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https://www.ncbi.nlm.nih.

gov/books/NBK557783/#:~:text=Iron%20deficiency%20anemia%3A%20It
%20is,iron%20absorption%20from%20the%20gut.

https://healthmatch.io/anemia/pathophysiology-of-anemia#overview

Pathophysiology

What is the pathophysiology of anemia?

At a biological level, anemia results from an imbalance between erythrocyte loss subject to production
or issues with hemoglobin. This occurs due to the following:

Absolute anemias:

 Decreased red cell production: Acquired, hereditary


 Increased red cell destruction: Acquired (mechanical, antibody-mediated, hypersplenism, RBC
membrane disorders, chemical injury), hereditary
 Blood loss and blood redistribution

Relative anemias:

 Macroglobulinemia, pregnancy, athletes, postflight astronauts


 The pathophysiology of anemia differs significantly depending on the underlying etiology. For
example, restoring blood volume with intracellular and extracellular fluid in acute hemorrhagic
anemia dilutes the remaining RBCs and can cause anemia.
 The bone marrow produces RBC and releases it into circulation. An imbalance in production to
destruction or removal of RBC can result in anemia.

Pathology
Iron deficiency anemia: It is the most common pathological cause of anemia during pregnancy. It may
result from insufficient dietary intake, blood loss from menstruation or previous pregnancies, increased
demand for iron during pregnancy, or impaired iron absorption from the gut.

Clinical manifestation with rationale

Clinical Manifestations

In general, the more rapidly the anemia develops, the more aggressive is its symptoms.

Anemia Clinical Manifestations

 Decreased hemoglobin. A patient with anemia has hemoglobin levels between 9 to 11 g/dL.
 Fatigue. Fatigue occurs because there is inadequate oxygen levels in the tissues that should have
been carried by hemoglobin.
 Tachycardia. The heart compensates for the decrease in oxygen by pumping out more blood so
it can reach peripheral tissues in the body.
 Dyspnea. Difficulty of breathing occurs because of the decreased concentrations of oxygen in
the blood.
 With decreased hemoglobin that serves as the pigment in the red blood cells, the patient may
become pale because of the lack or decrease in the pigment that is hemoglobin.

Progression of disease

How does iron-deficiency anemia develop?

Normally, your body brings in a steady flow of iron from the food you eat. Your body stores
excess iron so it’s available as needed to make hemoglobin. Iron-deficiency anemia develops when your
body uses the iron stores faster than they can be refilled, or when the flow of iron into your system has
slowed. This occurs in three stages:

First stage: Iron stores are depleted. In this stage, the supply of iron to make new hemoglobin and red
blood cells is dwindling but hasn’t yet affected your red blood cells.

Second stage: When iron stores are low, the normal process of making red blood cells is altered. You
develop what’s called iron-deficient erythropoiesis, sometimes called latent iron deficiency.
Erythropoiesis is the medical term for the process of producing new red blood cells. In this stage, your
bone marrow makes red blood cells without enough hemoglobin.

Third stage: Iron-deficiency anemia develops because there isn’t enough iron to make hemoglobin for
red blood cells. In this stage, the hemoglobin concentration will drop below the normal range. This is
when you may begin noticing iron-deficiency anemia symptoms.

Who’s likely to develop iron-deficiency anemia?

Almost anyone can develop iron-deficiency anemia. That said, women who have menstrual cycles or
who are pregnant or breastfeeding are more likely to develop iron-deficiency anemia than women
who have gone through menopause or men. Here are other groups of people who have an increased
risk of developing iron-deficiency anemia:

Some infants between ages 6 months and 12 months: Babies are born with iron they received from
the person who carried them through gestation. That iron supply runs out after four to six months.
Babies who are breastfed only or drink unfortified formula may not get enough iron.

Children between ages 1 year and 2 years: Many times, young children who drink a lot of cow’s milk
may not get enough iron.

Teenagers: Growth spurts may use up iron reserves more quickly, causing iron deficiency.

Adults over age 65: Older people may not get as much iron as they need because they’re eating less
food.

Individuals with certain chronic medical conditions, bone marrow disorders or autoimmune disorders.

Complications

You may notice symptoms immediately, or they may develop gradually if your anaemia is caused by a
long-term problem, such as a stomach ulcer.

The most common symptoms include:

 tiredness and lack of energy (lethargy)


 shortness of breath
 noticeable heartbeats (heart palpitations)
 a pale complexion
 Less common symptoms include:
 headache
 hearing sounds that come from inside the body, rather than from an outside source (tinnitus)
 an altered sense of taste
 feeling itchy
 a sore or abnormally smooth tongue
 hair loss
 a desire to eat non-food items, such as ice, paper or clay (pica)
 difficulty swallowing (dysphagia)
 painful open sores (ulcers) on the corners of your mouth
 spoon-shaped nails

Prognosis

What can I expect if I have iron-deficiency anemia?

