Detailedapproa

THYROID AND PARATHYROID DISORDERS
BY DR. MAGDI AWAD SASI 2013

1 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013
Thyroid Gland Anatomy
Largest endocrine gland; high rate of blood flow
Anterior and lateral sides of trachea
o Two large lobes connected by isthmus
Thyroid follicles
o Filled with colloid and lined with simple cuboidal epithelial

(follicular cells) that secretes two hormones, T3 and T4 .
Thyroid Gland physiology:

Synthesis and release of thyroid hormones is influenced by TSH from the
pituitary.
Two kinds of hormones are produce in the thyroid gland triiodothyronine

(T3) and thyroxine (T4).
Concern the regulation of the metabolic and oxidation rates in all the
tissues of the body except the brain.

At physiological levels, they stimulate growth and development with
synthesis of many enzymes.
At pharmacological levels, increased heat production and O2

consumption related in part to uncoupling of oxidative phosphoryiation.
Many of the effects appear to be mediated by way of sympathetic

nervous system.
The sympathetic overactivity seen in many patients with anxiety states

accounts for the frequent mistakes in diagnosis.
Hypothalamus - the highest control of thyroid function((TRH)).
Thyroid hormone
o Bodys metabolic rate and O2 consumption
o Calorigenic effect - heat production
o heart rate and contraction strength
o respiratory rate
o Stimulates appetite and breakdown CHO, lipids and proteins
o Alertness, bone growth/remodeling
C (calcitonin or parafollicular) cells
o Produce calcitonin blood Ca2+ , promotes Ca2+ deposition and

bone formation especially in children
What is Hyperthyroidism ?
Increased synthesis and production of too much thyroid hormones is

called hyperthyroidism. This leads to thyrotoxicosis.
Thyrotoxicosis is the over production of thyroid hormones without
increased synthesis. Thyrotoxicosis could be a result of thyroditis or too
much intake of exogenous thyroid hormone.
What Causes Hyperthyroidism?
Hyperthyroidism can be that the whole gland is producing too much

hormones or there is only a single nodule producing more than enough
hormones. When this happens, the single nodule is called "hot nodule".
causes of hyperthyroidism and thyrotoxicosis:
1. Too much iodine intake

2. Autoimmune --Graves' disease-the most common
Thyroiditis-Hashimoto's, DeQuervain's, reidls thyroiditis.
3. Noncancerous growths of thyroid or pituitary gland
4. Toxic thyroid adenoma
5. Toxic multinodular goiter
6. Postpartum thyroiditis
7. TSH-secreting tumors (pituitary)
8. HCG-producing tumors
9. Hyper functioning ovarian teratoma.
10.Overmedicating with synthetic thyroid hormone.
11.DrugsAmidarone.
12.Thyrotoxicosis factitia
Symptoms of thyrotoxicosis:
Hyperthyroidism can either be symptomatic or asymptomatic. It can be
acute or chronic depending on the length with which the thyroid gland
has been producing more than normal amounts of the hormones. The
symptoms usually begin slowly and are not noticeable as can be largely
attributed to stress only. As time goes , the symptoms will become more
pronounced.
The paradoxical association of loss of weight with normal or increased

appetite is particularly suggestive of hyperthyroidism.

D/D Diabetes mellitus--------Defective alimentary absorption.
The weight is gained if increased appetite is more than the metabolic rate
I. Heat production increased:

Heat intolerance
increased sweating
II. CNS--- pt cant keep still.
Undue fatigability , proximal muscle weakness( thyrotoxic
myopathy) ,hyperkinesiasexaggerated and purposeless
movements ,Difficulty concentrating ,tremors , Emotion
liability.(mysthenia gravis association 10% ).
III. Psychiatric:
Nervousness and anxiety, Irritability, sleep disturbance,
Psychosis , insomnia.
IV. CVS--- palpitation , dyspnea on exertion , chest pain,CCF
The elderly patient usually present with cardiovascular symptoms
((predominant or alone)).
Unexplained heart failure after middle age should always arouse
suspicion of hyperthyroidism.
Failure of digitalis in normal dosage to control the rapid heart rate
is very suggestive.
Many of the effects appear to be mediated by way of sympathetic
nervous system sensitivity.
Difficulty in stabilizing a diabetic patient is sometimes the first clue
to the thyroid disorder.
V. GIT---Weight loss despite an increased appetite, diarrhea,
heartburn. For weight variation according to age,
Young increased weight /// Elderly- weight decreased.
VI. Musculoskeletal system and growth:

Pain in the backthyrotoxic kyphosis resulting from osteoporosis
Hypercalcemia with its clinical squeal is very rare, arthralgia ,
proximal muscle weakness.
VII. Integument:
Loss of hair. Nails may show recession from the nail bed.
Polyuria and polydypsialess common.
NECK---- A visible enlargement of the thyroid gland in the neck (goiter)
EYES---Exophthalmos - protruding eyes, diplopia, chemosis, swelling
Menstrual cycle variations lightening of menstrual flow and less

frequent periods.
CLINICAL FINDING :
If there is neck swelling (GOITER) ,it is a must to pass through 4 steps.
1. Inspection---site,size ,shape,skin changes,surface .

ASK THE PATIENT TO SWALLOWPATHOGNOMIC
2. Palpation- contirm , temperature, borders, consistency,tendenrness
3. Percussion----for retrosternal extension
4. Auscultation--- for bruit
Exam the eyes for eye signs --is it Graves.
Skin feels warm , moist skin with fever.
CVS
PULSEcollapsing , sleeping heart rate 80/min , atrial fibrillation
BLOOD PRESSURE--- systolic HTN with high pulse pressure.

CCF--- raised JVP , pedal edema, systolic murmurs
CNS---hyperactive reflexes
CLINICAL SIGNS IN GRAVES DISEASE:
Increase in thyroid gland size
Soft to slightly firm
Non-nodular / nodular
Bruit and/or thrill
Mobile
Non-tender
Without prominent adenopathy
EYE SIGNS:
Ophthalamic Graves disease:
1. Swelling of the eyelids-
Due to overfilling of orbit.
The lids appear congested and

edematous congestive
ophthalmopathy.
2. Irritation of the conjunctivae:

.Grittiness and soeness of the eyes.
.Edema of conjunctiva( chemosis)

.It may ulcerate and may prolapse between the lids.
.Corneal Damage may occure.
.The appearance of prominent vessels at the lateral canthi is usually a
sign that the ocular manifestation are going to be trouble some.
3. Exophthalmos:
Appearance of sclera B/W the lower lid and limbus of cornea .
Means protrusion of the eye ball.
Symmetrical in Graves disease with hyperthyroidism.
Caused by increased bulk of orbital contents.
The fat is increased and the muscles enlarged, infiltrated with
lymphocytes and contain increased amounts of water and
mucopolysccharides.
Usually alters little with treatment and may be remarkably persistent.
In some, it is progressive and may cause loss of vision if effective
treatment not given ((malignant exophthalmos )).
Unilateral exophthalmos causes:

1.Retro-orbital aneurysm
2.Retro-orbital tumor
3. Involvement from outside
4. Chronic myopia
4. Lid retraction:
Recognized by the appearance of sclera B/W The upper lid and the limbus of
the cornea when the patient is looking straight a head and not staring.
2types:
1.Spastic lid retraction:
It is diagnostic of Graves disease.

It is present in all positions of gaze

It is one of the commonest eye signs of Graves disease
It is due to spasm of the elevator palpebrae superioros and sympathetic
stimulation of the superior orbital muscle of muller.
2.Paralytic lid retraction:
Not specific for Graves disease.

