OUR LADY OF FATIMA UNIVERSITYCOLLEGE OF NURSINGVALENZUELA CAMPUS

Anemia UnspecifiedIn Partial Fulfillment of requirements of NCM 107B RLE leading to the degree of Science in

Nursing

Presented to:

Mr. Fred Ruiz

Presented by:Bungay, Maria Paula M.

BSN 4Y 2-1 Group 1B

August 28, 2015

TABLE OF CONTENTS

I. Introduction

II. Objectives

III. Patient’s Profile

IV. Anatomy and Physiology

V. Pathophysiology

VI. Laboratory Examination Results

VII. Gordon’s Assessment

VIII. Nursing Care Plans

IX. Drug Study

X. Health Teachings

I. INTRODUCTION

The main function of a red blood cell or erythrocyte is to carry and transport oxygen to the different parts of the body. The normal RBC count is 4-6 million/mm3. Hemoglobin (Hgb), an iron-bearing protein, is found inside an erythrocyte. Molecules of this iron containing protein are responsible for transporting the bulk of oxygen that is carried in the blood.

The more hemoglobin molecules the RBC contain, a higher amount of oxygen will they be able to carry. If the hemoglobin is defective, the erythrocyte will also malfunction. A red blood cell is just a vessel; the one that performs the oxygen transportation is the hemoglobin. Normal hemoglobin is 13-18 grams/dl in males and 12-16 grams/dl in females. A decrease in the RBC or hemoglobin or the oxygen-carrying ability of a blood is termed as anemia.

Erythrocyte Formation

RBC’s are produced by the bone marrow a process known as erythropoiesis. Before a red blood cell is formed, the hematopoietic stem cell first produces an uncommitted stem cell to be formed to committed progenitor cell. Progenitor cells are not only the precursor of RBC, but also of lymphocytes and megakaryocytes (antecedent of platelets). Before an erythrocyte is formed the progenitor cells develop an erythroblast, then a reticulocyte, and finally erythrocyte (RBC). A hormone, erythropoietin, which is secreted by the kidney, also controls RBC production by stimulating the bone marrow.

Types of anemia

Hypoproliferative Anemias

This type of anemia covers all condition where the bone marrow incapable of producing enough cells to develop to erythrocyte. Lack of erythropoietin may also be a contributing factor of the abnormality. The following types of anemia are under this classification:

Aplastic anemia –In this condition, the precursor cells (stem or progenital cells, which is responsible in forming components of blood) are extremely deficient, thereby, production of all formed elements (including RBC, lymphocyte, megakaryocytes) are reduced. Because of the depressed bone marrow function, it is replaced by fat cells leading to anemia, excessive bleeding (thrombocytopenia) and infections (depressed WBC count). This type of anemia is also a common example of a pancytopenic disorder.

Iron-deficiency anemia – It is also called microcytic, hypochromic anemia. This is type of anemia is the most common form among all ages, and is characterized by a low iron concentration in the body.

Megaloblastic anemia – A macrocytic, normochromic anemia results as the essential factors (vitamin B12 and folic acid) for normal DNA synthesis are missing causing suppression of mitosis in the bone marrow and allowing the RNA or protein synthesis to take place for the progression of cell growth without cell division. The resulting cells remain enlarged (because mitosis is absent).

1. 1. Vitamin B12 deficiency – Vitamin B12 or cobalamin is required for normal DNA synthesis. It is not synthesized in the tissues of but solely depends on the dietary intake of meat, liver, dairy products and sea foods.

2. 2. Folic Acid Deficiency – folic acid is also important for the DNA synthesis of cells. The dietary sources of folate are meats, eggs, leafy vegetables which are easily available.

Hemolytic Anemias

This type of anemia refers to the state where hemolysis(erythrocyte destruction) causes symptoms of anemia. Classification of this condition is further narrowed into intrinsic (inherited) or extrinsic (damage in erythrocyte is caused by environmental factors).

Intrinsic Hemolytic Anemia

1. Sickle Cell anemia – an inherited disorder on the beta chain of the hemoglobin resulting to abnormally shaped red blood cells. In this condition an abnormal hemoglobin S (HbS) is contained in the RBC’s causing distortions or sickling of the red blood cells.

