Pediatrics Final

Neurology

Developmental Milestones

• Social Smile: Onset normally 2 months (may be delayed to 3 months). Delayed smile can indicate cognitive issues. Hypoglycemia/maternal hypothyroidism can cause delay.

• Head Control: Full head support established by 4 months; no head lag expected.

• Rolling: Prone to supine around 6 months. Roll over by 5-6 months.

• Sitting: Sits with pelvic support ~6 months. Sits without support ~8-9 months.

• Object Transfer: Hand-to-hand transfer not expected at 4 months.

• Mouthing Objects: Starts around 4-6 months.

• Stranger Anxiety: Develops around 6-9 months.

• Pincer Grasp: Immature pincer grasp around 9-10 months.

• Standing/Walking: Stands alone ~12 months. Walks few steps with hand held ~12 months. Walks alone (normal range 9-15 months). Runs ~18 months. Runs stiffly at 18 months is noted. Goes upstairs with alternating feet ~30 months (2.5 years).

• Language:
  • Says “mama/dada” specifically ~10-12 months.
  • 1 year: 1-3 words besides mama/dada.
  • 15 months: Can say two words other than mama/dada.
  • 18 months: Speaks at least 10 single words. Points to body parts.
  • 2 years: 50+ words, 2-word sentences. Two-year-old unable to form a two-word sentence is unacceptable.
  • 2.5 years (30 months): Knows full name. Speaks pronouns (I/me/you).
  • 3 years: Knows age and sex.
  • 4 years: Tells stories. Refers to self by pronoun “I”.
  • Language delay: Deafness is a common cause.

• Fine Motor/Drawing:
  • Puts objects in mouth by 6 months.
  • Releases toy on demand ~12 months. Puts 2 cubes together.
  • Scribbles ~15-18 months. Draws vertical line ~18-24 months.
  • Draws horizontal line ~2 years.
  • Copies circle ~3 years.
  • Copies cross ~3.5-4 years. Copies square ~4 years.
  • Copies triangle ~5 years.

• Visual Tracking: Tracks 180 degrees by 2 months.

• Self-Care/Play: Eats with spoon ~18 months. Rides tricycle ~3 years. Hops on one foot ~4 years. Skips ~5 years. Knows heavier of two weights ~5 years.

• Corrected Age: Use for developmental assessment in premature infants until 2 years of age. (e.g., 7-month-old born at 28 weeks (12 weeks early) has corrected age of 4 months).

Seizures

• Febrile Seizures:
  • Simple: Generalized, <15 min, does not recur within 24 hrs. High recurrence risk in infancy. Low risk (<2%) of developing epilepsy.
  • Complex: Focal features, >15 min, or recurs within 24 hrs.
  • Management: Reassurance for simple seizures. Rectal diazepam if prolonged (>5 min). Antiepileptics generally not needed. Fever control may not prevent recurrence. Recurrence can happen even with lower fevers (e.g., 38°C).
  • Risk Factors for Epilepsy after Febrile Seizure: Complex features, neurodevelopmental abnormality, family history of epilepsy.
  • LP indicated if < 12 months old with first febrile seizure.

• Neonatal Seizures:
  • Causes: Hypoglycemia, Hypocalcemia, Hypomagnesemia, Hyper/Hyponatremia, infection (meningitis), HIE, ICH.
  • Types: Subtle (most common in preterms - eye deviation, lip smacking, apnea), Clonic, Tonic, Myoclonic. Generalized tonic-clonic is not typical.
  • Treatment: Phenobarbital is drug of choice.
  • Investigation: Rule out metabolic causes, meningitis. EEG helpful. Vital sign changes can suggest subtle seizures.

• Epilepsy Syndromes:
  • Absence Epilepsy: Staring spells, typical 3Hz spike-and-wave on EEG. Drug of choice is Valproic acid or Ethosuxamide. (Valproic acid preferred if also has GTCs). Good prognosis.
  • Infantile Spasms (West Syndrome): Spasms in clusters, often associated with Tuberous Sclerosis. EEG shows hypsarrhythmia. Treatment includes Vigabatrin. Poor prognosis for development.
  • Lennox-Gastaut Syndrome: Multiple seizure types, cognitive impairment, slow spike-wave on EEG. Poor response to treatment.
  • Juvenile Myoclonic Epilepsy: Myoclonic jerks, often in morning.
  • Rolandic Epilepsy: Benign focal epilepsy, often nocturnal facial/oral seizures. Good prognosis.

• Partial (Focal) Seizures:
  • Simple Partial: Consciousness preserved.
  • Complex Partial: Consciousness impaired. Often arise from temporal lobe. May have automatisms, staring. Can be difficult to distinguish from absence without EEG.
  • Gelastic Seizures: Recurrent attacks of laughter.

• Status Epilepticus: Seizure > 5-10 min or recurrent seizures without recovery. Medical emergency. Associated mortality (~5%). Can cause focal deficits. Intubate/ventilate if necessary.

• Non-epileptic Paroxysmal Events: Differentiated by history and physical, sometimes EEG. (e.g., Breath holding spells).

• Breath Holding Spells: Cyanotic or pallid, often triggered by frustration/anger/pain (age 6m-2y). May have brief clonic jerks after LOC. Benign. Parents need education/counseling.

Cerebral Palsy (CP)

• Non-progressive motor disorder. Often associated with prematurity, low birth weight, HIE, triplet gestation, TORCH. Periventricular leukomalacia is significant risk factor in premature infants.

• Types: Spastic (most common - diplegia, hemiplegia, quadriplegia), Choreoathetotic (associated with kernicterus), Ataxic, Mixed. Spastic diplegia is most common type overall. Quadriplegia often has worst prognosis, highest association with MR. Hemiplegia often spares cognition.

• Diagnosis: Based on history (risk factors) and abnormal motor exam (tone, reflexes, delayed milestones). Often presents as early hand preference (<1 yr), delayed walking, abnormal tone. Sensation usually intact.

• Associated Conditions: Epilepsy (~1/3), Mental retardation (variable, more common in quadriplegic), vision/hearing impairment, feeding difficulties.

• Management: Physiotherapy, Baclofen for spasticity.

• Prognosis: Motor deficit may improve slightly with therapy/growth but is generally static. Language skills do not typically deteriorate. Vaccination is NOT contraindicated.

Increased Intracranial Pressure / Meningitis

• Signs: Headache, vomiting, altered mental status, papilledema, bulging fontanelle (infants). Cushing’s triad (late sign).

• Meningitis Workup: LP for CSF analysis (cell count, diff, gram stain, culture, protein, glucose). Head CT before LP if focal neuro signs or signs of markedly elevated ICP.

• Bacterial Meningitis Prognosis Factors (Poor): Seizures after day 4, focal neuro deficit, gram-negative organism, low CSF glucose, very high CSF protein. Papilledema at presentation does NOT necessarily predict poor outcome.

• Management: Empiric antibiotics ASAP (e.g., Ceftriaxone + Vancomycin). Dexamethasone considered (esp. for Hib) given early. Monitor electrolytes (SIADH risk).

• Aseptic Meningitis: Often viral (Enterovirus). Diagnosis often by PCR of CSF.

Other Neurological Topics

• Hypotonia: Cerebral vs. spinal vs. muscle causes. Fasciculations suggest LMN lesion (e.g., SMA). Brisk reflexes suggest UMN lesion (central hypotonia).

• Acute Ataxia: Wide gait. Common causes include post-infectious cerebellitis, intoxication. Brain MRI is investigation of choice.

• Tuberous Sclerosis: Ash leaf spots (hypopigmented), subependymal calcifications/nodules, infantile spasms, developmental delay, seizures.

• Primitive Reflexes: Assess brainstem/basal ganglia. Should be symmetric. Asymmetry suggests focal neuro/peripheral nerve issue. Disappear at predictable ages (e.g., Moro 5-6m, Rooting 1-2m, Palmar grasp 2-3m, Tonic neck 6-7m). Parachute persists (appears ~9m). Babinski normal up to 2 years. Clonus normal up to ~2 months if unsustained.

• Neuro exam: Visual fixation at birth, follow to midline. Track 180 degrees by 2m. Acuity ~20/20 by 6 years (not months). Pupils react from birth. Color vision ~3 months.

• Valproic Acid: Side effects: Hepatotoxicity, thrombocytopenia, alopecia, weight gain (not loss), pancreatitis, teratogenicity. Drug of choice for absence with GTCs.

• EEG: Useful for diagnosing/classifying epilepsy, evaluating altered consciousness. Not routinely used for GDD without seizures.

Infectious Diseases & Vaccinology

Vaccinology

• Live Attenuated Vaccines: MMR, Varicella, Rotavirus, Oral Polio (OPV), BCG.
  • Contraindications: Severe immunodeficiency (e.g., SCID, high-dose steroids, chemotherapy, possibly siblings of chemo patients for OPV), pregnancy. MMR/Varicella generally withheld if recent IVIG. Varicella zoster vaccine contraindicated if recent IVIG within ~9 months in ITP patient.
  • MMR: Adverse effects (rare) - fever, rash, thrombocytopenia, encephalopathy. Not contraindicated by previous febrile seizure.
  • Rotavirus: Given orally (2, 3, 4 months in Jordan). Contraindicated >8 months old, history of intussusception. Prevents severe disease/dehydration. Highly contagious virus.
  • OPV: Used in outbreaks. Rare risk of vaccine-associated paralytic polio (VAPP). Contraindicated in household contacts of immunocompromised.