Occurs only in the presence of limitation of
upward gaze
I. Disorders of the muscles-Graves disease,
ocular myopathy
II. Mysthenia gravis
III. Upper brain stem lesions
It is thought to be caused by over innervations
of elevator palpebrae superioros when an
attempt is made to look up.
Lid retraction is the cause of a conjunctival
irritation and keratitis.
5. Lid lag: NORMAL

LID LAG
Occurs when the sclera B/W
upper eye lid and cornea
becomes visible as the
patient gaze follows the
examiner fingers down ward
from the position of
maximum elevation.
The eye moves not in close

contact with eye lid as a
delay in lid movement.

6.Ophthalmoplegia:
Paresis of one or more of

extraocular muscles usually
causes diplopia.
Upward and outwards
movements reduced 4 times.
Limitation of upward gaze may be due to tethering and
adhesions of inferior oblique and superior rectus muscle when
they decussate.
It is pathognomic in Graves disease .
It is one of the most unpleasant ocular complication of graves .
7.Congestive ophthalmopathy: malignant exophthalmos
IT IS A MEDICAL EMERGENCY REQUIRING IMMEDIATE ADMISSION.
The patient complain of severe pain in the eye or failure of vision.
It is a sever and progressive ocular changes in Graves characterized by:
1. Prominent eyes
2. Lids and conjunctiva swollen and inflamed
3. Marked ophthamoplegia
4. Retinal veins may be prominent.
5. Papilloedema may develop.
6. Oular tensions may be high.
7. Keratitis
8. Pressure on the optic nerve may be sudden and complete which
causes loss of vision even with normal fundus.

Clinical Differentiation of Lid
Retraction from Proptosis
Measurement using
prisms or special ruler
(exophthalmometer) Normal position
OR with sclera of eyelids
seen above iris :

Observing position of
lower lid (sclera seen
below iris = proptosis, Proptosis Lid retraction
lid intersects iris = lid
retraction)
SKIN SIGNS---PRETIBIAL
MYXEDEMA
5% of patients.
Usually affects the shins frontal

area
The swelling often extends over

the dorsum of the feet and toes
where it is associated with tissue
growth.
The skin is coarse ,purplish red ,

peaud orande appearance ,raised surface Thick, leathery consistency,
with coarse hair in the affected area.
The superficial layer of the skin is infiltrated with the mucopolysaccharide
hyaluronic acid.
Nodularity, sometimes.
Sharply demarcated
margins,Non-tender.
It tends to develop after

hyperthyroidism has been
treated by surgery or with
radioactive iodine.
The latent period take 4-

32months.
Soft tissue swelling that is

pigmented and
hyperkeratotic.
Thyroid Acropachy
Clubbing of fingers.
Painless.
Periosteal bone formation and

periosteal proliferation .
The subperiosteal new bone

formation resembles soap bubbles
on the surface of bone with coarse
spicules.

Onycholysis of Thyrotoxicosis
Distal separation of the
Nail plate from nail bed
Plummers nails)
Frequency of Neuromuscular Disorders Associated with Thyrotoxicosis:

Myopathy due to thyrotoxicosis >50
Usually proximal and mild to moderate
Hypokalemic periodic paralysis <1
Myasthenia gravis <1
Thyrotoxic Periodic Paralysis:

Most common cause of hypokalemic periodic paralysis
Flaccid paralysis
Lower extremities affected most often
Ocular and bulbar muscles uninvolved, respiratory muscles rarely
involved
Most often starts during sleep
Precipitated following exercise, high salt intake or high carbohydrate
diet
Hypokalemia during the paralysis .
Differential Diagnosis of a Painful Thyroid:
Subacute granulomatous thyroiditis Most common
Hemorrhage into a goiter, tumor or cyst
with or without demonstrable trauma Less common
Acute suppurative thyroiditis <1%
Anaplastic (inflammatory) thyroid carcinoma <1%
Hashimotos thyroiditis <1%
TB, atypical TB, amyloidosis <1%
Metastatic carcinoma
Diagnosis
Many symptoms of hyperthyroidism are the same as those of other
diseases, so hyperthyroidism usually cannot be diagnosed based on
symptoms alone. With suspected hyperthyroidism, you have to take a
medical history and perform a thorough physical exam. Several blood
tests confirm the diagnosis of hyperthyroidism and find its cause:
1. **TSH test**
The first test , The most accurate measure of thyroid activity available.
The TSH test is especially useful in detecting mild hyperthyroidism.
Generally, a TSH reading below normal means a person has
hyperthyroidism and a reading above normal means a person has
hypothyroidism.
2. **T3 and T4 test**
With hyperthyroidism, the levels of one or both of these hormones in
the blood are higher than normal
3. Thyroid-stimulating immunoglobulin (TSI) test
((Thyroid stimulating antibody test)) measures the level of TSI in the
blood. Most people with Graves disease have this antibody.

4. Ultrasound neck-
U/S more sensitive than physical examination , particularly for
nodules that are < 1 cm or located posteriorly in the gland.
U/S also more sensitive than thyroid scan
Thyroid U/S
Benign Malignant Characteristics
Characteristics
Regular border Irregular border
Halo (sonolucent rim) No Halo
Hyperechoic Hypoechoic
(more vascular)
Egg shell calcification Microcalcification
N/A Intranodular vascular spots

(color doppler)
5. **Radioactive iodine uptake test**

low levels of iodine uptake might be a sign of thyroiditis, whereas high
levels could indicate Graves disease.

Causes of Thyrotoxicosis
Divided by Degree of Radioiodine Uptake
High I123 Uptake Low I123 Uptake
Graves disease Subacute thyroiditis
I 123
Toxic nodular goiter Hashitoxicosis

I123
TSH-mediated thyrotoxicosis Drug-induced

Pituitary tumor Iodide
Pituitary resistance to Thyroid hormone
thyroid hormone Struma ovarii
HCG-mediated thyrotoxicosis Factitious
Hydatidiform mole
Choriocarcinoma
Other HCG-secreting tumors
Thyroid carcinoma (very rare)
6. **Thyroid scan**
A thyroid scan shows how and where iodine is distributed in the
thyroid. The images of nodules and other possible irregularities help to
diagnose the cause of a persons hyperthyroidism.
Thyroid Scan
Thyroid nodule: risk of malignancy 6.5%
only 5-10% of nodules
Cold Warm Hot Nodule

Tc-99m < 5%
nodule Nodule
(indeterminant) malignant
16-20% I123 < 1% malignant
5% malignant
malignant

7. FINE NEEDLE ASPIRATION
25G Needle, 10cc syringe

Done in Office
NOT INDICATED IN TOXIC PATIENTS .
+/- Local anaesthesia
3-5 passes
SEN 95-99% (False Negative rate 1-5%)
SPEC > 95%
Benign: macrofollicular or "colloid" adenomas, chronic autoimmune
(Hashimoto's) thyroiditis
Suspicious or Indeterminant: microfollicular or cellular adenomas
(follicular neoplasm)
Treatment:
Hyperthyroidism is treated with medications, radioiodine therapy, or thyroid

surgery. The aim of treatment is to bring thyroid hormone levels to a normal
state, thus preventing long-term complications, and to relieve uncomfortable
symptoms. No single treatment works for everyone.
Treatment depends on the cause of hyperthyroidism and how severe it is. When
choosing a treatment, consider
1. Patients age
2. Side effects of the medications
3. Pregnancy or heart disease
4. The availability of an experienced thyroid surgeon.
Medications
1. Beta blockers
Beta blockers act quickly to relieve many of the symptoms of
hyperthyroidism, such as tremors, rapid heartbeat, and nervousness, but
do not stop thyroid hormone production. Most people feel better within
hours of taking these medications.

