KING SAUD UNIVERSITY NURSING COLLAGE MASTER DEGREE1431-1432H

Nursing management for acute disease in:

Respiratory system Endocrine system

Hematology system Immunology system

Done by : maha alonazi

OBJECTIVE At the end of the lecture the master student

well be able to : Know the most common of acute respiratory

disease . Identify nursing management for RD . Know the most common of acute endocrine

disease . Identify nursing management for ED . Know the most common of acute

hematology & immunology disease . Identify nursing management for HD & ID .

OUTLINE RESPIRATORY DISEASE : Anatomy of respiratory system . Croup. Acute epiglottitis Broncholitis . Pneumonia. Aspiration pneumonia . ARDS Asthma. ENDOCRINE DISEASE : Anatomy of endocrine system .

Diabetes Mellitus Diabetic ketoacidosis . Diabetes Insipidus. SIADH . Hyperthyroidism. Hypothyroidism. Gigantism HEMATOLOGY & IMMUNOLOGY DISEASE : Anatomy of immune & hemato system .

Anemia Sickle cell disease DIC Hemophilia Leuckemia Thalasmia

ANATOMY OF RESPIRATORY SYSTEM

Upper airway . Lower airway . Thoracic cavity .

UPPER AIRWAY Ideally above larynx is the upper airway Practically speaking Nose, Larynx (Glottic

opening and vocalcords) and trachea (Up to Carina).

The upper airway is responsible forwarming, humidifying and filtering air before it reaches the trachea.

Nose

Pharynx

Larynx

LOWER AIRWAY (LUNG) Trachea

Lung

Conducting Airways

Gas exchange units (Alveoli)

THORACIC CAVITY Diaphragm

The chest wall

SPECTRUM OF RESP. DISEASES

Upper AW - Stridor, croup, laryngomalacia

Lower AW - Asthma, bronchiolitis

Lung Parenchymal - Pneumonia, Pulmonary edema

Pleural - Empyema, Pneumothorax

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WHEN WILL YOU SUSPECT UAW DIS?.

Stridor Neck retraction Suprasternal

retraction Sniffing position

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ACUTE LARYNGOTRACHEOBRONCHITIS (CROUP)

Definition : inflammatory swelling of the submucosa in the subglottic area & trachea ,bronchi ,bronchioles

Commonest cause of acute stridor usually occure for child from age 3 month to 5 yrs .

causes : Viruses: Parainfluenza. RSV . Sing & symptoms: barking cough. Hoarseness. stridor. Low fever. 14

( CROUP )MANAGEMENT

Mild: Stridor at rest, cough - Minimal handling

Moderate to severe: Stridor at rest. - Racemic epinephrine nebulization Dexamethazone IV or IM, also oral or Nebulized Budesonide

Severe: Impending respiratory failure Intubation for 2-3 days. Improves in a week.

Majority may not need intubation

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X-ray Neck in

croup

Sharpened pencil

appearance

NURSING MANAGEMENT

provide medication as order . Provide cool & humidified oxygen as needed Check vital sign . Monitor pulse oximetry. Minimal handling. Provide quit environment . Enteral feeding may be considered in pt. with

respiratory distress .

Definition :Is severe life threatening rapidly progressive infection of the epiglottis &aryepiglottic folds & surrounding tissue .

Usually occurs in children aged 2-6 yrs but can occurs any any age.

Caused: before the use of the HiB vaccine ( haemophilus influanzae type B) was the

moust commonly identified cause of acute epiglotittis ,the usual cause in the vaccinated child is now streptococcus pyogenes, S.pneumoniae ,or staphylococcus aureus .

Acute epiglottitis

Sing & symptom : Sudden onset of high fever. dysphagia. drooling,. muffled voice. soft stridor. inspiratory retractions.

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Normal Lateral neck

ACUTE EPIGLOTTITIS - MANAGEMENT

Intubation by a skilled person IV Ceftriaxone O2 and other supportive management Usually extubatable in 3-4 days Antibiotics for 10 days.

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NURSING MANAGEMENT

Close monitoring . Arm restraint to prevent self extubation . Decreased movement of the ETT in the

larynx . Deliver oxygen as necessary .

CROUP EPIGLOTTITIS

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Age: Younger infants No fever Harsh stridor

Parainfuenza virus Usually no

antibiotics, no intubation

Age: older children High fever, toxic Soft stridor,

Drooling, muffled H

influenza(Bacteria) Needs antibiotics

and intubation

DO AND DON’T IN UAW DIS.

Allow the patient in his position of comfort Do not separate the child from mother Do not force the child to lie down Do not make the child cry? Do not send the child for X-ray without

accompanied by medical team Continuously monitor for the need for

intubation.

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BRONCHOLITIS

Definition : acute inflammatory disease of the lower tract that result in obstruction of small airways .

Causeas : viral infection . Sing & symptom : Cough. Wheezing . Prolong expiration. Irritability . Low grade fever . Tachypnea . Retraction .

NURSING MANAGEMENT

Maintained fluid & nutritional requirement Monitor child closely for respiratory failure. provide medication as order . Provide oxygen as needed or M.V if

respiratory failure ,hypoxemia or apnea are developed .

Check vital sign . Monitor pulse oximetry Prevent nosocomial infection by good HW.

PNEUMONIA Pneumonia is infection of the lung caused most often by

bacteria or viruses . Mode of transmission: 1-Inspiration.

2-Aspiration.

3-Circulation. Bypass of nasal defense Pulmonary aspiration )CNS, GER, TEF( Abnormal secretions or mucociliary clearance Underling chronic disease/nutrition Defect in the immune system

Sign & symptom : Chills, fever and cough Stuffy nose Irritability Resp distress: expiratory grunting, nasoflaring,

retraction, tachypnea, tachycardia. Cyanosis, air hunger, and occasionally apnea

NURSING MANAGEMENT

Monitor V\S ,ABG level ,oxygen saturation . Administered nebulization & oxygen at

concentration as prescribed . Placed in high fowler position . Rendered chest physiotherapy . Encourage pt. to deep breathing & cough . Encourage pt. to increased fluid intake to

liquefy secretion . Assess lung sound . Administered antibiotic as ordered . Avoid contact with people with URTI .

ASPIRATION PNEUMONIA Definition :inflammation caused by pulmonary

aspiration of gastric fluid produced direct injury to the mucosal surface of the respiratory tract .

Causes :see table Sing & symptom : Cough ,fever . acute dyspnea. wheezing , crackles or absent breathing sound in

the effected lobes , cyanosis, retraction , tachypnea .

