Vitamin A

Vitamin A
Vitamin A is an essential micronutrient because it cannot be biogenerated de novo by animals. It must be obtained from plants in the form of provitamin-A carotenoids: α-, β-, and γ-carotenes and β-cryptoxanthin. These substances can be converted to vitamin A compounds in the body. The term vitamin A refers to all-trans-retinol, the alcohol form of the vitamin. The storage form of vitamin A is retinyl palmitate. The aldehyde form of vitamin A is retinal and functions in vision. The physiologically most important vitamin A metabolite is the acid derivative, retinoic acid. Retinoic acid functions at the gene level as a ligand for specific nuclear transcription factors that regulate many genes involved in fundamental biologic activities of the cell. The term retinoids includes both natural and synthetic compounds with vitamin A activity and is most often used in the context of vitamin A action at the gene level.Absorption, Transport, Metabolism, Storage
The body acquires vitamin A either as preformed vitamin A (usually as esters) or as provitamin-A carotenoids. In the USA, grains and vegetables supply approximately 55% and dairy and meat products supply approximately 30% of vitamin A intake from food. Vitamin A and the provitamins-A are fat-soluble, and their absorption depends on the presence of adequate lipid and protein within the meal. Chronic intestinal disorders or lipid malabsorption syndromes can result in vitamin A deficiency. Ingested and absorbed provitamins-A are bioconverted to vitamin A molecules in the small intestine by the carotene cleavage enzyme dioxygenase; β-carotene provides twice the vitamin A activity of the other provitamins-A. Further processing in the enterocyte involves the esterification of vitamin A to retinyl palmitate for incorporation into chylomicrons, which are released into lymph and transported via the circulation to the liver for storage or to other tissues. The vitamin A content in the liver is low at birth, but it increases 60-fold during the first 6 mo of life. If the growing child has a well-balanced diet and obtains vitamin A from foods that are rich in vitamin A or provitamin-A the risk of vitamin A deficiency is small. However, even subclinical vitamin A deficiency can have serious consequences. Stored vitamin A is released from the liver into the circulation as retinol bound to its specific transport protein, retinol-binding protein (RBP), which binds to the thyroid hormone transport protein, transthyretin; this complex delivers retinol (as well as the thyroid hormone) to tissues. Normal plasma levels of retinol are 20-50 mug/dL in infants and 30-225 mug/dL in older children and adults. Uncleaved provitamin-A carotenoids in the intestine are also incorporated into chylomicrons and delivered to various tissues. Malnutrition, particularly protein deficiency, can cause vitamin A deficiency by the impaired synthesis of retinol transport protein. However, if dietary vitamin A is provided in the absence of RBP, vitamin A is transported to the tissues via chylomicrons and almost completely alleviates the symptoms of vitamin A deficiency. In developing countries, subclinical or clinical zinc deficiency can increase the risk of vitamin A deficiency. There is also some evidence of marginal zinc intakes in children in the USA.Function and Mechanism of Action
Vitamin A is required throughout the life cycle, beginning with embryogenesis. Except for its role in vision, the pleiotropic actions of this micronutrient include many systemic functions that are mediated at the gene level by all-trans-retinoic acid (RA), which is a ligand for specific nuclear transcription factors, the retinoid receptors: RARs and RXRs. When an RAR is activated by the presence of RA, it combines with an RXR, and the resulting heterodimer binds to target genes that have specific recognition sites. Thus, vitamin A, via its active form, retinoic acid, regulates many genes that are involved in the fundamental biologic activities of cells, such as cell division, cell death, and cell differentiation. Retinoic acid is among the most important signaling molecules in vertebrate ontogenesis. It affects many physiologic processes, including reproduction, growth, embryonic and fetal development, and bone development, in addition to respiratory, gastrointestinal, hematopoietic, and immune functions. The role of vitamin A in immune function and host defense is particularly important in developing countries, where vitamin A supplementation or therapy reduces the morbidity and mortality rates of various diseases, such as measles  The best understood function of vitamin A is its nongenomic role in vision. The human retina has two distinct photoreceptor systems: the rods, containing rhodopsin, which can detect low-intensity light, and the cones, containing iodopsin, which can detect different colors. The aldehyde form of vitamin A, retinal, is the prosthetic group on both visual proteins. The mechanism of vitamin A action in vision is based on the ability of the vitamin A molecule to photoisomerize (change shape when exposed to light). Thus, in the dark, low-intensity light isomerizes the rhodopsin prosthetic group, 11-cis retinal, to all-trans-retinal, generating an electrical signal that is transmitted via the optic nerve to the brain and results in visual sensation.

