ASTHMA
Asthma is a chronic inflammatory condition of the lung airways resulting in episodic airflow obstruction
Etiology:
1. Genetics
2. Environmental: recurrent wheezing episodes and offending allergens
Epidemiology:
Fifteen percent of boys compared to 13% of girls have had asthma
Pathogenesis
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In the small airways, the airway lumen gets blocked by the small muscles encircling the tract as they
constrict.
It may also get obstructed by inflammatory molecules (IL-4,5,13;T-lymphocytes and/or cytokines).
Hyper-reactivity can cause airway inflammation, edema, basement membrane thickening or mucous gland
hypertrophy.
Risk factors:
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Parental asthma
Allergy:
Atopic dermatitis (eczema)
Allergic rhinitis
Food allergy
Inhalant allergen sensitization
Food allergen sensitization
Severe lower respiratory tract infection:
Pneumonia
Bronchiolitis requiring hospitalization
Wheezing apart from colds
Male gender
Low birthweight
Environmental tobacco smoke exposure
Reduced lung function at birth
Differential Diagnosis
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Vocal cord dysfunction. Vocal cords involuntarily close during inspiration/expiration and this causes S.O.B,
coughing, throat tightness and laryngeal wheezing.
Chronic, intermittent cough could be due to gastroesophageal reflux or rhinosinusitis.
Asthma patterns:
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TRANSIENT NONATOPIC WHEEZING
Common in early preschool years
Recurrent cough/wheeze, primarily triggered by common respiratory viral infections
Usually resolves during the preschool and lower school years, without increased risk for asthma in later life
Reduced airflow at birth, suggestive of relatively narrow airways.
AHR near birth. Improves by school age
PERSISTENT ATOPY-ASSOCIATED ASTHMA
Begins in early preschool years
Associated with atopy in early preschool years:
Clinical (e.g., atopic dermatitis in infancy, allergic rhinitis, food allergy)
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Biologic (e.g., early inhalant allergen sensitization, increased serum immunoglobulin E, increased blood
eosinophils)
• Highest risk for persistence into later childhood and adulthood
• Lung function abnormalities:
• Those with onset before 3 yr. of age acquire reduced airflow by school age
• Those with later onset of symptoms, or with later onset of allergen sensitization, are less likely to experience
airflow limitation in childhood
3. ASTHMA WITH DECLINING LUNG FUNCTION
• Children with asthma with progressive increase in airflow limitation
• Associated with hyperinflation in childhood, male gender
Asthma Management types:
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Intermittent
Persistent:
Mild
Moderate
Severe
CONTROL CLASSIFICATION*
Clinical assessment while asthma being managed and treated
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Well controlled
Not well controlled
Very poorly controlled
MANAGEMENT PATTERNS
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Easy-to-treat: well, controlled with low levels of daily controller therapy
Difficult-to-treat: well, controlled with multiple and/or high levels of controller therapies
Exacerbators: despite being well controlled, continue to have severe exacerbations
Refractory: continue to have poorly controlled asthma despite multiple and high levels of controller
therapies
Asthma triggers:
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INDOOR ALLERGENS
Animal dander
Dust mites
Cockroaches
Molds
SEASONAL AEROALLERGENS
Pollens (trees, grasses, weeds)
Seasonal molds
AIR POLLUTANTS
Environmental tobacco smoke
Ozone
Nitrogen dioxide
Sulphur dioxide
STRONG OR NOXIOUS ODORS OR FUMES
Perfumes, hairsprays
Cleaning agents
OCCUPATIONAL EXPOSURES
Farm and barn exposures
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Formaldehydes, cedar, paint fumes
Cold dry air
Exercise
Crying, laughter, hyperventilation
COMORBID CONDITIONS
Rhinitis
Sinusitis
Gastroesophageal reflux
DRUGS
Aspirin and other nonsteroidal anti-inflammatory drugs
β-Blocking agents
Sulfiting agents
Tartrazine
Evaluation of Asthma:
Treatment:
Management of asthma should have the following components:
(1) assessment and monitoring of disease activity;
(2) education to enhance patient and family knowledge and skills for self-management;
(3) identification and management of precipitating factors and comorbid conditions that worsen asthma; and
(4) appropriate selection of medications to address the patient’s needs.
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Inhaled corticosteroids: prednisolone
Leukotriene receptor antagonists: zafirlukast
Theophylline
Immunomodulators: omalizumab
Long-acting beta agonists: salbuterol
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NSAIDS: cromolyn
ATOPIC DERMATITIS:
Atopic dermatitis (AD), or eczema, is the most common chronic relapsing skin disease seen in infancy and childhood.
Pathogenesis:
Two forms of AD have been identified. Atopic eczema is associated with IgE-mediated sensitization (at onset or
during the course of eczema) and occurs in 70-80% of patients with AD. Nonatopic eczema is not associated with
IgE-mediated sensitization and is seen in 20-30% of patients with AD
Clinical Manifestations:
Occurs between 1-5 years of age
Diagnosis is based on 1 major and 2 minor features being present
MAJOR FEATURES
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Pruritus
Facial and extensor eczema in infants and children
Flexural eczema in adolescents
Chronic or relapsing dermatitis
Personal or family history of atopic disease
ASSOCIATED FEATURES
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Xerosis
Cutaneous infections (Staphylococcus aureus, group A streptococcus, herpes simplex, coxsackievirus,
vaccinia, molluscum, warts)
Nonspecific dermatitis of the hands or feet
Ichthyosis, palmar hyper linearity, keratosis pilaris
Nipple eczema
White dermatographism and delayed blanch response
Anterior subcapsular cataracts, keratoconus
Elevated serum immunoglobulin E levels
Positive results of immediate-type allergy skin tests
Early age at onset
Dennie lines (Dennie-Morgan infraorbital folds)
Facial erythema or pallor
Course influenced by environmental and/or emotional factors
Adolescents who present with an eczematous dermatitis but no history of childhood eczema, respiratory allergy, or
atopic family history may have allergic contact dermatitis
Laboratory findings:
Peripheral blood eosinophilia and increased serum IgE level
Treatment:
1. Cutaneous Hydration: patients with AD have impaired skin barrier function from reduced lipid levels, they
present with diffuse, abnormally dry skin, or xerosis. Moisturizers are first-line therapy. Lukewarm soaking
baths for 15-20 min followed by the application of an occlusive emollient to retain moisture provide
symptomatic relief.
2. Topical Corticosteroids
There are 7 classes of topical glucocorticoids, ranked according to their potency as determined by vasoconstriction
assays. Group 1 is strongest.
GROUP 1
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Clobetasol propionate (Temovate) 0.05% ointment/cream
Betamethasone dipropionate (Diprolene) 0.05% ointment/lotion/gel
GROUP 2
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Mometasone furoate (Elocon) 0.1% ointment
GROUP 3
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Fluticasone propionate (Cutivate) 0.005% ointment
GROUP 4
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Mometasone furoate (Elocon) 0.1% cream
GROUP 5
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Fluocinolone acetonide (Synalar) 0.025% cream
GROUP 6
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Desonide (DesOwen) 05% ointment/cream/lotion
GROUP 7
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Hydrocortisone (Hytone) 2.5%, 1%, 0.5% ointment/cream/lotion
3. Tropical calcineurin inhibitors
4. Systemic corticosteroids (rarely)
5. Antihistamine
ATRIAL SEPTAL DEFECT
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Atrial septal defects (ASDs) can occur in any portion of the atrial septum (secundum, primum, or sinus
venosus), depending on which embryonic septal structure has failed to develop normally
Less commonly, the atrial septum may be nearly absent, with the creation of a functional single atrium.
An isolated valve-incompetent patent foramen ovale (PFO) is a common echocardiographic finding during
infancy. It is usually of no hemodynamic significance and is not considered an ASD; a PFO may play an
important role if other structural heart defects are present.
An isolated PFO does not require surgical treatment, although it may be a risk for paradoxical (right to left)
systemic embolization. Device closure of these defects has been considered in young adults with a history of
thromboembolic stroke
OSTIUM SECUNDUM DEFECT
An ostium secundum defect in the region of the fossa ovalis is the most common form of ASD and is associated with
structurally normal atrioventricular (AV) valves. Mitral valve prolapse has been described in association with this
defect but is rarely an important clinical consideration.
Clinical Manifestations:
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A child with an ostium secundum ASD is most often asymptomatic; the lesion is often discovered
inadvertently during physical examination.
Even an extremely large secundum ASD rarely produces clinically evident heart failure in childhood.
However, on closer evaluation, in younger children, subtle failure to thrive may be present; in older children
varying degrees of exercise intolerance may be noted.
Examination of the chest may reveal a mild left precordial bulge.
A right ventricular systolic lift may be palpable at the left sternal border.
Sometimes a pulmonic ejection click can be heard.
characteristic finding is that the 2nd heart sound is widely split and fixed in its splitting during all phases of
respiration.
Diagnosis:
The echocardiogram shows findings characteristic of right ventricular volume overload, including an increased right
ventricular end diastolic dimension and flattening and abnormal motion of the ventricular septum
Treatment:
Transcatheter or surgical device closure is advised for all symptomatic patients and also for asymptomatic patients
with a Qp : Qs ratio of at least 2: 1 or those with right ventricular enlargement.
VENTRICULAR SEPTAL DEFECT
VSD is the most common cardiac malformation and accounts for 25% of congenital heart disease. Defects may occur
in any portion of the ventricular septum, but most are of the membranous type. These defects are in a
posteroinferior position, anterior to the septal leaflet of the tricuspid valve.
Clinical manifestations:
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The clinical findings of patients with a VSD vary according to the size of the defect and pulmonary blood flow
and pressure.
Small VSDs with trivial left-to-right shunts and normal pulmonary arterial pressure are
the most common. These patients are asymptomatic, and the cardiac lesion is usually found during routine
physical examination.
Characteristically, a loud, harsh, or blowing holosystolic murmur is present and heard best over the lower
left sternal border, and it is frequently accompanied by a thrill.
