is a periodic fainting spell in which ... - 1 file download
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is a periodic fainting spell in which there is a periodic onset and offset of blockage of heart due to disorder of heart rhythm that may last for seconds, hours, days, or even weeks before the conduction returns.
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AV block – High grade (ie, complete or Mobitz type II second degree) AV block, an event sometimes called a Stokes-Adams attack. In general, complete AV block and Mobitz type II AV block are more unstable and can be associated with syncope. Conversely, Mobitz type I (Wenckebach) second degree AV block is usually benign and not associated with syncope. When Mobitz type II second degree or third degree AV block is present in conjunction with syncope, a permanent pacemaker is indicated.
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Typically an attack occurs without warning leading to sudden loss of consciousness.Prior to an attack, a patient may be pale with hypoperfusion. Normal periods of unconsciousness last approximately thirty seconds; if seizures are present, they will consist of twitching after 15–20 seconds (seizures occur because of brainstem hypoxia and not due to cortical discharge as evident by EEG findings which show no epileptiform activities). Breathing continues normally throughout the attack, and so on recovery the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into a systemic circulation which has become dilated due to hypoxia.As with any syncopal episode that results from a cardiac dysrhythmia, the faints do not depend on the patient's position. If they occur during sleep, the presenting symptom may simply be feeling hot and flushed on waking.
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Shigella organisms can survive transit through the stomach since they are less susceptible to acid than other bacteria; for this reason as few as 10 to 100 organisms can cause disease. Seizures are the most common neurologic complication associated with Shigella infection●Fever – 30 to 40 percent●Abdominal pain – 70 to 93 percent●Mucoid diarrhea – 70 to 85 percent●Bloody diarrhea – 35 to 55 percent●Watery diarrhea – 30 to 40 percent●Vomiting – 35 percent
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Legg-Calve-Perthes (LCP) disease. Although LCP can have associated hip or knee pain, it is commonly known as “the painless limp.” The peak age of onset is 3 to 8 years. Slipped capital femoral epiphysis (SCFE) is incorrect because the peak age range of this disorder is peripubertal, approximately ages 8 to 14 years. SCFE typically has pain associated. Septic arthritis is usually acute in presentation and has associated pain, fever, inability to walk, and elevations of C-reactive protein and erythrocyte sedimentation rate. Juvenile idiopathic arthritis (JIA) rarely presents in the hip; the most common location is the knees. Morning stiffness is a common complaint with JIA.
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Legg-Calvé-Perthes and secondary avascular necrosis — LCP is a syndrome of idiopathic osteonecrosis (avascular necrosis) of the hip. It typically presents as hip pain and/or limp of acute or insidious onset in children between the ages of 3 and 12 years, with peak incidence at five to seven years of age. LCP is bilateral in at least 10 to 20 percent of patients. Clinical features of LCP and secondary avascular necrosis of the hip include insidious onset of hip pain with limp and activity-related pain.Diagnosis of LCP demands a high index of suspicion. Initial radiographs are often normal. Early in the course, bone scan shows decreased perfusion to the femoral head, and MRI reveals marrow changes highly suggestive of the diagnosis.Later in the course, radiographs show fragmentation and then healing of the femoral head, often with residual deformity. Gradual revascularization occurs subsequently.Children diagnosed with LCP should be made nonweight bearing and referred to an experienced pediatric orthopedist for management. Therapy for LCP is poorly defined because no large controlled trials are available, and long-term consequences become evident only after decades of follow-up. Treatment focuses on containing the femoral head within the acetabulum through the use of splints or occasionally surgery.Almost all children do well in the short term. However, long-term outcome depends upon age at time of disease onset and degree of involvement of the femoral head
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J wave causes: many conditions such as hypothermia; hypercalcemia; brain injury; vasospastic angina; acute ischemia, especially in true posterior myocardial infarction with occlusion of the left circumflex
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This infant has the features of pyloric stenosis, a condition four times more common in males and more common in first-born children. Affected infants usually present between the third and eighth weeks of life with increasing projectile emesis. Abdominal examination may reveal an olive-shaped mass and visible peristaltic waves. Serum electrolyte levels usually reveal hypochloremic metabolic alkalosis. Ultrasonography is useful in confirming the diagnosis.
