This document discusses hyperthyroidism and its treatment. It defines hyperthyroidism as increased secretion of thyroid hormones due to various stimuli. It then describes the clinical types of hyperthyroidism including diffuse toxic goitre (Graves' disease), toxic nodular goitre, and toxic nodule. The document outlines the symptoms, diagnosis, and principles of treatment for hyperthyroidism including anti-thyroid drugs, radioactive iodine therapy, and surgery. Treatment options depend on factors like the type and severity of hyperthyroidism, patient age and preferences.
Hyperthyroidism (overactive thyroid) occurs when your thyroid gland produces too much of the hormone thyroxine. Hyperthyroidism can accelerate your body's metabolism, causing unintentional weight loss and a rapid or irregular heartbeat
Hypothyroidism (underactive thyroid) is a condition in which your thyroid gland doesn't produce enough of certain crucial hormones.
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Hyperthyroidism (overactive thyroid) occurs when your thyroid gland produces too much of the hormone thyroxine. Hyperthyroidism can accelerate your body's metabolism, causing unintentional weight loss and a rapid or irregular heartbeat
Hypothyroidism (underactive thyroid) is a condition in which your thyroid gland doesn't produce enough of certain crucial hormones.
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Hyperparathyroidism is medical condition where overactivity of one or more of the body's four parathyroid glands leads to excess of parathyroid hormone in the bloodstream.
Thyroiditis is a general term that refers to “inflammation of the thyroid gland”. Thyroiditis includes a group of individual disorders causing thyroidal inflammation but presenting in different ways. For example, Hashimoto's thyroiditis is the most common cause of hypothyroidism in the United States.
Hyperparathyroidism is medical condition where overactivity of one or more of the body's four parathyroid glands leads to excess of parathyroid hormone in the bloodstream.
Thyroiditis is a general term that refers to “inflammation of the thyroid gland”. Thyroiditis includes a group of individual disorders causing thyroidal inflammation but presenting in different ways. For example, Hashimoto's thyroiditis is the most common cause of hypothyroidism in the United States.
thyrotoxicosis in special situation the let.pptHamedRashad1
how thyroid hyperfunction affects children and elderly , when to suspect and how to treat Summary of clinical manifestations and how to peck and diagnose and methods of treatment
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
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Prix Galien International 2024 Forum ProgramLevi Shapiro
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The prostate is an exocrine gland of the male mammalian reproductive system
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2. DEFENITION
What is hyperthyroidism?
Increased secretion of Thyroid hormones due to various
stimuli.
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What is thyrotoxicosis??
Symptoms and signs produced by Increased secretion of
Thyroid hormones due to various stimuli.
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3. TODAY’S MENU
Clinical types
Symptomatology
Diagnosis of thyrotoxicosis
Principles of treatment of thyrotoxicosis
Choice of therapy
Hyperthyroidism due to other causes
Surgery for thyrotoxicosis
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14. SYMPTOMATOLOGY
Loss of weight despite a good
appetite
Heat intolerance
Palpitations.
Tachycardia
Hot, moist palms
Exophthalmos
Eyelid lag/retraction
Agitation
Thyroid goitre and bruit.
Tiredness
Emotional lability
Weight loss
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15. PRIMARY VS SECONDARY
Symptom 1st Goitre next
Diffuse and vascular
Large or small
Firm or soft
Thrill and a bruit
Abrupt onset
Frequent Remissions &
exacerbations
More severe
No Cardiac manifestations
All eye signs
Goitre 1st symptoms next
Nodular
Insidious
Less severe
Cardiac manifestations more
Only Lid lag & Lid spasm
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16. CARDIAC RYTHM
Fast heart rate during sleep
Cardiac arrhythmias
Stages Of Development Of Thyrotoxic Arrhythmias:
1. multiple extrasystoles
2. paroxysmal atrial tachycardia
3. paroxysmal atrial fibrillation
4. persistent atrial fibrillation, not responsive to digoxin.
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17. MYOPATHY
Weakness of the proximal limb muscles
Thyrotoxic myopathy
Recovery proceeds as hyperthyroidism is controlled.
