PEDS EXAM @

NR 330 — COMPLETE MASTER STUDY GUIDE

Test 1 + Quiz 2, rebuilt around mechanisms, contrasts, and named traps — the way you actually retain this material

Built from your official exam PDFs, course outline, and PPT lecture notes

How This Guide Is Organized

Part 1 = Foundations (screening, growth, vitals, assessment, immunizations, nursing philosophy) — the concepts everything else builds on.

Part 2 = Body Systems (GI, respiratory, cardiac, cognitive/neuro, sensory, communicable disease) — Test 1 territory.

Part 3 = Acute & Chronic Conditions (neuro emergencies, endocrine, heme, renal, ortho, oncology) — Quiz 2 territory.

★ Purple boxes connect a concept back to something earlier in the guide — that's intentional. Most of peds nursing is the same handful of patterns (trend-over-snapshot, mechanism-explains-symptom, contrast pairs) showing up in a new body system each time.

PART 1: FOUNDATIONS

Newborn Screening & Levels of Prevention

PKU vs. Galactosemia — same mechanism, different clock

Both are autosomal recessive — missing enzyme → substance builds up → toxic. PKU: missing phenylalanine hydroxylase → protein-derived phenylalanine builds up. Baby looks normal AT BIRTH (silent damage — why screening exists). Galactosemia: missing GALT → milk sugar (galactose) builds up. Symptoms appear FAST, within days of feeding.

★ 'P before G, 48 before 72' — PKU screens at 24-48hrs, galactosemia at ≤72hrs. Alphabetical order matches numeric order. Galactosemia positive = STOP breastfeeding immediately, the one exception to 'breastfeeding is always encouraged.'

Primary / Secondary / Tertiary Prevention

Primary = PREVENT (before disease exists) — immunizations, safe sleep, car seats. Secondary = SCREEN (disease exists, catch it before symptoms) — PKU/galactosemia/lead screening. Tertiary = TREAT (manage what's established) — CF chest PT, cardiac rehab.

★ Test yourself with: does the disease already exist and you're catching it early? → Secondary. Are you stopping it from existing at all? → Primary.

Growth & Developmental Milestones

Weight — one repeating rhythm

Doubles by 6mo → Triples by 12mo → Quadruples by 2-2.5yr. Say it as a countdown: 6 → 12 → 2.5 (12 is exactly double 6, so the second number is 'free' once you know the first).

Gross Motor — 2-4-6-9-12

★ Picture a birthday cake with candles at 2-4-6-9-12 — each candle is a mobility level-up.

Development Across the Lifespan — the stages, and what drives each one

Newborn (0-28 days): reflexes dominate behavior before voluntary control exists — rooting, sucking, Moro, tonic neck, grasp, Babinski, stepping. Each disappears on its own schedule (3-6mo typically) as the cortex matures and takes over from brainstem-level reflexes.

Infant (1mo-1yr): cognitive development moves outward — first the infant notices faces/contrast (1-2mo), then their own body (2-6mo, staring at hands), then object permanence and cause-effect (6-12mo). That's a literal expanding radius of awareness: self → immediate world → objects with permanence.

Toddler (1-3yr): Erikson's autonomy vs. shame/doubt — negativism ('no!') and ritualism (need for sameness) are the child asserting control over a world that mostly controls them. Toilet training readiness is physical AND cognitive AND psychological — pushing it before all three align just creates conflict, not progress.

Preschool (3-6yr): Piaget's preoperational stage — symbolic thinking, but faulty logic (a tall skinny glass 'has more' than a short wide one with equal volume). Erikson's initiative vs. guilt — purposeful planning emerges. Play shifts from parallel (toddler, side-by-side) to associative (sharing activities/ideas).

School-age (6-12yr): Piaget's concrete operational stage — logical thinking, but only about concrete/tangible things, not abstractions yet. Erikson's industry vs. inferiority — self-worth becomes tied to competence and peer comparison for the first time.

Adolescent (12-20yr): Piaget's formal operational stage — abstract reasoning finally comes online. Erikson's identity vs. role confusion. Puberty: adrenarche (adrenal hormones → pubic/underarm hair) is a SEPARATE process from gonadarche (gonadal hormones → breast/genital development) — they don't have to happen in lockstep, which is why puberty timing looks so different kid to kid.

Notice the whole lifespan is one continuous story: reflexes hand off to voluntary control, parallel play hands off to cooperative play, concrete thinking hands off to abstract thinking. Nothing here is a random new fact — it's each stage building the capacity the next stage needs.

Colic — Rule of 3's

>3hrs/day, >3days/week, >3wks, in an infant under 3-5mo. Baby is FINE between episodes — that's what separates colic from GERD, milk allergy, infection, or hernia, which all show signs OUTSIDE the crying spells (poor weight gain, fever, blood in stool, rash).

★ Safety teaching: it's okay for an overwhelmed parent to place baby safely in the crib and step away — this is a real safeguard against shaken baby syndrome, not just a comfort tip.

Failure to Thrive

Diagnosed by TREND on a growth chart over multiple visits, not one low number. A baby tracking steadily along ANY percentile (even a low one) is not FTT — the red flag is crossing two major percentile lines downward.

Lead Poisoning

No safe blood lead level exists. Screening ~12 & 24mo. Classic case of primary prevention beating treatment — there's no way to reverse the neurodevelopmental damage once it happens.

Pediatric Health Assessment

Communication by age — matches the cognitive stages you just learned

Birth-2yr: eye contact, toys/comfort items, keep the parent holding the child, include the child even though they won't understand words — the goal is nonverbal trust-building.

2-7yr: simple explanations, familiarize with equipment before using it, encourage questions — this is the preoperational/magical-thinking stage, so concrete, non-scary framing matters a lot (a child this age can genuinely believe a blood draw will 'let all their blood out').

7-11yr: more detailed explanations, more involvement — concrete operational thinking can now handle real information, not just simplified versions.

11yr+: privacy, self-concept, participation — adolescent identity development means being talked AT feels different (worse) than being included.

This is the same developmental ladder from the lifespan section, just applied to how you talk to a patient instead of how they grow — cognitive stage dictates both.

Assessment sequence and why it's ordered this way

For the abdomen specifically: inspect → auscultate → percuss → palpate — palpation goes LAST because pressing on the belly can artificially change bowel sounds, so you listen before you touch.

Vital signs: temperature, pulse, respiratory rate, oxygen saturation, blood pressure — equipment and technique both have to flex by age (e.g., cuff size, counting respirations for a full 60 seconds in infants since their breathing pattern is irregular).

★ Hearing screen: before hospital discharge, no later than 1 month of age — same urgency logic as the CCHD pulse-ox screen, catching a problem before it silently affects development.

Nutrition — the one number worth anchoring

Birth-1yr caloric need: roughly 700-1,000 calories/day, from breast milk or iron-fortified formula. Iron fortification matters because a baby's own iron stores (from mom, during pregnancy) run out around 4-6 months — that's WHY iron-rich complementary foods get introduced around then, and why iron-deficiency anemia peaks at 9-24 months.

This directly explains the iron-deficiency anemia pattern in Part 3 — same mechanism, just showing up as a diagnosis instead of a nutrition guideline.

Vital Signs by Age

Pattern: HR and RR trend DOWN as a child grows (a bigger, stronger heart/lungs need fewer beats/breaths to move the same amount of blood/air). BP trends UP (bigger vessels need more pressure to push blood through a larger system). Temperature is the one vital that stays flat at every age.

★ A number is only 'normal' relative to age — HR 90 is abnormal (low) for an infant but perfectly normal for a teenager. Always match the number to the age range before judging it.

Immunization Schedule

★ MMR/Varicella wait until 12mo because they're LIVE — the immune system needs to mature and maternal antibodies can block a live vaccine from working before then. Hib = a BACTERIA (Haemophilus influenzae type b), not the flu — historically a major cause of epiglottitis and meningitis. PCV protects against pneumonia, meningitis, bloodstream infections, AND ear infections.

Foundations of Pediatric Nursing

Atraumatic Care

Reduce stressors, limit separation from parents, support the child's sense of control.

