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Pedi Exam 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Glands

A 
Pituitary
Hypothalamus
Thyroid
Parathyroid
Adrenal
Pancreas
Ovaries/Testes
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2
Q

Pituitary

A

pea sized gland at base of cranium

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3
Q

Hypothalamus

A

In brain around pituitary

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4
Q

Thyroid

A

2 Large lateral lobes below larynx

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5
Q

Parathyroid

A

4-5 small bodies on thyroid

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6
Q

Adrenal

A

Cap like glands on top. of kidneys

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7
Q

Pancreas

A

Islets of langerhans

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8
Q

Ovaries/Testes

A

Female pelvis/male scrotum

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9
Q

Components of Endocrine

A

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

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10
Q

Endo: Cells

A

Sends the chemical messages by the means of hormones

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11
Q

Endo: Target cells

A

End organs, receive that chemical message

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12
Q

Endo: Environment

A

Defined as through which the chemical is transported such as blood, lymph, ECF

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13
Q

Hormone types

A

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

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14
Q

Local hormones

A

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

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15
Q

General hormones

A

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

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16
Q

Job of endocrine

A

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

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17
Q

Diabetes Insipidus: Differentiation of types

A

Done by CAT scan and MRI

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18
Q

Hormone control

A

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

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19
Q

Endocrine malfunction

A

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

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20
Q

Endocrine malfunction: Treatment

A

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

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21
Q

Endocrine: Diagnostic tests

A

Lab screening
Radiology screening
Accurate Ht.Wt measurements
Genetic studies

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22
Q

Endocrine: Labs

A 
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
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23
Q

Growth hormone deficiency (hypopituitarism): Cause

A

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

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24
Q

Growth hormone deficiency (hypopituitarism):

A

Some of the disease of manifestations that you will see are things like Turners syndrome, renal disease, Prader willi

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25
Q

Turner Syndrome

A 
Chromosomal disorder
Females are affected
Short stature
Short neck 
Webbied features 
1x chromosome is missing from the cells
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26
Q

Prader Willi

A

Chromosome 15
Morbidly obese
Cognitive involvement
Genetic mutation or deletion

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27
Q

Release of GH from pituitary is controlled by

A

Hypothalamus and inhibitory factors

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28
Q

GH stimulates

A

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

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29
Q

GH deficiency results from

A

Failure of the pituitary or the hypothalamus to produce sufficient GH
Children with GHD are deficient in other hormones

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30
Q

Growth hormone deficiency: Causes

A

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

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31
Q

Growth hormone deficiency: Manifestations in Infants

A

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

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32
Q

Growth hormone deficiency: Manifestations in Children

A 
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
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33
Q

Growth hormone deficiency: Diagnostics

A

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

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34
Q

Growth hormone deficiency: Treatment

A

Replacement therapy
Growth monitoring
Testosterone injections
Estrogen injections

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35
Q

Creutzfeldt-Jakob disease

A

When GH was being derived from cadaver pituitaries
Virus
Progressive and fatal and is a neurological disorder
Unable to test for

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36
Q

Growth hormone deficiency: Treatment: replacement therapy

A

Expensive

Administered SubQ 3 times a wk or daily until the bone plates close or the patient reaches their predicted final height

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37
Q

Growth hormone deficiency: Treatment S/E of GH replacement

A

Rare
Increased ICP, HA needs work up
Early diagnosis and treatment are important to ensure attainment of maximum adult height potential

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38
Q

Growth hormone deficiency: Nursing care

A

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

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39
Q

Growth hormone deficiency: Education

A

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

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40
Q

Hyperpituitarism

A

Excessive secretion of the GH
Excess GH increases the growth rate in the child
Rare

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41
Q

Hyperpituitarism: Causes

A

Pituitary adenoma or a tumor of the hypothalamus

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42
Q

Gigantism

A

Grow up to 7-8ft tall when over secretion occurs before the closure of the epiphyseal plates

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43
Q

Acromegaly

A

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

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44
Q

Hyperpituitarism: can cause..

A

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

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45
Q

Hyperpituitarism: Diagnosis

A

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

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46
Q

Hyperpituitarism: Treatment

A

Treat the cause
Removal of tumor
Radiation therapy
Oral administration of Bromocriptine or Somanavert

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47
Q

Hyperpituitarism: Treatment: Bromocriptine

A

Dopamine agonist that suppresses the secretion of the GH

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48
Q

Hyperpituitarism: Treatment: Somanavert

A

New drug that blocks the action of the excessive GH

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49
Q

Precocious puberty: Normal puberty

A

Controlled by the pituitary
Girls: 8-13yr (10-12)
Boys: 9.5-14yr (11-14)

