Thyroid Disorders

Objectives:

● How to evaluate a patient with thyroid disease

● Hypothyroidism and hyperthyroidism
❏ Causes
❏ pathogenesis
❏ diagnosis
❏ treatment
● Other thyroid disorders

​Team Members:​ Saad AL-qahtani + alaa alakeel + hamad alkhudairy + ghada alskait
Team Leader:​ Haneen Alsubki

Revised By:​ Yara aldigi and Basel almeflh

Resources: ​435 team + Davidson + kumar

● Editing file
● Feedback

Color index:​ ​IMPORTANT ​- ​NOTES ​- ​EXTRA ​- Books

 Basic Review of Thyroid Gland

★ Recall synthesis of thyroid hormones​ ​(or don’t)

1. Endoplasmic reticulum synthesizes thyroglobulin (contains tyrosine), Golgi apparatus packages and
sends the thyroglobulin to the colloid.
2. In the basolateral surface, iodide(-) is picked up from blood and trapped into the follicular cell via NIS
(sodium-iodine-symporter).
3. On the apical surface, (Pendin) transporter transports iodide into the colloid, in the colloid iodide(-) is
oxidized into iodine via Thyroid Peroxidase.
4. Now iodine will bind to the Tyrosine ring on the thyroglobulin.
When;
5. One iodine binds to tyrosine --> MIT (monoiodotyrosine)
6. Two iodine bind to tyrosine --> DIT (diiodotyrosine)
7. After that, MIT & DIT or DIT & DIT can form bonds with each
other;
8. MIT + DIT = T3 (Triiodothyronine)
9. DIT + DIT = T4 (Thyroxine)
10. Not done yet -_- because T3 & T4 are still attached to the
thyroglobulin. The compound gets endocytosed back into the
follicular cell. Then it combines with a lysosome to hydrolyze the
peptide chain & release the thyroid hormones (T3& T4).
11. T4 & T3 are sent to the circulation bounded to thyroid binding
proteins (Thyroxine binding globulin TBG). (Because they're lipid
hormones)
Note that:
· T4 is more secreted from the thyroid than T3.
· However T3 is 5x more active than T4.
· Once reaching the target cells T4 is converted to T3 via iodinase enzyme.
· Because thyroid hormones are lipid soluble, they enter the nucleus of target cells to initiate their
actions.

★ Physiological effects of thyroid hormones:

 Hyperthyroidism and thyrotoxicosis

● Hyperthyroidism​: ​hyperactivity of the thyroid gland​ . ​ ​Overproduction (increase synthesis and

release) of thyroid hormone, due to primary (thyroid itself) or secondary (pituitary) cause.
● Thyrotoxicosis:​ is the clinical syndrome that results when tissues are exposed to high levels of
circulating thyroid hormone .​ is a metabolic state caused by elevated circulating FT4 & FT3

★ Conditions Associated with thyrotoxicosis :

● Diffuse toxic goiter (Grave’s disease) ​most common
● Toxic Adenoma
● Toxic multinodular goiter
● Subacute Thyroiditis ​2nd most common. initially causes hyper then hypo.
● Hyperthyroid phase of hashimoto’s thyroiditis
● Thyrotoxicosis factitia ​thyroxine ingested to decrease weight
● Rare:Ovarian struma , metastatic thyroid carcinoma (follicular) , hydatidiform mole ,
TSH secreting pituitary tumor , pituitary resistance to T3 and T4 .

★ Diffuse toxic goiter ​(Grave’s disease) ​we will focus on this mainly ​: ​watch!
● Most common form of thyrotoxicosis
● females > males
● Features :
❏ thyrotoxicosis
❏ goiter
❏ orbitopathy(Exophthalmos)
❏ dermopathy(pretibial myxedema)
❏ thyrotoxicosis + exophthalmos = graves disease

★ Etiology:
- Most common cause of hyperthyroidism (up to 80% of all cases of hyperthyroidism).
- ​Autoimmune disease​ of unknown cause .
-peak incidence in the 20 to 40 year age group .