★ Never perform a painful procedure in the child's own hospital bed — use a separate treatment room so the bed stays a 'safe space.'

Family-Centered Care

The family is a PARTNER, not a visitor. Four elements: dignity/respect, information sharing, participation, collaboration.

Role of the Pediatric Nurse

Care provider, educator, advocate (critical since kids can't always speak for themselves), family coordinator, case manager.

Family & Social Context

Family structure (single-parent, blended, foster/adoptive), childrearing/discipline styles, culture, religion, and social determinants of health (SDOH) all shape a child's care needs and must be actively assessed, not assumed.

★ Cultural competence is a skill set with layers: Awareness (recognizing your own bias) → Knowledge (learning about other frameworks) → Skills (applying it) → Humility (staying open, since you'll never fully 'complete' this). It's a process, not a checkbox.

PART 2: BODY SYSTEMS (TEST 1)

GI Disorders

Congenital malformations — each has a signature phrase

Esophageal atresia/TEF: excessive drooling + choking/cyanosis WITH FEEDING, can't pass NG tube.

Pyloric stenosis: projectile non-bilious vomiting, hungry 2-8wk old, olive-shaped RUQ mass.

Hirschsprung: no meconium in 24-48hrs, distension, ribbon stools.

Cleft Lip & Palate

Lip repair ~2-3mo, palate repair ~9-12mo (later, protects speech timing).

★ Elbow restraints protect the suture line post-op — removed one at a time to check skin/ROM.

Dehydration

Mild 3-5%, Moderate 6-9%, Severe ≥10% body weight lost. Weight = single most objective fluid-status indicator.

Intussusception

Peak 6-12mo. Triad: colicky pain + knees drawn up, currant-jelly stools, sausage mass. Air/contrast enema is diagnostic AND often therapeutic.

Appendicitis

Pain migrates to RLQ (McBurney's). Pain BEFORE vomiting (opposite of gastroenteritis).

★ Sudden pain relief = possible perforation, a red flag NOT reassurance. Never heat or laxatives/enemas.

Celiac Disease

Testing must happen WHILE still eating gluten. Only treatment: strict lifelong gluten-free diet.

Respiratory Disorders

Recognizing distress

Early: tachypnea, flaring, mild retractions. Late: grunting, head bobbing, cyanosis, bradycardia (a LATE pre-arrest sign in kids, unlike adults).

★ A child who suddenly looks 'calmer' with normalizing RR may be TIRING OUT toward failure, not improving.

Throat anatomy, top to bottom

Pharynx (strep pharyngitis) → Tonsils → Epiglottis (epiglottitis) → Larynx (croup) → Trachea → Lungs.

Croup vs. Epiglottitis

Bronchiolitis & RSV

Viral, most commonly RSV, infants under 2.

★ Bronchodilators/steroids do NOT work for bronchiolitis — opposite of asthma, where they're first-line. In young/premature infants, APNEA can be the FIRST sign of RSV, before classic cough/wheeze.

Asthma

SABA (albuterol) = rescue, fast, during an attack. LABA + inhaled corticosteroids = daily control, prevent attacks.

Pneumonia

★ In infants, presentation can be subtle — poor feeding/lethargy alone, without classic fever/cough.

Cystic Fibrosis

CFTR mutation → thick mucus in lungs AND pancreas. Salty skin/sweat → sweat chloride test (gold standard).

★ Airway clearance BEFORE meals, not after. CF patients avoid contact with OTHER CF patients — cross-infection risk.

Cardiac Disorders

Acyanotic vs. Cyanotic

Acyanotic (L→R shunt, no cyanosis): VSD, ASD, PDA, coarctation. Cyanotic (R→L shunt/obstruction, cyanosis): the 5 T's — Tetralogy of Fallot, Transposition, Truncus arteriosus, Tricuspid atresia, Total anomalous pulmonary venous return.

★ Classic infant CHD/HF sign: diaphoresis WITH FEEDING — feeding is 'exercise' for an infant. Tet spell fix: KNEE-CHEST position — increases systemic vascular resistance, reduces R→L shunt.

Hypertension

No single fixed number — judged against age/sex/height percentile charts. Younger kids with HTN are MORE likely to have an identifiable secondary cause than teens.

Heart Failure

Usually from underlying CHD (unlike adults' acquired causes). Daily weights + strict I&O are the core monitoring tools.

Cognitive & Neurodevelopmental

ASD

★ Single highest-yield intervention: maintain ROUTINE/predictability. Unexpected change is the biggest distress trigger.

ADHD

★ On stimulant meds, monitor GROWTH (appetite suppression) and CARDIOVASCULAR status.

Down Syndrome

Extra chromosome 21. Hypotonia is often the earliest sign.

★ Routine screening for cardiac, hearing, vision, thyroid isn't optional — it's core standard of care for this diagnosis.

Sensory Disorders

Otitis Media

★ Kids get this more than adults because eustachian tubes are shorter and MORE HORIZONTAL — drain less effectively.

Strabismus

★ Untreated = brain SUPPRESSES the misaligned eye's input → permanent amblyopia. Not cosmetic — a true time-sensitive window.

Communicable Diseases & Immunizations — Vaccine Concepts

Attenuation: reducing a pathogen's virulence while keeping its ability to trigger immunity — this is what makes a vaccine 'live but weakened.' Live-attenuated vaccines (MMR, Varicella) give strong, long-lasting immunity but are generally contraindicated in significantly immunocompromised kids, since even a weakened pathogen can replicate out of control without a working immune system.

Antitoxins: pre-made antibodies that neutralize a toxin directly (tetanus, botulism) — different from a vaccine, which trains the body to make its OWN antibodies over time. An antitoxin is immediate borrowed protection; a vaccine is the body learning to protect itself.

PART 3: ACUTE & CHRONIC CONDITIONS (QUIZ 2)

Seizures — Epilepsy & Febrile Seizures

Epilepsy: 2+ UNPROVOKED seizures, ≥24hrs apart — nothing obvious triggers it. EEG + MRI/CT to diagnose. Start with ONE medication when possible.

★ Never restrain during a seizure, nothing in the mouth, time it, document the pattern (aura, movement, LOC, post-ictal).

Febrile seizure: triggered by a FAST rise in temp (>38°C), not the height. Ages 6mo-5yr.

★ A single simple febrile seizure does NOT significantly raise future epilepsy risk — a genuine reassurance point for terrified parents.

Head Injuries & Glasgow Coma Scale

Big head + weak neck = more force transmitted in a fall — explains why pediatric head injury risk is elevated.

★ Arteries = high pressure = fast bleed = fast crash. Veins = low pressure = slow bleed = slow symptoms. Reason from the vessel type, don't just memorize the table.

GCS: Eye(4)+Verbal(5)+Motor(6)=15. Motor gets the most points because it's the most reliable indicator in a young/nonverbal child. ≤8 = severe (protect airway). TRENDED scores matter more than one number.

Shaken Baby Syndrome causes subdural hematomas + retinal hemorrhages — same venous-bleed mechanism as any subdural, just from abusive mechanism instead of accidental trauma.

Hydrocephalus

CSF production/absorption imbalance → ventricles enlarge → pressure builds.

★ In an infant, sutures aren't fused, so the SKULL EXPANDS instead of pressure building silently — bulging fontanel, split sutures, enlarging head circumference. Once sutures fuse (older kids), pressure has nowhere to go, so symptoms shift to headache/vomiting/vision changes instead.

VP shunt redirects CSF to the abdomen. Post-shunt, watch for TWO different problems: malfunction (ICP signs return) vs. infection (fever, redness along tract) — same urgency, different cause.

Diabetes Mellitus

Type 1: pancreas CAN'T make insulin (autoimmune destruction). Type 2: pancreas makes insulin, body stopped RESPONDING (resistance). That one distinction generates the rest of the topic.

Hyper vs. Hypoglycemia — mechanism drives the symptoms

Hyperglycemia (3 P's): sugar pulls water into urine (polyuria) → thirst (polydipsia) → cells still starving despite sugar around (polyphagia). Fruity breath = ketones, body burning fat instead.