CAUSES OF ASPIRATION PNEUMONIA

Altered level of consciousnessDrugs, alcohol, anesthesia, seizures, CNS disorders

Altered anatomy or function of trachea or esophagus

Traceal or esophageal abnormalities, ETT, tracheostomy

Altered function of swallow or esophageal motility

Loss of normal reflexes which prevent aspiration of stomach contents, GER )worse with neuro or anatomical impairment(

Inhalation injuryInhalation of toxic substances

NURSING MANAGEMENT

Monitor V\S ,ABG level ,oxygen saturation . Administered nebulization & oxygen at

concentration as prescribed . Placed in high fowler position . Rendered chest physiotherapy . Encourage pt. to deep breathing & cough . Encourage pt. to increased fluid intake to

liquefy secretion . Assess lung sound . Administered antibiotic as ordered .

ARDS

Definition :acute lung injury & noncardiogenic pulmonary edema .

Causes : Gastric aspiration. Toxic inhalation . Pulmonary infection . FBA .

Sing & symptom : Stage 1 :(1-2 day) : mild tachypnea,

hypoxemia,anxiety or restlessness. Stage2 :(2-3 day) :cyanosis in room

air ,tachycardia,retraction . Stage 3:(3-10 day ):symptom change from

distress to failure (inability to oxygenate & ventilate,alveolar collapse desaturation ,high oxygen requirement .

Stage 4 : (after 10 day ):development of pulmonary fibrosis & progressive impairment of oxygenation are observed .

NURSING MANAGEMENT Encourage coughing & deep breathing in awake pt. Frequent position change with CPT as needed . Reduce abdominal distention by NGT if necessary . Check vital sign . Monitor pulse oximetry . Do VBG & ABG analysis . Provide supplemental oxygen for pt. with adequate

ventilation . Provide medication such as

sedative ,analgesic ,neuromuscular blocking agents ,bronchodilator as ordered .

Provide high calories & high protein diet.

ASTHMA (CHRONIC DISEASE )

Definition :obstructive pulmonary disease characterized by airway inflammation with mucosal edema,thick secretion that cause plugging & hyperreactivity of the tracheobronchial tree that result in bronchospasm of the smooth muscle .

Causes :inflamatory mediators are thought to stimulate the vagus nerve ( cholinergic stimulation )causing smooth muscle constriction & increased production of mucus.

Sing & symptom:Tachycardia.Tachypnea.Cynosis.Expiratory wheezing in severe case. Inspiratory & expiratory wheezing .Hypoxemia .

NURSING MANAGEMENT

Monitor pattern of breathing & V\S at regular interval .

Assess S & S of respiratory distress . Administer oxygen & nebulization as

indicated . Assess lung sound . Monitor pulse oximetry & ABG level as

indicated . Encourage rest in between activity to prevent

fatigue & encourage deep breathing .

1- Endocrine glands : secrete hormones directly into the bloodstream ( adrenal , pancreas ,thyroid glands)

2-Exocrine glands :secrete biochemical substances that are released into ducts to be delivered to target organs ( salivary ,sweat glands )

Major glands : 1-Hypothalamus-pituitary complex .

(ACTH,TSH,ADH,Oxytocin ) 2-Thyroid gland.(T3,T4) 3-Parathyroid gland.(PTH) 4-Adrenal gland.(sex hor.

Cortisol,epinephrine,norepinephrine)

5-Islets of langerhans in the pancreas.insullin-beta cell, glucagon-alpha cell, somatostatin-delta cells

6-Gonads.estrogen,progesterone,testosterone .

FIG 1. PITUITARY HORMONES AND THEIR TARGET ORGANS.

DIABETES MELLITUS

Definitions

Type I: Insulin-dependent mellitus (IDDM) It is autoimmune disease that result in the T-cell-

mediated destruction of the beta pancreatic cells .it is the most common form of diabetes in infants & children & requires insulin replacement therapy .

Type II: Non-insulin-dependent diabetes mellitus (NIDDM) Is associated with obesity ,strong family history & older

age .it is not autoimmune process but instead due to insulin resistance enough insulin is produced to prevent ketoacidosis. it can treated by oral hypoglycemia agents , diet.exercise .

DIABETES MELLITUS

Diabetic ketoacidosisIs the absence of insulin & cellular

uptake of glucose is inhibited & glucose production by the liver is increased & glucose utilization decreased resulting in hyperglycemia .

Etiology :is related to inadequate endogenous

insulin secretion . Acute stress, infection ,trauma , high dose of steroide .

TABLE 1. SIGNS AND SYMPTOMS

SymptomsSymptoms

HyperglycemiaHyperglycemia

Metabolic acidosis (gap acidosis)Metabolic acidosis (gap acidosis)

Dehydration, shockDehydration, shock

Kussmaul breathingKussmaul breathing

Cardiac arrhythmiaCardiac arrhythmia

Sodium imbalanceSodium imbalance

Potassium imbalancePotassium imbalance

Mental status changesMental status changes

HyperosmolalityHyperosmolality

KetonuriaKetonuria

GlucosuriaGlucosuria

Management

FluidElectrolytesInsulinMonitoring

NURSING MANAGEMENT

Monitor V\S & blood sugar level . Provide 3 regular diabetic meals with in

between snacks as tolerated . Check weight daily \weekly as indicated . Observed for circulation on feet . Monitor intake & output . Check urine for protein & ketones . Monitor S\S of hypo & hyperglycemia . Administered insulin regimen as prescribed .

TABLE 3. CLINICAL OBSERVATION IN DEHYDRATION

Older Child:Older Child:

3% (30mL/kg)3% (30mL/kg)6% (60mL/kg)6% (60mL/kg)9% (90mL/kg)9% (90mL/kg)

ExaminationExaminationInfantInfant

5% (50mL/kg)5% (50mL/kg)10% (10mL/kg)10% (10mL/kg)15% 15% (150mL/kg)(150mL/kg)

DehydrationDehydration

Skin turgorSkin turgor

Skin (touch)Skin (touch)

Buccal Buccal mucosa/lipsmucosa/lips

Eyes Eyes

TearsTears

FontanelleFontanelle

CNSCNS

Pulse ratePulse rate

Pulse qualityPulse quality

Capillary refillCapillary refill

Urine outputUrine output

MildMild

NormalNormal

NormalNormal

MoistMoist

NormalNormal

PresentPresent

FlatFlat

ConsolableConsolable

NormalNormal

Normal Normal

NormalNormal

Normal Normal

ModerateModerate

TentingTenting

DryDry

DryDry

Deep setDeep set

ReducedReduced

SoftSoft

IrritableIrritable

Slightly Slightly increasedincreased

WeakWeak

=2 sec=2 sec

DecreasedDecreased

SevereSevere

NoneNone

ClammyClammy

Parched/Parched/crackedcracked

SunkenSunken

NoneNone

SunkenSunken

Lethargic/Lethargic/obtundedobtunded

IncreasedIncreased

Feeble/Feeble/impalpableimpalpable

>3 sec>3 sec

AnuricAnuric

TABLE 4. INSULIN PREPARATION

InsulinInsulinOnset (hr)Onset (hr)Peak (hr)Peak (hr)Duration Duration (hr)(hr)

