Académique Documents
Professionnel Documents
Culture Documents
BY DR.
1
2013
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.
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II.
III.
IV.
V.
VI.
VII.
Integument:
Loss of hair. Nails may show recession from the nail bed.
Polyuria and polydypsialess common.
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---
CNS---hyperactive reflexes
EYE SIGNS:
Ophthalamic Graves disease:
1. Swelling of the eyelidsDue 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)
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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
8
NORMAL
5. Lid lag:
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 .
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Normal position
of eyelids
Proptosis
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.
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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.
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Onycholysis of Thyrotoxicosis
Distal separation of the
Nail plate from nail bed
Plummers nails)
Myasthenia gravis
<1
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.
14
Thyroid U/S
Benign
Characteristics
Malignant Characteristics
Regular border
Halo (sonolucent rim)
Irregular border
No Halo
Hyperechoic
Hypoechoic
(more vascular)
Microcalcification
N/A
Causes of Thyrotoxicosis
Divided by Degree of Radioiodine Uptake
High I123 Uptake
Graves disease
I
Toxic nodular goiter
TSH-mediated thyrotoxicosis
Pituitary tumor
Pituitary resistance to
thyroid hormone
HCG-mediated thyrotoxicosis
Hydatidiform mole
Choriocarcinoma
Other HCG-secreting tumors
Thyroid carcinoma (very rare)
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I123
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
nodule
16-20%
malignant
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Warm
Nodule
(indeterminant)
5% malignant
Hot Nodule
Tc-99m < 5%
malignant
I123 < 1% malignant
1.
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Patients age
Side effects of the medications
Pregnancy or heart disease
The availability of an experienced thyroid surgeon.
Medications
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
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.
2.
3.
4.
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Toxic Goiter
Preparing hypetthyroid for surgery
Preparing elderly fo RAI
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
Treatment of Hyperthyroidism
Surgery
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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
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23
1.Radioactive iodine
Propraolol, thiourea
A.Permenant hypothyroid
1/3 of pt by 8 yr afterRAI
3.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.
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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
Uss guided FNA biopsy is reserved for pts with nonpalpable nodules 1.5cm in
diameter with H/O head-neck irradiation.
TOXIC MULITNODULAR GOITER
2. RAI should be given after stopping T.U./ 3days 4.High doses 0f RAI required.
And reender patient euthyroid.
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Symptoms:
o
o
o
o
o
o
o
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))
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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.
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
ETIOLOGY
A.
B.
C.
D.
PRIMARY CAUSES
Autoimmune hypothyroidism:
-Hashimotos thyroiditis
- Atrophic thyroiditis
Drugs :
-Antithyroid drugs,
amiodarone, lithium,
interferon
Iatrogenic:
-Radio-iodine therapy
- Thyroidectomy
- External radiation to the
neck (lymphoma/CA)
Congenital hypothyroidism:
-Thyroid agenesis
- Dyshormogenesis
- TSH-R mutation
Iodine deficiency
Infiltrative disorder
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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 .
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2.CNS disorders:
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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
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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.
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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.
35
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!
36
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!)
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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
CHRONIC, HASHIMOTOS
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IMMUNOLOGICAL FACTORS
PRESENCE OF IMMUNOGLOBULINS &
ANTIBODIES DIRECTED AGAINST THE
THYROID
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.
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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.
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THYROID TUMORS:
1. Follicular cancer:
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
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Anaplastic carcinoma
Medullary carcinoma:
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.
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Need to be followed by
1.Periodic palpation
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NON-TOXIC GOITER
TREATMENT:
COMMON IN
WOMEN:
ADOLESCENT
PREGNANT
LACTATING
MENOPAUSE
IODIZED OIL IM
IODINE TABLETS
SALT
FORTIFICATION
WITH IODINE
EDUCATE ABOUT
INTAKE OF:
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SEAWEEDS
SHELLFISH
FISH- TAMBAN, HITO,
DALAG
47
PARATHYROID GLAND
48
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:
49
CAUSE:
HEREDITARY
IDIOPATHIC
SURGICAL - most common (transient, permenant)
PARATHYROID ADENOMA RESECTION
suppression of PTH
50
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
Ca in ECF
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52
Po4
PH
Hypovitamniosis D
Resistance vit D
Malabsorption
hypoparathyroism
Hypocalcemia hypercalciuria
Acute pancreatitis
Osteoblastic metastases-----prostate, breast
Chemotherapy for leukemia and lymphoma.
LABORATORY:
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.
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COMPLICATION:
1)
2)
3)
4)
5)
D/D OF HYPOCALCEMIA:
I.
II.
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III.
IV.
D/D OF HYPOPARATHYRODISM:
V.
VI.
VII.
VIII.
Ideopathic epilepsy
Choreoathetosis
Asthma
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.
57
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
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II.
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Intake or absorption
a. Milk alkali syndrome
b. VIT D or A excess 25 HCC helpful to confirm DX.
Endocrine disorders
1.HPT (1RY OR 2RY)
2.Acromegally
MAGDI AWAD SASI
III.
IV.
3.Adisson disease.
4.Hyperthyrodism
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.
Miscellaneous
1. Thiazide
2. Sarcoidosis
3. Pagets disease
4. Immobilization
5. Hypophosphatasia
6. Acute ill patient (ICU)
7. Renal transplant
8. Familial hypocalcemic hypocalcinuria
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).
60
USS neck
CT scan neck
MRI NECK
T C- 99m seastamibi
Thallium/technetium subtraction scan
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).
X ray changes
Osteopenia
Osteitis fibrosa
Calciphylaxis
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Osteosclerosis
THYROID AND PARATHYROID DISORDERS 2013
bodies is called
Cardiac arrhythmia
Respiratory failure
Ca may precipitate in the cornea(band keratopathy) & soft tissues(calciphylaxis)
COMPLICATIONS OF HYPERCALCEMIA:
1.
2.
3.
4.
5.
6.
Peptic ulcer
Pancreatitis
Coma
Azotemia
Arrhythmia
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).
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ECG----short QT
SUMMARY:
S.Ca , Urinary Ca, CL & Uric acid, Urinary PO4,
MANAGEMENT:
TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC TISSUE
INDICATIONS1. 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
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Immobilization
Thiazid
VIT A/D
Ca. antaacids
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