thyroid disases final.pdf111

Ala’a Aljohan

Sara Aljaouni

Family medicine

Neck masses

Hyperthyroidism disorder

Hypothyroidism disorder

Case simulation

Overview:

neck masses

Family physicians frequently encounter neck masses in adult patients. A careful medical history should be obtained, and a thorough physical examination should be performed. The patient's age and the location, size, and duration of the mass are important pieces of information. Inflammatory and infectious causes of neck masses, such as cervical adenitis and cat-scratch disease, are common in young adults. Congenital masses, such as branchial anomalies and thyroglossal duct cysts, must be considered in the differential diagnosis. Neoplasms (benign and malignant) are more likely to be present in older adults. Fine-needle aspiration and biopsy and contrast-enhanced computed tomographic scanning are the best techniques for evaluating these masses.

American academy of family physician. 2015

Central Neck

is the most common duct cyst thyroglossalThe

congenital anomaly of the central portion of the neck .This

anomaly is caused by a tract of thyroid tissue along the

pathway of embryologic migration of the thyroid gland from

the base of the tongue to the neck. The thyroglossal duct

cyst is intimately related to the central portion of the hyoid

bone and usually elevates along with the larynx during

swallowing. It may contain the patient's only thyroid tissue.

vtg9huFWWP8https://www.youtube.com/watch?v=

Video shows thyroglssal cyst

https://www.youtube.com/watch?v=8huFWWP9vtg





procedure, which Sistrunkis the The treatment of choice

involves complete excision of the thyroglossal duct cyst,

including the central portion of the hyoid bone. If necessary,

excision extends to the base of the tongue.

Thyroid nodule Thyroid nodules are common in the general population,

especially in women. Nonpalpable nodules are often found

when patients undergo diagnostic imaging such as

ultrasonography and computed tomography of the chest

and neck. For these incidentalomas, current guidelines

recommend the same diagnostic strategy that is

recommended for palpable nodules. Although the risk of

malignancy in any given nodule is small, thyroid cancer must

be considered in the differential diagnosis. Family physicians

should understand the rationale for the evaluation of

nodules and be able to perform an evidence-based

assessment.


presentation Thyroid nodules are often noticed by patients as a lump or

protrusion in the lower anterior neck. Large nodules can

cause compressive symptoms, such as difficulty swallowing

or a choking sensation. Nodules may be single or multiple,

hard or soft, and tender or nontender.

Nodules may also be found by physicians on routine

examination. Clinical examination of the thyroid is difficult

in persons with large necks. Nodules 1 cm or smaller are

rarely detected by palpation.


Thyroid nodule

palpated

Thyroid u/s

Multiple

nodule

Single

nodule

Single nodule

TSH Suppressed: radioactive iodine scan:

1- hot nodule : benign FNA unnecessary.

2- cold nodule: perform FNA.

TSH normal or elevated: perform FNA.

Multiple nodule TSH suppressed: radioactive iodine scan

1- diffuse hetro uptake: benign FNA

unnecessary .

2- cold nodule :FNA

TSH normal or elevated: perform FNA.

Radioactive scan

Red flags:

1- patient aged >65y

2-solitary nodule increasing in size.

3-history of neck irradiation.

4-unexplained hoarseness of voice .

5- cervical lymphadenopathy.

6- very young patient.

Screening for Thyroid Dysfunction: Clinical Summary of the

USPSTF Recommendation

Population

Nonpregnant, asymptomatic adults

Recommendation

No recommendation

Grade: I statement (insufficient evidence)

Risk assessment

Risk factors for an elevated thyroid-stimulating hormone (TSH) level include female sex,

advancing age, white race, type 1 diabetes, Down syndrome, family history of thyroid disease,

goiter, previous hyperthyroidism, and external-beam radiation in the head and neck area. Risk

factors for a low TSH level include female sex; advancing age; black race; low iodine intake;

personal or family history of thyroid disease; and ingestion of iodine-containing drugs, such as

amiodarone.

Screening tests

The primary screening test for thyroid dysfunction is serum TSH testing. Multiple tests over 3 to

6 mounth should be performed to confirm or rule out abnormal findings. Follow-up testing of

serum thyroxine (T4) levels in persons with persistently abnormal TSH levels can differentiate

between subclinical (normal T4) and “overt” (abnormal T4) thyroid dysfunction.

Introduction The proper treatment of hyperthyroidism depends on

recognition of the signs and symptoms of the disease and

determination of the etiology. The most common cause of

hyperthyroidism is Graves’ disease. Other common causes

include thyroiditis, toxic multinodular goiter, toxic

adenomas, and side effects of certain medications.


