Endocrine Flashcards
Glands
Pituitary Hypothalamus Thyroid Parathyroid Adrenal Pancreas Ovaries/Testes
Pituitary
pea sized gland at base of cranium
Hypothalamus
In brain around pituitary
Thyroid
2 Large lateral lobes below larynx
Parathyroid
4-5 small bodies on thyroid
Adrenal
Cap like glands on top. of kidneys
Pancreas
Islets of langerhans
Ovaries/Testes
Female pelvis/male scrotum
Components of Endocrine
Cells
Target cells
Environment
The endocrine system controls or regulates metabolic processes governing energy production, growth, fluid and electrolyte balance, response to stress and sexual reproduction
Endo: Cells
Sends the chemical messages by the means of hormones
Endo: Target cells
End organs, receive that chemical message
Endo: Environment
Defined as through which the chemical is transported such as blood, lymph, ECF
Hormone types
Complex chemical substance produced and secreted into body fluids by a cell or group of cells that exert a physiological controlling effect on other cells
Local hormones
General hormones
Local hormones
Create the effects near the point of secretion
Acetylcholine is released at the parasympathetic of skeletal nerve endings mediates the synaptic activity of the nervous system
General hormones
Produced in one organ or part of the body and carried through the bloodstream to a distant part of the body where the initiate or regulate physiological activity of an organ for a group of cells
Job of endocrine
Differentiation of fetal reproductive and central nervous systems- determine the sex
Regulation of the pace of growth and development of the CNS throughout childhood and adolescence
Coordination of the male and female reproductive systems enabling sexual reproduction
Maintenance of homeostasis in the presences of a constantly changing external environment
Diabetes Insipidus: Differentiation of types
Done by CAT scan and MRI
Hormone control
Lacks until 12-28 months
Infants may exhibit imbalance in the concentration of fluids and electrolytes, amino acids, trace substance
Normal hormonal levels are related to age and stage of puberty
Endocrine malfunction
Present at birth, either observed at birth or detected with in the first year of life
Not diagnosed and treated early these conditions can lead to delayed growth and development, mental retardation and occasionally death
Endocrine malfunction: Treatment
Consists of a supplementation of what is missing such as what hormone is missing or an adjustment of levels of dietary control
Most are treated in an outpatients basis
Endocrine: Diagnostic tests
Lab screening
Radiology screening
Accurate Ht.Wt measurements
Genetic studies
Endocrine: Labs
Thyroid function Growth hormone (time specific, must be NPO, and an agent like insulin must be given to stimulate GH level BG test CB, Serum chemistry, urine studies
Growth hormone deficiency (hypopituitarism): Cause
Decreased activity of the pituitary gland
inadequate production of the secretion of the growth hormone which results in poor growth and short stature
Can be an isolated event or there could be an underlying cause of hypopituitarism such as brain tumors or cranial irradiation
Growth hormone deficiency (hypopituitarism):
Some of the disease of manifestations that you will see are things like Turners syndrome, renal disease, Prader willi
Turner Syndrome
Chromosomal disorder Females are affected Short stature Short neck Webbied features 1x chromosome is missing from the cells
Prader Willi
Chromosome 15
Morbidly obese
Cognitive involvement
Genetic mutation or deletion
Release of GH from pituitary is controlled by
Hypothalamus and inhibitory factors
GH stimulates
growth of all body tissues, synthesis of proteins in the lover
among them the insulin like growth factor, IGF, promotes glucose utilization by the cells and cell proliferation
GH deficiency results from
Failure of the pituitary or the hypothalamus to produce sufficient GH
Children with GHD are deficient in other hormones
Growth hormone deficiency: Causes
Infection or infarction of the pituitary gland sometimes related to Sickle cell disease
CNS disease
Pituitary or hypothalamus tumors
Psychosocial dwarfism (caused from psychosocial deprivation)
Dominant or recessive inheritance
Something that doesn’t happen or malformed during fetal development
50% of cases have unknown cause
Growth hormone deficiency: Manifestations in Infants
Normal weight and length at birth
Neonatal jaundice
Delay of the closure of the anterior fontanel
A 1: infant height is in the <5% for one’s age and sex, grow at a rate of <5cm per year
Hypoglycemia: might lead to seizures
Microprenis which undescended testicles
Pale optic discs in the eyes
