Thyroid disease Dr . Bandar - PowerPoint Presentation

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Thyroid disease

Dr

. Bandar

ghazal

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Normal mass of thyroid about 30 g

Highly vascularized , receive about 120 ml blood / min .

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Follicular cells secret :

Thyroxine

(

tetraiodothyronine

) T4

Contains 4 ions of iodine

Tri

iodothyronine

T3

Contains 3 ions of iodine .

it also produce thyroglobulin

Parafollicular

cells secret :

calcitonin

Thyroid gland secret and store thyroxin up to 100 days supply .

Thyroglobulin essential for production (iodination by

thyroperoxidase

)and storage of hormone into colloids

With stimulation , release hormone and thyroglobulin .

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Stimulators of thyroid gland :

Thyrotropine

releasing hormone . TRH

Thyroid stimulating hormone . TSH

T4 is longer half life than T3 (which is 3 – 4 times more potent )

Released in the blood approximately 14:1 .

T4 is converted into T3 within cells .

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Function

Regulate oxygen consumption , basal metabolism , growth and development

Regulate protein , fat and carbohydrate metabolism

Increase sensitivity to catecholamine's

Neural maturation .

Heat generation

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Hyperthyroidism and thyrotoxicosis

Thyrotoxicosis :

Exposure of tissues to high level of circulating thyroid hormones from any cause

Hyperthyroidism :

thyrotoxicosis caused by excessive endogenous production of thyroid Hormones .

Primary : thyroid gland is the anatomical site of dysfunction

Secondary : increased secretion of TSH is a rare secondary cause of hyperthyroidism .

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Clinical manifestations

General

: Fatigue , weight loss , heat intolerance

Neuropsychiatric

: Anxiety , insomnia , decreased concentration

Hyperreflexia

, tremor , lid lag (, due to high adrenergic tone )

Cardiovascular

:

Palplitation

, tachycardia , high systolic BP , high output heart failure

Gastrointestinal

:

Hyperphagia

, increased frequency of bowel movement , loose stool , diarrhea

Genitourinary

:

Oligomenorrhea

, amenorrhea

Musculoskeletal

:Muscle weakness

Cutaneous

:Hair loss , increased sweating

Increased oil production , acne ,

periorbital

edema

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Lid lag

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Investigation

TSH , F T4 , T T3 .

CBC , KFT , LFT , CPK ,

RAIU :

High in hyperthyroidism

Low in other causes of thyrotoxicosis .

In case of pregnancy , lactation ,

amiodarone

, lithium intake ????

TSI (thyroid stimulating immunoglobulin )

TRAP

thyrotropin

receptor antibodies

In case of suspected Graves disease .

U/S : to assess vascularity

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Causes

Graves disease

Common (presence of autoantibodies )

Toxic multinodular goiter

common

Toxic adenoma

common

Thyroiditis ( acute , sub acute , chronic )

Common , thyroid inflammation causing

release of

stored hormones

Medication induced

Amiodarone

, lithium , interferon alpha , tyrosine kinase inhibitor

Thyrotoxicosis

factitia

Common (

thyroxine

abuse , contaminated beef

)

Struma

ovarii

Rare (autonomous function thyroid

tissue in ovarian

teratoma

)

Thyrotrope

adenoma

Rare , TSH

secreting pituitary adenoma

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GRAVES DISEASE

Most common cause of thyrotoxicosis .

Autoimmune disorder affecting thyroid gland , increasing synthesis and production of thyroid hormones .

F: M 8:1

Onset : 20– 60 years

Thyroid gland is typically hyperplastic and enlarged

Maybe associated with other pernicious anemia , myasthenia gravis , DM , celiac disease .

It has a familial tendency maybe accompanied by graves

opthalmopathy

,

dermopathy

.

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Pathogenesis

T lymphocytes become sensitized to thyroid antigen and stimulate B lymphocyte to produce antibodies against TSH receptor

TSI thyroid stimulating immunoglobulin .

TRAB

thyrotropin

receptor antibodies .

Thyroid hormone production increase

Gland is diffusely enlarge

May have bruit , firm with smooth texture on examination .

Cervical lymphadenopathy can occur .

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Graves opthalmopathy

Graves

opthalmopathy

affects 25 % of PT .

Smoking is a risk factor .

Periorbital

edema

Chemosis

Proptosis

Diplopia (

oculomotor

paresis )

Vision loss

This condition does not respond to treatment of hyperthyroidism , and often needs steroids therapy and surgery

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Pretibial myxedema

Rare infiltrative

dermopathy

of graves disease affecting 2 - 3 % of

pt

Non pitting edema

Indurated with

peau

d orange appearance typically on shins

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Toxic adenoma

Single

Multiple (

plummers

disease

)

Usually affect old age ,as prevalence of thyroid nodule increase with age .