Radiology Masterclass Tutorials

Posted: 17 Apr 2013 09:33 AM PDT

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Tutorials

Chest X-ray Tutorials

·         Chest X-ray - Anatomy

·         Chest X-ray - Abnormalities

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Abdominal X-ray Tutorials

·         Abdominal X-ray - System and anatomy

·         Abdominal X-ray - Abnormal bowel gas pattern

·         Abdominal X-ray - Abnormal calcification

·         Abdominal X-ray - Abnormal soft tissues and bones

Musculoskeletal X-ray Tutorials

·         Musculoskeletal X-ray - General principles

·         Introduction to Trauma X-ray

·         Trauma X-ray - Upper limb

·         Trauma X-ray - Lower limb

·         Trauma X-ray - Axial skeleton 

General Radiology Tutorials

·         Basics of X-ray physics

·         OSCE presentation tips

·         OSCE scoring and check lists

AcePGMed: NEET 2013 Practice Question Paper

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CONGENITAL HEART DISEASE

                        

CONGENITAL HEART DISEASE

Etiology

            Environmental

            genetic

            multifactorial causes

Chromosomal abnormalities

trisomy 21, 13 or 18.

40% of those with Down syndrome can have a cardiac defect, with atrioventricular septal defect and ventricular septal defect accounting for approximately 80% of lesions.

Cardiac defects are common in trisomy 18 (Edwards’ syndrome) and 13 (Patau’s syndrome).

Turner’s syndrome, 45XO, left heart lesions with Coarctation of the aorta in 10% of cases.

autosomal abnormalities = low birthweight, mental retardation, small stature and

Single gene defects

Pompe’s disease = causes cardiomyopathy,

Marfan’s syndrome = aorta root dilation

Noonan’s syndrome, = pulmonary valve or artery stenosis,

CATCH 22 syndrome: cardiac defects, abnormal facies, thymic aplasia, cleft palate, hypocalcemia.

DiGeorge syndrome

Teratogens

maternal infection

illness

ingestion of certain drugs

congenital rubella syndrome = peripheral pulmonary stenosis or an arterial duct.

offspring of diabetic mothers,

uncontrolled maternal phenylketonuria

Maternal ingestion of therapeutic drugs

lithium =Ebstein’s anomaly

phenytoin =semilunar valve stenosis, coarctation, arterial duct

isotretinoin

fetal alcohol syndrome

Syndromes

de Lange= VSD

Williams = supravalvar aortic stenosis,

Friedreich’s ataxia =hypertrophic cardiomyopathy

Jervell and Lange-Nielsen =prolonged QT

Holt–Oram = atrial septal defect,

VATERL=VSD

Recurrence Risk

risk for another pregnancy rises to about 2% if one previous child is affected

If two previous children are affected the risk rises to 6–8%

if the mother is affected there is an even higher risk (5–15%)

Fetal echocardiography provides an accurate means of diagnosing fetal cardiac abnormalities from about 18 weeks’ gestation

Nomenclature Of Congenital Heart Disease

heart has three parts –

            Atrial chambers

            Ventricular chambers

            Arterial trunks

Connections and relationships of these can be determined

Determine of how each of the three basic components or segments of the heart are connected.

Determine the arrangement and connections of the atrial chambers

Then to analyze the atrioventricular and ventriculoarterial junction.

Then position of the heart.

Atrial arrangement

atrial arrangement or situs has first to be determined.

This does not always follow the situs of the abdominal viscera

but usually that of the thoracic viscera and

thus the bronchial morphology.

analyse of the bronchial anatomy on X-ray, - with a penetrated film.

The right main bronchus is more vertical and shorter than the left,

branching above the lower lobe pulmonary artery while the left branches below it.

The right atrium lies on the same side as the right bronchus.

The usual atrial arrangement is described as solitus

its mirror image as inversus.

When the atrial situs is uncertain it is frequently called ambiguous

Careful analysis may show bilateral manifestations of right or left atrial morphology, which can then be described as right or left atrial isomerism.

            In the former, (right atrial isomerism) asplenia is the usual association

            in the latter, polysplenia.

Atrial arrangement or situs is summarized as follows:

            solitus: right atrium on right, left atrium on left

            inversus: left atrium on right, right atrium on left

            isomerism – right: bilateral right atria

            isomerism – left: bilateral left atria

            ambiguous: used if arrangement cannot be identified.