Growth hormone deficiency: Manifestations in Children
Immature/cherubic facies which are angel/youthful facial features High pitch voice Delayed puberty Delayed dentition Hypoglycemia Overweight Ripply abdominal fat Delayed skeletal maturation Delayed sexual maturation
Growth hormone deficiency: Diagnostics
Monitor the growth measurements, see if he/she falls off the charts
Initial screening: thyroid function tests or see if the IGF 1 levels are low
CBC and bone age x-rays are also done
Somatomedin-C: indirect measurement of GH level
MRI: brain is done to rule out a pituitary lesion and abnormality
Rule out familial short stature of the parent or family members, pt also has a constitutional growth delay: skeletal dysplasia or psychosocial dwarfism
Growth hormone deficiency: Treatment
Replacement therapy
Growth monitoring
Testosterone injections
Estrogen injections
Creutzfeldt-Jakob disease
When GH was being derived from cadaver pituitaries
Virus
Progressive and fatal and is a neurological disorder
Unable to test for
Growth hormone deficiency: Treatment: replacement therapy
Expensive
Administered SubQ 3 times a wk or daily until the bone plates close or the patient reaches their predicted final height
Growth hormone deficiency: Treatment S/E of GH replacement
Rare
Increased ICP, HA needs work up
Early diagnosis and treatment are important to ensure attainment of maximum adult height potential
Growth hormone deficiency: Nursing care
Assessment of entire family
Provide psychosocial adjustment and support, might need financial assistance
S/E is that there may be an increased BG level and local infection
Growth hormone deficiency: Education
Its temporary
Keep a growth chart at home allow them to see whats going on and to take some responsibility for that
Proper med admin and how to give an injection
Need to give an injection at bedtime which approximates physiological release of GH (45-90 minutes after falling asleep)
Accurate height and weight measurement
Academic problems resulting from learning disabilities and from below average intelligence
Encourage the child to participate in sports such as swimming, martial arts, gymnastics
Grow at a slower rate, treatment resulting in self esteem issues
Counseling may be needed for the child
Hyperpituitarism
Excessive secretion of the GH
Excess GH increases the growth rate in the child
Rare
Hyperpituitarism: Causes
Pituitary adenoma or a tumor of the hypothalamus
Gigantism
Grow up to 7-8ft tall when over secretion occurs before the closure of the epiphyseal plates
Acromegaly
hypersecretion of the GH after the epiphyseal closure
Causes an increase of facial features such as a prominent super over do ridgem a prominent jaw, and generally enlarged facial features
Hyperpituitarism: can cause..
An increased strain on the organs leading to cardiomegaly or diabetes die to a strain on pancreas
Can also cause hypogonadism and or vision loss
Hyperpituitarism: Diagnosis
Increased level of IGF-1 which is an insulin like growth factor
A bone scan to see if epiphyseal plates have begun to fuse
Xray look for any tumors
Assessment: large feet, hands, facial features
Hyperpituitarism: Treatment
Treat the cause
Removal of tumor
Radiation therapy
Oral administration of Bromocriptine or Somanavert
Hyperpituitarism: Treatment: Bromocriptine
Dopamine agonist that suppresses the secretion of the GH
Hyperpituitarism: Treatment: Somanavert
New drug that blocks the action of the excessive GH
Precocious puberty: Normal puberty
Controlled by the pituitary
Girls: 8-13yr (10-12)
Boys: 9.5-14yr (11-14)
Precocious puberty
Hyperfunctioning of the pituitary
Girls: before 7, 6 in AA
Boys: Before 9-10
Precocious puberty: Signs
Child will appear taller than his or her peers but will reach skeletal maturity and the closure of the epiphyseal plates early resulting in an overall short stature later on
Precocious puberty: Speculated causes
from a disorder in the gonad, adrenal glands, or the hypothalamic pituitary gonadal access
Precocious puberty: Premature activation
Produces early maturation and development of the gonads, the secretion of sex hormones, the development of secondary sex characteristics, mature sperm or ova, early acceleration of a normal course
Precocious puberty: Other types
No early secretion of the gonadotropin
Early overproduction of the sex hormoones caused by a tumor, ovaries, testes, adrenal glands
Getting exogenous sources pf androgens or estrogens
Precocious puberty: Commercial products
Many of these facial creams or hair products contain estrogen hormones or placental extracts
Shampoos made specifically for AA contain hormones that are readily absorbed into the body that can even lead to some of the precocious puberty that we are seeing