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Clinical Manifestations:Projectile nonbilious vomiting is the cardinal feature of the disorder. Physical findings vary with the severity of the obstruc- tion. Dehydration and poor weight gain are common when the diagnosis is delayed. Hypokalemic, hypochloremic metabolic alkalosis with dehydration is seen secondary to persistent emesis in the most severe cases. The classic finding of an olive- sized, muscular, mobile, nontender mass in the epigastric area occurs in most cases but may be difficult to palpate. Visible gastric peristaltic waves may be seen. Ultrasonography reveals the hypertrophic pylorus. Upper GI study may show the classic “string sign.”
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Treatment :Initial treatment involves nasogastric tube placement to de- compress the stomach, and correction of dehydration, alkalosis, and electrolyte abnormalities. Pyloromyotomy should take place after the metabolic anomalies are corrected.
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Gastrointestinal manifestations include pancreatic insufficiency, bowel obstruction and rectal prolapse, diabetes, and hepatic cirrhosis. Loss of pancreatic enzyme secretion leads to decreased fat absorption; parents may notice that the child’s stools are large, bulky, and foul smelling. Later, stool becomes extremely dense, sometimes leading to distal intestinal obstruction. Failure to thrive is the most common manifestation of untreated CF in infants and children. Meconium ileus (neonatal intestinal obstruction in the absence of anatomic abnormalities) is virtually pathognomonic for CF.
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A patient with SCD with fever (with or without vaso-occlusive crisis) can have a medical emergency. Any SCD child presenting with a fever greater than 38.5°C is evaluated emergently, because SCD causes functional asplenia and predisposes patients to invasive encapsulated organisms (typically pneumococcal disease). In such situations complete blood count (CBC) and blood cultures are warranted, and if the screening results are concerning for infection without obvious source, empiric antibiotics are typically initiated (usually with ceftriaxone).
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Recurring infections in this patient presenting with oral lesions, weight loss, and lymphadenopathy are concerning for immune system dysfunction. He may have a primary immunodeficiency due to an inheritable defect or an acquired (secondary) immunodeficiency related to HIV infection, malignancy, malnutrition, or other disorder. The maternal history of IV drug use makes pediatric HIV infection a strong likelihood, probably due to vertical transmission
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HIV may present in infants and children with any one or several of the following signs and symptoms: generalized lymphadenopathy, hepatomegaly, splenomegaly, failure to thrive, recurrent or chronic diarrhea, oral candidiasis, parotitis, and developmental delay. Respiratory manifesta- tions include lymphoid interstitial pneumonia (LIP) and Pneumocystis jiroveci pneumonia (PCP). Regression in devel- opmental milestones and progressive encephalopathy may occur. Recurrent, often severe, bacterial and opportunistic (fungal, disseminated HSV or CMV, and Mycobacterium avium) infections are the hallmark of the acquired helper T-lymphocyte immunodeficiency. A significant percentage of infected adolescents presents with a mononucleosis-type syndrome within 6 weeks of HIV acquisition. Symptoms and signs include sore throat, fatigue, fever, rash, and cervical or diffuse lymphadenopathy. PCP and LIP are two of several AIDS-defining illnesses in the pediatric population. When any of these conditions occurs, the child is considered to have AIDS regardless of the absolute CD4+ T-lymphocyte count.
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secondary infection with Staph aureus from the dry scaly skin, leading to erosion and staph infection with inguinal lymph nodes dissemination and fever.
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Another common form of MD is myotonic muscular dystrophy, the second most common type of MD in the United States. It is inherited as an autosomal dominant trait. Infants born with this condition may have an inverted V-shaped upper lip, thin cheeks, and wasting of the temporalis muscles. The head is abnormally narrow, and the palate is high and arched. In the ensuing years weakness of the distal muscles leads to progressive challenges in walking. A variety of other findings arise including speech difficulties, gastrointestinal tract problems, endocrinopathies, immunologic deficiencies, cataracts, intellectual impairment, and cardiac involvement.
