Nursing Assessment of the Endocrine System (Test 2) Flashcards
(612 cards)
1
Q
What are lipid soluble hormones also known as?
A
Steroid hormones.
2
Q
Classifications and functions: lipid soluble hormones- ?
A
Adrenal cortex, sex glands, thyroid
3
Q
What are water soluble hormones also known as?
A
Protein base.
4
Q
Classifications and functions- water soluble hormones?
A
All other hormones
5
Q
What is the third group of hormones?
A
Reproduction/stress/metabolism/growth
6
Q
Hormone transport
A
Lipid soluble hormones are bound to plasma proteins for transport
7
Q
What are the 2 types of hormone receptors?
A
Steroid “ “ and Protein “ “
8
Q
Where is the steroid hormone receptor located?
A
Inside the cell
9
Q
What does the protein hormone receptor do?
A
Hormone attaches to receptor on cell membrane “first messenger” which stimulates the production of a “second messenger” that activates intracellular activity
10
Q
What is simple feedback?
A
Gland increase/decreases the secretion of a hormone based on feedback (ex: insulin/glucose)
11
Q
What is positive feedback?
A
Increases target organ action beyond normal
12
Q
What is complex feedback?
A
Communication among several glands to regulate hormone secretion (ex: thyroid)
13
Q
What is nervous system control?
A
Initiated by CNS and implemented by sympathetic nervous system (ex: stress/catecholamines)
14
Q
What are rhythms?
A
Hormones fluctuate in predictable patterns during 24 hour period (ex: cortisol)
15
Q
What hormones types make up the hypothalamus?
A
Inhibiting and releasing hormones
16
Q
What do inhibiting hormones do?
A
Inhibit the secretion of hormones from the anterior pituitary.
17
Q
What are examples of inhibiting hormone?
A
Somatostatin; prolactin-inhibiting hormone
18
Q
What do releasing hormones do?
A
Stimulates the secretion of hormones from the anterior pituitary.
19
Q
What are examples of releasing hormones?
A
Corticotropin-releasing hormone; growth hormone-releasing factor
20
Q
What hormones are in the anterior pituitary?
A
Tropic hormones, growth hormone, prolactin
21
Q
What do tropic hormones do?
A
Control the secretion of hormones by other glands
22
Q
What are examples of tropic hormones?
A
Thyroid-stimulating hormone (TSH); adrenocorticotropic hormone (ACTH); follicle-stimulating hormone (FSH)
23
Q
What hormones are in the posterior pituitary?
A
Antidiuretic hormone (ADH), and oxytocin
24
Q
What does ADH do? What is this stimulated by?
A
Regulates fluid volume by stimulating reabsorption of water in the renal tubules. Stimulated by increased plasma osmolality.
25
ADH also is...?
A potent vasoconstrictor.
26
What does oxytocin do?
Stimulates milk secretion and uterine contraction.
27
What hormones are in the thyroid gland?
Thyroxine (T4), triiodothyronine (T3), and calcitonin
28
What do T4 and T3 do?
Regulate metabolic rate of all cells and processes of cell growth
29
What do low levels of T4 and T3 cause?
Stimulate pituitary gland to release TSH
30
What does calcitonin do?
Inhibits calcium loss from bone, increases calcium storage in bone, and increase renal excretion of calcium and phosphorus
31
What hormone is in the parathyroid gland?
Parathyroid hormone (PTH)
32
What does PTH stimulate?
Stimulates bone desorption and inhibits bone formation; stimulates renal conversion of vitamin D
33
What does PTH increase?
Calcium reabsorption and phosphate excretion in kidneys
34
What 2 things make up the adrenal gland?
Adrenal medulla and adrenal cortex
35
What hormones are in the adrenal medulla?
Catecholamines (epinephrine, norepinephrine, dopamine); stress response
36
What hormones are in the adrenal cortex?
Cortisol, aldosterone, adrenal androgens
37
What does cortisol do?
Regulates blood glucose concentration, anti-inflammatory action, promotes metabolism
38
What does aldosterone do?
Maintains extracellular fluid volume, promotes renal reabsorption of sodium and excretion of potassium
39
What do adrenal androgens?
Promotes masculinization in men and growth and sexual activity in women
40
What hormones are in the pancreas?
Glucagon and insulin
41
What does glucagon do?
Increases blood glucose by stimulating glycogenesis, glycogenesis, and ketogenesis
42
What is insulin stimulated by?
Increased blood glucose level
43
What does insulin facilitate?
Glucose transport into cells
44
Normal aging results in what 4 things?
Decreased hormone production and secretion, altered hormone metabolism and biologic activity, decreased responsiveness of target tissue to hormones, alterations in circadian rhythms
45
*Changes of aging often mimic what?
The manifestation of endocrine disorders
46
What system is less developed at birth than any other system in the body?
Endocrine
47
Hormonal control of many body functions is lacking until when?
12-18 months
48
Infants may manifest what as a result of lack of hormonal development?
Imbalances in fluids, electrolytes, amino acids, glucose, and other trace substances as a result of this lack of development
49
What things are important to know about past health history?
Previous or current endocrine abnormalities, abnormal patterns of growth and development
50
What medications are important to know they are taking?
Hormone replacement, insulin, corticosteroids
51
What is important to know when gathering info about surgery/other treatment?
Neck or brain involvement of increased importance
52
If kids aren't getting good growth and weigh percentile numbers, it leads us to what?
Endocrine problems
53
ADH is released by what?
The pituitary gland
54
Where is ADH made?
Hypothalamus
55
What does ADH prevent?
The production of dilute urine
56
What is something to remember about COPD patients when gathering medication info?
A lot are on long term steroids
57
In what assessments may you find abnormalities when assessing the system of a person with endocrine problems?
Vital signs, height and weight, mental-emotional status, integument, head, neck, thorax, abdomen, extremities, genitalia (esp. hair distribution)
58
Common assessment abnormalities?
Changes in skin texture, exophthalmos, moon face, polyuria/polydipsia, goiter, changes in weight, lethargy, thermoregulation
59
What are the changes in skin texture caused by?
Hypo/hyperthyroidism
60
What is exophthalmos caused by?
Hyperthyroidism
61
What is moon face caused by?
Cushing syndrome
62
What is polyuria/polydipsia caused by?
DM, DI
63
What are goiters caused by?
Hypo/hyperthyroidism
64
What are changes in weight caused by?
Hypo/hyperthyroidism; DM
65
What is lethargy caused by?
Hypothyroidism
66
What are thermoregulation problems caused by?
Hypo/hyperthyroidism
67
What are MRIs used for?
Used to find tumors?, measure tumors, and evaluate for metastasis
68
What should you inform the patient about MRIs?
That the test is painless and noninvasive, and they will need to lie still
69
What is a computed tomography (CT scan) used for?
To identify tumors or cysts
70
What do you need to tell the patient about the CT scan?
They will need to lie still
71
What should you do if an IV contrast will be used?
Check for iodine allergy
72
Questions to ask for MRIs?
Are you claustrophobic? Do you have on any jewelry? Do you have metal implants or staples? Etc.
73
What do ultrasounds do?
Evaluates thyroid nodules to determine if they are cysts or tumors
74
What do you need to explain about ultrasounds?
Explain the painless procedure will take about 15 minutes
75
Do you need to fast or be sedated for ultrasounds?
No
76
What is the most sensitive diagnostic test for evaluating thyroid dysfunction?
TSH
77
What is the normal range of TSH?
0.4-4.2 microunits/milliliter
78
What should you explain about the TSH test?
