Exam 1 Endocrine Flashcards

1
Q

What changes can a patient experience with disruption to hormone function?

A

energy level
tolerance to heat or cold
weight
thirst
frequency of urination, bowel function
body proportions, muscle mass, fat and fluid distribution
secondary sexual characteristics (e.g., loss or growth of hair)
menstrual cycle
memory, concentration, sleep patterns
mood
vision
joint pain
sexual dysfunction

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2
Q

What is exophthalmos?

A

abnormal protrusion of one or both eyeballs

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3
Q

What a examples of physical changes d/t hormone disruption that can be assessed?

A

appearance of facial hair in women
“moon face,”
“buffalo hump,”
exophthalmos
vision changes
edema
thinning of the skin
obesity of the trunk
thinness of the extremities
increased size of the feet and hands
hypo- or hyperreflexia.

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4
Q

What is a pheochromocytoma?

A

a tumor of the adrenal medulla

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5
Q

What is the MOA of insulin? What are 6 functions of insulin?

A

Ianabolic, or storage, hormone. When a person eats a meal, insulin secretion increases and moves glucose from the blood into muscle, liver, and fat cells.

*Transports and metabolizes glucose for energy

*Stimulates storage of glucose in the liver and muscle (in the form of glycogen)

*Signals the liver to stop the release of glucose

*Enhances storage of dietary fat in adipose tissue

*Accelerates transport of amino acids (derived from dietary protein) into cells

*Inhibits the breakdown of stored glucose, protein, and fat

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6
Q

How does the production of insulin in the pancreas differ during periods of fasting (such as overnight)? What is the purpose of insulin and glucagon working together? What is the function of the liver in the production of glucose? What occurs if fasting last longer than 8-12 hours?

A
  • the pancreas continuously releases a small amount of insulin (basal insulin)
  • and glucagon (secreted by the alpha cells of the islets of Langerhans) is released when blood glucose levels decrease

glucagon stimulates the liver to release stored glucose.

2 To maintain a constant level of glucose in the blood by stimulating the release of glucose from the liver.

3 the liver produces glucose through glycogenolysis (the breakdown of glycogen).

4 the liver switches to form glucose from the breakdown of noncarbohydrate substances, including amino acids, through the process of gluconeogenesis.

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7
Q

What is the patho of DM 1? When excess glucose is in the bloodstream, how does it affect the kidneys? What happens when glucose is excreted in urine? without insulin what glucose-producing processes function unhibited?

A

the destruction of the pancreatic beta cells resulting in decreased insulin production, increased glucose production by the liver, and fasting hyperglycemia, and glucose derived from food cannot be stored in the liver but instead remains in the bloodstream

the kidneys are unable to filter all of the excess glucose; glycosuria then occurs

osmotic diuresis: when excess glucose is excreted in the urine, it is accompanied by excessive loss of fluids and electrolytes

glycogenolysis and gluconeogenesis

contribute further to hyperglycemia
and
fat breakdown occurs excessively in the liver, resulting in an increased production of ketone bodies

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8
Q

What makes ketone bodies problematic when they are in excessive amounts? Result?

A

They are highly acidic, throws off homeostasis causing metabolic ascidosis

DKA

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9
Q

What are the 2 dysfunctions occurring with type 2 diabetes and their pathos?

A

insulin resistance and impaired insulin secretion

Insulin resistance refers to a decreased tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism. In type 2 diabetes, these intracellular reactions are diminished, making insulin less effective at stimulating glucose uptake by the tissues and at regulating glucose release by the liver

To overcome insulin resistance and to prevent the buildup of glucose in the blood, increased amounts of insulin must be secreted to maintain the glucose level and can have difficulty keeping up

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10
Q

What is metabolic syndrome? Resulting in what conditions? What constitutes a diagnosis of metabolic syndrome?

A

Insulin resistance leading to a constellation of symptoms

hypercholesterolemia, abdominal obesity
high blood pressure
high serum glucose (prediabetes)
High triglyceride levels
Low HDL levels

presence of 3 of the conditions

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11
Q

What other conditions can hasten Type 1 diabetes?

A

Cushing’s syndrome
pancreatitis

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12
Q

When insulin levels is controlled, the risk for developing what 3 complications is improved?

A

retinopathy (damage to small blood vessels that nourish the retina)
nephropathy (damage to kidney cells)
neuropathy (damage to nerve cells)

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13
Q

What is the therapeutic goal of diabetes management? What are the 5 components to achieving this?

A

to achieve euglycemia (normal blood glucose levels) without hypoglycemia while maintaining a high quality of life

nutritional therapy
exercise
monitoring
pharmacologic therapy
education

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14
Q

What are clinical manifestations of type 1 or 2 diabetes (essentially manifestations of hyperglycemia)?

A

3 Ps: polyuria, polydipsia, polyphagia
1: sudden weight loss
N/V
abdominal pain
blurred vision
paresthesia
fatigue
weakness
slow wound healing
dry skin
recurrent infections (bladder, vaginitis)
dehydration
hypotension
sexual dysfunction

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15
Q

What are the goals of dietary management for diabetes? Nurse’s role?

