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Module 5 (Pediatrics) > Endocrine Dysfunction > Flashcards

Endocrine Dysfunction Flashcards

1
Q

S/S of T1DM

A

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)

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2
Q

Monitoring of Blood Glucose Levels using

A

self-monitoring and control of insulin (tolerate)

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3
Q

Glycosylated hemoglobin monitoring

A

Reflects the glucose level in the blood from 2-3 months
- assess control and effectiveness
- detects nonadherence

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4
Q

Nondiabetic levels for A1C

A

4-6%

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5
Q

Diabetic child’s A1C acceptable level

A

6.5-8%

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6
Q

It is recommended that urine ketone tests be done every ____ hours during an illness.

A

3

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7
Q

When should you check for ketones in the urine?

A

illness
glucose level is over 240 without an illness

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8
Q

What are acceptable ways to monitor diabetes?

A

Blood glucose tests (finger)
Hemoglobin A1C

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9
Q

Hypoglycemic episodes most commonly occur

A

before meals or when insulin effect is at its peak

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10
Q

Hypoglycemic S/S

A

rapid (minutes)
labile, irritable, nervous
difficulty concentrating
shaky
hunger
COLD AND CLAMMY
Tachycardia
tremors

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11
Q

Hypoglycemia is when the glucose is below

A

60

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12
Q

Hyperglycemia s/s

A

High and dry, sugar high
gradual over days
lethragic
confused
thirtst, weak
N/V
flushed and dry (dehydrated)
low hr
KUSSMAUL BREATHING

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13
Q

Hyperglycemia with s/s occurs when the glucose is

A

greater than 250

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14
Q

Rule of thumb for hypoglycemia

A

15-15-15 rule
15g of simple arb
wait 15 to check glucose
15g protein and fat

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15
Q

Mild hypoglycemia

A

fruit juice

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16
Q

Severe hypoglycemia

A

glucagon
- vomiting can occurs so caution aspirations

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17
Q

Rebound hyperglycemia

A

Somogyi effect
- elevated glucose at bedtime and drop at 0200 and rebound later

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18
Q

Endocrine System controls and regulates

A

metabolism
- energy production
- growth
- fluid and electrolyte balance
- response to stress
- sex development

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19
Q

Hormones are

A

Chemical substances which control/regulate activities of other cells/organs

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20
Q

Hormones are regulated by

A

endocrine glands into bloodstream
feedback mechanism

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21
Q

What is the master gland of the endocrine system?

A

Anterior Pituitary

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22
Q

Anterior pituitary gland is controlled by

A

hypothalamus

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23
Q

What hormone is regulated by other mechanisms

A

Insulin - glucose regulated

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24
Q

Hypopituitarism is caused by 1+ of these hormones

A

Gonadotropin deficiency
-Absence of secondary sex hormones
Growth hormone (GH) deficiency
Thyroid-stimulating hormone (TSH) deficiency
Adrenocorticotropic hormone (ACTH) deficiency

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25
Q

Gonadotropin deficiency causes

A

Absence of secondary sex hormones

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26
Q

Hypopituitarism Caused by

A

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

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27
Q

The s/s of hypopituitarism of the GH deficiency shows what after the 1st year?

A

below the 3rd percentile

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28
Q

GH

A

stimulate linear growth across growth
BUT stops growing height after 1st year

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29
Q

S/S of GH deficiency

A

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

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30
Q

Hypopituitarism is mainly the deficiency of what hormone?

A

growth

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31
Q

What teeth are delayed in hypopituitarism?

A

permanent
- overvrowded and mispositioned becuase of the smaller underdeveloped jaw

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32
Q

Sexual development is delayed till when with hypopituitarism?

A

30-40

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33
Q

What needs to be ruled out before dx hypopituitarism?

A

Failure to Thrive

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34
Q

Dx of Hypopituitarism

A

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

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35
Q

To truly diagnose GH deficiency then need

A

-poor linear growth
- delayed bone age
- abnormal GH stimulation test

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36
Q

Growth Hormone stimulation test

A

Baselines with fluids
Over hours they will give medications to stimulate the GH and draw labs afterwards
- to show responses

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37
Q

Hypopituitarism Tx

A

correct underlying (tumors)
Growth Hormone replacement – 80% success
- Biosynthetic growth hormone - SQ daily at bedtime (natural)
- Very expensive (insurance partial if doc deficiency sometimes)

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38
Q

Child and Family Support in Hypopituitarism

A
  • parents have anger or guilt towards not growing bc disease
    Human Growth Foundation
    Research, education, support groups, bully prevention
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39
Q

Why are X-rays used for Hypopituitarism?