Explain blood draw procedure to patient
79
What is a T4 test used for?
To evaluate thyroid function and monitoring thyroid function
80
What is the normal range of T4?
4.6-11.0 micrograms/deciliter
81
What should you explain about the T4 test?
Explain blood draw procedure to patient
82
What is a T3 test helpful in?
Diagnosing hyperthyroidism in T4 levels are normal
83
What is the normal T3 range for ages 20-50?
70-204 nanograms/deciliter
84
What is the normal T3 range for ages 50 plus?
40-181 nonograms/deciliter
85
What should you explain to the patient about T3 tests?
Explain blood draw procedure to patient
86
What is a thyroid scan used for?
To evaluate thyroid nodules
87
What is given during a thyroid scan?
Radioactive isotopes are given orally or IV thyroid is scanned
88
What does a normal thyroid look like in a scan?
Homogenous pattern
89
What do benign nodules look like in a scan?
Appear as warm spots
90
What do malignant nodules look like in a scan?
Appear as cold spots (meaning they won't absorb meds)
91
What should you check before doing a thyroid scan?
Check for iodine allergy
92
What should patients not have before a thyroid scan?
Shouldn't have supplemental iodine for several weeks before
93
For what tests should you minimize salt intake (iodine)?
Thyroid scan and radioactive iodine uptake (RAIU)
94
What do RAIUs provide?
Direct measurement of thyroid activity
95
What is the patient given for a RAIU?
Radioactive iodine orally or IV
96
When is the thyroid scanned during a RAIU?
At several time intervals
97
What should you check for before a RAIU?
Check for iodine allergy
98
What should be avoided before a RAIU?
No supplemental iodine for several weeks before the test
99
What can interfere with RAIU results?
Thyroid medications
100
Which is more common, RAIU or blood draws?
Blood draws, RAIUs aren't used much
101
What does cortisol evaluate?
Adrenal cortex function
102
What is the normal range of cortisol at 8am?
5-23 micrograms/deciliter
103
What is the normal range of cortisol at 4pm?
3-16 micrograms/deciliter
104
What time is the most accurate cortisol test collected?
In the morning
105
What is important to remember to write on the sample?
Mark sample time of specimen vial
106
What does fasting blood glucose measure?
Measures circulating glucose level
107
What is the normal range for a fasting blood glucose test?
70-99 milligrams/deciliter
108
How long should they fast for a FBG test?
4-8 hours
109
Is water intake allowed for a FBG test?
Yes
110
What should you ensure when giving a FBG test?
Ensure no dextrose in IV solution
111
What is a Glycosylated Hemoglobin test also known as?
HGB A 1 C
112
What does Hgb A1C measure?
Glucose control during previous 3 months
113
What is the normal range for a Hgb A1C test?
4-6%
114
Is fasting necessary for an Hgb A1C?
No
115
What does a ketone test measure?
Amount of acetone secreted in urine as result of incomplete fat metabolism
116
What does a positive ketone result indicate?
Can indicate lack of insulin and diabetic acidosis
117
How is a ketone test done?
Completed with freshly voided urine sample
118
What other test is a ketone test often done with?
Glucose test
119
When do we usually see ketones?
In diabetics without insulin
120
How else can ketones be tested for?
Blood
121
Theories link cause of DM to single/combo of what factors?
Genetic, autoimmune, environmental, viral
122
What are the two most common types of DM?
Type 1 and 2
123
What other types of DM are there?
Gestational, prediabetes, secondary diabetes
124
Normal insulin metabolism is produced by what?
The beta cells (weird B looking letter)
125
What are the beta cells made of?
Islets of Langerhans (pancreas)
126
How is normal insulin released?
Released continuously into the bloodstream in small increments with larger amounts released after food intake
127
What does normal insulin stabilize glucose range to? (Aka what's the ideal glucose range?)
70-120 mg/dl
128
What is the average daily secretion of normal insulin?
0.6 units/kg body weight
129
What does insulin promote? What does this cause?
Glucose transport from bloodstream across cell membrane to cytoplasm of cell. Causes decrease of glucose in the bloodstream.
130
What does increased insulin after a meal stimulate?
Storage of glucose as glycogen in liver and muscle
131
What does increased insulin after a meal inhibit?
Gluconeogenesis
132
What does increased insulin after a meal enhance?
Fat disposition
133
What does increased insulin after a meal also increase?
Protein synthesis
134
What are insulin dependent tissue examples?
Skeletal muscles and adipose tissues
135
What are non insulin dependent tissue examples?
Brain, liver, blood cells
136
What is the definition of non insulin dependent tissues?
Do not depend directly on insulin for glucose support
137
What do counterregulatory hormones oppose?
Oppose effects of insulin
138
What do counterregulatory hormones increase?
Blood glucose levels
139
What do counter regulatory hormones provide?
A regulated release of glucose for energy
140
What do counter regulatory hormones help?
Help maintain normal blood glucose levels
141
What are examples of counterregulatory hormones?
Glucagon, epinephrine, growth hormone, cortisol
142
What is the incidence rate of DM?
15 per 100,000 people in North America
143
What are the peak ages of onset for females and males?
Between 10 and 12 for girls, and 12 to 14 for boys (puberty)
144
What factor increases the risk for DM?
If the child or adolescent has a first degree relative or identical twin with the disease, but it's not for sure going to happen though
145
What type of diabetes may show a familial tendency?
Type 1
146
Theories for DM disease development include?
Genetic components, environmental influences such as viruses, and an autoimmune response that causes the destruction of insulin-secreting cells of the pancreas in the islets of Langerhans
147
What is type 1 DM formerly known as?
Juvenile onset or insulin dependent diabetes
148
What age bracket does type 1 usually occur in?
Most often occurs in people under 30 years of age
149
When is the peak onset of type 1?
10-14
150
What do the body's T cells do?
Attack and destroy beta cells which are the source of insulin
151
What do antibodies to the islet cells cause?
80-90% reduction of normal beta cell function leads to hyperglycemia and diagnosis of type 1 DM
152
What is the onset of disease like for type 1?
Long preclinical period
153
What are present before symptoms occur for type 1?
Antibodies present for months to years before symptoms occur
154
When do manifestations develop for type 1?
When pancreas can no longer produce insulin
155
After manifestations of type 1, what happens?
Rapid onset of symptoms and present as ER with ketoacidosis
156
What does type 1 history include?
Recent, sudden weight loss
157
What are classic symptoms of type 1?
Polydipsia, polyuria, polyphagia
158
What is polydipsia?
Excessive thirst
159
What is polyphagia?
Excessive hunger
160
Does eating more stop the weight loss of type 1 onset?
No, even though you eat a lot, you are still losing weight (15-20 pounds)
161
What does type 1 diabetes require?
Exogenous insulin to sustain life
162
When does DKA occur?
Occurs in absence of exogenous insulin (absolutely no insulin)
163
Is DKA life threatening?
Yes
164
What does DKA result in?
Metabolic acidosis
165
When is prediabetes also known as?
Impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)
166
Fasting blood glucose levels
Higher than normal (over 100 mg/dl, but under 126 mg/dl)
167
Impaired glucose tolerance 2 hour plasma glucose
Higher than normal (between 140 and 199 mg/dl)
168
Why is pre diabetes not just diabetes?
Not high enough for diabetes diagnosis
169
What does having pre diabetes increase your risk for?
Type 2
170
If no preventative measure is taken about the pre diabetes, what usually happens?
Develop diabetes within 10 years
171
Does damage occur with pre diabetes?
