Thyroid disorders

Presented by
Shagufta Emmanuel (NI)
CON, UCHS, Lahore
Objectives of Thyroid Disorders
 Understand anatomy & physiology of the thyroid gland and its hormones (T3, T4,
calcitonin).
 Identify causes & risk factors of common thyroid disorders (goiter,
hypothyroidism, hyperthyroidism, thyroiditis, thyroid cancer).
 Recognize clinical manifestations (signs & symptoms) of thyroid dysfunction.
 Differentiate between hypothyroidism & hyperthyroidism based on clinical
features and lab values.
 Describe diagnostic methods (TSH, T3, T4, antibodies, imaging, biopsy).
 Explain medical & surgical management of thyroid disorders.
 Discuss nursing management including patient education, medication compliance,
and monitoring.
 Identify complications (e.g., thyroid storm, myxedema coma, airway obstruction in
goiter, malignancy).
 Apply preventive strategies (iodine intake, screening high-risk groups).
 Anatomy of Thyroid Gland
• Location: Anterior neck, below the larynx, in front
of trachea.
• Shape: Butterfly-shaped with 2 lobes (right & left)
connected by an isthmus.
• Blood supply:
– Superior thyroid artery (from external carotid
artery)
– Inferior thyroid artery (from subclavian artery)
• Histology: Made of follicles filled with colloid
(thyroglobulin), lined by follicular cells.
• Parafollicular (C) cells produce calcitonin.
Physiology of Thyroid Hormones
1. T3 (Triiodothyronine) & T4 (Thyroxine)
• Produced by follicular cells.
• Synthesis: Requires iodine + thyroglobulin.
• Regulation:
– Hypothalamus → TRH Thyrotropin-Releasing Hormone
– Pituitary → TSH
– Thyroid → T3 & T4
• Functions:
– Control basal metabolic rate (BMR)
– Stimulate growth & development (esp. brain in childhood)
– Regulate carbohydrate, protein, and fat metabolism
– Increase heart rate, cardiac output, and oxygen consumption
2. Calcitonin
• Produced by parafollicular (C) cells.
• Function:
– Lowers blood calcium by inhibiting bone resorption (osteoclast activity)
– Works opposite to parathyroid hormone (PTH)
Iodine
• Definition:
Iodine is a trace mineral (micronutrient) that the body needs in very small
amounts for normal growth and development.
• Role in the Body:
– Essential for the production of thyroid hormones (T3 & T4).
– Without iodine, the thyroid cannot make enough hormones → leads to goiter
and hypothyroidism.
• Sources of Iodine:
– Iodized salt (main preventive measure for goiter worldwide)
– Seafood, fish, dairy products, eggs
– Seaweed (kelp, nori)
• Daily Requirement (Adults):
~150 micrograms/day (more in pregnancy & lactation).
Hypothyroidism
Definition: Deficiency of thyroid hormone production.
Causes:
– Autoimmune (Hashimoto’s thyroiditis)
– Iodine deficiency
– Post-surgery or radioiodine therapy
– Congenital hypothyroidism
Clinical features:
– Fatigue, weight gain, cold intolerance
– Dry skin, constipation, bradycardia
– Puffy face, slow reflexes, depression
HPT Axis
• Normal Function:
• Hypothalamus → releases TRH
(Thyrotropin-Releasing Hormone)
• Pituitary gland → releases TSH
(Thyroid-Stimulating Hormone)
• Thyroid gland → releases T3 & T4 →
regulate metabolism
• Feedback: High T3/T4 → inhibits
TRH & TSH
In Hypothyroidism (Low Thyroid
Hormone)
• Primary (thyroid problem):Thyroid
cannot make enough T3/T4
• TSH ↑, TRH ↑ (pituitary tries to
stimulate thyroid)
• Secondary (pituitary
problem):Pituitary fails to release
enough TSH
• T3/T4 ↓, TRH ↑
Diagnosis
• Primary Hypothyroidism: ↑ TSH, ↓ T4
• Secondary Hypothyroidism: ↓ TSH, ↓ T4
• Imaging (Ultrasound/Scintigraphy): if goiter or nodules present