Rapid actingRapid acting

NovoLogNovoLog

HumalogHumalog

0.17-0.330.17-0.33

0.25-0.50.25-0.51-31-3

0.5-1.50.5-1.53-53-5

6-86-8

Short actingShort acting

RegularRegular0.5-10.5-11-51-53-103-10

Intermediate Intermediate actingacting

NPHNPH

LenteLente

1-41-4

1-41-44-144-14

4-144-1410-2410-24

12-24+12-24+

Long actingLong acting

UltralenteUltralente4-104-108-308-3018-3618-36

BasalBasal

LantusLantus55No pronounced No pronounced peakpeak20-24+20-24+

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

Characterized by inappropriate, excessive secretion of ADH

Occurs in the face of low serum Na and low serum osmolality

Clinical signs and symptoms are secondary to increased blood volume and hyponatremia.

PATHOPHYSIOLOGY OF SIADH

ETIOLOGY AND RISK FACTORS

Conditions associated with SIADH

Meningitis, Head trauma, Cerebral tumors, Cerebral hemorrhage, Chornically ill or malnourished, Spinal surgery

SIGNS AND SYMPTOMS

Low urine output and the absence of hypovolemia

Headache, confusion, lethargy, altered LOC, coma or seizures

Nausea and vomitingWeight gainFilling pressures (normal or increase)

Hypertension and tachycardia

MANAGEMENT

Serum sodium: normalized over 24 to 48 hours

Monitoring: intake & output , specific gravity, serum electrolytes and osmolality, & daily weights.

NURSING MANAGEMENT

Monitor intake & output Monitor specific gravity. Monitor serum electrolytes and

osmolality daily weights.

DIABETES INSIPIDUS Characterized by a decrease in both urine

concentrating ability and water conservation. Types of DI

CentralCommon form in children and critical care environment, deficiency of ADH due to failure of the hypothalamus to synthesize or failure of the posterior pituitary to secrete or both .

Nephrogenic Characterized by normal secretion of ADH by the posterior pituitary but the distal tubule & collecting ducts in the kidney are resistant to the effects of ADH .

DIABETES INSIPIDUS Etiologyy :

Central Pituitary and head trauma, CNS infections, cerebral edema, cerebral hemorrhage or infarct, congenital, familial, idiopathic

NephrogenicChronic renal disease, polycystic kidney disease, pregnancy, starvation

SIGNS AND SYMPTOMS

Large quantity of dilute urineHypernatremiaSerum hyperosmolalityPolyuriaUrine osmolalityPolydipsiaSigns of dehydrationAltered mental status

DIABETES INSIPIDUS Management

Central Use fluid or ADH replacement therapy

Nephrogenic Difficult to treat, Sodium-restricted diet

NURSING MANAGEMENT

Monitor intake and output.Daily weights.Frequent hemodynamic.Neurologic assessments.Assess signs of dehydration.Assess urine & electrolytes result .Monitor specific gravity.

DIFFERENTIATION BETWEEN DI AND SIADH

DISIADH

Serum sodium>145 mEq/L<135 mEq/L

Urine sodiumLow High

Serum osmolality>300 mOsm/kg<275 mOsm/kg

Urine osmolality<300 mOsm/L>800mOsm/L

Urine specific gravity

<1.005>1.020

Urine outputHighLow

THYROID GLAND

It is the largest endocrine gland. It lies in front of the neck; it is formed two lobes connected by an isthmus which crosses the trachea.

 

THYROID GLAND

The thyroid gland secretes the following hormones:

1-Thyroxine (tetraiodothyronine = T4) and (triiodothyronine, = T3) both hormones are iodine containing amino acid.

2-Calcitonin: it is a calcium lowering hormone, polyeptide in nature, secreted from parafollicular cells of thyroid gland. It lowers the plasma calcium level.

Actions of T4 and T3:  Increase oxygen consumption and enhances

the metabolism of all the body tissues. Increase protein synthesis in the kidney,

muscle and liver. They stimulate growth. They increase activity of most of enzymes in the cells.

Increase the rate of glucose absorption, uptake, and utilization by tissues.

Increase the metabolism of fat from its stores and use its fat for production of energy and it decreases the level of plasma cholesterol.

Accelerates the heart rate and it is an erythropoietic factor.

It increases appetite, the motility and secretions of gastro – intestinal tract.

Are important for normal development and maturation of Central Nervous System.

HYPERTHYROIDISM

Hyperthyroidism(Grave’s disease): Overactivity of the Thyroid Gland, In healthy people, the thyroid makes just the right amounts of two hormones, T4 and T3.

Hyperthyroidism is a condition caused by the effects of too much thyroid hormone on tissues of the body.

CAUSES

There are several causes of hyperthyroidism. Most often, the entire gland is overproducing thyroid hormone. This is called Graves' disease.

Less commonly, a single nodule is responsible for the excess hormone secretion. We call this a "hot" nodule. 

Thyroiditis (inflammation of the thyroid) can also cause hyperthyroidism.

SYMPTOMS AND SIGNS Palpitations Heat intolerance Nervousness Insomnia Breathlessness Increased bowel movements Light or absent menstrual periods Fatigue Fast heart rate Trembling hands Weight loss Muscle weakness Warm moist skin Hair loss Enlargement of the thyroid gland (goiter). Protrusion of the eye balls due to excessive growth and

degeneration of tissues behind the eye.

TREATMENT

Anti-thyroid Drugs Radioactive Iodine Treatment Surgical Removal of the Gland or Nodule

NURSING MANAGEMENT

Monitor V\S . Assess skin turgor & mucous

membrane for signs of fluid deficit . Monitor intake & output . Monitor weight daily . Provide high calorie food . Provide quiet ,calm ,cool environment Inspected skin frequently

HYPOTHYROIDISM condition leading to the deficiency in the

production of thyroid hormone. Iodine deficiency is the most common cause

of hypothyroidism worldwide but it can be caused by any number of other causes such as several conditions of the the thyroid gland, or less commonly, the pituitary gland or hypothalamus.

Before Puberty (cretinism): Mal development or complete absence of gland in

a new born gives the signs and symptoms of cretinism at the age of about 6 months when the mother’s milk becomes deficient in thyroxin, it is characterized by:

Mental retardation due to defective of nerve fibers, which lead to delayed mile stones as (sitting walking and speech).