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The most common muscular dystrophy occurring in boys is Duchenne muscular dystrophy (DMD). In boys with DMD, the CK level can be elevated up to 20-times normal. DMD is an X-linked recessive muscular dystrophy which results from absence of dystrophin. Weak- ness begins in the proximal muscle groups; the calf muscles appear hypertrophied, and the child rises from a sitting position by leaning on the calves and using the arms to “climb” up the legs (Gower’s sign). Becker muscular dystrophy has similar clinical manifestations due to abnormalities in the dystrophin protein, but the onset is later (adolescence), and the disease is generally milder. Cerebral palsy is a nonprogressive disorder of movement and posture resulting from a static brain lesion acquired in the fetal or perinatal period. Spinal musular atrophy is an inherited disorder that results in the progressive degradation of anterior horn cells. Patients vary in presentation from the infant with profound hypotonia (Wernig-Hoffman) to motor delays. Typically, the examination is significant for tongue fasiculations, proximal greater than distal weakness, and areflexia. Multiple sclerosis is an autoimmune disorder involving demyelination in the brain and spinal cord. Onset is later in life and more common in females, with waxing and waning of symptoms. Adrenoleukodystrophy is X-linked and occurs primarily in boys; this peroxysomal disorder is a neurode- generative condition involving the white matter of the brain.
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Tuberous sclerosis, like neurofibromatosis, is a progressive au- tosomal dominant neurocutaneous disorder, although sporadic cases are more common than inherited ones. Two separate genes have been identified for tuberous sclerosis (chromosome sites 9q34 and 16p13). The normal genetic product is tuberin, a protein thought to suppress the development of tumors. Disease severity varies greatly. Typical skin lesions include ash-leaf spots (flat, hypopigmented macules), shagreen patches (areas of abnormal skin thickening), sebaceous adenomas, and ungual fibromas. Ash-leaf spots are the earliest manifestation and are best detected by Wood lamp examination. Neuroimaging demonstrates the distinctive periventricular knob-like areas of localized swelling, or tubers. Subependymal nodules and giant cell astrocytomas may also be present. Mental retardation and seizures (including infantile spasms) are common. Tumors also have a predilection for the kidney, heart (particularly cardiac rhabdomyomas), and retina. Treatment consists of antiepileptic therapy and surgical removal of related tumors when indicated.
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Neurofibromatosis types 1 (von Recklinghausen disease) and 2 (bilateral acoustic neuromas) are the most common variants in children. Neurofibromatosis type 1 is a clinical diagnosis based in part on the presence of six or more cafe-au-lait spots of a specific size. A large gene on chromosome 17 coding for neurofibromin has a high spontaneous mutation rate. Patients with neurofibromatosis type 1 are at increased risk for optic pathway gliomas and other low-grade gliomas in the central nervous system. They typically require evaluation and treatment for the associated seizures, learning disorders, renovascular hypertension, and scoliosis. Routine vision screening is critical. Neurofibromas that cause impairment may be surgically removed; however, most will recur. Bilateral acoustic neuromas are the hallmark of neurofibromatosis type 2. Complications include hearing loss and vestibular disorientation. Brain MRI demonstrates bilateral eighth cranial nerve masses. Neurofibromas, meningiomas, schwannomas, and astrocytomas are also associated with type 2 neurofibromatosis. Cataracts and retinal hamartomas are not uncommon. Surgical debulking is appropriate when hearing impairment becomes pronounced. Cochlear implants have restored hearing in some patients. The genetic abnormality occurs on chromosome 22
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■ TABLE 15-9 Diagnosis of Neurofibromatosis Type 1 Two of the following must be present: 1. Six or more cafe-au-lait spots, .5 mm in size in children and .15 mm in adolescents or adults 2. Axillary or inguinal freckling 3. Two or more Lisch nodules (hamartomas) in the iris 4. Two or more neurofibromas or one plexiform neurofibroma 5. A distinctive osseous lesion, such as sphenoid dysplasia 6. Optic gliomas 7. Affected first-degree relative based on the preceding criteria
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The most common cause of juvenile or acquired hypothyroidism is Hashimoto thyroiditis, which is a chronic lymphocytic thyroiditis that results in autoimmune destruction of the thyroid gland. Hypothyroidism is treated with synthetic levothyroxine.
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A posterior urethral valve is an obstructing membrane in the posterior male urethra as a result of abnormal in utero development. It is the most common cause of bladder outlet obstruction in male newborns. The disorder varies in degree, with mild cases followed conservatively.