2. Thalassemia – group of genetic disorders that involve a defective hemoglobin- chain synthesis. Thalassemia majoris threatening disease characterized by severe anemia, hemolysis and ineffective erythropoiesis. Thalassemia minor is a mild form of anemia. The affected individual has only one defective gene and is asymptomatic.

Extrinsic Hemolytic Anemia

1. Immune hemolytic anemia – a person’s own antibodies destroy his own red blood cells (hemolysis).

2. Mechanical hemolytic anemia – hemolysis is caused by trauma or physical injuries that disrupt red blood cells altering and tearing them through the small vessels.

II. OBJECTIVES

Nurse – Centered

1. Describe factually, the personal and pertinent family history of the patient and relate it to the present condition.

2. Perform comprehensive physical assessment. 3. Trace the book-based and client-centered pathophysiology 4. Determine the predisposing and precipitating factors and the signs and symptoms and

relate to the disease process. 5. Enumerate and describe the diagnostic and laboratory procedures as well as the nursing

responsibilities in relation to the disease condition 6. Enumerate the different treatment modalities and their indication specifically for the

patient’s condition. 7. Identify the pharmacologic treatment provided to the patient, relate the actions of each

drug with the disease process and evaluate the patient’s response to the medications given.

8. Identify nursing diagnoses, formulate short-term goals, carry out appropriate interventions and evaluate the plan.

9. Appraise the effectiveness of medical and surgical nursing management in treating the patient.

10. List the preventive measure for the occurrence of Anemia.

Patient – Centered1. Report understanding of the disease process. 2. Understand the indications of the different diagnostic procedures and medical management involved in her care. 3. Cooperate with the necessary medical and nursing interventions. 4. Adhere with the health teachings provided. 5. Understand the different ways of health promotion and prevention in relation to the disease condition. 6. Demonstrate improved conditions as evidenced by absence of further complications.

III. PATIENT'S PROFILE

Name: MS. AC

Age: 16 years old

Nationality: Filipino

Religion: Roman Catholic

Civil Status: Single

Date Admission: August 16, 2015

Time of Admission: 10:54 PM

Ward: Pediatric Ward

Initial Diagnosis: Blood Dyscrasia probably ALL

Diagnosis: Anemia, Unspecified

HISTORY OF PAST ILLNESS

Ms. AC usually had conditions such as coughs and colds as well as fever, which they

treated, as stated by her father, by giving her BIOGESIC or other over the counter drugs. Father

stated that she already experienced serious infections such as chickenpox and measles. The last

time she was admitted to the hospital was June 15, 2015. Ms. AC has no family history of

Anemia. She has no known food and drug allergies. Ms. Ac is not fond of eating meat and

vegetables and she would often miss her mealtime. At the young age she started working as a

maid and stop going to school due to financial problem. As stated by Ms. AC her sleeping

pattern is usually at 2 A.M.

PHYSICAL ASSESSMENT

Physician’s Physical Assessment done by the Resident on Duty (August 16, 2015), lifted

from the patient's chart)

Height: 59 cm

Weight: 41 kg

Vital Signs as follows:

T: 36.6°C PR: 112 bpm RR: 42cpm BP: 110/60 mmHg SAO2: 98%

GENERAL SURVEY

Ms. AC, Assessed/received patient lying on bed, sleeping, conscious with GCS 15. With the following vital signs:

Temperature: 36.6 °C

Heart rate: 112 bpm

Respiratory rate: 20 bpm

Blood Pressure: 110/70 mmHg

SAO2: 99%

IV. ANATOM Y AND PHYSIOLOGY

The production of red blood cells is referred to as erythropoiesis. Mature red blood cells

develop from hemocytoblasts. This development takes about 7 days and involves three to four

mitotic cell divisions, so that each stem cell gives rise to 8 or 16 cells. The various cell types in

erythrocyte development are characterized by the gradual appearance of hemoglobin and

disappearance of ribonucleic acid (RNA) in the cell

the progressive degeneration of the cell's nucleus which is eventually extruded from the cell the

gradual loss of cytoplasmic organelles, for example mitochondria a gradual reduction in cell size.