Precocious puberty: CNS abnormalities
Tumors, surgery, inflammation, hydrocephalus, cysts
Precocious puberty: Androgel, Android
Topical testosterone products
Precocious puberty: Obesity
Common line and a positive correlation
Precocious puberty: Other gland
Makes steroid hormones is the adrenal gland
Diabetes Insipidus
Rare disorder of the posterior pituitary gland
Characterized by deficiency of the ADH or vasopressin
2 forms: True or central, Familial or nephrogenic
Diabetes Insipidus: True or central
Actual ADH deficiency
Diabetes Insipidus: Familial or nephrogenic
Which the kidneys are unable to respond to the ADH that are present
X-ray linked transmission
Diabetes Insipidus: Is the inability
To concentrate urine due to the deficiency of vasopressin or ADH
Diabetes Insipidus: ADH job
Concentration of the urine by stimulating the reabsorption of the water from the distal renal tubule from the kidney
ADH is inadequate, tubules do not reabsorb the water leading to polyuria, passage of a large volume of urine in the given time
Diabetes Insipidus: Primary causes
Familial or idiopathic
Diabetes Insipidus: Secondary causes
Results from head trauma, tumors, or infection in the area of the hypothalamus
Diabetes Insipidus: Results in
Meningitis, encephalitis, vascular anomalies such as an aneurysm can occur
Diabetes Insipidus: Causes
Craniopharyngioma: a tumor involving the hypothalamus
Head trauma or surgical resection
Diabetes Insipidus: Normally …
Hypothalamus→AHD→Pituitary→Blood→Kidneys→Distal tubules
Diabetes Insipidus: Low serum osmolality
Less solute and more water
Decrease in ADH slows down the reabsorption in the water and makes the urine less concentrated, making more suring
Diabetes Insipidus: Normal function and compensatory action
Hypothalamus releases ADH to the pituitary which will then go to the blood, kidneys, then the distal tubules causing an increase reabsorption of free water to concentrate the urine and decrease the urinary output
Diabetes Insipidus: Osmoreceptors
Pituitary react to serum osmolality
Low serum osmolality leads to a decrease in ADH production leads to an increase in urine output normalizing osmolarity
High serum osmolality: lead to an increase of ADH production, which can then lead to water retention and decreased urine output
Diabetes Insipidus: Deficiency of ADH
Body is unable to conserve water causing an increase in volume of dilute urine which is then voided
Loss of free water leads to an increase of serum Na concentration
Child has an intact thirst center than he or she may be able to compensate for the large fluid loss by increase their oral fluid intake
Unable to drink enough resulting in high serum Na level
Diabetes Insipidus: Manifestations
Polyuria Polydipsia Nocturia Na level >150 mEq Urine specific gravity <1.005
Diabetes Insipidus: Manifestations: infants
Excessive urination, insatiable thirst
First sign may be enuresis
Diabetes Insipidus: Manifestations: Children
Irritable, relieved with feeding water, not milk
Prone to dehydration, electrolyte imbalance, hyperthermia, circulatory collapse
Diabetes Insipidus: Diagnostic test: Water deprivation
Leave the child without any water and then you draw frequent blood lab levels
If child continues to have a large amount of dilute urine, a low specific gravity and an increased serum Na level
4-7hr
Normal response: decrease in urine output
Abnormal response: Dilute urine
Wt loss of 3-5% indicates a significant dehydration that requires termination of the test
Small children need to be monitored so they dont drink from places that they shouldnt
Diabetes Insipidus: Diagnostics: Unresponsive to water deprivation
Indicates that the child has nephrotic or nephrogenic DI
Diabetes Insipidus: Treatment
Life long in some cases or until the cause for DI goes away Fluid balance Synthetic vasopressin (0.05-0.2ml IN, SQ, IM, PO)
Diabetes Insipidus: Treatment: Concentrations- Intranasally
Squirt or through a soft flexible tube with permarked doses twice a day
DDAVP needs to be mixed thoroughly with the oil by holding it under warm water for 10-15 minutes and shaking it vigorously before having it drawn ip into the syringe
Diabetes Insipidus: Treatment: Concentrations- SubQ injection
lasts 48-72hr
Require frequent injections Q2-3days
See effects with in 8-20 hr
Watch for signs of overdose such as water intoxication
Diabetes Insipidus: Nursing care
Assessment and looking at their weight, I&O, electrolyte monitoring
Education on what S/S to watch for
DDAVP admin
Teaching S/S of excessive or insufficient DDAVP
S/S of hyper/hypoNa
Urine measurement and specific gravity teaching
