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Thyroid Gland
Butterfly-shaped endocrine gland
Located in the midline anterior neck, anterior to the trachea
requires dietary iodine for hormone synthesis (T3, T$)
Thyroid hormone
Tetraiodothyronine (T4)
Inactive; converted to T3
Trilodothyronine
Active; more potent
Hormone regulation
Controlled by TSH (thyroid-stimulating hormone) from the anterior pituitary
Negative feedback loop with T3/T4 levels
Physiologic effects
regulates metabolism
increases heart rate and cardiac output
affects body temperature
supports growth and development
Clinical correlations
Hypothyroidism: weight gain, fatigue, cold intolerance, bradycardia
Hyperthyroidism: weight loss, heat intolerance, tachycardia
Iodine deficiency→ goiter
Hypothyroidism
Prevalence:
most common in women >50 and elderly
Pathophysiolgy
low T3/T4 → slow metabolism
Clinical Manifestations
fatigue, lethargy
Bradycardia
Weight gain
Constipation
Dry skin/ hair loss
cold tolerancy
high cholesterol
Complication
myxedema coma (severe, life-threatening hypothyroidism)
Treatment
Thyroid hormone replacement (levothyroxine)
Hyperthyroidism
Prevalence
More common in women, typically ages 20–40
Often caused by Graves Disease
Pathophysiology
High T3/T4 → increased metabolic rate
Clinical Manifestations
Nervousness, anxiety
Tachycardia
Weight loss
Heat intolerance
Diarrhea
Warm, moist skin
Hair thinning
↓ Cholesterol
Complication
Thyroid storm (severe, life-threatening hyperthyroidism)
Treatment
Antithyroid medications
Radioactive iodine
Surgery (if indicated)
Levothyroxine (Drug Classification: Thyroid Hormones)
Prototype: Levothyroxine
Indications: Replacement hormone therapy for patients with hypothyroidism
MOA: Acts as a synthetic form of thyroid hormones, increasing metabolism of all nutrients and promoting cell growth and protein synthesis
Side effects: When dose is too high, hyperthyroidism symptoms, including:
Anxiety
GI upset
Sweating
Weight Loss
Heat intolerance
Nursing considerations: Monitor Thyroid hormones
Patient teaching: Take on an empty stomach before breakfast with a full glass of water. This is a lifelong treatment. Full effects may not be felt for weeks. Report chest pain, heart palpitations, dizziness, or excess weight loss
Methimazole/Propylthiouracil Drug claasification: Antithyroid agents
Prototypes:Methimazole/Propylthiouracil
Indications: treatment for hyperthyroidism often used to control hyperthyroidism in preparation for thyroidectomy or radioactive iodine therapy.
Mechanism of Action: Blocks the synthesis of thyroid hormones.
Side Effects: GI upset, rash. When dose is too high, the patient will have symptoms of hypothyroidism, including:
Lethargy and depression
Weight gain
Cold intolerance
Bradycardia
Adverse Effects: Hepatotoxicity, agranulocytosis (sore throat, fever, signs of infection), and methimazole is teratogenic and PTU would be used in early pregnancy.
Nursing Considerations: Monitor CBC and liver function tests. Assess for agranulocytosis. If patient has sore throat and fever, stop the medication and call the provider.
Patient Teaching: Monitor weight and notify health care provider of significant changes, report sore throat, fever, and laboratory tests will be done frequently. Report palpitations, nervousness, and insomnia (thyroid storm/thyrotoxicosis).
Drug Classification: Strong Iodine Solution
Prototypes: strong iodine solution
Indications: Short term treatment for hyperthyroidism often used to control hyperthyroidism, thyrotoxicosis
(thyroid storm), and in preparation for thyroidectomy.
• Mechanism of Action: Blocks release of thyroid hormones. Decreases thyroid gland vascularity and size.
• Side Effects: GI upset, hypothyroidism (prolonged use), iodism. Hypersensitivity (rash and pruritic)
• Iodism (eye-oh-diz-um)
• Metallic taste, excessive salivation
• Stomatitis
• Severe GI upset
• Nursing Considerations: Short term use, monitor thyroid function tests, and assess for signs of iodism.