Atrioventricular connection

            The atrioventricular connection then describes the way the atria communicate with the ventricles at the atrio-ventricular junction.

            If the connections follow the normal pattern they are said to be concordant, e.g. right atrium to right ventricle and left atrium to left ventricle,

            Discordant atria connect with the contra-lateral ventricle.

            When both atrio-ventricular valves enter one ventricular chamber, the connection is described as double inlet

            if one or other atria is not directly connected to a ventricle, then that atrio-ventricular connection is said to be absent.

            it may not be possible to state exactly the atrio-ventricular connection which is then described as ambiguous.

These are summarized as follows:

            concordant: right atrium to right ventricle, left atrium to left ventricle

            discordant: right atrium to left ventricle, left atrium to right ventricle

            ambiguous: with atrial isomerism and one atrium entering each ventricle

            double inlet: both atria connect to the same ventricle

            absent right or left: no true or potential connection from the right or left atrium to a ventricle.

Ventriculoarterial connection

            This describes the means by which the great arteries take origin from the ventricular chambers.

            If an artery overrides the septum, and thus arises from both ventricles, it is assigned to that from which more than half takes origin.

Connections can thus be:

            concordant: pulmonary trunk from right ventricle, aorta from left

            discordant: aorta from right ventricle, pulmonary trunk from left

            double outlet: both great arteries from one ventricle

            single outlet: single great artery.

Three further steps

            are then necessary to complete the analysis: a statement of the relationship of structures; tabulation of associated lesions; and description of the cardiac position within the chest.

Relationships

These are described in simple terms,

            such as right/left,

            anterior/posterior,

            superior/inferior,

            side by side.

These relationships neither imply nor give any information on morphology or connections.

Additional abnormalities

These will include factors such as

            venous drainage,

            Septal defects,

            Stenosis or atresia of valves, and great artery anomalies such as coarctation.

Cardiac position

            When the heart is on the left side this is not usually stated if there is situs solitus,

            should be described as levocardia where there is an abnormal situs.

            Dextrocardia describes the situation in which more than half of the cardiac shadow on X-ray is in the right side of the chest

            it makes no assumptions as to the atrial situs or intracardiac anatomy.

            Mesocardia is used when the heart appears to be in the center of the thorax.

Comment

nomenclature may seem complicated

not required in the majority of patients who have normal chamber connections,   morphology and relations.

it simplifies assessment and description of complex defects

prevents any ambiguity in communication between different cardiologists and surgeons.

use the terms which have been in use for some time

Thus atrial situs solitus, atrioventricular concordance and ventriculoarterial discordance is simply to say  transposition of the great arteries.

Medical Care Of Congenital Heart Disease

cardiologist use interventional catheterization techniques to undertake corrective procedures for some less complex lesions

role of the physician is to provide general medical care

use the appropriate investigations to make an accurate diagnosis

refer the patient to the surgeon at the appropriate time.

The Newborn Infant With Congenital Heart Disease

The patient with congenital heart disease who survives beyond infancy has a good outlook,

Nowadays surgery generally carry a low risk.

With modern surgery, up to 15–20% of live-born children in whom a defect is recognized in infancy can die in the first year of life,

Infant with congenital heart disease may show rapid progression to severe cardiac failure or cyanosis with hypoxia and acidosis

Heart disease in the newborn is usually recognized by the presence of cyanosis or heart failure.

Early detection of cyanotic heart disease is difficult

hyperoxic test is useful where there is uncertainty

in response to hyperoxia (80–100% oxygen)  -  a _PO₂ of over 150 mmHg (21 kPa) from the upper body excludes a major right to left shunt and a failure to rise suggests a cardiac defect.

important early signs of heart failure are

            tachycardia       >160/min

            tachypnea         >50/min

            hepatomegaly

Palpation of the pulses

compare not only the right arm and the leg pulse but also the pulses in both arms.

With coarctation of the aorta or hypoplastic left heart syndrome the femoral pulses may feel normal initially when the ductus is open.

Low volume pulses occur with obstruction to left ventricular output such as hypoplastic left heart syndrome or severe aortic stenosis.

A parasternal or subxiphoid heave may indicate the presence of a significant defect in a patient where there is no abnormality on auscultation.

A single second heart sound should be considered abnormal after the first day of life.

Gallop rhythm indicates cardiac failure.

Many infants with significant heart disease have no murmur

When a murmur is heard it is not diagnostic but suggests the presence of an underlying defect.