Hypoglycemia: sympathetic/adrenaline panic response — sweating, shaking, tachycardia — because the brain's only fuel is running out right now.

★ Rule of 15: 15g fast carb, recheck in 15min, repeat if still low.

DKA vs. HHS

DKA: NO insulin → can't use sugar → burns fat → ketones → acidosis. Kussmaul respirations, fruity breath. HHS: SOME insulin present → less ketosis, but sugar climbs extremely high → massive dehydration instead.

★ Sick-day rule: NEVER stop insulin even when not eating — stress hormones still raise glucose regardless of food intake.

Drowning

Submersion → can't breathe → hypoxia → hypoxia drives all downstream damage. Every intervention is really just 'fix the hypoxia fast.'

★ Cold water slows metabolism/O2 use — resuscitation continues longer in cold-water submersion ('not dead until warm and dead').

★ 'Secondary drowning': a child can look fine at rescue and still develop pulmonary edema hours later — monitor even if asymptomatic.

Childhood Cancer — Bone & Soft Tissue

★ Chemo hits every fast-dividing cell, not just cancer — that's WHY you see myelosuppression, mucositis, and hair loss together. Fever + ANC <500 = emergency, call immediately.

Spinal Curvature

Lordosis = inward (swayback). Kyphosis = outward (hunchback). Scoliosis = sideways, S-shaped.

★ Scoliosis treatment is one clean escalating sequence: <25° observe → 25-45° brace (16-23hr/day) → >45-50° surgery.

Torticollis: one tight SCM muscle → head tilts TOWARD tight side, chin rotates AWAY. Untreated → plagiocephaly (flattened skull on that side).

Fractures & Overuse Injuries

Kid bones are more flexible (more collagen) — explains greenstick (bends/splinters one side) and buckle/torus (compression bulge) fractures, which don't really occur the same way in adult bone.

★ The growth plate is the WEAKEST point in a child's bone — opposite of adults. Compartment syndrome 5 P's (Pain out of proportion, Pallor, Paresthesia, Pulselessness, Paralysis) are roughly in order of appearance — don't wait for all 5.

Spiral fracture + story that doesn't match = classic abuse red flag.

★ Both = same mechanism (repetitive growth-plate stress), different location. Both self-limiting.

Hip Dysplasia, Clubfoot & Hypospadias

★ Barlow = 'Bad' (pushes hip OUT/dislocates it, tests instability). Ortolani = 'Okay again' (puts hip BACK IN, you feel the 'clunk').

Pavlik harness keeps hips flexed/ABDUCTED — opposite of tight swaddling, which is exactly why overly tight swaddling is a DDH risk factor.

Clubfoot — Ponseti sequence: serial casting → Achilles tenotomy → bracing (years, to prevent relapse).

★ Hypospadias: circumcision must be AVOIDED before repair — the foreskin is needed for reconstruction.

Cerebral Palsy & Duchenne Muscular Dystrophy

CP: NONPROGRESSIVE brain injury → PERMANENT movement disorder. The injury itself doesn't worsen; its effects are lifelong.

★ Motor red flags = the milestones you already know, showing up LATE: poor head control after 3mo, can't sit unsupported by 8mo.

DMD: X-linked recessive → almost exclusively males. Progressive weakness starting proximal (hips/thighs) and spreading outward.

★ Gower sign: child uses hands to 'walk up' their legs because proximal muscles are too weak to push them upright directly. Calf 'pseudohypertrophy' = fat/fibrous tissue replacing muscle, not real strength. Elevated CK = muscle breakdown leaking into blood.

Hematologic Disorders

Sickle Cell Anemia

Triggers: hypoxia, dehydration, acidosis, fever — this list doubles as the prevention checklist.

★ Dactylitis often the FIRST sign in infants. Splenic sequestration and acute chest syndrome are EMERGENCIES, not routine crisis pain. Hydroxyurea boosts fetal hemoglobin, which resists sickling.

Iron Deficiency Anemia

Peak 9-24mo — rapid growth + excess cow's milk (low iron, blocks absorption, displaces iron-rich foods).

★ Give iron WITH vitamin C, NEVER with milk/antacids. Dark/greenish stools = EXPECTED, not a red flag.

ITP

Autoimmune, usually 1-4wks AFTER a viral illness — immune system misfires onto platelets after fighting the virus.

★ Child otherwise looks WELL — isolated platelet problem, no fever/systemic illness. That's what separates it from something like leukemia on an exam question.

UTI, Glomerulonephritis & HUS

Three different starting points, same endpoint (kidney function affected): UTI = simple ascending infection. Glomerulonephritis = the kidney's FILTER inflamed (post-strep). HUS = full-body clotting disaster starting from a GI infection.

★ UTI: fever may be the ONLY sign in infants. Glomerulonephritis: happens 1-3 WEEKS after strep — it's immune complexes depositing in the kidney, not the bacteria itself. Tea-colored urine + periorbital edema + HTN.

★ HUS: bloody diarrhea FIRST, kidney/blood picture 5-10 days LATER. Two counterintuitive avoidances: no antibiotics (kills bacteria, releases MORE toxin) and no anti-diarrheals (traps toxin longer) — both normal instincts are wrong here.

MASTER GUIDE ADDENDUM

Fills the 3 gaps + strengthens 4 thin spots identified against your topic checklist

1. Head Injury Triad — the piece that was missing

All three sit on one severity spectrum, from functional to structural to actively bleeding:

★ The spectrum in one sentence: concussion = function only, contusion = tissue damage, hematoma = active bleeding on top of tissue damage. Severity and danger increase in that exact order.

2. Insulin Therapy Types — the piece that was missing

Organize by SPEED, not name — that's the whole trick:

★ Relay analogy: rapid/short handle the sugar spike from a specific meal; basal handles the 'keep the lights on' need that exists whether or not the child eats. NEVER hold basal insulin on a sick day just because the child isn't eating — the body still makes glucose from stress hormones.

3. Drowning — Nursing Care & Treatment (the piece that was missing)

Priority order, no exceptions:

• 1. Basic life support / CPR — before anything else, including rewarming in cold-water cases

• 2. Airway/oxygenation support — hypoxia is the actual injury; fixing it fast is the whole goal

• 3. Continued monitoring for several hours, even if the child looks fine

★ 'Secondary drowning' — a child can look completely normal right after rescue and still develop pulmonary edema HOURS later from aspirated water. That delayed risk is why monitoring continues even in an asymptomatic child.

★ Cold water is oddly protective — it slows metabolism/O2 use, so resuscitation efforts continue longer than usual in cold-water submersion ('not dead until warm and dead').

Prevention teaching (this is where most exam content on this topic actually lives): pool fencing (self-latching, self-closing, all 4 sides), a dedicated 'water watcher' doing nothing else, swim lessons, life jackets for boating, no alcohol while supervising.

4. Strengthening 4 Thin Spots

Epilepsy — full nursing management, not just seizure precautions

• During a seizure: never restrain, nothing in the mouth, time it, position on side if possible, document the pattern (aura → movement → LOC → post-ictal)

• Between seizures: medication adherence teaching (missed doses are the #1 cause of breakthrough seizures), monitor for medication side effects, seizure diary for the family to track triggers/frequency

• Safety/lifestyle: helmet for high-risk activities, shower instead of bathe alone, swim only with supervision, medical alert bracelet

Cancer — full neutropenic precaution list

• Private room, strict hand hygiene for all visitors/staff

• Avoid raw/unwashed produce and fresh flowers/plants (bacterial sources)

• NO live vaccines while immunocompromised

• Avoid crowds and anyone with active illness

★ The single most urgent family teaching point: fever + ANC under 500 = call immediately or go to the ER. That combination is a medical emergency, not a 'wait and see.'

UTI — the why behind the pattern

Girls are at higher risk after infancy specifically because of a SHORTER urethra — less distance for bacteria (usually E. coli) to travel from the perineal area up into the bladder. That's a mechanical/anatomical fact, not a coincidence.

★ In infants of either sex, fever may be the ONLY sign — no verbal complaints of burning/urgency are possible yet, so unexplained infant fever often triggers a UTI workup specifically because of this.