A

less than 3 = entire body
3+ = hands and wrists
mature and body age and if delayed then GH deficiency

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40
Q

What is the growth rate of GH replacement therapy for hypopituitarism?

A

initially, significant growth then tapers off with slow continues
Continue till bone maturation (boys 16 and girls 14)

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41
Q

Hyperpituitarism

A

overproduction of anterior pit. gland

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42
Q

Hyperpituitarism caused by

A

Hyperplasia of pituitary cells - over growth or tumor formation
Primary hypothalamic defect

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43
Q

Hyperpituitarism complications

A

Gigantism – excess growth
Hyperthyroidism -
Hypercortisolism – Cushing’s
Precocious puberty

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44
Q

S/S of Hyperpituitarism Before GROWTH PLATE CLOSURE

A

Proportional overgrowth of long bones (8ft tall)
Rapid & increased muscle development
Weight increase in proportion to height
Proportional head enlargement
Delayed fontanel closure

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45
Q

S/S of Hyperpituitarism After GROWTH PLATE CLOSURE

A

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

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46
Q

Hyperpituitarism and Acromegaly grow how?

A

not taller grow transverse
- slow and gradually
overtime look different

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47
Q

If Acromegaly is untreated

A

high mortality due to cardiovascular, metabolic and respiratory complications

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48
Q

Hyperpituitarism Dx

A

History of excessive growth
Increased levels of GH
Normal bone age
Enlargement of bones
Endocrine studies – excess of thyroid, cortisol, and sexual

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49
Q

Hyperpituitarism Tx

A

Removal of tumor/lesion if present
External radiation/radioactive implants
Pharmacologic agents
Transphynode surgery
suppression of GH drugs
emotional support

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50
Q

What famous person has acromegaly?

A

Lincoln

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51
Q

Precocious puberty

A

early onset of sexual development
- more in girls

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52
Q

Hyperpituitarism puberty onset when a boy

A

before 9

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53
Q

Hyperpituitarism puberty onset when a caucasian girl

A

before 7

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54
Q

Hyperpituitarism puberty onset when an AA girls

A

before 6

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55
Q

What are the different precocious puberty types

A

Central (80%)
Peripheral
Incomplete

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56
Q

Central Precocious puberty

A

the hypothalamus releases puberty hormones too early and matures faster
- idiopathic

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57
Q

Peripheral Precocious puberty

A

release of androgens by glands cause secondary sexcharacteristics, testes and ovaries produce – no maturation of gonads

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58
Q

Incomplete Precocious puberty

A

one random secondary sex characteristics

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59
Q

Precocious Puberty Tx

A

Treat specific causes if known (usually regress later on)
MRI
Synthetic hormones
Lupron Depot injections (1-3 months depending)
histrelin implant (1-2 years)

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60
Q

Precocious Puberty Therapy goal

A

Slow/stop pubertal progression (shorter than peers to reach normal ht)
Allow for normal adult height

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61
Q

Precocious Puberty Nursing Considerations

A

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

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62
Q

What side effects of Lupron Depot injections (1-3 months depending)

A

mood swings or hot flashes

63
Q

What would you say to a child going through hypopituitarism and precocious puberty if they are self-conscious?

A

Everything is normal it is just happening at a quicker rate than usual

64
Q

Juvenile Hypothyroidism
is caused by
- Congenital
- Acquired

A

congenital = underdeveloped thyroid gland
acquired =
Partial/complete thyroidectomy
Following radiation treatment
Infectious processes
Dietary iodine deficiency

65
Q

Thyroid levels in Juvenile Hypothyroidism in congenital

A

low T3-4
High TSH

66
Q

Congenital Juvenile Hypothyroidism may not show until

A

at growth spurts because their body may only have the bare minimum and not ready for more

67
Q

Juvenile Hypothyroidism has a more profound ________ than GH hormone and increases TSH

A

growth

68
Q

Acquired Juvenile Hypothyroidism S/S

A

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

69
Q

Congenital Juvenile Hypothyroidism S/S**

A

thick tongue
jaundice
floppy
umbilical hernia
hoarse cry
constipation
dry skin
large fontanel opening
mental decline

70
Q

Juvenile Hypothyroidism Tx

A

Oral thyroid hormone replacement - levothyroxine
Prompt treatment in infants
Lifelong treatment