Retarded growth, the height is less than one meter. Intolerance to cold weather and decrease BMR. Abdominal muscle weakness, with protruded

viscera and protruded enlarged tongue. Infantile sexual organs. Thick skin. Raised serum cholesterol level.

After Puberty Myxoedema:

This due to atrophy of the thyroid glands or due to thyroidectomy for any reason. It is characterized by:Slow mental activity. Increase sensitivity to cold, the BMR decreased

(30 to 40).The hair is coarse and sparse, dry skin, firm non

pitting oedema.Sexual hypo function in female, there is

irregular cycle, in male there is impotence.Loss of appetite and decrease motility of the

gastrointestinal tract which leads to constipation.

Deficient erythropoiesis leading to anaemia.

SING & SYMPTOM Fatigue. Cold intolerance increased sensitivity to cold Constipation Depression. muscle cramps and joint pain Thin, brittle fingernails Coarse hair Decreased sweating Dry, itchy skin Weight gain and water retention Bradycardia. Thinning of the outer third of the eyebrows (sign

of Hertoghe). Abnormal menstrual cycles.

CAUSES Iodine deficiency is the most common cause

of hypothyroidism worldwideor a deficiency in stimulating hormones from the hypothalamus or pituitary.

Congenital hypothyroidism is very rare accounting for approximately 0.2‰

Hypothyroidism can result from postpartum thyroiditis, a condition that affects about 5% of all women within a year of giving birth.

Hypothyroidism can also result from sporadic inheritance, sometimes autosomal recessive.

CLASSIFICATION

Primary: Thyroid gland: The most common forms include Hashimoto's thyroiditis (an autoimmune disease) and radioiodine therapy for hyperthyroidism.

Secondary: Pituitary gland: Occurs if the pituitary gland does not create enough thyroid-stimulating hormone (TSH) to induce the thyroid gland to produce enough thyroxine and triiodothyronine. Although not every case of secondary hypothyroidism has a clear-cut cause, it is usually caused by damage to the pituitary gland, as by a tumor, radiation, or surgery.[Secondary hypothyroidism accounts for less than 5% or 10% of hypothyroidism cases.

Tertiary: Hypothalamus: Results when the hypothalamus fails to produce sufficient thyrotropin-releasing hormone (TRH). TRH prompts the pituitary gland to produce thyroid-stimulating hormone (TSH). Hence may also be termed hypothalamic-pituitary-axis hypothyroidism. It accounts for less than 5% of hypothyroidism cases.

TREATMENT

Hypothyroidism is treated with the levorotatory forms of thyroxine (levothyroxine) (L-T4) and triiodothyronine (liothyronine) (L-T3).

NURSING MANAGEMENT

Monitor vital signs . Monitor ECG tracing to detect

arrhythmias . Provide warm environment. Provide high fiber diet . Administered prescribed stool softener . Administered medication as prescribed . Encourage increase intake of fluids . Provided warm drink .

GROWTH HORMONE (SOMATOTROPIN)

HGH is synthesized and secreted from the anterior pituitary gland Effects of growth hormone on the tissues of the body can generally be described as anabolic (building up).

In addition to increasing height in children and adolescents, growth hormone has many other effects on the body:

Increases calcium retention, and strengthens and increases the mineralization of bone

Increases muscle mass through sarcomere hyperplasia

Promotes lipolysis

Increases protein synthesis Stimulates the growth of all internal organs

excluding the brain Plays a role in homeostasis Reduces liver uptake of glucose Promotes gluconeogenesis in the liver Contributes to the maintenance and function

of pancreatic islets Stimulates the immune system

High levels of growth hormone may indicate:

Acromegaly Gigantism Growth hormone resistance Pituitary tumor. Low levels of growth hormone may

indicate: Growth hormone deficiency. Hypopituitarism.

EXCESSIVE GROWTH HORMONE SECRETION

Gigantism is the result of excessive growth hormone secretion that begins in young children or adolescents. It is a very rare disorder, usually resulting from a tumor of somatotropes. One of the most famous giants was a man named Robert Wadlow. He weighed 8.5 pounds at birth, but by 5 years of age was 105 pounds and 5 feet 4 inches tall. Robert reached an adult weight of 490 pounds and 8 feet 11 inches in height. He died at age 22.

Acromegaly results from excessive secretion of growth hormone in adults.

GROWTH HORMONE DEFICIENCY

The effects of growth hormone deficiency vary depending on the age at which they occur. In children, growth failure and short stature are the major manifestations of GH deficiency, with common causes including genetic conditions and congenital malformations. It can also cause delayed sexual maturity.

Dwarfism: It is deficiency of growth hormone in young

age. The rate of development is decreased so the child who has reached the age of 10 years has the body of 4 years. The dwarf is short and mentally normal.

 

TREATMENT

For excessive secration : drugs like octreotide (somatostatin agonist) and bromocriptine (dopamine agonist) can be used to block GH secretion because both somatostatin and dopamine negatively inhibit GHRH-mediated GH release from the anterior pituitary.

For deficiency: injection of GH.

NURSING MANAGEMENT

provide medication as order . Measure weight & height . Check weight daily \weekly as indicated . Assess GH level . Educate pt. & family about the important of

follow up .

ADRENAL GLAND DYSFUNCTION

Hypo function of adrenal cortex: (Addison disease): It is due to adrenal cortical

insufficiency. It is characterized by:Loss of appetite, vomiting, and diarrhea

i.e. gastro intestinal disturbances.Muscle weakness due to decrease of

anabolic effect of androgens.

Decrease sodium and increase potassium in the blood. (Water moves intracellular, ----- the blood volume decreases and hypotension occur.

Hypoglycemia.Decrease sexual function.The Bronze hyper pigmentation of the skin

due to high level of ACTH secondary to low level of glucocorticoids. ACTH has melanocytic stimulating activity.

CUSHING'S SYNDROME

Cushing's syndrome is a hormone disorder caused by high levels of cortisol in the blood.

This pathology was described by Harvey Cushing in 1932.[The syndrome is also called Itsenko-Cushing syndrome, hyperadrenocorticism or hypercorticism)

Hyper function of Adrenal Cortex (Cushing's Syndrome):  It is characterized by:

Wasting and weakness of muscle, (catabolic effect).

Increase sodium and water retention in the blood (leading to oedema and hypertension with decrease level of plasma potassium).

Redistribution of fat, the extremities are thin, there are accumulation of fat in the abdominal wall, face (MOON) and the upper back (buffalo trunk).

Hyperglycemia.Gonadal disturbances.

