Module 5- PEDI > UNIT 3 ENDOCRINE > Flashcards

UNIT 3 ENDOCRINE Flashcards

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1
Q

What are the functions of the endocrine system?

A

Controls & requlates metabolism
1. energy production
2. growth
3. fluid and electrolyte balance
4. response to stress
5. sexual development

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2
Q

What are hormones?

A

Chemical substances which control/regulate activities of other cells/organs
1. Released by endocrine glands into blood stream
2. Regulated by feedback mechanism

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3
Q

What is the master gland of the endocrine system?

A

Anterior pituitary which is controlled by the hypothalamus

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4
Q

What is hypopituitarism?

A

Diminshed secreation of pituitary hormones
1. gonadotropin deficency
2. Growth hormone (GH) deficiecny
3. Thyroid-stimulating hormone (TSH) deficiecny
4. Adrenocorticotropic hormone deficiency

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4
Q

Clinical manifestions of hypopituitarism include?

A
  1. Depends on the hormones involved and the age of onset
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5
Q

What causes hypopituitarism?

A
  1. Tumors: in the brain around hypothalmic /pituitary
  2. Incomplete/underdevelopment of pituitary gland or hypothalamus
  3. congenital: newborn infants..familial… alot of the time they will have hypoclycemia and seizure activity
  4. Surgery: any brain surgery in the area of the hypothalmus or pituitary gland
  5. Radiation
  6. Trauma: Brain trauma during delievery, maltreatment, skill fractures from car accidents
  7. Autoimmune
  8. Idopathic
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5
Q

What are clinical manifestations of GHD

A
  1. 1st year-normal growth
  2. After 1st year children fall below the 3rd percentile
  3. Height stunted more than weight– with good nutrition they may appear overweight due to short stature
  4. Skepetal proportionals normal for age
  5. Primary teeth-normal age
  6. Permanent teeth-delayed
  7. Teeth overcrowded and malpositioned because they have a smaller underdeveloped jaw
  8. Delayed sexual development– otherwise normal unless they also have a deficiency in the gonadtropin hormone alsoe
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6
Q

How might GHD affect the teeth?

A
  1. Primary teeth- normal age
  2. Permanant teeth-delayed
  3. Teeth may be overcrowded and malpositioned because they have a smaller underdeveloped jaw
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7
Q

How is GHD diagnosed?

A
  1. Family history
    • find out growth patterns of family members or if there is a parental hx of GHD,
    • r/o malabsorption disorders. Chronic illness like congenital heart disease neuro illness that can also effect growth.
  2. Physical exam
    • Accurate height and weight
  3. Xray/MRI
    • 3 and below will get a full xray if older they will just get xray of hands and wrist looking at bone age with GHD… age will be delayed
  4. Endocrine studes
    • Absent of low level of GH
  5. Genetic testing

**OVERALL- poor linear growth, delayed bone age and abnormal growth hormone stiumlation tested needed for diagnosis. **

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8
Q

Therapeutic managment of GHD includes?

A
  1. Correct the underlying disease process
  2. Growth hormone replacement
    • Biosynthestic growth hormone
    • Very Expensive
  3. Child and famiy support
    • Parents may be angry for not treating sooner thinking that there child will eventually have a growth spurt
    • Human growth fondation can provide resources on research,education, support groups and bully prebention.
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9
Q

What should we know about growth hormone replacement therapy?

A
  1. It is the definitive treatment
  2. Given subq on a daily basis.
  3. Expensive
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10
Q

When is the best time to give growth hormone replacement therapy?

A

At bedtime due to the natural release of pituitary hormones

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11
Q

What would the expected growth pattern be after growth hormone replacement therapy?

A

Significant growth within the 1st year and then it tapers off with gradual growth. They will continue to take growth hormones until bone age is caught up. For boys that is around age 16 and for girls age 14

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12
Q

What is Hyperpituitarism?

A

Overproduction of anterior pituitary hormone

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13
Q

What causes hyperpituitarism?

A
  1. Hyperplasia of pituitary cells
  2. Primary hypothalamic defect
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14
Q

What are clinical manifestations of hyperpituitarism?

A
  1. Gigantism —> excess growth hormone during childhood
  2. Hyperthyroidism—> excessive TSH
  3. Hypercortisolism —> cushing’s syndrome
  4. Precocious puberty
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15
Q

What are clinical manifestions of Growth Hormone Excess (BEFORE) growth plate closure?

A
  1. Proportional overgrowth of long bones
    • What causes some kids to reach 8ft tall
  2. Rapid & Increased muscle developement
  3. Weight increase in proportion with height
  4. Proportional head enlargement
    • Delayed fontanel closure
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16
Q

What are clinical manifestations of growth hormone excess (AFTER) growth plate closure?