2. Antithyroid medications :
Treatment of hyperthyroidism
Antithyroid drugs
Carbimazole 10 mg tid
Reduce to maintenance after 4 weeks
Rash, GI, agranulocytosis
Graves withdraw drugs after course of
treatment
Carbimazole, thiouracil ,methimazol
Antithyroid medications interfere with thyroid hormone production but dont

usually have permanent results. Antithyroid medications are not used to treat
thyroiditis.
Once treatment with antithyroid medications begins, thyroid hormone levels

may not move into the normal range for several weeks or months. The average
treatment time is about 1 to 2 years, but treatment can continue for many
years.
Side effects in some people, including:

1. Allergic reactions such as rashes and itching
2.Agranuloctosis- decrease in the number of white blood cells in the body.
3. Liver failure, in rare cases
Ask the patient to stop antithyroid medication if he develop:
1. Fatigue & weakness
3.Vague abdominal pain & Loss of appetite
5. Skin rash or itching & Easy bruising
7. Jaundice
8. . Fever & persistent sore throat.

Antithyroid medications and pregnancy
Radioiodine therapy is contraindicated . propylthiouracil (PTU), is
available for women in this stage of pregnancy or for women who are
allergic to methimazole and have no other treatment options.
Some women are able to stop taking antithyroid medications in the last 4
to 8 weeks of pregnancy due to the remission of hyperthyroidism that
occurs during pregnancy. However these women should continue to be
monitored for recurrence of thyroid problems following delivery.
Methimazole:
Advantage 1.less frequent doses , fewer pills & more convenient.
2. lower incidence of acute hepatic necrosis.
Complications:
Serum sickness
Cholestatic jaundice
Hypoglycemia
Loss of taste
Alopecia
Nephritic syndrome
Dose (10mg)
30---60 mg once daily
Indications :
1. Toxic Goiter
2. Preparing hypetthyroid for surgery
3. Preparing elderly fo RAI
4. Mild toxicosis

3. Radioiodine Therapy
In radioiodine therapy, patients take radioactive iodine-131 by mouth.
Because the thyroid gland collects iodine to make thyroid hormone, it will
collect the radioactive iodine from the bloodstream in the same way. The
radioactive iodine gradually destroys the cells that make up the thyroid
gland but does not affect other body tissues.
Treatment of hyperthyroidism
Radio-iodine
Inflammatory response followed by
fibrosis
May be used for Graves, TMG or TA
? Need for drug treatment before and
after
May need retreatment
Long term risk of hypothyroidism
Treatment with beta blockers can control symptoms.

women wait a year after treatment before becoming pregnant.
4. Thyroid Surgery((least-used))
Surgery may be used to treat:
1.Pregnant women who cannot tolerate antithyroid medications
2.Large goiters and Cancerous thyroid nodules
Before surgery, we may prescribe antithyroid medications to temporarily
bring a patients thyroid hormone levels into the normal range. This
presurgical treatment prevents a condition called thyroid storma
sudden, severe worsening of symptomsthat can occur when
hyperthyroid patients have general anesthesia.

Treatment of Hyperthyroidism
Surgery
Rarely used nowadays
Need to be rendered euthyroid before
surgery
Lugols iodine 0.1-0.3 mls tid for 10 days
before surgery
DRUGS USED IN THYROTOXICITY

After surgery:
A. When part of the thyroid is removed, T3T4 levels may return to normal
B. Some patients may still develop hypothyroidism, need thyroxine.
C. If the entire thyroid is removed, lifelong thyroxine is necessary.
D. After surgery, patients thyroid hormone levels should be monitored.
Facts TO REMMEBER:
Hyperthyroidism is a disorder that occurs when the thyroid gland makes
more thyroid hormone than the body needs.
Hyperthyroidism is most often caused by Graves disease, an autoimmune
disorder.
Hyperthyroidism is much more common in women than men.
Hyperthyroidism is also more common in people older than age 60 and is
often caused by thyroid nodules. Hyperthyroidism in this age group is
sometimes misdiagnosed as depression or dementia. For people older
than age 60, subclinical hyperthyroidism increases their chance of
developing atrial fibrillation , heart failure.
Hyperthyroidism is treated with medications, radioiodine therapy, or
thyroid surgery. No single treatment works for everyone.
Treatment by medication- antithyroid and B blockers .
Hyperthyodism will not cause carcinoma.
Exophthalmos is characteristic for graves disease.
After RAI therapy, hypothyroidism is the rule and TR is thyroxine lifelong.
Treatment of Hyperthyroidism IN USA:
Make diagnosis, get RAI uptake.
Beta block (inderal 40-80 mg tid).
If RAI uptake is high treat with RAI.
If RAI is low symptomatic

Graves Eye Disease
Usually mild Tx, protective glasses, elevate head of bed, conjunctival

lubricants
High dose steroids
External radiotherapy
Orbital decompression
Toxic Solitary Adenoma
Rare cause (< 2% of patients

with hyperthyroidism)
Younger people 30s and 40s
Scan
Benign follicular adenomas

Toxic solitary nodule
Less than 40year more than 40year
1.Make pt euthyrod by: 1.Radioactive iodine
Propraolol, thiourea A.Permenant hypothyroid
2.Before 10 days of O.T.
Iodine therapy. 1/3 of pt by 8 yr afterRAI
3.Surgery B. Nodule remain in50%
C.10% of pt may grow.
Post operative hypothyroidism
-Trsnsiet.14% become hypothyroid
By 6 years after surgery.
MULTINODULAR GOITER:
Older
Usually less severe hyperthyroidism
May have subclinical
hyperthyroidism.
May have long history of goitre
A thyroid containing multiple
nodules is likely to be benign MNG.
Fine needle biopsy is performed on
any nodule that is growing /
dominant/ hard inconsistency.

Larger retrosternal goiter rarely harbor a malignancy but can be followed by CT.
1.Surgical resection=compression 2 .Thyroxine useful in pt TSH
or Continuous growth
Thyroxine should not be prescribed

3.Pt found be toxic may have RAI scan For pt w suppressed TSH since may
IF I123 is a therapeutic consideartion Add to autonomous secretion and
cause thyrotoxicosis
Uss guided FNA biopsy is reserved for pts with nonpalpable nodules 1.5cm in
diameter with H/O head-neck irradiation.
TOXIC MULITNODULAR GOITER
1.Symptomatically with propranolol/thiourea 3.PT follow a low iodine diet to
Enhance thyroid uptake of RAI
95% recurrence rate after they are stopped. Which may be relatively low .
2. RAI should be given after stopping T.U./ 3days 4.High doses 0f RAI required.
And reender patient euthyroid. 5.Pt should be followed closely
Hyper and hypo are common
6.SURGERY FOR COSMOTIC AND PRESSURE SYMPTOMS