• Inactivated/Killed/Subunit/Toxoid Vaccines: DTaP/Tdap, IPV, Hib, PCV (conjugate), Hepatitis A, Hepatitis B, HPV.
  • DTaP: Acellular pertussis component. Common side effects: local reaction (pain, swelling), fever. Absolute contraindication: Anaphylaxis to previous dose or component, encephalopathy within 7 days of previous dose. Relative contraindications/precautions: high fever (>40.5), collapse/shock-like state, persistent crying >3hrs, seizures within 3 days (evaluate before giving next dose). Pertussis component given Tdap booster in pregnancy to protect newborn. Diphtheria/Tetanus toxoid content reduced in adult formulations (Td).
  • Hib: Conjugate vaccine. Prevents invasive disease (meningitis, epiglottitis, pneumonia). Not needed after 5 years old. Not effective <6 weeks old.
  • PCV (Pneumococcal Conjugate): Protects against common invasive serotypes. Prevents nasopharyngeal carriage. Pure polysaccharide vaccine (PPSV23) used for older children/adults at risk, not effective <2 years.
  • Hepatitis B: Recombinant surface antigen. Given at birth, 1-2m, 6m. Post-exposure prophylaxis for infant of HBsAg+ mother: Hep B vaccine + HBIG within 12 hours. Vaccine not contraindicated in prematurity.
  • Hepatitis A: Killed virus. Recommended >12 months. Not routinely given in Jordan.
  • IPV: Inactivated polio vaccine. Used in routine schedule. No risk of VAPP.

• General Principles: Immunized individuals can sometimes still carry/transmit organisms (e.g., Diphtheria). Polysaccharide vaccines generally poorly immunogenic in infants <2 years unless conjugated.

• Jordan National Schedule Points: Rota at 2,3,4 months. Hib/PCV at 2,3,4 months + booster. MMR at 1 year and 18 months. HAV not routine.

Specific Infectious Diseases

• Meningitis: (See Neurology section for CSF/Management).
  • Causes by Age: Neonates (GBS, E. coli, Listeria), Infants/Children (S. pneumoniae, N. meningitidis, Hib - less common now).
  • N. meningitidis: Gram-negative diplococci. Causes meningitis and/or meningococcemia (purpuric rash). Adrenal hemorrhage (Waterhouse-Friderichsen). More severe in complement deficiency. Rifampin or Ceftriaxone prophylaxis for close contacts. Penicillin/Ceftriaxone treatment.
  • S. pneumoniae: Most common cause post-neonatal period. Increased risk in asplenia, skull fracture. Penicillin resistance common (use Vancomycin empirically).
  • Hib: Was leading cause before vaccine. Epiglottitis also common. Rifampin prophylaxis for young/unimmunized household contacts.

• Sepsis:
  • Neonatal: Early onset (<72h) usually vertical transmission (GBS, E. coli). Late onset (>72h) vertical or horizontal. Empiric treatment: Ampicillin + Gentamicin. Coagulase-negative staph common cause of late-onset sepsis, esp. with lines.
  • Older children: S. pneumoniae, N. meningitidis most common.

• Pneumonia: (See Respiratory section)

• Gastroenteritis: (See GI section)

• Varicella (Chickenpox) / Herpes Zoster: VZV latency in dorsal root ganglia. Reactivation causes Zoster (shingles). Chickenpox milder in children than adults/immunocompromised/newborns. Rash starts on trunk, spreads centrifugally (macule -> papule -> vesicle -> crust). Acyclovir for severe disease/complications (encephalitis). Vaccine effective post-exposure (within 3-5 days).

• Measles: Prodrome (cough, coryza, conjunctivitis, Koplik spots) followed by maculopapular rash starting on face/hairline, spreading downwards. Highly contagious (respiratory droplets). Complications: Otitis media, pneumonia, encephalitis, SSPE (late). Vitamin A reduces morbidity/mortality. Vaccine effective post-exposure. Contraindicated in pregnancy, severe immunodeficiency.

• Mumps: Parotitis. Complications: Aseptic meningitis (most common), orchitis (esp. post-pubertal), pancreatitis, oophoritis. Antiviral therapy not effective. Vaccine contraindicated in severe immunodeficiency.

• Rubella: Mild illness usually. Characteristic rash (starts face, rapid spread). Posterior auricular/suboccipital lymphadenopathy. Major risk is Congenital Rubella Syndrome (CRS) if primary maternal infection in 1st trimester (cataracts, deafness, heart defects - PDA/PS, microcephaly). Vaccine contraindicated in pregnancy.

• Pertussis (Whooping Cough): Bordetella pertussis. Catarrhal, paroxysmal (whoop), convalescent stages. Severe in infants <6 months (apnea, cyanosis). Lymphocytosis characteristic. Diagnosis by PCR/culture. Treatment: Macrolides (Azithromycin preferred <1m). Vaccine protects against severe disease. Acellular less effective long-term than whole cell but fewer side effects. Antitoxin not proven beneficial.

• Diphtheria: Corynebacterium diphtheriae (toxigenic strains). Pharyngeal membrane, myocarditis, neuropathy. Antitoxin crucial (give early). Penicillin/Erythromycin eradicate carriage. Vaccine is toxoid.

• Poliomyelitis: Fecal-oral transmission. Mostly asymptomatic/minor illness. Paralytic (<1%) involves anterior horn cells (LMN signs - asymmetric flaccid paralysis). No sensory loss. VAPP risk with OPV.

• Hepatitis A: Fecal-oral. Usually asymptomatic/mild in young children. More severe in adults. Contagious in pre-icteric phase. Vaccine (killed) recommended >1 year. Post-exposure prophylaxis: Vaccine or Ig. Rarely acquired via transfusion.

• Hepatitis B: (See Vaccinology section). Parenteral/sexual/perinatal transmission. High risk of chronic carriage if infected perinatally. Associated with hepatocellular carcinoma. Core antibody not protective.

• Rotavirus: (See Vaccinology/GI sections). Most common cause of severe GE in young children. Osmotic diarrhea.

• Salmonella: Gastroenteritis usually self-limited (antibiotics not needed unless infant/immunocompromised/invasive). Can cause bacteremia (esp. infants), osteomyelitis (esp. sickle cell). S. Typhi (typhoid fever) acquired from human carriers. S. enteritidis from eggs/poultry.

• Otitis Media: S. pneumoniae, H. influenzae (non-typable), M. catarrhalis. S. Pneumo most common cause in agammaglobulinemia.

• Epiglottitis: Historically Hib. Now other bacteria possible. Thumb sign on lateral neck X-ray. Airway emergency.

• Botulism: Infant botulism from C. botulinum spores (e.g., honey). Constipation, hypotonia, weakness. Prevented by avoiding honey <1 year.

• Tetanus: Clostridium tetani (anaerobic, spore-forming). Toxin-mediated (tetanospasmin). Trismus, muscle rigidity, spasms. Wound management crucial. Tetanus vaccine (toxoid) + TIG for contaminated wounds if inadequately immunized. Antibodies don’t cross placenta well. Bacteremia does not occur. Isolation not required (not contagious).

Neonatology

Jaundice (Hyperbilirubinemia)

• Physiologic: Appears after 24h, peaks day 3-5 (term) or 5-7 (preterm), resolves by 1-2 weeks. Bilirubin <15 mg/dL (term). Due to increased RBC breakdown, immature liver conjugation (UGT enzyme), increased enterohepatic circulation. Rate of rise <5 mg/dL/day. Direct bili <2 mg/dL.

• Pathologic: Appears <24h, rises >5 mg/dL/day, total bili >15 (term), direct bili >2 mg/dL or >20% of total, persists >1-2 weeks. Requires investigation.

• Causes of Unconjugated (Indirect) Hyperbilirubinemia:
  • Increased Production: Hemolysis (ABO/Rh incompatibility - positive Coombs test, G6PD deficiency, spherocytosis), Polycythemia, Cephalohematoma/bruising. Hemolysis is most common cause of jaundice <24h.
  • Decreased Conjugation: Physiologic, Crigler-Najjar syndrome, Gilbert syndrome, Hypothyroidism, Breast milk jaundice.
  • Increased Enterohepatic Circulation: Breastfeeding jaundice, intestinal obstruction, pyloric stenosis.

• Causes of Conjugated (Direct) Hyperbilirubinemia: Always pathologic. Biliary atresia, neonatal hepatitis (TORCH, metabolic), sepsis, TPN cholestasis, Alagille syndrome, Choledochal cyst, CF, Tyrosinemia, Galactosemia. Gilbert syndrome causes UNconjugated.

• Breastfeeding vs. Breast Milk Jaundice:
  • Breastfeeding Jaundice: Early onset (1st week), due to inadequate intake/dehydration/increased enterohepatic circulation. Prevented by frequent, effective feeding.
  • Breast Milk Jaundice: Later onset (after 1st week), peaks at 2-3 weeks, may persist 1-3 months. Due to substance in milk inhibiting UGT. Baby thriving. Diagnosis of exclusion. Usually benign, rarely needs interruption of breastfeeding.

• Kernicterus (Acute Bilirubin Encephalopathy): Risk depends on bilirubin level, gestational age, presence of hemolysis, sepsis, acidosis, hypoalbuminemia. High levels in breast milk jaundice generally not associated with neurotoxicity.

• Assessment: Visual estimation is inaccurate. Measure TSB or TcB. Assess risk factors (prematurity, hemolysis, sepsis, feeding). Direct bilirubin needed if jaundice prolonged or ill infant.

