Pathophysiology: Iron Deficiency Anemia | Free Essay Example

Pathophysiology: Iron Deficiency Anemia

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Iron Deficiency Anemia (IDA) is an abnormal body condition characterized by lack of enough erythrocytes in the blood (McCance et al, 2010). The disease is brought about by low amounts of iron in the body which then hinder the production of hemoglobin. Thus, oxygen transportation to the body tissues is negatively affected. IDA is the commonest type of anemia affecting 2 billion people in the world and 3.4 million individuals in the US (Huch & Schaefer, 2006). The condition affects twenty percent of reproductively active women and two percent of adult males.

The trend may be explained by menstrual bleeding in addition to poor dietary intake and parasitic infections among other issues. According to Springhouse (2006), the disease is found in all parts of the world and it affects over eleven million people on yearly basis. In 1999, 118 deaths related to IDA were reported in the US. People with IDA condition may have some degree of coldness and conditions like pica. Additionally, victims may have various complications which hamper their participation in productive activities (Springhouse, 2006). Thus, the disease is of major importance in human society.

The case study in this paper involves a forty seven years old male who presents with the gradual onset of dyspnea on exertion and fatigue. He also complains of frequent dyspepsia with nausea and occasional epigastric pain. He has as a history of alcohol abuse. The patient states that he has not had his usual energy level for the past three to four months. His dyspnea has become much worse in the past few weeks. He denies chest pain, orthopnea, edema, cough, wheezing, or recent infections. He states that he has had occasional episodes of hematemesis after drinking heavily, and subsequently had several days of dark stools. He consumes two 6-packs of beer per day for the past 8 years since losing his job. Nothing seems to make his breathing any better, but antacids help relieve his epigastric discomfort and dyspepsia.

On assessing his medical history, the patient denies any case of cardiac or pulmonary disease. He was diagnosed with a duodenal ulcer in the past and was on three drugs at once for a while 2 years ago, but stopped taking them due to the cost. His only surgery was a childhood tonsillectomy. He is a nonsmoker and takes no medications except over-the-counter antacids. He has no known allergies.

As such, further investigations on his medical history need to be conducted to ascertain cases of critical diseases and major hospitalizations. In addition, the client’s past hematologic setbacks, liver problems and bleeding abnormalities may be examined (Collins, 2003). Moreover, caregivers should investigate any cases of petechie and renal or splenic disease and establish if the patient bruises easily.

Physical examinations reveal that he is a thin pale, white male in no acute distress, but appears older than stated age. His vital signs are as follows; temperature is 37 Celsius orally, pulse is 95 beats/min, respiratory rate is 16 breaths/min and unlabored, and blood pressure is 120/72 mmHg in the right arm (sitting). His skin is pale without rashes or spider angiomas. His sclera are pale, but without icterus. Cheilosis is present. His pharynx is clear and without postnasal drainage. There is no thyromegaly, adenopathy, or bruits. His nails are brittle and thin. His abdomen is not distended and bowel sounds present. He bears some pain in the upper middle part of the stomach (epigastric tenderness). His prostate is not tender or enlarged. His stool is guaiac positive. He has no joint deformity, muscle tenderness, or edema.

According to the laboratory tests, the hemoglobin is 8 g/dL and hematocrit is 29%. The average corpuscular volume is typical, but the average corpuscular Hb content is reduced. In addition, the erythrocyte distribution width is amplified, and the reticulocyte count is less than two percent. On the smear, there are mixed microcytic/hypochromic and macrocytic/normochromic erythrocytes. The appearance of white blood cells platelet is normal.

The results of the prothrombin time, liver function tests, electrolytes, and amylase are normal. Partial thromboplastin time is unaltered. Serum ferritin, transferrin saturation, total iron-binding capacity, folate, and red cell folate levels are decreased. The serum B12 level is normal. A bone marrow biopsy shows megaloblastic changes and low iron stores. An upper endoscopy reveals a 2 cm duodenal ulcer with evidence of recent but not acute hemorrhage.

The patient was suspected to suffer from iron deficiency anemia. IDA is said to be an advanced stage of iron deficiency in the body (McCance et al, 2010). Low amounts of iron can be attributed to increased body demand as a result of rapid development, excessive blood loss (during menstruation or accidents) and reduced iron intake in the ileum (Huch & Schaefer, 2006). In addition, deficiency may result from consumption of foods that lack iron or that contains non heme iron.

