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ALLERGYDr. Geraldine Anne S. RamirezDepartment of Pediatrics
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Allergy
- Untoward physiological event where there is anacquired specific change in the reactivity of the host,mediated by an immune system.
IgE antibody
role in immediate hypersensitivity Rxn
- detected clinically in atopic individual by the whealand flare formation
- Ascariasis and occupational allergens
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Immunologic Basis of Allergic
Diseases
Immunologic system
detect and eliminate anything foreign to the body
Immunitybeneficial
Allergyharmful
Foreign material external environment
- Internal environment
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Component of host vs. foreign
substances
1. Environment
2. Target cells ( B lymphocytes and T lymphocytes )
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Immunologic Response of the Host
in Eliminating Foreign Material
1. Primary (Non-specific) the most primitiveresponse; phagocytosis and inflammation
2. Secondary (specific) 2 possible mechanisms:
a. B cell response with elaboration of antibodies
(IgE, IgM, IgG, IgA, IgD)b. T- cell response of cell-mediated or delayed
hypersensitivity
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In patient with genetic defect in processing Ag,and the Ag persists-host is immunologicallyimbalance
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Genetics
Chromosome autosomal dominant
Both parent atopic 33% risk
One parent atopic (24%-29%)
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Allergy and Infection
- Most common infection viral RSV, parainfluenzaand corona virus
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Emotional Factors
- trigger or exacerbate an allergic attack
(autonomic nervous system)
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Physical Factors
- cold, heat, exercise, changes in barometricpressure (parasympathetic ns)
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Characteristics of the Allergic Child
- Hay fever
- Urticaria
- Asthma
- Others: diarrhea, headache, conjunctivitis
Diagnosis
- RAST
- Skin test
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Lab. Exam
- CBC increase eosinophilia (3-7%)
- ESR
- Radiography
- Stool Exam- Urinalysis
- Total IgE (PRIST)
- Provocation or Challenge test- Patch Test
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Principles of Therapy in Allergic
Disease
- Based on effect of adequate identified causativeallergens (hx taking and skin testing)
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Non-IgE Mechanism of Allergy
Complement Pathway
C3a }anaphylaxis can induce histaminerelease from Basophiles and from mast cellsin the skin, producing wheal and flare rxns.
C5a } may result in Urticaria
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Neurogenic Pathway
- Non-adrenergic, non cholinergic (NANC) Pwregulates upper and lower airway function through thesecretion of small neuropeptides that have pro-inflammatory activities.
- Stimulation of exposed norepinephrine in the airwaytriggers cause increased nasal activity and secretion ofneuropeptides as reflex response.
- May cause bronchoconstriction, airway edema, andmucus production
ex. Asthma
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Modern Concept of Allergy
Allergic diseasesabnormal intense immunologicalreaction to the usual environment allergens.
Signs and Symptoms
1st month vomiting, diarrhea, bloody stools
2nd and 3rd monthskin eruptions
4 mos. yr. sneezing or wheezing
Initial exposure to allergen elicits a temporaryinflammatory response
Repeated exposure chronic inflamed with tissue damage,
hypersensitivity of the affected organ
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1st Allergy at about 6 mos. of life
Food allergy
Atopic dermatitis upper airway allergies
Bronchial hypersensitivity Lower airway allergies
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3. Tissue damaging responses (tertiary) will comeinto play
- these responses are no longer beneficial tothe host
If the tertiary response is ineffective, the Ag stillpersists then a more harmful or deleteriousand self-perpetuating response will be sustained(Autoimmune disease)
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4 Types of Immunologic or
Hypersensitivity Rxn
Type I or Anaphylaxis IgE mediated or anaphylacticreaction: e.g. rhinitis, sinusitis, asthma, hypersensitivitypneumonitis, urticaria, eczema, dermatitis, angioedema
Type II or Cytotoxic
Type III or Immune complex
Type IV or Granulomatous rxn
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Mediators of Allergy
Rapidly released mediators:
1. Mast cellsPreformed mast cells mediators vasoactiveamine (histamine and serotonin), adenosine,
proteases (kinase, tryptase), proteoglycans
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* Most significant biologic activity of thesemediators:
Vasodilatation with vascular leakage, smoothmuscle contraction, goblet and glandularsecretion as well as stimulation of the irritant
(itch and sneeze) nerve receptors.