• Management:
  • Phototherapy: Converts bilirubin to water-soluble isomers. Side effects: rash, loose stools, dehydration, bronze baby syndrome, retinal damage (cover eyes). Corneal ulcers not a typical side effect.
  • Exchange Transfusion: For critically high levels or signs of kernicterus. Consider if failure of phototherapy. Risks associated.
  • IVIG: Can reduce need for exchange transfusion in isoimmune hemolysis (ABO/Rh).
  • Phenobarbital: Induces UGT enzyme, rarely used now.
  • Hydration: Ensure adequate intake. Water supplementation not needed.

• Prolonged Jaundice (>2 weeks term, >3 weeks preterm): Investigate - check direct/indirect bili, LFTs, thyroid function, urine for reducing substances/culture, sepsis screen.

Respiratory Distress in Newborn

• Respiratory Distress Syndrome (RDS): Primarily in premature infants due to surfactant deficiency. Presents soon after birth with tachypnea, grunting, retractions, cyanosis. CXR: low lung volumes, diffuse reticulogranular pattern (“ground glass”), air bronchograms. Management: Antenatal steroids (most effective prevention), surfactant replacement, CPAP/mechanical ventilation, oxygen. Risk increased with maternal diabetes, C-section without labor. Risk decreased with chorioamnionitis, IUGR, prolonged ROM. Usually worsens over first 48-72h then improves. Apnea suggests more severe disease. Dexamethasone postnatally not standard due to neurodevelopmental concerns.

• Transient Tachypnea of Newborn (TTN): Delayed resorption of fetal lung fluid. Presents within hours of birth with tachypnea, mild distress. Usually term/near-term infants, esp. after C-section or precipitous delivery. CXR: normal/increased lung volumes, perihilar streaking, fluid in fissures. Usually resolves within 48-72 hours with supportive care (oxygen, sometimes CPAP). Surfactant not needed.

• Meconium Aspiration Syndrome (MAS): Primarily term/post-term infants. Intrauterine hypoxia leads to meconium passage and gasping. Causes chemical pneumonitis, airway obstruction, PPHN. CXR: coarse patchy infiltrates, hyperinflation, possible pneumothorax. Requires resuscitation, ventilation, possibly surfactant/iNO. Routine suctioning below cords no longer recommended for vigorous infants. Meconium itself is sterile, but risk of secondary infection exists.

• Pneumonia: GBS, E. coli. Presents similar to RDS. CXR may show infiltrates/consolidation. Requires antibiotics.

• Persistent Pulmonary Hypertension of Newborn (PPHN): Failure of normal postnatal drop in PVR. Right-to-left shunting via PDA/PFO. Associated with MAS, RDS, pneumonia, sepsis, asphyxia. Requires supportive care, oxygen, often iNO.

• Other Causes: Congenital heart disease, pneumothorax, congenital diaphragmatic hernia, choanal atresia.

Prematurity

• Definition: Born <37 weeks GA. Post-term >42 weeks. Low birth weight (LBW) <2500g, VLBW <1500g, ELBW <1000g.

• Survival Factors: Gestational age (most accurate isolated factor), birth weight, antenatal steroids, surfactant availability.

• Complications: RDS, apnea of prematurity (treat with caffeine), PDA, IVH, PVL (risk factor for CP), NEC, ROP, BPD (chronic lung disease), sepsis, hypothermia, hypoglycemia, hyperbilirubinemia, feeding difficulties, FTT, osteopenia of prematurity (check Alk Phos, Phos).

• Long-term Sequelae: Cerebral palsy, developmental delay, learning disabilities, visual/hearing impairment, chronic lung disease, ADHD.

• Management: Thermoregulation (incubator, plastic bag/wrap for ELBW), fluid/nutrition management (TPN, enteral feeds), respiratory support, infection prevention, developmental care. Correct for prematurity when assessing development until age 2.

Birth Asphyxia & Resuscitation

• APGAR Score: Assesses Appearance, Pulse, Grimace, Activity, Respiration at 1 and 5 minutes. Score 0, 1, or 2 for each. Used to guide resuscitation needs and response, not predict long-term outcome. Acrocyanosis scores 1 for color. HR <100 needs intervention. Irregular/slow breathing scores 1. Grimace scores 1. Some flexion scores 1. Good cry scores 2 for respiration. Active motion scores 2 for activity. Sneeze/cough on suction scores 2 for grimace.

• Resuscitation Steps (NRP): Initial steps (Warm, dry, stimulate, position airway, suction if needed) -> Assess HR and breathing. If HR <100 or gasping/apnea -> Positive Pressure Ventilation (PPV) -> Reassess. If HR <60 despite effective PPV -> Chest compressions (3:1 ratio with ventilation) -> Reassess. If HR remains <60 -> Epinephrine (IV/IO or ET). Volume expansion considered for shock/blood loss.

• Key Points: Skilled person needed at every delivery. Initial steps within 30-60 seconds. PPV is crucial step for bradycardia/apnea. Don’t delay compressions if HR <60 after ~30s effective PPV. Atropine not used for neonatal bradycardia. 0.9% NS for volume. Glucose not usually given acutely unless hypoglycemia documented. All newborns assessed, not all sent to radiant warmer.

Neonatal Examination & Common Findings

• Timing: Brief assessment at birth. Full exam within 24 hours. Discharge exam.

• Normal Variations: Erythema toxicum, Mongolian spots, milia, Epstein pearls, Vernix caseosa, lanugo, acrocyanosis, breast engorgement, vaginal bleeding/discharge (maternal hormone withdrawal), caput succedaneum (crosses sutures), pulsating umbilical cord, bluish spot on back (Mongolian). Bifid uvula can be normal or associated with submucous cleft. Posterior fontanelle may be present/small.

• Abnormal Findings: Cephalohematoma (subperiosteal, doesn’t cross sutures, risk for jaundice), Craniotabes (soft skull bones, can be normal in preterms or suggest rickets/OI), Wormian bones (intrasutural bones, assoc. syndromes), True cyanosis, Jaundice <24h, Single umbilical artery (assoc. anomalies), Ambiguous genitalia, White pupillary reflex (leukocoria - RB, cataract), Omphalitis (erythema extending around umbilicus), Bulging fontanelle, Hepatosplenomegaly, Congenital heart murmurs (though absence doesn’t rule out CHD), Choanal atresia (cyanosis relieved by crying).

Other Neonatal Topics

• Sepsis: (See Infectious Diseases). Empiric Tx: Ampicillin + Gentamicin.

• Hypoglycemia: Risk factors: Prematurity, SGA, LGA, infant of diabetic mother (IDM), asphyxia, sepsis, hypothermia, CAH, hyperinsulinism. IDMs have hyperinsulinemia -> hypoglycemia post-birth. Also at risk for macrosomia, RDS, cardiac defects, polycythemia, hypocalcemia. Breast milk jaundice does not cause hypoglycemia.

• Hypothermia: Significant risk, esp. in preterms. Maintain neutral thermal environment.

• Feeding: Breastfeeding initiated ASAP. Feed on demand. Colostrum important first milk. Vitamin D supplement needed for exclusively breastfed infants (400 IU/day). Iron supplement needed after 4-6 months for breastfed infants. Formula-fed infants generally don’t need Vit D/Iron supplement if formula is fortified. Signs of good feeding: audible swallowing, 6-8 wet diapers/day (after day 3-4), 3-4 stools/day, appropriate weight gain.

• Fluids/Electrolytes: Maintenance fluids calculated based on weight (Holliday-Segar). Preterms have higher insensible losses. Sodium usually not added on Day 1. Glucose 5% or 10% used. Maintenance KCL (20 meq/L) added once urine output established. Fluids may be restricted with PDA.

• Necrotizing Enterocolitis (NEC): Most common GI emergency in neonates, esp. preterms after starting feeds. Abdominal distension, bloody stools, feeding intolerance, apnea, shock. X-ray: pneumatosis intestinalis, portal venous gas, free air (perforation). Management: NPO, NG decompression, broad-spectrum antibiotics, supportive care, surgery if perforated. Strictures are late complication. Infectious etiology likely plays role, but exact cause complex. Rate inversely related to GA. Jaundice is not a primary presentation.

• Osteopenia of Prematurity: Due to inadequate Ca/Phos intake/stores. Dx labs: Elevated Alk Phos, Low Phos. Requires supplementation.

• Vitamin K Deficiency Bleeding (VKDB): Prevented by routine Vit K injection at birth. Presents with bleeding (GI, ICH, umbilical). Breastfed infants at higher risk if no prophylaxis.

Cardiology

Congenital Heart Disease (CHD) - General

• Cyanotic vs. Acyanotic: Differentiated by presence of central cyanosis.

• Increased vs. Decreased Pulmonary Blood Flow (PBF): Assessed clinically and on CXR.

• Ductal Dependency: Some lesions require PDA for pulmonary blood flow (e.g., Pulmonary Atresia, severe TOF, Tricuspid Atresia) or systemic blood flow (e.g., HLHS, Critical Coarctation/AS, Interrupted Aortic Arch). PGE1 infusion maintains ductal patency.

• Foramen Ovale Dependency: Some lesions require PFO for mixing or survival (e.g., TGA, Tricuspid Atresia, HLHS, TAPVR).

• Fetal Circulation: High PVR, low SVR. RV is dominant ventricle. PFO allows R -> L atrial shunt. Ductus arteriosus allows pulmonary artery -> aorta shunt. Umbilical vein carries most oxygenated blood. Umbilical arteries carry deoxygenated blood.

