Peds Sessions Flashcards
Look over Brandau CIS
DO it now.
Vitamin D
25-hydroxyvitamin D diffuses across the placental barrier so that the infant’s levels depend upon the mother
There is a correlation between the mother and infant for 1,25 dihydroxyvitamin D but fetal levels come from the fetal kidney
stages of rickets
STAGE 1-D3 deficiency leading to decreased Ca absorption and Ca levels begin to decrease resulting in the INCREASE of PTH levels and mobilization of Ca from bone
STAGE 2-Phosphorus reabsorption in the kidney decreases increasing the renal tubular concentration of phosphorus. At this time there is decreased amounts of 25-D3 thus no conversion to 1,25-D3 so reabsorption of Ca from the gut does not take place meaning Ca levels are maintained by the action of PTH on bone
STAGE 3-As the calcium levels continue to fall calcification of the bony matrix becomes inadequate i.e. the solubility product (calcium x phosphorus) is not exceeded and normal mineralization of bone cannot take place.
Common findings: protruding forehead, pigeon chest, depressed ribs, kyphosis, curved humerus, large head, “ricketic rosary”, curved tibia and fibula
Vit D dependent rickets:
Predisposing factors:
Lack of sunlight exposure
Lack of commercial milk products
Anticonvulsive therapy (phenobarbital or phenytoin)
Intestinal malabsorption syndromes/particularly those that cause malabsorption of fat
Clinical Features: Tetany Growth retardation Frontal bossing Rachitic rosary Widening of the wrists or knee joints Seizures
Lab findings: **Low serum calcium **Low serum phosphorus High level of alkaline phosphatase **High serum level of PTH Low serum level of 25-D3
hypophosphatemic Rickets/ Vit D resistant rickets
Not vitamin D metabolism problem but rather a phosphate leak at the level of the proximal tubule
Inherited as an autosomal dominant or X-linked dominant
Problem causes low serum phosphorus
Solubility product of calcium and phosphorus is < 35 mg/dL so no mineral precipatation occurs in the cartilaginous matrix
Lab findings:
Low serum phosphorus**
Normal level of serum calcium
Normal or slightly elevated level of PTH
**Pathognomonic finding
Renal insufficiency Rickets
Both vitamin D and PTH systems are broken
Phosphorus excretion is decreased
Serum phosphorus levels increase
Synthesis of 1,25-D3 decreases
Ca absorption from the gut becomes severely reduced
Lab findings: **High serum level of phosphorus **Low serum level of calcium High level of PTH Serum alkaline phosphatase is elevated **Elevated serum creatinine and BUN
transient hypoparathyroidism
- low serum calcium, elevated phosphorus… but normal PTH levels
hx: infant born w/ seizures and low calcium levels
Causes are diverse and represent disruptions in the steps controlling maintenance and secretion of the hormone
Transient hypoparathyroidism can occur in the offspring of mothers with hyperparathyroidism or hypercalcemia of any cause
Always keep in mind Di-George Syndrome when see hypocalcemia:
Catch 22
- 22q11.2 deletion
- cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, hypocalcemia
Chvostek’s sign
= sign of hypocalcmia - tap on the facial nerve - will elicit twitching at the lip at the corner of the mouth and spasm of fascial mm. depending on severity
DDx of neonatal hypocalcemia
Maternal diabetes
Birth Asphyxia
Sepsis (macrophage-generated cytokines that effect PTH secretion)
Preterm birth – levels can be all over the place
Increased calcitonin
Resistance to PTH
Decreased PTH secretion
presentation of neonatal hypocalcemia can be confused with…
Hypoglycemia Sepsis Meningitis Asphyxia Intracranial bleed Narcotic withdrawal
clinical signs of hypocalcemia of newborn?
Jitteriness Generalized convulsions Focal seizures Lethargy Poor feeding Vomiting abdominal distention
exanthem
skin eruption due to an illness
enanthem
an eruption of lesions in mucous membranes
rocky mountain spotted fever
- tick born disease
- Rickettsia rickettsii
- most common symptoms are high fever (> 102° F), headache, rash, and myalgias.
- petechial rash typically begins on the wrists and ankles but may be found anywhere, including the oral mucosa, as in this child
meningococcemia
- gram-negative diplococcus Neisseria meningitidis
- basically develop DIC : see large dark red patches/erythema and blisters
- 50% of patients developing meningitis only, 10% developing septicemia only, and 40% developing both.
- Children with meningitis are usually febrile and ill-appearing, with symptoms of lethargy, vomiting, and nuchal rigidity.
- Septicemia leads to capillary leak, coagulopathy, profound acidosis, and myocardial failure.
- Patients must be closely monitored for hypotension, shock, pericarditis, organ failure, and coagulopathy, usually in an intensive care unit setting.
** seen spreading in dorms **