The skin is thin.

the hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to release adrenocorticotropin (ACTH). ACTH travels via the blood to the adrenal gland, where it stimulates the release of cortisol. Cortisol is secreted by the cortex of the adrenal gland from a region called the zona fasciculata in response to ACTH. Elevated levels of cortisol exert negative feedback on the pituitary, which decreases the amount of ACTH released from the pituitary gland. Strictly, Cushing's syndrome refers to excess cortisol of any etiology.

One of the causes of Cushing's syndrome is a cortisol secreting adenoma in the cortex of the adrenal gland. The adenoma causes cortisol levels in the blood to be very high, and negative feedback on the pituitary from the high cortisol levels causes ACTH levels to be very low. Cushing's disease refers only to hypercortisolism secondary to excess production of ACTH from a corticotrophic pituitary adenoma. This causes the blood ACTH levels to be elevated along with cortisol from the adrenal gland. The ACTH levels remain high because a tumor causes the pituitary to be unresponsive to negative feedback from high cortisol levels.

Cushing's Syndrome was also the first autoimmune disease identified in humans.

CAUSES:

Exogenous vs. endogenous Hormones that come from outside the body

are called exogenous. hormones that come from within the body

are called endogenous.

The most common cause of Cushing's

syndrome is exogenous administration of glucocorticoids prescribed by a health care practitioner to treat other diseases (called iatrogenic Cushing's syndrome). This can be an effect of steroid treatment of a variety of disorders such as asthma and rheumatoid arthritis, or in immunosuppression after an organ transplant.

Administration of synthetic ACTH is also possible, but ACTH is less often prescribed due to cost and lesser utility.

Endogenous Cushing's syndrome results from some derangement of the body's own system of secreting cortisol. Normally, ACTH is released from the pituitary gland when necessary to stimulate the release of cortisol from the adrenal glands.

In pituitary Cushing's, a benign pituitary adenoma secretes ACTH. This is also known as Cushing's disease and is responsible for 70% of endogenous Cushing's syndrome.

In adrenal Cushing's, excess cortisol is produced by adrenal gland tumors, hyperplastic adrenal glands, or adrenal glands with nodular adrenal hyperplasia.

Finally, tumors outside the normal pituitary-adrenal system can produce ACTH that affects the adrenal glands. This final etiology is called ectopic or paraneoplastic Cushing's syndrome and is seen in diseases like small cell lung cancer .

SING & SYMPTOM

rapid weight gain particularly of the trunk and face "moon face “ with sparing of the limbs (central obesity ).

A common sign is the growth of fat pads along the collar bone and on the back of the neck (buffalo hump) .

Other symptoms include hyperhidrosis (excess sweating),.

Telangiectasia (dilation of capillaries).

Thinning of the skin (which causes easy bruising and dryness particularly the hands and other mucous membranes, purple or red striae (the weight gain in Cushing's syndrome stretches the skin, which is thin and weakened, causing it to hemorrhage) on the trunk, buttocks, arms, legs or breasts, proximal muscle weakness (hips, shoulders).

Hirsutism (facial male-pattern hair growth). Baldness and/or cause hair to become

extremely dry and brittle.

In rare cases, Cushing's can cause hypercalcemia which can lead to skin necrosis (osteoporosis ). The excess cortisol may also affect other endocrine systems and cause, for example, diabetes mellitus

menstrual disorders such as amenorrhea in women and decreased fertility in men infertility due to elevations in androgens.

signs include polyuria (and accompanying

polydipsia), persistent hypertension (due to cortisol's enhancement of epinephrine's vasoconstrictive effect) and insulin resistance (especially common in ACTH production), leading to hyperglycemia (high blood sugar) and insulin resistance which can lead to diabetes mellitus.

Patients frequently suffer various psychological disturbances, for example, euphoria , depression and anxiety.

Haematology and

Immunology

Haematology and

Immunology

Cell differentiation from stem cells

Anatomy and Physiology

1- Red blood cells (RBCs, erythrocytes): Develop from erythroid precursor cells

Reticulocytes represent the stage of maturation

Mature RBCs have a life span of 120 days

Hemoglobin: large, complex, iron-containing protein. Responsible for the RBCs oxygen-carrying abilities.

RBC: transport oxygen from the lungs to the tissues

Hgb A, normal adult hemoglobinHemoglobin F ( fetal Hgb) present in large concentrations in the fetus, decrease after birth and minimally present in children and adults.

Normal RBC production requires iron, folic acid and Vit B12.

THE IMMUNE SYSTEM

2-Leukocytes (white blood cells) group that serve to protect the organism. Neutrophils: the largest component of total

circulating WBCs, 60 – 70%.Originate and mature in bone marrowPolymorphonucleated (PMNs or poly): mature form

of neutrophilBand: unsegmented – appearing nucleusNeutrophilia: increased number of circulating

neutrophils

Anatomy

Neutropenia: decreased number of circulating neutrophils (<1500/mm3)

WBCs mature in bone marrow for 10 days

Eosinophils: 2 – 5% of the circulating WBC. Eosinophilia: increased number of eosinophilsEosinopenia: decreased number of eosinophils

Basophils: smallest portion of granulocytes, 1% of WBCBasophilia increased number of circulating basophilsBasopenia decreased number of circulating basophils

Mononuclear phagocytes Monocytes 3 – 8% of circulating WBCs

Monocytosis increase in the number of circulating monocytes

Monocytopenia decrease in the number of circulating monocytes

Macrophages: have long life span.

Lymphocytes (lymphoid lineage): primary immune cells Lymphocytes: 10 – 40% of the ciculating WBCs

Lymphocytosis: increase number of circulating lymphocytes

Lymphopenia: decrease in number of circulating lymphocytes

T lymphocytes or T cells: 65 – 85% of all lymphocytes Clusters of differentiation (CD) Helper T cells (CD4) Suppressor T cells (CD8) Cytotoxic or killer T cells (CD8)

Lymph nodes of the body

Anatomy B Lymphocytes or B cells: constitute up to 35%

NK cells constitute 5 – 8% of the total lymphocyte count

Memory cells – have CD. Programmed to recognize the original invading microorganism on subsequent invasions.

WBCFunctions

Defense: protect the body’s internal environment from “nonself” antigens or microorganisms invasion.

Assists the immune system in discriminating “self” from “nonself” or “altered self”

Second line of defense: involves the inflammatory response, phagocytosis .

3-Platelets (thrombocytes)1. Megakaryoblasts: mature into megakaryocytes2. Characteristics: minute, round or oval discs.

Platelet count: 150, 000 to 400, 000/mm3.

Maintain normal hemostasis & vascular integrity when a blood vessel wall is injured.