In a few instances, the murmur ends before the 2nd sound, presumably because of closure of the defect
during late systole.
A short, harsh systolic murmur localized to the apex in a neonate is often a sign of a tiny VSD in the apical
muscular septum.
In premature infants, the murmur may be heard early because pulmonary vascular resistance decreases
more rapidly.
Dyspnoea,
Feeding difficulties,
Poor growth,
Profuse perspiration,
Recurrent pulmonary infections, and cardiac failure in early infancy.
Cyanosis is usually absent, but duskiness is sometimes noted during infections or crying.
Diagnosis:
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In patients with small VSDs, the chest x-ray is usually normal, although minimal cardiomegaly and a
borderline increase in pulmonary vasculature may be observed
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In large VSDs, the chest x-ray shows gross cardiomegaly with prominence of both ventricles, the left atrium,
and the pulmonary artery
Echocardiography is also useful for estimating shunt size by examining the degree of volume overload of the
left atrium and left ventricle; in the absence of associated lesions, the extent of their increased dimensions is
a good reflection of the size of the left-to-right shunt.
Treatment:
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The natural course of a VSD depends to a large degree on the size of the defect. A significant number (3050%) of small defects close spontaneously, most frequently during the 1st 2 yr. of life.
Small muscular VSDs are more likely to close (up to 80%) than membranous VSDs (up to 35%).
The vast majority of defects that close do so before the age of4 yr., although spontaneous closure has been
reported in adults.
In infants with a large VSD, management has 2 aims: to get the symptoms of heart failure under control and
prevent the development of pulmonary vascular disease.
PATENT DUCTUS ARTERIOSUS
During fetal life, most of the pulmonary arterial blood is shunted right to- left through the ductus arteriosus into the
aorta. Functional closure of the ductus normally occurs soon after birth, but if the ductus remains patent when
pulmonary vascular resistance falls, aortic blood then is shunted left-to-right into the pulmonary artery.
Clinical manifestations:
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Retardation of physical growth may be a major manifestation in infants with large shunts.
A small PDA is associated with normal peripheral pulses,
large PDA results in bounding peripheral arterial pulses and a wide pulse pressure, due to runoff of blood
into the pulmonary artery during diastole.
The heart is normal in size when the ductus is small, but moderately or grossly enlarged in cases with a large
communication.
In these cases, the apical impulse is prominent and, with cardiac enlargement, is heaving.
A thrill, maximal in the 2nd left interspace, is often present and may radiate toward the left clavicle, down
the left sternal border, or toward the apex.
It is usually systolic but may also be palpated throughout the cardiac cycle.
The classic continuous murmur is described as being like machinery in quality
Diagnosis:
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Radiographic studies in patients with a large PDA show a prominent pulmonary artery with increased
pulmonary vascular markings.
Cardiac size depends on the degree of left-to-right shunting; it may be normal or moderately to markedly
enlarged.
The chambers involved are the left atrium and left ventricle
The clinical signs and echocardiographic findings are sufficiently distinctive to allow an accurate diagnosis by
non-invasive methods in most patients
Treatment:
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Irrespective of age, patients with PDA require catheter or surgical closure. (Transcatheter PDA closure)
In patients with a small PDA, the rationale for closure is prevention of bacterial endarteritis or other late
complications.
In patients with a moderate to large PDA, closure is accomplished to treat heart failure or prevent the
development of pulmonary vascular disease, or both.
TETRALOGY OF FALLOT:
Tetralogy of Fallot is one of the conotruncal family of heart lesions in which the primary defect is an anterior
deviation of the infundibular septum (the muscular septum that separates the aortic and pulmonary outflows).
The consequences of this deviation are the 4 components:
(1) obstruction to right ventricular outflow (pulmonary stenosis),
(2) a malalignment type of ventricular septal defect (VSD),
(3) dextroposition of the aorta so that it overrides the ventricular septum, and
(4) right ventricular hypertrophy
Clinical Manifestations:
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Cyanosis
The systolic murmur is usually loud and harsh; it may be transmitted widely, especially to the lungs, but is
most intense at the left sternal border. The murmur is generally ejection in quality at the upper sternal
border, but it may sound more holosystolic toward the lower sternal border. It may be preceded by a click.
The murmur is caused by turbulence through the right ventricular outflow tract.
Tet spells (Paroxysmal hyper cyanotic attacks, Spells are associated with reduction of an already
compromised pulmonary blood flow, which, when prolonged, results in severe systemic hypoxia and
metabolic acidosis.)
difficulty in feeding,
failure to gain weight,
retarded growth and physical development,
laboured breathing (dyspnoea) on exertion,
clubbing of the fingers and toes, and
polycythemia.
Diagnosis:
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The cardiac silhouette has been likened to that of a boot (“Coeur en sabot”)
The electrocardiogram demonstrates right axis deviation and evidence of right ventricular hypertrophy
Treatment:
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Infants with severe tetralogy require urgent medical treatment and surgical intervention in the neonatal
period. Therapy is aimed at providing an immediate increase in pulmonary blood flow to prevent the
sequelae of severe hypoxia
Intravenous administration of prostaglandin E1 (0.01-0.20 μg/kg/min), a potent and specific relaxant of
ductal smooth muscle, causes dilation of the ductus arteriosus and usually provides adequate pulmonary
blood flow until surgery can be performed
RHEUMATIC FEVER
Rheumatic fever is an inflammatory disease that can develop when strep throat or scarlet fever isn't properly
treated. Strep throat and scarlet fever are caused by an infection with streptococcus bacteria.
Rheumatic fever most often affects children who are between 5 and 15 years old, (at risk for GAS pharyngitis)
though it can develop in younger children and adults.
Rheumatic fever can cause permanent damage to the heart, including damaged heart valves and heart failure
Clinical Manifestations:
Initial attack: 2 major manifestations, or 1 major and 2 minor manifestations, plus evidence of recent GAS infection.
Recurrent attack: 2 major, or 1 major and 2 minor, or 3 minor manifestations
JONES CRITERIA
MAJOR MANIFESTATIONS
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Carditis: isolated mitral valvular disease or combined aortic and mitral valvular disease
Polyarthritis: larger joints, particularly the knees, ankles, wrists, and elbows. hot, red, swollen, and
exquisitely tender
Erythema marginatum: erythematous, serpiginous, macular lesions with pale centres that are not pruritic
primarily on the trunk and extremities, but not on the face
Subcutaneous nodules: consist of firm nodules approximately 1 cm in diameter along the extensor surfaces
of tendons near bony prominences.
Chorea: Emotional lability, incoordination, poor school performance, uncontrollable movements (milkmaids
grip), and facial grimacing, all exacerbated by stress and disappearing with sleep, are characteristic
MINOR MANIFESTATIONS
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Clinical features:
Arthralgia
Fever
Laboratory features:
Elevated acute phase reactants:
Erythrocyte sedimentation rate
C-reactive protein
Prolonged P-R interval
SUPPORTING EVIDENCE OF ANTECEDENT GROUP, A STREPTOCOCCAL INFECTION
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Positive throat culture or rapid streptococcal antigen test
Elevated or increasing streptococcal antibody titre
Treatment:
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Antibiotic therapy: orally administered penicillin or amoxicillin or a single intramuscular injection of
benzathine penicillin to ensure eradication of GAS from the upper respiratory tract
Anti-inflammatory therapy: Patients with typical migratory polyarthritis and those with carditis without
cardiomegaly or congestive heart failure should be treated with oral salicylates
Supportive therapies for patients with moderate to severe carditis include digoxin, fluid and salt restriction,
diuretics, and oxygen. The cardiac toxicity of digoxin is enhanced with myocarditis.
RHEUMATIC HEART DISEASE:
Rheumatic involvement of the valves is the most important sequelae single episode of acute rheumatic fever usually
results in complete healing of valvular lesions while repeated episodes, especially on previously affected valves
result in rheumatic heart disease of acute rheumatic fever.
PATTERNS OF VALVULAR HEART DISEASE:
Mitral insufficiency
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Mitral insufficiency is the result of structural changes that usually include some loss of valvular substance
and shortening and thickening of the chordae tendineae. During acute rheumatic fever with severe cardiac
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involvement, heart failure is caused by a combination of mitral insufficiency coupled with inflammatory
disease of the pericardium, myocardium, endocardium, and epicardium.
Auscultation reveals a high-pitched holosystolic murmur at the apex that radiates to the axilla.
The 2nd heart sound may be accentuated if pulmonary hypertension is present.
A 3rd heart sound is generally prominent.
A holosystolic murmur is heard at the apex with radiation to the axilla.
A short mi diastolic rumbling murmur is caused by increased blood flow across the mitral valve as a result of
the insufficiency
Treatment:
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In patients with mild mitral insufficiency, prophylaxis against recurrences of rheumatic fever is all that is
required.
Afterload-reducing agents (angiotensin-converting enzyme inhibitors or angiotensin receptor blockers) may
reduce the regurgitant volume and preserve left ventricular function.
Surgical treatment is indicated for patients who despite adequate medical therapy have persistent heart
failure, dyspnoea with moderate activity, and progressive cardiomegaly, often with pulmonary hypertension
Mitral stenosis:
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Mitral stenosis of rheumatic origin results from fibrosis of the mitral ring, commissural adhesions, and
contracture of the valve leaflets, chordae, and papillary muscles over time
Patients with mild lesions are asymptomatic.
More severe degrees of obstruction are associated with exercise intolerance and dyspnoea.
Critical lesions can result in orthopnoea, paroxysmal nocturnal dyspnoea, and overt pulmonary edema, as
well as atrial arrhythmias
The principal auscultatory findings are a loud 1st heart sound, an opening snap of the mitral valve, and a
long, low-pitched, rumbling mitral diastolic murmur with presystolic accentuation at the apex.
The mitral diastolic murmur may be virtually absent in patients who are in significant heart failure
A holosystolic murmur secondary to tricuspid insufficiency may be audible.
