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King saud university nursing collage master degree 1431-1432H


KING SAUD UNIVERSITY NURSING COLLAGE MASTER DEGREE 1431-1432H Nursing management for acute disease in: Respiratory system Endocrine system Hematology system – PowerPoint PPT presentation

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Title: King saud university nursing collage master degree 1431-1432H

King saud university nursing collage master
  • Nursing management for acute disease in
  • Respiratory system
  • Endocrine system
  • Hematology system
  • Immunology system
  • Done by maha alonazi

  • 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 .

  • Anatomy of respiratory system .
  • Croup.
  • Acute epiglottitis
  • Broncholitis .
  • Pneumonia.
  • Aspiration pneumonia .
  • ARDS
  • Asthma.
  • Anatomy of endocrine system .

  • Diabetes Mellitus
  • Diabetic ketoacidosis .
  • Diabetes Insipidus.
  • SIADH .
  • Hyperthyroidism.
  • Hypothyroidism.
  • Gigantism
  • Anatomy of immune hemato system .

  • Anemia
  • Sickle cell disease
  • DIC
  • Hemophilia
  • Leuckemia
  • Thalasmia

Pulmonary System
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 vocal
  • cords) and trachea (Up to Carina).
  • The upper airway is responsible for
  • warming, humidifying and filtering air before
  • it reaches the trachea.
  • Nose
  • Pharynx
  • Larynx

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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

When will you suspect UAW dis.?
  • Stridor
  • Neck retraction
  • Suprasternal retraction
  • Sniffing position

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.

(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
  • Severe Impending respiratory failure
    Intubation for 2-3 days. Improves in a week.
  • Majority may not need intubation

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 .

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

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.

Nursing management
  • Close monitoring .
  • Arm restraint to prevent self extubation .
  • Decreased movement of the ETT in the larynx .
  • Deliver oxygen as necessary .

Croup Epiglottitis
  • 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 DONT 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.

  • 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 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
Drugs, alcohol, anesthesia, seizures, CNS disorders Altered level of consciousness
Traceal or esophageal abnormalities, ETT, tracheostomy Altered anatomy or function of trachea or esophagus
Loss of normal reflexes which prevent aspiration of stomach contents, GER (worse with neuro or anatomical impairment) Altered function of swallow or esophageal motility
Inhalation of toxic substances Inhalation injury
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 .

  • 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 .

Endocrine System
  • 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,nor
  • 5-Islets of langerhans in the pancreas.insullin-be
    ta cell, glucagon-alpha cell, somatostatin-delta
  • 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
  • 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 ketoacidosis
  • Is 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
Hyperglycemia Metabolic acidosis (gap acidosis)
Dehydration, shock Kussmaul breathing
Cardiac arrhythmia Sodium imbalance
Potassium imbalance
Mental status changes Hyperosmolality Ketonuria Glucosuria
  • Fluid
  • Electrolytes
  • Insulin
  • Monitoring

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
9 (90mL/kg) 6 (60mL/kg) Older Child 3 (30mL/kg)
15 (150mL/kg) 10 (10mL/kg) Infant 5 (50mL/kg) Examination
Severe None Clammy Parched/cracked Sunken None Sunken Lethargic/obtunded Increased Feeble/impalpable gt3 sec Anuric Moderate Tenting Dry Dry Deep set Reduced Soft Irritable Slightly increased Weak 2 sec Decreased Mild Normal Normal Moist Normal Present Flat Consolable Normal Normal Normal Normal Dehydration Skin turgor Skin (touch) Buccal mucosa/lips Eyes Tears Fontanelle CNS Pulse rate Pulse quality Capillary refill Urine output
Table 4. Insulin preparation
Duration (hr) Peak (hr) Onset (hr) Insulin
3-5 6-8 1-3 0.5-1.5 0.17-0.33 0.25-0.5 Rapid acting NovoLog Humalog
3-10 1-5 0.5-1 Short acting Regular
10-24 12-24 4-14 4-14 1-4 1-4 Intermediate acting NPH Lente
18-36 8-30 4-10 Long acting Ultralente
20-24 No pronounced peak 5 Basal Lantus
Syndrome of Inappropriate antidiuretic hormone
  • Characterized by inappropriate, excessive
    secretion of ADH
  • Occurs in the face of low serum Na and low serum
  • 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 vomiting
  • Weight gain
  • Filling pressures (normal or increase)
  • Hypertension and tachycardia

  • Serum sodium normalized over 24 to 48 hours
  • Monitoring intake output , specific gravity,
    serum electrolytes and osmolality, daily

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
  • Central
  • Common 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
  • Nephrogenic
  • Chronic renal disease, polycystic kidney disease,
    pregnancy, starvation

Signs and symptoms
  • Large quantity of dilute urine
  • Hypernatremia
  • Serum hyperosmolality
  • Polyuria
  • Urine osmolality
  • Polydipsia
  • Signs of dehydration
  • Altered 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
Serum sodium gt145 mEq/L lt135 mEq/L
Urine sodium Low High
Serum osmolality gt300 mOsm/kg lt275 mOsm/kg
Urine osmolality lt300 mOsm/L gt800mOsm/L
Urine specific gravity lt1.005 gt1.020
Urine output High Low
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

Thyroid gland
  • The thyroid gland secretes the following
  • 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(Graves 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.

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  • 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

  • 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

  • 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
    mothers 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
  • 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
  • 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.