Medical alert bracelet
Give free access to water and bathrooms
Teach child how to care for self
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Opposite of DI
Excessive production or release of ADH/vasopressin at the posterior pituitary gland
SIADH: results in
Filtered water to be reabsorbed in the kidneys back to central circulation
SIADH: Caused by
Disorder of the CNS including infections such as meningitis, head trauma, brain tumors, after brain surgery, initially the pt will get DI and SIADH then back to DI
SIADH:
Transient and will resolve when the underlying condition is corrected
Increase of ADH that causes the kidneys to reabsorb too much free water leading to a decreased output of concentrated urine, an increase fluid circulatory volume and a decreased serum Na
SIADH: Manifestations
Decreased urine output Increased urine specific gravity: more concentrated (1.030) Fluid retention with no edema Wt gain Increased BP Hypotonicity Increased urine osmolality HypoNa Hypochloremia Serum osmolality
SIADH: Treatment
Fluid restriction to correct hypoNa
Correct the underlying cause
Severe hypoNa: IV NaCl with slow careful monitoring of hypertonic saline
Chronic: consists of lithium and demeclocycline treatment which blocks the action of ADH at the renal collecting tubules
SIADH: Nursing care
Assess of recognizing the S/S with PICU pt
Accurate I&O
Daily wt
S/S of fluid volume overload
Children develop an expanded circulatory volume but do not form edema. excess of bother water and Na
Be aware of the fluid and what it contains. Irrigate all the tubes with NaCl not water, to prevent the pulling of NaCl thurs creating a greater imbalance
Congenital hypothyroidism
Present from birth where the thyroid gland does not produce enough thyroid hormone to meet the metabolic needs of the baby
Part of the mandatory newborn screenings that is present: to be done 24-48 hr or before discharge
Congenital hypothyroidism: Caused by
Spontaneous gene mutation and autosomal recessive genetic transmission of an enzyme or from iron deficiency
Congenital hypothyroidism: Manifestations
Prolonged jaundice, lethargy, constipation Feeding problems Cold to touch, skin mottling, bradycardia, small metabolic rate Umbilical hernia Hypotonia/slow reflexes Large tongue Thick lips Dull appearance Short trunk and neck Large fontanels Distended abdomen Hoarse cry Excessive sleeping
Congenital hypothyroidism: Treatment
Lifelong replacement
Synthetic thyroid hormone
Routine T4 and TSH levels and bone scans
Prognosis is good when there is a compliance with treatment
Diagnosed before 3 mo, then optimal mental development will occur, some mild delays but they will play catch up by the 6th grade
Congenital hypothyroidism: Nursing care
Good newborn assessment
Routine follow up assessments (G/D, Ht, Wt, FOC)
Congenital hypothyroidism: Parental education
Medication administrations
Can be dissolved in a small amount of water and given through a syringe or nipple
Never put it in the whole bottle incase its not completed
If vomits within 1 hr then administer it again
S/S of hyper and hypothyroidism
frequent missed doses can lead to a developmental delay and poor growth
How to take pulse, how to hold the dose if greater than said by the provider and contact the provider
Genetic counseling
Dress the child appropriately: will tend to be cold
Increase fruits and bulk to help towards constipation
Medical alert bracelet
Acquired hypothyroidism
Much like congenital hypothyroidism
inadequate thyroid hormone to meet the metabolic needs of the body
Acquired after 2-3 yr
Reversible
Acquired hypothyroidism: Causes
Hashimoto’s thyroiditis associated with goiter
Surgical resection
Radiation therapy for any type of malignancy
Excessive iodine ingestion because too much iodien could destroy the thyroid tissue
Iodine meds
Isolated thyroid stimulating hormone deficiency
Goiter sometimes present
Goiter at birth
Causes respiratory distress so we as nurses want to prepare for ER ventilation such as supplemental O2 and tracheostomy tube set
Hyperextension of the neck facilitates the breathing if there is a larger goiter
Acquired hypothyroidism: Causes: Congenital
Iodine or antithyroid drugs during pregnancy
Acquired hypothyroidism: Causes: Acquired
decrease of iodine, tumor, or inflammation
Acquired hypothyroidism: Manifestations
Goiter Dry thick skin abd course hair Hair loss Tiredness/fatigue Cold intolerance Constipation Wt gain Decreased growth Irregular menses Edema of the face, eyes, and hands High TSH Low T4
Acquired hypothyroidism: Treatment
Thyroid hormone replacement same dose as congenital
Acquired hypothyroidism: Nursing care