Common Etiology and Clinical Diagnosis

of Hyperthyroidism:

Graves’ disease

Toxic adenoma

Toxic multinodular goiter

Thyroiditis

Hyperthyroidism

T = Tremor

H = Heart rate up

Y =Yawning [fatigability]

R = Restlessness

O = Oligomenorrhea & amenorrhea

I = Intolerance to heat,

D =Diarrhea

I = Irritability

S = Sweating

M = Musle wasting & weight loss

E = Exophthalmos

Graves’ disease (thyroid-stimulating

antibody)

Pathophysiology:

Increased glandular stimulation (substance causing

stimulation).

Gland size:

Increased.

Nodularity:

None.

Tenderness:

Nontender.

GRAVES’ DISEASE

1-Graves’ disease is the most common cause of

hyperthyroidism, accounting for 60 to 80 percent of all

cases.

2- It is an autoimmune disease caused by an antibody, active

against the thyroid-stimulating hormone (TSH) receptor,

which stimulates the gland to synthesize and secrete excess

thyroid hormone. It can be familial and associated with

other autoimmune diseases.

3-An infiltrative ophthalmopathy accompanies Graves’

disease in about 50 percent of patients.


ophthalmopathy

1- periorbital edema.

2-conjunctival edema (chemosis).

3- poor lid closure.

4- extraocular muscle dysfunction ( diplopia).

5- proptosis ( exophthalmos) .

6- lid lag sign (von Graefes sign): lagging of the upper eyelid

on downward rotation of the eye.

7- lid retraction : sclera is visible above the superior corneal

limbus.

Toxic adenoma

PATHOPHYSIOLOGY:

Autonomous hormone production.

GLAND SIZE:

Decreased.

NODULARITY:

Single nodule.

TENDERNESS:

Nontender.

Toxic adenoma

Toxic adenomas are autonomously functioning nodules that

are found most commonly in younger patients and in

iodine-deficient areas.



PATHOPHYSIOLOGY:

Autonomous hormone production.

GLAND SIZE:

Increased.

NODULARITY:

Multiple nodules.

TENDERNESS:

Tender.



1-Toxic multinodular goiter causes 5 percent of the cases of

hyperthyroidism in the United States and can be 10 times

more common in iodine-deficient areas.

2-It typically occurs in patients older than 40 years with a

long-standing goiter, and has a more insidious onset than

Graves’ disease.


Lymphocytic thyroiditis, postpartum

thyroiditis, medication-induced

thyroiditis

Pathophysiology:

Leakage of hormone from gland.

Gland size:

Moderately increased.

Nodularity:

None.

Tenderness:

Nontender


Thyroiditis

Thyroiditis is a general term that refers to inflammation of

the thyroid gland and encompasses several clinical

disorders. The family physician will most commonly

diagnose thyroiditis because of abnormal results on thyroid

function testing in a patient with symptoms of thyroid

dysfunction or anterior neck pain.


Subacute thyroiditis

Leakage of hormone from gland.

Gland size:

Increased.

Nodularity:

None.

Tenderness:

Tender


Subacute thyroiditis (subacute

granulomatous thyroiditis, giant cell

thyroiditis, de Quervain thyroiditis)

Presentation:

Thyroid pain; hyperthyroidism followed by transient

hypothyroidism most commonly.

Etiology:

Post viral.

Diagnosis:

Thyroid function tests; elevated TPO antibody levels; low

radioactive iodine uptake in the hyperthyroid phase.


Complication:

Euthyroidism is generally achieved by 18 months, but up to

15% of patients become permanently hypothyroid; rarely

recurs.

Treatment:

Beta blockers can be considered for significant hyperthyroid

symptoms (in the hyperthyroid phase); levothyroxine for

symptomatic hypothyroidism (in the hypothyroid phase) and

permanent hypothyroidism.


TREATMENT-INDUCED

HYPERTHYRIODISM

1- Amiodarone. 2- interferon alfa. 3-interlukin 2 4- excess iodine.


KEY RECOMMENDATIONS FOR PRACTICE

1-Patients with subacute thyroiditis should be started on high-dose acetylsalicylic acid or nonsteroidal anti-inflammatory drugs as first-line therapy. C

2-Corticosteroid therapy for subacute thyroiditis should be initiated in patients with severe neck pain or minimal response to acetylsalicylic acid or nonsteroidal anti-inflammatory drugs after four days. C

3-Patients with severe thyroid pain and systemic symptoms (e.g., high fever, leukocytosis, cervical lymphadenopathy) should undergo fine-needle aspiration to rule out infectious thyroiditis. C


Diagnosing Hyperthyroidism

interpretation

TSH: 0.05-4.70 mIU/mL.