A

Control of total caloric intake/maintain a reasonable body weight
Control of blood glucose levels
Normalization of lipids and blood pressure to prevent heart disease
Increase fiber in diet which can lower cholesterol levels
Use of artificial sweeteners
Reduce intake of saturated and trans fats

Be knowledgeable about dietary management
Communicate with a dietician
Reinforce client understanding
Support dietary and lifestyle changes

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16
Q

What is lipodystrophy? How can it be prevented? What are the best locations?

A

localized changes in fatty tissue d/t repeated insulin administration

systemic rotation of injection sites

back of upper arm, belly, upper glute/hip, top of thigh

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17
Q

What are the 4 dysfunctions that can occur and cause type 2 diabetes?

A

impaired insulin secretion
absorption of glucose from the GI tract
increased hepatic glucose production
decreased insulin-stimulated glucose uptake in the muscles

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18
Q

What are criteria for diabetes diagnosis?

A

Symptoms : polyuria, polydipsia, polyphagia, eight loss
casual (any time of day regardless of meal) plasma glucose concentration > 200 mg/dL
Or
Fasting (not intake for 8 hrs) plasma glucose >126 mg/dL
Or
Two-hour postload glucose >200 mg/dL during an oral glucose tolerance test
Or
Hemoglobin A1C ≥6.5% (glucose attached to the hemoglobin)

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19
Q

What are some dietary client teaching?

A

eat small amounts of fresh fruit
fill plate 1/4 of whole grain
Drink skim or 1% milk
fill 1/4 plate with lean protein
fille 1/2 plate with non-starchy vegetables

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20
Q

What are nutritional consideerations for meal planning with diabetes?

A

Carbohydrates: 45% to 50%
Emphasize whole grains
Non-starchy vegetables
Fat: 20% to 35% unsaturated, low saturated fats to reduce LDL
Non-animal sources of protein: 15%-20%
Legumes
Whole grains
Increase fiber
Increase omega-3 fatty acids

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21
Q

How does the glycemic index measure food sources? What are some findings when evaluating the glycemic index?

A

A value from 0-100 of any carbohydrate (based on rise of serum glucose at 2 hours after eating)

The lower the index the better for preventing spikes in blood glucose with diabetes

Raw or whole foods tend to have lower glycemic index than cooked, chopped, or pureed foods

Eat whole fruits rather than juices; they have a lowerglycemicindex because of fiber (slowing absorption)

Adding food with sugars may produce a lower glycemic index if eaten with foods that are more slowly absorbed

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22
Q

How does alcohol react with insulin and diabetes?

A

Do not drink alcohol on an empty stomach
Alcohol doesn’t require insulin to provide the body with energy
Excessive alcohol consumption can lead to dangerous episodes of hypoglycemia

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23
Q

What is the benefit of exercise and managing diabetes? What are considerations to implement to ensure success with exercise and diabetes management?

A

Lowers blood glucose
Aids in weight loss, easesstress, and maintainsa feeling of well-being
Lowers cardiovascular risk

Exercise when serum glucose is between 80-250 mg/dL, not too high or low
Do not exercise if ketones present in urine
If performing high-intensity activity, consider having a prior snack
Have high quality, comfortable shoes

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24
Q

What are exercise precautions with diabetes?

A

those who require exogenous insulin should it a 15g carb before moderate exercise

type 2 may not need extra food before exercise

post exercise hypoglycemia can occur up to 24hrs after intense exercise

exercise stress test can be administered prior to starting an exercise program

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25
Q

What are the 4 categories and examples of insulin?

A

rapid acting: lispro, aspart, gluisine
short acting: regular
intermediate acting: NPH
long acting: no peak glargine, detemir

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26
Q

What are complications of insulin therapy?

A

local allergic reaction
systemic allergic reaction
insulin lipodystrophy
resistance to exogenous insulin
morning hyperglycemia

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27
Q

What is the major side effect of antidiabetic agents that stimulate insulin secretion?

A

hypoglycemia

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28
Q

What are the sites of action for the following antidiabetic agents (and examples)?
biguanides and thiazolidinediones

amylin analogs incretins and insulin secrelagogues incretins

glucosidase inhibitors and amylin analogs

A

Metformin
liver: hepatic glucose output and muscle: peripheral glucose uptake

pancreas: glucagon and insulin secretion

GI: glucose absorption

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29
Q

What are the most common SE with metformin? Most severe? Nursing considerations?

A

GI upset, nausea, diarrhea

lactic acidosis

does not cause hypoglycemia
hold 24-48hrs prior to IV contrast

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30
Q

What is the MOA of sulfonylureas (glyburide, glipizide)? What is the risk? Who should avid?

A

Stimulates insulin secretion by pancreas. Often used with metformin to control serum glucose

Risk of significant hypoglycemia
Sulfa antibiotics have similar structure, so can cause hypoglycemia together

Avoid in client allergic to sulfa
Avoid prolonged sunlight since sulfa groups cause photosensitivity

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31
Q

What is the MOA of anagliflozin? Drug class? What is the increased risk with this med?

A

Prevent the reuptake of glucose in the kidney, lowering serum glucose

sodium-glucose co-transporter inhibitors

The glucose in urine increases risk of UTIs

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32
Q

What is the MOA of pioglitazone/rosiglitazone? Drug class? Side effects? What should be monitored?