Long term damage already occurring to heart and blood vessels
172
How does pre diabetes appear?
Usually present with no symptoms
173
What do you need to do with a patient that has pre diabetes?
Must watch for diabetes symptoms
174
What is the most prevalent type of diabetes?
Type 2
175
What is the percentage of patients with type 2 of all diabetes types?
Over 90%
176
What age bracket does type 2 usually occur in?
Over 35
177
How many patients with type 2 are overweight?
80-90%
178
Type 2 prevalence increases with...?
Age
179
What type of basis does type 2 have?
Genetic basis
180
What ethnic populations have an increased rate of type 2?
African Americans, Asian Americans, Hispanic Americans, and Native Americans
181
What ethnic populations have the highest rate of diabetes in the world?
Native Americans and Alaskan Natives
182
What are HCPs finding more and more of?
Children with type 2 diabetes, a disease usually diagnosed in adults aged 40 years and older
183
What may be major contributors to the increase in type 2 diabetes during childhood or adolescence?
The epidemics of obesity and the low level of physical activity among young people
184
Why is type 2 difficult in children?
It can go undiagnosed for a long time and children often have mild/no symptoms
185
In type 2 what does the pancreas do?
Continues to produce some endogenous insulin
186
The insulin produced in a patient with type 2 is...?
Is either insufficient or poorly utilized by tissues
187
What is the most powerful risk factor for type 2?
Obesity (abdominal/visceral)
188
???What genetic mutations are related to type 2?
Lead to insulin resistance and increased risk for obesity
189
What are the 4 major metabolic abnormalities r/t type 2?
Insulin resistance, pancreas' decreased ability to produce insulin, inappropriate glucose production from liver, and alteration in production of hormones and adipokines
190
What happens in insulin resistance?
Body tissues don't respond to insulin and insulin receptors are either unresponsive or insufficient in number
191
What happens when pancreas has decreased ability to produce insulin?
Beta cells are fatigued from compensating and beta cells mass lost
192
What happens from inappropriate glucose production from liver?
Liver's response of regulating release of glucose is haphazard, and it is not considered a primary factor in development in type 2
193
What does alteration in production of hormones and adipokines do?
Play a role in glucose and fat metabolism and contribute to pathophysiology of type 2; two main adipokines- adiponectin and leptin
194
What kind of onset is type 2?
Gradual onset
195
A person may go with with undetected..?
Hyperglycemia
196
What from hyperglycemia may become severe?
Osmotic fluid/electrolyte loss or hyperosmolar coma
197
What is probably the number one way people get diagnosed as type 2?
Improper wound healing
198
What are clinical manifestations of type 2?
Nonspecific conditions (may have classic symptoms of type 1), fatigue, recurrent infections, recurrent vaginal yeast or candida infections, prolonged wound healing, visual changes
199
When does gestational diabetes develop?
During pregnancy
200
When is gestational diabetes detected?
At 24 to 28 weeks
201
Usually normal glucose levels at...?
6 weeks postpartum
202
What does GD increase risk for?
Increased risk for C section, perinatal (baby) death, and neonatal complications
203
Why do these increased risks exist?
Because these babies grow at much faster rates and causes those risks
204
After having GD, it increases risk for what?
Risk for developing type 2 in 5 to 10 years
205
What is therapy for GD?
1st nutritional, 2nd insulin
206
What puts you at higher risk for GD?
Excessive weight gain and family diabetes history
207
Secondary diabetes results from what?
Another medical condition: Cushing syndrome, hyperthyroidism, pancreatitis, parenteral nutrition, cystic fibrosis, hematochromatosis, corticosteroids (Prednisone), thiazides, phenytoin (Dilantin, which is a long term antiseizure)
208
When does secondary diabetes resolve?
Usually resolves when underlying condition is treated
209
Diagnosing diabetes- Hgb A1C level
over 6.5%
210
Diagnosing diabetes- fasting plasma glucose level
Over 126 mg/dl
211
Diagnosing diabetes- OGTT 2 hour plasma glucose level
200 mg/dl
212
Diagnosing diabetes- random plasma glucose level
Over 200 mg/dl in a patient with classic symptoms of hyperglycemia
213
Nursing history type of assessment for DM patients?
Past health history (viral infections, medications (esp. steroids, antibiotics, etc.), recent surgery), positive health history, obesity
214
If a patient with DM is obese, what will the doctor probably do?
Probably start yearly fasting glucose checks and more often if they have a family history
215
Stress and sugar relationship?
Stress of illness or injury makes sugar levels increase, if you keep it between 70-120 mg/dl it helps wound healing
216
What do you say if a patient asks why they are getting fingersticks and they're not diabetic?
Stress of illness or injury makes sugar levels increase, if you keep it between 70-120 mg/dl it helps wound healing
217
What do we assess during physical assessment for DM patients?
Weight loss, thirst, hunger, poor healing, Kussmaul respirations (rapid breathing and a sign of DKA)
218
Nursing diagnoses for DM?
Ineffective therapeutic regimen management, risk for injury, risk for infection, powerlessness, imbalanced nutrition: more than body requirements
219
What is important to remember about DM as a nurse?
Managing diabetes takes a lot of discipline, so put yourself in your shoes before you judge
220
What are overall goal examples during the planning period for DM?
Active patient participation (and family and SO's if applicable), few or no episodes of acute hyperglycemic emergencies or hypoglycemia, maintain normal blood glucose levels, prevent or delay chronic complication, lifestyle adjustments with minimal stress
221
Health promotion for implementation phase for DM?
Identify those at risk, routine screening for overweight adults over age 45 (FPG is preferred method in clinical settings
222
Acute intervention for implementation phase for DM?
Hypoglycemia, DKA, Hyperosmolar hyperglycemic nonketotic syndrome
223
Acute intervention for stress of illness and injury for DM?
Increase blood glucose level, continue regular meal plan, increase intake of noncaloric fluids, continue taking oral agents and insulin, frequent monitoring of blood glucose at least every 4 hours and ketone testing if glucose is over 240 mg/dl
224
Patients undergoing surgery or radiologic procedures requiring contrast medium should...?
Hold their metformin (glucophage) day of surgery and 48 hours, (begun after serum creatinine has been checked and is normal???)
225
What is the overall goal of ambulatory and home care?
To enable patient or caregiver to reach an optimal level of independence
226
When implementing insulin therapy and oral agents in ambulatory and home care what do you need to do?
Provide education of proper administration, adjustment, and side effects; assessment of patient's response to therapy
227
When implementing personal hygiene in ambulatory or home care what do you need to do?
Regular bathing with emphasis on foot care, and daily brushing/flossing (dentist should be informed about diabetes diagnosis*)
228
What is important about medical identification and travel card for DM patients?
Must carry id indicating diagnosis of diabetes
229
What is important about patient and family teaching for DM?
Educate on disease process, physical activity, medications, monitoring blood glucose, diet, resources; enable patient to become most active participant in his/her care
230
What is exogenous insulin?
Insulin from an outside source
231
Who may take exogenous insulin?
Required for type 1, prescribed for type 2 who can't control blood glucose by other means
232
What is the only type of insulin used today?
Human insulin
233
How is human insulin prepared?
Prepared through genetic engineering- common bacteria (Escherichia coli) and yeast cells using recombinant DNA technology
234
Insulins differ in regard to what 4 things?
Onset, peak, action, and duration
235
What are insulins characterized as?
Rapid, short, intermediate, and long acting
236
Different types in insulin may be used for...?
