Difference between Anemia and Polycythemia

Difference between Anemia and Polycythemia

Red blood cells are the vital cells of blood that carries oxygen to all parts of the body. Red blood cells disorders(anemia) are the condition in which there is a problem with red blood cells that affect their function

Types of red blood cells disorders:

A number of red blood cells disorders that are discussed below:

  1. ANEMIA
  2. POLYCYTHEMIA

Anemia is the disorder that inability of the red blood cells to carry enough oxygen to meet needs of the body or a condition in which a person has a lower than the normal number of red blood cells or hemoglobin. A lack of the mineral iron in your blood commonly causes this disorder. There are low levels of hemoglobin in blood is a cause of anemia but if any defect in the production of red blood cells that produced faulty hemoglobin or red blood cells also cause anemia.

Difference between Anemia and Polycythemia

 Anemia is classified depending on the cause:

  • A production of insufficient or defective erythrocytes
  • Blood loss or excessive loss of erythrocytes

Another and common classification of anemia is based on mean cell volume (MCV) of red blood cells

Microcytic anemia (low cell volume <80)
Normocytic anemia (normal cell volume range of 80 to 100)
Microcytic anemia large cell volume

SIGN & SYMPTOMS OF ANEMIA

It’s related to inability of the red blood cell to supply enough oxygen to the other body cell

  • Tiredness
  • Fatigue
  • Pale appearance
  • Shortness of breath
  • Breathlessness
  • Palpitation

TYPES OF ANEMIA

  1. Iron deficiency anemia
  2. Vitamin B12 /Folic acid deficiency anemia
  • Aplastic anemia
  1. Hemolytic anemia
  2. congenital hemolytic anemia
  3. Sickle cell anemia
  4. Thalassaemia
  5. Hemolytic disease of the newborn
  6. Acquired hemolytic anemia

IRON DEFICIENCY ANEMIA:

This is the most common form of anemia in many parts of world .when your body does not have enough iron or insufficient red blood cells or hemoglobin, that cause iron deficiency anemia.  Our body needs iron to make hemoglobin. In iron deficiency anemia, the red blood cell count often normal, but cells are small size that contains less hemoglobin than normal. A poor diet or certain intestinal disease that affect body absorbs iron can also cause iron deficiency anemia.  Dietary iron comes mainly from red meat and highly colored   vegetables. Daily iron requirement in male about 8miligram per day and for women 18miligram per day it’s higher to compensate for menstrual losses.

SYMPTOMS:

Weakness
General fatigue
Pale skin
Shortness of breath
Dizziness
Cold hands and feet
Fast or irregular pulse
Brittle nails
Headaches

CAUSES:

Inadequate iron intake
Pregnancy or blood loss due to menstruation
Internal bleeding
Inability to absorb iron

RISK FACTORS:

Women of childbearing age
Pregnant women
Poor diet
Donate blood frequently
Prematurely born child

DIAGNOSTIC EVALUATION:

  • Red blood cell size and color
  • Hematocrit
  • Hemoglobin
  • Ferritin( protein helps store iron in our body)

TREATMENT:

  • Iron supplements:

Take iron tablets on an empty stomach
Don’t take iron with antacids
Take iron tablets with vitamin C

Vitamin B12 / folic acid deficiency anemia:

Deficiency of vitamin B12  and/ or folic acid impairs erythrocytes maturation and abnormally large erythrocytes (megaloblasts) are found in the blood circulation. During normal erythropoiesis abnormal cell division occurs the cells grow larger than normal between divisions, and circulating cells are immature, larger than normal and some are nucleated (usually normal RBC  haven’t  nucleus). This situation cause reduces lifespan to between 40 to 50days (normally 120days), and depressed production and early lysis cause anemia.

If we don’t get enough vitamin B12 in our diet from foods like milk, eggs, and meat, our intestines absorb vitamin B12  from food. A protein in our stomach makes called “intrinsic factor” helps our body absorb it. When we don’t have enough, we have a type of vitamin B12   deficiency anemia called “pernicious anemia”

PERNICIOUS ANEMIA:

This is the most common form of vitamin B12 deficiency anemia. It is commonest in female over 50. It is an autoimmune disease in which autoantibodies destroy intrinsic factor and parietal cells in the stomach.