  • Iodine deficiency is the most common cause of
    hypothyroidism worldwideor a deficiency in
    stimulating hormones from the hypothalamus or
  • 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.

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

  • 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
  • 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

  • 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

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

  • Hyper function of Adrenal Cortex
  • (Cushing's Syndrome)
  •  It is characterized by
  • Wasting and weakness of muscle, (catabolic
  • 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
  • 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.

  • 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
  • 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
  • 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,
  • 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
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
  • RBC transport oxygen from the lungs to the

  • Hgb A, normal adult hemoglobin
  • Hemoglobin 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 marrow
  • Polymorphonucleated (PMNs or poly) mature form
    of neutrophil
  • Band unsegmented appearing nucleus
  • Neutrophilia increased number of circulating

  • Neutropenia decreased number of circulating
    neutrophils (lt1500/mm3)
  • WBCs mature in bone marrow for 10 days
  • Eosinophils 2 5 of the circulating WBC.
  • Eosinophilia increased number of eosinophils
  • Eosinopenia decreased number of eosinophils
  • Basophils smallest portion of granulocytes, 1
    of WBC
  • Basophilia increased number of circulating
  • Basopenia decreased number of circulating

  • Mononuclear phagocytes
  • Monocytes 3 8 of circulating WBCs
  • Monocytosis increase in the number of circulating
  • Monocytopenia decrease in the number of
    circulating monocytes
  • Macrophages have long life span.

  • Lymphocytes (lymphoid lineage) primary immune
  • Lymphocytes 10 40 of the ciculating WBCs
  • Lymphocytosis increase number of circulating
  • Lymphopenia decrease in number of circulating
  • T lymphocytes or T cells 65 85 of all
  • Clusters of differentiation (CD)
  • Helper T cells (CD4)
  • Suppressor T cells (CD8)
  • Cytotoxic or killer T cells (CD8)

Lymph nodes of the body
  • 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
  • WBC
  • Functions
  • Defense protect the bodys internal environment
    from nonself antigens or microorganisms
  • Assists the immune system in discriminating
    self from nonself or altered self
  • Second line of defense involves the inflammatory
    response, phagocytosis .

  • 3-Platelets (thrombocytes)
  • Megakaryoblasts mature into megakaryocytes
  • 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.

  • 4-Plasma factors
  • Procoagulants aka plasma clotting factors.
    Promotes coagulation.
  • Anticoagulants inhibit coagulation
  • Circulating anticoagulants antithrombin III,
    protein C, protein S
  • Coagulation depends on the balance between the
    procoagulants and the anticoagulants

Nomenclature for coagulation factors
Factor Synonym
I Fibrinogen
II Prothrombin
III Tissue thromboplastin
IV Calcium
V Proaccelerin
VI Not assigned
VII Proconvertin
VIII Antihemophilic factor (AHF)
IX Plasma thromboplastin component (Christmas factor
X Stuart factor (Stuart-Prower factor)
XI Plasma thromboplastin antecedent (PTA)
XII Hageman factor
XIII Fibrin-stabilizing factor (FSF)
  • 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
  • Etiologic factors.
  • Morphologic factors.

  • I. Etiologic Factors
  • Anemias resulting from impaired or decreased
  • The production of the RBCs and Hb can be
    impaired by
  • Nutritional deficiency (e.g.folate, iron, B12).
  • Bone marrow failure (e.g. irradiation,
  • 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
  • Defect in cell enzyme G6PD deficiency.
  • Defect in cell hemoglobin Sickle cell anemia,
  • Extracorpuscular causes
  • Immune blood transfusion.
  • Non- immune - burns. - Snake venoms.
  • Anemias resulting from excessive blood loss
  • Acute blood loss (bleeding)
  • Alteration in vital signs doesnt occur unless
    20 or more of blood lost occur. Shock occurs
    with losses of 40 of blood volume.
  • Chronic blood loss (occult bleeding,

  • 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.

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  • 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.

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  • 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
  • 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
  • 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
  • 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
  • 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
  • Expected Outcomes
  • Child receive at least minimum dailyrequirement
    of iron.

  • Nursing Diagnosis
  • 2-Risk for injury related to abnormal
    hemoglobin, decreased ambient oxygen, and
  • Patient Goal 1
  • Will maintain adequate tissue
  • 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 childs fluid requirements on
    this minimum amount (specify) to ensure adequate
  • Increase fluid intake above minimum requirements
    during physical exercise/emotional stress and
    during crisis to compensate for additional fluid
  • Give parents written instructions regarding
    specific quantity of fluid required to encourage
  • 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
  • Choose appropriate roommate of similar age and
    interests who requires restricted activities.
  • Plan nursing activities to provide sufficient
  • Assist with activities requiring exertion.
  • Expected Outcomes
  • Child plays and rests quietly and engages in
    activities appropriate to capabilities.

  • 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.

  • 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

  • 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
  • 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

  • ß-Thalassemia Major(Cooleys 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 a and two ß- polypeptide chains, in
    thalassemia major there is a partial or complete
    deficiency in the synthesis of ß- chain of Hgb
  • Consequently, there is a tremendous increase in
    the synthesis of a- chains and ? 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-
  • 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.

  • 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,
  • 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 .

  • Is a disorder of hemostasis of one or more
    clotting factor.
  • Type
  • 1-hemophilia A deficient in factor VIII,called
    classic hemoph