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19. Specific to Graves Disease
1. Diffuse painless and firm enlargement of thyroid gland
2. Ophthalmopathy – Eye manifestations – 50% of cases
Classification of Eye Changes in Graves' Disease
0) No signs or symptoms.
1) Only signs, no symptoms. (Signs limited to
upper lid retraction, stare, lid lag.)
2) Soft tissue involvement (symptoms and signs).
3) Proptosis (measured with Hertel exophthalmometer)
4) Extraocular muscle involvement.
5) Corneal involvement.
6 Sight loss (optic nerve involvement).
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20. Eye Signs in Toxic Goitre
In early stages, may be unilateral but later may
become bilateral.
Order of appearance of signs
Stellwag's sign : Absence of normal
blinking—so staring look.
Von Graefe`s sign : Upper eye lid lags behind
the eye ball as the patient is asked to look
downwards.
Dalrymphe's sign : Upper sclera is visible due
to retraction of upper eye lid.
Joffroy's sign : Absence wrinkling in the
forehead on looking upwards with the face
inclined downwards.
Moebius sign : Inability or failure to
converge the eye balls
Gifford's sign: Difficulty in eversion of the
upper lid.
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21. Specific to Graves Disease……..
3. Thyroid dermopathy
consists of thickening of the skin,
particularly over the lower tibia, due to
accumulation of glycosaminoglycans
(pre tibial myxedema)
Is usually bilateral
4. Thyroid Acropachy
Thyroid acropachy is clubbing of fingers and
toes in primary thyrotoxicosis.
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24. Thyroid imaging
Radionuclide imaging
Size, shape & function of gland assessed
Increased uptake=“hot", less risk of
malignancy,<5%
Decreased uptake=“cold" higher risk of
malignancy,15-20%
Ultrasound
CT/ MRI good for assessment of retrosternal
extension.
pathology
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DIAGNOSIS
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25. Algorithm for Hyperthyroidism
Measure TSH and FT4
TSH, FT4
Measure FT3
Primary (T4)
Thyrotoxicosis
High
Pituitary Adenoma FNAC, N
Scan
Normal
TSH, FT4 N TSH, FT4 N TSH, FT4 N
T3 Toxicosis
Sub-clinical Hyperthyroidism
Features of Grave’s
Yes
Rx.
Grave’s
No
Single Adenoma,
MNG
Low RAIU RAIU
Sub Acute Thyroiditis, I2, ↑ Thyroxine
F/u in 6-12 wks
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28. Choice Of Therapy
• Type of thyrotoxicosis
• Age of the patient
• Co existing medical illness
• Severity of thyrotoxicosis
• Goitre size
• Presence of ophtalmopathy
• Patient preference
Factors
influencing
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29. ANTITHYROID DRUGS
Indications for antithyroid drugs:
Patients with high likelihood of remission
the elderly or others with comorbidities increasing
surgical risk or with limited life expectancy
Toxicity in pregnant women
moderate to severe active Graves’ ophthalmopathy
(GO)
Before surgery, to make the patient euthyroid
Soon after starting radioactive I131therapy for 6 to 12
weeks
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30. How long to give ATD ?
improved symptoms in 2 weeks and euthyroid in about 6 weeks
Check TSH and FT4 every 4 to 6 weeks
In Graves, remission after 12-18 months
Monitor every 3 months for the 1st year, and then annually after ATD
40% recurrence in 1 yr.
MNG and Toxic Adenoma will not get cured by ATD.
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31. Adjuvants
Beta blockers
Inhibit adrenergic effects
Indications
Prompt control of symptoms;
treatment of choice for thyroiditis;
first-line therapy before surgery, radioactive iodine, and
antithyroid drugs;
Contraindications
Use with caution in older patients and in patients with pre-
existing heart disease, chronic obstructive pulmonary disease,
or asthma
Propranolol is the most commonly prescribed medication in
doses of about 20 to 40 mg four times daily
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32. Iodides
Block the conversion of T4to T3 and inhibit hormone release
Indications
preoperatively when other medications are ineffective or
contraindicated;
to reduce gland vascularity before surgery for Graves’ disease
during pregnancy when antithyroid drugs are not tolerated;
Complications
Paradoxical increases in hormone release with prolonged use;
common side effects of sialadenitis, conjunctivitis, or acneform rash;
Adjuvants
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33. RADIOIODINE THERAPY
Radioactive iodine
Concentrates in the thyroid gland and destroys thyroid
tissue
High cure rates with single-dose treatment (80 percent);
treatment of choice for
Graves’ disease
Multi nodular goitre, toxic nodules in patients older
than 40 years, and
In recurrent thyrotoxicosis
It is effective, safe, and does not require hospitalization.