Synthesis and secretion of hormone is independent of TSH

Not accompanied by

opthalmopathy

or

dermopathy

AntI

thyroid antibodies usually absent .

Exposure to contrast media or very high iodine intake may convert non toxic adenoma into toxic adenoma

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Subacute thyroiditis

Moderately enlarged tender gland

Thought to be due to viral infection

Maybe not tender called silent thyroiditis

Thyrotoxicosis result from released stored hormone resulting from destruction of follicles

Thyrotoxicosis followed by hypothyroidism then into

euthyroid

.

First 2 phases may last up to 3 months

During thyrotoxicosis there is low grade of thyroid uptake

Increased risk of recurrence

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Thyrotoxicosis

factitia

Due to ingestion of excessive amounts of exogenous thyroid hormone whether as form or replacement or abuse .

Consumption of contaminated beef

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Struma ovarii

Thyroid tissue is contained in about 3 % of ovarian

dermoid

tumor and

teratoma

.

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Pituitary tumor

Rare

No

opthalmopathy

seen

Antibodies are normal

TSH is high or in normal range

Secondary hyperthyroidism

Due to pituitary adenoma , neoplasm or hyperplasia .

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Management

B –blocker

:

Atenelol

,

metoprolol

, propranolol

To reduce sympathetic symptoms

Propranolol non selective , decrease peripheral conversion of T4 to T3

But requires to be administered 2 – 3 times a day

cardio selective such as

atenelol

,

metoprolol

is daily one dose , better adherence by PT

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Thioamides

: ( inhibit

thyroperoxidase

)

Methimazole

Propylthiouracil

In graves :

50 % will have spontaneous remission within 24 months .

Recurrence of hyperthyroidism is likely when TRAB is high at time of drug discontinuation . So if occur ablation or surgery

Radioactive iodine ablative therapy :

Pregnancy should be avoided 6 – 12 months after therapy

First line for toxic adenoma and multinodular

Thyroidectomy

:

Choice of therapy depends on

pt

status age and preference and the cause of thyrotoxicosis

For example

pt

above 65 years with cardiovascular and other comorbidities , we start short term

thioamide

to normalize thyroid function then RAIT or surgery .

First line for toxic adenoma , multinodular and malignancy

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In PT with graves

opthalmopathy

there is an escalation of antibodies following RAIT

That may exacerbate the ocular symptoms

So pretreatment is required by steroids

And thyroid surgery is better than RAIT .

For destructive thyroiditis :

B blocker

NSAIDS

High dose of Steroids

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Thyroid storm

Rare

High mortality 30 %

sever form of thyrotoxicosis

Presence of hemodynamic decompensating ( shock ) .

Clinical status > lab value of T4 . 3

Higher risk

pt

with Graves disease .

high fever

Tachycardia

Altered mental status

Cardiac and hepatic dysfunctions

Abdominal pain , nausea , vomiting , diarrhea .

ICU

Supportive measure , b blocker

Propythiouracil

then switch to

methimazole

.

Steroids ,

Plasmapheresis , surgery

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Subclinical hyperthyroidism

It’s a condition where TSH LOW with normal T4, 3

25 % of PT will return to normal TSH value after 6 weeks .

1-7 % of PT will progress to hyperthyroidism / year

Persistent subclinical

status

may predispose

pt

to AFIB , cardiovascular complications , hip fracture

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Treat

IF PERSISTENT TSH <0.1 MU/L and with symptoms or

cardiac risk factors

osteoporosis

Observe

If TSH >0.1 TO 0.5 .

IF TSH < 0.1

Without symptoms or risk factors .

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Hypothyroidism

Insufficient synthesis of thyroid hormones

Female : .male is 10 : 1

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Causes

Hashimoto

thyroiditis

Autoimmune

associated with TPO antibody

Post thyroidectomy

Ex. Surgery

due to cancer , Graves disease , goiter

Occur in all PT post

thyrodectomy

In 20% after lobectomy

Post radioactive iodine therapy

Treatment of Graves

disease , toxic adenoma .

Occur in 90 % of graves disease after (RAIT ) within one year .

Occur in 60 % in toxic multinodular goiter with onset delayed to many years .

