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NRSG 213 > Lecture 6 - Endocrine System > Flashcards

Lecture 6 - Endocrine System Flashcards

1
Q

Thyroid hormones regulate

A
  1. Lipid and Carbohydrate metabolism
  2. Growth and development
  3. Heat regulation
  4. Effects of CV, endocrine, and neuromuscular systems
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2
Q

Thyroid gland is stimulated by

A

Thyroid stimulating Hormone (TSH), which is made by the pituitary gland

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3
Q

The thyroid produces which two hormones

A

T3. Triiodothyronine (4x more potent than T4)

T4. Thyroxine

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4
Q

Hypothyroidism – Caused when (3 different types)

A
  1. Thyroid gland doesn’t make enough hormone (T3 and T4)
  2. No stimulation by pituitary gland
  3. Low levels of thyrotropin-releasing hormone from the hypothalamus
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5
Q

Hypothyroidism leads to what? And what are its signs and symptoms?

A 
Slowing of body processes. 
S/S --> 
- Constipation
- Lethargy 
- Thick skin, loss of hair 
- Bradycardia, hypotension 
- Feeling cold 
- Weight gain

Non PC: Slow, fat, dry and cold

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6
Q

Hyperthyroidism is caused by

A
  1. Thyroid gland makes too much hormone

2. Too much stimulation by the pituitary gland

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7
Q

Hyperthyroidism leads to what? What are its S/S?

A

Speeding up of body processes!

S/S:

  • Diarrhea
  • Feeling hot, sweaty
  • Increased appetite
  • Nervousness, insomnia
  • Hypertension, tachycardia
  • Lose weight

not pc: Hot thin and fast

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8
Q

Thyroid replacement therapy & S/E & Med to remember

A

Medications that replace what the thyroid gland cannot produce. Returns the body systems to normal once dose is regulated.

S/E: Usually related to overdose (Systems speeding up, heart, GI, etc)

Med: Levothyroxine (Synthroid)….1 Tab a day, need lower doses as you age.

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9
Q

Antithyroid agents & S/E & Med

A

Medications that suppress the thyroid gland. Hyperthyroid is often treated with radioactive iodine (I131) or surgically very effectively.

S/E: Liver and bone marrow toxicity

Med: Propylthiouracil….Given temporarily until ready for surgery

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10
Q

Important guidelines for thyroid medications

A
  1. Don’t stop taking
  2. Take at same time each day
  3. Don’t take OTC meds without checking with MD
  4. Keep a log of behavior/mood, weight changes, Pulse
  5. Avoid iodine foods (soy, tofu, seafood, iodized salt)
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11
Q

Corticosteroids Definition & Uses

A

Similar to hormones secreted by the adrenal glands (AKA steroids) – Not the same as anabolic steroids

Uses:

  • decreases inflammation (Itching, swelling)
  • Suppresses the immune system (Autoimmune diseases, organ rejection, etc)
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12
Q

Corticosteroids meds to remember

A

Hydrocortisone - short acting (30 min - 2 hrs)…..PO, IM/IV, Topical (OTC) which is most common

Prednisone - intermediate acting (few hours)…given PO

Longer acting corticosteroids last 3 -4 days or more

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13
Q

Common side effects of corticosteroids

A
  1. Suppresses immune system – risk for infection
  2. Increased appetite
  3. Weight gain/change in fat metabolism (moon face and buffalo hump)
  4. Pulls calcium out of bones - osteoporosis
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14
Q

Function of the pancreas

A
  1. Secretes digestive enzymes

2. Secretes two hormones that control the metabolism of glucose (insulin and glucagon)

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15
Q

Pancreatic hormones - Glucagon functions

A

Glucagon: Hormone that retrieves stored glucose (glycogen) from the liver and converts it back to glucose (glycogenolysis). Made by the alpha cells of the islet of lagerhands in the pancreas.