Fractures — nursing care checklist

• Neurovascular checks (the 5 P's) distal to the injury/cast — pain, pallor, paresthesia, pulselessness, paralysis — checked and documented regularly, not just once

• Elevate the extremity, ice for the first 24-48 hrs to control swelling

• Cast care teaching: keep dry, don't insert objects to scratch, report increasing pain/numbness/swelling/foul odor immediately

• Pain management scheduled, not just PRN, especially in the first 24-48 hrs

• Kid bones are more flexible than adult bones (more collagen, less mineralized). That single property is why kids get fracture types that adults basically don't.

• Greenstick — the bone bends and splinters on one side only, without breaking all the way through. Picture bending a young, flexible tree branch too far — it cracks on the outside of the bend but doesn't snap in two. Classic in kids under 10.

• Buckle (Torus) — a compression bulge, where the bone deforms/buckles under force but doesn't actually break through. Same flexibility principle — the bone absorbs the force by deforming rather than snapping. Most common in the forearm, usually stable.

• Growth plate (physeal) fracture — happens at the physis, the cartilage growth zone near the end of a long bone. Big deal because this is the weakest point in a child's bone — the opposite of adults, where the growth plate is long gone and the surrounding bone is actually the weaker point. Injury here can affect all future growth of that bone, not just the immediate break.

• Complete fracture — breaks all the way through, same as an adult fracture. Less unique to kids, but still happens.

• Spiral fracture — comes from a twisting force. Not unique to kids mechanically, but worth flagging: a spiral fracture in a young child whose story doesn't match the injury (e.g., "she fell off the couch") is a classic red flag for abuse, since twisting injuries don't usually happen from simple falls.

★ Any of the 5 P's showing up — especially pain out of proportion to the injury, or pain with passive stretch — is treated as a possible compartment syndrome emergency, not routine post-fracture discomfort.

NR 330: Parent-Child Nursing

Peds Quiz 2 Study Guide

Dominican University | ABSN Summer 2026

SECTION 1: SEIZURES, EPILEPSY & FEBRILE SEIZURES

Epilepsy

Definition: Chronic neurological disorder characterized by two or more unprovoked seizures occurring at least 24 hours apart; classified as generalized, focal, combined, or unknown

Diagnosis: Electroencephalogram (EEG); MRI/CT to identify a structural cause

Etiology & Risk Factors

• Genetic mutations

• History of trauma, infection, developmental disorders, or alcohol exposure

• Structural changes in the brain

• Occurs more often in children than in young adults

Clinical Manifestations

• Recurrent seizures with motor and/or non-motor manifestations

• Generalized seizures: jerking, weakness, spasms, eyelid movements, staring (absence)

• Focal seizures: may begin with an aura, impaired awareness, automatisms, muscle spasms

Nursing Interventions & Management

• Anti-seizure medications — start with a single medication (monotherapy) when possible

• Ketogenic diet: high fat, low carbohydrate, moderate protein

• Vagus nerve stimulation

• Surgery if seizures are severe and unresponsive to medication

• Seizure precautions: padded rails, suction and oxygen at bedside, nothing placed in the mouth during a seizure

• Time the seizure and document characteristics (aura, movement type, LOC, post-ictal state)

• Educate family to identify and avoid triggers (sleep deprivation, flashing lights, missed medication doses)

• Recommend a medical alert bracelet

Febrile Seizures

Definition: A seizure triggered by a rapid rise in body temperature (>38°C/100.4°F) in a child without a CNS infection or other defined cause; classified as simple or complex

Risk Factors

• Ages 6 months to 5 years

• Temperature over 38°C (100.4°F)

• Previous febrile seizure and family history of febrile seizures

Clinical Manifestations

• Seizure activity occurring with a fever; usually brief, lasting up to 2 minutes

• Simple febrile seizure: generalized, resolves within 15 minutes, does not recur within 24 hours

• Complex febrile seizure: focal, lasts longer than 15 minutes, or recurs within 24 hours

Nursing Interventions & Management

• Identify and treat the underlying cause of the fever

• Fever reduction: antipyretics (acetaminophen/ibuprofen), remove excess clothing

• During the seizure: lay the child on their side with the head tilted back, protect from injury, do NOT restrain the child, do NOT place anything in the child's mouth, and time the event

• Hospitalization indicated for serious infection, prolonged seizure activity, or if the child remains unresponsive afterward

• Vaccinations can help prevent illnesses that trigger febrile seizures

• Reassure parents — most children outgrow febrile seizures, they typically do not cause brain damage, and a single simple febrile seizure does not significantly increase the risk of developing epilepsy

SECTION 2: HEAD INJURIES & GLASGOW COMA SCALE

Head Injury

Types: Concussion (mild traumatic brain injury), Contusion/Laceration (bruising or tearing of brain tissue), Hematoma — Epidural (between skull and dura, typically arterial, rapid deterioration) and Subdural (between dura and arachnoid, typically venous, slower onset)

Etiology: Head or neck trauma from falls, motor vehicle collisions, sports, or abuse

Pediatric Considerations: Large head size relative to body and weak neck muscles increase risk of injury; head injuries are more common in males and carry a high mortality rate

Clinical Presentation

• Concussion: nonspecific, temporary symptoms — headache, dizziness, confusion, nausea, brief loss of consciousness

• Contusion/Laceration: more severe and persistent neurologic deficits than a concussion

• Hematoma: rapid development and sudden onset — decreasing LOC, unequal pupils, vomiting

Lab Testing & Diagnostic Studies

• Serial neurological assessments and pupillometry

• CT or MRI to assess for bleeding

• Monitor CBC if hemorrhage is suspected

Treatments & Nursing Management

• Concussion: rest (physical and cognitive), NSAIDs/acetaminophen for pain

• Contusion/Laceration: manage intracranial pressure, control external bleeding

• Hematoma: surgical drainage (burr hole or craniotomy)

• Mortality rates increase as GCS scores decrease

• Encourage socialization about 48 hours after a mild TBI, but limit environmental noise and stimuli initially

• Educate parents about manifestations to watch for, management strategies, required rest, and a gradual return-to-activity/return-to-learn plan

• Prevention: helmets for sports and biking, proper car seat/booster/seatbelt use

• Shaken Baby Syndrome (Abusive Head Trauma): caused by violent shaking of an infant; can result in subdural hematomas and retinal hemorrhages — educate caregivers on safe ways to cope with a crying infant and to NEVER shake a baby

Glasgow Coma Scale (GCS) — Pediatric Modifications

The GCS assesses three components — Eye Opening, Motor Response, and Verbal Response — with age-adjusted criteria for infants and young children. Total score ranges from 3 to 15.

Clinical Use

• Score ≤ 8 = severe injury/coma — airway protection required

• Score 9–12 = moderate injury

• Score 13–15 = mild injury

• Serial (trended) GCS assessments are more clinically valuable than a single isolated score

• Lower GCS scores correlate with worse prognosis and higher mortality

SECTION 3: HYDROCEPHALUS

Definition: Enlargement of the cerebral ventricles due to an imbalance in production and absorption of cerebrospinal fluid (CSF); types include congenital, acquired, communicating, obstructive (non-communicating), and ex-vacuo

Risk Factors: Usually affects infants and young children; strong genetic link; may occur with neural tube defects (spina bifida), intraventricular hemorrhage of prematurity, tumors, or infection

Screening: Serial head circumference measurements; large or rapidly increasing head size; "sunset sign" (eyes deviated downward with sclera visible above the iris)

Clinical Presentation

• Infants: enlarging head circumference, bulging/tense anterior fontanel, split sutures, sunset sign, high-pitched cry, irritability, poor feeding, low muscle tone

• Toddlers and older children: headache (often worse in the morning), vomiting, vision changes, developmental delay or poor school performance, personality changes, ataxia

Lab Testing & Diagnostic Studies

• Neuroimaging — head ultrasound in infants with an open fontanel, CT, or MRI

Treatments & Nursing Management

• Treatment goal: restore normal CSF flow and reduce pressure on the skull and brain

• Ventriculoperitoneal (VP) shunt placement is the most common treatment, directing CSF flow to the abdominal cavity; ventriculoatrial shunt is an alternative; endoscopic third ventriculostomy (ETV) is used in select cases

