MED. SURG. STUDY GUIDE – TEST 3 LATEST PAPER 2021/2022

MED. SURG. STUDY GUIDE – TEST 3
E. Thyroid disorders: hypo/ hyper, medications, labs, and treatments – Surgery,
radioactive iodine.

 Thyroid gland
o Principal actions te
 Stimulation of energy use
 Stimulation of the heart
 Promotion of growth and development
 Thyroid gland is all about metabolism
o Hormones secreted
 T – 4 thyroxine
 T – 3 triiodothyronine
 T3, t4 influence heart and increased levels can causes palpitaions
 Calcitonin
 Works with the parathyroid gland to manage calcium levels
 Iodine is necessary for production of thyroid hormones
 Low iodine in diet can result in hypertrophy of gland – simple
goiter
o The goiter itself doesn’t tell if the patient has hyper or
hypothyroidism
 Physiological Role of the Thyroid Hormones
 They have a diffuse effect and do not seem to have any specific
target organ
o Negative Biofeedback controls the thyroid system
 When too much of the hormone is present, biofeedback slows down the
release
 When too little, the release is sped up
 There are 3 levels of Neg. biofeedback
 When T3, T4 are low:
o 1. Hypothalamus recognizes low levels, releases TRH
o 2. TRH stimulates the anterior pituitary gland to release
TSH
o 3. TSH stimulates the thyroid gland to increase production
of T3, T4
 When T3, T4 are high:
o 1. Hypothalamus recognizes high levels, stops or slows
down release of TRH
o 2. Anterior pituitary will then stop/slow down release of
TSH
o 3. Thyroid will then stop/ slow down release of T3, T4
 Hypothyroidism
o Not enough production/release of T3, T4
o Slow metabolic rate
o More common in women than men
o Deficiency of thyroid hormone causes:
 Myxedema: face swelling

,MED. SURG. STUDY GUIDE – TEST 3
 Cretinism
 Occurs in children and can lead to mental growth deficiencies
o Pathology
 Primary hypothyroidism
 Caused by destruction of thyroid tissue or defective hormone
synthesis
 Most common cause in U.S is atrophy pf thyroid gland
o Atrophy occur after autoimmune disease such and
hyperthyroidism like graves and hasimoto
 Secondary hypothyroidism
 Caused by pituitary or hypothalamic dysfunction (↓ TSH or TRH)
o Etiology
 Iodine deficiency – most common cause worldwide
 Atrophy of the gland
 Treatment for hyperthyroidism
 Drugs
 amiodarone (Cordarone) (which contains iodine) and lithium
(which blocks hormone production)
 Cretinism if occurs in infancy
 Caused by thyroid hormone deficiencies during fetal or early
neonatal life.
 All infants in the United States are screened for decreased thyroid
function at birth.
o Clinical Manifestations
 Regardless of the cause, hypothyroidism has systemic effects
characterized by a slowing of body processes.
 Manifestations vary depending on the severity and the duration of thyroid
deficiency, as well as the patient’s age at the onset of the deficiency.
 The onset of symptoms may occur over months to years unless
hypothyroidism occurs after a thyroidectomy, thyroid ablation, or during
treatment with anti-thyroid drugs.
 Cardiovascular system
 ↓ Cardiac contractility and output
 Angina, heart failure, myocardial infarction
 Anemia
o Erythropoietin levels may be low or normal. Because the
metabolic rate is lower, oxygen demand is reduced.
 Cobalamin, iron, folate deficiencies
o May cause patient to bruise easily
 ↑ Serum cholesterol and triglycerides
o Can cause coronary atherosclerosis
 Respiratory system
 Low exercise tolerance
 Shortness of breath on exertion
 Myxedema

,MED. SURG. STUDY GUIDE – TEST 3
o Physical swelling of skin and subcutaneous tissue
o This edema causes puffiness, facial and periorbital edema,
and a masklike affect.
o Individuals with hypothyroidism may describe an altered
self-image related to their disabilities and altered
appearance.
o Myxedema coma – Medical emergency
 Impaired consciousness or come
 Precipitated by infection, drugs, cold, trauma
 Characteristics are subnormal temperature,
hypotension, hypoventilation
 Cardiovascular collapse
 results from hypoventilation, hyponatremia,
hypoglycemia, and lactic acidosis
 Treat with IV thyroid hormone
o Medications and Treatment
 Replacement therapy
 Levothyroxine (T4)(Synthroid): Highly protein bound, drug of
choice
o Each different strength of the medication is represented by
a specific color of pill
o Half-life 7 days
o Uses
 All forms of hypothyroidism
o When thyroid hormone therapy is initiated, it is important
that the initial dosages are low to avoid increases in resting
heart rate and blood pressure.
o Interactions: Coumadin, Insulin, Digoxin
o Pharmacokinetics: Best taken on empty stomach
o Adverse effects
 Tachycardia
 Angina
 Tremors
o Must use caution
 Overdosing can occur if the dose is too high
 Symptoms would be similar to
hyperthyroidism
 Underdosing can also occur if not enough med
 Symptoms would be similar to
hyperthyroidism
 Liothyronine (T3)(Cytomel
o Labs
 Low T –3, T-4
 High TSH with primary

, MED. SURG. STUDY GUIDE – TEST 3
 Production of T3 and T4 decreased due to gland problem /
damage
o Body tries to correct low level by sending out more TSH
but gland doesn’t work properly
 These labs could also indicate dose of med (like not enough
medication)
 Low TSH with Secondary
 Low because damage to either pituitary or hypothalamus
o NO TSH released so thyroid cannot be stimulated to
release T3 or T4
 Constant blood test, every couple of months, are required to monitor
levels of T3 and T4 to ensure the current dose is still effective
 If not, the dose can be increased or decreased
o Nursing Management
 Compliance is essential and life-long
 Each patient will have their one personalized and individual dosing
strength
 Patient shouldn’t switch the brand of medication
 Caution with elderly – need frequent with labs
 Elderly have a decreased metabolism; the levels of T3/T3 may
start to rise too high. The dosage may need to be decreased
 Hyperthyroidism
o Excess production/release of T3, T4
o A sustained increase in synthesis and release of thyroid hormones by thyroid
gland
 Occurs more often in women
 Highest frequency between ages 20 to 40 years
o Types
 Graves’ disease (Most Common Form)
 Excessive thyroid hormone secretion
 Etiology - unknown
o In Graves’ disease the patient develops antibodies to the
TSH receptor.
o These antibodies attach to the receptors and stimulate the
thyroid gland to release T3, T4, or both.
o The excessive release of thyroid hormones leads to the
clinical manifestations associated with thyrotoxicosis.
o The disease is characterized by remissions and
exacerbations with or without treatment.
o It may progress to destruction of the thyroid tissue,
causing hypothyroidism.
 Pathology
o Autoimmune disease
 Diffuse thyroid enlargement
 Excessive thyroid hormone secretion