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2. PAF- platelet activating factor a peptide that isproduced with pro-inflammatory
properties
- Isolated in the bronchial airway and skin
- ability to aggregate and degranulate platelets, a
feature of allergic immunity
- Acts pro anti-inflammatory mediators inallergy
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3. Cytokine very patent pro-inflammatory
mediators
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Pharmacotherapy
1. Antihistaminesprevent symptoms of IgE-mediatedallergic diseases, atropine like effect, asthmaprophylaxis
HI receptor antagonist useful in allergic disorders complete or block the action of histamine byreversible competitive antagonism at HI receptor
H2 receptor antagonist ex. Cimetidine, ranitidine-can inhibit cell-mediated immune skin responses
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2 Types of Histamines
1. Classical rapidly absorbs after oral orparenteral administration relief appreciatedwithin 15-30 min. e.g. meclizine- 12-24 hrs.,
mequitazine 36 hrs.- passed BBB and placenta, metabolized inthe liver
SE: sedation, nausea and vomiting,suppression of parkinsonismlikesyndrome
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2 Types of Histamines
2. Newer Nonclassical HI anatagonists
Terfenadine, astemizole lack of sedationand anti-cholinergic effects
- long acting, good compliance
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2. Adrenergic Agents
- relax airway smooth muscle, inhibit release of
chemical mediators from mast cells causingbronchoconstriction, increase mucociliarytransport by ciliary activity
Beta 2 adrenergic agents e.g. salbutamol,terbutaline, tolbuterol
Epinephrine stimulate alpha B1 and B2receptors given SQ 0.1 ml/kg of 1:1 dil, Rapid
onset, counteracts asthmaticbronchospasm
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3. Methylxanthine
- Theophylline- relaxes bronchial smooth
muscle, stimulate ciliary motility, acts as CNSrespiratory stimulant, improve diaphragmaticand other respiratory muscle contractility in thedistressed asthmatic
- phosphodiesterase inhibition which increasethe tissue levels of cyclic AMP
- inhibition of neural transmission at certainsynapses
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SE: narrow range between clinically effected bloodlevels and levels producing side effects which
include:anorexia, nausea, vomiting, heartburn,diarrhea, neurologic
effects: headache, restlessness, insonia,muscle spasm, seizure, cardiovascular
effects: (palpitations, tachycardia, arrhythmia),allergy
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4. Corticosteroid
- anti-inflammatory, potentiate the effects of
beta adrenergic drugs decrease airwayobstructions
- long term side effects: adrenal suppressionleading to inhibition of linear growth andposterior subscapsular cataract
- long term use inhaled corticosteroid safeand effective e.g. Budesonide
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5. Muscarinic Antagonist
- obviates the systemic atropine effects
- competitively inhibit the effect of acetylcholineat muscarinic receptor causing relaxation of theairway smooth muscles and dec. secretion of
mucus ex. Ipatropium bromide
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6. Cromolyn Sodium
- non-steroidal, inhaled anti-inflammatory drug,prevents both antibody-mediated mast celldegranulation and the transmembrane influx ofCa provoked by IgE antibody-antigen mediator-
selective suppressive effect on anti-inflammatorycells like macrophages, eosinophils, neutrophilsand monocytes.
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7. Ketotifen
- prophylaxis for asthma, a potent anti -anaphylactic activity, inhibit release and effect ofmediators, acts as Ca channel antagonists andoptimizes the beta adrenergic responses.
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ENDOCRINE DISORDERS
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Disorders of the Pituitary Glands
Hypothalamic and Pituitary hormones
Pituitaryloc at sella turcica
Ant. Pituitarysecrete trophic hormones
1. ACTH2. TSH
3. GH
4. LH5. FSH
6. PRL
7. Betalipotropin
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Primary hormone defwhen failure is due toorgan failure
Secondary hormone def lack of stimulationby the pituitary, which may result fromeither def. of hypothalamic releasinghormone or to an intrinsic pituitary disease
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Hypopituitarism
- Growth hormone defgrowth failure
EtiologyCongenital
Acquired
P ibl C f Pit it r nd r
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Possible Causes of Pituitary and or
hypothalamic dysfunction leading to
Growth failure:
1. Developmental Defects2. Idiopathic Hypopituitarism3. Tumors and Infiltrative lesions
4. Psychosocial Dwarfism5. Unresponsive to GH6. Empty Sella Syndrome7. Iatrogenic
8. Infections9. Vascular lesions10. Autoimmune causes
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Clinical Manifestations
- Short, growth velocity is subnormal, BW andlength are normal
- Doll like, cherubic
- External genitalia in boys are underveloped,penis is small
- Delay in skeletal and dental devt.
- Hypoglycemia
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Differential Diagnosis
- Proportionate Dwarfism
- Gonodal dysgenesis
- Turner syndrome- Constitutional short stature
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Diagnosis
- History and PE, Measurements
- Abnormal GH and other Pituitary function tests
- Investigation of other target organs like:
Thyroid functionserum thyroxine andTSH
Gonodal function measure serum LH,FSH, estradiol and
testosterone, prolactin
Adrena glandsplasma or serum cortisol
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Roentgenography and Imaging
studies:
Skull X-ray
MRI
CT Scans
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Treatment
Organic lesions treat primary cause
Surgery
Growth hormone defHigh Growth Hormone
Di b I i id
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Diabetes Insipidus
- Disorder characterized by extreme thirst, polydipsia,
polyuria, and episodes of dehydration is due toabsence of ADH
- Etiology: idiopathic
- Takes 95% of the post. lobe of pituitary to cause DI
- Craniopharyngiomamost common cause inchildren up to 14 yrs.