Combination therapy
237
Examples of rapid acting insulin?
Lispro (Humalog), Aspart (Novolog), and glulisine (Apirdra)
238
Examples of short acting insulin?
Regular
239
Examples of intermediate acting insulin?
NPH (cloudy)
240
Examples of long acting insulin?
Glargine (Lantus), detemir (Levemir)
241
What is a basal-bolus regimen?
Closely mimics endogenous insulin production
242
What is given for a basal-bolus?
Long acting (basal) once a day and rapid/short acting (bolus) before meals
243
How are rapid acting (bolus) prepared/onset?
Injected 0-15 minutes before meals, onset of action 15 minutes
244
How are short acting (bolus) prepared/onset?
Injected 30-45 minutes before meal, onset of action 30-60 minutes
245
Do patients have to wait to eat after getting insulin?
No????
246
How are long acting (basal) prepared/peak action?
Injected once a day at bedtime or morning, no peak action
247
What insulin cannot be mixed with any other insulin or solution?
Long acting (basal)
248
How may insulin be stored?
In use vials may be left at room temp up to 4 weeks, Lantus only for 28 days, extra insulin should be refrigerated
249
How should insulin not be stored?
Do not heat/freeze, avoid exposure to direct sunlight
250
Study graph on page 13
Study graph on page 13
251
Are oral agents insulin?
No!
252
What are oral agents?
Work to improve mechanisms by which insulin and glucose are produced and used by the body
253
What do oral agents work on?
Insulin resistance, decreased insulin production, increased hepatic glucose production
254
What are examples of oral agents?
Sulfonylureas, meglitinides, biguanides, alpha-glucosidase inhibitors thiazolidinediones
255
What do sulfonylureas do to insulin production?
Increase production from pancreas
256
What do Sulfonylureas do to chance of prolonged hypoglycemia?
Decrease chance
257
How many experience decreased effectiveness after prolonged use of Sulfonylureas?
10%
258
What are examples of Sulfonylureas?
glipizide (glucotrol), glimepiride (amaryl)
259
What do Meglitinides do to insulin production?
Increase production from pancreas
260
When are Meglitinides taken?
30 minutes before each meal up to time of meal
261
When should Meglitinides not be taken?
If meal is skipped
262
What are examples of Meglitinides?
Repaglinide (Prandin), Nateglinide (Starlix)
263
What do Biguanides do to glucose production?
Reduce glucose production by liver
264
What do Biguanides do to insulin sensitivity?
Enhance it at tissues
265
What do Biguanides do to glucose transport?
Improve glucose transport into cells
266
Why are Biguanides popular?
Do not promote weight gain
267
What is an example of Biguanides?
Metformin (Glucophage)
268
What are Alpha-Glucosidase Inhibitors also called?
"Starch blockers"
269
What do AGIs do?
Slow down absorption of carbohydrates in small intestines
270
What is an example of AGI?
Acarbose (Precose)
271
What are Thiazolidinediones most effective with?
In those with insulin resistance
272
What do Thiazolidinediones improve?
Improves insulin sensitivity, transport, and utilization at target tissues
273
What are examples of Thiazolidinediones?
Pioglitazone (Actos), Rosiglitazone (Avandia)
274
What is Amylin analog secreted by?
Hormone secreted by beta cells of pancreas
275
What is Amylin analog cosecreted with?
Insulin
276
What is Amylin analog indicated for?
Type 1 and 2
277
How is Amylin analog administered?
Subq in thigh or abdomen
278
What does Amylin analog do to GI related things?
Slows gastric emptying, reduces postprandial glucagon secretion, increases satiety (fullness)
279
What is an example of Amylin analog?
Pramlintide (Symlin)
280
What does post prandial mean?
After meals
281
What is Incretin mimetic?
Synthetic peptide
282
What does Incretin mimetic stimulate?
Release of insulin from beta cells
283
How is Incretin mimetic administered?
Subq injection
284
What does Incretin mimetic suppress?
Glucagon secretion
285
What does Incretin mimetic reduce?
Food intake
286
What does Incretin mimetic slow?
Gastric emptying
287
Can Incretin mimetic be used with insulin?
No
288
What is an example of Incretin mimetic?
Byetta
289
What happened to a lot of people while taking Incretin mimetic?
Lost weight
290
What do Beta Adrenergic blockers mask?
Symptoms of hypoglycemia
291
What do Beta Adrenergic blockers prolong?
Hypoglycemic effects of insulin
292
What can Thiazide/loop diuretics do?
Potentiate hyperglycemia by inducing potassium loss
293
What is an example of Thiazide/loop diuretics?
Lasix
294
What is pancreas transplantation used for?
Patients with type 1 who also have end stage renal disease and had/plan to have a kidney transplant
295
How are pancreas transplants usually done?
With kidney transplants, alone is rare
296
What does a pancreas transplant eliminate the need for? What else can it also eliminate?
Exogenous insulin; can eliminate hypoglycemia and hyperglycemia
297
What is the cornerstone of care for a diabetes patient?
Nutritional therapy
298
What is the most challenging part of therapy for many people?
Nutritional therapy
299
Who is recommended to be part of a diabetic's team?
Recommended that diabetes nurse educator and registered dietitian with diabetes experience be members of team
300
What do American Diabetes Association (ADA) guidelines indicate?
That within context of an overall healthy eating plan, person with diabetes can eat same food as person who doesn't have diabetes
301
What is the ADA's overall goal?
Assist people in making changes in nutrition and exercise habits that will lead to improved metabolic control
302
What is type 1's meal plan?
Based on individual's usual food intake and is balanced with insulin and exercise patterns
303
Type 1 insulin regimen?
Managed day to day
304
What is type 2's emphasis on?
Based on achieving glucose, lipid, and blood pressure goals
305
What is a focus on for type 2's?
Calorie reduction
306
What is essential for a diabetic diet?
Nutrient balance
307
What should be balanced for a type 2?
Nutritional energy intake should be balanced with energy output
308
How much should carbohydrates and monosaturated fats provide of total energy intake?
45-65%
309
What kind of diet is not recommended for diabetics?
Decreased carb diet
310
What does the Glycemic Index term used to describe?
Rise in blood glucose levels after consuming carb containing food
311
What should be considered when formulating a meal plan?
The GI
312
What diet systems are based on the GI?
Nutrisystem, weight watcher's
313
How much fat should make up a meal plan's total calories for a diabetic?
No more than 25-30%
314
How much of the total fat comes from saturated fats?
7%
315
How much protein should contribute the total energy consumed?
Less than 10%
316
What kind of intake should be significantly less than the general population?
Protein intake
317
Does alcohol have any nutritive value?
No
318
What does alcohol promote?
Hypertrigylceridemia
319
What does alcohol have a detrimental effect on?
Liver
320
What can alcohol cause?
Severe hypoglycemia
321
Who initially provides diet teaching?
Dietician
322
What should be included during diet teaching?
Family and SO's
323
What is an appropriate basic teaching tools for diabetics?
USDA MyPyramid Guide
324
What is the plate method?
Helps patient visualize the amount of vegetable, starch, and meat that should fill a 9 inch plate
325
What is an essential part of diabetes management?
Exercise
326
What does exercise do to insulin receptor sites?
Increase
327
What does exercise do to blood glucose levels?
Lowers
328
What contributes to weight loss?
Exercise
329
What can be taken during exercise?
Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia
330
When is exercise best done?
After meals
331
When should exercise plans be started?
After medical clearance and slowly with gradual progression
332
What should exercise be?