A

Growth happens in the transverse direction
1. Acromegaly
- Enlarged facial features
- Separation and malocclusion of teeth
- Enlarged hands/feet
- Thickened, deeply creased skin
- Deep husky voice
- increased tendency toward hyperglucemia & DM
- Any additional growth will be in a transverse way… Prominent jaw, nose, forehead

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17
Q

True or false: The clinical manifestions of excess growth hormone after plate closure happen so slowly that it may not be recognized very quickly?

A

True- People who see the person daily may not even realize it until they look back at pictures.

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18
Q

True or false: Growth hormone excess after growth plate closure tends to have a higher mortality rate?

A

True

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19
Q

How is growth hormone excess diagnosed?

A
  1. History of excessive growth
  2. Increased levels of GH
  3. NOrmal bone age
  4. Enlargement of bones
  5. Endocrine studies
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20
Q

What is our therapeutic managment of Growth hormone excess?

A
  1. Removal of tumor/lesion if present
  2. External radiation/radioactive implants
  3. Pharmocologic agents
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21
Q

What is Precocious Puberty

A

Early onset of sexual development

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22
Q

At what ages is puberty considered precociuous puberty in boys, white females and african american grils?

A
  1. Before age 9 in boys
  2. Before age 7 in caucasian girls
  3. Before age 6 in Afriacan-American girls
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23
What are the 3 types of precocious puberty?
1. Centeral 2. Peripheral 3. Incomplete
24
What is central precocious puberty?
1. HYpothalmus is activated to release those gonadotropin releasing hormones too early 2.Natural process of puberty just happen to early 3.Early maturation and development of the gonads w/secreation of sex hormones 4.They develop secondary sex characteristics and sometimes can even produce mature sperm and ove Cause: idiopathic
25
What is Peripheral Percocious puberty?
1. Not caused by the release of hormones from the hypothalmus instead their is a release of androgens by the adrenal gland that is going to cause secondary sex characteristics 2. The testes and overaies may also release strogen/testosterone 3. Breast development, facial hair,body hair may occur 4. Testes and overies DO NOT MATURE
26
What is incomplete precocious puberty?
1. Random sex characterist that may appear in a child. Usually dosent go on to develop "actual precocious puberty"
27
How is precocius puberty managed?
1. Treat specific cause if known - MRI to r/o cyst or tumor 2. Synthetic hormones - Lupron depot injection - Histerlin implant
28
What should we know about the adminstration and MOA synthetic hormones in the therapuetic management of precocious puberty?
Synthetic hormones stop the pituitary gland from releasing gonadatropins Lupron depot injections -- every 1 to 3 months depending on the preperation they use Histerlin implant-- placed in the arm and lasts 1-2 years.
29
What is the goal of therapy for precocius puberty?
1. Slow/stop pubertal progression 2. Allow for normal adult hight - Growth plates close prematurely which is why we want to stop/slow but may appear taller at 1st
30
How long do we treat precocious puberty?
1. We will continue treatment until normal age of puberty then stop and allow puberty to occur normally
31
What education should we provide parents/patients that have precocious puberty?
1. Education regarding injections & side effects 2. Family education - expression of concerns by the child - dress accroding to chronological age - reassurance regarding physiologic changes - childs social, cognitive and emtional development match chronological age.
32
What are some nursing considerations for precocious puberty?
1. Provide emotional support (body changes can be scary and they may be embarressed) 2. Provide privacy during physical examinations 3.
33
What is the main function of the thyroid?
Main physiologic action of the thyroid hormone is to regulate metabolism, control the processes of growth and tissue regeneration. More profound effect than growth hormone.
34
What are two types of juvenille hypothyroidism?
1. Congenital 2. Aquired
35
What is congential hypothyroidism?
"Newborn Period" 1. Hypoplastic thyroid gland-- underdeveloped thyroid which causes low levels of thyroid hormone and incrased levels of TSH 2. May have enough thyroid hormone to manage the 1st couple years of life but as growth rapidly increase the demand for the hormone increase and their might not be enough
36
If congential hypothyroidism is left untreated it can cause....
Severe permanant intellectual disability
37
How soon will you start seeing symptoms of congenital hypothyroidism? and What symptoms might you see?