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Fetal USG assists in the prenatal diagnosis of urinary tract obstruction. Sonographic findings include bilateral hydronephrosis with bladder distention with a “keyhole” appearance, particularly in a male fetus. In severe cases, oligohydramnios is found and may lead to poor fetal lung development with pulmonary insufficiency and congenital contractures. Prenatal USG leads to the diagnosis in most cases of PUV. Urethral valves are leaflets of tissue located in the lumen of the distal urethra from the prostate to the external sphincter. Posterior urethral valves are the most common cause of severe urinary tract obstruction in boys, occurring in 1 of every 5000 to 8000 newborn male infants; 25% to 30% ultimately have end-stage renal disease or chronic renal insufficiency. Neonates may present with respiratory distress secondary to lung hypoplasia from oligohydramnios, distended bladders, poor or dribbling urinary streams, palpable kidneys, reduced renal function, or UTI. Older infants have failure to thrive, renal dysfunction, or UTI. Older boys may present with voiding difficulty, such as diurnal enuresis or frequency. Posterior urethral valve is confirmed with VCUG or postnatal USG. The evaluation of the boy who has UTI includes VCUG and renal USG. Radionuclide scans are done to assess the renal parenchyma and the degree of obstruction. The diagnosis is confirmed with cystoscopy which allows for direct visualization of the PUV and ablation. Immediate relief of PUV obstruction includes bladder catheterization through the urethra with a small feeding tube. If UTI is suspected, antimicrobial therapy is initiated. Serum electrolytes, blood urea nitrogen (BUN), and creatinine levels are measured with correction as needed. Hemodynamic status is monitored because sepsis or renal failure can lead to cardiovascular collapse. After acute obstruction is relieved and the patient has been stabilized, endoscopic transurethral valve ablation may be performed if the serum creatinine level is normal and urethral size permits. If the serum creatinine remains elevated, the urethral lumen is too narrow, or the UTI does not respond to antibiotics, emergent vesicostomy may be necessary. Following ablation, VUR and persistent hydroure- teronephrosis may occur.
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Venous hum is a benign phenomenon. At rest, 20% of the cardiac output flows to the brain via the internal carotid and vertebral arteries. This drains via the internal jugular veins. The flow of blood can cause the vein walls to vibrate creating a humming noise which can be heard by the subject. Typically, a peculiar humming sound is heard in the upper chest near the clavicle.This may be confused with a heart murmur. The venous hum is heard throughout the cardiac cycle. The difference is easily detected by placing a finger on the jugular vein when listening to the heart, which will abolish or change the noise. A true heart murmur will be unaffected by this manoever. The murmur also disappears when the patient is in the supine position or may disappear if the subject turns their head to one side.
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Common Variable presents in adolescence with a lack of antibodies which leads to infections with encapsulated organisms (Strep Pneumo, H. Influ).
ICP leads to absence of venous pulsationsfrom low to high ur pons will die.from high to low ,ur brain will blow(cerebral edema )
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so in DKA serum osmolarity is high and when u give treatment rapidly ,it will cause cerebral edema
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Acute fluid overload leads to dilutional hyponatremia, which leads to a relative decrease in Na in the blood. This causes higher Na+ gradient in the cells pulling water in and leading to cerebral edema. So have to be careful giving too much fluid too quickly.
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The VSD will shift blood from left to right, this will lead to more blood entering the Pulmonary circulation causing Pulmonary HTNOn the other hand, the blood to the periphery will be reduced, including the kidneys. This will stimulate EPO release from the kidneys causing more RBCs to be released into the circulation ----> Polycythemia
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In children with lower airway FBA, the most common radiographic findings in lower airway FBA are :●Hyperinflated lung (lucency distal to the obstruction) – This is caused by partial airway obstruction with air trapping, such that air passes with inspiration, but not with exhalation ●Atelectasis – This is usually caused by complete obstruction of an airway, since air is resorbed from the distal alveoli over time. ●Mediastinal shift – The mediastinum tends to shift away from the lung field containing the foreign body (FB).●Pneumonia – Infection often develops distal to an obstructed airway. Therefore, a consolidated infiltrate is also a possible/ S: UTD
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Aplastic anemia causes pancytopenia and fever. Lymphadenopathy, arthralgias, bone pain, and hepatosplenomegaly are unusual findings.