➔ Pathophysiology:​ The thyrotoxicosis in Grave’s disease results from the production of IgG
antibodies directed against the TSH receptor (​TSH receptor antibodies, TSH stimulating
antibodies​), stimulation of TSH receptor on the thyroid follicular cells increases thyroid hormone
production & cell proliferation (​Diffuse​ goiter in most cases).​but we can’t control it . unlike the TSH
released from the pituitary .
➔ Pathogenesis:​ ​Local viral infection → inflammatory reaction leading to the production of IFN-g
and other cytokines by non-thyroid-specific infiltrating immune cells → will induce the
expression of HLA class II molecules on the surface of thyroid follicular cells.→ Subsequently,
thyroid specific T-cells will recognize the antigen presented on the HLA class II molecules and
will be activated →The activated thyroid-specific T-cells stimulate B cells to produce → ​TSH
receptor-stimulating antibodies → hyperthyroidism
 ★ thyroid function test:

Hyperthyroidism
Types Clinical Hyperthyroidism Subclinical Hyperthyroidism TSH Mediated Hyperthyroidism
Secondary hypothyroidism

Blood -FT4 high FT4 normal FT4 high

Test -FT3 high FT3 normal FT3 high
-TSH low (upper borderline!) TSH high
-you can make the diagnosis by TSH low TSH secreting tumor
TSH alone , but we do T4 to the pituitary is sensing the (not responding to - feedback)
make sure the grade of graves overproduction of thyroid
isn’t really severe .
hormones so TSH decreases
❏ If there is ​Eye signs
before the level T3, T4 get
exophthalmus ​ :
high
No further tests
❏ If there is No eye
signs :
Do thyroid scan

★ Thyroid Scan​ ‫ﻧﻄﻠﺐ‬ ‫ اﻟﺨﻄﻮة اﻟﺜﺎﻧﯿﺔ إﻧﻨﺎ‬,‫​ﻏﺎﻟﺒًﺎ ّﻟﻤﺎ ﻧﻠﻘﻰ زﯾﺎدة ﺑﺎﻟﺜﺎﯾﺮوﯾﺪ ﻫﻮرﻣﻮن وﻣﺎ ﻛﺎن اﻟﺘﺸﺨﯿﺺ واﺿﺢ اﻛﻠﯿﻨﯿﻜﯿًﺎ‬
Radioiodine uptake test

Hot: low risk of Warm: low risk of Cold:Higher risk of malignancy

malignancy. malignancy. (although most cold nodules are
benign).

❖ Examples :
-Spontaneous resolving hyperthyroidism
❖ Examples : -Subacute Thyroiditis​ , inflammation the gland
-​Grave’s disease is destroyed , so low uptake
-TMN -Thyrotoxic phase of hashimoto’s thyroiditis
-Iodine loaded patients
-Patients on LT4 therapy
-Struma ovarii

● Nodules detected by thyroid scans are classified as cold, hot, or warm. If a nodule is composed of cells that do not make thyroid
hormone (don't absorb iodine), then it will appear "cold". A nodule that is producing too much hormone will show up darker and is
called "hot." If appearing “warm” it’s producing normal amount of hormones.
 ★ Symptoms

Clinical Manifestation Of Hyperthyroidism (↑ Thyroxine​)

skin sweating , moist , thin hair .

Brain Hyperthermia, Heat intolerance, Increase appetite, Anxiety, Hand tremor

GIT Hyperdefecation, Loose bowel motion, Increase gluconeogenesis (Failure of controlling a known DM)

Renal Urinary frequency

Heart Palpitation, Sinus tachycardia, Atrial fibrillation

Eye Eyelid lag, Eyelid retraction (staring gaze) Why? because thyroid hormones potentiate the effect of
sympathetic innervation on the eyelid muscle (levator palpebra) → contraction.

