Endocrine Dysfunction Flashcards
S/S of T1DM
3 Ps (polyphagia, polyuria, polydipsia)
wt loss
bed wetting to nocturia
irritable (not themselves)
short attention
low frustration
dry, flushed skin
blurred vision
poor wound healing w/ infections
fatigue
HA
Hyperglycemia (glucosuria)
Diabetic ketosis ( ketones and glucose in urine, dehydration)
DKA (dehydration, electrolyte imbalance, acidosis, deep, rapid breathing)
Monitoring of Blood Glucose Levels using
self-monitoring and control of insulin (tolerate)
Glycosylated hemoglobin monitoring
Reflects the glucose level in the blood from 2-3 months
- assess control and effectiveness
- detects nonadherence
Nondiabetic levels for A1C
4-6%
Diabetic child’s A1C acceptable level
6.5-8%
It is recommended that urine ketone tests be done every ____ hours during an illness.
3
When should you check for ketones in the urine?
illness
glucose level is over 240 without an illness
What are acceptable ways to monitor diabetes?
Blood glucose tests (finger)
Hemoglobin A1C
Hypoglycemic episodes most commonly occur
before meals or when insulin effect is at its peak
Hypoglycemic S/S
rapid (minutes)
labile, irritable, nervous
difficulty concentrating
shaky
hunger
COLD AND CLAMMY
Tachycardia
tremors
Hypoglycemia is when the glucose is below
60
Hyperglycemia s/s
High and dry, sugar high
gradual over days
lethragic
confused
thirtst, weak
N/V
flushed and dry (dehydrated)
low hr
KUSSMAUL BREATHING
Hyperglycemia with s/s occurs when the glucose is
greater than 250
Rule of thumb for hypoglycemia
15-15-15 rule
15g of simple arb
wait 15 to check glucose
15g protein and fat
Mild hypoglycemia
fruit juice
Severe hypoglycemia
glucagon
- vomiting can occurs so caution aspirations
Rebound hyperglycemia
Somogyi effect
- elevated glucose at bedtime and drop at 0200 and rebound later
Endocrine System controls and regulates
metabolism
- energy production
- growth
- fluid and electrolyte balance
- response to stress
- sex development
Hormones are
Chemical substances which control/regulate activities of other cells/organs
Hormones are regulated by
endocrine glands into bloodstream
feedback mechanism
What is the master gland of the endocrine system?
Anterior Pituitary
Anterior pituitary gland is controlled by
hypothalamus
What hormone is regulated by other mechanisms
Insulin - glucose regulated
Hypopituitarism is caused by 1+ of these hormones
Gonadotropin deficiency
-Absence of secondary sex hormones
Growth hormone (GH) deficiency
Thyroid-stimulating hormone (TSH) deficiency
Adrenocorticotropic hormone (ACTH) deficiency
Gonadotropin deficiency causes
Absence of secondary sex hormones
Hypopituitarism Caused by
Tumors (brain or in the pituitary gland)
Incomplete/underdevelopment of the pituitary gland or hypothalamus
Congenital (with hypoglycemia and seizures)
Surgery in the brain or near
Radiation
Trauma
Autoimmune
Idiopathic
The s/s of hypopituitarism of the GH deficiency shows what after the 1st year?
below the 3rd percentile
GH
stimulate linear growth across growth
BUT stops growing height after 1st year
S/S of GH deficiency
After 1st year - below 3rd percentile
**Height stunted more than weight
-appear overwt**
Skeletal proportions normal for age
Primary teeth - normal age
Permanent teeth – delayed
Teeth overcrowded and mispositioned – smaller underdeveloped jaw
Delayed sexual development till 30-40
Hypopituitarism is mainly the deficiency of what hormone?
growth
What teeth are delayed in hypopituitarism?
permanent
- overvrowded and mispositioned becuase of the smaller underdeveloped jaw
Sexual development is delayed till when with hypopituitarism?
30-40
What needs to be ruled out before dx hypopituitarism?
