Introduction

Pheochromocytomas are neoplasms of the chromaffin cells of the adrenal medulla or paraganglial cells of extramedullary sites (paragangliomas) 

-These tumors secrete excessive amounts of epinephrine, norepinephrine, or both or even dopamine

-Most pheochromocytomas secrete norepinephrine 

-Pheochromocytoma was classically referred to as the “tumor of tens” because it was considered that 10% are hereditary, 10% are malignant, 10% are asymptomatic, 10% are extra-adrenal, 10% are extra-abdominal,10% are multiple, 10% are bilateral

– They can occur at any age, have no gender predilection

-Peak incidence: in the fourth and fifth decades of life

-Familial causes: Multiple Endocrine Neoplasia type 2 (MEN 2), von Hippel-Lindau disease, von Recklinghausen neurofibromatosis type 1 (NF-1) 

Symptoms & Signs 

-The classic pentad of symptoms: Episodic headache, palpitations, unusual sweating, pallor and orthostasis

-Other symptoms: Anxiety, irritability, flushing, chest pain, shortness of breath, nausea, vomiting, abdominal pain

-The most common clinical sign: Hypertension 

-Typical paroxysm: Sudden headache, palpitations, and sweating produced by anxiety or activities that compress the tumor (bending, defecation, deep palpation of the abdomen etc) 

Diagnosis 

24-hour urinary tests: Catecholamines, Fractionated metanephrines, total metanephrines

Plasma tests: Catecholamines, Free metanephrines

Imaging: CT, MRI, MIBG scintigraphy, Somatostatin receptor scintigraphy

Most sensitive test: Plasma fractionated free metanephrines

Most specific test: Urinary total metanephrines 

Treatment 

Definitive treatment: Surgery 

First administer alpha blockers, then beta blockers

α-blockers: Phenoxybenzamine, prazosin, terazosin, doxazosin

beta blockers: Propranolol, atenolol, metoprolol, carvedilol, bisoprolol, esmolol 

Calcium channel blockers: Nicardipine 

Introduction 

Primary aldosteronism occurs when the adrenal glands produce too much of the steroid hormone aldosterone, which helps control sodium and potassium excretion 

-Excessive aldosterone production increases sodium retention and suppresses plasma renin 

-It increases renal potassium excretion, which can lead to hypokalemia 

-The most common cause of refractory hypertension in young and middle-aged adults: Primary aldosteronism 

-Most frequent cause of primary aldosteronism: Bilateral adrenal cortical hyperplasia 

Symptoms & signs

Fatigue, edema, tingling, muscle weakness, excessive thirst, frequent urination, visual disturbances, normotension, hypertension, paresthesias with tetany, headache, polyuria and polydipsia 

Diagnosis

Labs: low plasma renin; low potassium;  Elevated plasma and urine aldosterone levels, sodium bicarbonate levels 

Imaging: Adrenal CT 

Treatment 

Unilateral Adrenal adenoma: usually treated by adrenalectomy 

Bilateral adrenal hyperplasia: usually treated with medical therapy 

Medications: Spironolactone, Eplerenone, Amiloride

Primary aldosteronism (Conn’s syndrome)

Introduction 

Primary aldosteronism occurs when the adrenal glands produce too much of the steroid hormone aldosterone, which helps control sodium and potassium excretion 

-Excessive aldosterone production increases sodium retention and suppresses plasma renin 

-It increases renal potassium excretion, which can lead to hypokalemia 

-The most common cause of refractory hypertension in young and middle-aged adults: Primary aldosteronism 

-Most frequent cause of primary aldosteronism: Bilateral adrenal cortical hyperplasia 

Symptoms & signs

Fatigue, edema, tingling, muscle weakness, excessive thirst, frequent urination, visual disturbances, normotension, hypertension, paresthesias with tetany, headache, polyuria and polydipsia 

Diagnosis

Labs: low plasma renin; low potassium;  Elevated plasma and urine aldosterone levels, sodium bicarbonate levels 

Imaging: Adrenal CT 

Treatment 

Unilateral Adrenal adenoma: usually treated by adrenalectomy 

Bilateral adrenal hyperplasia: usually treated with medical therapy 

Medications: Spironolactone, Eplerenone, Amiloride

Introduction

Cushing syndrome is a hormonal disorder which occurs when body has too much of the hormone cortisol over time 