A

Reduces insulin resistance on cells

thiazodinedones

Side-effects are mainly metabolic: weight gain, hyperlipidemia, edema, and liver dysfunction

Monitor LFTs, weight, lipids

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33
Q

What impact does hypoglycemia have on the nervous system? What is the glucose level threshold for hypoglycemia? What can cause hypoglycemia? What is the adrenergic response?

A

acitvate the sympathetic nervous system (fight or flight)

below 70 mg/dL

Too much insulin or oral hypoglycemic agents
Excessive physical activity
Not enough food

Sweating
Tremors
Tachycardia
Palpitations
Nervousness
Hunger

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34
Q

What is the most significant effect of hypoglycemia? S/S? S/S of severe hypoglycemia?

A

the brain needs glucose to work so hypoglycemia causes significant CNS interruption

Inability to concentrate
Headache
Confusion
Memory lapses
Slurred speech
Drowsiness

Disorientation
Seizures
Loss of consciousness
Death

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35
Q

How should episodes of hypoglycemia be managed? What is client is unconsious?

A

Give 15 to 20 g of fast-acting, concentrated carbohydrate if alert/awake
Three or four glucose tablets
4 to 6 ounces of juice or regular soda (not diet soda)
6 to 10 hard candies
1 tbsp honey

Subcutaneous or intramuscular glucagon (1 mg)
25 to 50 mL of 50% dextrose solution IV

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36
Q

What is the dysfunction occurring with DKA? What are the 3 main dysfunctions occuring?

A

Absence or inadequate amount of insulin resulting in abnormal metabolism of carbohydrate,protein, and fat
Mainly a complication of type 1 diabetes, rarely type 2

Hyperglycemia
Dehydration
Acidosis

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37
Q

What are assessment findings of DKA? ABGs?

A

blood glucose of 300-800
ketone bodies in the urine from fat breakdown
elevated K, Hg, BUN and Cr
low Na

lower pH, low bi-card
when PCO2 lowers it is d/t respiratory compensation (Kussmaul respirations)

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38
Q

How is DKA managed? what hapens to the potassium with treatment? What should be monitred?

A

rehydration with NS initially, at glucose of 250 add dextrose
* bolus of regular insulin then continuous IV
* reverse acidosis w/ insulin and bi-carb
* treat hyperkalemia with insulin, bi-carb and albuterol

rehydration increased volume which decreases serum potassium ratio.
Insulin enhances the movement of potassium into the cell because it rides along with the insulin

blood glucose
renal functions and urinary output
ECG
electrolytes
VA
lung assessments for Kussmaul and fluid overload

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39
Q

What are sick day rules with diabetes? When should you call the provider?

A

Notify healthcare provider if ill
Monitor BS every 2-4 hrs.
Continue taking insulin/oral meds during illness
Consume liquids every hour to prevent dehydration
Meet carbohydrate needs through soft food 6-8 times per day
Test urine for ketones every 3-4 hrs of if BS is >240 mg/dL

Call the provider for:
Moderate to large ketones in urine
BS >250 mg/dL that does not respond to treatment
Fever greater than 101.5°F, does not respond to acetaminophen, or lasts >24 hrs.
Feeling disoriented/confused
Experience rapid breathing
Persistent N/V or diarrhea
Inability to tolerate liquids
Illness lasts longer than 2 days

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40
Q

What is HHS? Patho? 2 manifestations? Differences in lab findings from DKA? Manifestations? Mortality rate?

A

hyperglycemic hyperosmolar syndrome

lack of sufficient insulin
Ketosis/acidosis is minimal or absent since insulin is still present but not enough

Severe hyperglycemia (greater than 600 mg/dL) causes an osmotic diuresis, loss of water and electrolytes, hypernatremia, and increased serum osmolality
* HHS causes profound dehydration, often up to 10-12 liters of fluid loss

Typically, no hyperkalemia, no acidosis, but increased BUN and creatinine from dehydration

Manifestations include hypotension, profound dehydration, tachycardia, and variable neurologic signs caused by cerebral dehydration

High mortality rate, more than DKA since it occurs more gradually over days, so clients stay home longer

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41
Q

What are a few differences in lb values between DKA and HHS?

A

lack of acidosis in HHS

Hyperkalemia is uncommon in HHS

Serum glucose is higher in HHS

Serum osmolality is higher in HHS

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42
Q

What triggers HHS? How is HHS managed?

A

infections, heart attack, stress, sepsis in type 2 diabetics

rehydrate with NS (loads of fluids)
IV regular insulin to pull glucose into cells
monitor fluid volume and electrolytes
assess self-care managment

43
Q

What are long-term complications of diabetes?

A

Macrovascular damage:
Accelerated atherosclerotic changes in large arterial vessels
Coronary artery disease (MIs)
Cerebrovascular disease (strokes)
Peripheral vascular disease (loss of toes/limbs)

Acceleratedatherosclerotic changes in small arterial vessels
sexual dysfunction
Diabetic retinopathy: leading to vision loss
Nephropathy: leading to reduced renal function and chronic renal failure
Peripheral neuropathy: leading to loss of skin sensation,skin ulcers,and cellulitis

44
Q

What are nursing considerations for diabetic foot care?

