Endocrine Issues and Disorders Flashcards
Type 1 diabetes
acute onset
human leukocyte antigens strongly associated
destruction of pancreatic islet cells by isle tell antibodies (autoimmune process)
ketones in blood and urine
s/sx of type 1 DM
polyuria, polydipsia and polyphagia nocturnal enuresis weight loss, with increased hunger fatigue and weakness, paraesthesia LOC changes ranging from irritability to coma (most present with this for the first time) loss of SQ fat and muscling waiting suggestive of insidious onset dysfx of peripheral sensory nerves evidence of dehydration
s/sx of type 1 DM in advance disease
ophthalmic exam may reveal micro aneurysms or cotton wool spots
evidence of peripheral visceral insufficiency
diminshed DTRs
Labs of Type 1 DM
- looks dehydrated
serum fasting blood sugar >/= 126 on 2 separate occasions
random blood sugar >/=200 and polydipsia, polyuria, and weight loo indicate the need to confirm the dx by fasting studies
glycosuria and ketonuria
plasma ketones
BUN and creatinine may be increased (dehydrated)
increased hgb A1c
impaired glucose tolerance: fasting >/=100 and =125
Dietary teaching of Type 1 DM
total carb intake: 50-60% of total caloric intake
fats: 25-30% of total calories
fiber: 25g/1000 calories
protein: 10-20% of total calories
Patients presenting with ketones in type 1 DM must start ______.
insulin
**begin with 0.5 u/kg/day, giving 2/3 of dose in morning and the remaining 1/3 in the evening
Somogyi Effect
**think tsunami, go up and down
when nocturnal hypoglycemia stimulates a surge of counter regulatory hormones that raise blood sugar–pt is hypoglycemic at 3 am and rebounds with an elevated blood sugar at 7 am (so hyperglycemic)
treat by reducing or eliminating the HS dose of insulin
Dawn phemomenon
tissue become desensitized to insulin nocturnally. Blood sugar gets progressively higher through the night and is elevated at 7 am. This desensitization is felt to be d/t the presence of growth hormone that spikes at night
treat by adding or increasing the dose of HS insulin
Type 2 diabetes mellitus
previously referred to as non0insulin dependent DM or adult onset
not linked to human leukocyte antigen system
no islet cell antibodies identified
presence of obesity or family history increases risk
S/sx of type 2 DM
insidious onset of hyperglycemia may be asymptomatic
generalized pruritus
recurrent vaginits is often the first symptom in women
peripheral neuropathies and recurrent blurred vision are more common than in DM1
chronic skin infections
acanthosis nigricans
polydipsia, polyphagia, polyuria may be present but less common symptoms DM2
in early disease, physical findings are unremarkable
Labs for type 2 DM
same as for type 1 DM except no ketones in blood and urine
What circumstances should you consider screening for DM2
obesity and has 2 of the risk factors:
family hx of type 2 DM
race/ethnicity of african american, native american, hispanic or asian/pacific islanders
signs associated with insulin resistance
screening if done should begin at age 10 or onset of puberty (whatever occurs first) and repeat every 2 years
Signs of insulin resistance:
acanthosis nigricans
hypertension
dyslipidemia
polycystic ovarian disease
Oral antidiabetics for type 2 DM
metformin (FDA approved in children)
850 mg twice a day or 500 mg 3x/day
reduces gluconeogenesis
do not give to hepatic or renal failure or to those prone to hypoxia
significant GI upset
little or no hypoglycemia
discontinue 48 hours prior to a procedure
Hyperthyroidism
increased T3
increased T4
decreased TSH
Grave’s disease
most common in children associated with diffuse enlargement of thyroid, hyperactivity of the gland, and presence of antibodies against different fractions of the thyroid gland
Causes/incidence of hyperthyroidism
more common in females
onset between 12-14 years of age
other causes: toxic adenoma, thyroiditis, TSH secreting pit tumor, high dose amiodarone)
Signs and symptoms of hyperthyroidism
everything sped up
nervousness, restlessness heat intolerance, increased sweating, warm moist skin muscle cramps frequent basilar migraine weight changes (usually a loss0 palpitations, chest pain menstrual irregulatories fine hair
a.fib tachycardia thyroid goiter (often without bruit) grave's opthalmopathy may be present hyperactive DTR
Labs for hyperthyroidism
TSH decreased
T4 increased
T3 increased
ANA usually elevated without evidence of lupus
Management of hyperthyroidism
Refer to endocrine
Meds: propranolol and thiourea drugs (PTU and tapazole)
other treatments: radioactive iodine, thyroid seizure, 2-3 gets of lugol’s solution
Hypothroidism
T3 decreased
T4 decreased
TSH increased
d/t disease in thyroid gland or deficiency of pituitary thyroid stimulating hormone or hypothalamic thyrotropin releasing hormone
most often due to autoimmune thyroiditis
Congenital cause of hypothyroidism
may affect fetus in first trimester
absence or underdevelopment of thyroid gland
inherent dysfunction in transport/assimilation of iodine
hypothalamic of pit disorder
occurs in 1:4000 live births
Juvenile cause of hypothyroidism
hashimoto's thyroiditis pituitary deficiency of TSH hypothalamic deficiency of TRH iodide deficiency damage to the gland
Signs and symptoms of hypothyroidism in neonates/infants
no obvious symptoms in the first month of life
lethargy, poor feeding, prolonged bilirubin elevation
growth deceleration
large fontanels
bradycardia
hypotonia
Signs and symptoms of hypothyroidism in older children
weakness, muscle fatigue arthralgias, cramps cold intolerance constipation weight gain mental/physical sluggishness, poor motor coordination delayed bone age, poor growth dry skin, thinning hair, brittle nails puffy eyes and thick tongue edema of the hands and face, ascites slowed DTRs diminished heart sounds
Lab tests for hypothyroidism
newborn screening is mandatory
Elevated TSH Dec T4 Dec Free Tr increased serum cholesterol and liver enzymes hyponatremia, hypoglycemia anemia
Management of hypothyroidism
refer to endocrine
treat with synthroid (not generic)
Short stature
height falling> 2 SD below mean or a marked devotion from perviously established growth curve
failure to grow more than 4 cm per year
Normal variants for short stature
familial genetic variant: normal linear growth velocity and a short target height
constitutional delay: bone age consistent with height age–slow growth rate for first 2-3 year of life, then a low-normal growth velocity
family history of short stature and delayed puberty are often present
Conditions with disproportionate short stature
dwarfism
rickets
Conditions with proportionate short stature
IUGR maternal/fetal infection chromosomal abnormalities FTT variety of endocrine disease: hypopituitarism, GH deficiency, diabetes, hypothyroidism
Labs for short stature
CBC, LFT, electrolyte, ESR, bone age, UA, thyroid function test, celiac disease, stool for ova and parasites, growth hormone level, sweat test if recurrent bronchitis (rule out CF)