ECG

Difficult to interpret in the first few days of life

            an infant with severe congenital heart disease can have a normal ECG.

chest X-ray is useful.

            contour of the heart and the great arteries and the effect of the anatomical abnormality on the pulmonary vascularity

            typical appearances are not always found.

            A large thymus may cause difficulty in interpretation of the cardiac silhouette

            increased pulmonary blood flow is not always reflected in the X-ray appearances.

Echocardiography may be more accurate

Catheterization is usually only required for interventional procedures such as atrial septostomy.

This is easily performed through the umbilical vein within the first 2 days of life.

Transfer to the cardiac centers should be as rapid as possible in a suitable transport incubator.

General care of temperature, acidosis and electrolyte imbalance is essential.

Prostaglandin therapy

The use of E-type prostaglandins to dilate the ductus arteriosus is an essential part in the management of the newborn infant with a ductus dependent circulation. T

his occurs either when there is

            marked obstruction to pulmonary blood flow (such as pulmonary atresia)

            in aortic arch abnormality (such as critical aortic stenosis or coarctation).

Prostaglandin E2, which is readily available in most obstetric hospitals, is cheaper than prostaglandin E1, and equally effective

Prostaglandins should be administered as a peripheral venous infusion

a suitable initial rate being 0.02 mg/kg/min

the dose being increased up to 0.05–0.10 mg/kg/min

depending on the clinical response.

serious complication of prostaglandin therapy is respiratory depression,

normal respiration rapidly returns when the infusion is stopped.

It should then be restarted at a reduced dosage.

Other side-effects include fever, tachycardia and jitteriness.

                       

Channelopathies (Myotonias and Periodic Paralysis)

Channelopathies (Myotonias and Periodic Paralysis)

Channelopathies
= disorders of ion channels that result in altered excitability of cellular membranes.
Most of channelopathies are disorders of muscle membrane ion channels.
Results in muscle membrane hyper excitability leading to sustained contraction = myotonia
May result in muscle membrane hypoexcitability leading to weakness seen in periodic paralysis
Muscle channelopathies are sodium, calcium, and chloride channel disorders
May be Inherited channelopathies OR
Acquired channelopathies (Acquired channelopathies are autoimmune)
myotonias
            dystrophic
            nondystrophic disorders.
In dystrophic myotonia, myotonia is one of several muscle symptoms
            with muscle atrophy and weakness being most prominent.
These include
            dystrophia myotonica
            proximal myotonic myopathy
in nondystrophic myotonias the most prominent symptom is myotonia
periodic paralyses - divided into those associated
with a high or normal serum potassium concentration (i.e., hyperkalemic periodic paralysis)
those associated with a low serum potassium concentration (i.e., hypokalemic periodic paralysis).
the abnormal serum potassium concentration is the consequence rather than the cause of the periodic paralysis.
Skeletal Muscle Channelopathies
Channel and disease     are -
SODIUM
            Hyperkalemic penodic paralysis           
            With myotonia 
            Without myotonia        
            With paramyotonia congenita   
            Paramyotonia congenita           
            Sodium channel myotonia         
            Myotonia fluctuans       
            Myotonia permanens   
            Acetazolamide-responsive myotonia     
CALCIUM
            Skeletal muscle calcium channel alpha-1 subunit
            Hypokalemic periodic paralysis
CHLORIDE
            Skeletal muscle chloride channel           
            AD myotonia congenita (Thomsen's)    
            AR myotonia congenita (Beeker's)       

Pathogenesis and Pathophysiology of Sodium Channelopathies
sodium channelopathies result from point mutations in a gene, situated on the long arm of chromosome 17.
reduced inactivation of the sodium channel, followed by
            either increased muscle excitability with myotonia
            or increased muscle inexcitability with hyperkalemic periodic paralysis.
Pathogenesis and Pathophysiology of Chloride Channelopathies.
reduced muscle membrane chloride conductance ( i.e.rate of flow of chloride is decreased) resulting in muscle membrane hyper excitability à repetitive firing, à leads to the myotonia.
Eg -Thomsen's and Becker's diseases
Pathogenesis and Pathophysiology of Calcium Channelopathies.
In hypokalemic periodic paralysis, the weakness is related to the calcium channel.
There is an influx of potassium into the muscle fiber with an accompanying influx of extracellular water.
 influx of potassium may account for the precipitation of hypokalemic periodic paralysis with large carbohydrate meals.
influx of potassium in hypokalemic periodic paralysis causes the muscle fibers to become depolarized and inexcitable.
Clinical Features and Associated Disorders of Sodium Channelopathies.
            paramyotonia congenita
            hyperkalemic periodic paralysis
            sodium channel myotonias.
Paramyotonia Congenita.
            The predominant symptom is paradoxical myotonia, which is present from birth and persists throughout life.
            The myotonia is paradoxical because unlike classic myotonia, it increases with repetitive movements.
            It is exacerbated by cold temperatures, which cause weakness.
            In warm environment, patients may have no symptoms
            attacks are precipitated by potassium ingestion
Hyperkalemic Periodic Paralysis.
            appears in infancy or early childhood
            paresis - brief and mild
            lasting 15 minutes to 4 hours
            precipitated by rest following exercise
            by ingestion of potassium-rich foods
            by administration of potassium compounds
            attacks commonly start in the morning before breakfast
            stress provokes them more easily
            Weakness is mainly proximal

