemolytic, Aplastic, and Acute sequestration.

VASO-OCCLUSIVE CRISIS

This crisis is due to obstruction of blood flow in the smaller venules, capillaries and even in medium-sized or large arteries, as a result of the increased viscosity and sludging associated with sickling.

The increased adhesiveness of sickled reticulocytes worsens occlusion. Vaso-occlusion is the pathophysiologic basis of most of the clinical.

HAEMOLYTIC CRISIS

Hemolytic crisis makes RBCs are broken down at a more rapid rate than during the steady-state of the disease, it is precipitated by malaria and bacterial infections.

Features include:

*Severe anemia, Cardiac failure
*Jaundice, hepatomegaly.
*Encephalopathy-seizures, altered sensorium
*The terms ‘ hemolytic’ and ‘hyper haemolytic’s are often used interchangeably, but the latter technically refers to the co-existence of SCA and G6PD[glucose 6-phosphate dehydrogenase deficiency].
APLASTIC CRISIS

There is a shut down of the bone marrow which is usually limited to the red blood cell precursors, making the patient become profoundly anemic and may go into high-output cardiac failure.

Anemia reoccurs after blood transfusions until the crisis is over, Several viruses are associated with this syndrome most especially parvovirus B19.

ACUTE SEQUESTRATION

The Pooling of blood in the spleen is a frequent occurrence in children with sickle cell anemia, particularly in the first few years of life, resulting in splenic sequestration crisis.

They are often associated with viral or bacterial infections; acute chest syndrome occurred in 20% in one series.

The usual clinical manifestations are sudden weakness, pallor, tachycardia, tachypnea, and abdominal fullness.

DIAGNOSIS OF SICKLE CELL ANEMIA

Clinical …….80% of cases.
Laboratory diagnosis:
Electrophoresis…cellulose acetate

DIAGNOSTIC METHODS INCLUDE:

Full blood count, blood film and reticulocyte count, bilirubin.
Hb electrophoresis using cellulose acetate or agar gel
High-performance liquid chromatography (HPLC)
Isoelectric focusing (IEL)
Polymerase chain reaction (PCR)
Supplementary genetic tests

MANAGEMENT FOR A STEADY-STATE

Determine and record physical/Haematol Parameters.
Avoid factors that encourage sickling.
Folic acid supplementation.
Malaria prophylaxis.

Treatments

ANTISICKLING AGENTS

Hydroxycarbamide, formerly known as Hydroxyurea.

15mg/kg/24 hrs. gradually increase to max of 30mg/kg/24hrs. Monitor FBC, LFT and HbF. Increase in HbF is usually 10-15%
Trade name –Hydrea
*5-Azacytidine,
*decitibine
*Histone deacetylase inhibition: short-chain fatty acids –butyric acid.
*Recombinant human erythropoietin (rhEPO)

It is important to note that hydroxycarbamide is the most successful drug therapy for scd.

It is a cytotoxic and cytoreductase antimetabolite that acts via inhibition of DNA synthesis by inhibiting ribonucleotide reductase. Known pharmacological effects that may contribute to the drug’s efficacy in SCD include:

Hydroxycarbamide

1.increase in red cell content of Hb F.
2.dose related cytoreductase effects on neutrophils.
3.increase in water content of red cells.
4.increased deformability and successful microvascular navigation of sickled cells.
5.altered adhesion of RBCs to endothelium by decreasing the expression of endothelial adhesion molecules.
Treatment with hydroxycarbamide shows significant reduction in bone pain crises, admissions, and need for blood transfusion#

Gene therapy

The term gene therapy is applied to any maneuver in which genes or genetically modified cells are introduced into a patient for therapeutic benefit. Gene therapy corrects sickle cell disease in mice, scientists report therapies designed to treat genetic disease in humans.

The therapy transfers an anti-sickling variant of the faulty gene to the bone marrow, where it incorporates itself into the stem cells that give rise to red blood cells. In two mouse models, the new gene was rapidly expressed in 99 percent of all circulating red blood cells, preventing sickling and other signs of the disease, Leboulch said.

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