Treatment:
Surgical valvotomy or balloon catheter mitral valvuloplasty generally yields good results; valve replacement is
avoided unless absolutely necessary
Aortic Insufficiency
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In chronic rheumatic aortic insufficiency, sclerosis of the aortic valve results in distortion and retraction of
the cusps.
The large stroke volume and forceful left ventricular contractions may result in palpitations.
Sweating and heat intolerance are related to excessive vasodilation.
Dyspnea on exertion can progress to orthopnoea and pulmonary edema; angina may be precipitated by
heavy exercise.
Nocturnal attacks with sweating, tachycardia, chest pain, and hypertension may occur
An apical presystolic murmur (Austin Flint murmur) resembling that of mitral stenosis is sometimes heard
and is a result of the large regurgitant aortic flow in diastole preventing the mitral valve from opening fully.
Chest x-rays show enlargement of the left ventricle and aorta.
Treatment:
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Unlike mitral insufficiency, aortic insufficiency does not regress.
Treatment consists of afterload reducers (angiotensin-converting enzyme inhibitors or angiotensin receptor
blockers) and prophylaxis against recurrence of acute rheumatic fever.
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Surgical intervention (valve replacement) should be carried out well in advance of the onset of heart failure,
pulmonary edema, or angina, when signs of decreasing myocardial performance become evident as
manifested by increasing left ventricular dimensions on the echocardiogram.
MYOCARDITIS:
Acute or chronic inflammation of the myocardium is characterized by inflammatory cell infiltrates, myocyte necrosis,
or myocyte degeneration and may be caused by infectious, connective tissue, granulomatous, toxic, or idiopathic
processes.
Etiology:
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Viral infections: Coxsackievirus and other enteroviruses, adenovirus, parvovirus, Epstein-Barr virus, par
echovirus, influenza virus, and cytomegalovirus are the most common causative agents in children, though
most known viral agents have been reported.
Bacterial infections: Diphtheritic myocarditis
Clinical Manifestations:
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Infants and young children more often have a fulminant presentation with fever, respiratory distress,
tachycardia, hypotension, gallop rhythm, and cardiac murmur.
Associated findings may include a rash or evidence of end organ involvement such as hepatitis or aseptic
meningitis.
Patients with acute or chronic myocarditis may present with chest discomfort, fever, palpitations, easy
fatigability, or syncope/near syncope.
Cardiac findings include overactive precordial impulse, gallop rhythm, and an apical systolic murmur of
mitral insufficiency.
Hepatic enlargement, peripheral edema, and pulmonary findings such as wheezes or rales may be present in
patients with decompensated heart failure
Diagnosis:
Cardiac MRI is a standard imaging modality for the diagnosis of myocarditis; information on the presence and extent
of edema, gadolinium-enhanced hyperemic capillary leak, myocyte necrosis, left ventricular dysfunction, and
evidence of an associated pericardial effusion assist in the cardiac MRI diagnosis of myocarditis
Treatment:
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use of inotropic agents, preferably milrinone, should be entertained but used with caution because of their
proarrhythmic potential.
Diuretics are often required as well.
angiotensin-converting enzyme inhibitors, and
Angiotensin receptor blockers
In patients manifesting with significant atrial or ventricular arrhythmias, specific antiarrhythmic agents (for
example, amiodarone) should be administered and implantable cardioverter defibrillator placement
considered.
SYSTEMIC LUPUS ERYTHEMATOUS
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by multisystem inflammation
and the presence of circulating autoantibodies directed against self-antigens. SLE occurs in both children and adults,
disproportionately affecting females of reproductive age. Although nearly every organ may be affected, most
commonly involved are the skin, joints, kidneys, blood-forming cells, blood vessels, and the central nervous system
Aetiology:
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Genetic
Environnmental factors: Epstein Barr virus
Clinical manifestations:
The presence of 4 features establishes SLE
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Constitutional Fatigue, anorexia, weight loss, fever, lymphadenopathy
Musculoskeletal Arthritis, myositis, tendonitis, arthralgias, myalgias, avascular necrosis, osteoporosis
Skin Malar rash, discoid (annular) rash, photosensitive rash, cutaneous vasculitis, livedo reticularis,
periungual capillary abnormalities, Raynaud phenomenon, alopecia, oral and nasal ulcers, panniculitis,
chilblains, alopecia
Renal Hypertension, proteinuria, hematuria, edema, nephrotic syndrome, renal failure
Cardiovascular Pericarditis, myocarditis, conduction system abnormalities, Libman-Sacks endocarditis
Neurologic Seizures, psychosis, cerebritis, stroke, transverse myelitis, depression, cognitive impairment,
headaches, migraines, pseudotumor, peripheral neuropathy
Pulmonary Pleuritis, interstitial lung disease, pulmonary haemorrhage, pulmonary hypertension, pulmonary
embolism
Hematologic Immune-mediated cytopenia (hemolytic anemia, thrombocytopenia or leukopenia), anemia of
chronic inflammation, hypercoagulability, thrombocytopenic thrombotic microangiopathy
Gastroenterology Hepatosplenomegaly, pancreatitis, vasculitis affecting bowel, protein-losing
enteropathy,peritonitis
Ocular Retinal vasculitis, scleritis, episcleritis, papilledema, dry eyes, optic neuritis
Diagnosis
Laboratory findings: A positive ANA test result is present in 95-99% of individuals with SLE along with direct Coombs
positivity.
Treatment:
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Hydroxychloroquine (5-7 mg/kg/day up to 400 mg/day) is recommended for all individuals with SLE if
tolerated.
In addition to treating mild SLE manifestations such as rash and mild arthritis, hydroxychloroquine prevents
SLE flares
Corticosteroids are a mainstay for treatment of significant manifestations of SLE and work quickly to improve
acute deterioration
Steroid-sparing immunosuppressive agents often used in the treatment of pediatric SLE include
methotrexate
Infections commonly complicate SLE, so routine immunization is recommended, as well as annual influenza
vaccination and administration of the 23-valent pneumococcal vaccine
JUVENILE IDIOPATHIC ARTHRITIS:
The most common rheumatic disease in children and one of the more common chronic illnesses of childhood.
JIA is an autoimmune disease associated with alterations in both humoral and cell-mediated immunity. T
lymphocytes have a central role, releasing proinflammatory cytokines favouring a type 1 helper T-lymphocyte
response.
Criteria for classification of JIR
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Age at onset: <16 yr.
Arthritis (swelling or effusion, or the presence of 2 or more of the following signs: limitation of range of
motion, tenderness or pain on motion, increased heat) in ≥1 joint
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Duration of disease: ≥6 wk.
Onset type defined by type of articular involvement in the 1st 6 mo.
after onset:
Polyarthritis: ≥5 inflamed joints
Oligoarthritis: ≤4 inflamed joints
Systemic-onset disease: arthritis with rash and a characteristic quotidian fever
Exclusion of other forms of juvenile arthritis
Clinical Manifestations:
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Morning stiffness with a limp or gelling after inactivity.
Easy fatigability and poor sleep quality may be associated.
Involved joints are often swollen, warm to touch, and painful on movement or palpation with reduced range
of motion, but usually are not erythematous.
Arthritis in large joints, especially knees, initially accelerates linear growth and causes the affected limb to be
longer, resulting in a discrepancy in limb lengths.
Continued inflammation stimulates rapid and premature closure of the growth plate, resulting in shortened
bones.
Treatment:
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NSAIDS
disease-modifying antirheumatic drugs (DMARDs),
methotrexate,
TNF inhibitors.
REACTIVE ARTHRITIS:
Reactive and postinfectious arthritis are defined as joint inflammation caused by a sterile inflammatory reaction
following a recent infection. We use reactive arthritis to refer to arthritis that occurs following enteropathic or
urogenital infections and postinfectious arthritis to describe arthritis that occurs after infectious illnesses not
classically considered in the reactive arthritis group, such as infection with group A streptococcus or viruses.
Pathogenesis:
Reactive arthritis typically follows enteric infection with Salmonella sp., Shigella flexneri, Yersinia enterocolitica,
Campylobacter jejuni, or genitourinary tract infection with Chlamydia trachomatis
Clinical manifestations:
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The classic triad of arthritis, urethritis, and conjunctivitis is relatively uncommon in children.
The arthritis is typically oligoarticular, with a predilection for lower extremities.
Dactylitis may occur, and enthesitis is common (affects as many as 90% of patients.
Cutaneous manifestations can occur and may include circinate balanitis, ulcerative vulvitis, oral lesions,
erythema nodosum, and keratoderma blennorrhagica, which is similar in appearance to pustular psoriasis
Systemic symptoms may include fever, malaise, and fatigue
Treatment:
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NSAIDS
In articular steroid injections
Penicillin prophylaxis
BLOOD SYSTEM
Anemia: Reduction of the hemoglobin concentration or RBC volume. Normal: 12-15mg/dl, 4.5-6 million/microL,
<45% hematocrit
Physiologic adjustments: Increased cardia output, increased 2,3 BPG, blood flow more to vital organ, right shift of O2
curve
Types:
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Hemopoetic
Hemolytic
Hemorrhagic
Mechanism:
Anemia due to RBC size: MCV- mean corpuscular volume; average volume of RBCs
Anemia by colour of RBC: MCHC- mean corpuscular hemoglobin concentration; average concentration of
hemoglobin in RBC. G/dL
MCH- Mean corpuscular hemoglobin; average weight of hemoglobin in RBC. g/dL. At birth 31-37, Adults 26-34.
Reticulocyte count: immature RBCs, gives indication on the level of bone marrow activity. At birth 1.8 to 8%, Adults
1 to 2%.
• Hypo-regeneration, norm-regeneration, hyper-regeneration
Red cell distribution width: measure of the variation in red blood cell size. 11.5 to 14.5%. >14,5% increased variation
in size; anisocytosis.