EMERGENCY THYROID STATUS ((THYROID STORM))
It is an exacerbation of hyperthyroidism.
IT is an acute life threatening , hypermetabolic state which may be the
initial presentation of thyrotoxicosis.
Less than 10% of hospitalized thyrotoxicosis.
Mortality 20---30%
Can be caused by all causes of hyperthyroidism but Graves the most
common.
Precipitating event:
I. Systemic insultsurgery, trauma ,myocardial infarction ,pulmonary

embolism, severe infection, DKA.
II. Discontinution of antithyroid drugs
III. Excessive iodine ( amiodarone , radiocontrast dyes)
IV. Radioiodine therapy
Symptoms:
o Increased all vital signs

o Increased body temperature, sweating
o Tachycardia, Arrythmia, atrial fibrillation
o Vomiting/ nausea, dyspnea, tacchypnea
o Diarrhea, epigastric discomfort
o Heart failure/ pulmonary odema
o Confusion
LABORATORY:
o Increased free T4 AND T3

o Decreased TSH
o Hyperglycemia , elevated alkaline phosphatase, leukocytosis, Mild
hypercalcemia , and elevated liver enzymes.
o Cortisol increase (( NORMAL LEVEL = ADRENAL INSUFFICIENCY))

Treatment:
A. TREATMENT DIRECTED AT THYROID GLAND AND HORMONES--
Inhibition of new hormone synthesis with Thioamide drugs such as PTU and
methimazole.
Inhibition of hormone release with Iodine & potassium iodide(Lugols solution)

& Lithium carbonate.
B. TREATMENT DIRECTED AT PREVENTING HORMONES AFFECTS ON THE

BODY
PTU , Corticosteroids ,B blockes( propanolol),Amiodarone, Plasmapheresis.
C. TREATMENTS DIRECTED AT MAINTAINING HOMEOSTASIS

Hyperthermiaacetaminophen , cooling , blankets
Fluid and electrolyte testing / replacement
Glucose
Vasopressors
Digoxin and diuretics if appropriate.
BETA BLOCKERSdecrease adrenergic hyperactivity
PTU------------------blocks the peripheral conversion of T4 TO T3.
GLUCOCORTICOIDSinhibit hormone production and decrease peripheral
conversion from T4 to T3.
SODIUM IODIDE SOLUTION(LUGOLS)high levels of iodide will initially

suppress release of thyroid hormone
Treat cardiac symptoms , fever and hypertension.
Apathetic Hyperthyroidism Common symptoms:
Weight loss, anorexia

Constipation despite thyrotoxic
Tachycardia, Atrial fibrillation , Heart failure, angina
Cognitive Dysfunction

Hypothyroidism
Definition:
Hypometabolic state due to deficiency of thyroid hormones .
Hypothyroidism results specially from glandular destruction and

underproduction of thyroid hormones.
It is characterized by Accumulation of mucopolysaccharides in the SC

tissue ((non pitting edema )).
Incidence : middle -50s female:male ratio 10:1
ETIOLOGY
A. PRIMARY : THYROID FAILURE (95%)
B. SECONDARY : PITUITARY TSH DEFICIT
C. TERTIARY : HYPOTHALAMIC DEFICIENCY OF TSH
D. PERIPHERAL RESISTANCE TO THE ACTIONS OF THYROID HORMONES
PRIMARY CAUSES
Autoimmune hypothyroidism: Drugs :

-Hashimotos thyroiditis -Antithyroid drugs,
- Atrophic thyroiditis amiodarone, lithium,
interferon
Iatrogenic:
-Radio-iodine therapy Congenital hypothyroidism:
- Thyroidectomy -Thyroid agenesis
- External radiation to the - Dyshormogenesis
neck (lymphoma/CA) - TSH-R mutation
Iodine deficiency
Infiltrative disorder
Infiltrative disorders: amyloidosis, sarcoidosis, hemochromatosis

Transient hypothyroidism:
1. Silent thyroiditis , including postpartum thyroidtis

2. Subacute thyroiditis
3. Withdrawal of thyroxine trt
B. Secondary hypothyroidism:
1. Hypopituitarism: tumors, pituitary surgery or irradiation, infiltrative

disorders, Sheehans syndrome, trauma
C.3ry -Hypothalamic disease: tumors, trauma, infiltrative disorders .
Clinical manifestations:
There will be systemic symptoms which may delay the diagnosis.
It is diagnosed either at first sight or not at all.
Myxedema enters into D/D of unexplained heart failure not responding to

diuretics and digoxin.
Myxedem enters into D/D unexplained ascitis(protein content high).
The pituitary is often quite enlarged in 1ry hypothyrodism due to reversible

hyperpalsia of TSH- secreting cells.
The concomitant hyperprolactinemia seen in hypothyrodism can lead to

mistaken diagnosis of pituitary adenoma.
CNSTiredness ,weakness, Difficulty concentrating and poor memory

thought and movements are retarded, parasthesia , thyroid maddness,speech is
slow , hoarse voice , depression, psychosis, confusion, Perceptive
deafness(40%)of all cases.
CVSFatigue , Dyspnea , lose of effort , legs swelling , syncopy
Angina pectoris , CCF,pericardial sffusion.
GIT---lose of apetite , abdomenal distention ,constipation .

SKIN- Dry skin , feeling cold , thick coarse skin.
Endo----Weight gain , cold intolerance , hair loss
MENSTRAUL CYCLE----menorrhagia , Dysmenorrhea.
Amenorrhea may be the presenting feature in young patients.
They have a tendency for fluid collection in negative spaces even in the
absence of bilateral leg swellings. The patient may present with unexpained
symptomatic pleural effusion or ascitis or pericardial effusion .Hypothyrodism
can be subclinical for long time as the patient may be at risk of coronary heart
disease as low thyroid hormones elevate the cholestrol . Pericardial effusion
may be huge and result into cardiac tymponade with heart failure symptoms .
The commonest presentation:
1. Tingling and numbness in the fingers due to carpel tunnel syndrome.

2. Muscular aches & pains is a prominent feature following thyrodectomy.
3. Too much reliance should not be placed on thining of outer third of the
eyebrows---------------uncommon in normal people
Rare presenting features:
1.Hoffmans syndrome:
Patient presents with stiff,aching ,swollen muscles

2.CNS disorders:
Epilepsy ,drop attacks ,dementia ,cerebellar ataxia ,peripheral
neuropathy.
All of which may in large part recover with thyroxine treatment.
3.Coma with hypothermia:
Especially elder patient living alone with inadequate blanket.
Precipitated by phenothiazine.
In mild hypothyrodism, the symptoms are usually minor and non specific.
Tiredness, Depression ,Puffiness of face , Periorbital swelling and
constipation.
May be present singly or in combination with out H/O thyroid diseases.
CLINICAL SIGNS:
Dry skin ,coarse ,thick and rough, distinict yellowish tint.
Malar flush, cool peripheral extremities &cyanosis of ears
Enlarged tongue D/D Amyloidosis.
Puffy face,periorbital edema,pallor.
Puffy hands and feet (non pitting thickning of S/C tissue) .
Diffuse alopecia-dry ,brittle, sparse,come out easily.
Hands reynauds phenomena
Bradycardia
Delayed tendon reflex relaxation
Carpal tunnel syndrome
Delayed Deep Tendon Reflex
Achilles tendon reflex time most

commonly sought but may also be
effectively tested on brachioradialis or
biceps
Achilles tendon reflex timing is best elicited with patient kneeling.
COMPLICATIONS OF HYPOTHYRODISM:
1. Mostly cardiac----CAD , CCF

2. Increased susceptibility to infections
3. Megacolon in long standing hypothyroidism
4. Organic psychosis with paranoid delusions (madness)
5. Infertility (rare cause)
6. Adrenal crisis may be precipitated by thyroid therapy.
7. Convulsions
8. Deep stupor & coma
9. Refractory hyponatremia in sever myxedema.
10 .Myxedematous pt are sensitive to opiates.
11. Inappropriate secretion of ADH has been observed
12. Sellar enlargement & TSH secreting tumors may develop in untreated
pt which decrease in size after replacement therapy.
LABORATORY INVESTIGATION:
Suspicion of hypothyroidism in the appropriate clinical context is the key to

diagnosis.
A. Family history of thyroid disease, Goiter , vitiligo ,autoimmune disease.