Failure to Thrive
Dx of Hypopituitarism
Family Hx – parents appearance, growth hx, siblings
- Prenatal = maternal disorder r/o
- Chronic illness – congenital heart defects
- Physical exam – accurate ht and wt to watch trends
X-rays/MRI – <3 y/o
If 3+ then just the arms for maturity of the bones (delayed)
- Brain lesions
Endocrine studies
- Low GH stimulation test
Genetic testing
To truly diagnose GH deficiency then need
-poor linear growth
- delayed bone age
- abnormal GH stimulation test
Growth Hormone stimulation test
Baselines with fluids
Over hours they will give medications to stimulate the GH and draw labs afterwards
- to show responses
Hypopituitarism Tx
correct underlying (tumors)
Growth Hormone replacement – 80% success
- Biosynthetic growth hormone - SQ daily at bedtime (natural)
- Very expensive (insurance partial if doc deficiency sometimes)
Child and Family Support in Hypopituitarism
- parents have anger or guilt towards not growing bc disease
Human Growth Foundation
Research, education, support groups, bully prevention
Why are X-rays used for Hypopituitarism?
less than 3 = entire body
3+ = hands and wrists
mature and body age and if delayed then GH deficiency
What is the growth rate of GH replacement therapy for hypopituitarism?
initially, significant growth then tapers off with slow continues
Continue till bone maturation (boys 16 and girls 14)
Hyperpituitarism
overproduction of anterior pit. gland
Hyperpituitarism caused by
Hyperplasia of pituitary cells - over growth or tumor formation
Primary hypothalamic defect
Hyperpituitarism complications
Gigantism – excess growth
Hyperthyroidism -
Hypercortisolism – Cushing’s
Precocious puberty
S/S of Hyperpituitarism Before GROWTH PLATE CLOSURE
Proportional overgrowth of long bones (8ft tall)
Rapid & increased muscle development
Weight increase in proportion to height
Proportional head enlargement
Delayed fontanel closure
S/S of Hyperpituitarism After GROWTH PLATE CLOSURE
Acromegaly
Enlarged facial features
Separation and malocclusion of teeth
Enlarged hands/feet
Increased facial hair
Thickened, deeply creased skin
Deep/husky voice
Increased slow tendency toward hyperglycemia & DM
Hyperpituitarism and Acromegaly grow how?
not taller grow transverse
- slow and gradually
overtime look different
If Acromegaly is untreated
high mortality due to cardiovascular, metabolic and respiratory complications
Hyperpituitarism Dx
History of excessive growth
Increased levels of GH
Normal bone age
Enlargement of bones
Endocrine studies – excess of thyroid, cortisol, and sexual
Hyperpituitarism Tx
Removal of tumor/lesion if present
External radiation/radioactive implants
Pharmacologic agents
Transphynode surgery
suppression of GH drugs
emotional support
What famous person has acromegaly?
Lincoln
Precocious puberty
early onset of sexual development
- more in girls
Hyperpituitarism puberty onset when a boy
before 9
Hyperpituitarism puberty onset when a caucasian girl
before 7
Hyperpituitarism puberty onset when an AA girls
before 6
What are the different precocious puberty types
Central (80%)
Peripheral
Incomplete
Central Precocious puberty
the hypothalamus releases puberty hormones too early and matures faster
- idiopathic
Peripheral Precocious puberty
release of androgens by glands cause secondary sexcharacteristics, testes and ovaries produce – no maturation of gonads
Incomplete Precocious puberty
one random secondary sex characteristics
Precocious Puberty Tx
Treat specific causes if known (usually regress later on)
MRI
Synthetic hormones
Lupron Depot injections (1-3 months depending)
histrelin implant (1-2 years)
Precocious Puberty Therapy goal
Slow/stop pubertal progression (shorter than peers to reach normal ht)
Allow for normal adult height
Precocious Puberty Nursing Considerations
Family Education injections & side effects
Emotional support
Provide privacy during physical examination (self-conscious)
Expression of concerns by the child
Dress = chronological age
Reassurance regarding physiologic changes
Child’s social, cognitive, & emotional development match chronological age
What side effects of Lupron Depot injections (1-3 months depending)
mood swings or hot flashes
What would you say to a child going through hypopituitarism and precocious puberty if they are self-conscious?