71
Q

Juvenile Hypothyroidism Edu for Family

A

Daily compliance with medication - provide resources
Periodic blood work monitoring of serum thyroid levels

72
Q

Juvenile Hypothyroidism needs to maintain

A

compliance with medication
the quicker the Tx the better development (1st 3 months)

73
Q

Alpha cells produce what

A

glucagon
- raises sugar

74
Q

Beta cells produce what

A

insulin -lower sugar

75
Q

Delta cells produce what

A

sumadostatin
- increases glucagon and insulin depending on what is needed
(Balance)

76
Q

Pancreatic Hormone Functions with what system in the pancreas

A

Islet of Langerhans

77
Q

Islet of Langerhans produce what cells

A

Alpha
Beta
Delta

78
Q

DM is a

A

chronic disorder of metabolism
with hypo and hyperglycemia
- can not use food for energy

79
Q

Does DM have a cure?

A

no

80
Q

What is the PATH of DM?

A

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

81
Q

Type 1 DM is the

A

absolute destruction of pancreatic beta cells

82
Q

Which type of DM has absolute insulin deficiency?

A

Type 1

83
Q

What are the different forms of T1DM?
Trigger?

A

Immune-mediated – autoimmune destruction
Idiopathic – Not simply inherited
- Genetic predisposition + trigger event (virus)

84
Q

S/S T1DM

A

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

85
Q

T1DM management

A

Insulin-dependent
Monitor glucose levels
Lifestyle changes
Nutrition
Exercise
Team Approach - family members for education with multiple lessons

86
Q

What animal is used for Diabetes Education in Pediatrics?

A

Coco the monkey from Disney
- books with it

87
Q

What is the DM for relative insulin deficiency?

A

Type 2
- resistance and body failure to use insulin properly

88
Q

What pts have an increased risk of T2DM?

A

adults > 45 years of age
overweight
sedentary lifestyle (lack of exercise and poor nutrition)
family history of DM

89
Q

T2DM has an increasing prevalence in

A

children/adolescents
- eating habits and lack of exercise

90
Q

T2DM S/S

A

Polyuria
Polydipsia
Polyphagia
Fatigue
Blurred vision
Slow-healing sores
Frequent infections
Polycystic ovary syndrome
Areas of darkened skin (acanthosis nigricans)

91
Q

acanthosis nigricans

A

areas of darkened skin

92
Q

T2DM Tx

A

Lifestyle changes
Nutrition
Exercise
Oral medication - Metaformin
Possibly insulin – if hyperglycemic
Monitor glucose levels

93
Q

What is the oral medication for T2DM

A

Metformin
- decrease absorption of sugar in the body
- decrease usage of insulin

94
Q

T2DM Dx

A

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%

95
Q

T2DM if 8-hour fasting blood glucose level

A

≥126 mg/dl

96
Q

T2DM if random blood glucose is

A

≥ 200 mg/dl with classic signs of hyperglycemia

97
Q

T2DM if oral glucose tolerance test

A

≥ 200 mg/dl in the 2-hour sample

98
Q

T2DM if Hemoglobin A1C

A

≥ 6.5%

99
Q

Mixed insulin is the combination of

A

intermediate & rapid-acting

100
Q

What are the different types of insulin?

A

rapid
short
intermediate
long

101
Q

What is the most important need to remember with insulin?

A

timing of food and insulin

102
Q

With rapid insulin, you need to eat within

A

15 minutes of food

103
Q

With short insulin, you need to eat within

A

30 minutes before meal

104
Q

What insulin is cloudy looking?

A

intermediate

105
Q

What insulin can not be mixed in a syringe with other insulins and must be given separately at a different site?

A

long-acting

106
Q

When do you dilute insulin?

A

less than 12 months
and extremely young infants because of small body

107
Q

Conventional mgmt in insulin dosing means

A

twice daily dosing (before breakfast and supper)
- rapid/short-acting mixed with intermediate

108
Q

Intensive therapy mgmt in insulin dosing means

A

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

109
Q

Insulin Administration DM

A

Subcutaneous administration
- PINCH METHOD WITH LIMITED ADIPOSE TISSUE
Rotate sites
Insulin absorption
Atraumatic care: shot blocker interferes with nerve transmissions

110
Q

What insulin site is the fastest rate of absorption and shortest to stop?

A

abdomen

111
Q

What insulin site is the longest to activate/absorb and lasts longer?