The young red cell is called a reticulocyte because of a network of ribonucleic acid

(reticulum) present in its cytoplasm. As the red cell matures the reticulum disappears. Between

2 and 6% of a newborn baby's circulating red cells are reticulocytes, but this reduces to less than

2% in the healthy adult. However, the reticulocyte count increases considerably in conditions in

which rapid erythropoiesis occurs, for example following hemorrhage or acute hemolysis of red

cells. A reticulocyte normally takes about 4 days to mature into an erythrocyte. In health,

erythropoiesis is regulated so that the number of circulating erythrocytes is maintained within a

narrow range. Normally, a little less than l% of the body's total red blood cells are produced per

day and these replace an equivalent number that have reached the end of their life span.

However that still represents a huge 200,000,000,000 cells. Erythropoiesis is stimulated by

hypoxia (lack of oxygen).

However, oxygen lack does not act directly on the hemopoietic tissues but instead

stimulates the production of a hormone, erythropoietin. This hormone then stimulates

hemopoietic tissues to produce red cells. Erythropoietin is a glycoprotein. It is inactivated by the

liver and excreted in the urine. It is now established that erythropoietin is formed within the

kidney by the action of a renal erythropoietin factor erythrogenin on plasma protein,

erythropoietinogen. Erythrogenin is present in the juxtaglomerular cells of the kidneys and is

released into the blood in response to hypoxia in the renal arterial blood supply.

Various other factors can affect the rate of erythropoiesis by influencing erythropoietin

production. Thyroid hormones, thyroid-stimulating hormone, adrenal cortical steroids,

adrenocorticotrophic hormone, and human growth hormone (HGH) all promote

erythropoietin formation and so enhance red blood cell formation (erythropoiesis). In thyroid

deficiency and anterior pituitary deficiency, anemia may occur due to reduced erythropoiesis.

Polycythemia (excess red blood cell production) is often a feature of Cushing's

syndrome. However, very high doses of steroid hormones seem to inhibit erythropoiesis.

Androgens (male hormones) stimulate and estrogens (female hormones) depress the

erythropoietic response. In addition to the effects of menstrual blood loss, this effect may

explain why women tend to have a lower hemoglobin concentration and red cell count than

men. Plasma levels of erythropoietin are raised in hypoxic conditions (low oxygen levels).

This produces erythrocytosis (increase in the number of circulating erythrocytes) and

the condition is known as secondary polycythemia. A physiological secondary polycythemia is

present in the fetus (and residually in the new-born) and in people living at high altitude

because of the relatively low partial pressure of oxygen in their environment. Secondary

polycythemia occurs as a result of tissue hypoxia in diseases such as chronic bronchitis,

emphysema and congestive cardiovascular abnormalities associated with right-to-left

shunting of blood through the heart, for example Fallot's of tetralogy. Erythropoietin is also

produced by a variety of tumors of both renal and other tissues. The oxygen carrying capacity of

the blood is increased in polycythemia but so is the thickness (viscosity) of the blood. The

increased viscosity produces circulatory problems such as raised blood pressure. There is a

condition known as primary polycythemia (polycythemia rubra vera), where there are increases

in the numbers of all the blood cells, and plasma erythropoietin levels are normal. The cause of

this condition is unknown. The underlying cause of secondary polycythemia is treated with the

aim of eliminating hypoxia. Vene section (blood letting) is sometimes employed to

reduce red cell volume to normal levels. Frequently blood is removed,

centrifuged to remove cells and the plasma returned to the patient (plasmapheresis). In anemia

there is a reduction in blood hemoglobin concentration due to a

decrease in the number of circulating erythrocytes and/or in the amount of hemoglobin they co

ntain. Anemia occurs when the erythropoietic tissues cannot supply enough normal

erythrocytes to the circulation. In anemia due to abnormal red cell production, increased

destruction and when demand exceeds capacity, plasma erythropoietin levels are increased.

However, anemia can also be caused by defective production of erythropoietin as, for example,

in renal disease.

A. Definition

Anemia is a condition where red blood cells are not providing adequate oxygen to body

tissues. Red blood cells provide oxygen to body tissues. There are many types and causes of

anemia.