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50
Q

Precocious puberty

A

Hyperfunctioning of the pituitary
Girls: before 7, 6 in AA
Boys: Before 9-10

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51
Q

Precocious puberty: Signs

A

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

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52
Q

Precocious puberty: Speculated causes

A

from a disorder in the gonad, adrenal glands, or the hypothalamic pituitary gonadal access

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53
Q

Precocious puberty: Premature activation

A

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

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54
Q

Precocious puberty: Other types

A

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

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55
Q

Precocious puberty: Commercial products

A

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

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56
Q

Precocious puberty: CNS abnormalities

A

Tumors, surgery, inflammation, hydrocephalus, cysts

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57
Q

Precocious puberty: Androgel, Android

A

Topical testosterone products

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58
Q

Precocious puberty: Obesity

A

Common line and a positive correlation

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59
Q

Precocious puberty: Other gland

A

Makes steroid hormones is the adrenal gland

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60
Q

Diabetes Insipidus

A

Rare disorder of the posterior pituitary gland
Characterized by deficiency of the ADH or vasopressin
2 forms: True or central, Familial or nephrogenic

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61
Q

Diabetes Insipidus: True or central

A

Actual ADH deficiency

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62
Q

Diabetes Insipidus: Familial or nephrogenic

A

Which the kidneys are unable to respond to the ADH that are present
X-ray linked transmission

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63
Q

Diabetes Insipidus: Is the inability

A

To concentrate urine due to the deficiency of vasopressin or ADH

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64
Q

Diabetes Insipidus: ADH job

A

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

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65
Q

Diabetes Insipidus: Primary causes

A

Familial or idiopathic

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66
Q

Diabetes Insipidus: Secondary causes

A

Results from head trauma, tumors, or infection in the area of the hypothalamus

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67
Q

Diabetes Insipidus: Results in

A

Meningitis, encephalitis, vascular anomalies such as an aneurysm can occur

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68
Q

Diabetes Insipidus: Causes

A

Craniopharyngioma: a tumor involving the hypothalamus

Head trauma or surgical resection

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69
Q

Diabetes Insipidus: Normally …

A

Hypothalamus→AHD→Pituitary→Blood→Kidneys→Distal tubules

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70
Q

Diabetes Insipidus: Low serum osmolality

A

Less solute and more water

Decrease in ADH slows down the reabsorption in the water and makes the urine less concentrated, making more suring

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71
Q

Diabetes Insipidus: Normal function and compensatory action

A

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

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72
Q

Diabetes Insipidus: Osmoreceptors

A

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

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73
Q

Diabetes Insipidus: Deficiency of ADH

A

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

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74
Q

Diabetes Insipidus: Manifestations

A 
Polyuria
Polydipsia
Nocturia
Na level >150 mEq
Urine specific gravity <1.005
75
Q

Diabetes Insipidus: Manifestations: infants

A

Excessive urination, insatiable thirst

First sign may be enuresis

76
Q

Diabetes Insipidus: Manifestations: Children

A

Irritable, relieved with feeding water, not milk

Prone to dehydration, electrolyte imbalance, hyperthermia, circulatory collapse

77
Q

Diabetes Insipidus: Diagnostic test: Water deprivation

A

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

78
Q

Diabetes Insipidus: Diagnostics: Unresponsive to water deprivation

A

Indicates that the child has nephrotic or nephrogenic DI

79
Q

Diabetes Insipidus: Treatment

A 
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)
80
Q

Diabetes Insipidus: Treatment: Concentrations- Intranasally

A

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

81
Q

Diabetes Insipidus: Treatment: Concentrations- SubQ injection

A

lasts 48-72hr
Require frequent injections Q2-3days
See effects with in 8-20 hr
Watch for signs of overdose such as water intoxication

82
Q

Diabetes Insipidus: Nursing care

A

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

83
Q

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

A

Opposite of DI

Excessive production or release of ADH/vasopressin at the posterior pituitary gland

84
Q

SIADH: results in

A

Filtered water to be reabsorbed in the kidneys back to central circulation

85
Q

SIADH: Caused by

A

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

86
Q

SIADH:

A

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

87
Q

SIADH: Manifestations

A 
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
88
Q

SIADH: Treatment

A

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

89
Q

SIADH: Nursing care

A

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

90
Q

Congenital hypothyroidism

A

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

91
Q

Congenital hypothyroidism: Caused by

A

Spontaneous gene mutation and autosomal recessive genetic transmission of an enzyme or from iron deficiency

92
Q

Congenital hypothyroidism: Manifestations

A 
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
93
Q

Congenital hypothyroidism: Treatment

A

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

94
Q

Congenital hypothyroidism: Nursing care

A

Good newborn assessment

Routine follow up assessments (G/D, Ht, Wt, FOC)