Teach medication administration and compliance
Assessment of goiter to see if it is decreasing in size
Growth/development assessment, Ht, Wt assessment
Denver developmental
School performance
Hyperthyroidism (Graves disease)
Excessive thyroid hormone that is being produced because of an enlarged thyroid gland
Increased metabolism
Seen mostly in 6-15 yr olds
Higher incidence with girls
Hyperthyroidism (Graves disease): Caused by
Autoimmune response to TSh receptors which is stimulating thyroid to secrete more T3 and T4, highly a familial incident, immunoglobulin is produced by the B-lymphocytes that stimulates the over secretion of thyroid hormones
Hyperthyroidism (Graves disease): Manifestations
Goiter Wt loss Increased appetite Diarrhea Increased perspiration Nervousness Tremors Overheated/fatigued during physical activity Heat intolerance Increased HR Exophthalmos (protruding eyes) Wide eyed Staring expression Increased blinking Absences of the wrinkling of the forehead when looking up Lid lag Lack of convergence Declining performance in school Muscle weakness Difficulty sleeping and relaxing May not be able to cover the cornea with eyelids Behavioral problems Blurred vision and loss of visual acuity Poor attention span Enlarged thyroid gland will be up to 3-4x normal (goiter)
Hyperthyroidism (Graves disease): Treatment
Anti thyroid drug therapy (take for 1-2yr followed by remission, see initial improvement in 2 wk, if relapse then 2nd course is indicated or surgical intervention) Radioactive iodine (thyroid cancer)
Hyperthyroidism (Graves disease): Goal
Inhibi the excessive secretions of thyroid hormone
Thyrotoxicosis
Thyroid storm/crisis
Occur from a sudden release of the hormone
Unusual in children but is life threatening
Thyrotoxicosis: S/S
Acute onset of irritability, and restless Vomiting Diarrhea Hyperthermia Hypertension Tachycardia Progresses: Delirium, death, coma
Thyrotoxicosis: Caused by
Acute infection ,surgical emergencies or a discontinuation of antithyroid therapy
Thyrotoxicosis: Treatment
Administration of beta adrenergic blockers (propranolol) to provide relief from adrenergic hyperresponsiveness that produces the reaction
Hyperthyroidism (Graves disease): Nursing care
Assessment for compliance
Education of child and parents
Will be on life long medication if they had radiation or surgery
Medication administration and compliance
Fever/sore throat they need to see a doctor due to neutropenia and leukopenia
Limit contact sports
Rest periods because they are easily fatigued
Medication side effects: skin rash, pruritus, gastric intolerance
Promote increase calorie intake providing 5-6 meals per day due to an increased in metabolic rate
Heat intolerance
Hygiene teaching may need to be done due increases sweating
Cushing syndrome:
Adrenal cortical hyper functioning
Excessive circulating free cortisol
Uncommon
Due to malignant adrenal tumor
Comes from prolonged steroid therapy that produces a cushingoid appearance (moon face, chubby cheeks, double chin)
Occur form pituitary, adrenal problems, tumor, or food causing an over production of ACT which stimulates the cortisol secretion
Inhibits the action of the GH
Cushing syndrome: Manifestations
Excessive hair growth Moon face Pendulous abdomen Poor wound healing Temporal fat Red cheeks Ecchymoses Red abdominal striae Bruises Weight gain Hypertension
Cushing syndrome: Labs
Decreased K
Decreased PO4/Phosphate
Cushing syndrome: Tests
Adrenal suppression test
MRI, CT scan (tumor detection)
Cushing syndrome: Adrenal suppression test
Initial screening of children with suspected adrenal cortical hyperfunction
Test reveals that the adrenal cortisol output is not suppressed overnight after a dose of dexamethasone, then they are positive
Cushing syndrome: Treatment
Radiation or drug therapy
Wean the patient off of steroids slowly
Bilateral adrenalectomy with replacement therapy
Require cortisol replacement therapy need to take their meds early in the morning every other day because this mimics the normal pattern of the cortisol secretion
Medical alert bracelet!
Diabetes Mellitus
Most common
Disorder of the carbohydrate, protein, and fat metabolism
Type 1 is most common
Diabetes Mellitus: Type 1
Insulin deficiency
Diabetes Mellitus: Type 2
Insulin resistance
COntracted usually as an adult and associated with overweight but there is an increasing incidence with adolescents getting it. Diet, exercise, and oral hypoglycemics are used to treat T2DM
Diabetes Mellitus: Etiology
Genetic factors
Autoimmune Mechanisms
Environmental
Diabetes Mellitus: Etiology: Genetic factors
Not really inherited, Inherits a susceptibility to the disease rather than the disease itself.