● increased lymphocytes - viral infection
● increased leukocytes - bacterial infection
● increased eosinophils - allergy or parasite
●promyelocytes + blast cells - leukaemia
● leucocytosis + immature cells (metamye) - left shift
● increased leukocytes in baby is normal
●increased reticulocytes - adequate
● reduced reticulocytes – inadequate
● increased MCV - macrocytic
● reduced MCV - microcytic
● increased MCHC - hyperchromic
● reduced MCHC - hypochromic
IRON DEFICIENCY ANEMIA
• Common nutritional disorder
• Hypochromic, microcytic anemia
Etiology:
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Early cord clamping
Blood loss – adolescents
Chronic bleeding – peptic ulcer, hemangioma, IBD, whole cow’s milk protein
Infection – hookworm, plasmodium, H. pylori
Clinical manifestations:
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Pallor – not visible until Hb drops below 7g/dl,
Palms, palmar creases, nail beds, conjunctiva
Irritability, anorexia, lethargy
Systolic flow murmurs – cardiac compensation
Impaired neurocognitive function in infancy
Pagophagia- ingest ice, Pica- ingest non-nutritive substances
Lab findings:
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Reduced serum ferritin
Decreased MCV and MCH – microcytosis, hypochromic
Differential diagnosis:
Alpha or beta thalassemia, Lead poisoning,
Treatment:
Oral administration of ferrous salts
Prevention:
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Breastfeeding with iron supplements at 4 months of age
Iron fortified infant formula
Excessive intake of cow’s milk should be limited
THALASSEMIA SYNDROMES
• Genetic disorder of globin chain production
• Imbalance between alpha and beta globin chains
• In Beta thalassemia – decrease in beta globin chains, relative excess of alpha globin chains. Same vice versa
• Thalassemia syndrome requires mutation in both beta globin genes
• Carriers with single globin mutation are generally asymptomatic or microcytosis with mild anemia
Epidemiology:
o >200 different mutations, only 3% of world population carry allele for beta thalassemia, 5 to 10% alpha (southeast
Asia)
Pathophysiology:
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Inadequate beta globin gene production → decreased normal HbA and imbalance between alpha and beta
production. Alpha chains in excess → free alpha chains are unstable → precipitate in red cell precursor →
damage the membrane → short life span of RBC →anemia → increased erythroid production
In alpha thalassemia →excess of beta and gamma are produced → excess makes barts hemoglobin
(4xgamma chains) → very high oxygen affinity → cause extravascular hemolysis
If no alpha chain production at all → severe alpha thalassemia → Hydrops Fetalis
Clinical manifestation:
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Weakness, cardiac decompensation in 2nd 6 months of life
Growth failure, bone deformities, hepatosplenomegaly
Thalassemia face; maxillary hyperplasia, flat nasal bridge, frontal bossing
Cachexia
Lab findings:
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Microcytic, hypochromic
Anisopoikilocytosis, reticulocytopenia – hypo regenerative
Elevated unconjugated serum bilirubin
Bone marrow hyperplasia in radiographs
Diagnosis:
New born screening, DNA diagnosis for Beta thalassemia mutation
Management:
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Transfusion therapy
Iron overload monitoring
Chelation therapy
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Hematopoietic stem cell transplant
Complications:
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Secondary hemosiderosis induced organ injury
Iron deposition in endocrine system → hypothyroidism, growth hormone deficiency, diabetes mellitus
MICROCYTIC ANEMIA
FOLIC ACID DEFICIENCY ANEMIA
• Biologically active folates serve in biosynthetic pathways
• Folates must be reduced to tetrahydrofolates by dihydrofolate reductase
• Tetrahydrofolates are required in DNA replication and proliferation
• Sources: green vegetables, fruits, animal organ- liver, goat milk
• Cause megaloblastic anemia
Etiology:
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Inadequate intake – malnutrition
Decreased absorption – diarrhea, celiac disease, enteritis, drugs- phenytoin
Congenital – Hereditary folate malabsorption, autosomal recessive
Clinical manifestation:
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Anemia- pallor, irritability, chronic diarrhea, poor weight gain
Cognitive delays
Thrombocytopenia - hemorrhages
Lab findings:
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Macrocytic RBCs, variation in RBC shape and size
Increased lactate dehydrogenase
Hyper segmented neutrophils
Bone marrow hyperplasia – hyper regenerative
Treatment:
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Oral / parenteral administration of folic acid. 1mg/day
Transfusion only when severe anemia
VITAMIN B12 DEFICIENCY ANEMIA
• Biologically active, water soluble vitamin
• Needed in methylation of homocysteine to methionine and conversion of malonyl CoA to Succinyl CoA
• These products are needed in protein synthesis, DNA and RNA
• Sources: meat, milk, fish, eggs
Etiology:
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Inadequate intake – breast milk of B12 deficient mothers
Impaired absorption – decreased gastric secretion, pancreatic insufficiency, celiac disease
Congenital – Hereditary intrinsic factor deficiency
Absence of Vit B12 transporter protein
Inborn error of cobalamin metabolism – enzyme deficiencies
Clinical manifestation:
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Weakness, lethargy, irritability, failure to thrive
Pallor, glossitis, icterus, vomiting, diarrhea
Neurological symptoms – hypotonia, seizures, development delay, paresthesia
Lab findings:
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Macrocytic RBCs, hyper segmented neutrophils
Neutropenia & thrombocytopenia – simulate Leukemia
Increased serum lactate degehydrogenase
Homocysteinuria, homocysteinemia, and methylmalonic acid in blood
Increased serum bilirubin
Treatment:
Supplements 1-3 micrograms/day
HENOCH-SCHONLEIN PURPURA – VASCULITIS
• Most common cause of non-thrombocytopenic purpura in children
• Vasculitis caused due to the deposition of IgA immunoglobulins in small vessels of joints, skin, GI tract and kidneys
• Called “anaphalactoid purpura”
Epidemiology:
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Affect males more than females
90% cases occur in children aged 3-10 years
More common in winter and spring – more viral upper respiratory tract infections
Etiology:
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URI, mycoplasma, TB, rubella, measles, streptococcus, adenovirus
Cold exposure, food sensitivity, drugs: vancomycin, diclofenac
Clinical manifestation:
Classic tetrad: Palpable purpura, arthritis/arthralgia, abdominal pain, renal disease
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Rash – start with pink maculopapules → to petechiae → palpable purpura
Symmetrical distribution, mostly in lower extremities
Subcutaneous localized edema – periorbital, dorsum of hand & feet, lips, scrotum
Joints – knees and ankles, serous effusion
GI Tract – mild → nausea, vomiting, pain. Severe → Hemorrhage, bowel necrosis
Occult heam positive stools, diarrhea, hematemesis
Renal – hematuria, proteinuria, nephrotic syndrome
CNS – Seizures, CNS hemorrhage
Others – lymphadenopathy, hepatosplenomegaly, carditis, pulmonary hemorrhage
Diagnosis:
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Elevated IgA (50-70%)
C-reactive protein
Leukocytosis, elevated ESR
Treatment:
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Steroids
Supportive care for mild and self-limited HSP
Hydration, nutrition, analgesia
Complications:
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Renal disease
Prognosis:
Excellent
Last average of 4 weeks, symptoms are milder with each relapse
Renal disease occurs only in 1-2% of children
IDIOPATHIC (AUTOIMMUNE) THROMBOCYTOPENIC PURPURA
• Most common cause of acute onset thrombocytopenia in otherwise well children
Epidemiology:
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1-4 weeks after exposure to common viral infections
Peak age 1-4 years
Males and females equally affected
Other infections include H. pylori, HIV, hepatitis
Pathogenesis:
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Auto-immune Thrombocytopenia → antibodies against platelet glycoprotein complexes → circulating
antibody coated platelets are recognized by the fc receptors of splenic macrophages → ingested &
destroyed
Most common is EB virus
More often in winter and spring – viral respiratory illnesses
Clinical manifestation:
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Sudden onset/ happens overnight → generalized petichiae and purpura
Bleeding from gums and mucous membranes
Lab findings:
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Platelet count <20x109/L
Hemoglobin may be decreased due to nose bleeds
Increased number of megakaryocytes
Differential Diagnosis:
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Induced drug dependent antibodies
Splenic sequestration
Congenital thrombocytopenia syndrome
Treatment:
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For mild cases – education and counselling
Intravenous immunoglobulins
Can cause headache and vomiting
Corticosteroids – Prednisone
Intravenous anti-D therapy
HEMOPHILIA A OR B
Most common severe inherited bleeding disorder
Deficiency of factor 8 (A) or factor 9 (B)
Pathogenesis:
These factors participate in the complex required for the activation of Factor 10 → activated factor 10 converts
prothrombin into thrombin → inadequate thrombin production leads to failure to make crosslinking fibrin clot
→delayed formation of blood clot after injury.