Typically within the 1st could weeks if it is congenital Symptoms include 1. Jaundice, thick tongue, floopy, horse cry, dry skin, constipation, umbilical hernia, dry skin, constipation, large fontenal
38
What are causes of aquried hypothryoidism?
1. Partial/complete throidectomy 2. Following radiation treatment 3. Infectious processes 4. Dietary iodine deficeincy
39
What are clinical manifestations of juvenile hypothyoidism?
1. Thyromegaly 2. Decelerated growth-- Not as significant if it occurs later in life 3. Myxedematous skin changes 4. Constipation 5. Sleepiness 6. Lethargy 7. Mental Decline 8. Delayed puberty 9. Excessive weight gain
40
What is the therapeutic management of Juvenile Hypothyroidism?
1. Oral thyroid hormone replacement- Levothyroxine 2. Prompt tratment in infants 3. Lifelong treatment
41
What education might we provide about juvenille hypothyroidism?
1. Daily compliance with medication - make sure they have the resources to get the medication. 2. Periodic monitoring of serum thyroid levels - As the child grows theraputic levels will change
42
What are alpha cells? | Islets of langerhans
Produce glucagon which stimulates the liver and other cells to release stored glucose so it raises our blood sugar
43
What are beta cells | Islets of langerhans
Produce insulin
44
What are delta cells?
Produce the hormone somastatin which regulates the secreation of insulin and glucogon
45
What is diabetes?
1. Chronic disorder of metabolism characterized by hyperglycemia & insulin resistance. It impaires the body's ability to use food and energy
46
What is type 1 DM?
Destruction of pancreatic beta cells. It is an absolute insulin deficiecny
47
What are the two forms of type 1 DM?
Immune-Mediated which is an autoimmune destruction of the beta cells & Idiopathic
48
True or false: Type 1 DM is not simply inherited?
True- Genetic predisspotion pjus a trigger event. Most common trigger is a virus... like enterovirus
49
What are s/s of type 1 DM?
1. 3p's : Polyuria, Polydipsia, Polyphagia 2. Hyperglycemia 3. Rapid weight loss 4. Dry Skin 5. Irritability 6. Drowsiness/fatigue 7. Abdominal discomfort 8. Ketoacidosis
50
How do we manage Type 1 DM?
1. Insulin-- this will vary depending on what is going on with the child 2. Monitor glucose levels 3. Lifestyle changes - Nutrition - Exercise 4. Team Appropach-- We want to try and get as many family memeber as possibly to educate
51
What is Type 2 DM?
1. Relative insulin defiiency - Insulin resistance - Body fails to use insulin properly
52
Who is at increased risk for type 2 DM?
1. Adults > 45 years of age 2. Overweight 3. Sedentary lifestyle 4. Family history of DM
53
True or false: There is not an increase prevalence in children/adolescents in type 2 DM?
False: There is an increase prevalence in children/adolescnets
54
What are s/s of type 2 DM?
1. 3p's: Polyuria, Polydipsia, Polyphagia 2. Fatigue 3. Blurred vision 4. Slow-healing sores 5. Frequent infections 6. Polycystic ovary syndrome 7. Areas of darkened skin (acanthosis nigricans)
55
How can we treat type 2 DM?
1. Lifestyle changes - Nutrition - Excercise 2. Oral medications (metformin) 3. Possibly insulin 4. Monitor glucose levels
56
How is DM diagnosed?
1. 8-hour fasting blood glucose level >126mg/DL 2. Random blood glucose over 200mg/DL with classic signs of hyperglycemia 3. Oral glucose tolerance test equal to or greater than 200mg/dl in the 2-hour sample 4. Hemoglobin A1C equal to or greather than 6.5%
57
What are the 4 types of insulin?
1. Rapid 2. Short 3. Intermediate 4. Long
58
Insulin is based on ?
1. Onset 2. Peak 3. Duration
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What is mixed insulin?
Combination of intermediate and rpaid acting
60
True or false: TIme of insulin and coordination of food is important?
1. True
61
Rapid insulin is given w/in ____ mins. of a meal?
15
62
Short acting insulin is given w/in ____ mins before a meal?
30
63
Intermediate acting insulin is ____1___ in appearance?
Cloudy
64
True or false: Long acting insulin cannot be mixed in a syringe with any other insulin?
True
65
Conventional managment of insulin dosing includes....
Rapid/Short acting mixed with intermediate acting Given prior to breakfast and supper
66
True or false: We must dilute insulin for children 12 and under?
True- we risk young babies bottoming out
67
Intensive therapy of insuling dosing includes....
Multiple injections Long acting once or twice daiy plus rapid acting prior to each meal Better control, fewer long-term complications
68
What should we know about insulin administration?
1. Subq admin - Outer arm - Abdomen - Hip area - Thigh - May need to pinch with finger and thumb 2. Rotate sites 3. Insulin absorption 4. Atraumatic care
69
What is the rate and duration of a abdomen insulin injection?
Rate: Very Fast Duration: Very Short
70
What is the rate and duration of an insulin injection given in the arm?
Rate: Fast Duration: Short
71
What is the rate and duration of an insulin inejection given in the leg?
Rate: Slow DUration: Long