Radiation to neck

Head and neck malignancy ,

hodgkin

lymphoma

Thyroiditis (acute ,

subacute

, suppurative )

Transient hypothyroidism ,

Central hypothyroidism

TSH deficiency

due to

hypothalmus

or pituitary disease , TSH should not be used to assess therapy with

thyroxine

Congenital hypothyroidism

Iodine deficiency

Common in developing countries

Drug induced

Amiodarone

,lithium , interferon alpha

Iodine

thionamide

,

Tyrosine kinase inhibitor (

sunitinib

)

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Sensitivity to heat / cold

Fatigue

Hypoglycemia

Increased cholesterol level

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HASHIMOTOS THYROIDITIS

Primary condition of hypothyroidism

Autoimmune disorder characterized by diffuse infiltration of the thyroid gland by lymphocyte and plasma cells resulting in follicular atrophy and scarring

More common in

pt

with other autoimmune disorder and positive family history

of thyroid autoimmunity .

Diffuse goiter can be seen most commonly in younger

pt

90 % of

pt

have positive TPO antibody (thyroid

peroxidase

antibody )

Described by Hakaru Hshimoto

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TSH , T3 , T4 levels

TPO antibodies ( Thyroid peroxidase )

Positive ANA

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Levothyroxine

To normalize TSH

And to resolve signs symptoms of hypothyroidism

1.6 mcg / kg

Except for elderly

pt

and

pt

with cardiac disease

25 – 50 mcg / day

Absorbed in

jejenum

and

ileium

, taken 1 hour before breakfast or coffee

Absorption of

thyroxine

is about 70 – 80 %

Repeat TSH after 6 weeks .

Helps in both hypothyroidism and shrinkage of goiter

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CRETINISM

Hypothyroidism dating from birth

Thyroxine

is essential for growth and development of brain during first 3 years

Earlier onset greater brain damage

Causes :

Radio iodine

Post radiation

Iodine

deficiency

Drug induced

Hashimotos

throiditis

Congenital developmental defects

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Delayed dentation

Mental retardation

Large posterior

fontanelle

Hypotonia

Same other features of

hypothyrodism

Umbilical

hernia

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Investigation : cord blood T4 ,

Tsh

Serum t4 ,

tsh

RAIU

Xray

of knee , foot and

skull

Treatment :

Levothyroxine

15mcg /kg / d

Iodine rich food

Flollow

up

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MYXOEDEMA

Common

in women

Two

varient

:

Hyperthyrois

myxoedema

(

pretibia

myxoedma

)

Hypothyroid

myxoedema

Causes : increases deposition of

glycosamine

glycan

Hasimotos

thyroiditis

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Myxoedema coma

Life threatening form of untreated sever hypothyroid with hemodynamic compromise .

Occur in

pt

with long standing hypothyroidism

Mortality is high

Risk factors :

Advanced age

cold exposure ,

Female gender

Events in undiagnosed

pt

such as ( infection , drug therapy , myocardial ischemia , trauma , stroke

ICU care is required

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Lethargy

stupor delirium

Psychosis

Hypotension

Convulsion

Hypoglycemia

Bradycardia

,

Hyponatremia

Hypoventilation , hypoxemia ,

hypercapnia

Coma

Hypothermia ( temperature below 34.4 c ) most common clinical manifestation

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Examine the neck for scar

Tsh

, ft4 , t3

Serum

osmolaity

, electrolytes

Creatinine

Glucose

CBC

Pan cultures for sepsis

Cortisol level to assess for adrenal insufficiency

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Hemodynamics : Iv fluids , vasopressor

Hyperventilation if respiratory acidosis is significant

Passive warming rather than active warming to avoid vasodilatation

Thyoxine

I/V

Loading dose 200 – 400 mcg followed by 1.6mcg/kg oral daily dose , dose is reduced to 75 % if given I/V.

Lower dose of

thyroxine

in elderly and in cardiac

pt

Stress dose Hydrocortisone 100 mg every 8 hours

If random cortisol level > 18 mg / dl it can be stopped

Treatment of infection

Correction of

hyponatremia

with saline

Correction of hypoglycemia with iv dextrose

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Goal of therapy is

Improve mental status

Metabolic parameters

Cardiopulmonary functions

When

pt

is stable start oral dose of

thyroxine

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Subclinical hypothyroidism

Typically asymptomatic

Diagnosed by elevated TSH and normal T4

Affect 5- 10 % of population

Repeat TSH in 2 months ,

bz

it might be transient

progression rate from subclinical to

hypothyroidsm

is 2 -4 % / year

One third revert to normal thyroid function

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Normal TSH level increase with age , up to 10 mu/l for person 80 years of age

Subclinical hypothyroidism with TSH above 10mu/l maybe at risk for CAD . HF

There is no evidence of treating subclinical hypothyroidism will improve quality of life

BP , weight , cognitive function .. But in

pt

with high LDL level normalization of TSH will lower LDL

Llevel

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TSH > 10 mu/l should be treated

25 - 50 mcg / d