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Severe Hemophilia - <1% activity of clotting factors – spontaneous bleeding
Moderate Hemophilia - 1 to 5% activity – require mild trauma to induce bleeding
Mild Hemophilia - >5 to 25% activity – significant trauma to cause bleeding
Hemostatic levels – factor 8; >30 to 40%. Factor 9; >25 to 30%
Clinical manifestation:
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Easy bruising, intramuscular hematoma, hemarthroses – ankle, knees and elbows
Bleeding into the iliopsoas muscle(macular Hematoma) → hypovolemic shock →inability to extend the hip
Lab findings and diagnosis:
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Approx. 3 times longer PTT
Specific assay for factors 8 or 9
Platelet count & prothrombin time are normal
Differential Diagnosis:
Thrombocytopenia, von willebrand disease
Treatment:
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Transfusion of clotting factor
For mild to moderate cases factor 8 or 9 must be raised to hemostatic level; 35%
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For life threatening major hemorrhages must be raised to 100% activity
Desmopressin acetate – release endogenously produced factor 8
HEMOPHILIA C – FACTOR 11 DEFICIENCY
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Autosomal deficiency, cause mild to moderate bleeding symptoms
Frequently in Ashkenazi Jews
May have minimal symptoms during surgery
Oral cavity bleeding is the most common, dental extractions
Longer PTT
No factor 11 concentrate is available so Fresh frozen plasma needs to be given
Frequent infusions of plasma would be necessary to achieve higher levels
Half-life is >48hrs, therefore maintaining level is not difficult
Chronic joint bleeding might occurs in the presence of von willibrand disease
ACUTE LYMPHOBLASTIC LEUKEMIA
Epidemiology:
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Peak incidence at 2 to 3 years of age
More in boys than girls
More common in children with chromosomal abnormalities
Etiology:
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It’s unknown
Genetic and environmental factor associated with childhood leukemia
Morphology:
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Malignant cells in bone marrow
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85% cases → B lymphoblastic leukemia. 15% → T lymphoblastic leukemia. 1% → mature B cell
leukemia(Burkitt)
PCR → detect small amount of malignant cells → Minimal Residue Disease
Clinical Manifestation:
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Anorexia, fatigue, malaise, irritability
Low grade fever, bone/joint pain – lower extremities → pain wakes patient a night
Bone marrow failure, pallor, fatigue, bruising
Lymphadenopathy, hepatosplenomegaly, testicular enlargement
CNS – cranial neuropathies, headaches, seizures
Respiratory failure due to anemia
Blast cells in CSF
Diagnosis:
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Total leukocyte count <10000/microL
Bone marrow examination - >25% lymphoblasts
If lymphoblast present and CSF leukocyte count increase → meningeal leukemia
Elevation of lactate dehydrogenase
Treatment:
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Chemotherapy
Initial therapy – remission induction → eradicate the leukemic cells from the bone marrow
Prednisone
Remission is when there is less than <5% blast cells
Second phase – consolidation → intensive CNS therapy
Intrathecal chemotherapy given repeatedly by lumbar puncture
Delayed Intensification → phase of aggressive treatment
Maintenance → 2 to 3 years. Daily mercaptopurine and weekly oral methotrexate
Intermittent doses of corticosteroids
Treatment of relapse:
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Intensive chemotherapy with agents not used before
Stem cell transplantation
Supportive care:
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Antimicrobial therapy for sepsis (neutropenia)
Allopurinol for increased uric acid produced
Erythrocyte and platelet transfusion because chemotherapy cause myelosuppression
Prognosis:
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Improvement in therapy → 5yr survival around 90% cases
There could be chronic medical conditions → cardia, musculoskeletal, neurologic conditions
PYLORIC STENOSIS
Pyloric stenosis is a narrowing of the opening from the stomach to the first part of the small intestine (the pylorus)
Clinical manifestations:
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Nonbilious vomiting is the initial symptom of pyloric stenosis. The vomiting may or may not be projectile
initially but is usually progressive, occurring immediately after a feeding.
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Emesis might follow each feeding, or it may be intermittent.
The vomiting usually starts after 3 wk of age, but symptoms can develop as early as the 1st wk of life and as
late as the 5th months
As vomiting continues, progressive loss of fluid, hydrogen ion, and chloride leads to hypochloremic
metabolic alkalosis.
Hyperbilirubinemia is the most common clinical association of pyloric stenosis, also known as icteropyloric
syndrome
eosinophilic gastroenteritis
hiatal hernia
Diagnosis:
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Palpating the pyloric mass.
The mass is firm, movable, approximately 2 cm in length, olive shaped, hard, best palpated from the left
side, and located above and to the right of the umbilicus in the mid epigastrium beneath the liver’s edge.
The olive is easiest palpated after an episode of vomiting. After feeding, there may be a visible gastric
peristaltic wave that progresses across the abdomen
Elongated pyloric channel (string sign),
a bulge of the pyloric muscle into the antrum (shoulder sign), and parallel streaks of barium seen in the
narrowed channel, producing a “double tract sign”
Treatment:
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The preoperative treatment is directed toward correcting the fluid, acid–base, and electrolyte losses.
Correction of the alkalosis is essential to prevent postoperative apnea, which may be associated with
anesthesia.
Most infants can be successfully rehydrated within 24 hr.
Vomiting usually stops when the stomach is empty, and only an occasional infant requires nasogastric
suction.
The surgical procedure of choice is pyloromyotomy
GASTROESOPHAGEAL REFLUX DISEASE [GERD]
Gastroesophageal reflux (GER) signifies the retrograde movement of gastric contents across the lower esophageal
sphincter (LES) into the esophagus
Transient LES relaxation (TLESR) is the primary mechanism allowing reflux to occur, and is defined as simultaneous
relaxation of both LES and the surrounding crura.
Clinical manifestations:
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Infantile reflux manifests more often with regurgitation (especially postprandially), signs of esophagitis
(irritability, arching, choking, gagging, feeding aversion), Sandefer syndrome and resulting failure to thrive;
symptoms resolve spontaneously in the majority of infants by 12-24 mo.
GERD in infants can manifest as obstructive apnea or as stridor or lower airway disease in which reflux
complicates primary airway disease such as laryngomalacia or bronchopulmonary dysplasia.
Diagnosis:
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Contrast (usually barium) radiographic study of the esophagus and upper gastrointestinal tract
Extended esophageal pH monitoring of the distal esophagus
Endoscopy
intraluminal impedance
Laryngotracheobronchoscopy
Treatment:
A combination of
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Modified feeding volumes,
Thickening of feed
Hydrolyzed infant formulas,
Proper positioning, and
Avoidance of smoke exposure satisfactorily improve GERD symptoms in 24-59% infants with GERD
Antacids
PPIs
Prokinetic agents
DEHYDRATION:
PEPTIC ULCER DISEASE
Peptic ulcer disease, the end result of inflammation caused by an imbalance between cytoprotective and cytotoxic
factors in the stomach and duodenum, manifests with varying degrees of gastritis or frank ulceration.
Deep mucosal lesions that disrupt the muscularis mucosa of the gastric or duodenal wall define peptic ulcers. Gastric
ulcers are generally located on the lesser curvature of the stomach, and 90% of duodenal ulcers are found in the
duodenal bulb.
Primary ulcers are most often associated with Helicobacter pylori infection
Secondary peptic ulcers can result from stress caused by sepsis, shock, or an intracranial lesion (Cushing ulcer), or in
response to a severe burn injury (Curling ulcer) or result of using aspirin or nonsteroidal anti-inflammatory drugs
(NSAIDs)
Pathogenesis:
Acid secretion: By 3-4 yr. of age, gastric acid secretion approximates adult values. Excessive acid secretion is
associated with a large parietal cell mass, hypersecretion by antral G cells, and increased vagal tone, resulting in
increased or sustained acid secretion in response to meals
Mucosal defence: A continuous layer of mucous gel that serves as a diffusion barrier to hydrogen ions and other
chemicals covers the gastrointestinal (GI) mucosa.
Clinical Manifestations:
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Hematemesis
Melena
nausea
Dyspepsia
epigastric abdominal pain or fullness
feeding difficulty,
vomiting,
crying episodes
Diagnosis:
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Esophagogastroduodenoscopy
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Endoscopy
Treatment:
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Amoxicillin
Clarithromycin
Proton pump inhibitor
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Amoxicillin
Metronidazole
Proton pump inhibitor
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Clarithromycin
Metronidazole
Proton pump inhibitor
H2 receptor antagonists
Cytoprotective agents
or
or
For pylori ulcer: Antibiotics and Bismuth salts + PPI
ACUTE GASTROENTERITIS:
The term gastroenteritis denotes infections of the gastrointestinal tract caused by bacterial, viral, or parasitic
pathogens. Many of these infections are foodborne illnesses.
Pathogenesis and severity of bacterial disease depend on whether organisms have preformed toxins (S. aureus,
Bacillus cereus), produce secretory (cholera, E. coli, Salmonella, Shigella) or cytotoxic (Shigella, S. aureus, Vibrio
parahaemolyticus, C. difficile, E. coli, C. jejuni) toxins, or are invasive, and on whether they replicate in food.
Enteropathogens can lead to either an inflammatory or noninflammatory response in the intestinal mucosa
Pathogenesis:
Enteropathogens elicit noninflammatory diarrhea through enterotoxin production by some bacteria, destruction of
villus (surface) cells by viruses, adherence by parasites, and adherence and/or translocation by bacteria.
Inflammatory diarrhea is usually caused by bacteria that directly invade the intestine or produce cytotoxins with
consequent fluid, protein, and cells (erythrocytes, leukocytes) that enter the intestinal lumen.
Diagnosis:
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Clinical evaluation of diarrhea
Stool examination
Treatment:
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Oral rehydration therapy
Enteric feeding
Proper diet selection
Zinc supplementation
Antibiotic therapy
DIARRHEA
WHO plan A
WHO plan B
WHO plan C
PROTENURIA
While a small amount of protein is normally present in the urine, proteinuria greater than 100 mg/m2/day or an
elevated urine total protein/creatinine ratio are considered pathologic.
Detection
1. Urinary dipstick is the most frequently used method of screening for proteinuria and detects variable levels of
albuminuria.
a. False positives may result if the urine is very concentrated or if the patient has received certain medications (e.g.,
penicillin, aspirin, IV contrast imaging agents, oral hypoglycemic agents).
b. False negatives may result if the urine is very dilute.
2. Twenty-four–hour urinary protein collection (normal is <100 mg/m2 /day) is the most accurate method of
detecting proteinuria but is very difficult to obtain in children. Instead, a random spot urine total protein-tocreatinine ratio (TP/CR) is usually performed. An early morning sample correlates well with 24-hour urinary protein
excretion.
a. Normal urine TP/CR for infants of age 6–24 months is <0.5.
b. Normal urine TP/CR for children of age >2 years is <0.2.
Epidemiology.
Up to 10% of children have a single positive dipstick test for proteinuria at some point; however, <1% have
persistent proteinuria on repeated dipstick evaluations.
Classification
1. Benign transient proteinuria.
Increased urinary protein excretion may sometimes be associated with vigorous exercise, fever, dehydration, and
congestive heart failure (CHF).