Presence of HLA (human leukocyte antigen) - loci on short arm of the chromosome
Do with compatibility
Diabetes Mellitus: Etiology: Autoimmune Mechanisms
Presence of HLA causes defect in immune system making it susceptible to a trigger event such as a dietary source, a virus, bacteria, or a chemical irritant.
Gradually it destroys beta cells, without beta cells no insulin can be produced
Diabetes Mellitus: Etiology: Environmental
Viruses or chemicals damage the insulin producing beta cells
Diabetes Mellitus: Patho: Insulin
transport carbohydrates into the cells to become energy
Prevents outflow of glucose from the liver to the general circulation
Diabetes Mellitus: Patho
Beta cell in islets of langerhans are destroyed
Remaining are unable to maintain normal BG levels
Lack of insulin results in increased BG level and decrease glucose level in the cells
Renal threshold for glucose is exceeded, glycosuria occurs. Up to 1000 calories per day can be lost in urine
No glucose is available to the cells, free fatty acids provide alternate source of energy, which are metabolized by the liver producing acetyl coenzyme. Ketone bodies are byproducts of CoA metabolism and accumulate in the body resulting in ketoacidosis
Diabetes Mellitus: Clinical mainfestations
Hyperglycemia Glycosuria Polyuria Polydipsia Gluconeogenesis Polyphagia Ketoacidosis
Diabetes Mellitus: Complications
Microvascular complications because the protein in the blood becomes deposited in the basement membranes causing: Nephropathy, Retinopathy, Neuropathy, Heart disease, PVD
Diabetes Mellitus: Manifestations
Hyperglycemia Polyuria Polydipsia Polyphagia Weight loss Enurses Irritability Shortened attention span Fatigue Blurred vision Poor wound healing Flushed skin HA Frequent infections Dry skin
Diabetes Mellitus: Diagnostic tests
Serum glucose levels
Urine test strips to determine ketonuria
Hemoglobin A1C
Diabetes Mellitus: Diagnostic test: Serum glucose levels
Fasting >126 is indicative of DM
Random >200 is indicative of DM
Diabetes Mellitus: Diagnostic test: Hemoglobin A1C
A longer term index of a patient’s average blood glucose level. An increase occurs about 3 weeks after a sustained elevation in blood glucose level. Take about 4 wks to show. Decrease in A1C also after a decrease in BG. Good control is about 7%, fair control 10%, poor control 13-20%. Assess diabetic control
Less than 7.5% is good for a diabetic.
Diabetes Mellitus: Therapeutic managment
Balancing of things that will raise blood sugar with things that will lower blood sugar
Things that will raise blood sugar
Food- especially carbohydrates Stress due to adrenaline and cortisol Physical- infection, illness Emotional- worry, excitement Growth due to growth hormone Certain medication (hormone, steroids) Menstrual cycle due to estrogen
Things that lower blood sugar
Insulin- only hormone to decrease blood sugars
Exercise but most effective in well controlled state
Alcohol due to blocked glycogen breakdown in liver (eat before drinking)
Insulin
Composed of a series of amino acids Pork or human insulin is preferred Available in rapid, short, intermediate and long acting preparations Comes in 100 unit /mL concentrations Dosage is based on capillary BG level
Animal insulin
different from human insulin by 1 pork amino acid or 3 in beef amino acids
Human insulin
Made by recombinant DNA using E. coli or yeast
Diabetes Mellitus: Insulin in Kids
Usually dose 2x daily regimen or the use of an insulin pump (require site maintenance every 48-72 hr)
Diabetes Mellitus: Treatment Goal
Maintain near normal levels of less than 126mg/dL and a Hgb-A1C of 7% or less
Diabetes Mellitus: Regular insulin
Clinically and practically be mixed with any insulin however its action may be blunted by mixing with lente or ultralente
Diabetes Mellitus: NPH insulin
Cannot be mixed with any lente type insulin
Diabetes Mellitus: Humulin BR
Pump insulin, cannot be mixed with any insulin
IV administration of Insulin
Regular insulin only!
Special line priming (insulin attaches to the plastic polymers of the IV bag and tubing.