Individualized
333
When should blood glucose levels be monitored r/t exercise?
Before, during, and after
334
Why do people not follow their glucose plan?
Most don't because of cost
335
What does self monitoring of blood glucose (SMBG) enable?
Enables patient to make self management decisions regarding diet, exercise, and medication
336
What is SMBG important for?
Detecting episodic hyperglycemia and hypoglycemia
337
What is crucial for SMBG?
Patient training
338
What does SMBG supply?
Immediate info about blood glucose levels
339
What is more common than diabetes in elderly? (???)
Hypoglycemia unawareness
340
What must you consider for the elderly?
Patient's own desire for treatment and coexisting medical problems
341
What elderly limitations must you recognize?
Physical activity, manual dexterity, and visual acuity
342
What could interfere with treating hypoglycemia in the elderly?
Presence of delayed psychomotor function
343
What should education for the elderly be based on?
Their individual needs, using slower pace
344
What main things do you need to do for pediatric DM illness management?
Continue insulin treatment, stay close to the meal plan, give plenty of liquids, choose meds wisely, check blood glucose and ketone levels frequently
345
What does illness often do to diabetic kids?
Increase the amount of insulin the body needs
346
What should you instruct parents?
Insulin should never be withheld
347
What should you do if the child has an upset stomach and can't eat?
Give clear liquids that contain carbohydrates (sports drinks, juices, gelatin, broth, frozen fruit bars, regular pop)
348
What should you encourage the child to do?
Drink as much water and other non-caffeinated beverages as possible (caffeine dehydrates you
349
Many OTC meds contain what?
Sugar and alcohol
350
What in meds can rapidly add up?
Glucose
351
What should parents look for in meds? What if that's unavailable?
Parents should look for a glucose free version of the medication. If unavailable, carbs must be accounted for in the meal plan.
352
What can meds that contain alcohol do? What should you ensure?
Lower blood glucose levels; ensure the child eats something to prevent hypoglycemia
353
What medicines are better?
Alcohol free rather than including it
354
Many decongestants can do what?
Raise blood glucose levels
355
What should you check frequently?
Blood glucose and ketone levels
356
What becomes a danger when the child is sick?
DKA
357
To prevent DKA or catch it early, what should you do?
Check the child's blood glucose levels often (every few hours) while sick
358
How often should you check ketones for kids? When do you need to do it more often?
Check urine several times a day; more for when vomiting or diarrhea is present
359
5 facts about infants?
Very rapid growth, trusting relationship with the parents, erratic eating habits (food can become a power struggle), erratic sleep patterns, treatment schedule is difficult to keep
360
Why is a treatment schedule difficult to keep for infants?
Because of erratic feeding and sleeping patterns
361
When do peer issues begin to emerge?
Preschool age
362
When can kids begin to understand rules?
Preschool
363
What can preschool kids do about care?
Can perform more self care, including blood tests under parental supervision
364
Preschool eating behavior is...?
Less erratic
365
Preschoolers are at risk for what? Because?
Hypoglycemia because they are very energetic
366
How are preschoolers' sleeping patterns?
Regular
367
What is a challenge when dealing with preschoolers and food?
May be more challenging to provide snacks and meals that match what siblings and friends eat
368
What do school age kids fear?
Being different from other kids
369
What can school age kids do?
Can perform most self care, including blood tests and insulin injections
370
What are school age kids eager to do?
Learn
371
What are school age kids beginning to do?
Understand consequences of their actions
372
What do school age kids test?
Independent decision making
373
Where is most of school age kids' time spent?
Away from home
374
When is puberty well under way?
Adolescence
375
What are adolescents concerned with?
Physical appearance
376
What do adolescents have a clearer sense of than school age kids?
Clearer sense of self (can set goals)
377
What is increased in adolescence?
Autonomy
378
What are diabetic related adolescent risk taking behaviors?
Not taking insulin and not performing blood sugar tests
379
What is unpredictable about adolescents?
Many social activities are unpredictable
380
What counseling do adolescents need?
Regarding contraception, alcohol, and smoking
381
What is DKA caused by?
Profound deficiency of insulin
382
What is DKA characterized by?
Hyperglycemia, ketosis, acidosis, dehydration
383
In what type does DKA most likely occur?
Type 1
384
What are precipitating factors of DKA?
Illness, infection, inadequate insulin dosage, undiagnosed type 1, poor self management, neglect
385
What happens when supply of insulin is insufficient?
Glucose cannot be properly used for energy and body breaks down fat stores
386
What are ketones?
By products of fat metabolism
387
What do ketones/fat metabolism affect?
Alters pH balance which causes metabolic acidosis, ketone bodies excreted in urine, electrolytes become depleted
388
What are signs and symptoms of DKA?
Lethargy/weakness, dehydration, abdominal pain, Kussmaul respirations
389
What are the early symptoms of DKA?
Lethargy/weakness
390
What does dehydration lead to/cause?
Poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension
391
What are related to the abdominal pain symptom of DKA?
N/V
392
What do Kussmaul respirations include?
Rapid deep breathing, attempt to reverse metabolic acidosis, sweet fruity odor
393
They may or may not need hospitalization depending on what?
Signs and symptoms
394
Laboratory findings of DKA: blood glucose-
Over 300 mg/dl
395
Laboratory findings of DKA: arterial blood pH-
Below 7.30
396
Laboratory findings of DKA: serum bicarbonate level-
Under 15 mEq/l
397
Laboratory findings of DKA: What's the 4th finding?
Ketones in blood and urine
398
What may be included in treatment of DKA and signs and symptoms
Airway management- oxygen administration
399
What IV will be used to correct fluid/electrolyte imbalance for DKA? What does it do?
0.45% or 0.9% NaCl; Restore urine output and raise blood pressure
400
When blood glucose levels approach what, what do you do?
When they approach 250 mg/dl, 5% dextrose is added to regimen and the point is to prevent hypoglycemia
401
What electrolyte needs to be replaced?
Potassium
402
When do patients with DKA need sodium bicarbonate?
If it less than 7
403
What insulin therapy is used with DKA?
Withheld until fluid resuscitation has begun, bolus followed by insulin drip
404
Is Hyperosmolar hyperglycemic syndrome (HHS) life threatening?
Yes
405
Which is more common, HHS or DKA?
DKA
406
In what patient type does HHS often occur in?
Over 60 with type 2
407
Does ketoacidosis occur in HHS? Why?
Patient has enough circulating insulin so ketoacidosis doesn't occur
408
HHS earlier stages have...?
Less symptoms
409
Why do neurologic manifestations occur in HHS?
Due to increased serum osmolality
410
HHS patients usually have a history of what?
Inadequate fluid intake, increasing mental depression, polyuria
411
HHS laboratory values: blood glucose-
Over 400 mg/dl
412
HHS laboratory values: What is increased?
Serum osmolality
413
HHS laboratory values: What is absent/minimal?
Ketone bodies
414
What administrations of DKA and HHS patients should be closely monitored?
IV fluids, insulin therapy, electrolytes
415
What assessments of DKA and HHS patients should be closely monitored?
Renal status, cardiopulmonary status, level of consciousness
416
What else should the patient be closely monitored for?
Signs of potassium imbalance, cardiac monitoring, vital signs
417
Does HHS have a low mortality rate?
No, high
418
What is HHS therapy similar to?
DKA therapy, except HHS requires greater fluid replacement
419
Hypoglycemia is...?
Low blood glucose
420
Hypoglycemia occurs when?