-it more frequently affects women

-the most common cause of Cushing’s syndrome: use of glucocorticoids 

Symptoms & Signs 

General: fatigue, backache, headache, central obesity with a rounded, rosy face (moon face), a fat pad in the upper back between the clavicles (buffalo hump), protuberant abdomen  

CNS: irritability, emotional lability, depression, psychosis, insomnia   

Musculoskeletal: Proximal muscle weakness (Difficulty standing up from a seated position, or climbing stairs), osteopenia, osteoporosis 

Reproductive: Oligomenorrhea, amenorrhea, erectile dysfunction, infertility 

Cardiovascular: Hypertension, hypercoagulation 

Endocrine: Glucose intolerance, diabetes

Skin: purple striae, easy bruisability, hyperpigmentation, hirsutism

Diagnosis 

Labs: 24-hour urinary free cortisol and creatinine, Late-night (10–11 PM) salivary cortisol determinations, Petrosal sinus sampling, overnight dexamethasone suppression test, plasma ACTH level, plasma DHEAS (dehydroepiandrosterone sulfate (DHEAS) level

Imaging: CT of the adrenals, MRI of the pituitary

Treatment 

Medications: Spironolactone, eplerenone, flutamide, cabergoline, Pasireotide, Ketoconazole, Metyrapone, Mitotane 

Surgery: transsphenoidal selective resection of the pituitary adenoma (Pituitary Cushing disease), Adrenalectomy (Adrenal Cushing disease) 

Introduction

-Primary adrenocortical insufficiency (Addison disease) is a syndrome resulting from the chronic deficiency of cortisol caused by adrenocortical insufficiency 

-Secondary adrenocortical insufficiency is due to ACTH deficiency, caused by exogenous glucocorticoid therapy, pituitary or hypothalamic tumors 

-in primary adrenal insufficiency, low or absent cortisol level results in hypersecretion of ACTH by the pituitary

-ACTH stimulates melanocyte activity, resulting in generalized hyperpigmentation, which is the most specific sign of primary adrenal insufficiency

-Addison’s disease occurs when >90% of adrenal tissue is destroyed

-The most common cause is autoimmune destruction 

Symptoms & Signs 

General: Weakness, malaise, anorexia, weight loss, craving for salt 

Vascular: postural hypotension

GI: Nausea, vomiting, diarrhea, constipation, abdominal pain

Musculoskeletal: Myalgia, arthralgia 

Metabolic: Hypoglycemia, hyponatremia,hyperkalemia 

Psychiatric: Personality changes 

Dermatological: Hyperpigmentation of the buccal mucosa and gums preceded by generalized hyperpigmentation of the skin, loss of axillary and pubic hair, vitiligo,calcification of auricular cartilage (petrified ears), longitudinal pigmented bands in the nails  

Gynecological: Amenorrhea, ovarian failure, infertility

Obstetrical: preterm delivery, low-birth weight newborn, increase in cesarean delivery

Emergency: Shock, coma, and death, if untreated

Diagnosis 

Labs: hyponatremia, hyperkalemia, acidosis, elevated serum creatinine and blood urea nitrogen, hypoglycemia, hypercalcemia

Hematology: Normochromic, normochromic anemia, neutropenia, eosinophilia, and lymphocytosis

Best screening test/Definitive diagnosis: Failure to respond adequately to corticotropin stimulation test

-MRI to rule out pituitary or hypothalamic tumor 

-CT scan of the adrenal glands

-Secondary Adrenal insufficiency: Diminished pigmentation, Normal serum potassium 

Treatment 

-Register with a medical alert system 

-Patient should be instructed in the self-administration of steroids

-Lifelong replacement therapy of glucocorticoids and mineralocorticoids 

-Medications: Hydrocortisone, prednisone, dexamethasone, fludrocortisone 

-Acute adrenocortical insufficiency: Medical emergency, parenteral hydrocortisone, correction of fluid and electrolytes 

Introduction

Paget disease (Osteitis deformans) is a chronic, localized bone-remodeling disorder of abnormal osteoclasts that drive increased bone resorption accompanied by accelerated, disordered bone formation that results in disorganized, fragile bone