Everything is normal it is just happening at a quicker rate than usual
Juvenile Hypothyroidism
is caused by
- Congenital
- Acquired
congenital = underdeveloped thyroid gland
acquired =
Partial/complete thyroidectomy
Following radiation treatment
Infectious processes
Dietary iodine deficiency
Thyroid levels in Juvenile Hypothyroidism in congenital
low T3-4
High TSH
Congenital Juvenile Hypothyroidism may not show until
at growth spurts because their body may only have the bare minimum and not ready for more
Juvenile Hypothyroidism has a more profound ________ than GH hormone and increases TSH
growth
Acquired Juvenile Hypothyroidism S/S
Thyromegaly – enlarged thyroid gland
Decelerated growth - later age
Myxedematous skin changes (dry skin, change in hair)
Constipation
Sleepiness
Lethargy
Mental decline –
Delayed puberty
Excessive weight gain
Congenital Juvenile Hypothyroidism S/S**
thick tongue
jaundice
floppy
umbilical hernia
hoarse cry
constipation
dry skin
large fontanel opening
mental decline
Juvenile Hypothyroidism Tx
Oral thyroid hormone replacement - levothyroxine
Prompt treatment in infants
Lifelong treatment
Juvenile Hypothyroidism Edu for Family
Daily compliance with medication - provide resources
Periodic blood work monitoring of serum thyroid levels
Juvenile Hypothyroidism needs to maintain
compliance with medication
the quicker the Tx the better development (1st 3 months)
Alpha cells produce what
glucagon
- raises sugar
Beta cells produce what
insulin -lower sugar
Delta cells produce what
sumadostatin
- increases glucagon and insulin depending on what is needed
(Balance)
Pancreatic Hormone Functions with what system in the pancreas
Islet of Langerhans
Islet of Langerhans produce what cells
Alpha
Beta
Delta
DM is a
chronic disorder of metabolism
with hypo and hyperglycemia
- can not use food for energy
Does DM have a cure?
no
What is the PATH of DM?
Sugar stays in the bloodstream due to the insulin not taking it into the cells
- insulin does not block the amount of glucose - causes build up
Type 1 DM is the
absolute destruction of pancreatic beta cells
Which type of DM has absolute insulin deficiency?
Type 1
What are the different forms of T1DM?
Trigger?
Immune-mediated – autoimmune destruction
Idiopathic – Not simply inherited
- Genetic predisposition + trigger event (virus)
S/S T1DM
Polyuria
Polydipsia
Polyphagia
Hyperglycemia
Rapid weight loss due to breakdown of fat
Dry skin
Irritability
Drowsiness/fatigue
Abdominal discomfort
Ketoacidosis leads to GI s/s
T1DM management
Insulin-dependent
Monitor glucose levels
Lifestyle changes
Nutrition
Exercise
Team Approach - family members for education with multiple lessons
What animal is used for Diabetes Education in Pediatrics?
Coco the monkey from Disney
- books with it
What is the DM for relative insulin deficiency?
Type 2
- resistance and body failure to use insulin properly
What pts have an increased risk of T2DM?