FT4: 12,00- 22 pmol/L.

FT3:2,80-7.10pmol/L.

TSH: LOW , freeT4: normal , freeT3: normal

Mild ( subclinical ) hyperthyrodism.

TSH: LOW , free T4: high or normal, free T3: high or normal.

Hyperthyroidism.

Treatment of Hyperthyroidism:

)atenelol, propanololblockers( Beta

Inhibit adrenergic effects.

Indication:

Prompt control of symptoms; treatment of choice for

thyroiditis; first-line therapy before surgery, radioactive

iodine, and antithyroid drugs; short-term therapy in

pregnancy.

CONTRAINDICATIONS :

Use with caution in older patients and in patients with pre-

existing heart disease, chronic obstructive pulmonary

disease, or asthma.


Iodides

Block the conversion of T4 to T3 and inhibit hormone release.

Indication:

Rapid decrease in thyroid hormone levels; preoperatively when

other medications are ineffective or contraindicated; during

pregnancy when antithyroid drugs are not tolerated; with

antithyroid drugs to treat amiodarone induced hyperthyroidism.

Complication:

common side effects of sialadenitis, conjunctivitis, or acneform

rash; interferes with the response to radioactive iodine.


PTU)and methimazoledrugs ( Antithyroid

Interferes with the organification of iodine; PTU can block

peripheral conversion of T4 toT3 in large doses.

Indication:

Long-term treatment of Graves’ disease PTU is treatment

of choice in patients who are pregnant and those with

severe Graves’ disease; preferred treatment by many

endocrinologists for children and for adults who refuse

radioactive iodine; pretreatment of older and cardiac

patients before radioactive iodine or surgery; both

medications considered safe for use while breastfeeding.


Radioactive iodine

Concentrates in the thyroid gland and destroys thyroid

tissue.

Indication:

radioactive iodine is the treatment of choice for most

patients with Graves’ disease and multinodular goiter, toxic

nodules in patients older than 40 years, and relapses from

antithyroid drugs.

contraindicated in patients who are pregnant or

breastfeeding; can cause transient neck soreness, flushing,

and decreased taste.


Surgery (subtotal thyroidectomy)

Reduces thyroid mass.

Indication:

Treatment of choice for patients who are pregnant and children who have had major adverse reactions to antithyroid drugs, toxic nodules in patients younger than 40 years, and large goiters with compressive symptoms; can be used for patients who are noncompliant, refuse radioactive iodine, or fail antithyroid drugs, and in patients with severe disease who could not tolerate recurrence; may be done for cosmetic reason.

Complication:

Risk of hypothyroidism (25 percent) or hyperthyroid relapse (8 percent); temporary or permanent hypoparathyroidism or laryngeal paralysis (less than 1 percent).


Hypothyroidism is defined as failure of the thyroid

gland to produce sufficient thyroid hormone to meet the

metabolic demands of the body.

Under activity of the thyroid gland may be primary from

disease of thy thyroid gland or much less commonly

secondary to hypothalamic or pituitary diseases

(secondary hypothyroidism)

It is much more common in women& the incidence

increases with age

5th edition Essentials of Kumar&clark’s clinical medicine

American academy of family physician 2015

AUTOIMMUNE THYRODITIS IATROGENIC DRUG INDUCE IODINE DEFICIENCY SUBCLINICAL HYPOTHYRODISIM CONGINITAL HYPOTHYRODISM MYXEDEMA COMA

Common Etiology and Clinical

Diagnosis of Hypothyroidism:

Autoimmune thyroditis

((Hashimoto thyroiditis

The Most Common Cause of Hypothyroidism

The name Hashimoto's thyroiditis is derived from

the 1912 pathology report by Hashimoto

describing patients with goiter and intense

lymphocytic infiltration of the thyroid as "struma

lymphomatosa"

Uptodate

It is characterized clinically by gradual thyroid

failure, with or without goiter formation, due to

autoimmune-mediated destruction of the thyroid

gland involving apoptosis of thyroid epithelial

cells.