Complication
• Myxedema Coma → life-threatening emergency (↓LOC, hypothermia, bradycardia,
hypotension, respiratory depression).
Medical Management of Hypothyroidism
1. Hormone Replacement Therapy (Mainstay)
• Levothyroxine (L-thyroxine, T4)
– Drug of choice
– Start with low dose → gradually increase (esp. in elderly & cardiac patients)
– Lifelong therapy usually required
– Taken in the morning, empty stomach, with water
2. Monitoring
• Regular monitoring of TSH and T4 levels
• Dose adjusted to keep TSH in normal range
• Clinical monitoring: energy level, weight, heart rate, skin, hair
3. Special Considerations
• Elderly or cardiac disease patients → start low dose to avoid angina, MI, arrhythmias
• Pregnancy → increase levothyroxine dose (requirement ↑ in pregnancy)
• Avoid stopping abruptly → risk of myxedema coma
4. Emergency (Myxedema Coma)
• IV levothyroxine
• Supportive management (airway, oxygen, fluids, warming, corticosteroids if adrenal
insufficiency suspected)
Nursing Management of Hypothyroidism

1. Assessment
 Monitor vital signs (esp. HR, BP, temperature,
respirations).
 Assess for fatigue, weight gain, cold intolerance,
constipation, dry skin, and edema.
 Observe for signs of myxedema coma (↓LOC,
hypothermia, bradycardia).
2. Nursing Interventions
• Medication management:
– Administer levothyroxine as prescribed.
– Educate patient about lifelong therapy.
– Give on empty stomach, same time daily.
• Monitor response: TSH/T4 levels, improvement in energy, heart rate,
mental alertness.
• Prevent complications:
– Maintain airway and oxygen if needed.
– Watch for angina, arrhythmias in cardiac patients.
• Provide comfort: Warm environment, extra blankets (cold intolerance).
• Promote activity tolerance: Allow rest periods, avoid overexertion.
• Nutrition: Encourage high-fiber diet, adequate fluids → prevent
constipation; avoid goitrogenic foods (soy, cabbage, peanuts in large
amounts).
3. Patient Education
• Lifelong thyroid hormone replacement → do not stop suddenly.
• Importance of regular follow-up and blood tests.
• Report chest pain, palpitations, or weight changes.
• Teach symptoms of both hypo- and hyperthyroidism (to detect
under/overdose).
Myxedema Coma
• Definition: Life-threatening complication of severe, untreated hypothyroidism.
• Causes/Triggers: Infection, surgery, trauma, cold exposure, sedatives, stopping
thyroid meds.
• Features:
– Coma or altered mental status
– Hypothermia
– Bradycardia, hypotension
– Hypoventilation
– Puffy face, non-pitting edema
• Diagnosis: ↑TSH, ↓T4 (primary hypothyroidism), plus clinical features.
• Management:
– Airway + oxygen
– IV levothyroxine (± liothyronine)
– IV hydrocortisone
– Warming, fluids, electrolytes
– Treat precipitating cause
Hyperthyroidism/Thyrotoxicosis
• Hyperthyroidism, also called overactive thyroid, is a
condition where the thyroid releases high levels of thyroid
hormone tetraiodothyronine (T4) and triiodothyronine (T3),
which are two primary hormones that control how your cells
use energy, into the body. This condition can make the
metabolism speed up.
 Hypothalamus Pituitary Thyroid Axis
Normal Function:
[Link] → releases TRH (Thyrotropin-
Releasing Hormone)
[Link] gland → releases TSH (Thyroid-
Stimulating Hormone)
[Link] gland → releases T3 & T4 → regulate
metabolism
[Link]: High T3/T4 → inhibits TRH & TSH

In Hyperthyroidism (High Thyroid Hormone)

Primary (thyroid overactive):
Thyroid makes too much T3/T4
TSH ↓, TRH ↓ (feedback inhibition)
Secondary (pituitary problem):
Pituitary releases too much TSH → thyroid
overproduces T3/T4
TRH may be normal or ↓
Causes:
1. Primary Hyperthyroidism
In the thyroid gland itself. Thyroid makes too much hormone on its own.
Examples:
– Graves’ disease: Immune system tells thyroid to make more hormone.
– Toxic multinodular goiter: Several nodules in thyroid overproduce hormone.
– Thyroid adenoma: A small tumor in thyroid makes extra hormone.
– Taking too much thyroid medicine accidentally.
2. Secondary Hyperthyroidism
Outside the thyroid, usually in the pituitary gland. Pituitary releases too much TSH → tells
thyroid to make too much hormone.
Examples:
– Pituitary tumor (adenoma) that secretes TSH.
– Rarely, hypothalamus problems (makes too much TRH).
Clinical features:

• Clinical Features (in short):

• Nervousness, irritability, restlessness
• Heat intolerance, sweating, warm/moist skin
• Palpitations, tachycardia, ↑ systolic BP, atrial
fibrillation
• Exophthalmos (bulging eyes)
• Weight loss despite ↑ appetite
• Muscle weakness, fatigue, osteoporosis
• Amenorrhea, ↑ bowel movements
Clinical Features:
• General hyperthyroidism signs:
– Weight loss despite good
appetite
– Heat intolerance, sweating,
irritability, tremors
– Palpitations, tachycardia
• Specific signs of Graves’ disease:
– Exophthalmos (protruding
eyes)
– Pretibial myxedema (swelling
on shins)
– Diffuse goiter (enlarged
thyroid)
Management
 Diagnosis:
 ↓ TSH, ↑ T3/T4
 Thyroid scan for cause
 Management:
Antithyroid drugs (propylthiouracil, methimazole)
Beta-blockers (symptom control)
Radioiodine therapy or surgery

 Complication: Thyroid storm (life-threatening).