• Monitor for signs of increased ICP: bulging fontanel, irritability, high-pitched cry, vomiting, sunset sign, decreased LOC

• Post-shunt: monitor for shunt malfunction (signs of increased ICP) and infection (fever, redness/swelling along the shunt tract, abdominal pain)

• Position with the head of the bed elevated; support the head and neck during feeding and repositioning

• Measure head circumference at every visit and plot on the growth chart

• Family education: recognize signs of shunt malfunction/infection requiring immediate care; ongoing developmental follow-up

SECTION 4: DIABETES MELLITUS — TYPE 1 vs. TYPE 2

Type 1 vs. Type 2 Diabetes Mellitus — Comparison

Hyperglycemia vs. Hypoglycemia

Hyperglycemia ("the 3 P's")

• Polyuria, Polydipsia, Polyphagia

• Weight loss

• Dehydration

• Altered mental status

• Sweet, fruity-smelling (ketone) breath

Hypoglycemia

• Pallor

• Sweating (diaphoresis)

• Headache

• Irregular heartbeat / tachycardia

• Fatigue

• Irritability

• Dizziness, shakiness, hunger

Complications

• DKA (Diabetic Ketoacidosis): hyperglycemia, ketosis, and metabolic acidosis — Kussmaul respirations, fruity breath, abdominal pain, vomiting, dehydration; a medical emergency, most common in Type 1

• HHS (Hyperosmolar Hyperglycemic State): extreme hyperglycemia without significant ketosis; more common in Type 2

• Long-term complications: retinopathy, nephropathy, neuropathy, cardiovascular disease

Nursing Management & Insulin Therapy

Insulin Therapy

• Rapid-acting (lispro, aspart) — onset ~15 minutes

• Short-acting (regular) — onset ~30 minutes

• Intermediate-acting (NPH)

• Long-acting/basal (glargine, detemir) — no pronounced peak

• Basal-bolus regimens or continuous subcutaneous insulin infusion (insulin pump)

• Rotate injection sites to prevent lipohypertrophy

• Blood glucose monitoring via fingerstick before meals/bedtime or continuous glucose monitoring (CGM)

• Treat hypoglycemia with the Rule of 15: give 15g of fast-acting carbohydrate, recheck glucose in 15 minutes, repeat if still low

• Sick-day management: never stop insulin even when not eating; monitor for ketones

Nutrition & Lifestyle

• Carbohydrate counting with consistent meal timing and composition

• Balanced diet with adequate fiber and lean protein; controlled carbohydrate portions; avoid skipping meals

• Exercise: monitor blood glucose before and after activity; may need extra carbohydrates before exercise; risk of delayed hypoglycemia hours after activity

• Type 2 management: weight management, increased physical activity, dietary changes (portion control, reduced simple sugars/processed foods), metformin is often the first-line oral medication

Psychosocial & Family Education

• Address diabetes distress/burnout; involve the child in self-care as developmentally appropriate

• School accommodations (504 plan) for glucose monitoring and insulin administration

• Teach recognition and treatment of hypoglycemia and hyperglycemia

• Teach sick-day rules and when to call the provider or seek emergency care

SECTION 5: DROWNING

Definition: Respiratory impairment resulting from submersion or immersion in liquid

Risk Factors: Unprotected/unsupervised access to water (pools, bathtubs, open water); risk-taking behaviors during adolescence; seizure disorders; lack of swimming ability; alcohol use among teens

Epidemiology: Third most common cause of injury-related death in children worldwide; peak incidence in toddlers (bathtubs/pools) and adolescent males (open water)

Pathophysiology: Water temperature affects breath-holding time and cerebral oxygen use; hypoxia is the primary insult driving subsequent pulmonary and neurologic injury

Clinical Presentation

• Ranges from mild coughing and tachypnea to respiratory failure, hypoxia, altered LOC, and cardiac arrest; delayed pulmonary edema may develop

Lab Testing & Diagnostic Studies

• Arterial blood gases, chest x-ray, pulse oximetry, continuous cardiac monitoring

Treatments & Nursing Management

• Basic life support/CPR is the first priority; rescue breathing may begin in the water if the rescuer is trained

• Rapidly resolve hypoxemia — supplemental oxygen, may require intubation and mechanical ventilation

• Warm the child if hypothermic ("not dead until warm and dead" guides resuscitation efforts in cold-water submersion)

• Monitor for at least several hours even if asymptomatic, due to the risk of delayed pulmonary edema ("secondary drowning")

• Plan for rehabilitation as needed for neurologic injury from prolonged hypoxia

Prevention & Client Education

• Never leave a child unattended near water (bathtub, pool, bucket)

• Fence pools on all sides with a self-latching, self-closing gate

• Enroll children in swim lessons; require life jackets for boating

• Designate an adult "water watcher" for active, uninterrupted supervision

• Avoid alcohol use while supervising children near water

• Encourage caregiver CPR training

SECTION 6: CHILDHOOD CANCER — BONE & SOFT TISSUE TUMORS

Osteosarcoma

Definition: The most frequently occurring primary bone cancer in children, arising from bone-forming (osteoid) tissue; most common sites are the distal femur, proximal tibia, and proximal humerus, near the growth plate

Epidemiology: Peak incidence during the adolescent growth spurt

Clinical Presentation

• Localized bone pain, often worse at night or with activity

• Swelling over the site with a palpable mass

• A pathologic fracture may be the initial presentation

Diagnostics & Treatment

• X-ray (classic "sunburst" pattern), MRI, bone biopsy

• Neoadjuvant chemotherapy, limb-salvage surgery or amputation, adjuvant chemotherapy

Ewing Sarcoma

Definition: The second most common primary bone cancer in children, arising from neuroectodermal tissue in bone or soft tissue; most common in the diaphysis (shaft) of long bones and the pelvis

Clinical Presentation

• Swelling and discomfort at the site

• Increased pain at night

• Fever — may mimic infection

Treatment

• Chemotherapy, radiation, and/or surgical resection

Rhabdomyosarcoma

Definition: Cancer arising from skeletal (striated) muscle cells; the most common soft tissue sarcoma in children — often related to genetic disorders

Clinical Presentation

• Manifestations depend on tumor location and the child's age — head/neck (bulging eyes/proptosis, ear pain or drainage), genitourinary (painful urination, vaginal/urethral bleeding), abdomen (vomiting, palpable mass)

Treatment

• Surgery, chemotherapy, and/or radiation

Nursing Care & Interventions — Childhood Cancer

• Pain management using multimodal, age-appropriate approaches and pain scales

• Monitor for chemotherapy side effects: myelosuppression (neutropenia, anemia, thrombocytopenia), nausea/vomiting, mucositis, alopecia

• Neutropenic precautions: private room, strict hand hygiene, avoid fresh flowers and raw fruits/vegetables per protocol, monitor temperature closely, avoid live vaccines

• Nutrition support — high-calorie, high-protein diet; manage taste changes and mucositis-related feeding difficulty

• Psychosocial support — address body image concerns (hair loss, limb loss/amputation), support school reintegration and sibling needs, use therapeutic play and child life specialists

• Family education on home care and when to seek emergency care (fever with an ANC < 500, signs of bleeding)

• Health promotion — early evaluation of persistent, localized bone pain or swelling

SECTION 7: SPINAL CURVATURE — SCOLIOSIS & TORTICOLLIS

Spinal Curvature Overview

• Lordosis: exaggerated inward curve of the lumbar/cervical spine ("swayback")

• Kyphosis: exaggerated outward/forward curve of the thoracic spine ("hunchback")

• Scoliosis: lateral, side-to-side curvature of the spine, often "S"-shaped; may cause uneven shoulders/hips

Scoliosis

Etiology: Most commonly idiopathic (unknown cause); can also be congenital or neuromuscular (associated with cerebral palsy, muscular dystrophy)

Screening: Recommended during annual physical exams/school screenings; Adam's forward bend test looks for asymmetry of the rib hump or shoulder height

Clinical Presentation

• Uneven shoulders, uneven waist/hips, one shoulder blade more prominent, leaning to one side, asymmetric rib hump on forward bend