Too much insulin in proportion to glucose in the blood and blood glucose level is less than 70 mg/dl
421
Hypoglycemia common manifestations?
Confusion, irritability, diaphoresis, tremors, hunger, weakness, visual disturbances, and can mimic alcohol intoxication
422
Untreated hypoglycemia can progress to what?
Loss of consciousness, seizures, coma, and death
423
What is hypoglycemia unawareness?
Person does not experience warning signs/symptoms, increasing risk for decreased blood glucose levels, and this is related to autonomic neuropathy
424
Causes of hypoglycemia?
Mismatch in timing- food intake and peak action of insulin or oral hypoglycemic agents
425
At first sign of hypoglycemia what should you do?
Check blood glucose
426
Blood glucose level actions-
If under 70 mg/dl begin treatment, if over 70 investigate further for cause of signs/symptoms
427
What should done if blood glucose monitoring equipment is not available and there is a sign of hypoglycemia?
Treatment should be initiated
428
What is used for treatment of hypoglycemia?
If alert enough to swallow, 15 to 20 grams of a simple carb (ex: pb on graham crackers) with 4-6 ounces of fruit juice or regular soft drink
429
What food should be avoided with a hypoglycemic patient?
Foods with fat, it decreases absorption of sugar
430
Important things to do/remember about hypoglycemic treatment:
Do not overtreat, recheck blood sugar 15 min after treatment, repeat until blood sugar is under 70 mg/dl, patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia, check blood sugar again 45 min after treatment
431
If no improvement after 2 or 3 doses of simple carbohydrate or patient not alert enough to swallow, what treatment should you use?
Administer 1 mg of glucagon IM or subq
432
What side effect does glucagon have?
Rebound hyperglycemia
433
After recovery of hypoglycemia, what should you have the patient do?
Ingest a complex carb after recovery
434
In acute care settings what would you use for treatment?
25-50 ml of 50% dextrose IV push
435
What is macrovascular disease?
Diseases of large and medium sized blood vessels
436
Macrovascular disease and diabetes relationship?
Occurs with greater frequency and with an earlier onset in diabetics
437
What is macrovascular disease development promoted by?
Altered lipid metabolism common to diabetes
438
What can tight glucose control do for macrovascular disease?
May delay atherosclerotic process
439
Risk factors for macrovascular disease?
Obesity, smoking, hypertension, high fat intake, sedentary lifestyle
440
What should patients with diabetes be screened for?
Dyslipidemia at diagnosis of macrovascular disease
441
What does microvascular disease result from? In response to what?
Result from thickening of vessel membranes in capillaries and arterioles; in response to chronic hyperglycemia
442
Which is specific to diabetes: microvascular or macro vascular?
Microvascular is specific
443
Areas most noticeably affected by microvascular?
Eyes (retinopathy), kidneys (nephropathy), skin (dermopathy)
444
When do clinical manifestations of microvascular appear?
Usually after 10-20 years of diabetes
445
What is diabetic retinopathy?
Microvascular damage to retina, result of chronic hyperglycemia
446
What is diabetic retinopathy the most common cause of?
New cases of blindness in people ages 20 to 74
447
What is the most common form of diabetic retinopathy?
Nonproliferative
448
What is non pro. DR?
Partial occlusion of small blood vessels in retina
449
What does non pro. DR cause?
Causes development of microaneurysms
450
What happens in non pro. DR?
Capillary fluid leaks out, which leads to retinal edema and eventually hard exudates or intraretinal hemorrhages occur
451
What is the most severe form of DR?
Proliferative
452
What does pro. DR involve?
Retina and vitreous
453
When does pro. DR occur?
When retinal capillaries become occluded
454
What happens when retinal capillaries become occluded?
Body forms new blood vessels, vessels are extremely fragile and hemorrhage easily (produces vitreous contraction), and retinal detachment can occur
455
The earliest and most treatable stages of DR often?
Often produces no changes in vision
456
People with DR must get what yearly?
Annual dilated eye exams
457
Treatment types for DR?
Photocoagulation, Cryotherapy, Vitrectomy
458
What is photocoagulation?
Most common, laser destroys ischemic areas of retina which prevents further visual loss
459
What is Cryotherapy?
Used to treat peripheral areas of retina, probe creates frozen area until reaches specific point on retina
460
What is Vitrectomy?
Aspiration of blood, membrane, fibers from inside eye through small incision
461
When is Vitrectomy used?
Vitreal hemorrhage doesn't clear in 6 months and/or threatened or actual retinal detachment
462
What is diabetic neuropathy associated with?
Damage to small blood vessels that supply the glomeruli of the kidney
463
What is the leading cause of end stage renal disease?
Diabetic neuropathy
464
What are critical factors for prevention/delay of diabetic neuropathy?
Tight glucose control, blood pressure management, and yearly screening
465
What is involved in blood pressure management?
Angiotensin-converting enzyme (ACE inhibitors) (used even when not hypertensive), and angiotensin II receptor antagonists
466
What is the yearly screening for diabetic neuropathy consist of?
Microalbuminuria in urine and serum creatinine
467
How many patients with diabetes have some degree of neuropathy?
60-70%
468
What is diabetic neuropathy related nerve damage due to?
Metabolic derangements of diabetes
469
Which is more common- sensory or autonomic neuropathy?
Sensory
470
What is a part of sensory neuropathy?
Distal symmetric
471
What does sensory neuropathy affect?
Hands and/or feet bilaterally
472
Characteristics of sensory neuropathy?
Loss of sensation, abnormal sensations, pain, and paresthesias
473
When is sensory neuropathy usually worse?
At night
474
What can occur with sensory neuropathy?
Foot injury and ulcerations can occur without feeling pain
475
What is the treatment for sensory neuropathy?
Tight glucose control and drug therapy
476
What does drug therapy for sensory neuropathy include?
Topical cream, Tricyclic antidepressants, Selective serotonin and norepinephrine reuptake inhibitors, and antiseizure meds
477
What can autonomic neuropathy affect?
Nearly all body systems
478
What complications can be caused by autonomic neuropathy?
Gastroparesis (delayed gastic emptying), cardiovascular abnormalities, sexual functions, neurogenic bladder
479
What is the most common cause of hospitalization in diabetes?
Foot complications
480
What do foot complications result from?
Combination of microvascular and macro vascular disease
481
What are risk factors for foot complications?
Sensory neuropathy and peripheral artery disease
482
Other contributors to foot complications are?
Smoking, clotting abnormalities, impaired immune function, autonomic neuropathy
483
What integumentary complications can occur with diabetes?
Acanthosis nigricans and necrobiosis lipoidica diabeticorum
484
What is acanthosis nigricans?
Dark, coarse, thickened skin
485
What is necrobiosis lipoidica diabeticorum associated with?
Type 1
486
What does necrobiosis lipoidica diabeticorum appear as?
Red yellow lesions and skin becomes shiny, revealing tiny blood vessels
487
Diabetics are more susceptible to what?
Infections
488
What is the definition of infection?
Defect in mobilization of imflammatory cells and impairment of phagocytosis by neutrophils and monocytes
489
What may loss of sensation cause?
May delay detection of infection
490
Treatment of infections in diabetics must be what?
Prompt and vigorous
491
What is acromegaly caused by?
Caused by an overproduction of growth hormone usually caused by a benign pituitary tumor
492
What does acromegaly present as?
Presents as a thickening of bone and soft tissue
493
How many people have acromegaly?
Very rare, 3 out of 1 million in US
494
What is the onset of acromegaly?