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Hydroceles are fluid-filled sacs in the scrotal cavity consisting of remnants of the processus vaginalis. They are often diag- nosed in the newborn period or early childhood. Hydroceles communicate with the peritoneal cavity through a patent processus and are at risk for incarceration. These communi- cating hydroceles and hernias should be repaired as soon as possible to prevent the development of an incarcerated hernia. Most noncommunicating or simple hydroceles involute by 12 months of age. A varicocele is defined as dilation of the testicular veins and enlargement of the pampiniform plexus. Varicoceles become detectable in boys during adolescence, occur more commonly on the left, and are usually nontender. They are generally not visible when the patient is supine, but become evident upon standing when the veins distend and produce the characteristic “bag of worms” within the scrotum. Indications for surgical repair include pain, progressive enlargement, and discordant testicular growth. Unrepaired varicoceles may place the patient at an increased risk for infertility.
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A mass that bulges from the groin area (possibly extending into the scrotal sac) which increases in size with crying and straining may represent an inguinal hernia.
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Bullous impetigo, which is caused by a toxin-producing strain of S. aureus, begins as red macules that progress to bul- lous (fluid-filled) eruptions on an erythematous base (as seen on Color Plate 4). These lesions range from a few millimeters to a few centimeters in diameter. After the bullae rupture, a clear, thin, varnish-like coating forms over the denuded area. S. aureus can be cultured from the vesicular fluid. Bullous impetigo lesions can be mistaken for cigarette burns, raising the suspicion for abuse. Nonbullous impetigo, which is caused by both group A B-hemolytic streptococci and S. aureus, begins as papules that progress to vesicles and then to pustules measuring approximately 5 mm in diameter with a thin erythematous rim. The pustules rupture, leaving a honey-colored thin exudate that then forms a crust over a shallow ulcerated base. Local lymphadenopathy is common with streptococcal impetigo. Fever is uncommon. The causative organism can usually be isolated from the lesions. Limited nonbullous impetigo can be treated with topical antibiotics such as mupirocin ointment. If the lesions of bullous and/or nonbullous impetigo are numerous, they can be treated with a first-generation cephalosporin such as cephalexin, an oral drug that is effective against both Staphylococci and group A Streptococcus. In settings where methicillin- resistant S. aureus (MRSA) is suspected, agents such as clindamycin or trimethoprim-sulfamethoxazole may be more appropriate. The caretaker can remove any honey-colored crusts with twice-daily warm compresses.
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•In earlier stage of aspirin toxicity there will be primary respiratory alkalosis. This mainly explained by the direct effect of aspirin on the respiratory center, which stimulates the medulla oblongata- leading to hyperventilation and respiratory alkalosis ( this patient is having increased rate, so for sure respiratory alkalosis is there)--->(((but, wait, there's something else given in the question)))•2nd phase in aspirin toxicity is mixed respiratory alkalosis and metabolic acidosis (a key feature of salicylate poisoning). The latter will occur mainly due to uncoupling of oxidative phosphorylation in mitochondria leading to:1) increased metabolic rate2)increased oxygen consumption3)increased carbon dioxide formation4)increased heat production -----> this explains why the patient is having elevated temperature5)increased glucose utilizationIn addition, metabolic acidosis can be exacerbated by:-1) accumulation of organic acid metabolites2) lactic acidosis•3rd phase will be mixed metabolic and respiratory acidosis: this occurs when the child loses the respiratory drive and get fatigued, CO2 accumulation will occur.**These presentations won't be based on time at presentation, but more on the dose consumed, for such an effect to occur. =>To conclude;The patient is presenting with elevated temperature; lethargy; hyperventilation ==> mixed primary respiratory alkalosis and primary metabolic acidosis.
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in children, hypercholesterolemia is managed by 1. diet control 2. physical activity and weight loss and then pharmacotherapy if all else fails. SOURCE: Uptodate
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S pneumo is the most common cause of spontaneous bacterial peritonitis in kids.
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All levels of the respiratory tract may be affected, including the nasal passages, sinuses, and lower airways. Nasal polyps in any pediatric patient should prompt further testing for CF