Diagnostics

• Physical exam, x-ray to measure the Cobb angle, MRI/CT if an underlying cause is suspected

Treatment

• Curve < 25°: observation with serial x-rays

• Curve 25–45°: bracing, worn 16–23 hours per day, most effective in growing children

• Curve > 45–50°: surgical correction (spinal fusion with instrumentation)

Nursing Care

• Support body image concerns related to bracing during adolescence, reinforce brace-wear compliance, and provide post-op spinal fusion care (log-rolling, pain management, neurovascular monitoring, early ambulation)

Torticollis ("Wry Neck")

Definition: Rotation/tilting of the head to one side due to shortening or tightness of the sternocleidomastoid (SCM) muscle

Etiology

• Congenital muscular torticollis: intrauterine positioning, birth trauma to the SCM, or the SCM not developing properly — may involve a palpable fibrous "tumor"/nodule in the muscle

• Acquired torticollis: infection, trauma, or reflex (ophthalmologic or neurologic causes)

Risk Factors: Difficult or breech birth, trauma during pregnancy or delivery

Clinical Presentation

• Head tilted toward the affected side with the chin rotated to the opposite side; limited range of motion; possible facial/cranial asymmetry (plagiocephaly) if untreated

Diagnostics

• Physical exam, ultrasound of the SCM, MRI/labs if an acquired cause is suspected

Treatment

• Passive stretching exercises and positioning are the mainstay of treatment; physical therapy; tubular orthosis for torticollis (TOT) collar; surgical release if conservative treatment fails (typically after age 1)

Nursing Care

• Teach parents stretching exercises and repositioning techniques (tummy time, positioning toys/crib on the unaffected side to encourage active turning); refer early to physical therapy; monitor for plagiocephaly

SECTION 8: FRACTURES & OVERUSE INJURIES

Fracture Types

• Complete: bone broken all the way through into two pieces

• Incomplete: bone partially broken

• Plastic deformation: bone bends without fracturing

• Buckle (Torus): compression injury causing a bulge in the bone cortex without a complete break — most common in the forearm; typically stable

• Greenstick: bone bends and splinters on one side without breaking all the way through — common under age 10 due to flexible pediatric bone

• Simple (closed): skin intact over the fracture

• Compound (open): bone punctures through the skin — high infection risk

• Comminuted: bone breaks into two or more fragments

• Fracture lines: transverse (straight across), oblique (diagonal), spiral (twisting force — consider abuse if inconsistent with the reported history)

Pathophysiology: The growth plate (physis) is the weakest part of a child's bone and a common fracture site; injury here can affect future bone growth

Etiology/Risk Factors: Trauma, sports, weak bones from poor nutrition, obesity, and diseases affecting bone strength (e.g., osteogenesis imperfecta)

Clinical Presentation

• Pain, swelling, discoloration/ecchymosis, limping or refusal to bear weight, deformity, limited use of the extremity

Diagnostics

• X-ray, MRI, labs to evaluate for bone deficiencies if indicated

Treatment

• Reduction (closed or open) to realign the bone

• Immobilization: casting, splinting, boots

• Surgical intervention (open reduction internal fixation) for unstable or displaced fractures

Complications

• Impaired circulation and nerve compression; compartment syndrome (5 P's — Pain out of proportion, Pallor, Paresthesia, Pulselessness, Paralysis — a medical EMERGENCY); physeal (growth plate) involvement affecting future growth; nonunion/malunion; infection, especially with open fractures

Nursing Care

• Perform neurovascular checks (circulation, sensation, movement) distal to the injury

• Cast care: keep the cast dry, do not insert objects inside it, elevate the extremity, monitor for signs of compartment syndrome

• Provide pain management

• Client/family education: safety and fall prevention, nutrition for healing, when to seek care (increasing pain, numbness, or a cool/pale extremity)

• Promote normal development — encourage play, communication, and socialization during recovery; use distraction techniques

Overuse Injuries — Sever's Disease & Osgood-Schlatter Disease

Pathophysiology: High-intensity, repetitive activity without adequate rest causes microtrauma and inflammation to growth plates, tendons, muscles, and bones in growing children

Sever's Disease (Calcaneal Apophysitis): Inflammation of the heel (calcaneal) growth plate where the Achilles tendon attaches; common in active children ages 8–15, especially runners and soccer players

Osgood-Schlatter Disease: Inflammation/irritation of the tibial tuberosity (patellar tendon insertion site) from repetitive quadriceps traction; common in adolescents ages 10–15 during growth spurts, especially with jumping and running sports

Risk Factors

• Poor body mechanics, excessive training without rest, rapid growth spurts, ages 6–18, multiple sports that stress the same body parts

Clinical Presentation

• Localized pain and swelling/inflammation over the affected growth plate (heel for Sever's, below the knee for Osgood-Schlatter); pain worsens with activity and improves with rest; a visible/palpable bony prominence may develop with Osgood-Schlatter

Diagnostics

• Clinical history and physical exam; imaging to rule out fracture or other injury

Treatment

• Rest/activity modification, ice, NSAIDs, stretching and physical therapy, orthotics (heel cups/inserts), gradual return to activity; both conditions are generally self-limiting and resolve once the growth plate closes

Nursing Care

• Educate on activity modification, rest, and a home exercise program; reassure the family that these conditions are not long-term/health-threatening; promote continued social and peer engagement despite activity restriction; provide mobilization aids as needed (crutches to offload weight)

SECTION 9: HIP DYSPLASIA, CLUBFOOT & HYPOSPADIAS (Review)

Developmental Dysplasia of the Hip (DDH)

Definition: Abnormal development of the acetabulum resulting in improper fit/positioning of the femoral head, ranging from mild instability to complete dislocation

Etiology/Risk Factors: Maternal hormones (ligamentous laxity), breech position, family history, female sex, firstborn status, swaddling or in-utero positioning that restricts hip movement

Screening

• Physical exam at every well-child visit until walking age — Barlow maneuver (attempts to dislocate an unstable hip) and Ortolani maneuver (attempts to reduce a dislocated hip, felt/heard as a "clunk"); assess for asymmetric skin folds, limited hip abduction, and leg-length discrepancy (Galeazzi sign)

Diagnostics

• Ultrasound (preferred before 6 months, prior to ossification), x-ray (after approximately 4–6 months)

Treatment

• Pavlik harness maintains the hips in a flexed, abducted position for infants; a hip spica cast or surgical reduction is used for older infants or failed harness treatment

Nursing Care

• Teach proper harness application and wear schedule (typically continuous), perform skin checks under the straps, avoid restrictive swaddling/positioning that adducts and extends the hips, promote hip-healthy swaddling and babywearing, and provide developmental support during immobilization

Congenital Talipes Equinovarus (Clubfoot)

Definition: A congenital deformity in which the foot is turned inward and downward

Etiology: Idiopathic in most cases; associated with intrauterine positioning, genetic factors, or neuromuscular conditions (e.g., spina bifida)

Clinical Presentation

• Foot fixed in plantarflexion (equinus), inward turning (varus), and forefoot adduction; may be unilateral or bilateral

Diagnostics

• Clinical exam; may be detected on prenatal ultrasound

Treatment

• Ponseti method: serial casting and manipulation beginning shortly after birth, often followed by an Achilles tenotomy, then bracing (foot abduction brace) worn full-time initially and then during naps/nighttime for several years to prevent recurrence; surgery is reserved for resistant cases

Nursing Care

• Educate on cast care and brace-wear schedule, which is critical for preventing relapse; perform skin checks; provide emotional support for parents and ongoing developmental monitoring

Hypospadias

Definition: A congenital defect in which the urethral opening is located on the ventral (underside) of the penis rather than at the tip

Clinical Presentation

• Abnormally positioned urethral meatus; may be associated with chordee (downward curvature of the penis) and undescended testes

Management

• Circumcision should be AVOIDED prior to repair — the foreskin is often used in surgical reconstruction; surgical repair (urethroplasty) is typically performed between 6 and 12 months of age