-It was originally described by Sir James Paget in 1877 

-It most commonly involves the pelvis, vertebrae, skull, humerus, femur and tibia 

-it predominantly affects Caucasian individuals over the age of 40 

Symptoms & Signs 

-Most patients are asymptomatic 

-Most common presenting symptom is pain, often worse at night  

-Bowing of weight-bearing bones, stress fractures (Chalk stick fractures), 

-Enlargement of the parietal or frontal bones (frontal bossing), increased head size, softening of the base of the skull (platybasia)

Complications of Paget disease: 

Rheumatologic: Osteoarthritis, gout, vertebral collapse 

Neurologic: Basilar impression, peripheral nerve entrapment, spinal cord and root compression 

Otologic: Cranial nerve dysfunction (especially deafness) 

Ophthalmic: Loss of vision 

Neoplastic: Osteosarcoma, giant cell tumor 

Cardiac: High-output heart failure 

Metabolic: Hypercalcemia 

Diagnosis 

X rays: Focal lytic, radiolucent areas with a coarse trabecular pattern and bone thickening, described as osteoporosis circumscripta “cotton-wool” skull, enlarged “picture-frame” vertebrae, “ivory vertebrae”

Labs: Normal calcium, phosphate levels, Elevated serum alkaline phosphatase

Bone resorption markers: Elevated serum or urine N-telopeptide or C-telopeptide measured in the blood or urine

Treatment 

-Adequate calcium and vitamin D intake 

-Mainstay of pharmacologic therapy: Bisphosphonates 

-The treatment of choice: Zoledronic acid 

-Other medications: Pamidronate, Risedronate, Alendronate, Tiludronate

-Serial serum alkaline phosphatase determinations are done to evaluate the response to treatment 

Introduction 

Rickets: Defective bone mineralization in children before epiphyseal fusion

Osteomalacia: Defective bone mineralization in adults with fused epiphyses

-The most common cause of osteomalacia: Vitamin D deficiency 

-Drug-induced osteomalacia caused by phenytoin, carbamazepine, valproate, phenobarbital 

Calcipenic rickets occurs in 4 forms:

Nutritional rickets 

Vitamin D-dependent rickets type I

Hereditary vitamin D resistant rickets

Defects in vitamin D metabolism 

Hypophosphatemic rickets occurs in 2 forms: 

-nutritional hypophosphatemic rickets 

-X-linked hypophosphatemic rickets 

Symptoms & Signs 

-can be asymptomatic 

-Weakness, apathy, listlessness, bone pain, proximal muscle weakness

-spasms, convulsions, thickened and widened wrists and ankles 

-Craniotabes: thinning of the bones of the skull, soft, misshapen head, widened sutures, frontal bossing, muscle hypotonia, pronounced potbelly, bowing of the legs, waddling gait  

-Delayed eruption of teeth, pitted teeth 

-Rachitic rosary: Enlargement and cupping of the costochondral junctions resulting in widening of the chest 

-Genu Valgum: ‘Knock knees’ 

-Genu Varum: ‘Bowed legs’ 

-Harrison Groove: Tug of the diaphragm against the softened lower ribs may produce an indentation at the point of insertion of the diaphragm

Kyphoscoliosis or lumbar lordosis is common

-Hypocalcemia: fatigue,lethargy, irritability, depression, paresthesias in the circumoral area, muscle cramps, carpopedal spasm, convulsions, tetany, laryngospasm, and stridor 

-Hypophosphatemia: muscle weakness, reduced endurance, dysphagia, diplopia, cardiomyopathy, respiratory muscle weakness and impaired cognition

Diagnosis 

Histology: Transcortical bone biopsy 

Radiographs: bilateral bowing deformity of the femora, metaphyseal flaring, physeal widening 

Treatment 

-vitamin D 

Are you planning a trip to oversees which requires you to get Yellow Fever Vaccine?

Come and get your YF vaccine at your own convenience.

No Doctor’s referral or appointment required.