Anatomy

4-Plasma factors:1. Procoagulants: aka plasma clotting factors. Promotes

coagulation.

2. Anticoagulants: inhibit coagulation Circulating anticoagulants: antithrombin III, protein C,

protein S

3. Coagulation: depends on the balance between the procoagulants and the anticoagulants

Nomenclature for coagulation factors

FactorSynonym

IFibrinogen

IIProthrombin

IIITissue thromboplastin

IVCalcium

VProaccelerin

VINot assigned

VIIProconvertin

VIIIAntihemophilic factor )AHF|(

IXPlasma thromboplastin component )Christmas factor

XStuart factor )Stuart-Prower factor(

XIPlasma thromboplastin antecedent )PTA(

XIIHageman factor

XIIIFibrin-stabilizing factor )FSF(

ANEMIA

Anemia is defined as a reduction below normal in the volume of red blood cells volume or hemoglobin concentration.

 Classification of Anemias

Anemias can be classified by two approaches:

Etiologic factors. Morphologic factors.

I. Etiologic Factors: Anemias resulting from impaired or

decreased production: The production of the RBCs and Hb can

be impaired by:Nutritional deficiency (e.g.folate, iron, B12).

Bone marrow failure (e.g. irradiation, malignancy).

Interference with bone marrow activity (e.g. infection, chronic diseases).

Anemias resulting from accelerated destruction of RBCs (Hemolytic):

There are causes that can shorten the life span of the cell, which can be:

Corpuscular Causes: Defect in cell membrane: Hereditary erythrocytosis. Defect in cell enzyme: G6PD deficiency. Defect in cell hemoglobin: Sickle cell anemia, Thalassemia.

Extracorpuscular causes: Immune: blood transfusion. Non- immune: - burns. - Snake venoms. Anemias resulting from excessive blood loss: Acute blood loss: (bleeding) Alteration in vital signs doesn’t occur unless 20% or more of blood

lost occur. Shock occurs with losses of 40% of blood volume. Chronic blood loss: (occult bleeding, Ancylostoma)

II. Morphologic Factors: The characteristic changes in RBCs’ size,

shape, color is described as below: Cell size: for example, normocytes (normal),

microcytes (smaller than normal), or macrocytes (larger than normal).

Shape- irregularly shape RBCs; for example, poikilocytes (irregularly shaped cell), spherocytes (globular cells), and drepanocytes (sickle cells).

Staining characteristics or color: Reflects the hemoglobin concentration; for example, normochromic (Sufficient or normal amount) or hypochromic (reduced amount).

SING & SYMPTOM General Manifestation: Dyspnea on exersion. Muscle weakness. Easy fatigability.

Frequent resting.Shortness of breath.Poor sucking (infants).

Pale skin: waxy pallor seen in severe anemia. Tachycardia. Cardiac dilatation gradually develops.

Central nervous system manifestations: Headache. Dizziness. Night headache. Irritability. Slowed thought processes. Decreased attention span. Apathy. Depression.

Shock [blood loss anemia]: Poor peripheral perfusion. Skin is moist and cool. Low blood pressure. Increased heart rate.

Anemias Caused by Defect in Hemoglobin Formation

Sickle cell anemia (SCA). Thalassemia.

SICKLE CELL ANEMIA

This disorder is characterized by severe chronic hemolytic disease resulting from premature destruction of the brittle poorly deformable erythrocytes. In which normal adult hemoglobin A (Hgb A) is partly or completely replaced by abnormal sickle hemoglobin (Hgb S).

It is a genetically determined (autosomal reccesive) disease.

SICKLE CELL ANEMIA sickle cell anemia, the number of red blood

cells is low because sickle cells don't last very long. Sickle cells usually die after only about 10 to 20 days. The bone marrow can't make new red blood cells fast enough to replace the dying ones.

Normal red blood cells are disc-shaped and look like doughnuts without holes in the center. They move easily through your blood vessels. Red blood cells contain an iron-rich protein called hemoglobin. This protein carries oxygen from the lungs to the rest of the body.

Sickle cells contain abnormal hemoglobin called sickle hemoglobin or hemoglobin S. Sickle hemoglobin causes the cells to develop a sickle, or crescent shape.

Sickle cells are stiff and sticky. They tend to block blood flow in the blood vessels of the limbs and organs. Blocked blood flow can cause pain, serious infections, and organ damage.

CAUSES:

Sickle cell anemia is inherited from both parents. Sickle cell disease is much more common in people of African and Mediterranean descent. It is also seen in people from South and Central America, the Caribbean, and the Middle East.

Someone who inherits the hemoglobin S gene from one parent and normal hemoglobin (A) from the other parent will have sickle cell trait. People with sickle cell trait do not have the symptoms of true sickle cell anemia.

SING & SYMPTOM: Severe sudden chest pain . Splenomegaly in the young children . Impaied growth & development . Attacks of abdominal pain. Bone pain. Breathlessness. Delayed puberty. Fatigue. Fever. Paleness. Rapid heart rate. Ulcers. on the lower legs (in adolescents and adults). Yellowing of the eyes and skin (jaundice).

The main objectives of medical treatment are:

Bed rest to minimize energy expenditure and oxygen use.

Hydration through oral and intravenous therapy.

Electrolyte replacement. Analgesics for severe abdominal and joint

pain. Blood replacement to treat anemia. Antibiotics to treat any existing infection.

NURSING MANAGEMENT Administer blood products as ordered . Improve oxygenation . Prevent iatrogenic anemia . Provide adequate nutrition with high iron . Administered iron replacement as ordered . Monitor vital signs . Assess pt. for palpitation , SOB, dizziness. Administered parenteral vitamin B12 as prescribed . Assess knowledge of present condition .reinforced

importance of therapeutic home management & OPD follow up .

Assessed dietary intake . Provided diet high in iron . Advised to rest in between activities . Assessed level of fatigue , sleeping pattern , and

activity that causes fatigue

To reduce sickle cell crises, take the following precautions:

To prevent oxygen loss, avoid: Demanding physical activity (especially if the

spleen is enlarged) Emotional stress Environments with low oxygen (high altitudes,

nonpressurized airplane flights) Smoking Known sources of infection

To make sure you're getting enough fluids: Avoid too much exposure to the sun Have fluids on hand, both at home and away Recognize signs of dehydration.

To avoid infection: Consider having the child wear a Medic Alert

bracelet Have the child vaccinated as recommended by the

health care provider Share the above information with teachers and

other caretakers, when necessary

They should take supplements of folic acid (essential for producing red blood cells) because red blood cells are turned over so quickly.

Antibiotics and vaccines are given to prevent bacterial infections, which are common in children with sickle cell disease.

Blood transfusions are used to treat a sickle cell crisis.

