peads Flashcards
explain why children have a higher HR than adults
child
= lower blood volume
= lower stroke volume
= higher HR required for same amount of cardiac output
**high yield
what percentage of blood loss predisposes a child to hypovolemic shock?
mild hypovolemia: 15% –> early signs like increase HR
moderate hypovolemia: 15-30% –> decrease urine output, mild HYPOtension
severe hypovolemia: 30-40% –> significant HYPOtension, rapid pulse, confusion, lethargy
life threatening: >40%
do children or adults compensate for blood loss more effectively?
children compensate more effectively
= mask early signs of shock
= early monitoring and rapid intervention is crucial
for CVS… what are the 2 normal foetal structures
- patent ductus arteriosus
- patent ductus venosus
**high yield (can MEQ)
what happens if the PDA does not close soon after birth… what are the LT side effects?
PDA
**high yield (NEED TO REVISE CVS AGAIN)
what is the most common type f congenital heat defects
- tetraology of fallot
- cyanotic heart vs non cyanotic heart
**high yield CVS embryology
when do congenital heart defects usually arise?
in the FIRST TRIMESTER (when the heart tube starts to fold)
in second/ third trimester (if there are viral infections that occur here)
**impt big concept
children have a narrower airway compared to adults… what does that predispose them to?
respiratory distress
**high yield MEQ
how does a childn’s lung capcity differ from that of an adult? and what are the LT effects
- smaller size and volume
- smaller tidal volume
- higher respiratory rate = higher metabolic rate
- smaller number and size of aveoli
**HIGH YIELD ENDOCRINE
in children, which hormones are most important for growth? vs puberty?
growth: GH
puberty: estrogen and testosterone (sex hormones)
what is the significance of a child having to drink breast milk instead of solid food? (4 points)
- newborn immature digestive systems
= stomach produce lower level of digestive enzymes
= not capable of processing solid foods + intestine cannot handle digestion and absorption of nutrients from solid foods - breast milk produces necessary nutrients newborns need for growth and development
- lack of oral motor skills required to move solid food around their mouths & chew & swallow
- lack of swallowing reflexes
= increased risk of choking
what are some of the main killers of young children in their first months of life
- prematurity
- neonataal factors
why does prematurity cause neonatal death?
underdeveloped organs (list examples)
= nutritional, gastrointestinal, and immature immune system challenges
- BRAIN
= apnea
2/ LUNGS
- HEART
= PDA does not close
= shunting and heart failure - POOR TEMP REGULATION
= due to insufficient body fat
= - underdeveloped
**high yield microbiology
what are the main types of serious bacterial infections in a neonate?
vs viral infections
BACTERIAL
1. listeria
2. GBS
3. ecoli
VIRAL
1. influenza
2. RSV (respiratory syncytical virus)
3. enterovirus (HAND FOOT MOUTH DISEASE, rash on palms and soles, ulcers in the mouth)
4. Hep B and C (from maternal transmission)
hep B increases risk of liver cancer by 300X
5. varicella zoster (if mom catches primary infection within 2 weeks of giving birth)
in terms of percentage, what is the risk of serious bacterial infections when neonates have a fever?
15%
**high yield MEQ
what hakes a neonate more susceptible to infections?
SOCIOECOLOGICAL FACTORS
1. increase exposure to pathogens
- eg. putting soil on umbilical cord to dry it up
- a lot of people visiting the baby
2.
**high yield immunology
what are the different types of immunity
- maternal immunity
= newborns recieve passive immunity from maternal antibodies - innate and adaptive immunity
= innate immune system is developed at birth, but ADAPTIVE IMMUNITY IS UNDEVELOPED
**
newborns recieve passive immunity from mothers (via placenta & breast milk)
= recieve maternal Ab
=
**high yield MSK
what are some of the MSK growth issues in children
- juvinille arthritis
=. inflammation affects growth plate (SPECIFICALLY LONG BONES AND SPINE)
= children are stunted and do not achieve full height - chronic illness and medications can impair growth/ height (eg. medications for nephrotic syndrome)
how long do bones take to heal in children vs adults
children heal in half the time as adults
what is the definition of a neonatae?
up to 28 days
what is the definition of ‘early term babies’
37 weeks
how many babies in singapore have jaundice
60% of full term babies
85% of premature babies
what are the causes of neonatal jaundice?
how do we check for jaundice in babies?