Specific Acyanotic Lesions (L -> R Shunts / Obstruction)

• Ventricular Septal Defect (VSD):
  • Most common CHD overall.
  • Small VSD: Often asymptomatic, loud holosystolic murmur at LLSB. May close spontaneously.
  • Large VSD: Symptoms of HF (tachypnea, poor feeding, FTT) after PVR drops (4-8 weeks). Holosystolic murmur (may be softer if very large), loud P2, mid-diastolic rumble at apex (increased flow across MV). Displaced apical impulse, RVH/LVH on ECG/CXR. Cardiomegaly, increased PVM on CXR. Can lead to pulmonary HTN / Eisenmenger syndrome if unrepaired. Wide pulse pressure is NOT typical.

• Atrial Septal Defect (ASD):
  • Secundum ASD most common type. Primum ASD associated with AV canal defects.
  • Often asymptomatic until adulthood.
  • Exam: Wide, fixed splitting of S2. Soft systolic ejection murmur at LUSB (increased flow across PV). Possible mid-diastolic rumble at LLSB (increased flow across TV).
  • ECG: RAD, RVH, RBBB pattern (rsR’ in V1).
  • CXR: Cardiomegaly (RA/RV enlargement), increased PVM. LV dilatation is NOT typical.
  • Complications: Arrhythmias (atrial), paradoxical emboli, pulmonary HTN (late). Closure recommended even if asymptomatic. Gallop rhythm is NOT typical.

• Patent Ductus Arteriosus (PDA):
  • Connects pulmonary artery to aorta. Normal closure within days after birth.
  • Small PDA: Often asymptomatic. Continuous “machinery” murmur at L infraclavicular area.
  • Large PDA: Symptoms of HF/FTT. Continuous murmur, loud S2, bounding peripheral pulses, wide pulse pressure (e.g., 100/45). LVH, LAE on ECG/CXR. Cardiomegaly, increased PVM. Can lead to pulmonary HTN. Right atrial hypertrophy/dilatation is NOT typical.

• Coarctation of Aorta (CoA):
  • Narrowing of aorta, usually near ductus insertion.
  • Presents with upper extremity hypertension, decreased/delayed femoral pulses (radio-femoral delay), possible systolic murmur radiating to back (interscapular). Possible LVH on ECG.
  • CXR: Cardiomegaly, rib notching (due to intercostal collaterals, seen in older children), “3” sign. Wide mediastinum is NOT typical. May present with shock in neonates if ductus closes (ductal-dependent systemic flow).

• Aortic Stenosis (AS):
  • Obstruction to LV outflow.
  • Exam: Systolic ejection murmur at RUSB, radiating to suprasternal notch/carotids. Possible ejection click. Possible LVH. Critical AS presents with shock in neonates (ductal-dependent).

• Pulmonary Stenosis (PS):
  • Obstruction to RV outflow.
  • Exam: Systolic ejection murmur at LUSB, radiating to back. Possible ejection click (valvar). Possible RVH. Critical PS presents with cyanosis in neonates (ductal-dependent pulmonary flow).

Specific Cyanotic Lesions

• Tetralogy of Fallot (TOF): Most common cyanotic CHD beyond infancy.
  • Components: VSD, Overriding Aorta, Pulmonary Stenosis (RVOTO), RVH.
  • Presentation: Cyanosis (degree depends on severity of RVOTO), “Tet spells” (hypercyanotic episodes, often relieved by squatting). Loud, harsh systolic ejection murmur at LSB (due to PS, murmur may decrease during Tet spell). Single S2. RV heave.
  • ECG: RAD, RVH.
  • CXR: Normal heart size or mild cardiomegaly, “Boot-shaped” heart (upturned apex due to RVH, concave PA segment), decreased PVM. Cardiomegaly on CXR is NOT typical unless severe.
  • Clubbing develops over time. Polycythemia is compensatory. Clubbing not expected at 3 months.

• Transposition of Great Arteries (TGA): Aorta arises from RV, PA from LV. Requires mixing (ASD/PFO, VSD, PDA) for survival.
  • Presentation: Severe cyanosis from birth, often minimal respiratory distress initially. Loud, single S2. Often no murmur unless associated VSD/PS.
  • CXR: “Egg-on-a-string” (narrow mediastinum, oval-shaped heart), increased PVM.
  • Management: PGE1 to maintain PDA, balloon atrial septostomy if needed, arterial switch operation.

• Tricuspid Atresia: Absence of tricuspid valve, hypoplastic RV. Requires ASD/PFO for RA->LA shunt and VSD for pulmonary blood flow.
  • Presentation: Cyanosis. Possible murmur (VSD).
  • ECG: Left axis deviation (characteristic finding), LVH. NO RV heave expected.
  • Management: PGE1 often needed. Staged surgical repair.

• Truncus Arteriosus: Single great artery arises from heart, supplying systemic, pulmonary, and coronary circulations. Always has associated VSD.
  • Presentation: Variable cyanosis, signs of HF (due to excessive PBF). Loud single S2, systolic ejection murmur, possible diastolic murmur (truncal valve regurg). Bounding pulses.
  • CXR: Cardiomegaly, increased PVM.

• Total Anomalous Pulmonary Venous Return (TAPVR): Pulmonary veins drain into RA or systemic veins instead of LA. Requires ASD/PFO for survival.
  • Presentation: Variable cyanosis, signs of HF/pulmonary congestion. If obstructed, severe cyanosis and respiratory distress early.
  • CXR: Cardiomegaly, increased PVM. Possible “Snowman” sign (supracardiac type).

• Hypoplastic Left Heart Syndrome (HLHS): Underdevelopment of left-sided structures (MV, LV, Aortic valve, Ascending aorta). Requires PDA for systemic flow and ASD/PFO for RA->LA flow.
  • Presentation: Shock/cyanosis when ductus closes. Poor pulses. Single S2.
  • Management: PGE1 infusion, staged surgical repair (Norwood etc.) or transplant.

Cardiovascular Physiology & Assessment

• Normal Changes: Resting HR decreases with age. BP lowest at birth, increases with age. PVR high in utero, drops significantly after birth, reaches adult levels later. Preterm BP lower than term. HR 165 in crying 6m old is normal. S2 louder than S1 at base (pulmonary area) is normal. Visible apical impulse normal in infants.

• Heart Failure: Signs: Tachypnea, tachycardia, poor feeding, FTT, sweating (diaphoresis), hepatomegaly, pulmonary congestion (retractions, rales), cool extremities, gallop rhythm (S3). Low BP is a late sign.

• Murmurs:
  • Systolic Ejection: AS, PS, ASD flow murmur, Innocent (Still’s, PPS).
  • Holosystolic/Pansystolic: VSD, MR, TR.
  • Diastolic: AR, PR (regurgitation), MS, TS (stenosis). Early diastolic murmur at aortic area - likely AR. Diastolic murmur at LLSB - ?TR/TS or VSD diastolic rumble. Soft early diastolic murmur at aortic area = pathological.
  • Continuous: PDA. Venous hum (benign).
  • Innocent Murmurs: Common. Usually systolic, soft (Grade 1-3/6), vibratory/musical (Still’s) or blowing (PPS), change with position (louder supine, disappear standing/sitting - Still’s), no associated symptoms/abnormal findings. Reassurance needed. Still’s murmur often at LLSB. PPS at LUSB/axillae (disappears by 6-9m).

• Cardiac Output: CO = HR x SV. Increases with increased metabolic demand (fever, exercise), anemia. Decreases with increasing afterload. Sympathetic stimulation increases HR and contractility. Infants have limited ability to increase SV, rely more on HR.

• Volume Overload:
  • LV Volume Overload: VSD, PDA, MR, AR, Truncus. Causes LV dilatation/hypertrophy.
  • RV Volume Overload: ASD, TR, PAPVR. Causes RA/RV dilatation/hypertrophy.

• Pressure Overload:
  • LV Pressure Overload: AS, CoA, Systemic HTN. Causes LVH.
  • RV Pressure Overload: PS, Pulmonary HTN. Causes RVH.

• Cyanosis Management: Suspected ductal-dependent cyanotic lesion -> PGE1. Hyperoxia test helps differentiate cardiac vs pulmonary cyanosis (cardiac usually has poor response to 100% O2).

Respiratory

Common Respiratory Illnesses

• Pneumonia:
  • Causes: Neonates (GBS, E. coli, Listeria), Infants/Young Children (Viruses - RSV; Bacteria - S. pneumoniae), Older Children >5y (S. pneumoniae, Mycoplasma pneumoniae, Chlamydophila pneumoniae). Hib less common due to vaccine. S. aureus associated with empyema, pneumatoceles.
  • Mycoplasma: Common >5 years, less common in infancy. Drug of choice: Macrolide (e.g., Erythromycin, Azithromycin).
  • Hospitalization Criteria: Age <3-6 months, respiratory distress (tachypnea, retractions, hypoxia), dehydration, immunocompromise, severe pneumonia (lobar, effusion), failure of outpatient therapy, suspected resistant organism. Bilateral infiltrates often warrants admission.
  • Complications: Pleural effusion, empyema (S. aureus most common cause), lung abscess, pneumatocele.

• Bronchiolitis:
  • Most common cause: RSV (Respiratory Syncytial Virus). Peaks in winter. Most common <2 years.
  • Symptoms: URI prodrome followed by cough, wheezing, tachypnea, retractions, feeding difficulty. Apnea can occur, esp. <2 months.
  • Exam: Wheezes, crackles.
  • CXR: Hyperinflation, flattened diaphragms, peribronchial cuffing, atelectasis. Decreased lung volume is NOT typical.
  • Management: Supportive - hydration, oxygen, suctioning. Nebulized hypertonic saline may help inpatients. Bronchodilators/steroids generally NOT recommended. Ribavirin rarely used (severe cases/immunocompromised).
  • Complications: Apnea, respiratory failure. Increased risk of later reactive airway disease/asthma. Secondary bacterial pneumonia is uncommon.