This leads to a lower rate of absorption. Non heme iron has to be converted to ferrous iron before absorption (Cannobio, 2009). Iron in the blood system binds to transferrin which conveys it to erythroblast receptors and also to cells in the liver and placenta. The erythroblast mitochondria then converts iron to protoporphyrin and then to heme while transferrin is recycled (McCance et al, 2010). Iron that remains after this process is transported and stored as ferritin and hemosiderin (Springhouse, 2006).

More iron is recycled from dying erythrocytes by transferrin. When iron absorption is low, bone marrow stores are depleted so that production of erythrocytes is hampered (Crowley, 2009). Nevertheless, a major cause of IDA to this client may be prolonged bleeding from gastrointestinal tracts and extended intravascular hemolysis as evidenced by presence of an ulcer (Springhouse, 2006). Low levels of iron intake may also result from upper small bowel malabsorption or from gastrectomy. Extraordinarily, inadequate amounts of iron can be attributed to under nutrition.

Iron deficiency anemia leads to inadequate Hb levels and thus low amounts of oxygen are circulated. A decreased amount of oxygen in circulation makes the heart to overwork and this may lead to heart complications. In this situation, a person may feel exhausted, feeble and have shortness of breath and develop a pale skin (McCance et al, 2010). As the disease progresses, an individual may have cheilosis and brittle nails and suffer from dysphagia. Lack of timely treatment may lead to heart failure and this can be fatal (Crowley, 2009).

The disease can be detected through conducting Complete Blood Count (CBC) (Springhouse, 2006). The test is used to ascertain hematocrit and hemoglobin levels. Low levels signify an anemic condition. The test also assesses the amount of leukocytes, erythrocytes and blood platelets. Unusual results signify a blood disorder. Moreover, CBC test investigates the MCV and MCHC which give clues to possible causes of anemia. In addition, blood smears are made to observe the shape of erythrocytes (McCance et al, 2010).

Abnormal shapes of red blood cells signify lack of hemoglobin in the cell. Furthermore, reticulocyte count test may be conducted to assess the functionality of bone marrow. Quantity of iron in the body may be determined through testing serum ferritin and iron as well as investigating the concentration of transferrin (Cannobio, 2006). Moreover, red blood cell protoporphyrin tests and stool occult blood procedures are important in establishing an anemic condition. Clinical manifestations of this disease include fatigue, black stool, dizziness, dyspepsia and ulcers as well as hometochezia (McCance et al, 2010).

The client has all these symptoms and hence the need for treatment. Iron deficiency anemia can be cured through treatment of root causes such as hemorrhages and then taking iron supplements like ferrous sulphate (Springhouse, 2006). Such supplements are in form of non heme or heme iron and they can be taken orally or through an injection. Other treatments may include taking iron rich foods like fish, eggs and raisins. With such treatment, iron level should normalize within two months (Mosby, 2010). There are no associated complications although the disease may reappear. Therefore, one is advised to take regular medical check ups. For effective treatment of IDA, assessment tests ought to be interpreted clearly.

Physical tests revealed several abnormal conditions. The patient had a thin pale coloration and he appeared older than the stated age even though he suffered no stress. The normal color of the skin is lost due to lack of hemoglobin and oxygen stress (Cannobio, 2006). The patient might have seemed older due to prolonged exhaustion resulting from breathing difficulties caused by oxygen stress. Furthermore, the patient’s sclera was pale although it lacked icterus and his mouth’s corner had signs of cheilosis which results from iron deficiency (Springhouse, 2006).

In addition, his nails were brittle and thin in appearance. Finally, abdominal and rectal tests showed presence of moderate epigastric tenderness and guaiac positive stool. Guaiac positive stool may be caused by bleeding in the gastrointestinal tracts while epigastric tenderness indicates a bruise in the alimentary canal. These are physical manifestation of anemia (Crowley, 2009). Nevertheless, there were some encouraging results.

The patient had a standard body temperature (37 Celsius) and normal pulse rate (95 beats per min). In addition, respiratory rate was normal (16 breaths per minute) while the blood pressure was typical at 120/72 mmHg (Springhouse, 2006). The patient’s pupils were normal and his pharynx was clear and without any postnasal drainage. More encouraging results indicated that the patient suffered no cases of thyromegaly, adenopathy, or bruits. Moreover, the client had good bilateral lung expansion and lungs were clear to auscultation. Any cases of gallops, heaves or thrills were dispelled. In addition, the patient’s abdomen was non-distended and the liver span was 8cm at the midclavicular line. His prostate was health and he seemed to have stamina.