            no ocular or respiratory muscle weakness

            flaccid quadriplegia with absent reflexes and normal sensory examination.

            The potassium level may rise during the attack

            May cause cardiac dysrhythmias.

            between attacks-  patient has normal strength of muscles

Sodium Channel Myotonias.
            myotonia becomes worse with cold,
            not associated with weakness
            responds to acetazolamide (acetazolamide-responsive myotonia
Clinical Features and Associated Disorders of Chloride Channelopathies.
            two forms
            autosomal dominant disease (Thomsen's disease)
            autosomal recessive disease (Becker's disease).
Autosomal Dominant Myotonia Congenita (Thomsen's Disease).
            painless generalized myotonia,
            looks like muscle stiffness.
            first and second decades of life
            provoked by exertion following rest.
            ask the patient to rise from a chair after a period of quiet sitting.
            improves with exercise
            well-developed muscles with particular hypertrophy of the lower limbs, giving them an athletic appearance.
            Muscle strength may be normal, or even stronger than normal.
            normal reflexes,
            eyelid, grip, and percussion-induced myotonia can be demonstrated.
Autosomal Recessive Myotonia Congenita (Becker's Disease).
            similar to Thomsen's disease except that myotonia appears later in the first decade.
            Becker's disease -muscles are initially weak
            a period of activity is required before full strength returns.
            may have muscle hypertrophy, of the legs and buttocks,
Hypokalemic Periodic Paralysis.
            autosomal dominant disorder
            common in males
            begin at adolescence
            occur at night,
            the patient awakens with weakness.
            episodes may be precipitated by
                        carbohydrate or alcohol intake,
                        rest after exercise,
                        emotional stress.
            attacks 1 to 4 hours, may persist for up to 3 days.
            Prodromal symptoms of muscle stiffness, heavy limbs, or sweating
            followed by proximal lower limb weakness,
            spreads to become a tetraparesis.
            Ocular or bulbar involvement is rare.
            Fatalities are rare = injudicious treatment or hypokalemia-induced cardiac dysrhythmias.
D         uring severe attacks patients are flaccid and areflexic.
Differential Diagnosis Myotonias.
            The principal symptom of myotonia is
            muscle stiffness
            inability to relax contracted muscle
            sodium channel myotonia is not painful
            Stiffness may be confused with spasticity or rigidity.
            Muscle cramps, is a feature of a peripheral nerve disorder
            Dystonia results in abnormal postures
            Painless contractures may be a feature of metabolic myopathy such as McArdle's disease
            withdrawl of levodopa = muscle rigidity or stiffness with fever, an elevated creatine kinase (CK) level, and a high white blood cell count.
            pseudomyotonia = impaired relaxation without electrical evidence of myotonia
                        = acid maltase deficiency and Brody's disease
Differential diagnosis of  Periodic Paralysis.
            causes of a flaccid, areflexic tetraparesis without sensory signs like
                        Hypercalcemia
                        Hypocalcemia
                        Hypophosphatemia
                        Hypomagnesemia
                        rhabdomyolysis
                        Guillain-Barre syndrome
                        myasthenic syndrome
                        acute poliomyelitis
                        Secondary hypokalemic periodic paralysis
                        intracellular potassium depletion from either renal, endocrine, gastrointestinal, or drug-induced mechanisms
                        Thyrotoxic periodic paralysis
                        hyperthyroidism.
Evaluation Myotonias.
            Laboratory evaluations
            Serum CK level, - elevated in Thomsen's and Becker's diseases
            EMG - spontaneous myotonic discharges
Periodic Paralysis.
            blood tests for potassium, calcium, magnesium, phosphate, and CK should be obtained during an episode of weakness.
            electrocardiogram (ECG) may show changes consistent with hypokalemia or hyperkalemia
            EMG
            Nerve conduction studies are normal.
            Muscle biopsy
Management Myotonias.
            anesthesia should be planned
            potassium administration can exacerbate myotonia, potassium supplements should be given only when necessary
            myotonia congenita = membrane-stabilizing drugs such as procainamide and quinine
            Phenytoin is useful for chronic administration
Periodic Paralysis.
Hypokalemic -
                        prevented by a low-carbohydrate, low-sodium diet. A
                        cetazolamide prevents paralytic attacks
                        ECG for cardiac dysrhythmias.
hyperkalemic periodic paralysis,
            thiazide diuretics
            Carbohydrate-containing foods and fluid may aggravate the weakness,
            Inhaled beta-adrenergic agonists such as salbutamol are effective treatments in acute situations
a� 8 c o � � psychiatrist.