A

inspect daily
do not soak, pat dry
do not self-treat corn/calluses
consult podiatrist
closed-toe, comfortable shoes
try on new shoes at end of the day to prevent purchasing shoes that are too tight
clean cotton socks
no heating pads or hot water bottles
treat cuts promptly and well

45
Q

What is the main mechanism of the function of the endocrine system? What hormone is the exception?

A

negative feedback loop to maintain homeostasis

oxytocin, positive feedback

46
Q

What are the roles of the endocrine system? Glands involved?

A

orchestrating cellular interactions, metabolism, growth, reproduction, aging, and response to adverse conditions

hypothalmus
pineal
pituitary
thyroid
parathyroid
thymus
adrenals
islets of langerhans in the pancreas

47
Q

What is the relationship between the pituitary gland and the hypothalamus? How is the pituitary accessed if there is a tumor? Major function?

A

Mainly controlled by the hypothalamus
Anterior pituitary has a blood vessel communication with hypothalamus
Posterior pituitary has a nerve communication with hypothalamus

Notice the optic chiasm is next to pituitary gland
Pituitary gland is accessible through the nose for tumor removal

Known as the “Master Gland” for its role in producing multiple essential hormones
Anterior pituitary produces and secreteshormones
Posteriorpituitary stores and secretes hormones

48
Q

What are the hormones excreted from the anterior pituitary and their function?

A

Adrenocorticotropic hormone (ACTH): stimulate adrenal cortex
Growth hormone: stimulate growth of tissue and bones
Thyroid stimulating hormone (TSH): stimulate the thyroid gland/T4 secretion
FSH/LH: regulation of menstrual cycles/ovulation, testicular development/testosterone production
Prolactin: breast milk production

49
Q

What are the hormones excreted from the posterior pituitary?

A

Antidiuretic hormone (ADH)
Oxytocin: Contraction of uterus post-partum,milk ejection/let-down in breasts

50
Q

What is the difference between functional and non functional pituitary tumors? Clinical manifestations?

A

Mostly benign and slow growing tumors
Functional
Secrete pituitary hormones of the affected cells
Prolactinoma is the most common pituitary adenoma
Effects of tumors are from the secreting hormone and the local compression effects of optic chiasm (visual fields)

Non-functional
Do not secrete pituitary hormones

Clinical manifestations based upon endocrine dysfunction and/or dysfunctional effects on target organs

51
Q

What is a hypophysectomy? What else can it treat? Nursing considerations post-surgery?

A

Surgical removal of pituitary gland tumors

Treatment of choice for Cushing syndrome (excess ACTH production) caused by pituitary tumor

Transsphenoidal surgery post-op nursing care and client education
Monitor for temporary diabetes insipidus
Notify provider of clear watery drainage (possible CSF leak)
Maintain client in semi- to high-Fowler
Assess for meningitis manifestations
Headache and nasal congestion for ≈ 1-2 weeks
No tooth brushing
No blowing nose
No forceful coughing
Avoid straining or bending at waist

52
Q

What are the actions of the thyroid?

A

The thyroid gland is like the factory/controls energy level of bodily functions
regulates carb, lipid and protein metabolism
CNS activity and brain development
cardiovascular stimulation
bone and tissue growth
GI regulation
sexual maturation

53
Q

What hormone controls the thyroid? What else is contained within the hormone? What hormones a released from the thyroid?

A

TSH from the anterior pituitary controls the release of thyroid hormonend their functions?

Iodine is contained in thyroid hormone, and needed in diet for production

Triiodothyronine (T3):
Controls cellular metabolic activity
More potent and rapid-acting than T4
Thyroxine (T4):
Controls cellular metabolic activity
Calcitonin: Secreted in response to high plasma calcium level and increases calcium deposit in bone/reduces bone breakdown

54
Q

What is the typical origin of thyroid diseases?

A

Majorityof thyroid diseases are from disease of thyroid gland,not the pituitary gland

55
Q

What are common indicators of hypothyroidism?

A

Primary loss of thyroid function is the most common mechanism (autoimmune Hashimoto thyroiditis)

Females between 30-60 years old are the majority of clients

Metabolism is reduced with reduced levels of T3 and T4

Medications like lithium, amiodarone can directly reduce thyroid function

A disease with a spectrum of severity from mild symptoms to myxedema coma

56
Q

What is the nature of hypothyroidism? Primary loss? Secondary? What is a common condition of primary hypothyroidism? Patho?

A

Suboptimal levels of thyroid hormone production

Primary: Loss of thyroid hormone production
Secondary: Pituitary disease resulting inlack of TSH production

Hashimoto disease (primary hypothyroidism)

Autoimmune thyroiditis
Results in low levels of T3/T4 and elevated TSH levels

57
Q

What are clinical manifestations of hypothyroidism/Hashimotos’s? (13)

A

Fatigue and lethargy
Weight gain w/o increased caloric intake
Cold intolerance, subnormal body temperature
Dry skin and dry, brittle hair
Cardiovascular-related
Bradycardia
Cardiomegaly
Elevated serum cholesterol
Atherosclerosis and CAD
Menorrhagia
Constipation
Depression
Goiter from TSH stimulation

58
Q

What are nursing considerations of levothyroxine?