95
Q

Congenital hypothyroidism: Parental education

A

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

96
Q

Acquired hypothyroidism

A

Much like congenital hypothyroidism
inadequate thyroid hormone to meet the metabolic needs of the body
Acquired after 2-3 yr
Reversible

97
Q

Acquired hypothyroidism: Causes

A

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

98
Q

Goiter at birth

A

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

99
Q

Acquired hypothyroidism: Causes: Congenital

A

Iodine or antithyroid drugs during pregnancy

100
Q

Acquired hypothyroidism: Causes: Acquired

A

decrease of iodine, tumor, or inflammation

101
Q

Acquired hypothyroidism: Manifestations

A 
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
102
Q

Acquired hypothyroidism: Treatment

A

Thyroid hormone replacement same dose as congenital

103
Q

Acquired hypothyroidism: Nursing care

A

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

104
Q

Hyperthyroidism (Graves disease)

A

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

105
Q

Hyperthyroidism (Graves disease): Caused by

A

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

106
Q

Hyperthyroidism (Graves disease): Manifestations

A 
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)
107
Q

Hyperthyroidism (Graves disease): Treatment

A 
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)
108
Q

Hyperthyroidism (Graves disease): Goal

A

Inhibi the excessive secretions of thyroid hormone

109
Q

Thyrotoxicosis

A

Thyroid storm/crisis
Occur from a sudden release of the hormone
Unusual in children but is life threatening

110
Q

Thyrotoxicosis: S/S

A 
Acute onset of irritability, and restless
Vomiting 
Diarrhea
Hyperthermia
Hypertension
Tachycardia
Progresses: Delirium, death, coma
111
Q

Thyrotoxicosis: Caused by

A

Acute infection ,surgical emergencies or a discontinuation of antithyroid therapy

112
Q

Thyrotoxicosis: Treatment

A

Administration of beta adrenergic blockers (propranolol) to provide relief from adrenergic hyperresponsiveness that produces the reaction

113
Q

Hyperthyroidism (Graves disease): Nursing care

A

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

114
Q

Cushing syndrome:

A

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

115
Q

Cushing syndrome: Manifestations

A 
Excessive hair growth
Moon face
Pendulous abdomen
Poor wound healing 
Temporal fat
Red cheeks 
Ecchymoses
Red abdominal striae
Bruises
Weight gain
Hypertension
116
Q

Cushing syndrome: Labs

A

Decreased K

Decreased PO4/Phosphate

117
Q

Cushing syndrome: Tests

A

Adrenal suppression test

MRI, CT scan (tumor detection)

118
Q

Cushing syndrome: Adrenal suppression test

A

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

119
Q

Cushing syndrome: Treatment

A

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!

120
Q

Diabetes Mellitus

A

Most common
Disorder of the carbohydrate, protein, and fat metabolism
Type 1 is most common

121
Q

Diabetes Mellitus: Type 1

A

Insulin deficiency

122
Q

Diabetes Mellitus: Type 2

A

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

123
Q

Diabetes Mellitus: Etiology

A

Genetic factors
Autoimmune Mechanisms
Environmental

124
Q

Diabetes Mellitus: Etiology: Genetic factors

A

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

125
Q

Diabetes Mellitus: Etiology: Autoimmune Mechanisms

A

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

126
Q

Diabetes Mellitus: Etiology: Environmental

A

Viruses or chemicals damage the insulin producing beta cells

127
Q

Diabetes Mellitus: Patho: Insulin

A

transport carbohydrates into the cells to become energy

Prevents outflow of glucose from the liver to the general circulation

128
Q

Diabetes Mellitus: Patho

A

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

129
Q

Diabetes Mellitus: Clinical mainfestations

A 
Hyperglycemia
Glycosuria
Polyuria
Polydipsia
Gluconeogenesis 
Polyphagia
Ketoacidosis
130
Q

Diabetes Mellitus: Complications

A

Microvascular complications because the protein in the blood becomes deposited in the basement membranes causing: Nephropathy, Retinopathy, Neuropathy, Heart disease, PVD

131
Q

Diabetes Mellitus: Manifestations

A 
Hyperglycemia
Polyuria
Polydipsia
Polyphagia
Weight loss
Enurses 
Irritability
Shortened attention span 
Fatigue
Blurred vision
Poor wound healing 
Flushed skin
HA
Frequent infections
Dry skin
132
Q

Diabetes Mellitus: Diagnostic tests

A

Serum glucose levels
Urine test strips to determine ketonuria
Hemoglobin A1C

133
Q

Diabetes Mellitus: Diagnostic test: Serum glucose levels

A

Fasting >126 is indicative of DM

Random >200 is indicative of DM

134
Q

Diabetes Mellitus: Diagnostic test: Hemoglobin A1C

A

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.