Bone Bone fracture, Osteoporosis, Hypercalcemia

Muscles Muscle wasting & weakness, Hyperreflexia, Weight loss

Reproductive Female: Menstrual cycles disturbances (Oligo-or amenorrhea)/ Male: ED

★ Diagnosis

Diagnostic approach of Hyperthyroidism

- Atypical presentations:
Clinically ● Thyrotoxic periodic paralysis ​( most common in asians , they present with changes in
electrolyte and hypokalemia )
● Thyrocardiac disease
● Apathetic hyperthyroidism ​(in elderly , they present with weight loss only)​Symptoms
of hyperthyroidism are blunted in elderly people. they don’t present with ideal symptoms
of hyperthyroidism. some present with only depression, Afib, CHF, or weakness.​ ‫وﻣﻤﻜﻦ‬
‫ ﺗﻘﻮﻟﻪ ﻧﻜﺘﺔ ﻣﺎ ﯾﻀﺤﻚ‬،‫اﻟﻤﺮﯾﺾ ﯾﺠﯿﻚ ﺧﺎﻟﻲ ﻣﻦ اﻟﺘﻌﺎﺑﯿﺮ‬.
● Familial dysalbuminemic hyperthyroxinemia​ rare

-​TSH-R Ab (Stim) ​it increases in graves’ disease

Biochemically -​Free T3 ​in T3 toxicosis when T4 is normal

★ Complications:
Thyrotoxic crisis (thyroid storm)​ :
● Predisposing conditions
​Clinical features​:
● Fever / Agitation t​ hey can’t sit in the bed , very agitated !
● Altered mental status
● Atrial fibrillation / Heart failure
★ Treatment of graves’ disease

A. Antithyroid drug therapy : ​in severe graves’ disease you can only use meds! to
decrease the level of the gland to a level that you can deal with it
❏ Propylthiouracil “​is safe for pregnant ladies”​ or methimazole
-Spontaneous remission 20-40%
-Relapse 50-60%
-Duration of treatment 6 months years
-Reactions to antithyroid drugs ​rare
❏ b-blockers ​to treat symptoms
❏ SSKI​ ​Super saturated pottasium Iodine , it decreases synthesis of thyroid hormones

B. Surgical treatment:​If meds and radioactive iodine failed

-Subtotal thyroidectomy
-Preparation for surgery ​control his HR,BP, thyroxine levels
-Complications:
* hypothyroidism/ hypoparathyroidism a ​ nd hypocalcemia
* Recurrent laryngeal nerve ​injury hoarseness

C. Radioactive iodine therapy​: ​most common therapy . If you have exophthalmos its
contraindicated because it makes it worse .
- I​131 ​is most commonly used
-Dose:
​ I​131 ​(uci/g) x thyroid weight
----------------------------- x 100
​ 24-hr RAI uptake

● Treatment of Graves’ disease ​complications​:

-​Thyrotoxic crisis ​with high dose you need to first prevent the conversion of T4 to T3 with
steroids then you give propylthiouracil then you give IV fluid Beta blockers and Iodine.
- Orbitopathy ​refer to ophthalmologist / give eye drops
- Thyrotoxicosis and pregnancy ​some meds. affect the baby
● Treatment of ​other forms of thyrotoxicosis:
-Toxic adenoma ​if the thyroid has an adenoma producing thyroxine :
1)Meds 2)radio-Iodine(if it’s small) 3)surgery (preferably if it’s big)
-TMN ​toxic multinodular goiter , same approach .
-Amiodarone
-Subacute thyroiditis ​you have to differentiate it from graves because the treatment is different .
here you only treat symptomatically until the inflammation subsides .
-Thyrotoxicosis factitia ​take good history
-Struma ovarii

- how to treat exophthalmos?

1- if active > steroids
2- inactive > Refer to ophthalmology for decompression.

- if someone is taking Amiodarone and developed hyperthyroidism, Do not stop the medication! you should
treat the complications. treatment depend on the type of hyperthyroidism he developed:
1- if graves type → treat with anti-thyroid.
2- if thyroiditis type → symptomatic treatment (Beta-blockers, Aspirin, paracetamol)
- If i ask you how to treat toxic adenoma or toxic multinodular goitre, is it by medication, surgery
- or RAI ? you should answer ALL. medications to start with, then surgery or RAI
 Hypothyroidism​ ​Watch!