2. Orthostatic proteinuria
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Certain children and adults (especially athletic individuals) have increased urinary protein excretion while
upright but not while supine.
Orthostatic proteinuria is usually a benign condition, and its confirmation eliminates the need for further
workup.
The presence of orthostatic proteinuria is diagnosed with an elevated afternoon urine TP/CR and a normal
first morning urine TP/CR.
3. Persistent pathologic proteinuria
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Persistent pathologic proteinuria may be associated with significant renal disease and is considered a marker
for progression of renal disease.
Generally, the greater the magnitude of the proteinuria, the more serious the renal disease. The greatest
amounts of proteinuria are seen in patients with nephrotic syndrome .
Persistent pathologic proteinuria may have a glomerular origin or a tubular origin. Glomerular proteinuria is
more common.
1. Glomerular proteinuria is caused by increased permeability of the glomerular capillaries to large molecular
weight proteins, as seen in glomerulonephritis and in minimal change nephrotic syndrome.
2. Tubular proteinuria results from decreased reabsorption of low molecular weight proteins by the tubular
epithelial cells, or by the addition of inflammatory proteins to the tubular urine.
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Examples of tubular proteinuria include interstitial nephritis, ischemic renal injury (acute tubular necrosis,
acute kidney injury [AKI]), and tubular damage resulting from nephrotoxic drugs.
Laboratory findings include elevated levels of urinary β2 microglobulin,a good marker for tubular
proteinuria among others.
This small molecule, which is freely filtered at the glomerulus, is normally almost completely reabsorbed by
the tubular epithelial cells. Its presence therefore signifies tubular injury.
Glucosuria and aminoaciduria may also accompany diffuse injury to the tubular epithelial cells.
HAEMATURIA:
Hematuria is defined as the presence of at least 5 red blood cells (RBCs) per microliter of urine and occurs with a
prevalence of 0.5-2.0% among school-age children
Gross hematuria is when a person can see the blood in his or her urine, and microscopic hematuria is when a person
cannot see the blood in his or her urine, yet a health care professional can see it under a microscope.
Upper urinary tract sources of hematuria originate within the nephron (glomerulus, tubular system, or interstitium).
Lower urinary tract sources of hematuria originate from the pelvocaliceal system, ureter, bladder, or urethra
Etiology:
1.
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2.
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3.
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4.
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HEME POSITIVE
Hemoglobin
Myoglobin
HEME NEGATIVE: Drugs
Chloroquine
Deferoxamine
Ibuprofen
Iron sorbitol
Metronidazole
Nitrofurantoin
Phenazopyridine (Pyridium)
Phenolphthalein
Phenothiazines
Rifampin
Salicylates
Sulfasalazine
Dyes (Vegetable/Fruit)
Beets
Blackberries
Food and candy colouring
Rhubarb
Metabolites
Homogentisic acid
Melanin
Methaemoglobin
Porphyrin
Tyrosinosis
Urates
Clinical manifestations:
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Tea- or cola-coloured urine, facial or body edema, hypertension, and oliguria are classic symptoms of
glomerulonephritis
Recurrent episodes of gross hematuria suggest IgA nephropathy, Alport syndrome, or thin glomerular
basement
membrane disease
Hematuria associated with headache, mental status changes, visual changes (diplopia), epistaxis, or heart
failure suggests significant hypertension
Frequency, dysuria, and unexplained fevers suggest a urinary tract infection, whereas renal colic suggests
nephrolithiasis
•
A complete physical examination is critical to assess the cause of hematuria
Common causes of gross Haematuria:
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Urinary tract infection
Meatal stenosis
Perineal irritation
Trauma
Urolithiasis
Hypercalciuria
Coagulopathy
Tumour
Glomerular
Postinfectious glomerulonephritis
ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
Group A β-hemolytic streptococcal infections are common in children and can lead to the postinfectious
complication of acute glomerulonephritis (GN). Acute poststreptococcal glomerulonephritis (APSGN) is a classic
example of the acute nephritic syndrome characterized by the sudden onset of gross hematuria, edema,
hypertension, and renal insufficiency.
Etiology:
APSGN follows infection of the throat or skin by certain “nephritogenic” strains of group A β-hemolytic streptococci.
Poststreptococcal GN commonly follows streptococcal pharyngitis during cold-weather months and streptococcal
skin infections or pyoderma during warm-weather months.
Pathology and pathogenesis:
Glomeruli appear enlarged and relatively bloodless and show diffuse mesangial cell proliferation, with an increase in
mesangial matrix. Polymorphonuclear leukocyte infiltration is common in glomeruli during the early stage of the
disease.
Morphologic studies and a depression in the serum complement (C3) level provide strong evidence that ASPGN is
mediated by immune complexes
Clinical Manifestations:
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Poststreptococcal GN is most common in children ages 5-12 yr. and uncommon before the age of 3 yr.
The typical patient develops an acute nephritic syndrome 1-2 wk after an antecedent streptococcal
pharyngitis or 3-6 wk after a streptococcal pyoderma
Edema,
hypertension,
Oliguria
Hypertensive encephalopathy→ blurred vision, severe headaches, altered mental status, or new seizures.
Nonspecific symptoms such as malaise, lethargy, abdominal pain, or flank pain are common
Diagnosis:
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Urine Analysis: red blood cells, often in association with red blood cell casts, proteinuria, and
polymorphonuclear leukocytes.
Confirmation of the diagnosis requires clear evidence of a prior streptococcal infection.
Serum C3 level is significantly reduced .C4 is normal or only depressed.
Complication:
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Acute complications result from hypertension and acute renal dysfunction.
Hypertension (60%)→ hypertensive encephalopathy(10%) [severe prolonged hypertension → intracranial
bleeding.]
Heart failure, hyperkalemia, hyperphosphatemia, hypocalcemia, acidosis, seizures, and uremia.
Acute renal failure can require treatment with dialysis
Treatment:
Management is directed at treating the acute effects of renal insufficiency and hypertension
Differences between nephrotic syndrome and glomerulonephritis
NEPHROTIC SYNDROME;
Nephrotic syndrome is the clinical manifestation of glomerular diseases associated with heavy (nephrotic-range)
proteinuria. Nephrotic range proteinuria is defined as proteinuria >3.5 g/24 hr or a urine protein: creatinine ratio >2.
The triad of clinical findings associated with nephrotic syndrome arising from the large urinary losses of protein are
hypoalbuminemia (≤2.5 g/dL), edema, and hyperlipidaemia (cholesterol >200 mg/dL).
Etiology:
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Nephrotic syndrome may also be secondary to systemic diseases such as
systemic lupus erythematosus,
Henoch-Schönlein purpura,
malignancy (lymphoma and leukaemia),
and infections (hepatitis, HIV, and malaria)
α1-Antitrypsin deficiency
Fabry disease
Clinical manifestations:
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Edema
Hypercoagulability
Hyperlipidaemia
Increased susceptibility to infections
In nephrotic syndrome, the glomeruli are affected by an inflammation or a hyalinization (the formation of a
homogenous crystalline material within cells) that allows proteins such as albumin, antithrombin or the
immunoglobulins to pass through the cell membrane and appear in urine.
Albumin is the main protein in the blood that is able to maintain an oncotic pressure, which prevents the leakage of
fluid into the extracellular medium and the subsequent formation of edemas.
As a response to hypoproteinemia the liver commences a compensatory mechanism involving the synthesis of
proteins, such as alpha-2 macroglobulin and lipoproteins.[14] An increase in the latter can cause the hyperlipidemia
associated with this syndrome.
IDIOPATHIC NEPHROTIC SYNDROME:
Approximately 90% of children with nephrotic syndrome have idiopathic nephrotic syndrome. It is associated with
primary glomerular disease without an identifiable causative disease or drug.
Etiology:
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Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Glomerulonephritis associated with nephrotic syndrome–
membranoproliferative glomerulonephritis, crescentic glomerulonephritis, immunoglobulin A nephropathy
In minimal change nephrotic syndrome (MCNS) (approximately 85% of total cases of nephrotic syndrome in
children), the glomeruli appear normal or show a minimal increase in mesangial cells and matrix.
Findings on immunofluorescence microscopy are typically negative, and electron microscopy simply reveals
effacement of the epithelial cell foot processes.
More than 95% of children with minimal change disease respond to corticosteroid therapy
URINARY TRACT INFECTIONS
Etiology & Epidemiology :
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During the 1st yr of life, the male : female ratio is 2.8-5.4 : 1. Beyond 1-2 yr, →male : female ratio of 1 : 10
UTIs are caused primarily by colonic bacteria.
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In girls, 75-90% of all infections are caused by Escherichia coli, followed by Klebsiella spp. and Proteus spp.
Clinical Manifestation & Classification:
3 forms of UTI - pyelonephritis, cystitis, and asymptomatic bacteriuria
Clinical Pyelonephritis
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Most common serious bacterial infection in infants younger than 24 mo of age who have fever without an
obvious focus .
Symptoms: abdominal, back, or flank pain; fever; malaise; nausea; vomiting; and, occasionally, diarrhea.
Fever may be the only manifestation.
Newborns symptoms: such as poor feeding, irritability, jaundice, and weight loss.
Involvement of the renal parenchyma →acute pyelonephritis, no parenchymal involvement→ pyelitis.
Renal abscess can occur following a pyelonephritic infection caused by the usual uropathogens or may be
secondary to infection (Staphylococcus aureus).
Perinephric abscess can occur secondary to contiguous infection in the perirenal area (vertebral
osteomyelitis, psoas abscess) or pyelonephritis that dissects to the renal capsule.
Xanthogranulomatous pyelonephritis is a rare type of renal infection → granulomatous inflammation with
giant cells and foamy histiocytes.
a. Clinical manifest: as a renal mass or an acute or chronic infection.
b. Renal calculi, obstruction, and infection with Proteus spp. or E. coli contribute to the development of
this lesion usually requires total or partial nephrectomy.