CAUSES:

A lack of vitamin B12
Certain condition that make difficulties to absorb enough vitamin B12,
Chronic alcoholism
Crohn disease
Pernicious anemia
Gastrectomy (removal of stomach part)

SYMPTOMS:

Diarrhea or constipation
Fatigue
Loss of appetite
Pale skin
Shortness of breath during hard work

DIAGNOSTIC EVALUATION:

  • A complete blood cell count
  • Examination of a blood smear
  • Blood vitamin B12 measurement
  • Test for presence of autoantibodies to instric factor or stomach
  • Bone marrow biopsy

TREATMENT:

  • Vitamin B12 injection
  • Vitamin B12 supplements and multivitamins

APLASTIC ANEMIA:

Aplastic (hypoplastic) anemia results from bone marrow failure. In a rare condition when the body stops producing enough new blood or reduced numbers of erythrocytes.  Since the bone marrow also produces leukocytes and platelets, leucopenia (low white blood cell) and thrombocytopenia (low platelet count) are also likely. This condition is occasionally inherited. Usually no causes are identified, known causes including;

Drugs; cytotoxic therapy
Radiation therapy and chemotherapy for cancer
Certain medicines
Exposure to toxic chemicals
Autoimmune disorder
A viral infection
Pregnancy
Unknown factor

SYMPTOMS:

Fatigue
Shortness of breath with exertion
Rapid or irregular heart rate
Pale skin
Frequent or prolonged infection
Unexplained or easy bruising
Nosebleeds and bleeding gums
Skin rash
Dizziness
Headache

DIAGNOSTIC EVALUATION:

  • Blood test
  • Bone marrow biops

TREATMENT:

  • Blood transfusion
  • Stem cell transplant
  • Immunosuppressant
  • Bone marrow stimulants
  • Antibiotic, antiviral

HEMOLYTIC ANEMIA:

Hemolytic anemia occurs when circulating red blood cells are destroyed and removed prematurely from the bloodstream because of abnormal cells or the spleen is overactive. At the end of red blood cells lifespan their go-to spleen to destroy and converting in bilirubin but in such condition before their lifespan they destroyed. The bone marrow production of erythrocytes increases to compensate, so there may be ongoing hemolysis without anemia. However, if the bone marrow cannot compensate red blood cells numbers will fall and anemia results.

CAUSES:

Infection
Tumors
Autoimmune disorder
Medication side effect
Leukemia
Lymphoma
Splenomegaly (Enlarge spleen)
Hepatitis
Lupus (an inflammatory disease condition when the immune system attacks its own tissues)

SYMPTOMS:

Fever
Weakness
Confusion
Dizziness
Pale skin
A headache
Dark urine
Heart murmur
Enlarged spleen
Enlarged liver
Jaundice

DIAGNOSTIC EVALUATION:

  • Bilirubin measurement
  • Hemoglobin
  • Liver function test
  • Reticulocyte count

TREATMENT:

  • Blood transfusion
  • Intravenous immunoglobulin
  • Corticosteroid medication
  • surgery

CONGENITAL HEMOLYTIC ANEMIA

Congenital hemolytic anemia or hereditary hemolytic anemia refers to hemolytic anemia which is primarily due to congenital disorders. In this disease, genetic abnormality leads to the synthesis of abnormal hemoglobin and increased red blood cell membrane fragility, reducing their oxygen carrying capacity and lifespan. The most common forms are sickle cell anemia and Thalassaemia.

CAUSES:

Defective gene
Abnormal red cell membrane

SYMPTOMS:

Jaundice
Weakness
Low blood cell count
Lethargy
Nosebleed in child
Vomiting
Abdominal pain
Fever
A headache
Tiredness
Enlarge spleen
Anorexia

DIAGNOSTIC EVALUATION:

As same as hemolytic anemia’s diagnosis

TREATMENT: splenectomy 

SICKLE CELL ANEMIA:

The abnormal hemoglobin molecules become misshapen when deoxygenated, making the erythrocytes sickle-shaped (weapon used to cut wheat) or crescent moons. The lifespan of cells is reduced by early hemolysis; they usually die in 10 to 20days, which causes anemia. Sickle cells do not move smoothly through the circulation. They obstruct blood flow.