Introduction

Osteoporosis is a systemic skeletal disease characterized by low bone mass, microarchitectural deterioration of the bone tissue, compromised bone strength resulting in bone fragility and increased risk of fractures

-It is more common in women than in men

-The World Health Organization has established criteria for defining osteopenia and osteoporosis based on the T score: 

T score greater than or equal to –1.0, normal; 

T score –1.0 to –2.5, osteopenia 

T score less than –2.5, osteoporosis; 

T score less than –2.5 with a fracture, severe osteoporosis.

-Medication-induced osteoporosis: Glucocorticoids are the most common cause of medication-induced osteoporosis; diabetes medications, thiazolidinediones,SSRIs, proton pump inhibitors, warfarin 

Symptoms & Signs 

-Osteoporosis is often a ‘silent disease’

-Complications: loss of height from vertebral fractures, kyphosis from vertebral fractures, chronic back pain, restrictive lung capacity from thoracic vertebral fractures, hip fractures, low self-esteem, decreased quality of life and independence, isolation and depression

-Most important consequence of osteoporosis: Fractures 

-Most frequent sites of fractures: thoracic and lumbar vertebral bodies, proximal hip, pelvis, proximal humerus, and distal radius 

-The most common osteoporotic fracture: Vertebra

-the most disastrous osteoporotic fracture:Proximal femur

Diagnosis 

-CBC, CMP, 24-hour urine collection of calcium, serum 25-hydroxy vitamin D, PTH

-Most commonly used tool to determine bone density: Dual-Energy X-ray Absorptiometry (DEXA) 

-Other techniques: single-energy x-ray absorptiometry (SXA), quantitative CT, and ultrasound (US)

-Fracture risk increases with age at any T-score.

Treatment 

Lifestyle modifications: Discontinue smoking, alcohol consumption, Exercise, hip protectors 

Nutritional supplements: Calcium, Vitamin D, protein intake, good sun exposure 

Medications: 

Bisphosphonates: Alendronate, Risedronate, Ibandronate, Zoledronic acid 

PTH analogs: Teriparatide, Abaloparatide, limited to 2-year treatment

SERMS: Raloxifene,tamoxifen; up to 5-year treatment 

RANKL inhibitor: Denosumab; up to 10-year treatment 

Sclerostin inhibitor: Romosozumab; limited to 12 monthly doses 

Hyperparathyroidism is a common disorder of calcium, phosphorus, and bone metabolism caused by increased circulating levels of parathyroid hormone (PTH) 

– PTH decreases urinary excretion of calcium and increases urinary excretion of phosphate.

-it is the most common disorder of parathyroid function

-it is categorized as primary, secondary, or tertiary depending on the etiology

-Causes: solitary parathyroid adenoma (85%), hyperplasia, multiple adenomas, carcinoma 

Primary hyperparathyroidism: 

-The most common cause of hypercalcemia 

-in the outpatient setting: Primary hyperparathyroidism 

-in the inpatient setting: Malignancy 

-It occurs at all ages, affects women more than men, most commonly in the seventh decade 

Secondary hyperparathyroidism: 

-PTH levels are elevated in response to chronic hypocalcemia

-Most common causes are chronic renal failure, vitamin D deficiency

Tertiary hyperparathyroidism: 

-Autonomous hypersecretion of PTH and hypercalcemia 

Symptoms & Signs 

-Classic description: “bones, stones, abdominal groans, psychic moans, with fatigue overtones.”

-Primary hyperparathyroidism is often asymptomatic 

General: Fatigue, weakness, irritability 

Psychiatric: Depression, dementia, and confusion

Cardiovascular: Hypertension, palpitations,prolonged P-R interval, shortened Q-T interval, bradyarrhythmias, heart block, asystole  

Gastrointestinal: Anorexia, nausea, vomiting, heartburn, peptic ulcer, weight loss, constipation, abdominal pain, pancreatitis 

Bone: osteoporosis, bone pain, osteitis fibrosa cystica 

Rheumatologic: arthralgia, myalgia, and gout

Neurological: Paresthesias, headaches, diminished deep tendon reflexes, insomnia, irritability 

Dermatologic: Pruritus 

Renal: Nephrolithiasis, polyuria, polydipsia, and renal failure 

Diagnosis 

1. Laboratory findings: Elevated serum calcium, ionized calcium; Elevated PTH; Low or low-normal phosphate levels; Elevated alkaline phosphatase

2.Other tests: Radiographs: Extensive areas of demineralization with areas of increased bone density (“Salt and pepper” skull); Electrocardiography & echocardiography

Treatment 

Medications: Calcium mimetics such as Cinacalcet, Bisphosphonates, Denosumab, Vitamin D and vitamin D analogs

Surgical treatment: Parathyroidectomy 

Got the first dose of Covid vaccine at the beautiful Penn Highlands Hospital, Dubois, PA. Dont believe the myths and conspiracies about vaccines. Get it when you can.