Etiology of hypothyroidism

Primary causes Secondary causes Tertiary causes

-( MCQs)
primary = source of problem = thyroid itself Secondary = Source of problem = ❏ ​Hypothalamic
pituitary dysfunction rare .
❏ Hashimoto’s Thyroiditis​: ​most common cause recently , -​Pituitary → decreased TSH → TRH will be low
before it was iodine deficiency . ​characterized by formation of decreased thyroid hormones
antibodies against Thyroglobulin (thyroid hormone precursor) and
Thyroid peroxidase (important thyroid enzyme) destructive lymphoid ❏ Hypopituitarism​ due to:
infiltration of the thyroid, ultimately leading to a varying degree of
fibrosis and thyroid enlargement. (Diffuse goiter)
- Pituitary adenoma
-with goiter ​No iodide > No Thyroid Hormones (T4, T3) > Increase - pituitary ablative therapy
release TSH > Goiter - pituitary destruction
-”Idiopathic” thyroid atrophy , presumably end-stage
autoimmune disease , following either Hashimoto's thyroiditis or
graves disease .
-Neonatal hypothyroidism due to placental transmission of
TSH-R blocking antibodies .
❏ Radioactive iodine therapy for graves’ disease​ ​it causes
destruction of the gland .
❏ Subtotal thyroidectomy for graves’ or nodular goiter ​2nd
most common
❏ Excessive iodine intake (Kelp , radiocontrast dyes)
❏ Subacute thyroiditis​ ​its an inflammatory process that is
caused by viruses or chemicals …
❏ Iodide deficiency
❏ Other goitrogens such as lithium , amiodarone ,
antithyroid drug therapy .
❏ inborn errors of thyroid hormone synthesis , ​that’s why for
the last 5 years they screen all infants for TSH .

other causes:

peripheral resistance of the action of thyroid hormones :

mutation in thyroid hormone receptors in cells leading to High hormones in blood but symptoms of ​hypo​thyroidism

★ Pathogenesis:
- Thyroid hormone deficiency affects every tissue in the body,
so that the symptoms are multiple
- Accumulation of ​glycosaminoglycans-mostly ​hyaluronic acid
in interstitial tissues ​(accumulation causes edema in the face , heart which causes
pericardial effusion , hands which causes carpal tunnel syndrome because of compression on the nerves )
- Increase capillary permeability to albumin
- Interstitial edema ​can affect any part of the body ​(skin, heart muscle, striated muscle)
● Why does edema happen in hypothyroidism ?because TSH becomes high and that stimulates fibroblasts to
increase the deposition of glycosaminoglycan , which results in osmotic edema
 ★ Clinical Features:
● Common feature: easy fatigability, coldness, weight gain, constipation,
menstrual irregularities, and muscle cramps.​ common symptoms and can be associated with any
disease (not specific nor sensitive).
● Physical findings: cool rough dry skin, puffy face and hands, hoarse
husky voice, and slow reflexes, yellowish skin discoloration​.

Clinical Manifestation of Hypothyroidism

DECREASE FUNCTIONS OF THE ORGANS​ ​"except menstrual flow"

Anemia ● Impaired Hb synthesis

why? ● Iron deficiency
the gut has a ● folate deficiency
problem in ● pernicious anemia , with B12 deficient megaloblastic anemia.
absorption
because of edema

skin ● Scaliness of skin, Brittle hair and loss of outer eyebrow

Pulmonary ● Shallow and slow respiration

● respiratory failure

GIT ● Chronic Constipation

● Ileus
● malabsorption

Renal ● Impaired GFR ​Significantly decreased but when you treat Cr. level
returns to normal .
● Water intoxication

CNS ● Chronic fatigue

● lethargy
● decreased concentration
● Anovulatory cycles and infertility
● depression
● agitation
● memory loss

Heart ● Bradycardia
● Decreased cardiac output Low voltage ECG​ ​( because of pericardial
effusion , so the signals won’t reach the electrodes )
● Cardiomegaly
● Pericardial effusion

NeuroMuscular ● Proximal Myopathy

● Delayed Relaxation Reflexes
● Severe muscle cramps
● Paresthesias
● Muscle weakness
● Carpal tunnel syndrome

Reproductive ● Male → Loss of libido.