The sickle cell gene is passed from generation to generation it’s called autosomal recessive inheritance means both parents can pass on the defective form of the gene to the child.

Sickle cell trait: with one normal hemoglobin gene and one defective gene they can pass the gene to their child.

CAUSES:

The sickle cell anemia is an inheritance, passes from generation to generation called autosomal recessive inheritance.

SYMPTOMS:

Weakness
Anemia
Delayed growth
Vision impairment
Frequent infection
Fever
Pale skin
Pale nail beds

DIAGNOSTIC EVALUATION:

  • Blood test (hemoglobin S)

TREATMENT:

  • Medication
  • Blood transfusion
  • Vaccinations( prevent infection)
  • Bone marrow transplant

THALASSAEMIA:

This inherited condition involving lower amount of hemoglobin production, which is turn to reduced erythropoiesis and stimulate hemolysis. In most severe form of the disease, regular blood transfusion is required. This can lead to iron overload.

There are mainly two types of Thalassaemia

  • Alpha Thalassaemia: when genes related to the alpha globin protein are missing
  • Beta Thalassaemia: when similar gene defect affect the production of the beta globin protein
  • Mainly they both alpha and beta Thalassaemia includes two forms
  1. Thalassaemia major: inherit the gene defect from both parents.
  2. Thalassaemia minor: defective gene from only one parent

CAUSES:

Maturation in the DNA of cells that produce hemoglobin
Inheritance
Abnormal hemoglobin production

SYMPTOMS:

Weakness
Pale skin
Dark urine
Abdominal pain
Abdominal swelling
Slow growth
Facial bone deformities
Fatigue

DIAGNOSTIC EVALUATION:

  • Blood test for Thalassaemia

TREATMENT:

  • Mild Thalassaemia: occasionally blood transfusion
  • Moderate /severe Thalassaemia: frequent blood transfusion

Stem cell transplant

HEMOLYTIC DISEASE OF THE NEWBORN:

In this disorder, the mother’s immune system makes antibodies to the baby’s red blood cells, causing destruction of fetal erythrocytes. This antigen system involved is usually (not always) the rhesus (Rh) antigen.

CAUSES:

Rh incompatibility

Develops when an Rh –ve mother conceives a fetus which is Rh +ve

ABO incompatibility

Thalassemia

Autoimmune hemolytic anemia

SYMPTOMS:

Jaundice
Enlarge liver & spleen
Ascites
Generalized edema
Respiratory distress

DIAGNOSTIC EVALUATION:

Biochemistry tests for jaundice
Complete blood count
Bilirubin level

TREATMENT:

Feeding often & receiving extra fluids
Phototherapy
Antibodies
Medicines to raise blood pressure if it drops too low

ACQUIRED HEMOLYTIC ANEMIAS:

In this context ‘acquired’ means

Hemolytic anemia in which no familial or racial factors involved, there are several CAUSES.

Causes:

Chemical agents
Autoimmunity
Blood transfusion reaction
Hypersplenism (entrapment)

SYMPTOMS:

Dark urine
Pale skin
Heart murmur
Increase heart rate
Splenomegaly
Hepatomegaly (enlarged liver)

POLYCYTHAEMIA

This means an abnormally larger number of erythrocytes in the blood. Also decrease in the volume of plasma and it’s sometimes called erythrocytosis but usually it’s not referred.  This increases blood viscosity, slow blood flow and increases the risk of intravascular clotting ischemia and infarction.

Difference between Anemia and Polycythemia

CAUSES:

High Altitudes
Pulmonary disease
Hypoventilation
Cardiovascular diseases (congenital with the cyanosis)
Heavy cigarette smoking

SYMPTOMS:

A headache
Dizziness
Fatigue
Blurred vision
Joint pain
Numbness
Fever
Weight loss
Shortness of breath
Weakness
Itching (especially following a warm bath)
Bleeding

DIAGNOSTIC EVALUATION:

Blood test

Bone marrow aspiration
Test for the gene mutation that cause polycythemia Vera

TREATMENT:

Phlebotomy: removal of blood from the circulation.
Aspirin: reduce burning pain
Hydroxyurea:  to suppress bone marrow’s ability to produced blood cells.