Peds Sessions Flashcards
Look over Brandau CIS
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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 **
Measels
caused by rubeola virus
** measels rash starts from head and goes all the way down the body **
After exposure, the incubation period lasts for 7-14 days.
- Patients then develop a prodrome of high fevers, often > 104° F, with the classic triad of cough, coryza, and conjunctivitis.
** A couple of days later, Koplik spots develop on the buccal mucosa, appearing as white spots on an erythematous base.
leukemia
see petechial lesions – worry about these!!!!
- nonspecific symptoms of anorexia, irritability and lethargy
- Subsequently one may see progressive fatigue, weight loss, pallor, bone pain, fever and petechiae
HUS (TTP in adults)
associated with “bloody diarrhea” (E. coli O-157)
- patient develop progressive renal failure, anemia, thrombocytopenia.
ITP
Idiopathic thrombocytopenic purpura (ITP)
- Most common cause of thrombocytopenic purpura in childhood: present with little spots, and occur in places you wouldn’t expect
- associated with bleeding and bruising
- usually follows a viral illness, and then platelets drop <20,000 (consumptive coagulopathy - AI response from viral illness results in platelet drop)
- giant, normal looking platelets
- RARELY get intracrnial bleeds, b/c the platelets that are available are large and very effective
- self-limited, lasts a few weeks to a few months
NOTE: differentiate from leukemia, which normally has around 50,000 platelets
chicken pox
“dew drop on rose petal” = varicella virus
herpes
see vesicular lesions - can get encephalitis and hepatitis
encephalitis complications: stroke, seizures
- worry about brain and liver*
what infection can cause bullous?
staph infection
- “sandpaper rash”- peeling in antecubital spaces and groin
scarlet fever - bad sore throat, sandpaper type rash (maculopapular), in lower abdominal lesion
= Group A strep infection
urticaria
allergic reaction, viral reaction, strep, idiopathic causes
steven-johnson syndrome
involves mucus membranes,
form of toxic epidermal necrolysis, is a life-threatening skin condition - involves peeling and stripping of skin
Fifth’s disease
= “slapped cheek” syndrome
= parvovirus B19
this patient is nontoxic, often presents with this a maculopapular rash on the trunk and extremities, followed by the development of a lacy reticulated pattern on the trunk and extremity
who else can be affected by parvo?
- can cause problem with pregnant women: can cause hydrops fetalis and anemia in baby
- sickle cell patients: can have significant complications b/c it shuts down the bone marrow
roseola
- caused by HHV 6 and 7
- an infant or young child, presents with high fever, 103-105 lasting 3-4 days and usually nothing else clinically
- high fever, irritable, feel bad … then fever breaks and 24 hours later a diffuse rash shows up
- totally benign disorder, looks really sick in the beginning
see circular rashes, think what?
ringworm or nummular eczema - tx it with steroids if think its eczema or tx with lotramine if think its tinea - if it doesn’t get better then you switch!
do skin slideshow
do it now!
tuberous sclerosis
- see small white patch, shows up better under Wood’s lamp
- can see adenomas
** big problem: can grow tumors in the brain
classic lesions of TS are the ash leaf macule, shagreen patch (raised orange peel appearance) and adenoma sebaceum, (skin colored or pink lesion often present on face in late childhood to early adolescence) which is a misnomer as they are actually fibroadenomas and have nothing to do with the sebaceous glands.
the ash leaf lesion is often present at birth, most easily seen with a wood’s lamp.
sturge-weber lesion
port wine stain
- rare congenital neurological and skin disorder
- could have hemangiomas present in the brain- can cause seizures and big problems
- Do an MRI
- this can be a devastating disorder which is the result of a capillary hemangioma which involves the skin of the face, mucous membranes, meninges and choroid plexus. You may see seizures, hemiparesis, hemianopsia and intellectual impairment. Usually lesions are unilateral.
Neurofibromatosis
- presents with cafe au lait spots (greater than 1.5 cm)
- axillary freckling
- see neurofibromas, acoutstic neuromas, optic gliomas
** more than 6 lesions greater than 1.5 cm is pathognomonic for Neurofibromatosis.
Cutaneous and subcutaneous neurofibromas appear in late childhood or adolescence.
NOTE: One may also see large unilateral cafe au lait spots in Mccune Albright syndrome. This disorder includes polyostotic bone dysplasia, precocious puberty and multiple endocrine dysfunctions.