adults > 45 years of age
overweight
sedentary lifestyle (lack of exercise and poor nutrition)
family history of DM
T2DM has an increasing prevalence in
children/adolescents
- eating habits and lack of exercise
T2DM S/S
Polyuria
Polydipsia
Polyphagia
Fatigue
Blurred vision
Slow-healing sores
Frequent infections
Polycystic ovary syndrome
Areas of darkened skin (acanthosis nigricans)
acanthosis nigricans
areas of darkened skin
T2DM Tx
Lifestyle changes
Nutrition
Exercise
Oral medication - Metaformin
Possibly insulin – if hyperglycemic
Monitor glucose levels
What is the oral medication for T2DM
Metformin
- decrease absorption of sugar in the body
- decrease usage of insulin
T2DM Dx
8-hour fasting blood glucose level ≥126 mg/dl
Random blood glucose ≥ 200 mg/dl with classic signs of hyperglycemia
Oral glucose tolerance test ≥ 200 mg/dl in the 2-hour sample
Hemoglobin A1C ≥ 6.5%
T2DM if 8-hour fasting blood glucose level
≥126 mg/dl
T2DM if random blood glucose is
≥ 200 mg/dl with classic signs of hyperglycemia
T2DM if oral glucose tolerance test
≥ 200 mg/dl in the 2-hour sample
T2DM if Hemoglobin A1C
≥ 6.5%
Mixed insulin is the combination of
intermediate & rapid-acting
What are the different types of insulin?
rapid
short
intermediate
long
What is the most important need to remember with insulin?
timing of food and insulin
With rapid insulin, you need to eat within
15 minutes of food
With short insulin, you need to eat within
30 minutes before meal
What insulin is cloudy looking?
intermediate
What insulin can not be mixed in a syringe with other insulins and must be given separately at a different site?
long-acting
When do you dilute insulin?
less than 12 months
and extremely young infants because of small body
Conventional mgmt in insulin dosing means
twice daily dosing (before breakfast and supper)
- rapid/short-acting mixed with intermediate
Intensive therapy mgmt in insulin dosing means
multiple injections
Long-acting once or twice daily plus rapid-acting prior to each meal
- Better control, fewer long-term complications
- 20-24 hours: basal release morning or night
Insulin Administration DM
Subcutaneous administration
- PINCH METHOD WITH LIMITED ADIPOSE TISSUE
Rotate sites
Insulin absorption
Atraumatic care: shot blocker interferes with nerve transmissions
What insulin site is the fastest rate of absorption and shortest to stop?
abdomen
What insulin site is the longest to activate/absorb and lasts longer?
Buttocks
Insulin injection sites
outer arm
abdomen
hip area
thigh
Insulin Administration methods
Sub Q injections
Insulin Pen to smart
Insulin Pump (omnipod, i-Port)
An insulin pump site changed every
48-72 hours
- up to 75 injections
Atraumatic care
What is the drawback of an insulin pump?
tech does not always work
DKA
With DM, what is a must
self-monitoring
What alters insulin administration absorption?
exercise
illness
What is the goal level of blood glucose?
blood glucose 80-120 mg/dl
What is the goal level of hemoglobin A1C?
6.5-8% (younger people are able to run higher and older people are able to run lower <7.5%)
- over the last 3 months
Finger sticks atraumatic care
Warm the finger (warm water)
Use ring finger and thumb
Puncture side of finger pad
Press the lancet device lightly against the skin
Use a lancet device with adjustable-depth tips
Use glucose monitors that require small samples
Continuous Glucose Monitor (CGM) replacement of sensors
every 3-7 days
Hyperglycemia caused by
Too little insulin - missed dose
Illness/infection/immunizations
Injury
Stress- physical/emotional
Growth
Medications - steroids
Menses
Hyperglycemia S/S
Thirst
Polyuria (early)
Nausea
Blurred vision
Fatigue
DKA
Oliguria (later)
Hyperglycemia Tx
Drink fluids
Administer additional insulin
Monitor glucose more closely
Hypoglycemia S/S
Too much insulin
Diet
Exercise
Alcohol
Growth spurts
Puberty
Illness (esp. with vomiting)
In younger children is it okay to give insulin after they eat?
yes, because they won’ be honest about when they eat
Hypoglycemia S/S
Shaky/sweaty
Hungry
Pale
HA
Later=
- Confusion, Disorientation, Lethargy, slurred speech
- Change in behavior (glucose not getting into the brain - dizzy
cold and clammy need some candy
Hypoglycemia Severe S/S
Inability to swallow
Seizure/convulsion
Unconsciousness
Hypoglycemia Tx
Check blood sugar if possible
When in doubt, give 15g of simple carbohydrate (milk or juice)
WAIT and redo after 15 minutes
Followed by complex carbohydrate & protein
- reassess
Glucagon
If you cannot differentiate between hypo and hyperglycemia, what do you treat it as if you cannot get a glucose reading?