Cystitis
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Cystitis indicates that there is bladder involvement
Symptoms: dysuria, urgency, frequency, suprapubic pain, incontinence, and malodorous malodorous urine.
does not cause fever and does not result in renal injury.
Acute hemorrhagic cystitis often is caused by E.coli
Adenovirus cystitis →boys; it is self-limiting, with hematuria lasting approximately 4 days.
Eosinophilic cystitis is a rare form → symptoms -cystitis with hematuria.
a. On imaging: multiple solid bladder masses that consits of eosinophils.
b. Ureteral dilation with hydronephrosis also is common.
c. Cause: exposed to an allergen.
d. Bladder biopsy often is necessary to exclude a neoplastic process.
e. Treatment →antihistamines and nonsteroidal antiinflammatory agents.
Interstitial cystitis → urgency, frequency, and dysuria, and bladder and pelvic pain relieved by voiding with a
negative urine culture.
a. Most likely to affect adolescent girls and is
idiopathic.
b. Diagnosis: cystoscopic observation of mucosal ulcers
with bladder distention.
c. Treatments: bladder hydrodistention and laser
ablation of ulcerated areas, but no treatment
provides sustained relief.
Asymptomatic Bacteriuria
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positive urine culture,no manifestations of infection.
It is most common in girls.
benign and does not cause renal injury, except in pregnant women→ if left untreated, can result in a
symptomatic UTI.
Pathogenesis
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Nearly all UTIs are ascending infections. The bacteria arise from the fecal flora, colonize the perineum, and
enter the bladder via the urethra.
In uncircumcised boys, the bacterial pathogens arise from the flora beneath the prepuce.
In some cases, the bacteria causing cystitis ascend to the kidney to cause pyelonephritis.
Rarely, renal infection occurs by hematogenous spread, as in endocarditis or in some neonates.
Diagnosis
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a urine culture is necessary for confirmation and appropriate therapy
Nitrites and leukocyte esterase usually are positive in infected urine.
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Microscopic hematuria is common in acute cystitis
Pyuria (leukocytes on urine microscopy) suggests infection
Sterile pyuria (positive leukocytes, negative culture) → partially treated bacterial UTIs, viral infections, renal
tuberculosis, renal abscess
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With acute renal infection, leukocytosis, neutrophilia, and elevated serum erythrocyte sedimentation rate,
procalcitonin, and C-reactive protein are common
Treatment
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Acute cystitis: a 3- to 5-day course with trimethoprim-sulfamethoxazole (TMP-SMX) or trimethoprim(E. coli.)
Nitrofurantoin: Klebsiella and Enterobacter organisms
Clinical pyelonephritis: 7-14 day course of broad-spectrum antibiotics + rehydration
Aminoglycosides: Pseudomonas spp + alkalinization of urine with sodium →inc effectiveness
Oral third-generation cephalosporins such as → Gram-negative organisms other than Pseudomonas, →
considered by some authorities to be the treatment of choice for oral outpatient
VESICOURETERAL REFLEX
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Describes the retrograde flow of urine from the bladder to the ureter and kidney.
Occurs when the submucosal tunnel between the mucosa and detrusor muscle is short or absent,
congenital/familial usually.
Can let bacteria enter through ureter easily from bladder to upper urinary tract - predisposes to
pyelonephritis.
Causes renal scarring after infection - reflux nephropathy
Classification
VUR severity is graded using the International Reflux Study Classification of I-V and is based on the appearance of the
urinary tract on a contrast voiding cystourethrogram (VCUG) The higher the VUR grade the greater the likelihood of
renal injury.
Diagnosis
catheterization of the bladder, instillation of a solution containing iodinated contrast or a radiopharmaceutical, and
radiologic imaging of the lower and upper urinary tract: a contrast VCUG or radionuclide cystogram
Treatment
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Therapy revolves around preventing pyelonephritis and renal injury
The risk of recurrent UTI is highest in patients with grade III or IV reflux and those with bowel and bladder
dysfunction
CAN BE CORRECTED WITH SURGERY IF HIGH GRADE - Laparoscopy, inguinal incision surgery, or
endoscopically with subureteral injection.
NEUROLOGICAL EXAMINATION
Development
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Head Circumference→ av rate of head growth inpremature infant is 0.5 cm in the 1st 2 wk, 0.75 cm in the
3rd wk, and 1.0 cm in the 4th wk and every week thereafter until the 40th wk of development.
The head circumference of an average term infant measures 34-35 cm at birth, 44 cm at 6 mo, and 47 cm at
1 yr of age
Newborn reflexes
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Root Reflex→This reflex begins when the corner of the baby's mouth is stroked or touched. The baby will
turn his or her head and open his or her mouth to follow and "root" in the direction of the stroking.-->This
helps the baby find the breast or bottle to begin feeding.
Suck Reflex→Rooting helps the baby become ready to suck. When the roof of the baby's mouth is touched,
the baby will begin to suck.
Tonic Neck Reflex→When a baby's head is turned to one side, the arm on that side stretches out and the
opposite arm bends up at the elbow. This is often called the "fencing" position. This reflex lasts until the
baby is about 5 to 6 months old.
Moro Reflex→The Moro reflex is often called a startle reflex because it usually occurs when a baby is
startled by a loud sound or movement. In response to the sound, the baby throws back his or her head,
extends out the arms and legs, cries, then pulls the arms and legs back in.
Grasp Reflex→Stroking the palm of a baby's hand causes the baby to close his or her fingers in a grasp. The
grasp reflex lasts until the baby is about 5 to 6 months old.
Babinski Reflex→When the sole of the foot is firmly stroked, the big toe bends back toward the top of the
foot and the other toes fan out. This normal reflex lasts until the child is about 2 years of age.
Step Reflex→This reflex is also called the walking or dance reflex because a baby appears to take steps or
dance when held upright with his or her feet touching a solid surface. This reflex lasts about two months.
SEIZURES
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Seizure is a transient occurrence of signs and/or symptoms resulting from abnormal excessive or
synchronous neuronal activity in the brain
Classification →2 large categories:
a. In focal (formerly known as partial): initial activation of a system of neurons limited to part of 1
cerebral hemisphere.
b. Simple partial seizures: focal seizures with no alteration in consciousness.
c. complex partial seizures (focal dyscognitive): focal seizures with altered awareness of the
surroundings.
d. In generalized seizures: synchronous involvement of all of both hemispheres
An unprovoked seizure is one that is not an acute symptomatic seizure.
Remote symptomatic seizure: secondary to a distant brain injury, such as an old stroke.
Reflex seizures: sensory stimulus such as flashing lights
Epileptic syndrome is a disorder that manifests 1 or more specific seizure types and has a specific age of
onset and a specific prognosis.
Epileptic encephalopathy is an epilepsy syndrome: result in cognitive and other impairments in the patient.
An absence seizure causes you to blank out or stare into space for a few seconds. They can also be called
petit mal seizures
Evaluation of first seizure
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Assessment of the adequacy of the airway, ventilation, and cardiac function, as well as measurement of
temperature, blood pressure, and glucose concentration
determine whether the seizure has a focal onset or is generalized.
a. Focal seizures → include forceful turning of the head and eyes to 1 side, unilateral clonic
movements beginning in the face or extremities, or a sensory disturbance, such as paresthesias or
pain localized to a specific area.
Focal and generalized motor seizures may be tonic–clonic, tonic, clonic, myoclonic, or atonic.
a. Tonic: increased tone or rigidity
b. Atonic seizures: flaccidity or lack of movement during a convulsion.
c. Clonic seizures: rhythmic fast muscle contractions and slightly longer relaxations
d. Myoclonus: “shock-like” contraction of a muscle of <50 msec that is often repeated.
The duration of the seizure and state of consciousness (retained or impaired) should be documented.
The eyegrounds must be examined for the presence of papilledema, optic neuritis, retinal hemorrhages,
uveitis, chorioretinitis, coloboma, or macular changes, as well as retinal phakoma.
Febrile Seizures
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Occur between the age of 6 and 60 mo with a temperature of 38°C or higher
simple febrile seizure is a primary generalized, usually tonic–clonic, attack associated with fever, lasting for a
maximum of 15 min, and not recurrent within a 24-hr period.
A complex febrile seizure is more prolonged (>15 min), is focal, and/or reoccurs within 24 hr.
Febrile status epilepticus is a febrile seizure lasting longer than 30 min.
Risk factors
Evaluation
Febrile seizures causative agents may be otitis media, roseola and human herpesvirus (HHV) 6 infection, shigella
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Lumbar puncture
A lumbar puncture is an option in a child 6-12 mo of age who is deficient in Haemophilus influenzae type b and
Streptococcus pneumoniae immunizations or for whom immunization status is unknown & during administration of
antibiotics
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Electroencephalogram
if the patient does not recover immediately from a seizure, then an EEG can help distinguish between ongoing
seizure activity and a prolonged postictal period, sometimes termed a nonepileptic twilight state
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Blood Studies
Blood studies not routinely recommended
Blood glucose should be determined
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Neuroimaging
A CT or MRI is not recommended in evaluating the child after a first simple febrile seizure
Treatment
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If the seizure lasts for longer than 5 min, acute treatment with diazepam, lorazepam, or midazolam
Intravenous benzodiazepines, phenobarbital, phenytoin, or valproate may be needed in the case of febrile
status epilepticus
ACUTE BACTERIAL MENINGITIS
Etiology
Streptococcus pneumoniae and Neisseria meningitidis
Clinical Manifestations
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The onset of acute meningitis has 2 predominant patterns.
a. Common: Preceded by several days of fever, nausea and vomiting ,headaches and increasing
lethargy and irritability
b. Rare: sudden onset with rapidly progressive manifestations of shock, purpura, disseminated
intravascular coagulation, and reduced levels of consciousness → coma or death within 24 hr.
Nonspecific findings: fever,poor feeding, headache, petechiae, purpura, or an erythematous macular rash.