Analysis of diagnostic data revealed that the patient was suffering from iron deficiency anemia. The patient’s hemoglobin was shown to be 8 g/dl instead of 13-18g/dl for normal men (Springhouse, 2006). This signifies erythrocytes under production and this may lead to less oxygen in circulation thus fatigue and heart complications. The patient’s Mean Corpuscular Volume was normal. However, this condition may exist even in presence of normocytic anemia (Springhouse, 2006).

Additionally, the patient’s Mean Corpuscular Hemoglobin Content was slightly declined. This is associated with conditions like microcytic anemia and it is attributed to factors like iron deficiency, chronic blood loss and thalassemia (Springhouse, 2006). Moreover, the red cell distribution width was markedly increased while the MCV was normal. This presented possible cases of early stages of iron deficiency, vitamin B deficiency, and early folate deficiency as well as initial stages of anemic condition (Cannobio, 2009).

The diagnostic results also showed mixed microcytic/hypochromic and macrocytic/normochromic red blood cells. The findings can be associated with folate and iron deficiencies (Cannobio, 2009). This condition may also be responsible for normal MCV. The appearance of platelets was normal hence their function in blood clotting was not jeopardized. Further result revealed that “Prothrombin Time (PT), Partial Thromboplastin Time (PTT)”, liver function, electrolytes, and amylase were normal (Springhouse, 2006).

Normal PPT meant that coagulation factors such as fibrinogen and prothrombin as well as heparin were up to standard amounts (Springhouse, 2006). Normal PT implied that there was good interaction of prothrombin groups V, VII, X and fibrinogen which are useful in determining amounts of oral anti-coagulants. Serum ferritin levels were decreased and this is attributed to prolonged bleeding of the digestive tract, iron deficiency or deprived iron absorption due to abnormal intestinal conditions (Springhouse, 2006).

This may ultimately lead to anemia and it explains why the patient’s stool tested guaiac positive. The patient’s transferrin saturation was decreased and this is also associated with iron deficiency. Decreased levels of total iron binding capacity implied that the patient also suffered from anemia of chronic ailments (Springhouse, 2006). Folate and cell folate levels were decreased and this shows depletion of folate storage. More so, a bone marrow biopsy showed megaloblastic changes and low iron stores giving more clues to iron deficiency anemia as well as megaloblastic anemia (Cannobio, 2009). Finally, an upper endoscopy revealed a 2cm duodenal ulcer with evidence of recent but non acute hemorrhage. This could be attributed to Helicobacter pylori infection which may cause bleeding (Springhouse, 2006). All the findings are therefore contributing to iron deficiency anemia.

Treatment of iron deficiency anemia was initiated after the assessments. The basic objectives were to correct iron deficiency, cure the ulcers, address the underlying causes and ensure that Hb levels get back to normal (Springhouse, 2006). The patient was admitted for three days.

Initially, iron supplement (ferrous sulfate) was administered orally twice a day. The first dose (60mg) was given thirty minutes before meals and this was to be continued until Hb levels get back to normal. Iron is readily absorbed in an empty stomach (Springhouse, 2006). Supplemental iron was given together with vitamin C (500mg) since it improves iron uptake in the ileum. In addition, stool softer was prescribed as iron supplements are known to cause constipation in addition to dark stool, inflammation of gastrointestinal tracts and acidity. Furthermore, anti-acids were given 4 hours after meals. However, the patient failed to tolerate oral iron and reported no improvement.

A hematologist was consulted and cancelled oral supplements and opted for intravenous injections (I.V.). The hematologist argued that I. V. injections require less dosage and they are less painful although they offer the same remedy as oral supplements (McCance et al, 2010). However, there were concerns that parenteral iron may lead to unpleasant side effects like thrombophlebitis, anaphylactoid responses and blood ailments (Crowley, 2009). Antibiotics were prescribed so as to eliminate bacterial infections thus controlling ulcers.

The patient’s reaction to these remedies was assessed by continuous hemoglobin measure and the results were encouraging. The condition was likely to get cured within two months. Further consultations were made with a nutritionist who advised the patient to continue consuming iron rich meals. Such foods include fish, meat and vegetables which promote iron absorption in the body (Crowley, 2009). The patient had no complications as a result of this treatment. The anemia resource nurse was consulted and the patient was discharged home on day three with instructions to follow with the hospital primary care clinic in one week.