Learning and attention deficit disorders and mental retardation managed by a psychologist and educator.

Strabismus, nystagmus, and optic atrophy –consult with  ophthalmologist - in the initial assessment.

Lower urinary tract dysfunction should receive prompt assessment and treatment.

Several drugs have been used to treat Spasticity, including dantrolene sodium, the benzodiazepines, and baclofen.

            Intrathecal baclofen - used - in selected children with severe spasticity.

            Botulinum toxin - management of spasticity in specific muscle groups, - positive response in - patients studied.

            Patients with incapacitating athetosis occasionally respond to levodopa, and       children with dystonia may benefit from carbamazepine or trihexyphenidyl.

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Palpation

Applying the palm of the hand to the chest

Thrills

increased precordial pulsation (apical in left ventricular hypertrophy and basal and right sided in right ventricular hypertrophy)

diastolic shock (in the pulmonary area in pulmonary hypertension)

The apex beat, normally in the fourth or fifth intercostal space within the mid-clavicular line

pulse wrist (radial) or inguinal region (femoral).

Sinus arrhythmia (increase in rate on inspiration with decrease on expiration)

bounding pulse

weak pulse

collapsing (

femoral pulses may be absent, or delayed

Percussion

right cardiac border does not extend beyond the right sternal edge

the upper border is at the level of the second intercostal space

determine cardiac size

Diminished or absent cardiac dullness is found in emphysema and pneumothorax.

Auscultaition

The ranges for heart rate in infancy and childhood are:

Newborn          70/120  

Infant               80/160              

Preschool child 75/120  

School child 70/110

Auscultate areas -

Mitral

Tricuspid

Pulmonary

Aortic

3^rd & 4^th left intercostal spaces,below left clavicle.

Auscultatory assessment

cardiac rhythm

heart sounds

murmurs.

Third heart sound

ejection click

intensity of heart sounds

Description of murmurs should include

1)   site,

2)   intensity (graded 0—6) with point of maximum intensity,

3)   timing (systolic: pan, early or late; or diastolic: early diastolic, mid-diastolic or presystolic,

4)   propagation (mitral systolic murmurs radiate to the left axilla, aortic systolic to the neck, aortic regurgitant down the left sternal edge) and

5)   variation with position. Coarctation of the aorta may produce a murmur audible over the back.

6)  Variation with respiration

venous hum

pericardial friction rub

to his ear.

other systems, e.g. by hepatic enlargement in cardiac failure.

Cervical Lymphadenopathy

Cervical Lymphadenopathy

most common neck mass in children.

If - anterior to the sternocleidomastoid muscle.

Infection is the usual cause of enlargement; viral etiology and persist for months.

Acute suppurative submandibular adenitis occur in early childhood (6 mo-3 yrs), is preceded by pharyngitis or URI, the child develops erythema, swelling and cellulitis, and management is antibiotics and drainage.

Chronic adenitis: -

persistent node (> 3 wk., tonsillar),

solitary, non-tender, mobile and soft.

Generally no treatment if < 1 cm,

nodes above 2 cm sizes with rapid growth, clustered, hard or matted do biopsy.

Other causes are: (1) Mycobacterial adenitis- atypical (MAIS complex), swollen, non-tender, nor-inflamed, positive skin test, excision is curative,

(2) Cat-Scratch adenitis- caused by A. Fellis, transmitted by kittens, positive complement fixation test, minimally tender, fluctuant regional nodes, spontaneous resolution.

(3) Hodgkin's disease - teenage and young adults, , non-tender node, associated to weight loss, biopsy is diagnostic.