• Croup (Laryngotracheobronchitis):
  • Most common cause: Parainfluenza virus. Usually 6 months - 3 years. Peaks autumn/early winter.
  • Symptoms: URI prodrome, then barking cough, inspiratory stridor, hoarseness. Usually gradual onset.
  • Management: Cool mist, oral/IM dexamethasone, nebulized epinephrine for moderate/severe distress. Rarely needs intubation. Antibiotics not indicated (unless bacterial tracheitis suspected).
  • X-ray (AP neck): Steeple sign (subglottic narrowing).

• Epiglottitis:
  • Historically Hib, now other bacteria (Strep, Staph). Rare due to Hib vaccine.
  • Symptoms: Acute onset high fever, sore throat, dysphagia, drooling, muffled voice, tripod position, respiratory distress. Preceding coryza is NOT typical. Cough often absent/slight.
  • Management: Airway emergency! Keep child calm, avoid upsetting interventions (e.g., throat exam). Secure airway in OR (intubation). IV antibiotics (e.g., Ceftriaxone). Alert ENT/Anesthesia. Lateral neck X-ray shows “thumb sign” (swollen epiglottis) - do not delay airway management for X-ray if unstable.

• Bacterial Tracheitis: Superinfection of trachea, often after viral croup. Caused by S. aureus typically. Presents with high fever, toxicity, worsening respiratory distress despite croup treatment. Requires antibiotics, possible intubation.

Asthma

• Diagnosis: Recurrent episodes of wheezing, cough (esp. nocturnal, post-exercise), shortness of breath. Often triggered by URIs, allergens, exercise, cold air. PFTs show obstructive pattern (decreased FEV1, FEV1/FVC ratio), reversible with bronchodilator. Increased FRC.

• Triggers: URIs (most common in young children), allergens (dust mites, pollen, dander, mold), irritants (smoke), exercise, cold air, weather changes.

• Acute Exacerbation:
  • Assessment: Wheezing, tachypnea, retractions, accessory muscle use, ability to speak, PEFR, O2 saturation. Silent chest, cyanosis, altered mental status, Pulsus paradoxus, rising PaCO2 are signs of impending respiratory failure.
  • Management: Inhaled SABA (albuterol), systemic corticosteroids (oral/IV - hydrocortisone preferred IV), oxygen. Consider ipratropium bromide (anticholinergic) with SABA for severe exacerbations. IV Magnesium sulfate for severe, refractory cases. Aminophylline rarely used now. Inhaled corticosteroids are controller meds, not first-line rescue. Mast cell stabilizers (cromolyn) are for prevention, not acute treatment.

• Controller Therapy: Indicated if using SABA >2 days/week, >2 nights/month, or >2 exacerbations needing oral steroids/year (GINA guidelines). Inhaled corticosteroids (ICS) are cornerstone. Options include adding LABA, LTRA (montelukast), or increasing ICS dose based on severity. Check compliance/technique before stepping up therapy.

• Predictors of Persistence: Atopy (eczema, allergic rhinitis), parental asthma, wheezing apart from colds, eosinophilia, positive skin prick tests to inhaled allergens.

Cystic Fibrosis (CF)

• Genetics: Autosomal recessive (CFTR gene mutation, delta-F508 most common). Defective chloride channel. Inherited on chromosome 7 (not 9). Affects males/females equally.

• Diagnosis: Newborn screening (IRT - Immunoreactive Trypsinogen; elevated suggests possible CF, not diagnostic). Sweat chloride test (pilocarpine iontophoresis) is gold standard (>60 mmol/L is positive). Genetic testing confirms diagnosis.

• Manifestations:
  • Respiratory: Chronic cough, recurrent pneumonia (S. aureus early, Pseudomonas later), bronchiectasis, nasal polyps, sinusitis, pneumothorax (late complication), eventual respiratory failure. PFTs show obstructive pattern (can be mixed or restrictive late).
  • Gastrointestinal: Meconium ileus (newborn), pancreatic insufficiency (fat malabsorption - steatorrhea, FTT), rectal prolapse, distal intestinal obstruction syndrome (DIOS), cholestasis, CF-related diabetes (CFRD), hyperglycemia (not typically hypoglycemia). Delayed puberty common. Precocious puberty is NOT a feature.
  • Other: Salty sweat (salt wasting risk, esp. in heat - can lead to hyponatremic dehydration with metabolic alkalosis, not typically acidosis), infertility (males - CBAVD).

• Management: Airway clearance (physiotherapy, vests), inhaled medications (bronchodilators, DNase, hypertonic saline), antibiotics (oral, inhaled, IV for exacerbations), pancreatic enzyme replacement, high-calorie/high-fat diet, fat-soluble vitamin supplementation (A, D, E, K). Lung transplant for end-stage disease.

Other Respiratory Topics

• Airway Resistance: Major contributor in infants is nasal airway/mouth.

• Atelectasis: Mucous plugging common cause, esp. post-viral infection. CXR shows opacification, volume loss, possible mediastinal shift towards affected side.

• Pleural Effusion/Empyema: S. aureus common cause of empyema. Requires drainage + antibiotics.

• Primary Ciliary Dyskinesia (PCD): Chronic sinopulmonary infections, situs inversus (Kartagener’s), infertility. Dx requires electron microscopy of cilia.

• Laryngomalacia: Most common cause of congenital stridor. Inspiratory stridor, worse supine/crying/feeding. Due to floppy supraglottic structures. Usually benign, resolves by 1-2 years. Can be aggravated by GERD. Surgery is rarely needed.

• Sinusitis: Often follows URTI. Thick/purulent nasal discharge, cough, facial pain/pressure. Amoxicillin or Augmentin first line. CT not usually required unless complications suspected (orbital cellulitis, brain abscess). Chronic asthma is NOT a cause of sinusitis but can be associated.

• Pharyngitis: Viral most common overall. Group A Strep (GAS) bacterial cause. Sudden onset, fever, exudates, anterior cervical nodes more common in GAS. Penicillin treatment prevents rheumatic fever but not post-strep GN. AGN can follow skin or throat infection.

• Hypoxia Mechanisms: V/Q mismatch most common cause.

• OSA (Obstructive Sleep Apnea): Adenotonsillar hypertrophy most common cause in children.

Gastrointestinal

Nutrition & Feeding

• Breast Milk:
  • Composition: Whey predominant protein (easier to digest), lactose is main carbohydrate, fat content varies (provides ~50% calories). Lower protein, Ca, Phos than cow’s milk. Higher carbohydrate content than cow’s milk. Contains IgA, lactoferrin, lysozyme (protective). Vitamin D content low (supplementation needed). Iron low but highly bioavailable (supplement after 4-6m). Caloric content ~67 kcal/100ml. Protein component (casein, whey) is most antigenic. Hydrolyzed casein is NOT the protein component. Contents vary with maternal diet, stage of lactation.
  • Benefits: Optimal nutrition, easy digestion, reduced infection risk (diarrhea, otitis media, pneumonia), reduced SIDS risk, potential reduced risk of allergy/asthma/obesity/diabetes, promotes bonding. Does NOT protect against hemorrhagic disease of newborn (needs Vit K). Protects against ovarian cancer in mother.
  • Contraindications: Maternal HIV (in developed countries), active untreated TB, active herpes lesions on breast, certain medications, illicit drug use, infant galactosemia. Hepatitis B+ mother CAN breastfeed if infant receives HBIG + vaccine. Breast abscess may require temporary cessation on affected side. Severe psychosis.

• Formula: Cow’s milk based is standard. Special formulas:
  • Soy: For galactosemia, transient lactase deficiency, vegetarian preference. Cross-reactivity with cow’s milk protein allergy (CMPA) exists. Carbohydrate is sucrose.
  • Hydrolyzed (Extensively or Partially): For CMPA, malabsorption. Extensively hydrolyzed or amino acid-based for severe CMPA. Partially hydrolyzed is NOT for treatment of CMPA. Response usually seen in 2-3 days.
  • Lactose-Free: For primary or secondary lactase deficiency. NOT standard for CMPA.

• Cow’s Milk: Fresh cow’s milk not recommended before 12 months (low iron, high solute load, risk of GI blood loss). Low-fat milk not recommended before 24 months.

• Introducing Solids: Recommended around 6 months, when infant shows developmental readiness (good head control, sits with support, shows interest). Introduce single ingredients one at a time.

• Nutritional Assessment: Weight gain is best indicator of adequacy. Monitor length, head circumference. Calorie count less practical. Urine output helpful for hydration.

• Failure To Thrive (FTT): Weight <3rd-5th percentile or crossing >2 major percentiles downward.
  • Type 1: Weight affected first (inadequate intake, malabsorption).
  • Type 2: Weight and Height affected (endocrine, genetic, constitutional).
  • Type 3: Weight, Height, Head Circumference affected (CNS, chromosomal, TORCH).
  • Causes: Inadequate intake (poverty, poor feeding technique, neglect), malabsorption (CF, celiac, CMPA), increased metabolic demand (CHD, chronic illness), endocrine (hypothyroid), genetic/chromosomal. Vomiting alone less likely to cause Type 1 FTT unless severe/persistent. Chromosomal abnormality can cause FTT.