B. Causes

Anemia is caused by many different things at it has a lot of subtypes. However, the main

presenting factor is the lack of healthy circulating red blood cells to carry oxygen systemically.

Here is a quick overview of the different subtypes of anemia:

1. Iron Deficiency Anemia

Iron is needed for healthy production of red blood cells. Iron is a building block of healthy red

blood cells. A deficiency in iron would result in immature, microsomic, and hypochromic red

blood cells. Also, fewer RBCs will be produced by the marrow. This type of anemia is the most

common type of anemia.

2. Folic-Acid Deficiency Anemia

Folate is also known as Folic Acid. This type of anemia results from a deficiency of this B vitamin.

This particular type of anemia is particularly common among pregnant women as the developing

fetus uses up the mother’s folate stores. In folate deficiency anemia, the red blood cells are

macrosomic and are called megalocytes or megaloblasts. This is the reason why this form of

anemia is called Megaloblastic Anemia

3. Thalassemia

Thalassemia is a form of anemia that is inherited. In this type of anemia, the body makes an

abnormal form it hemoglobin, the major protein in RBCs that carry oxygen. In alpha-

thalassemia, the genes related to alpha globin are mutated or are missing. In beta thalassemia, a

gene defect also affects the production of beta globin. Thalassemia major is categorized if you

inherit the genetic defect from both parents. If only one parent however transmits the defect, it

is termed Thalassemia minor. Both conditions result to an abnormal form of hemoglobin and

leads to excessive RBC destruction leading to anemia.

4. Vitamin B12 Deficiency Anemia

This form of anemia is due to lack of sufficient cyanocobalamin or Vitamin B12. This type

of anemia results to macrocosmic, hypochromic RBCs. This is often referred to as Pernicious

anemia. The cause of this type of anemia could be a dietary deficiency, or a disease that impairs

its proper absorption such as Celiac disease or Crohn’s disease.

5. Hemolytic Anemia

Hemolytic Anemia is a type of anemia that results from excessive lysis or destruction of RBCs.

This type of anemia has a lot of causes and it also has different subtypes. The destroying factor

may be intrinsic, or extrinsic, depending on the specific cause. In this type of anemia, RBCs are

rapidly destroyed, resulting to a low number of oxygen-carrying RBCs leading to anemia. This

type of anemia does not occur though if the bone marrow is capable of producing much more

RBCs than those destroyed.

6. Aplastic Anemia

In Aplastic anemia, there is a deficiency in sufficient production of red blood cells by the bone

marrow. There are two types of this: idiopathic, or secondary. In idiopathic aplastic anemia,

there is no clear cause as to why the bone marrow is unable to produce new, mature red blood

cells. In secondary aplastic anemia, the failure results as a sequel from another disorder such as

renal disease (where there is decreased erythropoietin), chemotherapy, radiation, and others.

7. Sickle-Cell Anemia

This type of anemia is caused by a particular type of hemoglobin called hemoglobin S.

Hemogloin S changes the shape of red blood cells especially during times of low oxygen

saturation of the blood. Hemoglobin S causes cells to become shaped like sickles or crescents.

These RBCs are unable to properly carry oxygen, and they often get lodged into capillaries and

block them.

C. Symptoms

Symptoms of anemia may vary from the specific subtype, but these are some of the general

signs and symptoms:

Fatigue

Pallor

Cyanosis

Low hematocrit and RBC levels on a Complete Blood Count

Chest pain

Dizziness and Headaches

Paresthesia

Skin mottling

Shortness of Breath

Confusion and restlessness

Cold hands and feet

Tachycardia

D. Management

Management of anemia depends on the specific deficiency or the specific subtype. Nonetheless,

conventional management includes:

1. Supplementation with Iron, Folate, or Vitamin B 12

2. Use of corticosteroids in anemia’s where there is destruction of RBCs

3. Blood Transfusions

4. Erythropoietin supplementation

5. Rest

6. Treatment of the underlying condition that causes the anemia

E. Prevention

Prevention of anemia is possible. Ensuring that you eat a proper diet is one of the keys towards

prevention of this disease. Supplement your diet with foods rich in iron, folate, vitamin B12 and

vitamin C such as green leafy vegetables, dairy, eggs, organ meats, lentils, beans, meat, and

others. If there is an underlying medical condition that may cause anemia, consult your doctor

as to how to manage this condition.