● Women → Menorrhagia.
 ❖ Hypothyroidism patients are prone to develop Atherosclerosis. Why?​Because lack of Thyroid
hormone → decrease liver uptake of LDL and decrease secretion of cholesterol in bile →
Increase blood cholesterol → Atherosclerosis

★ Complications
1- Regarding​ ​myxedema coma​ ​:
➔ The end-stage of untreated hypothyroidism
➔ Progressive weakness , stupor , hypothermia , hypoventilation , hypoglycemia , hyponatremia ,
water intoxication , shock , and death .
➔ Associate illness and precipitating factors : pneumonia , MI , cerebral thrombosis , GI bleeding ,
ileus , excessive fluid administration , and administration of sedatives and narcotics .
➔ Three main issues : CO2 retention and hypoxia , fluid and electrolyte imbalance and hypothermia
2- ​Myxedema and heart disease​.​(patient with heart disease on levothyroxine treatment can get heart
problems , because he has low metabolism then sudden increase in the metabolism happens so the heart can get
ischemic)
3- ​Hypothyroidism and neuropsychiatric disease.​ ​you can't trust that he is going to take the meds. as
prescribed .

★ Diagnosis:
Hypothyroidism

Biochemical TRH stimulation test Serology

Not used anymore Thyroid Ab

- Primary Hypothyroidism​:​High TSH, The ​TRH test​ involves - Thyroid Peroxidase

Low T4. ​T3 is only important in administration of a small amount autoantibodies.
Hyperthyroidism when we suspect T3 of ​TRH​ intravenously, following - Anti-Thyroglobulin
thyrotoxicosis. which levels of TSH will be
Antibodies.
- Secondary Hypothyroidism​: Low measured at several subsequent
- we order thyroid AB if
time points using samples of
TSH, Low T4 we suspect autoimmune
blood taken from a peripheral
- If I had to choose one test I will choose thyroid disease.
vein. The ​test​ is used in the
TSH because it is the most important test - we can have
differential diagnosis of secondary
used to diagnose primary autoimmune thyroid
and tertiary hypothyroidism.
hypothyroidism. we order free T4 if we disorder with normal
suspect secondary hypothyroidism.So thyroid Antibodies , it’s
basically we first order TSH if it’s high not 100% specific .
then it’s hypothyroidism for sure . if it - Required if the patient
was normal or low , we order T4 to check has mildly elevated TSH
for secondary hypothyroidism . with normal T4.
 ● individual and median values of thyroid function tests
in patients with various grades of hypothyroidism.
Discontinuous horizontal lines represent upper limit (TSH) and
lower limit (FT4,T3) of the normal reference ranges.
Reproduced with permission from Ord WM: On myxedema, a
term proposed to be applied to an essential condition in the
"cretinoid" affection occasionally observed in middle-aged
women. Medico-Chir Trans 1878; 61: 57.

- Subclinical Hypothyroidism: High TSH with normal T4 and

T3.
- Mild Hypothyroidism: High TSH with low T3 and normal
T4.
- Overt Hypothyroidism: High TSH with low T3 and T4.
- Why are the T3 and T4 is normal in the blood?
to protect the tissue (heart, liver, and brain) there is an enzyme that
converts T4 to T3 in the tissue level just to preserve the function to
the important organs.

★ Treatment:
A- ​Levothyroxine (T4)​.
❏ Follow serum Free T4 and TSH. ​T3 is rarely used.
❏ Take dose in AM
❏ Do blood test fasting before taking the daily dose
❏ Adults: 1.7 ug/kg/d, but lower in elderly (1.6 ug/kg/d)​ in the elderly start with small doses
and increase the dose every two weeks and do a Thyroid Function Test.
❏ For TSH suppression (nodular goiters or cancer): 2.2 ug/kg/d
❏ Increase dose of T4 in malabsorptive states or concurrent administration of aluminum
preparations, cholestyramine, calcium, or iron compounds
❏ Increase dose of T4 in pregnancy and lactation
❏ The t1/2 of levothyroxine is 7 days.
❏ we need 6 weeks to follow up thyroid function test because the t1/2 of thyroxine is 7 days.
❏ Scenario : patient diagnosed with primary hypothyroidism you give her thyroxine , she follows up
after 6 months and the TSH was high , how will you approach her? first you have to ask if the
patient is taking her drugs properly “Compliance” then look for malabsorption state or pregnancy
in order to increase the dose.
❏ If the patient takes any medications that affects thyroxine absorption , you have to seperate them
by 4 hours .