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- Hereditaryautosomal dominant
- Differential Diagnosis:
Chronic Renal Disease - hypoplastic or polycystickidney, Chronic GN, Pyelonephritis
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Causes of Central or Neurogenic DI
Hypophysectomy
Tumors
Surgery to remove suprasellar tumors
Granuloma
Infiltrative disorder like leukemia andhistiocytosis x
Infections like encephalitis
Trauma Autoimmune causes
Hereditary/familial
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Laboratory Dx:
History and PE
Monitor I and O
Urine specific gravity1.001 1.005
Urine osmolality and plasma are taken
MRI
CT Scans
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Treatment
Central DIDDAVP a synthetic analogue ofVasopressin Chlorpropamide.
Nephrogenic DI treat underlying cause prevent dehydration, inc. water intake,Chlorthiazide, Indomethacin
S d f I i S i
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Syndrome of Inappropriate Secretion
of ADH
- Condition wherein ADH concentration isinappropriately high for the level of plasmaosmolality
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Diagnostic Criteria
1. Hyponatremia with hypo-osmolality
2. Urine inappropriately concentrated to greaterthan 100 mosm/kg
3. Euvolemia and absence of CHF, cirrhosis,Nephrotic syndrome
4. Absence of renal, adrenal or thyroidinsufficiency
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Etiology
Condition involving CNS: Trauma, infectiousand surgery for pituitary tumors
The following can produce S/S of SIADH:
- TB, Lung tumors, lymphomas, sarcomas ofduodenim, pancreas, prostate, thymus
- intake of drugs like Clofibrate,chlorpropamide, thiazide
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Clinical Manifestations
S/S of hypotonicity of body fluids and waterintoxication
N/V, irritability, and personality changes
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Treatment
Restrict fluids
Correct electrolytes imbalance
Demeclocycline
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Thyroid Disorders in Children
Congenital Hypothyroidism
- One of the most common preventable causes ofmental retardation
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Etiology
1. Thyroid dysgenesis
2. Thyroid dyshormogenesis
3. Hypothalamic or pituitary dysfunction
4. Maternal anti-thyroid drug ingestion
5. Maternal autoimmunity
6. Immaturity
D f t i C it l N d i
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Defects in Congenital Non endemic
Hypothyroidism
1. TSH receptor abnormality
2. Iodide trapping defect
3. Organification defect
4. Iodotyrosine deiodinase def.
5. Defects in thyroglobulin synthesis or transport leadsto failure of T3 and T4 release into the circulation
6. Failure of proteolytic enz. to digest the thyroglobulin- T4 complex
7. Peripheral thyroid hormone receptor defect
Cli i l M if t ti
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Clinical Manifestation Common S/S in Neonates:
Constipation, prolonged jaundice, lethargy, poorfeeding, hypothermia, good babies unusuallyquiet and seldom cry when wet
Other features:
Prolonged gestation with large birth size, large ant
fontanel and a post. fontanel > 1 cm, RDS,peripheral cyanosis, delayed onset of stooling,abdominal distention, vomiting and edema
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Long Term untreated CH-CRETIN
- Hollow empty eyes which appear far apart
- Swollen eyelids, broad nose with depressedbridge, open mouth with thick broad tongue,narrow chest with curved back
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Lab Dx
Low to nil serum thyroxin (T4), TSH assay
Newborn screening
Thyroid scanning
Radioactive iodine uptake
CBC with Periph smear, Bilirubin levels
EKG Bone Age
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Treatment
Early institution of treatment is the dictum
Na Levothyroxine
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Prognosis
Time of treatment is correlated withneurodevelopmental outcome. Treat within the1st 4-6 weeks of life augurs a very good mental
prognosis.
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Goiters in Children
Any enlargement of the lobe or lobes of thethyroid gland to at least the patients terminalphalanx of the thumb
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Endemic Goiter
- Iodine deficiency, endemic in the mountains
- Intake of goitrogens and a genetic metabolicdefects
- Compensatory hypertrophy of the glands in itseffort to produce adequate amounts of thyroidhormone
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Treatment
- Levothyroxin
- Potassium iodide or iodized oil
- Iodized salt as prophylaxis
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Hashimoto Thyroditis
CLTchronic lymphocytic thyroiditis
- autoimmune, inflammatory condition causing55-65% of all euthyroid goiters
- common in female more than male
- occurs frequently with chromosomalabnormality or syndromes
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Diagnosis
Increase titers of thyroid antibodies
RAI scan
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Simple Colloid Goiter
- Adolescent goiter, on toxic goiter, autoimmune,gland is normal
- Thyroid function test is normal
- Regression of goiter size with thyroxine therapy
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Congenital Goiter
- Occur in areas of iodine deficient
- Anti thyroid substances ingested by pregnantmothers
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Solitary Nodule
- Assoc. with malignancy
- Rare in children
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Etiology
Irradiation most common implicated
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Clinical Manifestation
Thyroid Ca - painless cervical amass in thethyroid area
- Cervical lymph node enlargement
- Majority are euthyroid
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Lab Dx
Normal thyroid function
USG
Radionuclide scan
FNAB
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