Inject the insulin into the bag and then let it run through the tubing for about 30-50mL run out of the tubing. This allows the patient to get all the insulin that they need instead of the insulin clinging to the walls of the tubing
Works rapidly, and clears the blood stream in about 30 minutes
IV administration of Insulin: Abrupt D/C
Will cause the BG to rise after 5-30 minutes
Be sure to give SubQ insulin when you are turning off the pump so the BG stays stable
Insulin pump
Regular insulin (humulin BR- buffered regular insulin- designed to withstand movement through the pump tubing)
Worn on a belt or shoulder harness
Needle and catheter are changed every 48-72 hr
New insulin Apidra can be used in pumps
Lispro can also be used (rapid acting)
Insulin program
Plan of 4 things
MOst are treated with 2 injections per day
Typical program is 30 minutes before breakfast NPH and regular, 30 minutes before supper NPH and regular
NPH peak
6-12hr
Regular Peak
30 minutes
Insulin absorption is determined by
Condition of the site
Temperature of the insulin (cold can be painful and absorbed more slow)
Location of the site (over exercising muscles can absorbed more quickly. The fastest is the abdomen and shortest in duration, slowest absorption is the leg or butt but the longest duration)
Diabetes Mellitus: Therapeutic management: Monitoring
SBGM (self blood glucose monitoring) is taught and used
Insulin dosage based on reading
Urine testing no longer routine
Normalization of BG level may prevent long term complications
Want it to be between 80-120
Diabetes Mellitus: Nutrition
Need consistent intake and timing of food especially CHOs which should be limited and kept constant in amount consumed and time consumed from day to day
Fruits are simple CHOs and will raise BG faster but effect is not sustained
Starches are complex CHOs that will raise BG slower and have a more sustained effect
Diabetes Mellitus: Starches
Certain veggies fall into starches: Potatoes, beans, pasta, corn, rice, peas
Diabetes Mellitus: Milk
Complex CHO
Will raise BG slow and last even longer, mainly due to the effect of protein and fat in the milk
Protein will eventually breakdown releasing some glucose
Protein is planned in the diet for moderate amounts
Time is regulated according to insulin type
Extra food is needed for extra energy
Exchange system consists of 6 basic food groups
Should allow calories for optimal growth
Diabetes Mellitus: Exercise
Vigorous exercise should be preceded by a CHO snack
Simple sugars should be made available at all times during exercise
Exercise is not indicated if DM is poorly controlled (BG is over 240 with positive ketones)
Child in insulin depleted and exercise would be an added stress resulting in even further gluconeogenesis and ketogenesis due to adrenaline
Diabetes Mellitus: Hypoglycemia control
Physical activity is associated with increased insulin sensitivity
Regular exercise and fitness improve metabolic control with a lower insulin use
Child must have adequate caloric intake to prevent hypoglycemia
Diabetes Mellitus: Illness management
Do not omit insulin during illness, amount might change
Supplemental Lispro or regular for hyperglycemia during illness
Watch for fluid balance
Child vomits more than one time let the provider know
Surgery: require alterations in the insulin needs of the child, the stress of surgery will increase the BG level- regular insulin is needed at this time
Diabetes Mellitus: Transplantation
Seen as a cure
Islet cells or whole pancreas transplantation
Viable insulin producing cells have been injected into portal veins where they are transported to the liver to produce 2/3 of the insulin
Diabetes Dilemmas: Hypoglycemia (mild): Brain symptoms
Consist of HA, hunger, confusion, dizziness, diplopia, mood changes, and behavioral changes
Diabetes Dilemmas: Hypoglycemia (mild): Adrenalin symptoms
Shakiness, pallor, tachycardia, dilated pupils, cold and clammy type of feeling
Diabetes Dilemmas: Hypoglycemia (mild): Treatment
Stop exercise, check BG level, giv milk or fruit juice or a carbonated beverage, candy, fruit or anything with high sugar
Wait 10-15 minutes to check effect then recheck BG, repeat fruit if still symptomatic
Give starch and a protein if the next meal or snack is more than an hour away
Diabetes Dilemmas: Hypoglycemia (severe): Symptomes
unconscious, extreme confusion, combativeness and or seizures
Diabetes Dilemmas: Hypoglycemia (severe): Treatment
Call for help
Give sticky food such as honey or gel or syrup into the side of the mouth
Glucagon by SubQ injection
Check BG during treatment
Following recovery: child may eat a snack of complex CHO to replenish the glycogen stores