A

Dose started low and slowly titrated until desired levels of serum TSH and free T4concentration are achieved

Take in the morning on an empty stomach

Treatment is lifelong since thyroid gland rarely recovers function in Hashimoto thyroiditis

Non-adherence to levothyroxine will cause hypothyroidism symptoms, low T4 and elevated TSH levels

59
Q

What is the nursing management for hypothyroidism?

A

Monitor for CV changes
Low BP, bradycardia, dysrhythmias

Monitor weight
Low-calorie, high-bulk diet

Encourage activity

Monitor respiratory status and encourage coughing/deep breathing

Administer stool softeners as needed
Avoid fiber laxatives which interfere with absorption of levothyroxine

Keep the client warm if they have decreased cold tolerance
No heating devices which can cause unrecognized burns

Monitor mental status and concerns regarding body image

Educate client to report chest pain/discomfort immediately

Educate client to adhere to medication regimen (time/dose/brand)

60
Q

What is myxedema coma? Cause?

A

Rare, life-threatening, severe form of hypothyroidism
40% mortality rate

Causes
Undiagnosed hypothyroidism
Medication noncompliance (levothyroxine)
Stressor (acute illness, surgery, chemotherapy, use of sedatives/opioids)
Occurs most often in older women during the winter months

61
Q

What are clinical manifestations of myxedema coma?

A

Initial symptoms
Depression, diminished cognitive status, lethargy
Lethargy may progress to stupor, reduced level of consciousness, coma
Hypoventilation progressing to respiratory failure
Hyponatremia
Hypoglycemia
Hypothermia
Bradycardia & hypotension – may progress to CV collapse

62
Q

What is the medical management of myxedema coma?

A

Goals: restoration of normal metabolic state and prevention of complications
Early recognition and aggressive intervention
Check for possible sources of infection (blood, sputum, urine)
ICU setting
ABG analysis and ventilatory support
Continuous VS and ECG monitoring
Cautious administration of replacement thyroid hormones (IV initially)
Passive rewarming
Monitor I&O and daily weights
Treat hypoglycemia with glucose
Administer corticosteroids
Initiate aspiration precautions
Avoid sedatives and opioids
Turn and reposition Q2H

63
Q

What is the dysfunction of hyperthyroidism? Causes?

A

Excessive synthesis and secretion of thyroid hormone (all systems are stimulated!)
Symptoms range from mild to life-threatening

Causes
Graves disease
Autoimmune thyroiditis
Most common cause of hyperthyroidism
Affects women 8x more than men
Age of onset normally 20s – 40s
Toxic multinodular goiter of thyroid gland
Toxic adenoma in thyroid gland
Excessive ingestion of thyroid hormone (levothyroxine)
Secondary hyperthyroidism from pituitary adenoma (excessive TSH)

64
Q

what are the CNS and cardiovascular manifestations of hyperthyroidism? GI? Other?

A

Related to the increase in metabolic rate and increased oxygen consumption
CNS effects
Anxiety, restlessness, irritability
Emotional instability
Fine hand tremors

Cardiovascular effects
Tachycardia and palpitations
Arrhythmias
Elevated SBP

GI effects
Diarrhea
Increased appetite
Weight loss

Other manifestations
Heat intolerance with increased perspiration
Exophthalmos (bulging eyes)
Muscle wasting and weakness
Thin skin
Oligomenorrhea
Osteoporosis
Goiter from overstimulation (autoantibodies)

Heart failure from chronic stimulation

65
Q

What is exophthalmos?

A

bulging of eyes caused by excessive tissue growth behind the eyes

66
Q

How is hyperthroid ism diagnosed?

A

Enlarged thyroid gland (goiter)
Bruit over thyroid arteries - sign of increased blood flow to the thyroid is possible
Decreased serum TSH
Increased serum free T4
Increased radioactive iodine uptake

67
Q

What are therapeutic options for treating hyperthyroidism?

A

Medications: Oral propylthiouracil (PTU) or methimazole

Radioactive Iodine therapy (destroys partially or fully the thyroid function)

Thyroidectomy (removal of thyroid gland)

B-blockers (treats the symptoms only, doesn’t affect thyroid function)

68
Q

That are thionamides? Commonly prescribed? MOA? Length of treatment? Nursing considerations?

A

Methimazole
Propylthiouracil (PTU)

Block the utilization of iodine, thus inhibiting one or more stages in thyroid hormone synthesis and release

Medications are used until client is euthyroid
May take several weeks until symptoms relief occurs
Gradually taper off dose once euthyroid state is achieved

Take with meals in divided doses at regular intervals- do not stop abruptly
PTU is preferred in a pregnant woman, less toxicity
Monitor CBC and LFTs prior to administration, most concerning adverse effect is bone marrow suppression (monitor for fevers,signs of infection, bruising from thrombocytopenia)

69
Q

What is radioactive iodine therapy? Dosing timeline? Contraindicated in who? When does therapeutic effect begin?

A

Irradiation by administration of radioisotope ᶦᶟᶦI (radioactive iodine)
Thyroid cells exposed to the radioactive iodine are destroyed

One dose may be sufficient; 2nd or 3rd dose may be needed
Degree of thyroid destruction varies and may require lifelong thyroid hormone replacement

Contraindicated in pregnancy

Effects of therapy take 6 to 8 weeks

70
Q

What are precautions needed for radioactive iodine therapy?