• Patient Teaching: Mix solution with juice or milk to improve bitter taste. Use a straw and rinse mouth. Report
signs of iodism
The role of the Pancreas in Glucose Regulation
Endocrine organ regulating blood glucose
Islets of Langerrhans
β (Beta) cells → insulin → ↓ blood glucose
α (alpha) cells → glucagon → ↑ blood glucose
Insulin released during a “fed” state
Glucagon released during a fasting state
Diabetes Mellitus
Type 1: β-cell destruction → no insulin
Type 2: insulin resistance + relative deficiency
Pharmacology Basics related to the Pancreas:
Insulin meds replace pancreatic insulin
Oral agents:
• ↑ insulin secretion
• ↑ insulin sensitivity
• ↓ hepatic glucose production
Role of the Liver in Glucose Regulation
Primary glucose storage organ
Stores glucose as glycogen
Maintains normal blood glucose between meals
Key Liver Functions
Glycogenesis: stores glucose as glycogen (after meals)
Glycogenolysis: breaks down glycogen → releases glucose (fasting)
Gluconeogenesis: produces glucose from non-carbohydrate sources
Hormonal Control
insulin: promotes glycogen storage (↓ blood glucose)
Glucagon: stimulates glucose release (↑ blood glucose)
Epinephrine: rapid glucose release during stress
Clinical Relevance
Liver is the main target of glucagon
impaired liver function → poor glucose control
Alcohol use increases risk of hypoglycemia
• Memory: Liver = glucose bank
The Hormones: Insulin
Hormone produced by β cells of the pancreas
Lowers blood glucose by acting like a key — it triggers GLUT4 (insulin-dependent transport protein) to move to the cell membrane, allowing glucose to enter the cell by facilitated diffusion.
Promotes:
Glucose uptake into cells
Glycogen synthesis (liver, muscle)
Fat and protein storage
Naturally released in patients with healthy glucose regulation in response to high blood glucose
Clinical Use
Required for Type 1 diabetes
Used in Type 2 diabetes when oral agents are insufficient
Nursing Focus
Match insulin administration with meals
Monitor for hypoglycemia
Know onset, peak, duration
Check blood glucose before administration
• Think: Insulin = “puts glucose into cells”
The Hormones: Glucagon
Hormone produced by α cells of the pancreas
Raises blood glucose by stimulating glycogen breakdown and glucose production in the liver.
Stimulates:
Glycogen breakdown (glycogenolysis)
Glucose production (gluconeogenesis)
Released during fasting or hypoglycemia
Clinical Use
Emergency treatment for severe hypoglycemia
Used when patient is hypoglycemic unconscious or unable to swallow
• Think: Glucagon = “emergency sugar release
The Hormones: Glycogen
Stored form of glucose
Found mainly in the liver and skeletal muscle
Allows rapid glucose availability
Key Functions
Liver glycogen: maintains blood glucose between meals
Muscle glycogen: used for local energy only (not released into blood)
Hormonal Control
Insulin: promotes glycogen storage (glycogenesis)
Glucagon: stimulates glycogen breakdown (glycogenolysis)
Epinephrine: rapid glycogen breakdown during stress
Clinical Relevance
Limited storage → depleted within ~24 hours of fasting
Liver disease → impaired glucose regulation
Essential for hypoglycemia prevention
Memory: Glycogen = stored glucose
Laboratory Findings for Glucose Imbalances
Hemoglobin A1C (HbA1c)
• Reflects average blood glucose over ~3 months
• Not affected by daily fluctuations
• Used to diagnose and monitor diabetes
• Reflects long-term control
A1C Values
• Normal: < 5.7%
• Prediabetes: 5.7–6.4%
• Diabetes: ≥ 6.5%
Blood Glucose Values
Fasting Blood Glucose
• Normal: 70–99 mg/dL
• Prediabetes: 100–125 mg/dL
• Diabetes: ≥ 126 mg/dL
Random Blood Glucose
• Normal: < 140 mg/dL
• Diabetes likely: ≥ 200 mg/dL with symptoms
Blood Glucose Imbalance: Hypoglycemia
Blood glucose < 70 mg/dL
Cause: Too much insulin/meds, missed meals, exercise, alcohol
Clinical Manifestations:
• Shaky, sweaty
• Tachycardia
• Hunger
• Confusion
• Clammy skin
• Seizures / Decreased Level of Consciousness (LOC)
(severe)
Treatment
• Conscious → 15 g fast sugar
• Recheck in 15 min
• Unconscious → Glucagon IM/SQ or IV dextrose
Nursing Considerations
• Check blood glucose before administering insulin
• Give carbs first, protein later
• Memory: Cold and clammy need some candy!