B- Myxedema coma ​first stabilize the pt.

❏ Acute medical emergency
❏ Monitor blood gases
❏ Patient may need intubation and mechanical ventilation
❏ Treat associated medical problems
❏ Avoid excessive hydration
❏ Assess adrenal function and treat if needed
❏ In pituitary myxedema, glucocorticoid replacement is essential
❏ IV levothyroxine: loading 300-400 ug, daily maintenance 50 ug
❏ Be cautious in patients with coronary artery disease ​they may develop MI .
 ❏ Active rewarming of the body in contraindicated. ​we use passive rewarming with blankets ,
because if we use active rewarming(we will drop the vascular resistant abruptly ) and it will
induce vasodilation and cause hypotension .
❏ confirm from the history of the patient + symptoms . ask the family , friends about compliance of
meds. is he out of meds.? is he skipping doses ?

C- Myxedema with heart disease

❏ Start treatment ​slowly​ in long standing hypothyroidism and in elderly patients
particularly those with known cardiovascular disease ​gradually !
❏ 25 ug/d x 2 weeks, increase by 25 ug every 2 weeks until a daily dose of 100-125 ug is
reached.

● Toxic effects of levothyroxine therapy ​thyroxine is the safest drug that you will come
upon in medical practice
❏ N​ o allergy has been reported to pure levothyroxine -
❏ If FT4 and TSH are followed and T4 dose is adjusted, no side effects are reported
❏ If FT4 is higher than normal ​if he is talking a higher dose than he needs :​ hyperthyroidism
symptoms may occur
-Cardiac symptoms
-Osteopenia and osteoporosis

● Recommendations for the treatment of myxedema coma

• hypothyroidism large initial intravenous dose of 300-500 μg T4; if no response within

48 hours, add T3

• hypocortisolemia intravenous hydrocortisone 200-400 mg daily

• hypoventilation don’t delay intubation and mechanical ventilation too long

• hypothermia blankets, no active rewarming: ​Giving the patient warm saline by an NGT
or a catheter.

• hyponatremia mild fluid restriction

• hypotension cautious volume expansion with crystalloid or whole blood

• hypoglycemia glucose administration

• precipitating event identification and elimination by specific treatment (liberal use of

antibiotics)

★ Other Thyroid disorders :

● Nontoxic goiter
● Subacute thyroiditis(De quervains)
● Chronic thyroiditis
● Acute Thyroiditis
● Thyroid nodules
● Thyroid cancer
 Hx & Physical Exam of Thyroid

1. lithium carbonate ​for psychiatric pts. It causes hypothyroidism mainly

2. Iodide -​is a substrate that is used by thyroid gland to produce hormones-​ ingestion (Kelp
seaweeds that contains iodine​, Iodide-containing cough preparation i​ n pts who have
History chronic cough ​, Iv iodide-containing contrast A ​ sk if the pt. had a recent cath for example.
Can cause both hypo and hyperthyroidism.
3. Residence in an area of low dietary Iodide
4. Radiation exposure ​it can cause thyroid cancer . Ask if they work in labs , Or if they had
many CT scans . Also, if they ever come upon a disaster that causes leak of radioactive
material .
5. family history
-Thyroid disorders
-Immunologic disorders(DM , rheumatoid , pernicious anemia ,
alopecia,vitiligo,myasethenia gravis , MEN2a )