Gradual onset, 7 to 9 years between onset of symptoms and final diagnosis
495
What are clinical manifestations of acromegaly?
Enlargement of hands and feet, joint pain, thick leathery oily skin, visual disturbances, headaches
496
What is the treatment of choice for acromegaly? What will the patient need?
Hypophysectomy (removal of pituitary gland) and the patient will require hormone supplements for life
497
What may a large tumor require?
Radiation or drug therapy in addition to hypophysectomy
498
Bone growth and soft tissues r/t acromegaly
Bone growth can usually be stopped and soft tissue hypertrophy reversed
499
What does SIADH stand for?
Syndrome of Inappropriate Antidiuretic Hormone
500
When does SIADH occur?
When ADH is released despite normal or low plasma osmolarity
501
What are causes of SIADH?
Most common is malignancy, the rest is on table 50-1
502
What does SIADH lead to?
Fluid retention, serum hypoosmolality, hyponatremia, hypochloremia, and concentrated urine
503
Pathophysiology map of SIADH?
1. Increased diuretic hormone leads to 2. increased water reabsorption in renal tubules which leads 3. to increased intravascular fluid volume which leads 4. to dilution hyponatremia and decreased serum osmolality
504
What are clinical manifestations of SIADH?
Muscle cramping, pain, and weakness (caused by hyponatremia); decreased urinary output; increased body weight; and lethargy, seizures, and coma (severe, late stage)
505
How is SIADH diagnosed?
Through measurement of urine and serum osmolality
506
Nursing and collaborative management for SIADH (Table 50-2, p. 1260)?
Restrict fluid intake to no more than 1000 mL a day (includes IV fluids too), position head of bed to flat, seizure precautions, and frequent oral care
507
What is diabetes insipidus?
Decrease in ADH production, secretion, or renal response
508
What are the 3 types of diabetes insipidus?
Central, nephrogenic, and primary
509
What is central diabetes insipidus caused by?
Caused by lesion of the hypothalamus or pituitary (most common cause)
510
What is nephrogenic diabetes insipidus? What is it caused by?
There is adequate ADH but the kidneys do not respond appropriately. Caused by meds (ex: Lithium which is long term usually)
511
What is primary diabetes insipidus associated with?
Associated with excessive water intake
512
What are clinical manifestations of diabetes insipidus?
Polydipsia and polyuria (5-20 L/day)
513
What is the diagnostic study for diabetes insipidus?
Water restriction test
514
What nursing and collaborative management is needed for diabetes insipidus?
Fluid and hormone replacement
515
What does DI fluid and hormone replacement include?
IV fluid titrated to replace urinary output (0.45% NS; D5W) and desmopressin acetate (DDACP)- chemical replacement for ADH
516
How many thyroid nodules are benign?
95%
517
What are clinical manifestations of thyroid cancer?
Painful, palpable nodule in an enlarged thyroid gland
518
What are diagnostic studies for thyroid cancer?
Ultrasound, Cat Scan or MRI
519
Nursing and Collaborative management for thyroid cancer?
Surgical removal of the tumor with or without radiation treatment (and the thyroid gland?) and monitor patient for hypocalcemia after surgery
520
Is true thyroid cancer common?
No it's rare
521
What is hyperthyroidism?
Increase in synthesis and release of T3, T4, or both
522
Does hyperthyroidism occur more often in males or females?
Females
523
What age is the highest frequency of hyperthyroidism?
20-40 years old
524
What is the most common type of hyperthyroidism?
Grave's Disease
525
What is Grave's Disease?
Autoimmune disease of unknown etiology; patient develops antibodies to TSH receptors. The antibodies then attach to the receptors and stimulate the thyroid gland to secrete T3, T4, or both
526
Clinical manifestations of hyperthyroidism?
Table 50-5 pg. 1264, increased appetite, weight loss, hair loss, thin brittle nails, fatigue, insomnia, menstrual irregularities
527
Complications of hyperthyroidism?
Thyrotoxic crisis
528
What is thyrotoxic crisis?
(When it releases way too much hormone?) It is life threatening and can cause serve tachycardia, heart failure, shock, hyperthermia, and coma
529
Why do we especially not palpate thyroids as student nurses?
We can cause thyrotoxic crisis
530
Diagnostic studies of hyperthyroidism?
Decreased TSH levels, and increased free T4 levels
531
Collaborative care for hyperthyroidism?
Antithyroid meds, radioactive iodine therapy, subtotal thyroidectomy (common), nutritional therapy
532
What does hyperthyroidism nutritional therapy include?
High calorie diet (4000-5000 calories a day) may be needed to satisfy hunger and prevent tissue breakdown
533
Nursing implementation for hyperthyroidism?
Elevate HOB to promote fluid drainage from periorbital area
534
Nursing implementation after thyroidectomy?
Assess patient every 2 hours for first 24 hours for signs of hemorrhage or tracheal compression, position patient's head to avoid tension on the suture line, monitor vital signs, monitor of signs and symptoms of hypocalcemia, control post op pain
535
Why does hypothyroidism occur?
Insufficient circulating thyroid hormones
536
How many people does hypothyroidism affect?
Approximately 1 in 50 women and 1 in 300 men
537
Clinical manifestations of hypothyroidism?
Onset of symptoms may occur over months to years, fatigue, lethargy, impaired memory, cold intolerance, muscle weakness, weight gain
538
Diagnostic studies for hypothyroidism?
High TSH indicates a defect in the thyroid gland, low TSH indicates a defect in the pituitary or hypothalamus
539
Collaborative care for hypothyroidism?
Levothyroxine (Synthroid) is very common, they are started on a low dose and increased every 4 to 6 weeks as needed and they need to have blood work checked
540
What is hyperparathyroidism?
Oversecretion of PTH
541
What is hyperparathyroidism most commonly caused by?
A benign tumor in the parathyroid gland
542
What does hyperparathyroidism lead to?
Hypercalcemia and hypophosphatemia
543
Clinical manifestations of hyperparathyroidism?
Muscle weakness, loss of appetite, constipation, fatigue, shortened attention span
544
What are diagnostic studies for hyperparathyroidism?
Elevated PTH and calcium levels
545
Collaborative care for hyperparathyroidism?
Surgical removal of parathyroid gland or nonsurgical therapy
546
What does hyperparathyroidism non surgical therapy include?
Fosamax- normalizes calcium levels; oral phosphate replacement
547
What is hypoparathyroidism?
Inadequate levels of PTH
548
What does hypoparathyroidism lead to?
Hypocalcemia and hyperphosphatemia
549
What are clinical manifestations of hypoparathyroidism?
Irritability, abdominal cramps, fatigue, weakness
550
What are hypoparathyroidism diagnostic studies?
Low PTH and calcium levels
551
What are hypoparathyroidism nursing and collaborative management?
Treat complications such as tetany, IV calcium may be needed, instruct patient on management of long term drug therapy and nutrition
552
What is Cushing Syndrome?
Spectrum or abnormalities caused by an excess of corticosteroids
553
What is the most common cause of Cushing Syndrome?
Administration of exogenous corticosteroids (ex: Prednisone)
554
What can Cushing Syndrome also be caused by?
ACTH secreting tumor
555
What are clinical manifestations of Cushing Syndrome?
Truncal obesity, "moon face", purplish red striae on abdomen, hirsutism in women, menstrual disorders, hypertension, unexplained hypokalemia, buffalo hump, and increase in axillary, chest, etc. hair in abnormal places
556
What are diagnostic studies for Cushing Syndrome?