Blood Glucose Imbalance: Hyperglycemia
High blood glucose, Usually > 180 mg/dL
Common in diabetes
Causes
• Too little insulin or meds
• Illness, infection, stress
• Excess carbohydrate intake
• Missed doses
Clinical Manifestations
• Polyuria, Polydipsia, Polyphagia
• Warm, dry skin
• Fatigue
• Blurred vision
• Severe form: Fruity breath (Linked to: Diabetic ketoacidosis [DKA])
Treatment
• Insulin
• IV fluids
• Monitor glucose & electrolytes
Nursing Pearls
• Check blood glucose before giving insulin
• Watch for diabetic emergencies: DKA or Hyperosmolar Hyperglycemic State (HHS)
• Treat early to prevent dehydration
• Hyper = hot and dry, may be high!
Type 1 Diabetes
• Autoimmune destruction of β cells
• No insulin production
• Usually, onset in childhood or adolescence
• Requires lifelong insulin
Key Features
• Prone to hypoglycemia
• High risk for DKA
• Weight loss, polyuria, polydipsia, polyphagia
Labs
• ↑ Blood glucose
• ↓ or absent insulin
• ↑ Ketones (with DKA)
Nursing Focus
• Never hold insulin
• Match insulin to meals, patient will often wear insulin pumps
and glucose monitoring devices
• Monitor for hypoglycemia
• Sick-day management is critical
• Teach management skills to prevent long-term complications
• Type 1 = makes no insulin naturally
Type 2 Diabetes
Insulin resistance + relative insulin deficiency
• Insulin present, but cells don’t respond effectively
• Usually onset in adulthood (increasing in youth)
• Strongly associated with obesity, inactivity, genetics
Key Features
•Gradual onset
•Hyperglycemia common
•Lower risk of DKA than Type 1
•High risk for HHS
Laboratory findings
•↑ Blood glucose
•Normal or ↑ insulin early, ↓ later
•Minimal or no ketones
• If not within long-term control, ↑ A1C
Treatment
• Lifestyle modification
• Oral antidiabetic agents
• Non-insulin injectables
• Insulin if needed
Nursing Focus
• Monitor blood glucose & A1C
• Assess for complications
• Encourage diet, exercise, weight loss
• Teach medication adherence to prevent long-term complications
Type 2 = insulin resistance
Medication Classification": Biguanides (Metformin)
Prototype: Metformin
Indications: Oral medication for the treatment of Type 2 Diabetes may be used with diet, insulin, or sulfonylurea oral hypoglycemic medications.
Mechanism of Action: Decrease glucose production in the liver, decrease intestinal
absorption of glucose, increase the insulin sensitivity of cell receptors.
Side Effects: GI Upset, metallic taste, lactic acidosis.
Adverse Effects: Lactic acidosis (nausea, vomiting, fatigue, muscle cramps, abdominal pain, tachypnea, and hypotension)
Nursing Considerations: Hold metformin before procedures that require contrast dye and for 48 hours after the procedure related to kidney damage. Monitor for signs of lactic acidosis. Not for patients with type 1 diabetes.
Patient teaching: Take with a meal. Do not consume alcohol. Follow prescribed diet and exercise. Report signs of lactic acidosis. Inform healthcare providers of medication before diagnostic procedures or surgery.