Diarrhea

• Acute Diarrhea: <2 weeks. Most common cause worldwide: Rotavirus. Other viral (norovirus, adenovirus), bacterial (Salmonella, Shigella, Campylobacter, E. coli, Yersinia), parasitic (Giardia, Amoeba). Antibiotic-associated diarrhea.
  • Rotavirus: Osmotic diarrhea, highly contagious, vaccine preventable. Most common cause overall. Diagnosed by stool antigen test.
  • Invasive/Bloody Diarrhea (Dysentery): Shigella, Salmonella, Campylobacter, EHEC O157:H7, Amoeba. Characterized by fever, cramps, stool PMNs. Vibrio cholera causes watery, non-bloody diarrhea.
  • Management: Oral Rehydration Therapy (ORT) is cornerstone. Continue feeding (including breastfeeding) + ORT. Avoid sugary drinks/juices. Antibiotics only for specific cases (Shigella, C. diff, severe cholera, sepsis, Giardia, Amoeba). Antidiarrheals generally not recommended.

• Chronic Diarrhea: >2-4 weeks.
  • Causes: Post-infectious (secondary lactase deficiency), toddler’s diarrhea (functional), Celiac disease, CF, CMPA/food allergies, Giardia, IBD, immune deficiency.
  • Investigation: Stool studies (pH, reducing substances, fat, O&P, culture, C. diff, Giardia antigen, calprotectin), blood tests (celiac serology, CBC, albumin), sweat test.
  • Stool pH <5.5 + reducing substances suggests carbohydrate malabsorption (e.g., lactose intolerance). Protein malabsorption does NOT cause acidic stool pH.
  • Steatorrhea suggests fat malabsorption (CF, cholestasis).
  • Secretory diarrhea persists with fasting.

Specific GI Conditions

• Celiac Disease: Immune-mediated enteropathy triggered by gluten (wheat, barley, rye). Rice is safe.
  • Associations: Type 1 DM, autoimmune thyroiditis, Down syndrome (Trisomy 21), Turner syndrome, IgA deficiency, family history. Trisomy 13 is NOT a typical association.
  • Presentation: Diarrhea, FTT, abdominal pain/distension, constipation, short stature, iron deficiency anemia, dermatitis herpetiformis (itchy rash). Vitamin D resistant rickets is NOT a typical presentation.
  • Diagnosis: Serology (Anti-TTG IgA is best screening test; check total IgA). HLA-DQ2/DQ8 testing. Gold standard: Small bowel biopsy showing villous atrophy (though often avoided now if serology/genetics strongly positive).
  • Management: Lifelong strict gluten-free diet. Sensitivity does NOT resolve after 5 years. TTG titers should decrease with adherence. At risk for Vit D deficiency.

• Cow’s Milk Protein Allergy (CMPA): Can present with vomiting, diarrhea (sometimes bloody), FTT, eczema, respiratory symptoms. Treat by eliminating cow’s milk protein (maternal elimination if breastfeeding, switch to extensively hydrolyzed or amino acid formula).

• Lactose Intolerance:
  • Primary: Rare congenitally. Develops in older children/adults (lactase non-persistence).
  • Secondary: Transient, follows gastroenteritis or other mucosal injury. Improves with lactose-free formula/diet. Oral lactase supplements may help. Dairy avoidance relieves symptoms. Does NOT typically cause worsening diarrhea unless intake is excessive. Condition is common, not rare.

• Gastroesophageal Reflux (GER) vs. GERD: GER common in infants, usually benign (“happy spitters”). GERD = GER + complications (FTT, esophagitis, respiratory problems).

• Biliary Atresia: Progressive obliteration of extrahepatic bile ducts. Presents in first few months with persistent jaundice (conjugated), acholic (pale) stools, dark urine, hepatomegaly. Requires Kasai procedure early, often eventual liver transplant.

• Galactosemia: Defect in galactose metabolism. Presents after milk feeding with jaundice, vomiting, hepatomegaly, E. coli sepsis, cataracts. Urine positive for reducing substances (non-glucose). Requires lifelong lactose/galactose-free diet (Soy formula used).

• Pancreatitis: Recurrent pancreatitis needs workup including sweat test (CF), metabolic screen, imaging. Anti-TTG not needed unless celiac suspected for other reasons.

• Abdominal Pain: Organic causes often associated with pain awakening from sleep, localized pain, weight loss, vomiting, fever, abnormal exam. Functional pain often periumbilical, vague, normal exam/growth.

Nephrology & Fluids/Electrolytes

Dehydration

• Assessment:
  • Mild (3-5%): Slightly decreased intake/output, thirsty, normal exam.
  • Moderate (6-9%): Lethargic/irritable, sunken eyes/fontanelle, decreased tears, dry mucous membranes, decreased skin turgor, prolonged capillary refill (2-3s), tachycardia, decreased urine output.
  • Severe (≥10%): Apathetic/comatose, very sunken eyes/fontanelle, no tears, parched membranes, tenting skin turgor, very prolonged capillary refill (>3s), tachycardia/bradycardia (late), hypotension (late), minimal/no urine output. Profound signs indicate severe dehydration.
  • Earliest sign often tachycardia or decreased urine output. Prolonged capillary refill is reliable sign.

• Types:
  • Isotonic (most common): Na 130-150 mEq/L.
  • Hypotonic: Na <130 mEq/L. Risk of cerebral edema during rehydration.
  • Hypertonic: Na >150 mEq/L. Doughy skin, irritability/lethargy, increased thirst. Risk of cerebral hemorrhage (due to dehydration) and cerebral edema/seizures if rehydrated too quickly. Correct deficit slowly over 48 hours.

• Fluid Calculation (Holliday-Segar Maintenance):
  • 100 mL/kg/day for first 10 kg
  • 50 mL/kg/day for next 10 kg (11-20 kg)
  • 20 mL/kg/day for weight >20 kg
  • Example: 12 kg child = (100x10) + (50x2) = 1000 + 100 = 1100 mL/day.
  • Example: 20 kg child = (100x10) + (50x10) = 1000 + 500 = 1500 mL/day.
  • Example: 25 kg child = 1500 + (20x5) = 1500 + 100 = 1600 mL/day (slide says 1625?).

• Fluid Management:
  • Oral Rehydration Therapy (ORT): Preferred for mild-moderate dehydration. Use commercial ORS. Give small frequent amounts. Continue breastfeeding/feeding.
  • Intravenous Fluids (IVF): For severe dehydration, shock, inability to take ORT.
    • Bolus: 20 mL/kg Normal Saline (0.9% NaCl) over 15-30 min (repeat as needed for shock). 7kg child needs 140ml bolus. 15kg child needs 300ml bolus.
    • Deficit Replacement: Calculate % dehydration x weight (kg) = deficit (L). Replace deficit + maintenance over 24h (usually half in first 8h, rest over 16h) OR over 48h for hypernatremia.
    • Fluid Choice: Maintenance usually D5 0.45% NaCl or D5 0.2% NaCl (+ 20 mEq/L KCl once voiding). Deficit often replaced with 0.45% or 0.9% NaCl. Initial resuscitation always with isotonic fluid (0.9% NS or LR). 10% dextrose water not appropriate for resuscitation/deficit. D5W is maintenance fluid for first 24h in newborn without complications.

Urinary Tract Infection (UTI)

• Incidence: High in first year, esp. uncircumcised males and females. Prolonged jaundice can be presentation in infants. Constipation is risk factor.

• Diagnosis:
  • Symptoms: Infants (fever, irritability, vomiting, poor feeding, jaundice), Older children (dysuria, frequency, urgency, incontinence, abdominal/flank pain, fever).
  • Urinalysis (Dipstick): Nitrite specific (most Gram-negatives convert nitrate->nitrite), but not sensitive (needs urine in bladder ~4h). Leukocyte esterase (LE) sensitive for pyuria, but not specific for UTI. Nitrite alone highly sensitive is wrong. LE+Nitrite most suggestive. Protein/blood non-specific.
  • Microscopy: Pyuria (>5 WBCs/hpf). Bacteriuria.
  • Culture (Gold Standard): Method matters. Suprapubic aspirate (any growth significant). Catheter specimen (>10^3 - 10^5 CFU/mL significant, depends on source). Clean catch midstream (>10^5 CFU/mL significant). Bag urine unreliable (high contamination rate).

• Imaging:
  • Renal Ultrasound (RUS): Done after first febrile UTI in infants/young children to look for structural abnormalities, hydronephrosis.
  • Voiding Cystourethrogram (VCUG/MCUG): To diagnose Vesicoureteral Reflux (VUR). Indications debated, often done after 2nd febrile UTI or first UTI with abnormal RUS/atypical organism/poor response. Not routine after first UTI. Can detect posterior urethral valves.
  • DMSA Scan: Detects acute pyelonephritis and renal scarring (gold standard for scarring). Usually done 4-6 months after UTI to assess for scarring. Should NOT be done in first month to assess scarring.

• Management: Antibiotics (7-14 days for pyelonephritis). Infants <2-3 months usually admitted for IV antibiotics. Older children with pyelonephritis may be treated outpatient if well-appearing/reliable. Treat asymptomatic bacteriuria ONLY in pregnancy (or before urologic procedure).

• Vesicoureteral Reflux (VUR): Retrograde flow of urine from bladder to ureters/kidneys. Graded I-V. Lower grades often resolve spontaneously (e.g., Grade II often resolves in 5 yrs). Higher grades associated with renal scarring/recurrent pyelonephritis. Prophylactic antibiotics controversial.