Healthcare providers typically treat iron-deficiency anemia by prescribing iron supplements and
suggesting ways you can add iron to your diet. There are times, however, when iron deficiency anemia is
a symptom of a serious medical condition. You may be losing blood or your body can’t absorb iron. If
that’s your situation, your healthcare provider will focus on treating the condition. Your healthcare
provider is your best resource for information.

When should I see my healthcare provider?

Depending on your situation, you should see your healthcare provider regularly so they can
monitor your iron levels and your overall health. You might see your healthcare provider every three
months for a year or longer.

We all have days when our daily responsibilities outweigh the amount of energy we have to get
things done. But if you have feelings of fatigue that you just can't shake, talk to your healthcare
provider. They’ll find out what’s draining your energy. Iron-deficiency anemia symptoms develop over
time. Left untreated, iron-deficiency anemia can cause serious medical issues. Fortunately, most people
who have iron-deficiency anemia feel better after taking iron supplements.

Diagnostec evaluation

Normally during pregnancy, erythroid hyperplasia of the marrow occurs, and red blood cell (RBC) mass
increases. However, a disproportionate increase in plasma volume results in hemodilution (hydremia of
pregnancy): hematocrit (Hct) decreases from between 38% and 45% in healthy women who are not
pregnant to about 34% during late single pregnancy and to 30% during late multifetal pregnancy. The
following hemoglobin (Hb) and Hct levels are classified as anemic:

 1st trimester: Hb < 11 g/dL; Hct < 33%


 2nd trimester: Hb < 10.5 g/dL; Hct < 32%
 3rd trimester: Hb < 11 g/dL; Hct < 33%

If Hb is < 11.5 g/dL at the onset of pregnancy, women may be treated prophylactically because
subsequent hemodilution usually reduces Hb to < 10 g/dL. Despite hemodilution, oxygen-carrying
capacity remains normal throughout pregnancy. Hct normally increases immediately after birth.
Anemia occurs in up to one third of women during the 3rd trimester. The most common causes
are

 Iron deficiency
 Folate deficiency
 Obstetricians, in consultation with a perinatologist, should evaluate anemia in pregnant
Jehovah's Witness patients (who are likely to refuse blood transfusions) as soon as possible.

Differential Diagnoses

 Alpha Thalassemia
 Aplastic Anemia
 Beta Thalassemia
 Hemolytic Anemia
 Iron Deficiency Anemia
 Low LDL Cholesterol (Hypobetalipoproteinemia)
 Megaloblastic Anemia
 Myelophthisic Anemia
 Pernicious Anemia
 Sickle Cell Disease (SCD)
 Spur Cell Anemia

Treatment and Management

First aid / Emergency care

Medical
Parmachological

Iron Products

Class Summary

These agents are used to provide adequate iron for hemoglobin synthesis and to replenish body
stores of iron. Iron is administered prophylactically during pregnancy because of anticipated
requirements of the fetus and losses that occur during delivery.

Ferrous sulfate (Feratab, Fer-Iron, Slow-FE)

Ferrous sulfate is the mainstay treatment for treating patients with iron deficiency anemia. They
should be continued for about 2 months after correction of the anemia and its etiologic cause in order
to replenish body stores of iron. Ferrous sulfate is the most common and cheapest form of iron utilized.
Tablets contain 50-60 mg of iron salt. Other ferrous salts are used and may cause less intestinal
discomfort because they contain a smaller dose of iron (25-50 mg). Oral solutions of ferrous iron salts
are available for use in pediatric populations.

Carbonyl iron (Feosol, Icar)

Carbonyl iron is used as a substitute for ferrous sulfate. It has a slower release of iron and is
more expensive than ferrous sulfate. The slower release affords the agent greater safety if ingested by
children. On a milligram-for-milligram basis, it is 70% as efficacious as ferrous sulfate. Claims are made
that there is less gastrointestinal (GI) toxicity, prompting use when ferrous salts are producing intestinal
symptoms and in patients with peptic ulcers and gastritis. Tablets are available containing 45 mg and 60
mg of iron.

Ferric citrate

Ferric iron is reduced from the ferric to the ferrous form by ferric reductase in the GI tract. After
transport through the enterocytes into the blood, oxidized ferric iron circulates bound to the plasma
protein transferrin, and can be incorporated into hemoglobin. Ferric citrate 1 g is equivalent to ferric
iron 210 mg. It is indicated in adults with iron deficiency anemia who have CKD and are not on dialysis.

Iron dextran Complex (INFeD)

Dextran-iron replenishes depleted iron stores in the bone marrow, where it is incorporated into
hemoglobin. Parenteral use of iron-carbohydrate complexes has caused anaphylactic reactions, and its
use should be restricted to patients with an established diagnosis of iron deficiency anemia whose
anemia is not corrected with oral therapy.

The required dose can be calculated (3.5 mg iron/g of hemoglobin) or obtained from tables in
the Physician's Desk Reference. For intravenous (IV) use, this agent may be diluted in 0.9% sterile saline.
Do not add to solutions containing medications or parenteral nutrition solutions.