Given orally as a single dose in a capsule or liquid form.
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34. RADIOIODINE THERAPY………
Drawbacks
Delayed control of symptoms;
post treatment hypothyroidism
contraindicated - pregnant or breastfeeding;
transient neck soreness, flushing, and decreased taste;
radiation thyroiditis in 1 percent of patients;
may exacerbate Graves’ ophthalmopathy;
may require pre treatment with antithyroid drugs in
older or cardiac patients
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35. Surgical Treatment
Surgical treatment is reserved
patient preference
Pregnant women who can’t tolerate ATD
child or adolescent intolerant of ATDs
large goiter, with or without compressive
symptoms
severe Graves’ ophthalmopathy
the presence of suspicious nodules
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36. SURGICAL………..
GRAVES DISEASE
Near-total or total thyroidectomy is the procedure of
choice
TMNG
Near- total or total thyroidectomy should be performed
TOXIC ADENOMA
an ipsilateral thyroid lobectomy, or
isthmusectomy
In patients with coexisting eye disease,
total thyroidectomy
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37. Other causes of Hyperthyroidism
Thyrotoxicosis factitia
Jod–Basedow thyrotoxicosis
Subacute/acute forms of autoimmune thyroiditis or of de
Quervain’s thyroiditis
Secondary carcinoma
Neonatal thyrotoxicosis
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39. Preoperative Preparation
Standard preparation
make the patient euthyroid/ near euthyroid using antythyroid drugs
Alternative method
rapid control of thyroid status can be achieved with a combination of
thionamides, SSKI, dexamethasone (1 to 2 mg twice daily), and beta
blockers
very rapid control=> operation within a week
Lugol’s iodide solution or saturated potassium iodide( three
drops twice daily) for 7 to 10 days
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40. SURGICAL TECHNIQUE
Extent of thyroidectomy
controversial, and determined by the desired outcome
Risk of recurrence Vs hypothyroid, and surgeons experience
Total or near thyroidectomy
for patients with coexistent thyroid cancer, sever ophthalmopathy, life
treating reactions to antythyroid drugs
Subtotal thyroidectomy is recommended for the rest
bilateral subtotal thyroidectomy in which 1–2 grams of thyroid tissue is
left on both sides.
Hartley Dunhill procedure
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42. Features
Control of toxicity
Return to euthyroid
state
Recurrence
Thyroid failure
Hypoparathyroidism
Followup
Total Thyroidectomy
Immediate
Immediate
None
100%
5%
Minimal
Subtotal
thyroidectomy
Immediate
Variable
5%
25%
1%
lifelong
Surgical options
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43. Postoperative management
Following surgery, thyroid hormone replacement should be
started
TSH should be measured every 1–2 months until stable, and
then annually
RAIT should be used for retreatment of persistent or
recurrent hyperthyroidism following inadequate surgery
Following thyroidectomy, serum calcium hormone levels be
measured, and oral calcium supplementation be
administered based on these results
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44. NOVEL MINIMALLY INVASIVE
THERAPIES
Percutaneous Ethanol Injection (PEI) for Nodules
Injections of ethanol can be administered directly to toxic thyroid
nodules, cysts and large nontoxic thyroid nodules
Ultrasound-Guided Laser Thermal Ablation (LTA) for
Nodules
Percutaneous laser thermal ablation is used to reduce both
hyperfunctioning and compressive nodule
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45. Treatments Under Investigation
Arterial Embolization
Indicated in patients with severe hyperthyroidism who cannot tolerate or
who prefer not to use conventional treatment methods
The Novel Molecule
a small-molecule antagonist that directly inhibits or prevents TSI antibodies from
activating the TSH receptor.