B. H/O previous destructive therapy
Diagnosis : serum TSH
: serum T4 total or free?
: thyroid autoantibodies
In outpatient setting serum TSH !!!
Dyslipidemia with elevated cholesterol and triglycerides
Anemia
CNOCLUSION:
TSH and FT4 normal: subclinical hypothyroidism
TSH and FT4:clinical hypothyroidism
TSH normal or and FT4 :secondary hypothyroidism
MANAGEMENT:
Aim: to make patient euthyroid clinically & biochemically.
Treatment with L-thyroxine is life-long ensure compliance!!
Monitoring:
Clinically & biochemically
Measure TSH and free T4 2-3 month after initiation of therapy

determine maintenance dose.

OVERT HYPOTHYROIDISM
Starting dose : 50-100 ug/d 100-200ug/d within 2 weeks
IHD / grossly hypothyroid / elderly:
Start at 25 ug/d
slowly within 2-4/52 according to pt response
Angina: withhold / dose. Proper Management of IHD
Hypopituitarism:
Cortisol: to avoid adrenal crisis
SUBCLINICAL HYPOTHYROIDISM:
L-thyroxine to risk of CAD
50-100 ug/d adjust to maintain TSH at normal level
Most asymptomatic & dont need Rx (monitor TSH q2-5y)
Treatment Indications:
A. Increased risk of progression
B. TSH > 10, Female > 50 year old.
C. Anti-TPO Ab titre > 1:100,000 ?
D. Goitre present ?
E. Dyslipidemia?
F. Total cholesterol (TC) 6-8% if TSH > 10 and TC > 6.2 nM
G. Symptoms?
H. Pregnancy, Infertility, Ovulatory Dysfunction.

PREGNANCY:
dose, especially in 2nd / 3rd trimester
Levothyroxine (T4)
Eltroxin (GSK)
Synthetically made
50 ug white pill no dye (hypoallergenic)
Most commonly prescribed treatment for hypothyroidism
No T3 (but 85% of T3 comes from T4 conversion)
All patients made euthyroid biochemically
Most (but not all) patients feel normal
Average dose 1.6 ug/kg
Age > 50-60 or cardiac disease: must start at a low dose (25 ug/d)
Recheck thyroid hormone levels every 4-6 weeks after a dose change
Aim for a normal TSH level
Medical situations where T4 medication may be affected.ex:
A. Estrogen: Pregnancy, OCP, HRT
i. Need to increase T4 dose!
B. Drugs that interfere with T4 absorption
i. Iron, Calcium
ii. Cholestyramine (cholesterol resin Rx)
At least 4h between T4 and these drugs!

Liothyronine (T3)
Cytomel (Theramed)
Shorter half-life
Fluctuating levels (i.e. need a slow-release pill)
Twice daily dosing often needed
10x more potent: palpitations & other cardiac side effects
High T3 levels, low T4 levels (not physiologic either!)
HYPOTHROID MEDICAL EMERGECY((MYXEDEMA COMA))
Severe, uncompensated form of prolonged hypothyroidism.
Precipitated by stress / infection / drug
Complication: signs of hypothyroidism with
1 Hypoventilation
2. Cardiac failure
3. Fluid & electrolyte imbalance
4. Coma 50% of cases

PLAN OF MANAGEMENT
1. Treat precipitating cause
2. Gradual rewarming blanket
3. Accurate core T rectal thermometer
Aim for slow in core T : 0.5 C/hr
4. Cardiac monitoring
5. Correction of electrolyte abnormalities
6. Adequate hydration & nutrition (dextrose)
7. L-thyroxine (300-400 ug oral/iv) &
tri-iodothyronine 10 ug 8 hrly
8. Hydrocortisone : blood cortisol
THYROIDITIS
CLASSIFICATION:
SUBACUTE, NONSUPPURATIVE
UNKNOWN CAUSE
ASSOC. WITH VIRAL URT INFECTIONS
CHRONIC, HASHIMOTOS
IMMUNOLOGICAL FACTORS
PRESENCE OF IMMUNOGLOBULINS &
ANTIBODIES DIRECTED AGAINST THE
THYROID

Inflammation of the thyroid gland (thyroiditis) comprises many common
disorders of the thyroid gland. Thyroiditis affects mainly women and can occur
at any age. Affected patients can be euthyroid, hypothyroid or hyperthyroid
depending on the cause. Many patients ultimately develop permanent
hypothyroidism.
Key learning points
Hashimotos thyroiditis is the most common form of thyroiditis.

Subacute or De Quervains thyroiditis is most likely due to a viral infection
Thyroiditis can often lead to hypothyroidism developing.
Amiodarone can cause hyperthyroidism or hypothyroidism
An enlarging or hard thyroid could also be due to a carcinoma.
Hashimotos Disease(( chronic lymphocytic thyroditis )):
Most common cause of hypothyroidism in North America (not idodine

defeciency!)& most common form of thyroditis.
Autoimmune
Its frequency is increased by dietary iodine.
Females > Males 6 times , Runs in Families.
Antithyroid antibodies:
Thyroglobulin Ab ,Microsomal Ab ,TSH-R Ab (block)
First preceded by subclinical hypothyroidism with normal thyroid
hormones levels and elevated TSH
Later ,FT4 levels fall and TSH levels rise further
Auto antibodies can be induced by amidarone, interferon ,IL 2,GCSF.
Anti TPO +++
C/F:
Diffusely enlarged ,firm, finely nodules
One lobe may be asymmetrically enlarged (D/D neoplasm)
Pt c/o neck tightness, pain &tenderness are not present.
10% of cases are atrophic ,fibrotic particularly in elderly female.
LAB.: antiperoxidase (95%) & antithyroglobulin(60%).

Treatment:
Thyroid Hormone Replacement
Levothyroxine (T4)
No benefit to giving iodine!
In fact, iodine may decrease hormone production
Variety :
1.Subclinical thyroditis:
Very common 40% female , antibodies 13% female
2.Postpartum thyroditis:
Transient hyperthyroidism followed by hypothyroidism.
Recovery is the rule.
Subacute thyroditis:
Common disorders De quervains thyroditis
Granulomatous thyroditis
Gaint cell thyroditis
Presented by acute painful enlargement of thyroid gland and dysphagia .
The pain may radiate to the ears.
Silent thyroditis -----no pain
Young and middle aged women are most commonly affected.
Viral infection has been suggested as the cause.
Clinically; the manifestation may persist for weeks or months and
associated with thyrotoxicosis.
LAB.:
ESR increased and antithyroid antibodies decreased.
I123 radioactive uptake is low
Fine needle aspiration-----Gaint multinucleated cells.

Suppurative thyroditis:
Rare disorder
C/F-Severe pain, tenderness& redness,
fluctuation in thyroid gland region.
Caused by pyogenic organisms.
Occurs in the course of systemic
infection.
Riedlels thyroditis(chronic fibrous thyroditis):
It is called woody thyroiditis,

ligamentous thyroiditis,riedles
struma.
It usually causes hypothyroidism and
may cause hypoparathyrodism .
Age middle age or elder women.
Enlargement is often asymmetric.
The gland is stony hard and adherent to the neck structures.
This leads to compression signs-Dysphagia, Dyspnea& hoarsness.
It is usually a manifestation of a multifocal systemic fibrosis with:
1.Retroperitoneal fibrosis
2.Mediastinal fibrosis
3.Biliary tract sclerosis
NOTES IN Thyroiditis:
Painful (subacute, de Quervains)
Painless (post partum)
Hyperthyroid, hypothyroid and euthyroid phases
Anti thyroid drug therapy does not work.