Meningeal irritation: nuchal rigidity, back pain, Kernig sign (flexion of the hip 90 degrees with subsequent
pain with extension of the leg), and Brudzinski sign (involuntary flexion of the knees and hips after passive
flexion of the neck while supine).
a. In children, particularly in those younger than 12-18 mo, Kernig and Brudzinski signs are not
consistently present
ICP is suggested by headache, emesis, bulging fontanel, widening of the sutures, oculomotor or abducens
nerve paralysis, hypertension with bradycardia, apnea or hyperventilation, decorticate or decerebrate
posturing, stupor, coma, or signs of herniation.
Seizures that persist after the 4th day of illness and those that are difficult to treat may be associated with a
poor prognosis.
Alterations of mental status: consequence of increased ICP, cerebritis, or hypotension
Diagnosis
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Confirmed by analysis of the CSF: microorganisms on Gram stain and culture, a neutrophilic pleocytosis,
elevated protein, and reduced glucose concentrations
Contraindications of CSF analysis:
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a. evidence of increased ICP → 3rd or 6th cranial nerve palsy with a depressed level of consciousness,
or hypertension and bradycardia with respiratory abnormalities
b. severe cardiopulmonary compromise requiring prompt resuscitative measures for
c. infection of the skin overlying the site of the LP
Blood cultures should be performed in all patients with suspected meningitis. Blood cultures reveal the
responsible bacteria in up to 80-90% of cases of meningitis
Treatment
A child with rapidly progressing disease of less than 24 hr duration, in the absence of increased ICP, should receive
antibiotics as soon as possible after an LP is performed
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S. pneumoniae: vancomycin
S. pneumoniae, N. meningitidis, and H. influenzae type b: cefotaxime or ceftriaxone
Patients allergic to β-lactam antibiotics and >1 mo of age: chloramphenicol
allergy to β-lactam: vancomycin + rifampin.
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Escherichia coli or P. aeruginosa: third-generation cephalosporin
a. E. coli: cefotaxime or ceftriaxone,
b. P. aeruginosa: ceftazidime
Side effects of antibiotic therapy of meningitis include phlebitis, drug fever, rash, emesis, oral candidiasis, and
diarrhea. Ceftriaxone may cause reversible gallbladder pseudolithiasis, detectable by abdominal ultrasonography.
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Rapid killing of bacteria releases cell wall endotoxin that precipitate the cytokine-mediated inflammatory
cascade. → dexamethasone (corticosteroid)
Complications
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seizures, increased ICP, cranial nerve palsies, stroke, cerebral or cerebellar herniation, and thrombosis of the
dural venous sinuses.
Subdural effusions are especially common in infants
Pericarditis or arthritis may occur in patients being treated for meningitis, especially that caused by N.
meningitidis.
Difference between bacterial and viral meningitis
Elevated levels of C-reactive protein, erythrocyte sedimentation rate, and procalcitonin → Bacterial
Differential Diagnosis
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Mycobacterium tuberculosis, Nocardia spp., Treponema pallidum (syphilis), and Borrelia burgdorferi (Lyme
disease); fungi, such as those endemic to specific geographic areas (Coccidioides, Histoplasma, and
Blastomyces) and those responsible for infections in compromised hosts (Candida, Cryptococcus, and
Aspergillus); para sites, such as Toxoplasma gondii
Determining the specific cause of CNS infection is facilitated by careful examination of the CSF with specific
stains (Kinyoun carbol fuchsin for mycobacteria, India ink for fungi), cytology, antigen detection
(Cryptococcus), serology (syphilis, West Nile virus, arboviruses), viral culture (enterovirus), and polymerase
chain reaction (herpes simplex, enterovirus, and others)
Pathology & Pathogenesis
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A meningeal purulent exudate of varying thickness → around the cerebral veins, cerebellum and spinal cord.
Ventriculitis with bacteria and inflammatory cells in ventricular fluid may be present (more often in
neonates) & subdural effusions and, rarely, empyema.
Perivascular inflammatory infiltrates also may be present, and the ependymal membrane may be disrupted.
cerebral changes characterized by polymorphonuclear infiltrates
Cerebral infarction, resulting from vascular occlusion because of inflammation, vasospasm, and thrombosis
is frequent
Increased ICP → cell death (cytotoxic cerebral edema), cytokine-induced increased capillary vascular
permeability (vasogenic cerebral edema), and, possibly, increased hydrostatic pressure (interstitial cerebral
edema) after obstructed reabsorption of CSF in the arachnoid villus or obstruction of the flow of fluid from
the ventricles
Hydrocephalus can occur as an acute complication of bacterial meningitis.
Raised CSF protein levels are partly a result of increased vascular permeability of the blood–brain barrier and
the loss of albumin-rich fluid from the capillaries and veins traversing the subdural space
Hypoglycorrhachia (reduced CSF glucose levels) is attributable to decreased glucose transport by the
cerebral tissue
CASES
You are examining 12 years old patients on vegetarian diet who complains feeding difficulties, vomiting, diarrhea
and paresthesia. You preform CBC , that show Hb 8 G/dl, Er 2,5 X1012, Rt-1 %, leucocytes 8 X109 hyper segmented
neutrophils. Methyl malonic acid and homocysteine is elevated.
VIT B12 DEFICIENCY
You are examining 12 years old patients with irritability, fatigue, palpitation, pagophagia. You preform CBC, that
show Hb 8 G/dl, Er 2,5 X1012, Rt-1 %, decreased ferritin level.
IRON DEFICIENCY ANEMIA
You are assessing 4 months old infant with jaundice, characteristic face - with maxilla hyperplasia and frontal
bossing, marked hepatosplenomegaly. CBC shows Hb 6 g/Dl, Er 2 X1012, MCV 70; MCH – 20; Rt 4 %; Elevated Serum
Iron and ferritin level and Indirect bilirubin. You will suggest
THALLASEMIA
The red blood indices of 2 years child CBC are following: Hb 9,4 g/dl; Er 3,0X10 12; MCV, MCH and MCHC are
decreased; Ret -1 %. How you will classify anemia?
microcytic, hypochromic anemia, with inadequate response
macrocytic, hypochromic anemia, with inadequate response
microcytic, hyperchromic anemia, with inadequate response
microcytic, hypochromic anemia, with adequate response
The red blood indices of 3 years child CBC are following: Hb 9,0 g/dl; Er 2,8X10 12; MCV is increased; Ret -1 %. How
you will classify anemia?
MACROCYTIC ANEMIA
You are examining 3 years child with pallor, irritability and pica. The red blood indices are following: Hb 8,5 g/dl; Er
2,5 X1012; MCV, MCH and MCHC are decreased Ret -1 %. What you would suspect?
IRON DEFICIENCY ANEMIA
Previously healthy child of 3 years is presented with symptoms of mucosal bleeding from gums, generalized
petechial rash. He is active and no decline in everyday activities is noted. Possible preliminary diagnosis can be
THROMBOCYTOPENIA
Mother shows you the 6 years old child CBC, that reveals Hb 12 g/dl, Er: 3,8 X10 12; Leucocytes 9 X109, bands 2 %,
segmented 50 %, eosinophils 12 %, monocytes 6% lymphocytes 30 %. What would you suggest?
ALLERGY OR PARASITE
Mother shows you the 10 years old child CBC, that reveals Hb 12g/dl, Er: 4,5 X10 12; Leucocytes 18 X10 9,
myelocytes 1 %, metamyelocytes 2 %, bands 8 %, segmented 40 %, eosinophils 4 %, monocytes 10 % lymphocytes 35
%. What is your opinion?
LEFT SHIFT, BACTERIAL INFECTION
You are assessing 6 years old child’s CBC, which decreased level of leucocytes and increased lymphocyte level. What
would you suspect? VIRAL INFECTION
Mother shows you the 3 days newborn CBC. Hb 21g/dl, Er: 6,5 X1012; Leucocytes 18 X109, myelocytes 1 %,
metamyelocytes 2 %, bands 6 %, segmented 42 %, eosinophils 4 %, monocytes 10 % lymphocytes 35 %. What is you
opinion?
THIS IS NORMAL
A gradual decline in hemoglobin levels so called physiologic anemia in preterm revealed in:
First 3 to 6 weeks of life
First days after the birth
6-8 weeks
9-12 months
Mother shows you the 12 years old child CBC, that reveals Hb 12g/dl, Er: 4,5 X10 12; Leucocytes 18 X10 9,
myelocytes 1 %, metamyelocytes 2 %, bands 8 %, segmented 40 %, eosinophils 4 %, monocytes 10 % lymphocytes 35
%. What is your opinion?
LEFT SHIFT, BACTERIAL INFECTION
4 years girl with splenomegaly, anemia, headaches, joint swelling was referred from PHC. In ED CSF examination was
performed. Lymphoblasts and elevated leukocyte count was revealed. How can you define this condition?
LEUKAEMIA
3 years boy is presenting with symptoms of fever, night time bone pains. Splenomegaly, lymphadenopathy, swelling
of joint on physical examination is reviled. In lab testing anemia and thrombocytopenia are seen. Your more relevant
diagnosis is
LEUKAEMIA
Results of an analysis of peripheral blood suggest the possibility of leukemia, it is important to perform:
BONE MARROW EXAMINATION
Most common viruses described in association with Idiophatic thrombocytopenic purpura is:
Flu virus
Corona virus
Epstein-Barr virus
Varicella zoster virus
Sudden head extension causing extension followed by flexion of the arms and legs, is called reflex of
MORO REFLEX
Placing a finger in palm resulting in flexing of the infant's fingers, accompanied by flexion at elbow and shoulder, is
called reflex of
GRASPING REFLEX
Analysis of the CSF revealing neutrophilic pleocytosis is characterized for:
BACTERIAL MENINGITIS
Analysis of the CSF revealing mild to moderate lymphocytic pleocytosis, normal or slightly elevated protein, and
normal glucose is characterized for:
VIRAL MENINGITIS