A

Prevent radiation exposure to others
Do not share toilet for 2 weeks
Flush the toilet 2 – 3 times
Wash clothing separate from others
Run washing machine for a full cycle after washing contaminated clothes
Do not share a toothbrush
Used disposable plates and utensils

71
Q

When is a thyroidectomy indicated?

A

Medication therapy failure or intolerance
Radiation therapy is contraindicated
Large goiter
Thyroid cancer

72
Q

Nursing post-operative thyroidectomy care?

A

Airway compromise from hemorrhage and edema can compress the trachea and usually occurs within the first 24 hours

Have tracheostomy and suction supplies available

Semi-Fowler position

Support the head and neck to avoid neck extension

Assess the dressing and the back of the neck for excessive bleeding

Check for laryngeal nerve damage by asking the client to speak as soon as awake and every 2 hours after

Assess for symptoms of hypocalcemia (loss of parathyroids)

Ensure calcium gluconate or calcium chloride is immediately available

73
Q

What is an early assessment to identify increasing edema, damage to the laryngeal nerve or hemorrhage after a thyroidecthomy?

A

voice changes

74
Q

What are the thyroid storm? What can cause it?

A

Severe, usually abrupt form of hyperthyroidism from a surge in thyroid hormones

uncontrolled Graves disease plus an additional stress to body
Usually precipitated by a stressful event:
Injury or infection
DKA
Pregnancy
Abrupt withdrawal of antithyroid medications
Extreme emotional stress
Thyroid surgery,releasing thyroid hormones

75
Q

What are clinical manifestations of a thyroid storm? CV effects? CNS?

A

Hyperpyrexia (temperature > 38.5⁰ C/101.3⁰ F)

CV effects
Tachycardia > 130 bpm
Hypertension
Chest pain
Palpitations
Dyspnea

CNS effects
Acute agitation
Delirium
Psychosis
Coma

76
Q

What is the medical management of a thyroid storm?

A

ICU setting
Provide as calm and quiet an environment as possible
Continuous VS and ECG monitoring (atrial fibrillation is very common)
Temperature reduction
Cooling blanket, cooling sponge baths
Acetaminophen
salicylates (aspirin) are contraindicated- increase free thyroxine levels
Heart rate reduction: Beta adrenergic blockers, Digoxin
Humidified oxygen
Dextrose-containing IV fluids
Administration of methimazole or PTU to reduce T4/T3 levels
IV fluids to maintain hydration from excessive sweating, monitor input/output
Provide supplemental oxygen due to increased oxygen demands

77
Q

What stimulates the adrenal cortex? What does it release? What stimulates the adrenal medulla? What does it release in return?

A

Adrenal cortex is stimulated by adrenocorticotropic hormone (ACTH)
Releases cortisol, aldosterone, and androgens

Adrenal medulla is stimulated by sympathetic nervous system
Functions as part of the autonomic nervous system (sympathetic system)
Releases catecholamines
Epinephrine
Norepinephrine
Dopamine

78
Q

What are the functions of the hormones secreted from the adrenal cortex? Which is the glucocorticoid and it’s function? What is the mineralcorticoid and its funnction? What are androgens?

A

Hormones secreted enable the body to adapt to stress (cortisol) and fluid balance (aldosterone)

Glucocorticoids
Cortisol
Affects cellular metabolism, maintains blood pressure,maintains serum glucose levels

Mineralocorticoids
Aldosterone
Maintains electrolyte balance and fluid balance by reabsorbing Na and secreting potassium in the kidney
Part of the RAAS

Androgens
Little effect when secreted in normal amounts
Excess secretion causes masculinization of women such as facial hair and acne

79
Q

what is cushing syndrome? Cause? what is cushing disease? Least common cause? How is it diagnosed?

A

exogenouscauseofincreased cortisol

Most common cause is the use of corticosteroid medications to treat other illnesses such as asthma, allergies, autoimmune disease

endogenous cause of increased cortisol
Can also occur from excessive glucocorticoid production secondary to adrenal cortex hyperplasia or adenoma (less common)

Lastly, can occur from ACTH secreting pituitary adenoma (least common)

Diagnostics
Serum cortisol are elevated
24-hour urinary cortisol are elevated
Low dose dexamethasone suppression test
Reduced serum potassium, increased serum sodium and glucose
CT scans of brain and abdomen if adrenal hyperplasia or pituitary tumor is felt to be cause

80
Q

What is the effect of long-term cortisol use?

A

osteoporosis

80
Q

What is the rapid method of dexamethasone supression testing for adrenal dysfunctions in cortisol? Prolinged method? Findings?

A

Rapid testing
The dose is given before sleeping
Blood sample is taken after waking and before getting out of bed
Stay overnight
Usually, the PO dose is given at 11 pm and the blood cortisol level is taken at 8 am
If there is no decrease in blood cortisol level, the test is repeated with a higher dose

Prolonged testing
Baseline 24-hr urine cortisol and blood cortisol
2 continuous days of urine collection while dexamethasone is administered every 6 hours
Monitor the client’s blood glucose and potassium levels for adverse effects

Expected finding is suppression of cortisol
Nonsuppression indicates Cushing disease

81
Q

What are 3 physical manifestations of cushing’s?