72
What is the rate and duration of an insulin injection given in the buttocks?
Rate: Very slow Duration: Very long
73
What are different insulin delivery devices?
1. Insulin pen 2. Insulin pump 3. Omnipod 4. I-port
74
What is an acceptable glycosylated hemoglobin (Hgb A1c)?
6.5-8% Younger kiddos A1C can be a little higher but as they age we want it to get lower than 7.5
75
What is a good self-monitoring blood glucose level?
80-120mg/dl
76
What should we know about DM monitoring using finger sticks?
Atrumatic care is important 1. Warm the finger 2. Use ring finger and thumb 3. Puncture side of finger pad 4. Press lancet device lightly against skin 5. Use lancet device with adjustable-depth tips 6. Use glucose monitors that require small samples
77
How often do you need to replace the CGM (continous glucose monitor) sensor
1. 3-7days
78
Complications of hyperglycemia are caused by?
1. Too little insulin 2. Illness/infection 3. Injury 4. Stress- physical and emotional 5. Growth 6. Medications 7. Menses
79
What are s/s of hyperglycemia?
1. Thirst 2. Polyuria (early) but as they become dehydrated the oppisite occurs 3. Nausea 4. Blurred vision 5. Fatigue 6. Diabetic ketoacidosis
80
What is the treatment of Hyperglycemia?
1. Drink Fluids 2. Administer additional insulin 3. Monitor glucose more closely
81
What are complication of hypoglycemia caused by?
1. Too much insulin 2. Diet 3. Exercise 4. Growth spurts 5. Puberty 6. Illness (esp w/vomiting)
82
What are symptoms of hypoglycemia?
1. Shaky/sweaty 2. Hungry 3. Pale 4. Headache 5. Confusion 6. Disorientation 7. Lethargy 8. Change in behavior
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What are severe symptoms of severe hypoglycemia?
1. Inability to swallow 2. Seizures/convulsions 3. Unconsciousness
84
How do we treat Hypoglycemia?
1. Check blood sugar if possible 2. When in doubt, give simple carbohydrate 3. Follow with complex ccarbohydrate & protien 4. If unconscious, seizes, or cannot swallow admin Glucagon
85
What should we know about glucogon?
1. Mixed and given IM/SQ or intranassally (baqsimi) 2. Releases stored glycogen from liver 3. should increase the blood glucose in 15 mins 4. Can cause n/v 5. Protect from aspiration
86
What are long-term complications affecting the vascular system?
1. Involves small and large vessels 2. Nephropathy 3. Retinopathy 4. Neuropathy 5. Cardiovascular- Hyperteniton and atherosclerosis
87
Altered thyroid function and limited mobility of small joints of the hand are complications in children with type 1 DM?
True
88
When might you start seeing long-term complications of DM?
Depends on how controlled the DM is. Can see it as early as 2-3 years or it can take as long as 20 to show up
89
DM education should include?
1. Explanantion of diabetes 2. meal planning 3. Admin insulin inj 4. Monitor hygiene 5. Promote exercise 6. record keeping 7. observe for complications 8. family support 9. Always carry glucose tablets, insta-glucose, surgar cubes, candy 10. Exercise-- with good control it can decrease insulin requirements. With poor control--- may stimulate ketoacidosis
90
What nutrition education should we provide a DM patient?
1. Sufficient calories to balance daily expenditure for energy and growth 2. Constant carbohydrate diet-exchange system 3. Consistent intake/timing of food 4. Timing of food coincides with time/action of insulin 5. Total # of calories/proportions of basic nutrients needs to be consistent day to day
91
Illness managment for DM includes...
1. Montior glucose every 3 hours 2. Monitor urine ketones eery 3 hours or when glucose in over 240 mg/dl (not for daily management)
92
What are the goals of illness management of DM?
1. Maintain normal glucose 2. Treat urinary Ketones 3. Maintain hydration
93
What is diabetic Ketoacidosis?
1. Most complete state of insuin deficeincy 2. Life-Threatening situation 3. Lack of insulin---> glucose unabailable for cellular metabolism---> body burns fat for energy---> fat breaks down into fatty acids---> glycerol in fat cells conerted to ketones in liver---> excess eliminated in urine (ketonuria) or lungs (acetone breath) 4. Ketones in blood (ketonemia) are strong acids lowering PH producing ketoacidosis
94
In DKA what happens with celluar death?
1. K+ released from cells into bloodstream and excreted by kidneys 2. Total body k+ decreased even though serum potassium may be elevated (decreased circulating fluid volume) 3. Alteration in serum and tissue K+ can lead to cardiac arrest 4. If not reversed by insulin therapy/fluid & electrolyte correction, progressive deterioration occurs (dehydration, electrolyte, imbalance, acidosis, coma, death)
95
How do we manage DKA?
1. Rapid assessment, adequate insulin, fluids, electrolyte replacement (esp. K+) 2. Managed in the PICU - Have 2 IV accesses - Cardiac monitor - Labs - Possible o2 - Possible NG (unconscious pt) - Possible antibiotics Happens most frequently w/infection
Module 5- PEDI
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