THYROID TUMORS:
1. Follicular cancer:
Common , 15% of thyroid malignancies.
Age-50 year
Female72%
More likely to have distant metastases
Invasion juxtanodal +
Blood vessels +++
Distant sites +++
Classified as differentiated thyroid carcinoma.
Death 24%
Resemble to normal thyroid +++
I 123 uptake +++
Degree of malignancy +++
C/F thyroid nodule =thyrotoxicosis
LAB.----------thyroglobulin levels high in metastatic follicular carcinoma.
Less common than papillary
Imaging extensive bones and soft tissue metastases may develop.
Total thyroidectomy (or near total).
Routine remnant ablation with RAI due to increased risk of metastatic
disease
2. Papillary Cancer
Most common (70% of all) and least aggressive.
Differentiated thyroid carcinoma.
Age 40year// female --- 70%
Death --- 7%
Invasion --juxtanodal ++++
Blood vessels +
Distant sites +
Resemble to normal thyroid +
I123 uptake -cold nodule +
C/F thyrotoxicosis with nodule
LABthyroglobulin levels are high in most metastatic papillar ca.
Imaging--- extensive bone and soft tissue metastasis may be
detected on radioisotope scans.
USS neck solid lesion // CXR-------puntate calcification.
Extent of surgery (near total thyroidectomy). Follow up with sTSH,
thyroglobulin exam and US.
Radioactive iodine ablation for high risk tumours. Follow up with
RAI scans plus the above.
Anaplastic carcinoma
Rare ,1% thyroid carcinoma
Age 57year// female 56%
Deaths ---98%
C/F: thyroid nodule
Signs of pressure or invasion of surrounding structures
Recurrent laryngeal nerve pulsy
Invasion -- juxta nodal +++
Blood vessel +++++
Distant sites ++++
I123 uptake O
Degree of malignancy +++++
Highly aggressive locally and systematically
Medullary carcinoma:
Uncommon , less than 5% of thyroid cancer

Average age50year // female 56%
Death 33%
Invasion tend to metastases locally
Juxta nodal ++++
Blood vessels +++
Distant ++
Of all cases- 1/3 sporadic , 1/3 familial , 1/3 MEN type II

I123 uptake O
C/F: thyroid nodule --- firm non tender
Anterior cervical lymph nodes may be enlarged.
1/3 Frequently secrete serotonin and PG leading to diarrhea and fatigue.
LAB.:TFT--- normal except in thyroditis 2ry to cancer.
Calcitonin levels may be elevated ,especially after stimulation by PG
infusion.
2/3 Familialchildren and siblings of patient with MC are advised to have
genetic testing to detect RET-PROTO-ONCOGENE mutation.
Imaging tend to calcify
Metastases may be detected by PET scan and MRI.
Degree of malignancy--------- ++++
Worse prognosis if tissue stains heavily with calcitonin or MM AG LEU
M1.
Solitary Thyroid Nodule
FNA
Benign no further intervention
Malignant or suspicious papillary or follicular.
Non-thyroidal illness
patients may have low T3 and/or T4 usually with a normal sTSH

Psychotic patients may have elevated T3 and/or T4.
Simple non-toxic goiter
Normal TFTs
No treatment required
Surgery if obstructive symptoms

SOLITARY THYROID NODULE
Call for fine needle aspiration biopsy.
1.NODULAR WITH BENIGN CYTOLOGY 2.SOLITARY THYROID NODULE IN PT
In a pt with H/O radiation therapy
Need to be followed by
1.Periodic palpation At high risk of malignancy-resection
2.Rebiopsied if further growth occurs
3.Cystic nodules can be managed by 4.Solitary nodule in thyrotoxic pt
removal of Fluid for cytology to are an indication of RAI scan
deflate the cyst.
To differentiate adenoma/graves
Cysts recur and need repeated aspirations
Thyroxine suppression therapy is ineffective
In shrinking nodules unless the pt has primary a hot nodule is usually benign
Hypothyroidism with increased TSH but resected to cure toxicity.

NON-TOXIC GOITER
TREATMENT:
IODIZED OIL IM
COMMON IN
IODINE TABLETS
WOMEN:
SALT
ADOLESCENT
FORTIFICATION
PREGNANT WITH IODINE
LACTATING EDUCATE ABOUT
MENOPAUSE INTAKE OF:
SEAWEEDS
SHELLFISH
FISH- TAMBAN, HITO,
DALAG

PARATHYROID GLAND

4 GLANDS
SECRETES PARATHORMONE (PTH) IN RESPONSE TO SERUM Ca & Ph

LEVELS
REGULATE CALCIUM & PHOSPHORUS METABOLISM
ORGANS AFFECTED:
BONES - resorption
KIDNEYS
Ca reabsorption
Ph excretion
GIT enhances Ca absorption
DIAGNOSTIC TESTS:
HEMATOLOGICAL
SERUM CALCIUM
SERUM PHOSPHORUS
SERUM ALKALINE PHOSPHATASE
URINARY STUDIES
URINARY CALCIUM
URINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATE
HYPOPARATHYROIDISM
DECREASED PTH PRODUCTION
HYPOCALCEMIA
CALCIUM IS:

DEPOSITED IN THE BONE
EXCRETED
CAUSE:
HEREDITARY
IDIOPATHIC
SURGICAL - most common (transient, permenant)
PARATHYROID ADENOMA RESECTION suppression of PTH
AND accelerated remineralization of skeleton
(Hungry bone syndrome)
CONGENITALLY ABSENT
HEAVY METALS- hemochromatosis, hemosiderosis, wilson disease
DYSEMBRYOGENESIS---Dogeorgs syndrome
INFECTION , GRANULOMA , SECONDARY
FUNCTIONAL DECREASE PTH BY MG DEFICIENCYmaabsorption.
NECK RADIATION
POLYGLANDULAR AUTOIMMUNE Type1-----APECED
Autoimmune poly endocrinopathy Candidiasis Ectodermal Dystrophy
Present in childhood with 2/3:
1.Candidiasis 2.Addison disease 3. Hypoparathyrodism
PT may develop cataract ,vitiligo, alopechia, uveitis, immune thyroid disease.

S/SX:
It is ionized calcium which under physiological regulation , is necessary for

muscle contraction and nerve function.
Hypocalcemia is a manifestation of reduced rate of bone resorption in the

absence of sufficient PTH.
Ca in blood Neuro excitibility and Tetany Ca in ECF
Affect the neuromuscular and cardiovascular sites.
It can manifested acutely as a medical emergency or chronic cold case.
Hypocalcemic tetany is manifested by:
1. Numbness and tingling in the fingers and toes and around the lips
2. Laryngeal stridor with crowing inspiration.
3. Dyspnea and cyanosis.
ACUTE HYPOCALCEMIA
TINGLING OF THE FINGERS
CHEVOSTEKS, TROUSSEAUS
In sever tetany , cramps of individual muscle

groups occurs in the hands and feet as
carpopedal spasm.

