Exam 3: Peds

Question 1

describe the anatomical changes in intussusception

Answer 1

Telescoping of the intestine. Ileocolic location most common though can occur in other locations

Question 2

Manifestations of intussusception

Answer 2

Healthy infant or toddler presents with periodic episodes of severe, crampy abdominal pain occurring in 20-minute intervals that worsen over time.
- inconsolable
- guarding position (knees up)
- pallor
- emesis: non bilious → bilious
- hematochezia + mucus → currant
jelly stool (Currant jelly a very late finding, when you get to this point, it means you have damage to the colon and its a late finding).
- Specific findings but less common: Scaphoid right lower abdomen and/or sausage mass in right mid or upper abdomen.

Question 2

epidemiology of intussusception

Answer 2

• age range usually 4 months to 36 months
• occurs in boys slightly more than girls

Question 3

describe the etiology of intussusception

Answer 3

a. Idiopathic in 75% of cases

b. Associated upper respiratory and adenovirus infections
precede intussusception in many cases. The why here is unknown but possibly related to enteric lymphatic swelling creating a lead point.

c. Lead point: Structure (localized swelling or polyp) that allows peristatic waves to drag one segment of the GI tract into the next

Question 4

diagnosis for intussusception

Answer 4

• Patient presentation
• ultrasound showing thickening and if obstruction, dilated loops of bowel

Question 5

what is compromised when the bowel intercepts on itself?

Answer 5

the blood supply

Question 5

what are the complications for Intussusception

Answer 5

intestinal obstruction caused by dilated loops of bowel

Question 6

what does scaphoid in RLQ mean?

Answer 6

scaphoid means theres a hollow in the RLQ
- as the large intestines fold over on itself and continues by peristaltic waves, its no longer in the RLQ (look at pic in outline)

Question 7

describe the anatomical changes of infantile hypertrophic pyloric stenosis

Answer 7

• hypertrophy of the pylorus which causes gastric outlet obstruction

**caused by hypertrophy or enlarging cells and tissues

**the pylorus sphincter doesnt only narrow, the muscles along the canal itself thickens–>when this happens, chyme or gastric content gets trapped in the stomach and cannot pass to the small intestines

Question 8

Epidemiology for Infantile hypertrophic pyloric stenosis

Answer 8

a. Infantile – 3-5 weeks, rare after 3 months–these kids persistently lose weight

b. boys>girls 5:1

c. Other: First born, preterm, and young maternal age.

Question 9

pathophysiology for Infantile hypertrophic pyloric stenosis

Answer 9

i. Circular muscle contraction narrowing sphincter opening

ii. Longitudinal muscle thickening narrowing pyloric canal

Question 10

what is the etiology/risk factors for pyloric stenosis?

Answer 10

Etiology not clearly understood. Risk factors include:
i. Intranatal or postnatal exposure to macrolide antibiotics (baseline rate ~ 2.3/1,000 → increases to 3-13/1,000 depending on antibiotic).
erythromycin, azithromycin, clarithromycin

ii. Others: maternal smoking during pregnancy, bottle feeding, genes

Question 11

what are the clinical manifestations for pyloric stenosis? (3)

Answer 11

i. Post-prandial, projectile, non-bilious vomiting followed by hunger/rooting ( this baby is starving b/c nothing is getting into the small intestines

ii. Fluid and electrolyte imbalances: Dehydration, hypochloremia, metabolic alkalosis
dehydration = decrease UO and no tears

iii. Olive sized mass right upper quadrant (hypertrophied tissue at gastric outlet). Late finding but diagnostic.

Question 12

diagnosis for pyloric stenosis

Answer 12

• history and presentation
• abd US
• upper GI series with barium

Question 13

describe the anatomical changes in Vesicoureteral reflux (VUR)

Answer 13

Anatomy: Normally, the ureters tunnel into the bladder and as the bladder fills the ureters are compressed which prevents reflux.