Iron sucrose (Venofer)

Iron sucrose is used to treat iron deficiency (in conjunction with erythropoietin) in adults with
chronic kidney disease (either with or without hemodialysis or peritoneal dialysis). Iron deficiency in
these patients is caused by blood loss during the dialysis procedure, increased erythropoiesis, and
insufficient absorption of iron from the GI tract. There is a lower incidence of anaphylaxis with iron
sucrose than with other parenteral iron products.

Ferric carboxymaltose (Injectafer)

Ferric carboxymaltose is a nondextran IV colloidal iron hydroxide in complex with


carboxymaltose, a carbohydrate polymer that releases iron. It is indicated for iron deficiency anemia
(IDA) in patients aged 1 year and older who have intolerance or an unsatisfactory response to oral iron.
It is also indicated for IDA in adults with nondialysis-dependent chronic kidney disease.

The FDA has also approved ferric carboxymaltose for iron replacement as treatment of iron
deficiency with heart failure and New York Heart Association class II/III to improve exercise capacity.

Ferrous gluconate (Fergon)

Ferrous gluconate replaces iron found in hemoglobin, myoglobin, and enzymes; allows the
transportation of oxygen via hemoglobin. It is indicated in the prevention and treatment of iron-
deficiency anemias.

Ferrous fumarate (Feostat, Ferro-Sequels, Nephro Fer)

Ferrous fumarate is a replacement of iron stores found in hemoglobin, myoglobin, and enzymes;
works to transport oxygen via hemoglobin. . It is indicated in the prevention and treatment of iron-
deficiency anemias.

Ferumoxytol (Feraheme)
Ferumoxytol is iron-carbohydrate complex released within macrophage vesicles; either enters
intracellular iron storage (eg, ferritin) or transferred to plasma transferrin for transport to erythroid
precursor cells for hemoglobin incorporation. It is indicated for iron deficiency anemia (IDA) in adults
who have intolerance to oral iron or have had unsatisfactory response to oral iron. Also, ferumoxytol is
indicated for IDA in adults who have chronic kidney disease (CKD).

Ferric maltol (Accrufer)

An oral iron replacement that delivers iron for uptake across the intestinal wall and transfer to
transferrin and ferritin. It is indicated for iron deficiency in adults.

Ferric derisomaltose (Monoferric)

Complex of iron (III) hydroxide and derisomaltose, an iron carbohydrate oligosaccharide that
releases iron. Iron binds to transferrin for transport to erythroid precursor cells to be incorporated into
hemoglobin. Ferric derisomaltose is administered IV and is indicated for iron deficiency anemia in adults
who are intolerant to or have had unsatisfactory response to oral iron.

Surgical

Procedures

If your anemia is severe, your doctor may recommend a medical procedure. Procedures include
blood transfusions and blood and marrow stem cell transplants.

Blood Transfusion

A blood transfusion is a safe, common procedure in which blood is given to you through an
intravenous (IV) line in one of your blood vessels. Transfusions require careful matching of donated
blood with the recipient's blood.

Blood and Marrow Stem Cell Transplant

A blood and marrow stem cell transplant replaces your faulty stem cells with healthy ones from
another person (a donor). Stem cells are made in the bone marrow. They develop into red and white
blood cells and platelets.
During the transplant, which is like a blood transfusion, you get donated stem cells through a
tube placed in a vein in your chest. Once the stem cells are in your body, they travel to your bone
marrow and begin making new blood cells.

Nursing care

Nursing Assessment

The assessment of anemia involves:

Health history and physical exam. Both provide important data about the type of anemia involved, the
extent and type of symptoms it produces, and the impact of those symptoms on the patient’s life.

 Medication history. Some medications can depress bone marrow activity, induce hemolysis, or
interfere with folate metabolism.
 History of alcohol intake. An accurate history of alcohol intake including the amount and
duration should be obtained.
 Family history. Assessment of family history is important because certain anemias are inherited.
 Athletic endeavors. Assess if the patient has any athletic endeavor because extreme exercise
can decrease erythropoiesis and erythrocyte survival.
 Nutritional assessment. Assessing the nutritional status and habits is important because it may
indicate deficiencies in essential nutrients such as iron, vitamin B12, and folic acid.

Preventive/Rehabilative care

Prenatal vitamins typically contain iron. Taking a prenatal vitamin that contains iron can help prevent
and treat iron deficiency anemia during pregnancy. In some cases, your health care provider might
recommend a separate iron supplement. During pregnancy, you need 27 milligrams of iron a day.
Good nutrition can also prevent iron deficiency anemia during pregnancy. Dietary sources of iron include
lean red meat, poultry and fish. Other options include iron-fortified breakfast cereals, dark green leafy
vegetables, dried beans and peas.

The iron from animal products, such as meat, is most easily absorbed. To enhance the absorption of iron
from plant sources and supplements, pair them with a food or drink high in vitamin C — such as orange
juice, tomato juice or strawberries. If you take iron supplements with orange juice, avoid the calcium-
fortified variety. Although calcium is an essential nutrient during pregnancy, calcium can decrease iron
absorption.

Insigths

Glossary reference

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