The small-molecule antagonist has not yet been studied in clinical trials
Therapeutic Peptides
antagonistic peptides that interfere with the action of TSH receptor antibodies as
well as peptides that bind to TSH receptor antibodies, preventing them from
reacting with the TSH receptor
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47. Choice of therapy
Diffuse toxic goitre
over 45 years, radioiodine.
under 45 years,
surgery for the large goitre and
anti-thyroid drugs or radioiodine
for the small goitre
Toxic nodular goitre
Surgery
Toxic nodule
Surgery or radioiodine(>45)
Recurrent thyrotoxicosis after surgery
radioiodine is the treatment of choice,
but anti-thyroid drugs may be used in
young women intending to havechildren.
Further surgery has little place.
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51. HEMORRHAGE
Incidence – 0.3-1%
Two types -
Deep to deep fascia
Subcutaneous
May be primary or reactionary
A deep bleeding produces tension hematoma. Usually due to slipping of
the ligature of the superior thyroid artery, though it can also be from a
thyroid remnant or a thyroid vein. This compresses on the airway &
potentially life threatening unlike the subcutaneous bleeding.
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52. HEMORRHAGE
GOOD INTRAOPERATIVE HEMOSTASIS
Don’t traumatize the thyroid
Avoid too much neck dressings
Suction drain ??
Do not waste time on imaging
A tension hematoma requires opening of the
wound, evacuation of hematoma & ligature of the
bleeding vessels
A subcutaneous hematoma can be aspirated.
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53. INFECTION
Cellulitis – erythema, warmth & tenderness
around the wound
Abscess – superficial / deep
Deep abscess associated with fever,
leucocytosis, tachycardia
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54. INFECTION
Pus for Gram’s stain & culture
CT for deep neck abscess
Can be prevented by proper hemostasis at the time
of surgery & using suction drain.
Per-operative antibiotics not recommended.
Once established
Antibiotics
Drainage of abscess.
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55. RECURRENT LARYNGEAL
NERVE PARALYSIS
Temporary paralysis is due to pressure of hematoma on
the nerve. Recovers in 3 weeks to 3 month.
Permanent paralysis is rare (<2%) and is due to undue
stretching or its inclusion in a ligature.
Unilateral –
1/3 rd are asymptomatic
Change in voice
Improves due to compensation by the healthy cord.
Bilateral- dyspnea & biphasic stridor
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56. RECURRENT LARYNGEAL
NERVE PARALYSIS
Prevent injury to the nerve by
Identify
ITA ligated far from lobe
Posterior layer of pretracheal fascia kept intact.
Laryngoscopy, laryngeal EMG
For unilateral paralysis no treatment is required.
For bilateral paralysis
Tracheostomy (with speaking valve.
Lateralization of cord
Arytenoidectomy
Through endoscope
Thyroplasty type 2
Cordectomy
Nerve muscle implant
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60. THYROID CRISIS / STORM
Acute exacerbation of hyperthyroidism as the patient has
not been brought to the euthyroid state before
operation.
Tachycardia, fever(>1050C) , restlessness, delirium
Mortality is 10%
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61. THYROID CRISIS / STORM
Ensure euthyroid state before
operation
Sedation – morphine / pethidine
Hyperpyrexia – ice bags. Tepid
sponging, hypothermic blanket,
rectal ice irrigation
Oxygen administration
IV glucose-saline for dehydration
Potassium for tachycardia
Cortisone – 100mg IV
Carbimazole – 10- 20 mg 6th hourly
Lugol’s iodine 10 drops 8th hourly by
mouth or potassium iodide 1g IV
Propranolol – 20-40mg 6th hourly
Digoxin for atrial fibrillation
Diuretics for cardiac failure
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62. RESPIRATORY
OBSTRUCTION
Laryngeal edema due to
Tension hematoma
Endotracheal intubation & surgical handling
More chance in vascular goiters.
Collapse / kinking of the trachea
Bilateral recurrent nerve paralysis can aggravate
obstruction if edema is present.