Nursing Care

• Post-op catheter/stent care, monitor urinary output, prevent pressure or kinking of the catheter, use a double-diapering technique, provide pain management, avoid tub baths until healed, restrict straddle-toy activity during healing, and provide family education and emotional support

SECTION 10: CEREBRAL PALSY & MUSCULAR DYSTROPHY (CPMD)

Cerebral Palsy (CP)

Definition: A group of permanent disorders of the development of movement and posture causing activity limitation, attributed to nonprogressive disturbances in the developing fetal or infant brain; the most common permanent physical disability of childhood

Epidemiology: Incidence of 1.5–3 per 1,000 live births; 15–60% of children with CP also have epilepsy

Etiology: About 80% are caused by unknown prenatal brain abnormalities; also linked to intrauterine infection (chorioamnionitis), prematurity (before 36 weeks), periventricular leukomalacia, and shaken baby syndrome

Types: Spastic (most common — increased muscle tone/stiffness), Dyskinetic (involuntary movements), Ataxic (poor coordination/balance), and mixed presentations

Clinical Manifestations — Motor Signs

• Poor head control after age 3 months, stiff or rigid limbs, arching the back or pushing away, floppy tone (hypotonia), unable to sit without support by age 8 months, clenched fists after age 3 months

Clinical Manifestations — Behavioral Signs

• Excessive irritability, no smiling by age 3 months, feeding difficulties, persistent tongue thrusting, frequent gagging or choking with feeds

Diagnostics

• Careful assessment of at-risk infants during early infancy, neurologic exam and history, neuroimaging, metabolic and genetic testing

Goals of Therapy

• Establish locomotion, communication, and self-help skills; achieve optimal appearance and integration of motor function; correct associated defects; provide adapted educational opportunities; promote socialization

Therapeutic Management

• Ankle-foot orthoses (braces), orthopedic surgery for spastic deformities, medications for pain related to spasms and seizures, botulinum toxin (Botox) injections for spasticity, dental hygiene, physical/occupational/speech therapy

Nursing Care Management

• Assist the family in adapting equipment and activities, administer medications, implement safety precautions, encourage recreational activities, and support the family

Muscular Dystrophy — Duchenne Muscular Dystrophy (DMD)

Definition: The largest group of muscular diseases in children — genetic, progressive degeneration of muscle fibers with increasing weakness, wasting, disability, and deformity; DMD (also called pseudohypertrophic muscular dystrophy) is the most common and most severe type

Etiology: X-linked recessive inheritance pattern affecting males; about one-third of cases are new/spontaneous mutations; incidence is approximately 1 in 3,500 male births

Clinical Manifestations

• Onset between ages 3 and 7; waddling gait, frequent falls, and a positive Gower sign (child uses hands to "walk up" the legs to stand from the floor due to proximal muscle weakness); lordosis; calf muscle hypertrophy ("pseudohypertrophy" — muscle replaced by fat/fibrous tissue); progressive generalized weakness through adolescence; some degree of cognitive impairment is common; death typically results from respiratory or cardiac failure

Diagnostics

• Genetic testing/PCR for the dystrophin gene mutation; confirmed by EMG, muscle biopsy, and elevated serum creatine kinase (CK); positive family history

Treatment

• No cure exists; the goal is to maintain function of unaffected muscles as long as possible — range of motion exercises, bracing, ADL support, and surgical release of contractures as needed; corticosteroids may slow progression; genetic counseling is recommended for the family

Nursing Care Management

• Help the child and family cope with a chronic, progressive, debilitating disease; design a program to foster independence and activity for as long as possible; teach self-help skills; arrange escalating levels of care as needs intensify (home health, skilled nursing facility, respite care); monitor respiratory and cardiac status

SECTION 11: HEMATOLOGIC DISORDERS — SICKLE CELL, IRON DEFICIENCY ANEMIA & ITP

Sickle Cell Anemia

Pathophysiology: An autosomal recessive disorder in which abnormal hemoglobin (HbS) causes red blood cells to become rigid and sickle-shaped under conditions of hypoxia, dehydration, acidosis, or fever; sickled cells clump together and obstruct blood flow, causing vaso-occlusion, tissue ischemia, and chronic hemolysis

Screening: Included in newborn metabolic screening

Etiology/Risk Factors: Most common among individuals of African, Mediterranean, Middle Eastern, and Indian descent; both parents must carry the sickle cell trait

Clinical Presentation

• Chronic anemia (fatigue, pallor, jaundice); vaso-occlusive (pain) crisis with severe pain in the bones, joints, abdomen, or chest; dactylitis (painful swelling of the hands/feet, often the first sign in infants); splenic sequestration crisis (sudden pooling of blood in the spleen — life-threatening); acute chest syndrome (fever, chest pain, hypoxia — a medical emergency); increased risk of infection from functional asplenia; stroke risk; priapism

Diagnostics

• Hemoglobin electrophoresis confirms the diagnosis; CBC shows low Hgb/Hct; peripheral smear shows sickled cells

Treatment & Nursing Management

• Pain management — around-the-clock scheduled analgesics (including opioids) during a crisis, plus nonpharmacologic comfort measures

• Hydration/rehydration with IV fluids to reduce blood viscosity and prevent further sickling

• Oxygen therapy as needed

• Medications: hydroxyurea (increases fetal hemoglobin and reduces the frequency/severity of crises), penicillin prophylaxis in young children (prevents infection due to functional asplenia), folic acid supplementation, and pain medications

• Blood transfusions for severe anemia, acute chest syndrome, or stroke prevention

• Bone marrow/stem cell transplant is the only potential cure

• Crisis prevention: adequate hydration, avoid extreme temperatures and high altitude, avoid strenuous exertion and dehydration, prompt treatment of infections, up-to-date immunizations including pneumococcal vaccine

• Family/client education: recognize early signs of a crisis, emphasize the importance of hydration, and offer genetic counseling

Iron Deficiency Anemia

Etiology/Risk Factors: The most common nutritional deficiency in children; peak incidence in infants 9–24 months due to rapid growth and inadequate dietary iron, especially with excessive cow's milk intake before age 1 or more than 24 oz/day in toddlers; also seen in adolescents (rapid growth, menstrual losses) and during pregnancy

Clinical Presentation

• Pallor (a common manifestation), fatigue, irritability, tachycardia, pica (craving/eating non-food items such as ice or dirt), decreased appetite, developmental/cognitive effects if prolonged and untreated, brittle nails, delayed growth

Diagnostics

• CBC shows decreased Hgb/Hct with microcytic, hypochromic RBCs (low MCV); decreased serum ferritin is the most sensitive indicator of iron stores; additional testing may be used to rule out other causes

Treatment & Nursing Management

• Oral iron supplementation — give with a source of vitamin C (e.g., orange juice) to enhance absorption; avoid giving with milk/dairy or antacids, which decrease absorption; give between meals if tolerated

• Educate that liquid iron may stain teeth — administer via straw or dropper toward the back of the mouth and brush teeth afterward

• Iron will turn stools dark or greenish-black — this is an expected finding; educate the family

• Dietary counseling: iron-rich foods include red meat, poultry, fish, iron-fortified cereals, leafy greens, and beans; limit cow's milk intake in toddlers to less than 24 oz/day; introduce iron-rich solid foods when starting solids

• Monitor for constipation/GI upset with iron supplementation

• Prevention: use iron-fortified formula for non-breastfed infants, provide iron supplementation for breastfed infants around 4–6 months, and delay whole cow's milk until 12 months

Immune Thrombocytopenia (ITP)

Pathophysiology: An autoimmune disorder in which autoantibodies target and destroy platelets, often triggered following a viral illness, resulting in thrombocytopenia

Etiology/Risk Factors: Often follows a viral infection by 1–4 weeks; the most common acquired bleeding disorder of childhood; typically affects children ages 2–5

Clinical Presentation

• Petechiae (pinpoint red/purple spots), purpura (larger bruised areas), easy bruising, epistaxis, bleeding gums; in severe cases, GI bleeding or intracranial hemorrhage may occur (rare but serious); the child otherwise appears well

Diagnostics

• CBC shows an isolated low platelet count with normal WBC/Hgb; peripheral smear; bone marrow exam is reserved for cases where the diagnosis is unclear