- heel prick test
what is the condition when bilirubin crosses the BBB?
kernicterus
why are jaundiced babies at risk of kernicterus, and not jaundiced adults
BBB in babies is undeveloped
= more porus
adults have a more robust BBB
= unlikely to have kernicterus
what is NNJ (neonatal jaundice)? what are the causes of NNJ?
- polycythemia (too much RBCs) –> infant of diabetic mom, poorly controlled
- incompatible blood type (ABO and Rh)
- breastfeedina & breastmilk
- lo birth weight
- internal bleeding
6.
what is breastfeeding jaundice? vs breastmilk jaundice
BREASTFEEDING JAUNDICE:
decrease feeding
= decrease stool production
= delayed bilrubin elimination from body
BREASTMILK JAUNDICE
1. inhibit enzyme UDP-glucuronosyltransferase
2.
**high yield
how is bile produced?
bile in intestine oxidised to sterobilin
what is blood type NNJ jaundice?
Cause:
Occurs when the mother has blood type O and the baby has type A, B, or AB.
The mother’s body produces anti-A or anti-B antibodies that can cross the placenta and destroy the baby’s red blood cells.
Prevalence:
More common than Rh incompatibility but usually less severe.
Symptoms:
Mild jaundice shortly after birth.
Rarely causes severe anemia or other complications.
Management:
Monitoring bilirubin levels.
Phototherapy for jaundice if needed.
2. Rh Incompatibility
Cause:
Occurs when the mother is Rh-negative and the baby is Rh-positive.
The mother’s immune system produces antibodies against the Rh antigen on the baby’s red blood cells.
Prevalence:
Less common due to the routine use of Rh immunoglobulin (RhIg).
Symptoms:
More severe than ABO incompatibility.
Can cause severe anemia, hydrops fetalis (fluid buildup in the baby’s tissues), or stillbirth.
Prevention and Management:
Preventive RhIg injections:
Given at 28 weeks of pregnancy and within 72 hours of delivery.
Prevents the mother from forming Rh antibodies.
Treatment for HDN:
Intrauterine transfusions in severe cases.
Phototherapy or exchange transfusion after birth for hyperbilirubinemia.
3. Other Blood Group Incompatibilities
Less common blood group antigens can also cause incompatibility, such as:
Kell (K antigen).
Duffy.
Kidd.
These can also lead to HDN but are rarer and depend on specific maternal and fetal blood types.
Diagnosis
Blood Typing:
Determine the mother’s and baby’s blood types and Rh status.
Indirect Coombs Test (Antibody Screen):
Detects antibodies in the mother’s blood that may attack the baby’s red blood cells.
Direct Coombs Test:
Performed on the baby’s blood after birth to detect antibodies bound to red blood cells.
Ultrasound or Doppler:
Used to monitor for anemia or hydrops fetalis during pregnancy.
**high yield
what is the type of jaundice in neonates?
unconjugated hyperbilirubinemia
**high yield
URINE:
urobilinogen is converted to urobilin
= excreted in urine (yellow coloured)
STOOL
bile is converted by gut bacteria
= into urobilinogen and stercobilinogen
what are the 3 conditions to look out for in neonataes that have jaundice lasting >2 weeks
- biliary atresia
- choledochal cyst
- alagille syndrome
- Biliary Atresia
Definition:
A rare, life-threatening condition where the bile ducts (intrahepatic and/or extrahepatic) are absent, underdeveloped, or scarred.
Results in obstruction of bile flow from the liver to the intestines.
Cause:
The exact cause is unknown, but it is believed to involve:
Congenital malformations.
Postnatal inflammatory or infectious damage.
Types:
Perinatal/Acquired: Most common, appearing after birth (2-8 weeks).
Embryonic/Fetal: Less common, associated with other anomalies (e.g., heart defects).
Symptoms:
Persistent jaundice beyond 2 weeks of life.
Pale or clay-colored stools (lack of bile pigments).
Dark urine.
Enlarged liver (hepatomegaly).
Poor weight gain or growth.
Diagnosis:
Blood Tests: Elevated conjugated bilirubin.
Ultrasound: Absence of bile ducts or abnormal bile flow.
HIDA Scan: No bile excretion into the intestines.
Liver Biopsy: Confirms absence or scarring of bile ducts.