Pseudohypoparathyroidism (PHP) is a genetic disorder of end-organ insensitivity to the effect of PTH, which results in hypocalcemia, hyperphosphatemia, and increased PTH levels

Symptoms & Signs 

-As the name implies, patients with pseudohypoparathyroidism have signs and symptoms characteristic of hypoparathyroidism

-PHP may be associated by a characteristic phenotype known as Albright Hereditary Osteodystrophy (AHO) which includes short stature, round facies, shortening of the fourth metacarpals (brachydactyly), and osteoma cutis 

-Examination of the clenched fist reveals a characteristic depression where the knuckle of the fourth metacarpal should be located.

Diagnosis 

-A high concentration of serum PTH, low serum calcium, high phosphate, and 

signs and symptoms of hypoparathyroidism

-patients with pseudohypoparathyroidism do not respond to infused PTH

Treatment 

Treatment is the same as for hypoparathyroidism

Get tested for Covid and Flu with results in 15 short minutes. Protect yourself and others.

Test Price $100

Our location: Dr.Paul’s Clinic, 1516 Martin St, State College, PA 16803

Test Price: $100

Introduction 

-The four parathyroid glands produce and secrete PTH

-Hypoparathyroidism develops when the parathyroid glands fail to secrete sufficient quantities of PTH, resulting in a low calcium level and a high phosphorus level 

-The most common cause of hypoparathyroidism is neck surgery with removal or destruction of the parathyroid glands

-Other causes include congenital abnormalities of the third and fourth pharyngeal pouches (DiGeorge syndrome), autoimmune or drug induced or radiation induced hypothyroidism 

Symptoms & Signs 

Skin: Dry, scaly skin, coarse hair

Ocular: Cataracts, Papilledema 

Dental: enamel hypoplasia, defective root formation, delayed teeth eruption

Respiratory: Bronchospasm, laryngospasm, stridor 

Cardiac: Heart failure, Prolonged QT interval on ECG

Psychological: Confusion, behavioral changes, psychosis 

Neuromuscular: numbness, tingling, carpopedal spasms, seizures, Parkinsonism

Tetany: Spontaneous tonic muscular contractions; Classically diagnosed by Chvostek sign and Trousseau sign

Chvostek sign: twitching or contraction of the facial muscles in response to tapping the facial nerve at a point anterior to the ear and above the zygomatic bone

Trousseau sign: it is elicited by inflating the sphygmomanometer with the cuff around the arm above the systolic blood pressure for 3 min; The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct

Diagnosis 

Labs: Inappropriately low or undetectable PTH level, low calcium level, high phosphorus level

EKG: a prolonged QT interval on the ECG

Treatment 

Recombinant PTH; IV or oral calcium, Vitamin D supplementation; correction of hypomagnesemia 

Thyroid cancer is the most common malignancy of the endocrine system

-Most thyroid cancers occur in the young with only one-third of cases occurring after age 55

-Thyroid cancer can be of follicular cell origin or C-cell origin or lymphoid origin. 

Originating from follicular cells 

Papillary 80% 

Follicular 11% 

Hürthle cell 3% 

Anaplastic 2% 

Originating from C-cells or parafollicular cells 

Medullary 4%

Originating from lymphoid cells 

Thyroid lymphoma 1% 

Most of these carcinomas are treated by surgery, radioiodine, and levothyroxine to suppress TSH

Introduction 

Toxic multinodular goiter refers to autonomous hyperfunctioning thyroid nodules that produce hyperthyroidism 

-it is more common in women over the age of 60 and in iodine-deficient regions

-it is the second most common cause of hyperthyroidism after Graves disease 

Symptoms & Signs 

Symptoms and signs of hyperthyroidism are similar to Graves’ disease: weight loss, nervousness, weakness, tremors, sweats, tachycardia, heart failure, arrhythmias, atrial fibrillation, congestive heart failure 