1. Observe the neck , especially as the patient swallows .

2. Examine from the front , rotating the gland slightly with one thumb while palpating
Examination the other lobe with the other thumb .
Do general 3. Examine from behind , using three fingers and the same technique
examination for the 4. determine the size of the thyroid lobes , consistency , presence of nodules .
whole body 5. Tachycardia or atrial arrhythmia ,Systolic hypertension with wide pulse pressure
,Warm, moist, smooth skin
6. Lid lag ,Stare
7. Hand tremor, Muscle weakness
8. Dermatologic examination:
- Pretibial myxedema
- non- pitting edema, erythema and thickening of the skin, without pain or pruritus

Thyroid uptake scan:

Anatomical - Technetium-99m (99m Tc)
- Iodine-123 (123 I)
 Summary
Thyroid Disorders:
➔ Hyperthyroidism Or Hypothyroidism
➔ Others: Nontoxic goiter, Subacute Thyroiditis, Acute thyroiditis, Chronic thyroiditis, Thyroid Nodules,
Thyroid Cancer.

Hyperthyroidism ​& Hypothyroidism

Thyrotoxicosis

Causes Primary:
- Diffuse toxic goiter (Graves’ - ​Hashimoto’s thyroiditis.
disease)
- Toxic adenoma (Plummer’s - Radioactive iodine therapy
disease) - thyroidectomy
- Toxic multinodular goiter - Excessive iodine intake (kelp, radiocontrast dyes)
- Subacute thyroiditis - Subacute thyroiditis
- Hyperthyroid phase of - Iodide deficiency
Hashimoto’s thyroiditis - Other goitrogens such as lithium, amiodarone,
- Iodine-induced hyperthyroidism antithyroid drug therapy

- Thyrotoxicosis factitia
- ovarian struma
Secondary: ​Hypopituitarism due to
a- Pituitary adenoma b- pituitary ablative therapy c- pituitary
destruction

Tertiary: ​Hypothalamic dysfunction

Peripheral resistance of thyroid hormone

Clinical Skin​: Sweating, Moist warm skin, General​: Myxedematous Appearance ​Weight gain
Manifestation palmar erythema, thin hair. Skin​: Scaliness of skin, Brittle hair.
Brain​: Hyperthermia, Heat intolerance, Brain​: Cognitive dysfunction, Hypothermia, Cold
Increase appetite, Anxiety, Hand tremor. Intolerance, Extreme Somnolence (sleepiness), Decrease
GIT​: Loose bowel motion Appetite​
Renal​: Urinary frequency. GIT​: Constipation
Heart​: Palpitation, Sinus tachycardia, Renal​: Oliguria​
Atrial fibrillation. Heart​: Bradycardia Eye Periorbital Edema
Eye​: eyelid lag, Eyelid retraction (staring Muscles​: Proximal Myopathy, Fatigue, Delayed Relaxation
gaze) Reflexes.
Bone​: bone fracture, Osteoporosis, Reproductive​:
Hypercalcemia. Male>Loss of libido. Women>Menorrhagia.
Muscles​: muscle wasting & weakness,
Hyperreflexia, Weight loss.
Reproductive​: Female: Menstrual cycles
disturbances (Oligo-or amenorrhea)/
Male: ED
 Specific manifestations in graves’
disease:
Orbitopathy (exophthalmos),
Dermopathy (pretibial myxedema)..

Diagnosis Biochemical: Biochemical:

- Clinical Hyperthyroidism: ​FT4 high, - Primary Hypothyroidism​:​High TSH, Low T4
FT3 high, TSH low - Secondary Hypothyroidism​: Low TSH, Low T4
- Subclinical Hyperthyroidism: ​FT4 Serology:​ Thyroid antibodies
normal, FT3 normal, TSH low. ECG
- TSH Mediated Hyperthyroidism​: FT4
high, FT3 high, TSH high.
Radiological:​Thyroid Scan
Serology: ​ Thyroid antibodies,​ ​TSH
Receptor antibodies.