Treatment:
Kasai Procedure (Hepatoportoenterostomy):
A surgical bypass that connects the liver directly to the small intestine.
Best results if done before 2 months of age.
Liver Transplant:
Required if the Kasai procedure fails or liver damage progresses.
2. Choledochal Cyst
Definition:
Congenital dilatation of the bile ducts, which can lead to bile flow obstruction, infection, and liver damage.
Cause:
Likely due to an abnormality in the pancreaticobiliary junction, allowing reflux of pancreatic enzymes into the bile ducts.
Types (Todani Classification):
Type I: Fusiform dilatation of the common bile duct (most common).
Type II: Diverticulum-like outpouching.
Type III: Cystic dilatation near the duodenal opening (choledochocele).
Types IV and V: Involve multiple intrahepatic or extrahepatic cysts.
Symptoms:
Jaundice (intermittent or persistent).
Abdominal pain or a palpable mass.
Dark urine and pale stools.
Recurrent cholangitis (bile duct infections).
Diagnosis:
Ultrasound: Detects cystic dilatations.
MRCP (Magnetic Resonance Cholangiopancreatography): Detailed visualization of the biliary tree.
ERCP (Endoscopic Retrograde Cholangiopancreatography): Diagnostic and sometimes therapeutic.
Treatment:
Surgical Removal of the Cyst:
Complete excision of the cyst to prevent complications like infection, stone formation, or cancer.
Biliary Reconstruction:
Roux-en-Y hepaticojejunostomy (reconstruction of bile flow).
3. Alagille Syndrome
Definition:
A rare genetic disorder characterized by abnormalities in the bile ducts, as well as multi-system involvement (liver, heart, eyes, skeleton).
Cause:
Mutations in the JAG1 or NOTCH2 genes, which are critical for bile duct development.
Autosomal dominant inheritance.
Symptoms:
Liver:
Reduced or absent intrahepatic bile ducts leading to cholestasis (bile flow obstruction).
Jaundice, pale stools, dark urine, and pruritus (itching).
Heart:
Congenital heart defects (e.g., pulmonary artery stenosis).
Skeletal:
Butterfly-shaped vertebrae.
Eyes:
Posterior embryotoxon (a specific corneal abnormality).
Facial Features:
Prominent forehead, deep-set eyes, and a pointed chin.
Diagnosis:
Liver Biopsy: Confirms paucity (reduction) of bile ducts.
Genetic Testing: Identifies JAG1 or NOTCH2 mutations.
Imaging and Echocardiography: Evaluate multi-organ involvement.
Treatment:
Symptom Management:
Cholestyramine or ursodeoxycholic acid for pruritus and cholestasis.
Supplementation with fat-soluble vitamins (A, D, E, K).
Liver Transplant:
For severe liver disease or cirrhosis.
Management of Heart and Other Systemic Issues:
Tailored based on the specific anomalies.
why is the influenza vaccination reccomended for children 6 months - 6 years old?
- higher risk of complications
- below 6 months, the mom’s antibodies would protect them
- children start going to daycare or preschool after 6 months
- herd immunity
what are the complications of strep throat
- post strep
how to treat strep throat
- penicillin V for at least 10 days
- amoxicillin
what is the difference between oseltamicir vs zanamivir
neuromidase cleavees the sliac acid of the infected cell membrane
= infected cell
common injuries that happen to children
- skin and soft tissue injuries
- MSK injuries
- head trauma
- mouth and teeth injuries
- foreign bodies
- drowning (most preventable)
why do children’s bones heal faster than adults?
childrens bones are
1. more vascular
2. more periosteum
common complications of fractures that pass through growth plates
growth plate fracture
= slower growth
= limb length discrepancy
what is the approximate healing time for fractures
what is the impro
what is the most common cause of damage to kidneys in children?
repeat episodes of pyelonephritis (UTI)
are the nephrons fully mature at birth + does the number of nephrons stay the same through adulthood?
of nephrons is established at birth
nephron maturation continues through adulthood
hows does GFR change through life?
newborns: low GFR
= less efficient renal tubule function
= fluid and electrolyte imbalances
= limited renal concentrating ability
= diluted urine
- GFR gradually increases during first years of life
adolescence: peak GFR
maturation of glomerular and tubular function
= increase GFR
= enhanced kidney efficiency