135
Q

Diabetes Mellitus: Therapeutic managment

A

Balancing of things that will raise blood sugar with things that will lower blood sugar

136
Q

Things that will raise blood sugar

A 
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
137
Q

Things that lower blood sugar

A

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)

138
Q

Insulin

A 
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
139
Q

Animal insulin

A

different from human insulin by 1 pork amino acid or 3 in beef amino acids

140
Q

Human insulin

A

Made by recombinant DNA using E. coli or yeast

141
Q

Diabetes Mellitus: Insulin in Kids

A

Usually dose 2x daily regimen or the use of an insulin pump (require site maintenance every 48-72 hr)

142
Q

Diabetes Mellitus: Treatment Goal

A

Maintain near normal levels of less than 126mg/dL and a Hgb-A1C of 7% or less

143
Q

Diabetes Mellitus: Regular insulin

A

Clinically and practically be mixed with any insulin however its action may be blunted by mixing with lente or ultralente

144
Q

Diabetes Mellitus: NPH insulin

A

Cannot be mixed with any lente type insulin

145
Q

Diabetes Mellitus: Humulin BR

A

Pump insulin, cannot be mixed with any insulin

146
Q

IV administration of Insulin

A

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

147
Q

IV administration of Insulin: Abrupt D/C

A

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

148
Q

Insulin pump

A

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)

149
Q

Insulin program

A

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

150
Q

NPH peak

A

6-12hr

151
Q

Regular Peak

A

30 minutes

152
Q

Insulin absorption is determined by

A

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)

153
Q

Diabetes Mellitus: Therapeutic management: Monitoring

A

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

154
Q

Diabetes Mellitus: Nutrition

A

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

155
Q

Diabetes Mellitus: Starches

A

Certain veggies fall into starches: Potatoes, beans, pasta, corn, rice, peas

156
Q

Diabetes Mellitus: Milk

A

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

157
Q

Diabetes Mellitus: Exercise

A

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

158
Q

Diabetes Mellitus: Hypoglycemia control

A

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

159
Q

Diabetes Mellitus: Illness management

A

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

160
Q

Diabetes Mellitus: Transplantation

A

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

161
Q

Diabetes Dilemmas: Hypoglycemia (mild): Brain symptoms

A

Consist of HA, hunger, confusion, dizziness, diplopia, mood changes, and behavioral changes

162
Q

Diabetes Dilemmas: Hypoglycemia (mild): Adrenalin symptoms

A

Shakiness, pallor, tachycardia, dilated pupils, cold and clammy type of feeling

163
Q

Diabetes Dilemmas: Hypoglycemia (mild): Treatment

A

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

164
Q

Diabetes Dilemmas: Hypoglycemia (severe): Symptomes

A

unconscious, extreme confusion, combativeness and or seizures

165
Q

Diabetes Dilemmas: Hypoglycemia (severe): Treatment

A

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

166
Q

Diabetes Dilemmas: Hypoglycemia: Severe reaction S/S

A

N/V and severe HA

No memory of what happened

167
Q

Somogyi Effect/Rebound

A

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

168
Q

Somogyi Effect/Rebound: Dawn phenomenon

A

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

169
Q

Somogyi Effect/Rebound: Hyperglycemia

A

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

170
Q

Diabetic ketoacidosis: Signs

A 
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
171
Q

Diabetic ketoacidosis: Pedi emergency

A

Priority is venous access

Also weigh, measure, put on a cardiac monitor and get labs

172
Q

Diabetic ketoacidosis: Treatment

A

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)

173
Q

Diabetic ketoacidosis: Insulin therapy

A

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

174
Q

Diabetic ketoacidosis: Fluid and electrolyte balance

A

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)

175
Q

Diabetic ketoacidosis: If not treated

A

Acidosis
Coma
Death

176
Q

Diabetic ketoacidosis: Nursing considerations

A 
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
177
Q

Diabetic ketoacidosis: Nutrition and meal planning

A

Learn to read the labels
Measure amounts
List of fast food restaurants with calories and fats listed
Avoid high fats, carbs, and sugars

178
Q

Diabetes: Nursing considerations: Insulin and injection techniques

A

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

179
Q

Diabetes: Proper hygiene

A

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

180
Q

Diabetes: Nursing diagnosis

A

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

181
Q

Addison’s disease

A

Adrenocortical insufficiency

182
Q

Addison’s disease: Cause

A

Infections
Destructive lesion of the adrenal gland or neoplasms
Autoimmune processes
Idiopathic

183
Q

Addison’s disease: Manifestations

A 
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
184
Q

Addison’s disease: Treatment

A

Replacement of glucocorticoids and mineralocorticoids
Triple dose during times of stress
Monthly injections of desoxycorticosterone acetate in implantation every 9-12 months

Pedi Exam 2 (6 decks)

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