There may be convulsions , abdominal pain , nausea and vomiting.
The seizures are of :
Grand mal type/ no aura / no loss of consciousness /no incontinence& trauma
Epileptiform attacks are striking and frequently described symptoms of

hypocalcemia.
CHRONIC HYPOCALCEMIA
Mental abnormalities
IRRITIBILITY & CONFUSION
PERSONALITY CHANGES
EMOTIONAL LIABILITY- DEPRESION
MEMORY IMPAIREMENT.

Papilloedema and increase intracranial pressure may accompany it.
CARDIAC ARRHYTHMIA
FATIGUE, WEAKNESS
CATARACT
Cataract is a characterized consequence of chronic hypoparathyrodism.
Ectopic calcifications lens, subcutaneous tissues, thickened calvarium.
XRAY: INCREASED BONE DENSITY
In idiopathic hypoparathyrodism,
Abnormalities of ectoderm- nails ,teeth , hairs , dry scaly coarse skin
Blunting of roots of teeth and dysplasia of tooth enamel
Nails- malformed ,brittle, transverse grooves
D/D OF TETANY:
1.HYPOCALCEMIA:
Ca Po4 PH
Hypovitamniosis D N
Resistance vit D N
Malabsorption N
hypoparathyroism N
2.Metabolic alkalosis----normal CA, PO4 , INCRESED PTH
Persistent vomiting
Hypokalemic alkalosis
Excessive alkali treatment

CRF over correction of acidosis
Hypokalemic alkalosis(( hyperaldosteronism/ corticosteroid analogue))
3. K Deficiency
4. MG Deficiency
D/D OF HYPOCALCEMIA:
1. Hypocalcemia hypercalciuria
2. Acute pancreatitis
3. Osteoblastic metastases-----prostate, breast
4. Chemotherapy for leukemia and lymphoma.
LABORATORY: Ca in blood and urine
Blood phosphate
Phosphate clearance
1. SERUM CALCIUM: low 9mg/dl
S.Ca is largely bound to albumin. The depressed level of S.Ca must be

correlated with the simultaneous concentration of serum albumin.
Low albumin ==== S.Ca is depressed.
(0.81 mg of Ca to 1gm of albumin).
Corrected S.Ca = S.Ca mg/dl + (0.8 X{4---ALBUMINg/dl})
Urine Ca approaches zero as the conc. Of Ca in blood less than 7mg/100ml.
2.SERUM CA low, SERUM PO4 high, ALP normal
Why increased phosphate?
B/C lack of hormone effect on phosphate clearance by the kidney.
The rate of excretion of urinary excretion of 3 5 AMP is reduced.

3.SERUM MG --low
Hypomagnesemia reduces both PTH RELEASE AND TISSUE RESPONSIVNESS

TO PTH---------HYPOCALCEMIA.
4. ECG-prolonged QT + T wave abnormalities.
5. SLIT LAMP EXAMINATION ---post. Lenticular cataract
6. IMAGING-----CT scan of skull ----basal ganglia calcification
Bones denser than normal
Spine showed the presence of lines parallel to the cortex of the vertebral
bodies giving rise to an image of a small copy of the vertebral body within the
body, a sign called bone within a bone.

COMPLICATION:
1) Acute tetany with stridor

2) Ossifications of paravertebral ligaments
3) Convulsions
4) Parkinsonism symptoms
5) Treatment related nephrocalcinosis and CRF
D/D OF HYPOCALCEMIA:
I. Decrease intake or absorption:

1.Malabsorptionno diarrhea
2.Small bowel bypass, short bowel
3. VIT D deficiency - absorption , 25 hydroxycolecalciferol
II. Loss
1.Alcoholim

2.Chronic renal insufficiency
3.Diuretic
III. Endocrine disease
1.Hypoparathyrodism
2.Sepsis
3.Pseudohypoparathyrodism
IV. Physiological
1.Decrease albumin
2.Decrease end organresponse to VIT D
3.Indued by loop diuretic,aminoglycoside, plicamycin
D/D OF HYPOPARATHYRODISM:
V. Ideopathic epilepsy
VI. Choreoathetosis
VII. Asthma
VIII. Brain tumors( convulsion and calcifications)
MANAGEMENT:
10% 20 - 30 ml 500- 1500 N/S
VIT D 50,00010,000U daily by mouth
1---2 gm Ca by mouth
Ca SUPPLEMENT
Ca carbonate (40%Ca) 500mg/ 5 times a day
Ca salts should be given orally as soon as possible to supply 1-2 gm Ca/d.
VIT D SUPPLEMENT LIQ FORM: WITH WATER, JUICE OR MILK.
Should be started as soon as oral Ca started.

Treatment of choice for chronic hypocalcemia is VIT D.
Ergocalciferol250,000-150,000U/D, slow acting
Toxicity takes weeks to disappear (6-18weeks).
Gives more stable serum Ca level.
Dihdrotachysterolfaster in onset, 3 times more potent
Daily dose 0.1251mg/d , expensive
Calcitriol (1, 5 DHCC)- RAPID , HIGH COST , TOXICITY 2 WKS
USED IN ACUTE HYPOCALCEMIA 4 MICOGM/D
Calcifedrolintermediate onset and duration of action 20mico/d
SEIZURE
LISTEN FOR STRIDOR OR HOARSENESS
TRACHEOSTOMY SET AT BEDSIDE
CaGLUCONATE AT BEDSIDE
HYPERPARATHYROIDISM
Increase PTH production.
Hypercalcemia with Hypophosphatemia.
Age-50year, sex- 3times in female more than male
PRIMARY adenoma OR hyperplasia or CA of the parathyroid gland.
Can be familial 5%( hyperplasia or adenoma)
Multiple endocrine neoplasia MEN I IIA IIB

SECONDARY compensatory over secretion of PTH in response to
hypocalcemia from :
CHRONIC RENAL DISEASE
RICKETS
MALABSORPTION SYNDROME
OSTEOMALACIA
TERTIARY-enlarged gland and become autonomus

CRF-----bone disease ---renal dystrophy.
PHYSIOLOGY OF PTH:
1. Renal tubule reabsorption of CA

2. Inhibits the net absorption of PO4 &HCO3 by renal tubule.
3. Stimulate the synthesis of 1,25 DHCC by the kidney.
4. Cause excretion of CA and PO4 by the kidney
PATHOLOGY OF INCREASED PTH:
1. Calculus formation within urinary tract- 5% of renal stones.
2. Diffuse parenchymal calcification (Nephrocalcinosis).
3. Osteoclastic activity in bone and increase CA delivery may produce diffuse

demineralization and pathological fractures cystic bone lesions
throughout the skeleton ===Osteitis fibrosa cystic
D/D OF HYPERCALCEMIA:
I. Intake or absorption
a. Milk alkali syndrome
b. VIT D or A excess 25 HCC helpful to confirm DX.
II. Endocrine disorders
1.HPT (1RY OR 2RY)
2.Acromegally

3.Adisson disease.
4.Hyperthyrodism
III. Neoplastic diseases
a. Tumor secreting PTH related proteins(ovary, kidney, lung)
b. Metastases to bone (breast )
c. Multiple myeloma ,leukemia ,lymphoma
d. Secretions of PG and osteolytic factors.
IV. Miscellaneous
1. Thiazide
2. Sarcoidosis
3. Pagets disease
4. Immobilization
5. Hypophosphatasia
6. Acute ill patient (ICU)
7. Renal transplant
8. Familial hypocalcemic hypocalcinuria
Leprosy , Tuberculosis, Berylliosis, Cocidomycosis, Histoplasmosis.
1,25Dihydrocholecalciferol---------CA
S/SX:
Most patients are asymptomatic.