Electrolyte Abnormalities

• Hyponatremia (Na < 135):
  • Hypovolemic: Renal losses (diuretics, adrenal insufficiency, RTA) or Extrarenal losses (GI - diarrhea/vomiting, sweat - CF, third spacing). Urine Na low (<20) in extrarenal, high (>20) in renal. Adrenal insufficiency causes hypovolemic hyponatremia with high urine Na. Gastroenteritis causes hypovolemic hyponatremia with low urine Na.
  • Euvolemic: SIADH (high urine Na, high urine osm), psychogenic polydipsia (low urine osm), hypothyroidism.
  • Hypervolemic: CHF, nephrotic syndrome, cirrhosis (low urine Na).
  • Cerebral Salt Wasting: Hyponatremia with volume depletion and high urine sodium, usually after CNS injury/surgery.
  • Management: Treat underlying cause. Fluid restriction for SIADH. Normal saline for hypovolemic. Hypertonic saline (3%) for severe symptomatic hyponatremia (seizures) - correct slowly. Oral salt supplements/steroids not primary tx for SIADH.

• Hypernatremia (Na > 145): Due to water loss > salt loss (DI, fever, burns, diarrhea) or excessive salt intake. See Dehydration section.

• Hypokalemia (K < 3.5): Causes: GI losses, diuretics, RTA types 1&2, alkalosis, insulin, beta-agonists. Manifestations: Weakness, fatigue, constipation, paralytic ileus, arrhythmias, ECG changes (U waves, flat T waves). Confusion less typical.

• Hyperkalemia (K > 5.5): Causes: Renal failure, adrenal insufficiency (Addison’s, CAH), acidosis, cell lysis (rhabdo, TLS), K-sparing diuretics, ACEi/ARBs. Manifestations: Weakness, paralysis, arrhythmias, ECG changes (peaked T waves, wide QRS). Management: Calcium gluconate (stabilize membrane), Insulin+glucose, Kayexalate, Bicarbonate, Albuterol, dialysis.

• Addison’s disease (Primary Adrenal Insufficiency): Causes hypokalemia, hyperkalemia, hyponatremia.

• SIADH: Hyponatremia, euvolemic, high urine Na (>40), high urine osmolality (>100), low serum osmolality. Often due to CNS or pulmonary disorders.

Other Nephrology Topics

• Nephrotic Syndrome: Characterized by heavy proteinuria (>3.5g/day or >40mg/m2/hr), hypoalbuminemia (<2.5 g/dL), edema, hyperlipidemia. Minimal Change Disease (MCD) most common type in children (responds well to steroids).
  • Features: Edema (scrotal, periorbital, generalized), ascites. Increased bleeding tendency is NOT typical (hypercoagulable state due to loss of antithrombin III - low levels expected).
  • Complications: Spontaneous Bacterial Peritonitis (SBP) - often pneumococcal, thrombosis, infections (loss of IgG), AKI (due to hypovolemia or diuretics).
  • Management: Steroids (prednisone) primary treatment for MCD (induces remission in >90%). Salt restriction, diuretics (carefully - risk of hypovolemia). Albumin infusion + Lasix for severe edema/anasarca. ACEi/ARBs for persistent proteinuria. Renal biopsy usually reserved for atypical features (age <1 or >12, hypertension, hematuria, low C3, steroid resistance). Angiotensin converting enzyme inhibitor is NOT acute management.

• Renal Tubular Acidosis (RTA): Metabolic acidosis with normal anion gap. Associated with FTT, rickets, nephrocalcinosis. Causes hypokalemia (Types 1 & 2) or hyperkalemia (Type 4).

• Glomerular Filtration Rate (GFR): Reaches adult levels (around 120 mL/min/1.73m2) by approximately 2 years of age.

• Asymptomatic Bacteriuria: Presence of bacteria in urine without symptoms. Generally benign in children, does not require treatment or increase risk of scarring. Can be normal finding in neurogenic bladder.

Endocrine

Growth & Puberty

• Normal Growth:
  • Weight: Doubles by 4-5 months, triples by 1 year. Average term birth weight 2.5-4.2 kg (mean ~3.5kg). Loses up to 10% in first week, regains by 10-14 days.
  • Length: Average birth length ~50 cm. Increases by ~25 cm in 1st year (gains 15-16cm by 6m). Doubles birth length by ~4 years (not 3 years).
  • Head Circumference: Increases by ~12 cm in 1st year. Major determinant of HC is brain growth. Macrocephaly >97th centile.
  • Growth Velocity: Fastest in infancy, slows in childhood, peak during puberty.
  • Segments: Upper:Lower segment ratio decreases with age, approaches 1.0 around age 10-12. Becomes <1 after puberty. High ratio in hypothyroidism, achondroplasia.
  • Contributors post-infancy: GH, Thyroxine, sex steroids (puberty), IGFs. Estrogen important for growth spurt/epiphyseal closure in both sexes.

• Short Stature: Height <3rd percentile or crossing percentiles downward.
  • Causes: Familial (Genetic) Short Stature (normal bone age, normal velocity, predicted height near parents), Constitutional Delay of Growth & Puberty (delayed bone age, normal velocity temporarily slowed before puberty, family hx delay, puberty delayed, predicted height normal), IUGR/SGA, Chronic illness (Celiac, IBD, renal failure, cardiac), Endocrine (Hypothyroidism, GH deficiency, Cushing’s), Genetic/Chromosomal (Turner, Down, skeletal dysplasias - Achondroplasia), Malnutrition. Nutritional obesity causes TALL stature initially. Klinefelter causes TALL stature. Cleft palate not direct risk factor. CNS infection can cause GH deficiency.
  • Evaluation: Growth chart plotting, parental heights (calculate Mid-Parental Height - MPH), bone age X-ray, screening labs (CBC, ESR, Chem, TSH/FT4, IGF-1/IGFBP3, Karyotype - girls, Celiac screen). GH stimulation testing if indicated. Random GH level is not useful.
  • Constitutional Delay: Often presents ~12 y/o with short stature, delayed puberty, delayed bone age. Growth velocity usually normal except for lack of pubertal spurt.

• Puberty:
  • Normal Onset: Girls 8-13 yrs (Breast budding - thelarche is first sign), Boys 9-14 yrs (Testicular enlargement >4ml or >2.5cm is first sign).
  • Delayed Puberty: Girls >13 yrs (no breast budding), Boys >14 yrs (no testicular enlargement). Constitutional delay commonest cause.
  • Precocious Puberty: Girls <8 yrs, Boys <9 yrs. Central (GnRH dependent - often idiopathic in girls, CNS pathology commoner in boys) vs Peripheral (GnRH independent - CAH, tumors).
  • Tanner Stages (SMR): Assesses breast, pubic hair (both sexes), genital development (males). Axillary hair is NOT part of formal Tanner staging.
  • Menarche: Usually Tanner stage 3-4 breast, ~2-2.5 yrs after thelarche. Correlates with maternal/sister onset. Occurs after peak height velocity. Earlier in obese girls, later in thin athletic girls.
  • Growth Spurt: Peak height velocity occurs earlier in girls (Tanner 2-3) than boys (Tanner 3-4). Minimal growth after menarche. Acceleration of linear growth occurs early (Stage 1-2) in boys.

• Mid-Parental Height (MPH):
  • Boys: [(Mother’s Ht cm + 13) + Father’s Ht cm] / 2
  • Girls: [Mother’s Ht cm + (Father’s Ht cm - 13)] / 2
  • Example: Mother 160cm, Father 177cm. Boy MPH = [(160+13) + 177]/2 = [173+177]/2 = 350/2 = 175 cm.

Thyroid Disorders

• Congenital Hypothyroidism:
  • Causes: Thyroid dysgenesis (agenesis, hypoplasia, ectopic - most common cause), dyshormonogenesis (autosomal recessive), maternal antithyroid drugs, iodine deficiency (endemic), TSH deficiency (central).
  • Screening: Routine newborn screening (TSH +/- T4). Jordan has screening program.
  • Clinical Features (often subtle/absent at birth, develop over weeks/months if untreated): Prolonged jaundice, poor feeding, constipation, lethargy, hypotonia, hoarse cry, umbilical hernia, large fontanelles, macroglossia, myxedema, broad hands/short fingers, short limbs, dry skin, coarse hair. Delayed development is consequence, not early sign. Early closure of fontanelle is NOT seen. Hypertonia NOT seen. Head size normal or large (myxedema). May look normal at birth. Fully developed picture by 3-6 months.
  • Diagnosis: High TSH, Low T4/FT4 (primary). Low/Normal TSH, Low T4/FT4 (central). Thyroid scan helps determine etiology.
  • Treatment: Levothyroxine lifelong. Early treatment prevents severe mental retardation.

• Acquired Hypothyroidism: Hashimoto’s thyroiditis most common cause. Goiter, growth failure, fatigue, constipation, cold intolerance etc.

Adrenal Disorders

• Congenital Adrenal Hyperplasia (CAH): Autosomal recessive enzyme defects in cortisol synthesis.
  • 21-Hydroxylase Deficiency (most common, >90%): Decreased cortisol & aldosterone, increased androgens.
    • Salt-Wasting form: Ambiguous genitalia (females), adrenal crisis (hypotension, hyponatremia, hyperkalemia, hypoglycemia, metabolic acidosis, shock) in first few weeks. Low renin is INCORRECT (renin is high due to low aldosterone).
    • Simple Virilizing form: Ambiguous genitalia (females), precocious pubic hair/phallic growth (males). No salt wasting.
    • Non-Classic (Late Onset): Hirsutism, menstrual irregularity, acne in later childhood/adulthood.
  • 11-β-Hydroxylase Deficiency: Decreased cortisol, increased androgens, increased mineralocorticoids (DOC -> hypertension). Ambiguous genitalia (females). Associated with hypertension.
  • Diagnosis: Elevated 17-OH Progesterone (for 21-OHD). Karyotype for ambiguous genitalia. Electrolytes, renin, cortisol levels.
  • Management: Glucocorticoid replacement (hydrocortisone), mineralocorticoid replacement (fludrocortisone for salt-wasters), salt supplementation (infancy). Stress dose steroids during illness/surgery.