Treatment & Nursing Management

• Many cases resolve spontaneously within weeks to months without treatment (observation for mild cases)

• IVIG (intravenous immunoglobulin) rapidly raises the platelet count

• Corticosteroids suppress the immune response

• Anti-D (RhoGAM) immunoglobulin is used in Rh-positive patients

• Platelet transfusion is reserved for life-threatening bleeding, since transfused platelets are rapidly destroyed

• Bleeding precautions: avoid contact sports and activities with injury risk, avoid IM injections and NSAIDs/aspirin (increase bleeding risk), use a soft toothbrush, and monitor for signs of bleeding

• Family education: activity restriction until the platelet count improves; seek emergency care for head injury or severe headache (possible intracranial bleed)

SECTION 12: URINARY TRACT INFECTION, GLOMERULONEPHRITIS & HEMOLYTIC UREMIC SYNDROME

Urinary Tract Infection (UTI)

Etiology: Most commonly caused by E. coli ascending the urinary tract; more common in girls after infancy due to a shorter urethra; uncircumcised infant boys are at higher risk during the first year of life

Risk Factors: Vesicoureteral reflux (VUR), voiding dysfunction, constipation, poor hygiene/wiping technique, sexual activity in adolescents, urinary catheterization

Clinical Presentation

• Infants/young children: fever (often the only sign), poor feeding, vomiting, irritability, foul-smelling urine, failure to thrive

• Older children: dysuria, urgency, frequency, suprapubic pain, foul-smelling/cloudy urine, new-onset enuresis; flank pain and fever suggest upper tract involvement (pyelonephritis)

Diagnostics

• Urinalysis (leukocyte esterase, nitrites, WBCs, bacteria); urine culture and sensitivity is the gold standard, with a clean-catch or catheterized specimen preferred in young children; renal/bladder ultrasound or voiding cystourethrogram (VCUG) for recurrent UTIs or suspected VUR

Treatment & Nursing Management

• Antibiotics based on culture and sensitivity — complete the full course even if symptoms resolve

• Increase fluid intake to flush the urinary tract

• Encourage frequent voiding and complete bladder emptying

• Education: proper front-to-back wiping technique for girls, avoid bubble baths and irritants, wear cotton underwear, avoid holding urine

• Follow-up urine culture to confirm resolution if indicated; monitor for recurrent infections and refer for VUR evaluation if recurrence occurs

Acute Glomerulonephritis (commonly Post-Streptococcal, APSGN)

Pathophysiology: Immune-complex-mediated inflammation of the glomeruli, most often occurring 1–3 weeks after a group A streptococcal infection (strep throat or a skin infection such as impetigo)

Clinical Presentation

• Hematuria — classically "tea-colored" or "cola-colored" urine; edema, especially periorbital and worse in the morning; hypertension; oliguria (decreased urine output); fatigue; mild proteinuria

Diagnostics

• Urinalysis shows hematuria, proteinuria, and RBC casts; elevated ASO titer indicates recent strep infection; decreased complement (C3) levels; elevated BUN/creatinine if renal function is affected

Treatment & Nursing Management

• Generally supportive care — most children recover fully

• Manage hypertension and fluid overload with sodium and fluid restriction and diuretics if needed

• Monitor strict intake and output, daily weights, and blood pressure

• Give antibiotics if an active streptococcal infection is still present

• Bed rest/activity restriction during the acute phase as needed

• Family education: monitor for worsening symptoms (severe hypertension, decreased urine output, respiratory distress from fluid overload); treat strep throat promptly to prevent recurrence

Hemolytic Uremic Syndrome (HUS)

Pathophysiology: A triad of hemolytic anemia, thrombocytopenia, and acute kidney injury, most commonly caused by Shiga toxin-producing E. coli (O157:H7) following a gastrointestinal infection

Etiology/Risk Factors: Ingestion of undercooked ground beef, unpasteurized milk/juice, or contaminated produce/water; most common in children under 5 years; the use of antimotility agents (anti-diarrheals) during the preceding GI infection may increase risk and should be avoided

Clinical Presentation

• Preceded by a prodrome of bloody diarrhea and abdominal cramping, followed (typically 5–10 days later) by pallor, fatigue, decreased urine output (oliguria or anuria), edema, hypertension, petechiae/bruising, irritability, and in severe cases seizures or altered mental status

Diagnostics

• CBC shows hemolytic anemia (schistocytes on smear) and thrombocytopenia; elevated BUN/creatinine; stool culture for E. coli O157:H7; low haptoglobin; elevated LDH

Treatment & Nursing Management

• Supportive care is the mainstay — antibiotics are generally AVOIDED for the underlying E. coli infection, as they may increase toxin release and worsen HUS

• Careful fluid and electrolyte management, monitoring for fluid overload given renal impairment

• Blood transfusion for severe anemia; platelet transfusion is generally avoided unless there is active bleeding

• Dialysis may be required for severe acute kidney injury

• Strict monitoring of intake/output, daily weights, blood pressure, and neurologic status

• Prevention/education: thoroughly cook ground beef, avoid unpasteurized dairy/juice, practice proper hand hygiene, and avoid anti-diarrheal medications during an acute bloody diarrheal illness

QUICK REFERENCE: KEY FACTS & MNEMONICS

Febrile Seizures

Ages 6 months–5 years | Simple: generalized, <15 min, no recurrence in 24 hr | Complex: focal, >15 min, or recurs in 24 hr

Glasgow Coma Scale

Eye (4) + Verbal (5) + Motor (6) = 15 max | Score ≤ 8 = severe — protect the airway

Head Injury Hematomas

Epidural = arterial, rapid deterioration | Subdural = venous, slower onset

Hydrocephalus

Watch for a bulging fontanel, sunset sign, and increasing head circumference | Shunt malfunction presents as signs of increased ICP

Type 1 vs. Type 2 DM

Type 1 = autoimmune, little/no insulin, high DKA risk | Type 2 = insulin resistance, lifestyle-related, low DKA risk

Hyper vs. Hypoglycemia

Hyperglycemia = the 3 P's (polyuria, polydipsia, polyphagia) + fruity breath | Hypoglycemia = sweating, shaking, pallor, irritability — treat with the Rule of 15

Drowning

Basic life support first | Monitor for several hours even if asymptomatic due to delayed pulmonary edema

Bone Cancers

Osteosarcoma = most common, distal femur/proximal tibia | Ewing Sarcoma = diaphysis/pelvis, can mimic infection

Scoliosis

Curve < 25° = observe | 25–45° = brace | > 45–50° = surgery

Fractures

Greenstick = bends and splinters, under age 10 | Buckle/Torus = forearm bulge | The growth plate (physis) is the weakest point

Overuse Injuries

Sever's disease = heel (calcaneus) | Osgood-Schlatter = below the knee (tibial tuberosity) — both are overuse injuries that resolve with rest

DDH Screening

Barlow maneuver dislocates, Ortolani maneuver reduces ("clunk") | Pavlik harness is the first-line treatment

Clubfoot

Ponseti method = serial casting → Achilles tenotomy → bracing

Hypospadias

NO circumcision before repair — the foreskin is used for reconstruction

Cerebral Palsy

A nonprogressive brain injury causing a permanent movement disorder | Spastic type is most common

Duchenne Muscular Dystrophy

X-linked, affects males, positive Gower sign, calf pseudohypertrophy, elevated CK

Sickle Cell Crisis

Hydrate + oxygenate + control pain | Hydroxyurea decreases crisis frequency

Iron Deficiency Anemia

Give iron with vitamin C, not milk | Stools turn dark green/black — this is expected

ITP

Petechiae + purpura + low platelets in an otherwise well child | Avoid contact sports, NSAIDs, and IM injections

UTI

E. coli is the most common cause | More common in girls after infancy | Clean-catch/catheterized culture is the gold standard

Glomerulonephritis

Tea-colored urine + periorbital edema + hypertension, occurring 1–3 weeks post-strep infection

HUS

Bloody diarrhea leads to anemia + thrombocytopenia + acute kidney injury | AVOID antibiotics and antidiarrheals for the causative E. coli infection