Hypoglycemia
- simple and complex carb (milk)
In HYPOGLYCEMIA, if the patient becomes unconscious, seizes, or cannot swallow (side lying)
Glucagon
- Mixed and given IM/SQ or Intranasally (baqsimi)
Releases stored glycogen from the liver
Should increase blood glucose in 15 minutes
Can cause nausea/vomiting (side lying)
Protect from aspiration
Vascular changes in DM long-term complications
Involves small and large vessels
Nephropathy
Retinopathy
Neuropathy
Cardiovascular
Hypertension
Atherosclerosis
Other long-term complications in children with T1DM
Altered thyroid function – at dx and poor controlled
Limited mobility – small joints of the hand (7-8 years old)
If the pt has a good control of DM, long term complications will develop in
20+ years
See a eye dr when after T1DM
2-3 YEARS AFTER DIAGNOSIS
See a eye dr when after T2DM
Initially after dx
DM Education
Explanation of diabetes
Meal planning
Administering insulin injections
Monitor hygiene - good health early on
Promote exercise
Record keeping
Observe for complications
Family support and camps
What does a diabetic always need to carry?
Glucose tablets
Insta-glucose
Sugar cubes
Candy
When should you exercise on DM?
WITH GOOD CONTROL
- decreases insulin requirements
When should you not exercise on DM?
Illness or With poor control if more than 240+
may stimulate ketoacidosis
Nutrition for DM
Sufficient calories to balance daily expenditure for energy and growth
Constant carb diet-exchange system
Consistent intake
Timing of food coincides with time/action of insulin
Total # of calories/proportions of basic nutrients needs to be consistent day-to-day
T1DM Education for toddlers and preschoolers needs to allow them to
make food choices and monitor carbs
- temper tantrums are s/s of possible hypoglycemia
snacks during increased activity
T1DM illness mgmt
glucose every 3 hours
urine ketones every 3 hours or when glucose is 240+
- always given insulin during illness and intake carbs
T1DM illness goals
Maintain normal glucose
Treat urinary ketones
Maintain hydration
rest
Diabetic Ketoacidosis is the complete state of
insulin deficiency
Patho of DKA
**Lack of insulin → glucose unavailable for cellular metabolism → body burns fat for energy → fat breaks down into fatty acids → glycerol in fat cells converted to ketones in liver → excess eliminated in urine (ketonuria) or lungs (acetone breath)
Ketonemia
ketones in the blood
- strong acids lowering of pH producing ketoacidosis
DKA with cellular death what is released and what are the aftereffects?
Potassium released from cells into the bloodstream and excreted by kidneys
Total body potassium decreased even though serum potassium may be elevated (decreased circulating fluid volume) - keep K in the body
Alteration in serum and tissue potassium can lead to cardiac arrest
If DKA is not reversed by insulin and electrolyte correction, then what will occur
progressive deterioration occurs (dehydration, electrolyte imbalance, acidosis, coma, death)
Mgmt of DKA
Rapid assessment
Adequate insulin to reduce elevated level
Fluids
NPO
Monitor renal functions
Electrolyte replacement (especially potassium)
- need renal function before administering
PICU mgmt of DKA
IV X2 – cont. insulin drip and K NS, dextrose with insulin
- slowly lower every hour check
Cardiac monitor bc low K
Labs
NPO
Hourly BG checks
Possible O2
Possible NG (unconscious pt)
Possible antibiotics
How do you bring down the blood sugar in DKA?
GRADUALLY and slowly
prevent cerebral edema
DKA happens frequently with DM having an
infection