Complications:

• Thyroid storm (life-threatening hyperthyroid crisis)

• Heart failure, atrial fibrillation
• Eye complications (corneal ulcer, vision loss if untreated)
Thyroid Storm
Definition
• A life-threatening emergency caused by severe,
uncontrolled hyperthyroidism, usually precipitated by stress,
infection, trauma, surgery, or sudden withdrawal of
antithyroid drugs.
Clinical Features
• High fever (> 38.5–40°C)
• Tachycardia (may lead to atrial fibrillation, heart failure)
• Hypertension → later hypotension, shock
• CNS: agitation, delirium, psychosis, seizures, coma
• GI: diarrhea, abdominal pain, vomiting
• Sweating, tremors
Cont.:
Diagnosis
• Clinical diagnosis (labs may show ↑T3, ↑T4, ↓TSH, but not needed to
start treatment).
Management (Emergency)
• Airway & supportive care (oxygen, IV fluids, cooling).
• Antithyroid drugs: Propylthiouracil (PTU) or Methimazole.
• Iodine solution (Lugol’s iodine / potassium iodide) → given after
antithyroid drugs to block hormone release.
• Beta-blockers (Propranolol): control tachycardia, tremor.
• Glucocorticoids (Hydrocortisone): reduce T4→T3 conversion, prevent
adrenal insufficiency.
• Treat precipitating cause (antibiotics if infection, etc.).
Nursing Management
• Common Nursing Diagnoses:
 Hyperthermia related to increased metabolic rate
 Imbalanced nutrition: less than body requirements related to hyper
metabolism
 Anxiety related to excessive thyroid hormone
 Risk for decreased cardiac output related to tachycardia or arrhythmias
 Disturbed sleep pattern related to hyperactivity
Nursing Goals:
 Maintain stable vital signs
 Prevent complications (thyroid storm, heart failure)
 Promote adequate nutrition and rest
 Reduce anxiety and restlessness
Nursing Interventions:
• Monitor Vital Signs:
– Check temperature, pulse, blood pressure frequently.
– Report tachycardia, arrhythmias, fever.
• Promote Nutritional Support:
– Provide high-calorie, high-protein diet.
– Offer small, frequent meals to meet increased metabolic demands.
• Manage Anxiety and Restlessness:
– Encourage quiet environment, relaxation techniques.
– Explain procedures clearly to reduce fear.
• Medication Management:
– Administer antithyroid drugs (e.g., Methimazole, Propylthiouracil) as prescribed.
– Monitor for side effects: rash, hepatotoxicity, leukopenia.
• Prevent Complications:
– Observe for thyroid storm: severe fever, tachycardia, hypertension, delirium.
– Administer beta-blockers to control tachycardia and palpitations if ordered.
• Patient Education:
– Teach medication adherence and importance of follow-up.
– Advise on dietary modifications and avoiding stimulants (caffeine).
– Educate about signs of worsening condition (e.g., palpitations, fever).
• Postoperative Care (if thyroidectomy):
– Monitor airway patency and bleeding.
– Assess for hypocalcemia (tingling, tetany) if parathyroid affected.
– Provide pain relief and emotional support.
Tumors of the Thyroid Gland
• Classification: Based on:
– Benign vs. malignant
– Presence of thyrotoxicosis (hyperthyroidism)
– Diffuse vs. irregular/nodular enlargement
• Goiter: Any thyroid enlargement large enough to be visible in the neck.
• Types of Goiter:
– Size: Ranges from barely visible to disfiguring.
– Shape: Symmetric and diffuse or irregular/nodular.
– Function:
• Toxic goiter: Associated with hyperthyroidism.
• Nontoxic goiter: Associated with a normal thyroid function (euthyroid).
Endemic (Iodine-Deficient) Goiter
• Definition: Most common type of goiter; occurs in regions with iodine deficiency.
Also called simple or colloid goiter.
• Causes:
– Iodine deficiency (most common).
– Intake of goitrogenic substances (e.g., excessive iodine, lithium) in susceptible
individuals.
• Pathophysiology:
– Low iodine → reduced thyroid hormone production → pituitary releases more
TSH → thyroid hypertrophy (enlargement).
• Symptoms: Usually none, except neck swelling; large goiters may compress the