Physical examination reveals a multinodular goiter which may extend substernally

Diagnosis 

Labs: low or undetectable TSH, elevation in serum serum T3 levels, with less striking elevation of serum T4

Radioiodine scan: multiple functioning nodules in the gland with iodine localized to active nodules

Treatment 

methimazole (preferable) or propylthiouracil followed by subtotal thyroidectomy; RAI therapy 

Introduction 

-Thyroid nodules is the most common endocrinopathy 

-They are extremely common, particularly among women

– About 90% of palpable thyroid nodules are benign adenomas, colloid nodules, or cysts, but some are malignancies 

-Most patients with a thyroid nodule are euthyroid, but some are hypothyroid or hyperthyroid 

-The most common neoplasm is the follicular adenoma (benign thyroid nodule) 

– A thyroid nodule is more likely to be a cancer in a man than in a woman and in young patients (under 20 years) and older patients (over 60 years)

Symptoms & Signs 

-Thyroid nodules usually are asymptomatic

-neck discomfort, dysphagia, choking sensation, hoarseness

-Large substernal goiters can cause superior vena cava syndrome, characterized by facial erythema and jugular vein distention that progress to cyanosis and facial edema when both arms are kept raised over the head (Pemberton sign)

Diagnosis 

-Serum TSH, thyroid ultrasound, Fine-needle aspiration (FNA)

-radionuclide thyroid scanning

-the diagnostic procedure of choice is FNA 

Treatment 

Medical therapy, levothyroxine suppressive therapy, surgery, RAI therapy, Ultrasound-guided radiofrequency ablation

-thyroid surgery is indicated for patients with Graves disease, toxic multinodular goiter, toxic adenoma, Reidel’s thyroiditis, goiter, thyroid nodules benign and malignant thyroid tumors 

-Complications of thyroid surgery: injury to recurrent laryngeal nerve with resultant vocal cord paralysis, hypoparathyroidism, injury to cervical sympathetic trunk resulting in Horner’s syndrome 

Radioactive iodine-131 is used for treatment of thyrotoxicosis, thyroid cancer and for diagnostic thyroid scanning

-It is effective in ablating the thyroid gland and producing permanent hypothyroidism

-In North America, RAI forms the mainstay of Graves’ disease 

– the only isotope used for treatment of thyrotoxicosis is 131I

-RAI is most often used in older patients or those who have relapsed after medical or surgical therapy or in whom medical or surgical therapy is contraindicated 

-Radioactive iodine should not be given to pregnant women due to the potential teratogenic effects for the fetus’s growth

-all women of childbearing age must have a negative pregnancy test prior to treatment

-After RAI, wait for 6 months before conceiving 

-Absolute contraindications to RAI: pregnancy or planning pregnancy within 6 months of treatment, breastfeeding 

-Relative contraindications to RAI: children, adolescents, those with ophthalmopathy 

-After RAI treatment, most patients become euthyroid within 2 months 

-The most common complication of RAI is hypothyroidism 

-RAI can exacerbate Graves’ ophthalmopathy especially if the patient is a smoker

Introduction 

Grave’s disease is an autoimmune thyroid disorder characterized

by circulating antibodies that stimulate the TSH receptor, resulting in the increase in synthesis and release of thyroid hormones 

-it is the most common cause of hyperthyroidism and thyrotoxicosis 

-It is more common in women than in men with onset usually between 20 and 40 years of age 

-Dietary iodine supplementation can trigger Graves disease

-Thyrotoxicosis: clinical state resulting from inappropriately high thyroid hormone levels

hyperthyroidism: thyrotoxicosis caused by elevated synthesis and secretion of thyroid hormone

Symptoms & Signs

General: fatigue, fever, heat intolerance, weight change, irritability, intolerance    

Thyroid: diffusely enlarged thyroid often with a loud bruit 

Eyes: infiltrative ophthalmopathy (Graves exophthalmos),spasm of the upper eyelid revealing the sclera above the corneoscleral limbus (Dalrymple’s sign) , lid lag with downward gaze (von Graefe sign), a staring appearance (Kocher sign), conjunctival swelling and congestion, keratitis, papilledema, permanent visual loss 