Nursing Diagnosis: 1. Altered nutrition, less than body requirements

related to reported inadequate iron intake, knowledge deficit regarding iron reach foods.

Goal: Patient will receive adequate supply of iron. Intervention: Provide diet counseling to care giver, especially in

regard to food source of iron (e.g. meat, liver, fish, egg yolks, green leafy vegetable, nuts, whole grains, infants cereals and dry cereals).

Expected Outcomes: Child receive at least minimum dailyrequirement of

iron.

Nursing Diagnosis: 2-Risk for injury related to abnormal hemoglobin, decreased

ambient oxygen, and dehydration. Patient Goal 1: Will maintain adequate tissue oxygenation. Nursing Intervention: Explain measures to minimize complications related to physical

exertion and emotional stress to avoid additional tissue oxygen needs.

Prevent infection. Avoid low-oxygen environment. Expected Outcome: Child avoids situations that reduce tissue oxygenation.   Patient Goal 2: Will maintain adequate hydration.

Nursing Intervention: Calculate recommended daily fluid intake (1600 ml/m3/day) and

base child’s fluid requirements on this minimum amount (specify) to ensure adequate hydration.

Increase fluid intake above minimum requirements during physical exercise/emotional stress and during crisis to compensate for additional fluid needs.

Give parents written instructions regarding specific quantity of fluid required to encourage compliance.

Encourage child to drink to encourage compliance. Teach family signs of dehydration to avoid delay in rehydration

therapy. Stress importance of avoiding overheating as source of fluid

loss. Expected Outcome: Child drinks an adequate amount of fluid and shows no

signs of dehydration.

Nursing Diagnosis: 3. Anxiety /fear related to diagnostic procedures, transfusion. Goal: Patient, family will become knowledgeable about the

disorder. Intervention: Prepare the child for tests. Remain with the child during tests and initiation of

transfusion. Explain purpose of blood components. Expected Outcomes: Child and family display minimal anxiety. Child and family demonstrate an understanding of the

disorders, diagnostic tests and treatment.  

Nursing Diagnosis: 4. Activity intolerance related to generalized weakness,

diminished oxygen delivery to tissues. Goal: Patient will receive adequate rest. Intervention: Provide diversional play activities that promote rest and

quite but prevent boredom and withdrawal. Choose appropriate roommate of similar age and interests

who requires restricted activities. Plan nursing activities to provide sufficient rest. Assist with activities requiring exertion. Expected Outcomes: Child plays and rests quietly and engages in activities

appropriate to capabilities.

THALASSEMIA

Thalassemia is a blood disorder passed down through families an inherited autosomal recessive blood disease in which the body makes an abnormal form of hemoglobin, the protein in red blood cells that carries oxygen.

The disorder results in excessive destruction of red blood cells, which leads to anemia.

CAUSES:

Hemoglobin is made of two proteins: Alpha globin and beta globin. Thalassemia occurs when there is a defect in a gene that helps control production of one of these proteins.

There are two main types of thalassemia: 1-Alpha thalassemia : occurs when a gene or

genes related to the alpha globin protein are missing or changed (mutated).

2-Beta thalassemia : occurs when similar gene defects affect production of the beta globin protein.

Alpha thalassemias occur most commonly in persons from southeast Asia, the Middle East, China, and in those of African descent.

Beta thalassemias occur in persons of Mediterranean origin, and to a lesser extent, Chinese, other Asians, and African Americans

There are many forms of thalassemia. Both alpha and beta thalassemia include the following two forms:

Thalassemia major Thalassemia minor Thalassemia major : occurs if the baby

receive the defective gene from both parents. Thalassemia minor: occurs if the baby receive

the defective gene from only one parent. Persons with this form of the disorder are

carriers of the disease and usually do not have symptoms.

β-Thalassemia Major(Cooley’s Anemia) It is most common form of thalassemia in the

world. More common in countries around Mediterranean Sea. It is inherited as autosomal genetic disorder of both genes controlling ß- chain synthesis (homozygous).

Normal postnatal hemoglobin (Hgb A) is composed of two α and two β- polypeptide chains, in thalassemia major there is a partial or complete deficiency in the synthesis of β- chain of Hgb molecule.

Consequently, there is a tremendous increase in the synthesis of α- chains and у chains.

SIGN & SYMPTOM The most severe form of alpha thalassemia

major causes stillbirth (death of the unborn baby during birth or the late stages of pregnancy).

Children born with thalessemia major (Cooley's anemia) are normal at birth, but develop severe anemia during the first year of life.

SINGS & SYMPTOM Unexplained fever.Poor feeding.Markedly enlarged spleen.Headache.Bone pain.Decreased exercise tolerance.Anorexia.Frequent epistaxis.Hemochromatosis.Hemosiderosis.

Other Features:Small stature.Delayed sexual maturation.Protrusion of the abdomen (hepato- spleno-

megaly).Bone Change (older children if untreated):

Enlarged head.Prominent frontal and parietal bosses.Flat or depressed bridge of the nose.Enlarged maxilla.Protrusion of the lip and upper central incisors

and eventual malocclusion.

:TREATMENT

Patients with thalassemia minor usually do not require any specific treatment unless they have very low HB.

Treatment for patients with thalassemia major includes chronic blood transfusion therapy.

iron chelation therapy to remove excess iron from the body.

splenectomy . Bone marrow transplant may help treat the

disease in some patients especially children.

THERAPEUTIC MANAGEMENT:

Blood Transfusion. Chelation Therapy

Nursing Diagnosis: Anxiety / fear related to diagnostic procedures,

transfusion. Activity intolerance and comfort altered related

to hematomas in tissues and joints. High risk for bleeding after minor hematomas

related to deficiency of coagulation factor. Pain related to bleeding in joints. Impaired physical mobility related to hemorrhage

in joints and tissues. Altered family process related to child with

chronic illness.  

Planning:The objectives of nursing care can be divided

into immediate needs and long-term goals: Prevent bleeding. Recognize and control bleeding. Prevent crippling effect of bleeding. Support family and prepare for home care. Identify persons at risk.

Implementation: 1. Prevent Bleeding: Prophylactic administration of AHF. Appropriate exercises to strengthen muscles and joints

and to allow age appropriate activity. To prevent oral bleeding, some readjustment in terms of

dental hygiene may be related to, minimize trauma to the gums such as use of a water-irrigating device, softening the toothbrush in warm water before brushing.

A peripheral fingerstick is better for blood samples and subcutaneous route is substituted for IM whenever possible.

Neither aspirin nor any aspirin- containing compound should be used. Acetaminophen (Tylenol) is a suitable aspirin substitute, especially for use during control of pain at home.