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63. RESPIRATORY
OBSTRUCTION
Open the wound & release the tension hematoma
Endotracheal tube if no improvement. INTUBATION TO
BE DONE BY AN EXPERIENCED ANESTHETIST as repeated
attempts cause more edema leading to cerebral anoxia.
The tube is left in place for several days & steroids given
to reduce the edema.
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64. PARATHYROID
INSUFFICIENCY
Due to removal of parathyroids or the parathyroid end artery.
Incidence – 1-3%
Occurs 2 – 5% after operation. Can be delayed for 2-3 weeks or hypocalcemia may be
asymptomatic.
Classic triad –
Carpopedal spasm
Stridor
Convulsions
Latent tetany
Trousseau’s sign
Chvostek’s sign
Persistant – grand mal epilepsy, cataracts, psychosis, calcification of basal ganglia,
papilledema.
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65. PARATHYROID
INSUFFICIENCY
Correct identification of the gland
Ligate vessels distal to the parathyroids.
Recognition of the parathyroid glands, which appear in a variety of shapes
and have a caramel-like color, is critical. When they lose their blood supply,
they turn black. The devascularized gland should be removed, cut into 1 to
2mm pieces, and reimplanted in the sternomastoid muscle or the forearm.
Monitor serum Ca for 72 hrs post-operatively.
20 ml 10% solution of calcium gluconate IV
10 ml injected IM
2.5-5 G calcium carbonate / day
PTH is unsatisfactory.
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66. THYROID INSUFFICIENCY
INCIDENCE :20-25% of patients subjected to subtotal thyroidectomy for diffuse
toxic goiter & toxic nodular goiters with internodular hyperplasia
Time: <2 yrs. May be delayed >5yrs.
Transient hypothyroidism may occur within 6 months which is asymptomatic.
Due to change in nature of autoimmune response.
More chance if less residual thyroid tissue
Cold intolerance, fatigue constipation, weight gain, myxedema.
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67. THYROID INSUFFICIENCY
Thyroxine – start with 50 mcg/d, 100mcg/d after 3 weeks,
and 150 mcg/d thereafter. Taken as a single daily dose.
Monitoring –
TSH in the lower end of reference range (0.15-3.5 mU / l)
T 4 normal or slightly raised. (10 – 27 pmol / l)
Manage ischemic heart disease with beta blockers &
vasodilators
Increase thyroxine during pregnancy. (50 mcg)
Myxedema coma: IV thyroxine 20mcg 8th hourly
followed by oral.
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68. RECURRENT
THYROTOXICOSIS
Incidence 5 – 10%
Due to inadequate removal or hyperplasia of
remaining thyroid tissue.
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69. RECURRENT
THYROTOXICOSIS
Less than 40 yrs – carbimazole
0-3wks 40-60mg/d
4-8wks 20-40mg/d
18-24 months 5-20mg/d
More than 40 yrs – radioiodine
5-10mCi oral; 75% respond in 4-12 weeks
Repeated after 12-24 weeks if no improvement.
Beta blocker / carbimazole cover during lag period.
Long term follow-up for hypothyroidism.
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70. PROGRESSIVE / MALIGNANT
EXOPHTHALMOS
Occurs even when thyrotoxic features are regressing.
Steroids & radiotherapy.
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71. HYPERTROPHIC SCAR /
KELOID
Platysma to be divided at a higher level
Occurs if scar overlies the sternum
Some persons are more susceptible.
May follow wound infection.
Intradermal steroids, repeated monthly.
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72. References
HYPERTHYROIDISM AND OTHER CAUSES OF THYROTOXICOSIS: MANAGEMENT
GUIDELINES OF THE ATA AND AACE Baskin HJ, Cobin RH, Duick DS, et al
(American Association of Clinical Endocrinologists) 2011
Klein I, Becker D, Levey GS.Treatment of hyperthyroid disease. Ann Int
Med.1994;121:281-288.
Schwartz’s Principles of Surgery, 9th ed.
William’s Text Book Of Endocrinology, 11th ed.
Bailey & Loves’ Short Practice of Surgery, 25th ed.
Greenspan’s Basic & Clinical Endocrinology, 8th ed.
Uptodate
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