V. PATHOPHYSIOLOGY

Anemia Schematic Diagram

Predisposing Factors-Sex (menstruation)-Genetics

Precipitating Factors

-Inadequate Iron intake & faulty diet-Blood Loss-Pregnancy

Decreased intake of iron rich foods, with blood loss

Iron in the body is used up

Decreased iron reserves needed for hemoglobin

production

Decreased RBC production due to lack of hemoglobin

Iron Deficiency Anemia

Decreased oxygen and hemoglobin

Pallor due to decreased hemoglobin

Weakness due to decreased overall oxygen supply

Headache due to decreased oxygen supply to the brain

If prolonged:*Chest Pain (Lack of oxygen in the heart)

*Shortness of Breath even with rest *Paresthesia (indicates nerve affectation)

*Disorientation and Confusion (if the brain is severely deprived of oxygen)

*Low RBC and Hematocrit levels

VI. LABORATORY EXAMINATION RESULTS

VII. GORDON'S ASSESSMENT

A. Health Perception and Management o Client can’t recall well if he was completely immunized.o Client was brought to the hospital for management.

B. Nutrition/ Metabolismo Fond of eating meats and fruits

C. Eliminationo Voids usually 5 times a dayo Urine color is yellowo Defecates usually every other day.

D. Activity/Exerciseo Bedrest with semi-fowlers position. o Minimal movements

E. Sexuality/Reproductiveo Singleo No history of STDS

F. Cognitive/Perceptualo Is not oriented to time due to post-op surgery.o Responds to stimuli physically.o Undergrado Not in a normal thought process due to condition and surgery.

G. Roles/Relationshipo Singleo Well-supported by the family

H. Self-Perception/ Self-Concepto Hopeful to be relieve and treatedo Manages healthy lifestyle before his condition

I. Value/Beliefo Born Again Christiano Has a strong faith in God

J. Coping/ Stresso S/P VPS in 2013o Copes up with problems

K. Sleep/Resto Difficulties in sleepingo Not enough rest intervals

L. Medication Historyo Meds for his previous hospitalization in 2013

VIII. NURSING CARE PLAN

#1

ASSESSMENT DIAGNOSIS OBJECTIVE INTERVENTION RATIONALE EVALUATION

Subjective:

♦ “Nanghihina ako,kadalasan hindi ko matapos ang mga gawain ko

(I’m feeling weak, I can’t even complete my chores

)” as verbalized by the patient.

Objective:

♦ Fatigue.

♦ Greater need for sleep and rest.

♦ Activity intolerance related to imbalance between oxygen supply (delivery) and demand.

Short term:

After 8 hours of nursing interventions the patient will:

♦ Report an increase in activity tolerance including activities of daily living.

♦ Demonstrate a decrease in physiological signs of intolerance.

♦ Display laboratory

Independent:

♦ Assess patient’s ability to perform normal task or activities of daily living.

♦ Note changes in balance/ gait disturbance, muscle weakness.

♦Recommend quiet atmosphere, bed rest if indicated.

♦Elevate the head of

♦Influences choice of interventions or needed assistance.

♦ May indicate neurological changes associated with vitamin B12 deficiency, affecting patient safety or risk of injury.

♦Enhances rest to lower body’s oxygen requirements, and reduces strain on the heart and lungs.

♦ Patient reveals an increase in activity tolerance, demonstrating a reduction in physiological signs of intolerance and laboratory values within normal range.

♦ V/S taken as follows: T: 36.9 P: 75 R: 18 BP: 100/80

values within acceptable range.

Long term:

After months of nursing interventions, the patient:

♦ Is free form weakness and risk for complications has been prevented.

the bed as tolerated.

♦Provide or recommend assistance with activities or ambulation as necessary, allowing patient to do as much as possible.

♦ Plan activity progression with patient, including activities that the patient views

♦ Enhances lung expansion to maximize oxygenation for cellular uptake.

♦ Although help may be necessary, self esteem is enhanced when patient does some things for self.