In patients with short ureter/tunnels, urine more easily refluxes into the ureter–> since the ureters is higher in the bladder, it does not compress when the bladder is filled with urine, which can cause reflux into the ureter

Question 14

classifications of Vesicoureteral reflux (VUR) 2

Answer 14

1. Primary: Congenital shortening of tunneled intravesicular ureter. (most common)
    Normal ureter comes down 2 cm into bladder so when bladder fills with urine it compresses and seals off. If ureters up higher it doesn’t pinch ureter off
   * Incompetent ureterovesical junction
2. Secondary: Conditions creating abnormally high voiding pressures such as bladder obstruction (stones) and neurogenic bladder
    This is an obstruction caused by;
   * Recurrent UTI- Causes inflammation of ureters
   * Posterior urethral valve disorder- Membrane forms at bottom on bladder, prevents urine passing through urethra
   * Neurogenic bladder- Bladder unable to contract

Question 15

epidemiology for vesicoureteral reflux (VUR) (4)

Answer 15

• girls more than boys
• race: white>black
• young children (<2 years) more than older children (growth lengthens the ureter)—when children get older, the bladder enlarges and wraps itself around the ureter
• genetic susceptibility: tends to run in families, no single gene identified

Question 16

what are the manifestations for VUR?

Answer 16

1. Prenatal fetal hydronephrosis buys the baby a work-up for VUR
2. Postnatal presentation: Febrile urinary tract infection. poor growth and development, irritability, feeding problems

Question 17

diagnostic workup for VUR

Answer 17

• KUB
• voiding cystogram to grade reflux and hydronephrosis (given radio opaque dye that collects in kidneys and shows the sign of renal pelvis and the ureters)

Question 18

Effect of lead on oxidative stress and physiologic element

Answer 18

• Pb+2 is chemically “similar” and competitive with divalent (elements that donate two electrons from their outer ring thus becoming +2 positive) ions involved in biological processes: Ca+2, Fe+2, and Zc+2. By competing, Pb+2 disrupts their associated physiologic processes
• Pb and cellular oxidative stress. Pb tips the scales in favor of reactive oxygen species (ROS) > antioxidant defenses (glutathione depletion mostly) leading cell death.

Question 19

what is an acceptable lead level?

Answer 19

<3.5 mcg/dL

Question 20

what does an increased level of lead affect?

Answer 20

brain development

Question 21

lead exposures and toxicity common in young children d/t:

Answer 21

a. “oral” exploration

b. immature blood brain barrier ( the effects on the brain is worse b/c the BBB is not mature until a year of age)

c. increased absorption from gut and recirculating lead stored in bones

d. nutritional deficits elevating lead levels (Gut is lined with divalent metal transporters. In the absence of iron and calcium, lead is preferentially absorbed)

Question 22

mechanism and manifestations of elevated lead levels on: the central & peripheral nervous system

Answer 22

lead is an imposter that alters neurotransmitters

a. Mechanism: Pb and neurotransmitters–> at all levels lead will interfere with calcium and interfere with neuronal functions

b. Pb and brain volume: complicated by lead and presence of ROS damages cell which causes shrinkage in the size of the brain

c. Pb and manifestations of neurological toxicity: lowest level may be asymptomatic or may have findings—> every findings have to do with central and peripheral nervous system

Question 23

mechanism and manifestations of elevated lead levels on: Pb and hematological system: Anemia

Answer 23

** lead interferes with iron in the formation of heme, heme without iron cannot attach oxygen to it**

a. Mechanism: Pb interference with heme synthesis
*lead interferes with two steps in the formations of heme-> interferes with ferrochelatase (ferric enzyme) by interfering with this enzyme iron cannot be incorporated into the cell

b. Hemolytic anemia develops at relatively high BLL (40 mcg/dL). Iron deficient anemia may overlap.

Question 24

what causes iron deficient anemia d/t lead?

Answer 24

nutritional deficit

-there are divalent metal transporters in GI tract that arent absorbing iron because its not present. so lead is absorbed

Question 25

mechanism and manifestations of elevated lead levels on: Pb and renal system

Answer 25

a. Mechanism: Oxidative stress damages nephron. Degree of damage determined by the duration and degree of exposure.

b. Progression from acute, reversible nephritis to chronic kidney disease.

Question 26

mechanism and manifestations of elevated lead levels on: Pb and impaired gastrointestinal system function

Answer 26

a. Mechanisms: Multifactorial – diminished absorption due to Pb presence, diminished peripheral nerve function, diminished peristalsis due to lead interference with ac+n- myosin-calcium muscle contraction

**contractile proteins are actin and myosin and calcium needs to cross over to contract–lead will compete with calcium and displace it so myosin and actin cannot cause muscular contraction
b. Pb and manifestations of gastrointestinal toxicity

Question 27

diagnosis for lead toxicity

Answer 27

• targeted screening. currently, United States Preventive Services Task Force
• symptomatic children and children in high risk areas
  **house built prior to 1978 (lead based paint)
  **common house sources of lead contamination
  **lead in drinking water

Question 28

preferred blood lead level sampling

Answer 28

capillary sampling is easily contaminated, venous sampling preferred