DISSEMINATED INTRAVASCULAR C OAGULATION

DIC

DIC is aserious bleeding disorder resulting from accelerated normal clotting with a subsequent decrease in clotting factors & platelets leading to uncontrolled bleeding .

Etiology : it is always a result of another disease or condition ,it is often associated with shock ,infection ,hemolytic processes such as transfusion of mismatched blood .

Sing & symptom : 1- bleeding: can occur any where in the body

following trauma or normal activity or spontaneously .

2- specific sing & symptom : Slow,persistent ,prolonged bleeding from minor

injuries . Uncontrollable hemorrhage subsequent to dental

extraction or irritation of the gums . Epistaxis especially after facial injury . Hematuria. Ecchymosis ( petechiae are rare ). Bleeding into joints (hemarthrosis )which may

lead to severe joint deformity .

HEMOPHILIA

Is a disorder of hemostasis of one or more clotting factor.

Type : 1-hemophilia A: deficient in factor VIII,called

classic hemophilia . 2- hemophilia B: deficient in factor IX : called

christmas disease . Etiology : sex link recessive traits occur

almost exclusively in male ,female carriers transmit the disease

Hemophilia (Classic Hemophilia) It is one of the commonest (95%)congenital

coagulation disorders due to deficiency or functional abnormality of factor VIII demonstrated as a sex- linked ressive trait (male is diseased and female is carrier).

Blood clotting occurring in 3 phases, each is dependent on the preceding phase.

The basic defect of hemophilia (A) is a deficiency of factor VIII (antihemophilic factor AHF).

AHF is produced by the liver and is necessary for formation of thromboplastin in phase I of blood coagulation. The less AFH in the blood, the more severe the disease.

The frequency and severity of bleeding are related to level of factor VIII deficiency:

  Clinical severity Factor VIII Activity Bleeding Tendency Severe 1% _Spontaneous bleeding without trauma. Moderate 1%-5% _Bleeding with trauma. Mild  5%- 50% _Bleeding with severe trauma or surgery.  

Sing & symptom : 1-Bleeding Skin : petechia ,purpura , hematoma . Head :gingival bleeding & epistaxis . GI: hematemesis & melena . Renal: hematuria . Nuro :headache , altered LOC. CV: symptom of shock . 2-platelet cunt is decreased . 3-prolong coagulation test .

TEATMENT The primary therapy for hemophilia is

replacement of the missing clotting factor. Vigorous therapy is instituted to prevent chronic

crippling effects from joint bleeding. If replacement therapy is begun immediately, local measures such as ice applications and splinting are seldom needed.

Other drugs may be included in the therapy plans depending on the source of the hemorrhage. Corticosteroids are used to treat inflammation in the joints; nonsteroidal antiinflammatory drugs such as aspirin, indomethasin (Indocin) and phenylbutazona (Burazolidin) should not be used because they inhibit platelet function.

NURSING DIAGNOSIS:

Anxiety / fear related to diagnostic procedures, transfusion.

Activity intolerance and comfort altered related to hematomas in tissues and joints.

High risk for bleeding after minor hematomas related to deficiency of coagulation factor.

Pain related to bleeding in joints.

LEUKEMIA It is a malignant disorder involving bone

marrow dysfunction manifested by anemia, thrombocytopenia, and abnormal proliferation of white cells, which results in harmful filtration into tissues. It is the most common malignancy in childhood (30%), peak incidence 2-8 years of age. Incidence among males is greater than females’ 2:1.

 

Etiology: Although the exact cause is unknown, but

multiple factors believed to be responsible: ionizing radiation, chemicals (benzene compound, heavy metals), drugs (Alkylating agents), and chromosomal abnormalities (Down syndrome), and familial predisposition.

Classification: Leukemia is classified according to its predominant

cell type and level of maturity as described by the following:

Lympho for Leukemias involving the lymphoid or lymphatic system.

Myelo for those of myeloid (bone marrow) origin. Blastic and acute for those involving immature cells. Cytic and chronic for those involving mature cells. In children two forms are generally recognized: Acute lymphoid leukemia (A.L.L.) and acute nonlymphoid

leukemia (A.N.L.L) or (A.M.L). A.L.L includes lymphatic, lymphocytic, lymphoblastic and

lymphoblastoid leukemia. A.N.L.L. type includes granulocytic, myelocytic, monocytic,

myelogenous, monoblastic and monomyeloblastic.

Common symptoms of chronic or acute leukemia may include:

Swollen lymph nodes that usually don't hurt. Fevers or night sweats. Frequent infections. Feeling weak or tired. Bleeding and bruising easily (bleeding gums,

purplish patches in the skin, or tiny red spots under the skin).

Swelling or discomfort in the abdomen (from a swollen spleen or liver).

Weight loss for no known reason. Pain in the bones or joints.

TREATMENT

pharmaceutical medications, typically combined into a multi-drug chemotherapy regimen.

Some are also treated with radiation therapy. In some cases a bone marrow transplant is

useful

Nursing diagnosis: 1. High risk for infection related to depressed body defenses. Goal: Patient will experience minimized risk of infection. Intervention: Place child in private room. Advise all visitors and staff to practice hand washing. Screen all visitors and staff for signs of infection. Use aseptic technique. Evaluate child for any potential sites or infections. Provide nutritionally complete diet for age. Administer antibiotics as prescribed. Expected Outcome: Child doesn’t come in contact with infected persons or contaminated

articles. Child consumes diet appropriate for age.  

Nursing diagnosis: 2. High risk for injury (hemorrhage) related to interference with

cell proliferation. Goal: Patient will exhibit no evidence of bleeding. Intervention: Use all measures to prevent infection, especially in ecchymotic

area. Use local measures to stop bleeding. Restrict strenuous activity that could result in accidental injury. Involve child in responsibility for limiting activity when platelet

count drops. Administer platelets as prescribed. Expected Outcome: Child exhibits no evidence of bleeding.  

Nursing diagnosis: 3. Altered nutrition less than body requirement

related to loss of appetite. Goal: Patient will receive adequate nutrition. Intervention: Encourage parents to relax pressure placed on

eating. Allow child any food tolerated. Improve quality

of food selections when appetite increases. Stress expected increase in appetite from

steroid.

Take advantage of any hungry period, sever small snakes.

Allow child to be involved in food preparation and selection.

Make food appealing. Remember usual food practices of children in

each age group. Expected Outcome: Nutrition intake is adequate.

REFERENCES

www.nlm.nih.gov/medlineplus/ency/hptt. Medical –surgical nursing ,health & illness

prespectives ,seventh edition . www.ar.wikipedia.org/wiki/ www.en.wikipedia.org/wiki/Thalassemia