Diabetes Dilemmas: Hypoglycemia: Severe reaction S/S
N/V and severe HA
No memory of what happened
Somogyi Effect/Rebound
During hypoglycemia, the body responds to the stress by secreting anti insulin hormones, which are counter-regulatory
Hormones released stored glycogen in the liver where it is converted to glucose
BG goes up often too high resulting in rebound hyperglycemia
Rebound refers to the hyperglycemia followed by hypoglycemia
Prevention of rebound requires increase in the amount of food or decreasing the insulin
Somogyi Effect/Rebound: Dawn phenomenon
Increase in blood sugar between 4 and 7am
Need to increase the insulin at bedtime
Its the big problem during puberty due to the release of cortisol and GH and other stimulants
Somogyi Effect/Rebound: Hyperglycemia
Common symptoms: polyuria, polydipsia, polyphagia
Blood sugar is over 240, requires urine ketone check
Persistent hyperglycemia necessitates an insulin change or evaluation of food intake
Hyperglycemia created an osmotic diuresis and dehydration
Oral fluids must be encouraged
Exercise may still be continued if there is not keotic or ketotic or spilling ketones in the urine
Diabetic ketoacidosis: Signs
Dehydration (decreased in Na, K, Cl, Ph, Mg, Serum pH and bicarb reflet degree of acidosis) Wt loss Tachycardia Flushed ears and cheeks Kussmaul respirations Acetone breath Decreased level of consciousness Hypotension Hyperglycemia Glycosuria BG >300 Ketones in serum Acidosis: pH <7.3 and bicarb: <15
Diabetic ketoacidosis: Pedi emergency
Priority is venous access
Also weigh, measure, put on a cardiac monitor and get labs
Diabetic ketoacidosis: Treatment
Start with treating dehydration: IV is NS, this decreases the risk for cerebral edema (over 24-48hr)
Serum K levels initially normal but check again after fluid bolus and insulin has been started
Fluid and insulin cause a rapid return of K to the cells and can severely deplete serum K levels
Start K replacement after the child voids (kidney functionality)
Diabetic ketoacidosis: Insulin therapy
Decrease serum glucose level
Not to exceed 100mg/dL/hr (usually 1U/kg/hr)
Faster than this could lead to cerebral edema
You want the BG to fall 50-100mg/dL/hr
When the BG level gets to 250-300, you begin to add dextrose to the fluid, either 5% or 10%
We want the goal to be 120-240
Diabetic ketoacidosis: Fluid and electrolyte balance
Important!
Give K after you know the level and after the first void to determine the kidney functionality
Monitor T waves as changes indicate hypoK or hyperK (elevated T waves, shortened OT interval)
Diabetic ketoacidosis: If not treated
Acidosis
Coma
Death
Diabetic ketoacidosis: Nursing considerations
Patient and parent teaching Blood glucose monitoring Record keeping S/S and treatment of hyper/hypoglycemia Family support Proper hygiene Insulin and injection techniques Nutrition and meal planning
Diabetic ketoacidosis: Nutrition and meal planning
Learn to read the labels
Measure amounts
List of fast food restaurants with calories and fats listed
Avoid high fats, carbs, and sugars
Diabetes: Nursing considerations: Insulin and injection techniques
Open bottles can be stored at room temp or refrigerated
Injection technique and rotation pattern
Give 4-6 injections per site before you change sites
Sites over active muscle absorb faster
Diabetes: Proper hygiene
Caution children to not let anyone use their lancet or their devices or needles or syringes
Teach methods to minimize the pain of BG testing
Holding the finger under warm water to stimulate blood flow to the area, puncture the finger on the side (less nerves), alternative site might be forearm
Apply Emla to the site to be punctured
Diabetes: Nursing diagnosis
Risk for injury related to insulin deficiency
Risk for injury related to hypoglycemia
Knowledge deficit related to care of a child with newly diagnosed DM
Altered family process related to management of a chronic disease
Addison’s disease
Adrenocortical insufficiency
Addison’s disease: Cause
Infections
Destructive lesion of the adrenal gland or neoplasms
Autoimmune processes
Idiopathic
Addison’s disease: Manifestations
Gradual onset Dehydration Anorexia Wt loss Muscle weakness Mental fatigue Irritability, apathy, negativism Increased sleeping Hypotension Small heart size Dizziness Syncope Hypoglycemia effects Unexplained seizures Craving salt Acute abdominal pain Electrolyte imbalance
Addison’s disease: Treatment
Replacement of glucocorticoids and mineralocorticoids
Triple dose during times of stress
Monthly injections of desoxycorticosterone acetate in implantation every 9-12 months