Plasma cortisol levels may be increased, 24 hour urine for free cortisol is often done
557
What is collaborative care for Cushing Syndrome?
Treatment depends on underlying cause and medication adjustments may be necessary if caused by corticosteroids by decreasing dose and alternate day dosing
558
What is Addison's Disease?
Caused by a lack of adrenal corticosteroids (glucocorticoids, mineral corticoids, androgens)
559
What is Addison's Disease most commonly caused by?
An autoimmune response
560
In what population is Addison's Disease most common?
White females under 60
561
Addison's Disease is often (blank) before diagnosis is made?
Advanced
562
Clinical manifestations of Addison's Disease?
Progressive weakness, fatigue, weight loss, anorexia, skin hyper pigmentation (especially around joints of arms, legs and knuckles and it looks like a bad self tanner)
563
Complications of Addison's Disease?
Addisonian crisis- acute adrenal insufficiency
564
Diagnostic studies for Addison's Disease?
Decreased cortisol levels
565
Collaborative care for Addison's Disease?
Replacement therapy with hydrocortisone usually through IV, increased salt in diet, increase in hydrocortisone dose during periods of high stress (surgery; hospitalization)
566
Effects of Corticosteroids?
Anti-inflammatory action, immunosuppression, maintenance of normal BP, carbohydrate and protein metabolism
567
Side effects of Corticosteroids?
Table 50-20 pg. 1283
568
Patient teaching guide for Corticosteroids?
Table 50-21 pg. 1283 (delayed wound healing, infections, can increase BP and blood sugar)
569
What is hyperaldosteronism?
Excessive secretion of aldosterone causing sodium retention and potassium excretion
570
What is hyperaldosteronism most commonly cause by?
Adrenocortical tumor in adrenal cortex
571
What are clinical manifestations of hyperaldosteronism?
Hypertension, headache, muscle weakness, cardiac dysrhythmias
572
What is Pheochromocytoma?
Excessive catecholamine production due to tumor of the adrenal medulla
573
What are clinical manifestations of Pheochromocytoma?
Severe hypertension, pounding headache, tachycardia with palpitations, profuse sweating, chest pain
574
Treatment for Pheochromocytoma includes what?
Surgical removal of the tumor and good BP management
575
When does Growth Hormone Deficiency occur?
WHen GH is absent or produced in inadequate amounts
576
What is hypopituitarism?
If other pituitary hormones are lacking + GHD
577
What is an important part of determining normal growth?
The child's growth pattern
578
When can GHD occur?
At any age
579
What are signs of GHD?
Growth of less than 2 inches per year between the ages of 2 and 11 years in girls or 2 and 13 years in boys; leveling off and slowing of growth progress; growth below the 5th percentile on standardized growth charts
580
Etiology of GHD?
Can be congenital, acquired, or idiopathic; tends to run in families but may occur with no family history,
581
What may congenital GHD be associated with?
An abnormal pituitary gland or be a part of another syndrome
582
What are acquired GHD causes?
Brain tumors (or other disorders), cranial irradiation, infections, trauma (head)
583
What are clinical manifestations of GHD?
Short height for child's age, increased amount of fat around waist and in face, emotional feelings about height or weight, younger appearance than children of same age, decreased muscle mass, delayed skeletal maturation, delayed onset of puberty, delayed tooth development, hypoglycemia
584
What are GHD diagnostic studies?
Thyroid panal, serum electrolytes, blood urea nitrogen, creatinine, complete blood count, insulin-like growth factor 1, insulin-like growth factor binding protein 3, karotyping (form of genetic testing), bone density scan
585
Management of GHD?
If the cause is a tumor, surgical removal or radiation therapy may be indicated. Replacement of deficient hormones is often required even after successful treatment of a pituitary tumor
586
What kind of injection is GH?
Most children receive subq injection
587
How often are GH injections given?
Daily or 3 to 4 times per week and have increased growth velocity at bedtime
588
Does GH need refrigerated?
Yes
589
How does growth need to be monitored?
Close monitoring of growth with endocrinology visits every 3 to 4 months and pediatric follow up
590
How long is GH replacement therapy given?
Continued until the child achieves an acceptable height or growth velocity drops to less than 1 inch per year
591
Nursing implications for GHD?
Assess compliance with medication regimen, assess and address issues of self esteem, monitor growth (accurate is impt), teach the child and family about the disorder, teach proper technique for administering meds (shots), educational resources for parents
592
What are educational resources for parents about GHD?
Magic Foundation www.magicfoundation.org/wwww, Human Growth Foundation www.hgfound.org, Child Growth Foundation www.childgrowthfoundation.org/ghd.htm
593
When is the onset of precocious puberty?
Before age 7 or 8 and before age 9 in boys
594
What is precocious puberty accompanied by?
The appearance of secondary sexual characteristics, advanced growth rate, and bone maturation
595
What does precocious puberty cause?
Short stature as an adult from premature closure of epiphyseal ends of the long bones
596
What is the etiology for precocious puberty?
Hormone-secreting tumors, brain injury caused by head trauma, infection, thyroid dysfunction, ovarian dysfunction, idiopathic
597
What is the most common etiology for precocious puberty?
Idiopathic
598
Clinical manifestations of precocious puberty in females?
Females: breast development, axillary hair, pubic hair, adult body odor, onset of menses, acne, deepening voice
599
Clinical manifestations of precocious puberty in males?
Testicular enlargement, acne, penile enlargement, axillary and chest hair, pubic hair, adult body odor, facial hair
600
Diagnostic studies for precocious puberty?
Bone density scan, gonadotropin0releasing hormone simulation test, pelvic and abdominal ultrasound, computed tomographic scan or MRI, Blood work of testosterone levels and estrogen fraction test
601
What is the treatment for precocious puberty?
Involves the suppression of puberty
602
What are clinical manifestations of Congenital Hypothyroidism?
Large for age despite having poor feeding habits and increased birth weight, puffy face, swollen tongue, hoarse cry, poor muscle tone, cold extremities, persistent constipation, bloated or full to the touch, lack of energy and sleeps most of the time, appears tired even when awake, little to no growth, often appears perfectly normal at birth
603
Why is screening forCongenital Hypothyroidism vital at birth?
They often appear perfectly normal at birth
604
What are Congenital Hypothyroidism diagnostic studies?
State required screening of TSH and T4 for every baby born, Low T4, elevated TSH, or both indicate hypothyroidism, positive test results ay be followed by scan for bone age, blood tests before 48 hours after birth may be falsely interpreted because of the rise in TSH immediately after birth
605
What indicates hypothyroidism in babies?
Low T4, elevated TSH, or both
606
What should you monitor in an infant with Congenital Hypothyroidism?
Monitor growth and development of the infant (serial measurements of height, weight, and head circumference and screens for developmental milestones)
607
What should you assess for in children with Congenital Hypothyroidism?
Assess for retarded physical growth and slow intellectual development, if cognitive impairment has occurred then provide support to the family
608
What should you teach the family about Congenital Hypothyroidism?
Teach importance of daily admin of meds, drug therapy is needed for life
609
When do we stop measuring head circumference?
18 months to 2 years because fontanelles close around 18 months
610
How can meds for infants with Congenital Hypothyroidism be prepared?
Crushed and added to a small amount of formula, food, or water, or can be offered mixed with formula through a syringe or a nipple
611
How must meds for infants never be prepared?
Never put in a full bottle of formula in case they don't finish it
612
What should you include instructions of about Congenital Hypothyroidism in kids?
Include instructions on taking pulse in the teaching plan to monitor for signs of drug overdose