♦ Promotes gradual return to normal activity level and improved muscle tone or stamina without undue fatigue.

essential. Increase levels of activities as tolerated.

♦ Identify or implement energy saving technique like sitting while doing a task.

Collaborative:

♦ Monitor laboratory studies. Hb or Hct and RBC count, arterial blood gases (ABGs).

♦ Encourages patient to do as much as possible, while conserving limited energy and preventing fatigue.

♦ Identifies deficiencies in RBC components affecting oxygen transport and treatment needs or response to therapy.

IX. DRUG STUDY

NAME OF DRUGS, GENERIC NAME, BRAND NAME

DATE ORDERED, DATE

TAKEN/GIVEN, DATE CHANGED

ROUTE OR ADMINISTRATION

DOSAGE AND FREQUENCY OF

ADMINISTRATION

GENERAL ACTION, MECHANISM OF

ACTION

INDICATION OR PURPOSES

CLIENT’S RESPONSE TO THE

MEDICATION

Generic name: Paracetamol

Brand name:Calpol

DO: August 26, 2015

DG: July 16,-21, 2015

Dosage:• 600mg

Route:•Oral

Frequency:• q 4hrs

General Action: Analgesics Muscle Relaxants

Mechanism of Action: -Decreases fever by inhibiting the effects of pyrogens on the hypothalamus heat regulating centers & by a hypothalamic

-Action leading to sweating & vasodilatation.

Relief of mild-to-moderate pain; treatment of fever.

Client’s response to medication is effective as evidence by lowering down the patient’s temperature

NAME OF DRUGS, GENERIC NAME, BRAND NAME

DATE ORDERED, DATE

TAKEN/GIVEN, DATE CHANGED

ROUTE OR ADMINISTRATION

DOSAGE AND FREQUENCY OF

ADMINISTRATION

GENERAL ACTION, MECHANISM OF

ACTION

INDICATION OR PURPOSES

CLIENT’S RESPONSE TO THE

MEDICATION

Generic name:Furosemide

Brand name:Lasix

DO: August 26, 2015

DG: July 16,-21, 2015

Dosage:• 20mg

Route:•IV

Frequency:• mid and post BT

Furosemide inhibits absorption of sodium and chloride from the proximal and distal tubules and ascending limb of the loop of henle. Leading to a sodium rich diuresis, thus reducing edema associated to renal disease resulting to decrease BP.

Indicated for the patient as he has elevated blood pressure and edema.

The patient improves her condition as he had a decreased BP after 30 mins. of administration.

Nursing Responsibilities

Before:

Observe 10 R’s of administration of drugs ' Check doctor’s order three times and verify the patient Check the label of the drug, its name and its expiration date Wash hands before handling the medication Assess patient’s vital signs prior to administering the medication

During: Administer as indicated (right drug, right dosage, right frequency) Clean the IV insertion for medication with a cotton ball with alcohol. Gradually inject the drug into the port. Slow IV push to prevent infiltration and phlebitis. Administer cautiously and slowly with aseptic technique.

After: Observe for the sensitivity and side effects to the drug Reassess patient’s level of pain at least 15 and 30 minutes after parenteral administration Monitor circulatory and respiratory status and bladder and bowel function. Caution ambulatory patient about getting out of bed or walking.

X. HEALTH TEACHINGS

MEDICATION: Folic Acid and Prednisone

EXERCISE: Perform passive ROM exercise like flexion, extension of the extremities.

Brisk walking every morning.TREATMENT:

Blood transfusion if blood count falls below normal. Folic acid injection if available.

HEALTH TEACHING: Encourage participation in recreation and regular exercise program Provide appropriate level of environmental stimulation (e.i;music, TV/ radio, personal

possessions and visitors) Suggest use of sleep aid/ promote normal sleep/rest.

OPD: Return to OPD for further check-up when there are changes on physical strength.

DIET: High fiber diet like vegetables and fruits. Protein rich diet Folic and vitamin B12 rich foods such as: liver, dried beans, peas, wheat products,

spinach, dark leafy vegetables, meat, eggs, milkSIGNS/SYMPTOMS:

Observe for signs and symptoms such as body weakness, poor skin turgor, pallor and weight loss