Medication Classification: Sulfonylureas (Glipizide/glyburide)
Prototype: Glipizide and Glyburide
Indications: Oral medication for the treatment of Type 2 Diabetes may be used with diet, insulin, or biguanide oral hypoglycemic medications.
Mechanism of Action: Lowers blood sugar by stimulating the release of insulin from the pancreas and increasing the sensitivity to insulin at receptor sites. May also decrease hepatic glucose production.
Contraindication: Use caution in patients with sulfa allergy (possible cross-sensitivity).
Side Effects: Photosensitivity, GI Upset.
Adverse Effects: Hypoglycemia
Nursing Considerations: Monitor glucose levels and A1C. Liver and renal studies. Not for patients with type 1 diabetes.
Patient teaching: Take 30 minutes before a meal. Do not consume alcohol. Follow prescribed diet and exercise. Report signs of hypoglycemia. Wear sunscreen
Medication Classification: Pancreatic Antihypoglycemic (glucagon)
Prototype: glucagon
Indications: Injectable medication for the acute management of severe hypoglycemia.
Mechanism of Action: Stimulates hepatic production of glucose from glycogen stores.
Side Effects: Increased heart rate and blood pressure, nausea, and vomiting.
Nursing Considerations: Hypoglycemia is most prevalent at the peak time of antidiabetic agents. Must monitor patient’s glucose after administration.
Patient teaching: Teach family members how to administer and if unconscious place patient in side-lying recovery position
Insulin Basics
Required for Type 1 diabetes mellitus , Used in Type 2 diabetes mellitus, if needed
Works in the same manner as naturally occurring insulin
Four categories of insulin that vary in onset, peak, and duration
Administration
High-risk medication – two nurses complete independent check of dose, type, and timing
Subcutaneous (most common)
IV: Regular insulin only
Use insulin syringes ONLY
Do not substitute with TB syringes
Injection Sites
Abdomen (preferred, fastest absorption)
Also, Upper arm, Thigh, Buttocks
Rotate sites
Prevents lipohypertrophy (fatty lumps in tissue)
Storage
Unopened insulin: refrigerate
Opened insulin: can be at room temperature for up to 28 days (most manufacturers)
Do not freeze
Protect from heat and sunlight
Check expiration date and appearance
Clear = should be clear
Cloudy = gently roll, do not shake
Major Risk
Hypoglycemia
Nursing Priorities
Check blood glucose before giving
Match insulin to meals
Know onset, peak, duration3
Insulin Categories and Information
Insulin Classifications (By Action)
Rapid-acting: Lispro
Short-acting: Regular
intermediate-acting: NPH (Neutral Protamine Hagedorn)
Long-acting: Glargine
Pre-mixed insulin is not covered in this course.
Key Concept
All insulins have the same mechanism of action
They differ by onset, peak, and duration
Insulin Timing Terms
Onset: time until insulin begins lowering blood glucose
Peak: time of maximum glucose-lowering effect
Duration: total time insulin continues to work
Basal vs Bolus Insulin
Basal insulin
Long-acting
Provides continuous background coverage
Controls glucose between meals and overnight
Bolus insulin
Rapid- or short-acting
Given with meals
Controls postprandial glucose spikes
Medication Classification: Rapid Acting Insulin (Insulin Lispro)
Prototype: insulin lispro (liss-pro)
Indications: Given as a subcutaneous injection for the treatment of diabetes mellitus and work rapidly to lower blood sugar. Used as a corrective (bolus) insulin due to rapid onset.
Onset: 5 – 15 minutes
Peak: 1 – 2 hours
Duration: 3 – 5 hours
Mechanism of Action: Lowers blood glucose by stimulating glucose uptake in skeletal muscle and fat.
Side Effects: Injection site redness and swelling, small bruise at injection site.
Adverse Effects: hypoglycemia, rebound hyperglycemia (Somogyi effect)
Nursing Considerations: Hypoglycemia is most prevalent at the peak time of antidiabetic agents. Check blood glucose before administration. Never give rapid acting insulin without food available or if patient cannot tolerate food (nausea and vomiting).