A

Moon face from fat redistribution to the face and central body with smaller limbs from muscle wasting

Striae from thinning of skin and exposure of deeper tissue/blood vessels

Buffalo hump also from fat redistribution

82
Q

What is medical managment of cushing syndrome? Meds? Least invasive? Secondary treatment/monitor?

A

Treatment depends upon the cause (exogenous or endogenous cause):
Hypophysectomy if syndrome is caused by anACTH pituitary tumor
Adrenalectomy for unilateral primary adrenal hyperplasia

Adrenal enzyme inhibitors
Ketoconazole…..also an antifungal medication, not a cure, but a treatment
Mitotane….destroys adrenal cells, used for adrenal cancers, less for adrenal hyperplasia

Attempt to reduce or taper dose of corticosteroids to the minimum dosage needed to treat the underlying disease process (asthma, colitis……etc.)

Monitor blood glucose and monitor blood pressure
Prevention of peptic ulcer disease with H-2 blockers or a PPI
Calcium and vitamin D to protect bones and prevent osteoporosis

83
Q

What is nursing managment of cushings?

A

Monitor I&O and daily weight
Assess for signs of hypervolemia
Maintain safe environment to decrease risk of fractures/skin trauma
Encourage activity within reason for the client
Prevent infection
Use surgical asepsis with dressing changes/invasive procedures
Monitor WBC count daily
Monitor skin integrity
Turn client every 2 hrs.
Meticulous skin care

84
Q

What is the most common adrenocortical insufficiency? Primary rreason? Secondary?

A

Addison’s disease

Primary adrenal insufficiency/Addison disease: resulting in reduced serum cortisol andaldosterone levels

Secondaryadrenal insufficiency:sudden cessation of exogenous corticosteroid therapy causes a rapid drop in serum cortisol levels; adrenal gland don’t have time to compensate by secreting cortisol (most common cause of adrenal insufficiency)

85
Q

What are addison disease clinical manifestations?

A

Weakness and fatigue
Salt cravings
Abdominal pain
N/V/D
Anorexia
Unintentional weight loss
Hypotension
Dark/bronze skin discoloration
Hypoglycemia
Hyponatremia
Hyperkalemia
Hypercalcemia
Increased WBC
Fluid volume deficit
Increased BUN and creatinine
Glucose within expected range or decreased

86
Q

What functions are cortisol need for? Aldosterone?

A

Cortisol is needed for maintaining blood pressure, blood sugar, and proper GI functioning

** Aldosterone is needed for reabsorbing NA and secreting K in the kidneys, plus maintaining fluid balance

87
Q

What does Addison’s usually destroy? Lifelong treatment?

A

autoimmune adrenal destruction

Lifelong therapy will be needed with a cortisol (hydrocortisone)and a mineralocorticoid (fludrocortisone)

88
Q

What is the primary nursing managment of Addison’s?

A

Primary goal is to prevent circulatory shock
Monitor F&E status
Measure orthostatic BP
Obtain daily weights
IV N/S fluid boluses for BP
Observe for dehydration
IV hydrocortisone infusion
Replace mineralocorticoid (fludrocortisone)
Monitor and treat hyperkalemia with sodium polystyrene,insulin/glucose,bicarbonate, calcium gluconate, and albuterol

89
Q

What is secondary treatment for Addions’s?

A

Administer hydrocortisone
Increase dose during periods of stress such as an illness
Administer with food to avoid gastric irritation
Taper dose to avoid acute adrenal insufficiency if discontinuing

Monitor for hypoglycemia
Administer glucagon as needed with reduced LOC
Administer oral glucose if awake

Monitor for signs of infection with cortisol causing immunosuppression

90
Q

What is an Addison crisis/adrenal crisis? Triggers?

A

Life-threatening complication of adrenal failure/insufficiency
May lead to circulatory collapse and shock

Triggering factors
Most common cause is abrupt withdrawal of glucocorticoid therapy
Or a client with known Addison disease,but needing more cortisol due to the following stressors:
Sepsis/ infection
Trauma
Stress
MI, surgery, anesthesia, hypothermia, volume loss, hypoglycemia

91
Q

What are clinical manifestations of a adrenal/addison crisis? Nursing managment?

A

Severe hypotension
Dehydration
Hyponatremia
Hyperkalemia
Increased BUN and creatinine
Profound fatigue
Confusion and restlessness

Place client in recumbent position with legs elevated
Administer IV fluids
Administer IV hydrocortisone
Administer vasopressors as needed to increase BP
Treat electrolyte imbalances (hyponatremia and hyperkalemia)
Administer insulin and dextrose to move K+ into cells
Administer Ca+ to counteract hyperkalemia and protect the heart
Treat underlying cause of the Addisonian crisis

92
Q

What is the nature of the adrenal medulla? What can occur with excessive hormone secretion?