Hypercalcemia is usually discovered accidently by blood biochemistry.
Nodules are almost never palpable.
Polyuria and constipation are the most characteristic symptoms.
1. Skeletal manifestation:
1-4%of patients
Osteitis fibrosa cystic may cause brown tumors.
Cysts of the jaw.
Pathological fractures -back.
Patients have bone pain, arthralgia ,diminished bone density (hip/radius).

2.Urinary tract manifestation
Polyuria and polydypsia may be present and due to increased CA
Kidney stones are seen in 18% of pts
Nephrocalcinosis
Renal failure
2. Hypercalcemic manifestation
Sever cases Thirst SOME PATIENT PRESENT W NEUROMUSCULAR
Polyuria muscle weakness
Anorexia easy fatigability
Nausea parasthesia
Vomiting depression
Constipation sleeping tendency
Anemia pruritis
Weight loss psychosis
HTN coma
CARDIAC ARRHYTHMIAS, HTN
XRAY: BONE DEMINERALIZATION
IMAGING:
I - To localize the gland:
Preoperative processes unsuccessful B/C so small 1 cm
1. USS neck
2. CT scan neck
3. MRI NECK
4. T C- 99m seastamibi
5. Thallium/technetium subtraction scan
ii- Angiography and selective venous sampling of PTH

iii- Bone x rays are normal and not required to make diagnosis.
There may be Demineralization
Subperiosteal resoption of bone (radial aspects of fingers)
Loss of lamina dura of teeth
Pathological fracture
Mottling of the skull(salt and pepper appearance).
Chondrocalcinosis(articular cartilage calcification).
Iv- patient with renal osteodystrophy:
Have ectopic calcifications around joints and soft tissues.
Dissiminated calcification in the X ray changes
Skin, soft tissues , arteries Osteopenia
Osteitis fibrosa
Calciphylaxis Osteosclerosis

Painful ischemic necrosis Osteosclerosis of the vertebral
Of skin and gangrene bodies is called
Cardiac arrhythmia RUGGER JERSEY SPINE
Respiratory failure
Ca may precipitate in the cornea(band keratopathy) & soft tissues(calciphylaxis)
COMPLICATIONS OF HYPERCALCEMIA:
1. Peptic ulcer
2. Pancreatitis
3. Coma
4. Azotemia
5. Arrhythmia
6. Fractures
Laboratory:
The hall mark of hypercalcemia is s.ca more than 10.5mg/dl
In hyperproteinemic state, total s.ca may be increased but ionized ca normal

where as in 1ry HPT , ionized calcium increased.
S O4 is often low 2.5

Urinary ca excretion may be high or normal (250mg/g creatinine)
An excessive loss of phosphate in urine
In 2ry HPT, s po4 is high.
ALP is elevated only if bone disease is present.
Plasma CL and uric acid levels may be elevated.
Elevated levels of PTH confirm the diagnosis.
Assay ---- immune radiometric assay (IRMA).

ECG----short QT
SUMMARY:
S.Ca , Urinary Ca, CL & Uric acid, Urinary PO4, S.PO4 and PTH.
MANAGEMENT:
TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC TISSUE
INDICATIONS-
1. S.Ca 1mg above upper limit of normal / U.Ca excretion more than
50mg/24hr.
2.U.Ca excretion 400mg/24hr
3.Cortical bone density 2SD below normal
4.Relative youth 30-60year
5.Symptomatic HPT
6.Difficult follow up
After surgery,pt. may develop parasthesia ,tetany as a result of rapid fall of

blood calcium .(although sCa normal).
So, frequent periodic monitoring of Ca and albumin recommended.
S.PTH postoperatively misleading//Transient thyrotoxicosis may occure.
MEDICAL TREATMENT:
Intensive hydration with normal saline.
Bisphonates-Pamidronate , Alendronate
30-90mg/o.9N/S over 4-12 hours
Preparing for surgery.
Estrogen replacementpostmenopausal
Avoid digoxin and give propranolol
Glucocorticoid is ineffective.
Renal osteodystrophy avoid hyperphosphatemiaCa acetate
&calcitriol

LOW Ca, HIGH Ph DIET
NO MILK, CAULIFLOWER & MOLASSES
STRAIN URINE FOR STONES
TO AVOID
1. Immobilization
2. Thiazid
3. VIT A/D
4. Ca. antaacids
CARE FOR PARATHYROIDECTOMY
FOLLOW UP:
CA, ALBUMIN---twice yearly
RFT +U.Ca--------once yearly
BONE DENSITY---1-2year
FAMILIAL HYPOCALCIURIC HYPERCALCMIA:
Autosomal dominant
Characterized by 1. Decrease urine CA 50 micro/24hr
2.Variable increase MG
3. Minimal PTH increase
DX family history + urinary Ca clearance
No surgery
Excellent prognosis

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THYROID AND PARATHYROID DISORDERS

BY DR. MAGDI AWAD SASI 2013

Largest endocrine gland; high rate of blood flow

Anterior and lateral sides of trachea

o Two large lobes connected by isthmus

o Filled with colloid and lined with simple cuboidal epithelial

Thyroid Gland physiology:

Two kinds of hormones are produce in the thyroid gland triiodothyronine

2 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013

At pharmacological levels, increased heat production and O2

Many of the effects appear to be mediated by way of sympathetic

The sympathetic overactivity seen in many patients with anxiety states

Hypothalamus - the highest control of thyroid function((TRH)).

o Bodys metabolic rate and O2 consumption

o Calorigenic effect - heat production

o heart rate and contraction strength

o Stimulates appetite and breakdown CHO, lipids and proteins

o Alertness, bone growth/remodeling

C (calcitonin or parafollicular) cells

o Produce calcitonin blood Ca2+ , promotes Ca2+ deposition and

Increased synthesis and production of too much thyroid hormones is

Hyperthyroidism can be that the whole gland is producing too much

causes of hyperthyroidism and thyrotoxicosis:

1. Too much iodine intake

The paradoxical association of loss of weight with normal or increased

4 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013

I. Heat production increased:

VI. Musculoskeletal system and growth:

NECK---- A visible enlargement of the thyroid gland in the neck (goiter)

EYES---Exophthalmos - protruding eyes, diplopia, chemosis, swelling

Menstrual cycle variations lightening of menstrual flow and less

1. Inspection---site,size ,shape,skin changes,surface .

Skin feels warm , moist skin with fever.

PULSEcollapsing , sleeping heart rate 80/min , atrial fibrillation

BLOOD PRESSURE--- systolic HTN with high pulse pressure.

6 MAGDI AWAD SASI THYROID AND PARATHYROID DISORDERS 2013

CLINICAL SIGNS IN GRAVES DISEASE:

Increase in thyroid gland size

Soft to slightly firm

Bruit and/or thrill

Without prominent adenopathy

Ophthalamic Graves disease:

1. Swelling of the eyelids-

Due to overfilling of orbit.

The lids appear congested and

2. Irritation of the conjunctivae:

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Unilateral exophthalmos causes:

It is diagnostic of Graves disease.

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2.Paralytic lid retraction:

Not specific for Graves disease.

5. Lid lag: NORMAL

The eye moves not in close

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Paresis of one or more of

7.Congestive ophthalmopathy: malignant exophthalmos

IT IS A MEDICAL EMERGENCY REQUIRING IMMEDIATE ADMISSION.

The patient complain of severe pain in the eye or failure of vision.

It is a sever and progressive ocular changes in Graves characterized by:

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seen above iris :

Usually affects the shins frontal

5. Radioactive iodine uptake test