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16
Q

Pancreatic hormones - Insulin

A
  1. Insulin: hormone that assists glucose to enter the cell for use as energy. Takes excess glucose from the blood and stores it in the liver. Made by the beta cells of the islets of Langerhans.
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17
Q

Diabtetes Mellitus - Type 1

A

Formerly known as insulin dependent diabetes. 10%.

  • Cause: Lack of insulin production or production of defective insulin. This person must have insulin injections to live!!!
  • Cannot store excess glucose –> glucose lost in urine –> damages the kidney. Excess glucose is also destructive of the retina and sensory nerves.
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18
Q

Onset & S/S on onset of Type 1 diabetes

A

Onset –> Sudden symptoms in childhood or adolescence

S/S on onset (signs of hyperglycemia) –>
- Polydipsia, polyphagia, polyuria

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19
Q

Profile of patient with type 1 diabetes

A
  1. Thin. Cannot gain weight.
  2. Episodes of hypoglycemia
  3. Is prone to complications from blood sugar too high (diabetic acidosis)
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20
Q

S/S of diabetic ketoacidosis (DKA)

A

Confusion, diaphoresis, irritability, dizziness, Blood sugar over 250, electrolyte imbalances, dehydration –> coma

21
Q

Type 2 diabetes & what its caused by

A

Formerly known as Non-Insulin dependent diabetes -NIDDM. 90% of all DM.

  • Caused by resistance to insulin and/or reduction in insulin production
  • This person may not need insulin injections
  • May be able to take an oral medication to stimulate the pancreas or decrease resistance to insulin
  • But may eventually need insulin –> During times of stress or illness –> or with advanced age/disease.
22
Q

Onset of type 2 DM

A

Slow onset of symptoms during adulthood (40s - 60s). Onset of 3 P’s but very slowly

23
Q

Profile of patient with type 2 DM

A
  1. Often obese
  2. Has hyperglycemia
  3. Symptoms start slowly
  4. Rarely has hypoglycemia
  5. Not prone to complicaitons from hyperglycemia untill glucose is over 600
  6. Many go undiagnosed (50%)
24
Q

Normal blood sugar level

A

70 - 130 mg/dL (ADA guidelines). Better for understanding patient’s insulin needs for the moment.

25
Q

Normal HGB A1C level is

A

<= 6.5%. Better for understanding long term effects of insulin.

26
Q

Insulin and mechanism of action

A
  • most insulin is a synthetic copy of human insulin (DNA tech) = Humulin
  • Formerly taken from pigs and cows
  • Action: Controls the storage and metabolism of carbohydrates, fats, and proteins.
    • Binding to receptor sites on cellular plasma membranes esp. liver, muscle, and fat tissue
27
Q

Goals of insulin therapy

A
  1. Replace insulin to keep glucose levels as normal as possible
  2. Avoid complications of too much or too little insulin
28
Q

Insulin administration

A
  1. Insulin must be injected to work – it is destroyed by HCL in the stomach
  2. No oral insulin
  3. IV, SQ, & via insulin pump
29
Q

4 types of insulin - Lispro or Spart or Humalog

A
  • Extremely fast acting
  • Pink top
  • Says lispro or aspart (humalog)
  • Immediate onset = 15 min
  • Peak = 1 - 2 hrs
  • Duration = 3 - 5 hrs
30
Q

4 types of insulin - Regular

A
  • Short acting. Has “R” on the bottle w/ orange top
  • Onset = 30 - 60 min
  • Peak = 2 -4 hrs
  • Duration = 6 - 10 hrs
31
Q

4 types of insulin - NPH

A
  • Intermediate acting. Has “N” + orange top + cloudy solution.
  • Onset = 1 - 2 hrs
  • Peak = 4 - 8 hrs
  • Duration = 10 - 18 hrs
32
Q

4 types of insulin - Glargine/Detemir

A
  • Long acting. Taller bottle/Clear liquid.
  • Onset = 1 - 2 hrs
  • Peak = none. Its steady.
  • Duration = 24 hrs
  • Usually once a day at bedtime
33
Q