A

Consider it part of the sympathetic nervous system

Secretes mainly epinephrine and norepinephrinefrom sympathetic stimulation

Excessive secretion of epinephrine/norepinephrine can occur from an adrenal tumor called a pheochromocytoma

With a pheochromocytoma, massive amounts of epinephrine/norepinephrine are sporadically secreted, resulting in a set of symptoms/signs

93
Q

What is a pheochromocytoma? Nature? Treatment?

A

Rare, usually benign tumor of the adrenal medulla

Cause of HTN in 0.1% of clients diagnosed with HTN

Fatal if undetected or untreated from strokes and heart attacks

Peak incidence between ages 40 –50

Males and females affected equally

Familial link

Definitive treatment is surgical removal of tumor (adrenalectomy)

94
Q

What is the classic triad of symptoms with a pheochromocytoma? The 5 Hs?

A

Classic triad
Episodic headache
Sweating
Tachycardia

“Five Hs”
HTN
Headache
Hyperhidrosis (excessive sweating)
Hypermetabolism
Hyperglycemia

95
Q

How is a phenochromocytoma diagnosed? What must be avoided before testing? What is preoperativetremant? Ontraoperative? Postoperative?

A

testing urine for epinephrine metabolites calledmetanephrines
also
clonidine suppression test

avoid caffeine or alcohol prior to test sincethese affect results

Surgical treatment:
Preoperatively
Bedrest with HOB elevated during a hypertensive crisis episode
Alpha blockers
Beta adrenergic blockers
Calcium channel blockers

Intraoperatively
Surgical manipulation of tumor may cause hypertensive crisis

Postoperatively
Corticosteroid therapy if bilateral adrenalectomy performed
IV immediately post-op
PO after recovering from acute stress of surgery

96
Q

What is the function of ADH? What are disorders of insufficient ADH and the resulting dysfunction? Excessive ADH?

A

reabsorbs fluid in the kidneys to maintain normal fluid levels,electrolyte levels, and urine concentration

diabetes insipidus. Results in massive loss of fluids in the urine, dehydration, dilute urine, and concentrated serum NA levels (hypernatremia)

syndrome of inappropriate ADH secretion. Results in excessive intravascular fluid volume, dilute serum, concentrated urine,and low serum NA levels (hyponatremia)

97
Q

What are the causes of neurogenic DI? Nephrogenic DI? What is ADH also know as?

A

hypothalamic or pituitary injury from trauma,meningitis,surgery
Results in a lack of ADH secretion

kidney injury not responding to ADH
Most common cause is lithium use which can cause damage to nephrons
Causes a deficiency of antidiuretic hormone (ADH)

ADH is also known as vasopressin

98
Q

What are manidestations of DI in the serum and urine?

A

Serum
Think CONCENTRATED
Increase in
Serum osmolarity
Serum sodium
Serum potassium

Urine
Think DILUTE
Decrease in
Urine specific gravity
1.001 – 1.005
Urine osmolarity
Urine sodium
Urine potassium

99
Q

What are clinical manifestations of DI?

A

Urine output > 250 mL/hr
Very dilute urine (<1.005)
Polydipsia
Polyuria
Thirsty
Hypotension
Tachycardia
Dehydration
Weight loss

100
Q

What is the medical managment of DI? Drug of choice? Route? Patient teaching?

A

Identify and treat underlying cause
Adequate fluid replacement in acute phase
Strict I & O monitoring, weigh daily
Frequent VS
Monitor for signs and symptoms of hyponatremia during treatment (desmopressin)

Desmopressin/DDAVP (synthetic vasopressin)
Drug of choice for central DI, life-long therapy

Given orally or intranasally

Use cautiously in clients with CAD (can cause vasoconstriction) or HF (fluid overload)
Dose is adjusted based on urine output and fluid balance in body
Monitor for headaches or confusion due to development of hyponatremia from ADH

101
Q

what is the medical managment of SIADH

A

treating underlying cause and restricting fluids

Restrict oral fluid intake < 1000 mL/day (avoids further hemodilution)

Strict I & O, daily weights
Frequent VS

Frequent monitoring of neurological status (hyponatremia)
headaches,confusion,seizures, and coma

Monitor for manifestations of hypervolemia
shortness of breath/lung crackles, hypertension

Administration of loop diuretics if fluid overload/heart failure

Administration of hypertonic saline (3%) if severely hyponatremic

102
Q

What are the meds of note for treating SIADH and their SEs?

A

Tetracycline derivatives (demeclocycline)
Blocks effect of ADH in the kidneys
Like tetracycline,avoid dairy products,antacids,and iron during ingestion
Can cause photosensitivity rashand oral thrush

ADH (vasopressin) antagonists
Tolvaptan blocks the effect of ADH in the kidneys

Furosemide (loop diuretic): to help remove excessive fluid if needed: monitor weight, sodium levels, renal function, and ototoxicity

3% N/S only for severe hyponatremia that may cause seizures

103
Q

What are complications associated with SIADH? What is central pontine myelinolysis?

A

Excessive fluid volume
Pulmonary edema/lung crackles, edema, hypertension
Report shortness of breath,monitor daily weights,restrict fluid

Hyponatremia
Monitor for N/V, seizures, confusion, altered level of consciousness, coma
Monitor serum electrolytes, especially sodium

**Central pontine myelinolysis:a complication of the rapid reversal ofhyponatremia : monitor serum sodium and any neurologic deterioration