Thyroid Diseases Flashcards
Consider Possibility of Endocrine / Thyroid Changes When Assessing the Older Adult
Normal aging
- Decreased hormone production/secretion
- Altered hormone metabolism/activity
- Decreased target tissue response
Alteration in circadian rhythm
Changes of aging can mimic endocrine disorders
Hypothyroid symptoms of fatigue, constipation, mental impairment often missed because of sole attribution to aging
Thyroid Stimulating Hormone (TSH)
Anterior pituitary hormone
Stimulates thyroid gland to release hormones
2 – 10 U / mL
Serum levels
High = Defect within thyroid
Low = Defect in pituitary or hypothalamus
Thyroid Hormones
Regulate:
Energy metabolism
Growth & development
Dietary iodine necessary for synthesis
Triiodothyronine (T3)
More potent; greater metabolic effect
20 – 50 years: 70 – 205 ng/dL
> 50 years: 40 – 180 ng/dL
Thyroxine (T4)
Most abundant
Female 5 – 12 mcg/dL
Male 4 – 12 mcg/dL
Thyroid Antibodies
Anti-thyroglobulin antibody (Thyroid auto-antibody)
Marker for autoimmune thyroiditis
Normal: < 116 IU / mL
Anti-thyroid peroxidase antibody (Anti-TPO)
Normal: < 9 IU / mL
Increased levels:
Hashimoto’s thyroiditis
Thyrotoxicosis
Hypothyroidism
Thyroid cancer
Myxedema
Rheumatoid arthritis & collagen disease
Pernicious anemia
HYPERthyroidism
Sustained increase: Synthesis & release of thyroid hormones by thyroid gland
Occurs more often in women between 20 - 40 years
Grave’s Disease most common form
Other causes
Toxic nodular goiter
Thyroiditis
Excess iodine intake
Pituitary tumors
Thyroid cancer
Subclinical
TSH below 0.4 m IU/L
Normal T3 & T4 levels
Overt
Low or undetectable TSH
Increased T3 & T4 levels
Symptoms may or may not be present
Thyrotoxicosis
Physiologic effects / syndrome of hyper-metabolism
Results from increased circulating levels of T3, T4 or both
Hyperthyroidism & thyrotoxicosis usually occur together
HYPERthyroidism: Diagnostics
Decreased TSH (less than 0.4mU/L)
Increased free Thyroxine (free T4)
Total T3 & T4 (not definitive)
Radioactive iodine uptake (RAIU)
- —Distinguishes Graves’ disease from other forms of thyroiditis
Diagnostic Findings
Increased T3 & T4
Increased T3 resin uptake
Decreased or undetectable TSH
Chest x-ray showing enlarged heart
ECG: Tachycardia
Graves’ Disease
Autoimmune disease
—-Diffuse thyroid enlargement
—–Excess thyroid hormone secretion
Causative factors interact with genetic factors
Patients with female natal sex 5 times more likely to develop than those with male natal sex
Clinical Manifestations of Grave’s Disease
Effect of thyroid hormone excess
Increased metabolism
Increased tissue sensitivity to SNS stimulation
Goiter
Inspection, Palpation
Auscultation: Bruits
Ophthalmopathy; Abnormal eye appearance or function
Exophthalmos
Increased fat deposits & fluid
Eyeballs forced outward
Cardiovascular system
- Graves Disease
Systolic hypertension
Bounding, rapid pulse; palpitations
Increased cardiac output
Cardiac hypertrophy
Systolic murmurs
Dysrhythmias
Angina
Respiratory system
- Graves disease
Dyspnea on mild exertion
Increased respiratory rate
GI system
- Graves disease
Increased appetite, thirst
Weight loss
Diarrhea
Splenomegaly
Hepatomegaly
Skin
- Graves disease
Warm, smooth, moist skin
Thin, brittle nails
Hair loss
Fine, silky hair
Premature graying in patients with natal male sex
Diaphoresis
Vitiligo
Acropachy; Soft-tissue swelling & clubbing of fingers; palmar erythema
Musculoskeletal system
- Graves disease
Fatigue
Weakness
Proximal muscle wasting
Dependent edema
Osteoporosis
Intolerance to heat
Elevated basal temperature
Lid lag, stare
Eyelid retraction
Rapid speech
Nervous system
- Graves disease
Hyperactive deep tendon reflexes
Nervousness, fine tremors
Insomnia
Difficulty focusing eyes
Lability of mood, delirium
Lack of ability to concentrate
Stupor, coma
Reproductive system
- Graves disease
Menstrual irregularities
Amenorrhea
Decreased libido
Decreased fertility
Impotence & gynecomastia in patients with natal male sex
Acute Thyrotoxicosis Thyrotoxic Crisis OR “Thyroid Storm”)
Excessive amounts of hormones released
Life-threatening emergency
Death rare when treatment started early
Results from stressors
Thyroidectomy patients at risk
Manifestations
Severe tachycardia, heart failure
Shock (Cardiogenic)
Hyperthermia (up to 106° F [41.1° C])
Agitation
Seizures
Abdominal pain, vomiting, diarrhea
Delirium, coma
Acute Thyrotoxicosis Thyrotoxic Crisis OR “Thyroid Storm”)
Excessive amounts of hormones released
Life-threatening emergency
Death rare when treatment started early
Results from stressors
Thyroidectomy patients at risk
Manifestations
Severe tachycardia, heart failure
Shock (Cardiogenic)
Hyperthermia (up to 106° F [41.1° C])
Agitation
Seizures
Abdominal pain, vomiting, diarrhea
Delirium, coma
Acute Thyrotoxicosis Thyrotoxic Crisis OR “Thyroid Storm”)
- interprofessional care
Therapeutic goals
Block adverse effects of thyroid hormones
Suppress hormone oversecretion
Prevent complications
Three primary treatment options
Anti-thyroid medications
Radioactive iodine therapy (RAI)
Surgery
Evaluation
Relief / control of symptoms
No serious complications r/t disease or treatment
Adhere to therapeutic plan
Maintain nutritional balance
Acute Thyrotoxicosis Thyrotoxic Crisis OR “Thyroid Storm”)
- medication therapy
Useful in treatment of thyrotoxic states
Not considered curative
Anti-thyroid medications
Iodine
β-Adrenergic blockers
Anti-thyroid Medications
Propylthiouracil (PTU)
Methimazole (Tapazole)
Daily dose usually divided in three, every 8-hours
Initial daily doses:
15 mg (mild)
30 - 40 mg (moderate)
60 mg (severe)
Maintenance: 5 - 15 mg daily
Inhibit thyroid hormone synthesis
Improvement 1 - 2 weeks
Results 4 - 8 weeks
Therapy for 6 - 15 months