trachea.
• Management:
– Correct iodine deficiency (e.g.,iodized salt).
– Preoperative treatment with antithyroid drugs and iodide if surgery is needed
to reduce goiter size and vascularity.
• Prevention: Provide iodine supplements to children in iodine-poor areas; iodized
salt is highly effective.
Nodular Goiter
Definition: Thyroid gland with nodules due to areas of overgrowth (hyperplasia).
• Symptoms: Often none initially.
• Progression:
– Nodules may gradually enlarge.
– Some may extend into the chest (thorax), causing local pressure symptoms.
• Complications:
– Some nodules may become malignant (cancerous).
– Some may cause hyperthyroidism (overactive thyroid).
• Management:
– Patients with multiple nodules may eventually require surgical removal of the thyroid.
 Thyroid Cancer
Definition:
• A malignant tumor of the thyroid gland, arising from follicular or
parafollicular (C) cells.
Epidemiology:
• More common in women than men.
• Most frequent in adults aged 30–50.
• Incidence increasing due to better detection.
Types:
• Papillary Thyroid Carcinoma (PTC) – ~80%
– Slow-growing, often spreads to cervical lymph nodes.
– Excellent prognosis.
• Follicular Thyroid Carcinoma (FTC) – ~10–15%
– Hematogenous spread (lung, bone).
– Prognosis good if detected early.
• Medullary Thyroid Carcinoma (MTC) – ~3–5%
– Arises from C cells; produces calcitonin.
– May be part of MEN 2 syndrome.
• Anaplastic Thyroid Carcinoma – <2%
– Very aggressive; poor prognosis.
Cont.
• Risk Factors:
• Radiation exposure (especially in childhood)
• Family history
• Iodine deficiency (for some types)
• Clinical Features:
• Painless thyroid nodule or mass
• Neck lymphadenopathy (especially in papillary type)
• Sometimes symptoms of thyroid dysfunction
• Rarely, compressive symptoms: dysphagia, hoarseness
Cont.
• Diagnosis:
• Ultrasound – first-line imaging
• Fine-needle aspiration (FNA) biopsy – confirms malignancy
• Thyroid function tests – usually normal
• Calcitonin – for medullary carcinoma
• Management:
• Surgery: Total or near-total thyroidectomy
• Radioactive iodine therapy: Mainly for papillary and follicular types
• Thyroid hormone suppression therapy
• Targeted therapy/chemotherapy: For advanced or metastatic disease
Cont.
Prognosis:
• Papillary and follicular: Excellent (10-year survival >90%)
• Medullary: Moderate, depends on stage
• Anaplastic: Poor (usually <6 months survival)
 Goiter
Definition: Enlargement of the thyroid gland (can occur in hypo, hyper, or euthyroid
states).
Types:
– Simple (iodine deficiency)
– Toxic (associated with hyperthyroidism)
– Nontoxic (without hormone imbalance)
Clinical features:
– Swelling in the neck
– Pressure symptoms if large (difficulty swallowing, breathing)
Management:
– Iodine supplementation (if deficient)
– Treat underlying cause
Thyroiditis
Definition: Inflammation of the thyroid gland.
Types:
– Hashimoto’s thyroiditis (autoimmune, hypothyroidism)
– Subacute (De Quervain’s) thyroiditis – painful, post-viral
– Postpartum thyroiditis
Clinical features:
– Pain, swelling, transient hyperthyroidism → hypothyroidism
– Fatigue, neck tenderness (in subacute)
Management:
– NSAIDs or steroids for inflammation
– Thyroxine if hypothyroid develops
Thyroid Nodules & Cancer
Types of cancer:
• Papillary carcinoma (most common, best prognosis)
• Follicular carcinoma
• Medullary carcinoma (MEN syndrome)
• Anaplastic carcinoma (most aggressive)
Clinical features:
– Solitary hard thyroid nodule
– Enlarged cervical lymph nodes
– Hoarseness, difficulty swallowing (advanced cases)
Diagnosis:
– Fine needle aspiration cytology (FNAC)
– Ultrasound, thyroid scan
Management:
– Surgery (thyroidectomy)
– Radioiodine therapy
– Lifelong thyroxine replacement
References
• Hinkle, J. L., & Cheever, K. H. (2022). Brunner
& Suddarth’s textbook of medical-surgical
nursing (15th ed., Endocrine Disorders, pp.
~1410–1415). Wolters Kluwer.