Patient teaching: Sick days require close monitoring. Recognize signs and symptoms ofhyper and hypoglycemia and be aware of self-treatment. Long-term effects of poor glycemic control include neuropathy, nephropathy, retinopathy, stroke, and myocardial infarctions
Medication Classification: Short Acting Insulin (regular insulin)
Prototype: regular (reg-yu-ler) insulin
Indications: Given as a subcutaneous injection for the treatment of diabetes mellitus to lower blood sugar. Used as a corrective (bolus) insulin due to fast onset.
Onset: 30 – 60 minutes
Peak: 90 - 120 minutes
Duration: 6 – 8 hours
Mechanism of Action: Lowers blood glucose by stimulating glucose uptake in skeletal muscle and fat.
Side Effects: Injection site redness and swelling, small bruise at injection site.
Adverse Effects: hypoglycemia, rebound hyperglycemia (Somogyi effect)
Nursing Considerations: This is the only insulin that can be administered intravenous (emergencies only). Hypoglycemia is most prevalent at the peak time of antidiabetic agents. Check blood glucose before administration.
Patient teaching: Sick days require close monitoring. Recognize signs and symptoms of hyper and hypoglycemia and be aware of self-treatment. Long-term effects of poor glycemic control include neuropathy, nephropathy, retinopathy, stroke, and myocardial infarctions
Medication Classification: Intermediate Acting Insulin (NPH)
Prototype: Neutral protamine Hagedorn [NPH] insulin
Indications: Given as a subcutaneous injection for the treatment of diabetes mellitus to lower blood sugar. Used to control glucose over time (basal insulin) and not corrective (bolus).
Onset: 1 – 4 hours
Peak: 4 – 8 hours
Duration: 12 - 18 hours
Mechanism of Action: Lowers blood glucose by stimulating glucose uptake in skeletal muscle and fat.
Side Effects: Injection site redness and swelling, small bruise at injection site.
Adverse Effects: hypoglycemia, rebound hyperglycemia (Somogyi effect)
Nursing Considerations: Hypoglycemia is most prevalent at the peak time of antidiabetic agents. Check blood glucose before administration.
Patient teaching: Sick days require close monitoring. Recognize signs and symptoms of hyper and hypoglycemia and be aware of self-treatment. Long-term effects of poor glycemic control include neuropathy, nephropathy, retinopathy, stroke, and myocardial infarctions
Medication Classification: Long-Acting Insulin (glargine)
Prototype: Glargine
Indications: Given as a subcutaneous injection for the treatment of diabetes mellitus to lower blood sugar. Used to control glucose over time (basal insulin) and not corrective (bolus).
Onset: 1 – 2 hours
Peak: none
Duration: ~24 hours
Mechanism of Action: Lowers blood glucose by stimulating glucose uptake in skeletal muscle and fat.
Side Effects: Injection site redness and swelling, small bruise at injection site.
Adverse Effects: hypoglycemia, rebound hyperglycemia (Somogyi effect)
Nursing Considerations: Hypoglycemia is most prevalent at the peak time of antidiabetic agents. Check blood glucose before administration. Cannot be mixed.
Patient teaching: Sick days require close monitoring. Recognize signs and symptoms of hyper and hypoglycemia and be aware of self-treatment. Long-term effects of poor glycemic control include neuropathy, nephropathy, retinopathy, stroke, and myocardial infarctions
Diabetes and Medication Interactions
Statins (HMG-CoA Reductase Inhibitors)r
↓ LDL, ↓ CV morbidity & mortality
Slight ↑ blood glucose
Benefit > risk in patients with diabetes
↓ MI and stroke risk
Corticosteroids - Endogenous (stress) or exogenous (medications)
↑ Hepatic glucose production
↑ Insulin resistance
Can cause significant hyperglycemia
Thiazide Diuretics - Used for hypertension
↑ Blood glucose (dose-dependent)
Common in patients with diabetes
Beta-Blockers
May mask hypoglycemia symptoms (tachycardia, tremor)
Non-selective beta blockers more than selective beta blockers
Use with caution in insulin-treated patients
Nursing Consideration
If blood glucose worsens → review non-diabetes medication list