Nervous: Restlessness, nervousness, fine resting tremors 

Cardiac: palpitations, angina,exertional dyspnea, atrial fibrillation, premature atrial contractions, atrial tachycardia, ischemic or valvular heart disease, pulmonary hypertension    

Gastrointestinal: dysphagia, frequent bowel movements, diarrhea  

Musculoskeletal: muscle weakness, cramps, osteoporosis  

Dermatologic: facial flushing, moist warm skin, pruritis, increased sweating, fine hair, onycholysis,bony involvement leads to subperiosteal bone formation and swelling in the metacarpals (thyroid acropachy), infiltrative dermopathy (pretibial myxedema)

Genitourinary: menstrual irregularities  amenorrhea, decreased fertility, and an increased incidence of miscarriages

Diagnosis 

Serum TSH: low or undetectable 

free T4 or T3: elevated 

Thyroid receptor antibodies (TRAbs): elevated 

RAI scan: elevated uptake and a homogeneous pattern 

Technetium scintigraphy: increased or normal thyroid uptake of technetium 

Treatment 

Symptomatic treatment: beta blockers, calcium blockers 

Antithyroid drugs: Methimazole, carbimazole, propylthiouracil 

Radioactive iodine (131I, RAI): the most commonly prescribed treatment in the United States, but is contraindicated in pregnancy or with breastfeeding 

surgery: a total resection of one lobe and a subtotal resection of the other lobe

Introduction 

Euthyroid sick syndrome is a clinical condition characterized by low thyroid hormone levels  in clinically euthyroid patients with nonthyroidal systemic illness

-it can be precipitated by stresses such as chronic liver failure, renal failure, malnutrition, fasting, starvation, anorexia, diabetic ketosis, and sepsis 

-The first testing abnormality to manifest is low T3 level

Symptoms & Signs 

No signs or symptoms of thyroid dysfunction 

Diagnosis 

Patient’s setting: critical illness, chronic illness, ICU admission etc

No clinical manifestations of thyroid dysfunction 

Labs: TSH: Normal or low 

T4 : Normal or low 

T3, total and free : Low 

Reverse T3 (rT3): High or normal 

Treatment: 

-Treat the underlying nonthyroid illness 

-Thyroid hormone replacement is not beneficial

Introduction 

Riedel’s thyroiditis is a chronic inflammatory disease associated with fibrosis or woody enlargement of all or part of the thyroid gland 

-it is now considered a IgG4-related systemic disease 

-Women in midlife are most often affected 

Symptoms & Signs 

-Symptoms of hypothyroidism when enough thyroid tissue is replaced by fibrous tissue; compressive symptoms of the esophagus, trachea such as dysphagia, dyspnea, hoarseness; a hard, ‘woody’ thyroid gland

Diagnosis 

Gross exam: hard, fixed, ‘woody’ thyroid gland 

Labs: normal or low thyroid hormones, normal or elevated TSH, normal or elevated IgG4 levels 

Open thyroid biopsy: a dense lymphoplasmacytic infiltrate rich in IgG4 plasma cells, storiform fibrosis, and obliterative phlebitis

Treatment 

Surgery: decompression through thyroidectomy Hypothyroidism: thyroid hormone replacement

subacute (de Quervain or Granulomatous) viral thyroiditis

Introduction 

Subacute thyroiditis is an acute painful disease of the thyroid probably caused by a virus or postinfectious inflammation 

-Measles, mumps, influenza, adenoviruses are among the commonly blamed viruses 

-It occurs between 30 and 50 years of age; it is three to five times more common in females than in males 

-It is often associated with HLA-B35

Symptoms & Signs 

Fever, anterior neck pain, aggravated by swallowing; pain frequently refers to the ear; a markedly tender thyroid gland upon palpation with one or more nodules; in the acute phase the patient may be euthyroid or hyperthyroid

Diagnosis 

Labs: Early hyperthyroidism is followed by a hypothyroid phase and later euthyroid phase

Biopsy: Lymphocytes and multinucleated giant cells

Treatment 

Aspirin, NSAIDS, glucocorticoids, β-adrenergic blockers; monitor TSH, T4 every two weeks; Complete recovery in most cases