Know the glucose infusion rate x per hours chart

A

It just shows how the different types of insulin peak and how long they last q

34
Q

Inhaled Insulin med name & time details

A
  • Afreeza
  • Speed = rapid acting insulin
  • Onset = rapid onset of action administered within 20 minutes of meals
  • Peak = 12 - 15 minutes
  • Duration = 2 - 3 hours
35
Q

Inhaled insulin precautions

A
  • Type II diabetics must be given in conjunction with long-acting insulins or oral diabetic agents
  • Precautions = Hypoglycemia, Cough, throat pain
  • Black box warning: Risk for acute bronchospasms…therefore not for use in smokers or chronic lung diseases
36
Q

Oral anti-diabetic agents – Many actions (4) depending on type

A
  1. Stimulates insulin secretion from the beta cells of the pancreas
  2. Helps with insulin resistance
  3. Enhances the action of existing insulin in the muscle, liver, and fat tissue (increased uptake)
  4. Prevent the liver from breaking down the existing insulin as fast
    - -> Cannot be used exclusively for type I - not the same as “oral insulin”
    - -> 6 types but we’ll focus on three in this class
37
Q

Sulfonylureas (earliest meds made) – Actions (3), S/Em, Med

A
  1. Stimulates inclusion production in beta cells
  2. Increases the action of existing insulin
  3. Prevents the liver from destroying insulin
    S/E: Can cause hyperglycemia
    Med to remember: glucotrol (Glipizide)
38
Q

Biguanides - First line medication for the treatment of Type II diabetes with lifestyle changes

A

Action: Decreases the production of glucose. But won’t cause hypoglycemia.
–> Med: Metformin

39
Q

Thiazolidinediones (Glitazones) – Also known as insulin sensitizing medications (Just the actions –>)

A
  1. Decrease insulin resistance by enhancing receptor sensitivity
  2. Stimulates peripheral glucose uptake and storage in the skeletal muscles
  3. Inhibits glucose production by the liver
40
Q

Thiazolidinediones (Glitazones) – Med to remember

A

Actos (dioglitazone) = only type still on the market

Concerns: increased risk fo heart failure and very expensive

41
Q

Nursing considerations for giving medications to diabetic patients

A
  1. Patient needs regular glucose monitoring
  2. Avoid switching brand of insulin
  3. Diet and exercise as important medications (consult a dietician)
  4. Recognize the signs and symptoms of hypoglycemia and hyperglycemia
  5. Sliding scales are common and individualized
42
Q

S/S of Hypoglycemia

A

Diaphoresis, Lightheaded, Irritable, HA, Tremor, Anxiety, blurred vision, pallor, difficulty concentrating, weakness

43
Q

S/S of Hyperglycemia

A

Polydipsia, polyphagia, polyuria, dehydration, fruity breath, dry mouth, weight loss, dry skin, N/V

44
Q

Quick fixes for insulin reactions (Hypoglycemia) – Conscious patient

A

3 glucose tabs, 4 oz of OJ, 6 -8 lifesavers, 1 small tube of cake frosting, 6 oz of non diet soda, 6 - 8 oz of milk, 3 graham crackers

45
Q

Quick fixes for insulin reactions (Hypoglycemia) – unconscious patient

A

50 mL of D50 IV or Glucagon IM, or SQ (if no IV in place)

46
Q

Additional Anti-diabetic meds – Dapafliflozin (Farxiga)

A

Class: Sodium glucose cotransporter inhibitor
Action: Blocks reabsorption of glucose in the renal tubules
– Oral 5 - 10 daily

47
Q

Additional Anti-diabetic meds – Sitagliptin (Januvia)

A

Class: Dipeptryl peptidase-IV inhibitors
Action: Increases incretins which help control blood sugar by increasing insulin release after a meal
– Oral 25 - 100 daily

48
Q

Additional Anti-diabetic meds – Dulaglutide (Trulicity)

A

Class: incretin mimetics
Action: Activates (glucagon-like peptide) GLP-1 receptor that leads to insulin release
– Injection 0.75 - 1.5 mg weekly

NRSG 213 (9 decks)

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