Thyroid Disorders Hyperthyroidism - PowerPoint Presentation

Slide1

Thyroid Disorders

Hyperthyroidism

Prepared by : Stephanie N. Ammari

Resources : Davidson ,

Medstudy

Slide2
Normal Physiology

Slide3

THYROID FUNCTION TESTS

TFTs

include TSH, FT4, and sometimes

FT3

.

When

screening for primary thyroid

disease:

start with a TSH to detect abnormalities of thyroid

function (both

hyper- and

hypothyroidism) .

If

the TSH is high, then order a

FT4

to assess for hypothyroidism.

If

the TSH is low, then order a FT 3 + FT 4 to assess

for hyperthyroidism .

Slide4
OTHER THYROID TESTS

Radioactive

iodine uptake (RAIU

) .

Thyroid

scan (also called "

scintigraphy

").

Ultrasound

.Biopsy (Fine needle aspiration (FNA) is a biopsy method used to evaluate a thyroid nodule ) .

Slide5

The thyroid RAIU and

scintigraphy

scan are essential in determining the cause of hyperthyroidism and are never used in the workup of a hypothyroid patient.

RAIU produces a

number ,

the scan produces a picture.

Slide6
Hyperthyroidism ( thyrotoxicosis )

The most common cause of hyperthyroidism is

autoimmune Graves

disease

.

Other causes :

toxic

multinodular

goiter (MNG

)toxic adenomas .thyrotoxicosis due to chronic autoimmune thyroiditis (hashitoxicosis).

Transient illnesses not associated with long-term primary hyperthyroid disease :

Subacute

and postpartum thyroiditis

.

Slide7

Symptoms

• Anxiety and restlessness

• Irritability

•

Insomnia

• Impaired concentration (even confusion or psychosis

) • Weight loss despite normal diet • Diarrhea

• Heat intolerance •

Alopecia

• Dyspnea

• Menstrual irregularities (

oligo

- or amenorrhea, impaired

fertility)

• In males:

gynecomastia

, decreased libido, impaired spermatogenesis, and/or erectile dysfunction

Slide8
Physical Exam

•

Warm

skin .

•

The "hyperthyroid stare"( exophthalmos

) .

• Lid-lag & lid retraction . • Hypertension . • Increased heart rate . • Atrial fibrillation or

ectopy in up to 20% of patients (more common in elderly) .Thyroid Acropachy .

In Goiter : diffuse enlargement of thyroid gland

Slide9
Graves Disease

The thyrotoxicosis results from the production of immunoglobulin G (

IgG

) antibodies directed against the TSH receptor on the thyroid follicular cell, which stimulate thyroid hormone production and proliferation of follicular cells, leading to

goitre

in the majority of patients

.

These antibodies are termed thyroid-stimulating

immunoglobulins or TSH receptor antibodies (TRAb) and can be detected in the serum of 80–95% of patients with Graves’ disease.

Slide10
Graves Disease

Graves’ disease has a strong genetic component

.

Genomewide

association studies have identified polymorphisms at the MHC, CTLA4, PTPN22, TSHR1 and FCRL3 loci as predisposing genetic

variants .

A suggested trigger for the development of thyrotoxicosis in genetically susceptible individuals may be infection with viruses or bacteria.

Slide11

Specific Graves disease physical

findings :

A diffuse, soft, symmetric goiter (but not always

) .

Ophthalmopathy

: Exophthalmos

and

periorbital edema with impaired extraocular movements diplopia

, corneal ulcerations, visual impairment. Dermopathy

: Pretibial

myxedema .

Immune-mediated

hematologic abnormalities, such as pernicious anemia and idiopathic thrombotic

purpura

.

Slide12

Slide13

Treatment is rarely required but in severe cases topical glucocorticoids may be helpful.

This infiltrative

dermopathy

occurs in fewer than 5% of patients with Graves’ disease

It takes the form of raised pink-

coloured

or purplish plaques on the anterior aspect of the leg, extending on to the dorsum of the foot

.

The lesions may be itchy and the skin may have a ‘

peau

d’orange

’ appearance with growth of coarse hair; less commonly, the face and arms are affected.

Slide14
Diagnosis

clinical exam + TFTs +

thyroid

uptake scan (TUS

).