Complications Thyrotoxic crisis (thyroid storm): 1- ​Myxedema coma

* Fever / Agitation 2- ​heart disease
* Altered mental status 3- ​neuropsychiatric disease
* Atrial fibrillation / Heart failure

Treatment ● Anti-thyroid medications​: Levothyroxine (T4) Replacement:

Propylthiouracil or - Lower dose in elderly and higher dose in pregnancy and
methimazole​. ​ lactation
● Radioactive iodine therapy​: (
131I )
● Beta Blockers
● SSKI
● Thyroidectomy
 ​Questions
Q1) A 30-year-old woman complains of palpitations, fatigue, heat intolerance, and insomnia. She is
otherwise healthy. She and her husband desire children and are not interested in contraception. On
physical examination, her extremities are warm and she is tachycardic. There is diffuse thyroid
enlargement and exophthalmos, as well as thickening of the skin in the pretibial area. Laboratory
testing reveals a free T4 value of 3.2 ng/dL (normal 0.9-2.4) with an undetectably low TSH level.
Radioiodine uptake at 24 hours is 42% (normal 10%-30%). What is the best treatment plan for this
patient?

A. Propylthiouracil
B. Radioactive iodine
C. Propranolol
D. Thyroid surgery
E. Oral corticosteroids

Q2)On routine physical examination, a 28-year-old woman is found to have a thyroid nodule. She
denies pain, hoarseness, hemoptysis, or local symptoms. Serum TSH is normal. Which of the
following is the best next step in evaluation?

A. Thyroid ultrasonography
B. Thyroid scan
C. Surgical resection
D. Fine needle aspiration of thyroid

Q3) A 60-year-old woman comes to the emergency room in a coma. The patient’s temperature is
32.2°C (90°F). She is bradycardic. Her thyroid gland is enlarged. There is diffuse hyporeflexia. BP
is 100/60. Which of the following is the best next step in management?

A. Await results of T4 and TSH.

B. Obtain T4 and TSH; begin intravenous thyroid hormone and glucocorticoid.
C. Begin rapid rewarming
D. Obtain CT scan of the head.
e. Begin intravenous fluid resuscitation.

Q4) which of the following is contraindicated in patient suffering from exophthalmos?

A.RAI
B.​propylthiouracil(PTU)
C.methimazole

Q5) which of the following tests is used to assess the severity of Graves disease ?
A.TSH
B.FREE T4
C.T3
D.UREA

Q6) A 25-year-old woman comes to the clinic for routine check up with no active symptoms. Serum
TSH is elevated. free T3 and T4 are normal. What is the diagnosis?
A.Subclinical Hypothyroidism.
B.Euthyroid.
C.Mild Hypothyroidism.

Q7) For the case above, What’s the next step in investigations?
A.Wait for symptoms to appear.
B.Start the patient on thyroxine.
C.Order thyroid Ab.

Q8) A 16-year-old girl presents to her GP complaining of a swelling in her neck which she has
noticed in the last 2 weeks. She has felt more irritable although this is often transient. On
examination, a diffuse swelling is palpated with no bruit on auscultation. The most likely diagnosis
is:
A.Hyperthyroidism.
B.Simple goiter.
C.Thyroid carcinoma.

Q9) A 60-year-old woman presents to a physician complaining of swelling in her neck. Her past
medical history is significant for rheumatoid arthritis and Sjogren syndrome. Physical examination
reveals a mildly nodular, firm, rubbery goiter. Total serum thyroxine (T4) is 10 mg/dL, and
third-generation thyroid-stimulating hormone (TSH) testing shows a level of 1.2 mIU/mL.
Antithyroid peroxidase antibody titers are high, which of the following is the most likely diagnosis?
A.Hashimoto thyroiditis.
B.Euthyroid sick syndrome.
C.Subacute thyroiditis
Q10) A 20-year-old woman presents after recent upper respiratory infection. She complains of neck
pain and heat intolerance. The thyroid is tender. Erythrocyte sedimentation rate is elevated; free
thyroxine value is modestly elevated. What is the most likely diagnosis?
A. Struma ovarii.
B.Euthyroid sick syndrome.
C.Subacute thyroiditis.

ANS: 1-A,2-D,3-B,4-A,5-B,6-A,7-C,8-B,9-A,10-C