A

Buttocks

112
Q

Insulin injection sites

A

outer arm
abdomen
hip area
thigh

113
Q

Insulin Administration methods

A

Sub Q injections
Insulin Pen to smart
Insulin Pump (omnipod, i-Port)

114
Q

An insulin pump site changed every

A

48-72 hours
- up to 75 injections
Atraumatic care

115
Q

What is the drawback of an insulin pump?

A

tech does not always work
DKA

116
Q

With DM, what is a must

A

self-monitoring

117
Q

What alters insulin administration absorption?

A

exercise
illness

118
Q

What is the goal level of blood glucose?

A

blood glucose 80-120 mg/dl

119
Q

What is the goal level of hemoglobin A1C?

A

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

120
Q

Finger sticks atraumatic care

A

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

121
Q

Continuous Glucose Monitor (CGM) replacement of sensors

A

every 3-7 days

122
Q

Hyperglycemia caused by

A

Too little insulin - missed dose
Illness/infection/immunizations
Injury
Stress- physical/emotional
Growth
Medications - steroids
Menses

123
Q

Hyperglycemia S/S

A

Thirst
Polyuria (early)
Nausea
Blurred vision
Fatigue
DKA
Oliguria (later)

124
Q

Hyperglycemia Tx

A

Drink fluids
Administer additional insulin
Monitor glucose more closely

125
Q

Hypoglycemia S/S

A

Too much insulin
Diet
Exercise
Alcohol
Growth spurts
Puberty
Illness (esp. with vomiting)

126
Q

In younger children is it okay to give insulin after they eat?

A

yes, because they won’ be honest about when they eat

127
Q

Hypoglycemia S/S

A

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

128
Q

Hypoglycemia Severe S/S

A

Inability to swallow
Seizure/convulsion
Unconsciousness

129
Q

Hypoglycemia Tx

A

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

130
Q

If you cannot differentiate between hypo and hyperglycemia, what do you treat it as if you cannot get a glucose reading?

A

Hypoglycemia
- simple and complex carb (milk)

131
Q

In HYPOGLYCEMIA, if the patient becomes unconscious, seizes, or cannot swallow (side lying)

A

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

132
Q

Vascular changes in DM long-term complications

A

Involves small and large vessels
Nephropathy
Retinopathy
Neuropathy
Cardiovascular
Hypertension
Atherosclerosis

133
Q

Other long-term complications in children with T1DM

A

Altered thyroid function – at dx and poor controlled
Limited mobility – small joints of the hand (7-8 years old)

134
Q

If the pt has a good control of DM, long term complications will develop in

A

20+ years

135
Q

See a eye dr when after T1DM

A

2-3 YEARS AFTER DIAGNOSIS

136
Q

See a eye dr when after T2DM

A

Initially after dx

137
Q

DM Education

A

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

138
Q

What does a diabetic always need to carry?

A

Glucose tablets
Insta-glucose
Sugar cubes
Candy

139
Q

When should you exercise on DM?

A

WITH GOOD CONTROL
- decreases insulin requirements

140
Q

When should you not exercise on DM?

A

Illness or With poor control if more than 240+
may stimulate ketoacidosis

141
Q

Nutrition for DM

A

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

142
Q

T1DM Education for toddlers and preschoolers needs to allow them to

A

make food choices and monitor carbs
- temper tantrums are s/s of possible hypoglycemia
snacks during increased activity

143
Q

T1DM illness mgmt

A

glucose every 3 hours
urine ketones every 3 hours or when glucose is 240+
- always given insulin during illness and intake carbs

144
Q

T1DM illness goals

A

Maintain normal glucose
Treat urinary ketones
Maintain hydration
rest

145
Q

Diabetic Ketoacidosis is the complete state of

A

insulin deficiency

146
Q

Patho of DKA

A

**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)

147
Q

Ketonemia

A

ketones in the blood
- strong acids lowering of pH producing ketoacidosis

148
Q

DKA with cellular death what is released and what are the aftereffects?

A

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

149
Q

If DKA is not reversed by insulin and electrolyte correction, then what will occur

A

progressive deterioration occurs (dehydration, electrolyte imbalance, acidosis, coma, death)

150
Q

Mgmt of DKA

A

Rapid assessment
Adequate insulin to reduce elevated level
Fluids
NPO
Monitor renal functions
Electrolyte replacement (especially potassium)
- need renal function before administering

151
Q

PICU mgmt of DKA

A

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

152
Q

How do you bring down the blood sugar in DKA?

A

GRADUALLY and slowly
prevent cerebral edema

153
Q

DKA happens frequently with DM having an

A

infection

Module 5 (Pediatrics) (27 decks)

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