• Adrenal Insufficiency (Addison’s Disease = Primary):
  • Causes: Autoimmune (most common in children), CAH, infection (TB, fungal), hemorrhage, adrenoleukodystrophy, withdrawal of long-term steroids (secondary/tertiary).
  • Clinical Features: Weakness, fatigue, anorexia, weight loss, salt craving, vomiting, abdominal pain, hyperpigmentation (primary only - due to high ACTH), postural hypotension.
  • Adrenal Crisis: Hypotension, shock, vomiting, dehydration, hypoglycemia, fever. Triggered by stress/illness.
  • Lab Findings (Primary): Hyponatremia, hyperkalemia, hypoglycemia, metabolic acidosis, Low cortisol, High ACTH, Low aldosterone, High renin. Low renin NOT seen. Hypernatremia NOT seen. ACTH stim test shows poor cortisol response. Antibodies (e.g., 21-hydroxylase Abs).
  • Lab Findings (Secondary/Tertiary): Low cortisol, Low ACTH. Aldosterone usually normal (renin-angiotensin controlled). No hyperpigmentation. No hyperkalemia.
  • Management: Glucocorticoid + Mineralocorticoid replacement (primary). Stress dose hydrocortisone IV/IM for crisis + fluid resuscitation (NS/D5NS). Emergency injection kit/education.

• Ambiguous Genitalia: Requires urgent evaluation: Karyotype, electrolytes, 17-OHP, pelvic ultrasound. Uterus present suggests 46,XX CAH or gonadal dysgenesis.

Diabetes Mellitus

• Type 1 DM: Autoimmune destruction of beta cells. Most common type in pediatrics. Presents with polyuria, polydipsia, polyphagia, weight loss. Can present with DKA. Requires insulin therapy. Antibody mediated. Screen for associated autoimmune (thyroid, celiac).

• Diabetic Ketoacidosis (DKA): Hyperglycemia, ketosis, metabolic acidosis. Management: IVF (isotonic initially, then add dextrose when glucose falls), insulin infusion (start after initial fluids), electrolyte monitoring/replacement (esp. K+). Monitor for cerebral edema.

• Hypoglycemia Management: Rule of 15s (15g fast-acting carb, recheck in 15min). Glucagon IM/SC if unable to take oral. IV dextrose if severe/unconscious. Give complex carb/protein snack after recovery. Do NOT omit subsequent long-acting insulin.

• Monitoring: HbA1c goal usually <7.5%. Home blood glucose monitoring.

• Sick Day Management: Never omit insulin. Monitor glucose/ketones frequently. Increase fluids. May need supplemental insulin.

• Exercise: Adjust insulin/carbs. Avoid competitive sports ONLY if poor control or significant complications (rare in children).

• Neonatal Diabetes: Can be transient or permanent, often genetic causes.

• MODY (Maturity Onset Diabetes of the Young): Autosomal dominant genetic defects.

Other Endocrine Topics

• Growth Hormone Deficiency: Can cause short stature, decreased growth velocity, delayed bone age. Neonatal signs (if severe/panhypopit): hypoglycemia, microphallus, prolonged jaundice, midline defects (e.g., cleft palate). Dx: Provocative GH testing after screening (IGF-1, IGFBP3). Treat with recombinant GH.

• Turner Syndrome (45,X): Female phenotype, short stature, gonadal dysgenesis (streak ovaries -> delayed puberty, infertility), webbed neck, low hairline, shield chest, coarctation/bicuspid aortic valve, renal anomalies, lymphedema (congenital), normal intelligence usually. Normal growth velocity is INCORRECT.

• Klinefelter Syndrome (47,XXY): Male phenotype, tall stature, small testes, gynecomastia, infertility, learning difficulties/behavioral issues. Occurs only in males. Short stature is INCORRECT.

• Obesity: BMI >95th percentile (or 85th-95th for overweight). Complications: Insulin resistance/Type 2 DM, hypertension, dyslipidemia, fatty liver disease, sleep apnea, pseudotumor cerebri, slipped capital femoral epiphysis (SCFE), earlier menarche (not late), psychosocial issues. Acanthosis nigricans (sign of insulin resistance). Lower risk of malignancy is INCORRECT (some cancers increased).

• Prader-Willi Syndrome: Neonatal hypotonia, FTT early, then hyperphagia/obesity, short stature, hypogonadism, developmental delay. Diagnosed by FISH/methylation studies.

Miscellaneous

Kawasaki Disease (KD)

• Acute febrile vasculitis, predominantly medium-sized arteries (esp. coronary). Leading cause of acquired heart disease in developed countries. Unknown etiology (?infectious trigger).

• Diagnostic Criteria: Fever ≥ 5 days PLUS ≥ 4 of 5:
  1. Bilateral non-purulent conjunctivitis
  2. Oral mucosal changes (strawberry tongue, red/cracked lips, pharyngeal erythema)
  3. Peripheral extremity changes (erythema/edema of hands/feet - acute; periungual desquamation - subacute)
  4. Polymorphous rash (maculopapular, morbilliform, targetoid; not vesicular)
  5. Cervical lymphadenopathy (usually unilateral, >1.5 cm)
  • Subcutaneous nodules are NOT a criterion.

• Phases: Acute (fever, criteria), Subacute (resolution of fever, desquamation, thrombocytosis, highest risk for coronary artery aneurysms - CAA), Convalescent (resolution of symptoms, labs normalize).

• Complications: Coronary artery aneurysms (occur in 20-25% untreated, <5% treated). Myocarditis, pericarditis, valvulitis, aseptic meningitis, arthritis, hydrops of gallbladder.

• Labs: Elevated ESR/CRP, leukocytosis, normocytic anemia, thrombocytosis (in subacute phase). Thrombocytopenia early can occur but is not typical. Elevated liver enzymes possible. Sterile pyuria.

• Management: Intravenous Immunoglobulin (IVIG) - single high dose (2g/kg). High-dose Aspirin (anti-inflammatory initially), then low-dose Aspirin (anti-platelet). Echocardiogram at diagnosis and follow-up to assess coronary arteries. IVIG reduces risk of CAA significantly. Admit for IVIG/monitoring. Anticoagulation may be needed if large aneurysms. Antibiotics not indicated.

Malnutrition

• Marasmus: Severe deficiency of calories. Severe wasting (loss of muscle/subcutaneous fat). Alert but irritable. Skin dry, thin, wrinkled. No edema. Most common form overall.

• Kwashiorkor: Severe deficiency primarily of protein (relative caloric excess possible). Edema (pitting, often starting in lower limbs), hypoalbuminemia, fatty liver, skin changes (flaky paint dermatosis), hair changes (flag sign), apathy, anorexia.

• Marasmic Kwashiorkor: Mixed features.

• Refeeding Syndrome: Complication during nutritional rehabilitation of severely malnourished patients. Rapid electrolyte shifts (esp. low PO4, Mg, K) leading to cardiac/neurologic/respiratory failure. Start feeding slowly, monitor electrolytes closely. Aggressive initial feeding is dangerous.

• Associated Deficiencies: Vitamins (esp. A, D), Minerals (Iron, Zinc, Calcium, Magnesium, Potassium).

Child Abuse

• Manifestations: Bruises (most common overall) - esp. patterned, multiple stages of healing, unusual locations (torso, ears, neck). Burns (immersion - stocking/glove, cigarette). Fractures (spiral fractures of long bones from twisting, posterior rib fractures, metaphyseal corner fractures, skull fractures, multiple fractures). Head trauma (subdural hematoma, retinal hemorrhages - shaken baby syndrome). Abdominal trauma (ruptured liver/spleen). Failure to thrive, neglect.

• Perpetrators: Parents/caretakers most frequent.

• Reporting: Mandatory reporting laws for suspected abuse.

Vitamin Deficiencies

• Vitamin A: Night blindness, xerophthalmia, Bitot’s spots, immunosuppression. Alopecia not typical.

• Vitamin D: Rickets (children), osteomalacia (adults). Bowed legs, rachitic rosary, delayed fontanelle closure, craniotabes.

• Vitamin E: Hemolytic anemia (esp. preterms), neurological deficits.

• Vitamin K: Deficiency bleeding (see Neonatology).

• Vitamin C: Scurvy. Gingivitis, bleeding gums, poor wound healing, perifollicular hemorrhage, corkscrew hairs.

• Vitamin B12 (Cobalamin): Megaloblastic anemia, neurological deficits (paresthesias, ataxia, memory loss). Deficiency from pernicious anemia, vegan diet, terminal ileum resection/disease (e.g., NEC, Crohn’s).

• Folic Acid: Megaloblastic anemia, neural tube defects.

• Zinc: Acrodermatitis enteropathica (rash - perioral, acral, perineal; alopecia; diarrhea; FTT). Inherited or acquired deficiency.

Other Miscellaneous Topics

• Anorexia Nervosa: Eating disorder with severe weight loss, distorted body image, fear of weight gain. Complications: Bradycardia (not tachycardia), hypotension, arrhythmias, osteoporosis, constipation, amenorrhea, lanugo hair.

• Acanthosis Nigricans: Velvety hyperpigmentation in flexural areas (neck, axillae). Associated with insulin resistance (obesity, T2DM, PCOS). Seen in 13 y/o obese hypertensive female.