Nursing care plans play a key role in the management of iron deficiency anemia. Nursing care plans for this patient were developed after interpretation of all the data collected. Conditions like exhaustion and weakness, lack of breath on exertion as well as low levels of perseverance during activity are signs of activity intolerance (Doenges, Moorhouse & Murr, 2010). Nursing diagnoses for activity intolerance has specific expected client outcomes.

As such, the levels of hemoglobin and hemocrit should get back to normal, breathing difficulties on exertion ought to be eradicated and the patient should exhibit more activity leniency as well as ADLs. This is achieved through nursing interventions aimed at energy management. Such interventions may include examining the patient’s breath rate, pulse rate and other conditions like dyspnea after activity. Scientifically, altered rates may arise if the heart and the lungs strain due to low oxygen supply (Springhouse, 2006). Over straining the heart may lead to its failure. Moreover, the nurse rested the patient in a calm surrounding and cancelled frequent visitations.

This helps to decrease body’s oxygen demand and thus the heart and lungs are not overworked (Cannobio, 2009). Furthermore, it helps the client to avoid visitors with upper respiratory diseases which can affect him through cross infection. In addition, the care provider allowed the patient to carryout light activities and ensured breaks between activities. This helps to preserve energy and also boost the client’s self confidence (Ackley & Ladwig, 2008). This care plan helped the patient to attain high levels of activity tolerance. Also, the levels of hemoglobin in the body were noted to rise slowly.

The other nursing diagnosis for this patient was malnutrition. This nursing care plan was a result of imbalanced diet and it was necessitated by conditions like exhaustion and weakness while performing minor duties (Doenges, Moorhouse & Murr, 2010). It was aimed at helping the client consume foods rich in iron so that body iron levels may normalize. To achieve this nutrition remedy, the care provider had to evaluate the client’s dietary history as it helps to establish the cause of malnutrition and possible ways of addressing it. Furthermore, the nurse had to teach both the client and relatives about the anemic condition and better ways of managing it. The rationale behind this was that the patient and home caregivers would appreciate the importance of foods which are rich in iron (Ackley & Ladwig, 2008). In addition, the nurse had to give iron supplements as required since they help to boost the amount of iron in the body.

The final nursing diagnosis involved the risk of infection. This is important as the patient had a lesion on the mouth which could lead to contamination (Doenges, Moorhouse & Murr, 2010). Furthermore, anemic individuals are prone to cross infections and they bruise easily. The expected client outcomes were improvement of body immunity and elimination of acts which may lead to infection. As such, nursing intervention included washing the client’s hands before meals to avoid contamination, covering lesions to avoid secondary infections and isolating the patient from persons with respiratory disease to avoid cross infection (Ackley & Ladwig, 2008).

The client had indicated that he was on three drugs at once and stopped taking them due to financial difficulties. Therefore, he should have been taught the importance of following treatment programs to the end. The patient could have obtained free medication from anti-anemia groups. More advice should have been given concerning insurance policies as well as their importance in health care. Furthermore, the client should have been informed about the hazards of consuming alcohol since it affects iron absorption and can also aggravate ulcers.

Iron deficiency anemia is a complex process and can be life threatening. However, with prompt treatment, it can be managed with a successful outcome for the patient. Nurses play a pivotal role in the prevention, detection, and treatment of IDA.

References

Ackley, B. J., & Ladwig, G. B. (2008). Nursing diagnosis handbook: An evidence- based guide to planning care. (8th Ed.). St Louis: Mosby Elsevier.

Cannobio, M. M. (2006). Mosby’s handbook of patient teaching. USA: Mosby Inc.

Collins, D. (2003). Algorithmic Diagnosis of Symptom. Web.

Crowley, L. V. (2009). An Introduction to Human Disease: Pathology and Pathophysiology Correlations. United Kingdom: Jones and Barrlett Publisher.

Doenges, M., Moorhouse, M., & Murr, A. (2010). Nursing Care Plans: Guidelines for Individualizing Client Car across the Life Span. Philadelphia: F. A. Davis Company.

Huch, R. & Schaefer, R. (2006).Iron deficiency and iron deficiency anemia: a pocket atlas special. Germany: Georg Thime Verlag KG.

McCance, K. L., Huether, S. E., Brashers, V., & Rote. (2010). Pathophysiology: The biologic basis for disease in adults and children. (6th Ed.). Maryland Heights, MO: Elsevier Mosby.

Springhouse. (2006). Professional Guide to Signs & Symptoms. (5th Ed.). Lippincott Williams & Wilkins.