The presence of serum thyroid autoantibodies

may be sufficient evidence for Hashimoto's

disease

Uptodate

Several antibodies and antigen-specific T cells directed

against thyroid antigens have been described in chronic

autoimmune thyroiditis. The major antigens are:

Thyroglobulin (Tg)

Thyroid peroxidase (TPO, historically known as the

“microsomal” antigen)

The thyrotropin (TSH) receptor

IATROGENIC

The second most common cause after treatment of

hyperthyroidism:

Thyroidectomy

Radioactive iodine

External neck irradiation for head and neck cancer

Blueprints family medicine 3rd edition

Drug induced

Carbimazole

Lithum

Amiodarone

interferon


Subclinical hypothyroidism

Subclinical hypothyroidism is a biochemical diagnosis

defined by a normal-range free T4 level and an elevated

TSH level


Investigation

TSH

Free T4 ( why?)

Thyroid antibodies

CBC

Lipid profile

biochemistry

Investigation

T3 T4 TSH

Low or normal

Low or normal increase 1ry

hypothyroidism

low low low 2ry

hypothyroidism

Normal normal slight Subclinical

hypothyroidism

5th edition Essentials of Kumar & clark’s clinical medicine

Screening

Family physician should evaluate for thyroid dysfunction in

all patient with symptoms of hypothyroidism.

Screening of asymptomatic patientmay be consider in

those with risk factors for hypothyroidism, such as history

of autoimmune disaes ,history of head or neck irradtion,

previous radioactive iodine therapy, presence of

goiter,family history of thyroid diseas or treatment with

drug known to influence thyroid function.


Sings &symptoms of hypothyroidism

High TSH TSH normal TSH low

Measure TSH

High TSH

•Measure T4

TSH normal

•Patient is euthyroid

TSH low

•Consider hyperthyriroidism

Free T4 below normal range

•1ry hypothyroidism

Free T4 is within normal range

•Subclinical hypothyroidism

T4 above normal range

•No 1ry hypothyroidism

Management

Most patient with hpothyroidism will require lifelong

thyroid hormone therapy

1.6 mcg\kg\day(initial dosage) Non pregnant

25-50 mcg daily starting dose increase by

25mcgevery three to four weeks until full

replacement

Older patient

+cardiac disease

increase to nine doses weekly (one extra dose on

two days of the week) at earliest knowledge of 2pregnancy; refer to endocrinologist

Pregnant patient

TSH < 10 mIU per L: 50 mcg daily, increase by

25 mcg daily every six weeks until TSH = 0.35

to 5.5 mIU per L

Patient with

subclinical

hypothyroidism

26mcg per kg per day6 .1mIU per L: 10 TSH ≥

http://www.aafp.org/afp/2012/0801/p244.html

http://www.aafp.org/afp/2012/0801/p244.html

Congenital hypothyroidism

Congenital hypothyroidism can cause mental retardation

(cretinism) unless thyroid therapy is initiated within two

weeks of birth

The condition typically is permanent, although transient

hypothyroidism can result from transmission of maternal

medications, maternal blocking antibodies, or iodine

deficiency or excess

dM6https://www.youtube.com/watch?v=TXVNSLgw

Baby with congenital hypothyrodisim

https://www.youtube.com/watch?v=TXVNSLgw6dM



MYXEDEMA COMA

. Myxedema coma is a rare but extremely severe

manifestation of hypothyroidism

most commonly occurs in older women who have a

history of primary hypothyroidism

Mental status changes including lethargy, cognitive

dysfunction, and even psychosis, and hypothermia are the

hallmark features of myxedema coma. Hyponatremia,

hypoventilation, and bradycardia can also occur


Investigation :

is given hormonbefore thyroid cortisol,& 4Serum TSH,T

Full blood count,serum ureaand electrolyes,blood glucose and

blood cultures

ECG monitoring for cardic arrhythmias

Treatment:

T3 orally or intravenously 2.5-5 microgram every 8 h

Oxygen (by mechanical ventilation if necessary)

Gradual rewarming

Hydrocortisone 100 mg i.v. 8 h

Glucose infusion to prevent hypoglycemia

Supportive management of comatose patient


American Academy of family physician

45 years old female known cases of DM on metformin 750

ml BID present to her family physician for her usual

follow up, her physician note that her weight continues

increase since she start her follow up.

Her weight in 1st visit was 60 kg

Her weight after 3 months 65 kg

Her weight after 6 months 72 kg

history

Examination

Investigation

Management

Follow up

Examination of thyroid gland

https://www.youtube.com/watch?v=ziaYBkgEZNU

thyroid disases final.pdf111

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