TSH is low (usually < 0.01

mU

/L

)

.FT3 and FT4 are elevated (rarely, only FT3 is increased with normal FT4) .

the TUS shows increased diffuse uptake.

Slide15

Other common lab abnormalities:

elevated alkaline phosphatase,

hypercalcemia

, anemia, and thrombocytopenia.

Autoantibodies

are generally not measured, but TSI (thyroid-stimulating

immunoglobulins

) are positive in > 90% of cases of Graves disease.

Slide16

Treatment

Treat with

antithyroid

drugs (

methimazole

[MMI] or

propylthiouracil

[PTU]) and/or thyroid ablation with

ᶦᶟᶥ I or surgery .

Slide17
Treatment

MMI

is

the preferred drug in non-pregnant patients because of lower toxicity than PTU.

PTU

:

is

still 1st line treatment for Graves disease in pregnant patients in the 1st trimester and is still used for thyroid storm.

PTU received a FDA boxed warning for increased risk of death due to acute liver failure or severe liver injury .

Slide18
Treatment

The most serious side effects of PTU and MMI are

hepatic toxicity and

agranulocytosis

, which are rare and unpredictable

.

LFTs and CBCs do not require monitoring

.

Check only if the patient becomes symptomatic (jaundice, dark urine, prolonged fever/sore throat). Side effects almost always disappear when the drug is promptly discontinued. Beta-blockers help patients with adrenergic symptoms while waiting on the effects of PTU or MMI.

Slide19
Treatment

Thyroid ablation using

ᶦᶟᶦ I

.

Virtually all patients are pretreated with beta-blockers, and many patients are treated with MMI (or PTU) prior to radioiodine ablation.

Most

patients become hypothyroid months to years after

ᶦᶟᶦ

I therapy.

Slide20

Surgery

Surgery may be indicated

in :

pregnancy

.

in patients with an associated cold nodule or relapse after

radiation . in some young patients with a large goiter.

# Worrisome complications of surgery are loss of all parathyroids and damage to recurrent laryngeal nerves .

Slide21

Thyroid Storm

Storm is the

2

nd

thyroid emergency that is associated with a high mortality rate (the other is myxedema coma

).

Storm

is most often a precipitated event in patients known or suspected to have undiagnosed or inadequately treated hyperthyroidism. Precipitating events include surgery, infections, or an

iodine load, such as amiodarone or contrast dye.

Slide22
Symptoms &

Dx

Symptoms of storm are identical to symptoms of hyperthyroidism, only more exaggerated:

Hypertension – tachycardia-

congestive heart

failure –fever – psychosis or

delirium.

Some

patients have constitutional symptoms of nausea, vomiting, and diarrhea

. Oddly, some patients develop jaundiceDiagnose

the condition with measurement of TSH and FT4: In virtually all cases, TSH is immeasurable and FT 4 markedly increased.

Slide23
Thyroid storm

Storm is characterized by a severe level of metabolic stress that the patient can no longer tolerate.

This

severe stress results in a relative adrenal insufficiency, even though the adrenal glands may be functioning perfectly and secreting a large amount of cortisol.

Patients

in storm die from cardiovascular collapse.

Slide24

Tx of Thyroid Storm

The most important aspect of treatment is large amounts of glucocorticoids.

Provide

supportive care in the ICU with diligent attention to volume status, temperature, and heart rate.

Give empiric broad-spectrum antimicrobial coverage until infection is excluded

.

Other aspects of treatment include the following

:

• Interrupt the physiologic response to excess thyroid hormone: IV propranolol or esmolol. • Block new hormone synthesis: high-dose

thionamide

(PTU or MMI

).

• Block release of preformed hormone from the gland: stable iodide

.

• Block peripheral conversion of T4 to T3 : iodinated contrast agent, propranolol, and corticosteroids. PTU also does this (but not MMI).

Slide25
Thyroiditis

# Thyroiditis

is divided into the following categories:

•

Acute: caused by bacterial infection of the gland (rare).

•

Subacute

: caused by viruses (also called "granulomatous").

•

Chronic: Autoimmune-mediated disease is the most common cause (Hashimoto's). Painless and postpartum thyroiditis are considered variants of "chronic."

Slide26

Subacute (de Quervain’s

)

thyroiditis

Subacute

thyroiditis is a transient inflammation of the thyroid gland occurring after infection with

Coxsackie, mumps or

adenoviruses . The condition can also be precipitated by drugs, including interferon-α and lithium . Affected patients are usually females aged 20–40 years.

In its classical painful form, There is pain in the region of the thyroid that may radiate to the angle of the jaw and the ears, and is made worse by swallowing, coughing and movement of the neck.

The

thyroid is usually palpably enlarged and

tender.

Systemic

upset is

common .

Painless transient thyroiditis can also occur after viral infection and in patients with underlying autoimmune disease.

Slide27

Slide28
Subacute

thyroiditis

Labs/studies

:

Initially, T3 and T4 are increased, TSH is suppressed, and RAIU is initially decreased.

ESR

is increased but is too nonspecific to use in diagnosis.

Over

time, temporary overt hypothyroidism develops in some with low T4 and increased TSH.

RAIU returns to normal. Eventually, T4 and TSH normalize

Slide29
Subacute

thyroiditis

The disorder is self-limited and usually does not require treatment

.

For severe cases, treat inflammation as needed with ASA or NSAIDs.

Glucocorticoids

are given as an 8-week taper in refractory/systemic cases.

Occasionally

, a patient may need beta-blockers to ameliorate the thyrotoxicosis symptoms or levothyroxine for overt hypothyroidism

. Reevaluate periodically until the patient's thyroid function normalizes.

Slide30
Postpartum thyroiditis

is fairly common, affecting up to 10-15% of postpartum women.

symptomatic thyrotoxicosis presenting for the first time within 12 months of childbirth is likely to be due to post-partum thyroiditis

The

clinical course and treatment are similar to those of painless

subacute

thyroiditis

.

Patients

present with hyper- or hypothyroid symptoms and a painless goiter. ESR is normal, but many patients do have anti-TPO antibodies.

RAIU is decreased. Don't hesitate to treat the hypothyroidism-or to give beta-blockers as needed for thyrotoxicosis

.

Patients universally recover but need annual follow-up because of the risk of

overt hypothyroidism

later.

Post-partum thyroiditis tends to recur after subsequent pregnancies, and eventually patients progress over a period of years to permanent hypothyroidism.

Slide31
Toxic Adenoma

A toxic thyroid adenoma is a benign area of autonomous

hyperfunctioning

thyroid

tissue .

Most occur as a single nodule of

hyperfunctioning

tissue within normal tissue that grows slowly, eventually becoming large enough to suppress TSH production

.

These are usually diagnosed by TFTs, which demonstrate overproduction of FT/FT4 and suppression of TSH, and thyroid scan (focal uptake in "hot" nodule).

Slide32
Treatment of thyroid adenomas

If the patient is hyperthyroid

, use ablative treatment or perform surgery.

Antithyroid

drugs

do not work long

term .

For the

euthyroid patient with a thyroid adenoma …. If the thyroid adenoma is compressing underlying structures or is cosmetically problematic, surgery is the best treatment.

Percutaneous ethanol injection of autonomous functioning thyroid nodules is an alternative to surgery and RAI, with restoration of normal thyroid function in the majority of cases .

Slide33

Multinodular Goiter

Toxic MNG .

Nontoxic MNG .

Slide34
Toxic MNG

refers to a MNG with thyrotoxicosis.

TSH

is suppressed, and FT3 and FT4 are often increased.

The thyroid

scan usually shows

1

or more hot nodules.

Toxic MNG may temporarily be treated with

antithyroid medications. Normal treatment is ablative therapy with radioactive iodine. This does not destroy all the nodules, but it does destroy those that are hyperfunctioning. Surgery is used in cases that are refractory, or in symptomatic cases, especially if a large goiter is compressing surrounding structures.

Slide35

Slide36
Subclinical Hyperthyroidism

a

low

or undetectable (

TSH)

level with a

normal serum free T4 and normal serum total T3 levels 

.

It can be caused by increased endogenous production of thyroid hormone (e.g., in Graves disease, toxic nodular goiter, or transient thyroiditis), by administration of thyroid hormone to treat malignant thyroid disease, or by unintentional excessive replacement therapy.The American Thyroid Association and the American Association of Clinical Endocrinologists recommend treating patients with

thyroid-stimulating hormone levels less than 0.1 mIU per L if they are older than 65 years or have comorbidities such as heart disease or osteoporosis.