Disorders of the Parathyroid Gland

7/27/2019 Disorders of the Parathyroid Gland

1/121

Disorders of the Parathyroid

Gland


2/121

EMBRYOLOGY AND ANATOMY


3/121

Parathyroid Embryology

In humans, thesuperiorparathyroid glandsare derived from the

fourth branchialpouch, which alsogives rise to thethyroid gland. Thethird branchial

pouches give rise tothe inferiorparathyroid glandsand the thymus


4/121


The position of normalsuperior parathyroid glands ismore consistent, with 80% ofthese glands being found nearthe posterior aspect of the

upper and middle thyroidlobes, at the level of thecricoid cartilage.

Enlarged superior glands may"descend by gravity" in thetracheoesophageal groove and

come to lie caudal to theinferior glands.


5/121


As the embryo matures, the thymus and

inferior parathyroids migrate together

caudally in the neck. The most common

location for inferior glands is within a distance

of 1 cm from a point centered where the

inferior thyroid artery and recurrent

laryngeal nerve cross.


6/121


The position of the inferior glands, however,

tends to be more variable as a consequence of

their longer migratory path.

Undescended inferior glands may be found

near the skull base, angle of the mandible, or

superior to the superior parathyroid glands,

along with an undescended thymus.


7/121

Parathyroid Anatomy

The usual weight, size, and fat content of a normalparathyroid gland vary.

The weight of a normal gland has been recorded to be aslow as 40 mg, and a limit of 50 to 60 mg has been

suggested Chronic illness, race, and other individual variations may

affect the weights of normal parathyroid glands. In patients with chronic illness, total glandular weights are lower

male and black patients, total glandular weights are higher.

Normal dimensions of 3 to 6 mm in length, 2 to 4 mm inwidth, and 0.5 to 2 mm in thickness, and an average ofthree dimensions of 5 mm 3 mm 1 mm have beenproposed.


8/121

Parathyroid Anatomy

The stromal fat content of parathyroid glands is the hallmark in theevaluation of their functional status.

Detailed studies of normal glands have shown wide variations in fatcontent

The variability of fat content reported by different studies suggests

that measurement of stromal fat within parathyroid glands hasbecome nearly useless as an indicator of function.

In children and adolescents, parathyroid glands contain very sparseamounts of fat.

After adolescence, stromal fat progressively increases until 25 to 30

years of age; subsequently fat content is largely determined byconstitutional factors.

Women seem to have a tendency to have higher glandular fatcontent, which may be related to total body fat concentrations.


9/121

Parathyroid Anatomy

The characteristic cellular content of the

normal gland is dominated by chief cells with

rare water clear cells.

Oxyphil cell concentrations tend to increase

with age and are noted to be rare in young

individuals.

Oxyphil cell concentrations seem to be more

common in adults older than 40 years.


10/121

Parathyroid Anatomy

Four parathyroid glands is the usual number found in humans

The presence of supernumerary parathyroid glands is rare, and mayhave important clinical consequences, especially with respect topatients with hyperparathyroidism resulting from multiple-glanddisease.

In a series of 2015 patients who were operated on for primaryhyperparathyroidism, a hyperfunctioning supernumerary ffith parathyroid gland was the source of hypercalcemia in 15 patients (0.7%).

Nine of these patients required reoperation to remove thesupernumeriary gland representing the parathyroid tumor. Most ofthese fifth gland tumors were located in the mediastinum, either in

the thymus (seven tumors) or related to the aortic arch (threetumors).


11/121

Parathyroid Anatomy

The location of parathyroid glands may vary, as aconsequence of the variation in degree ofmigratory descent during development.

Additional infuences on these variable locationsinvolves displacement of enlarged parathyroidglands during the development ofhyperparathyroidism.

Enlarged parathyroid glands tend to migrate in a

fbroareolar plane, which offers little resistance asa result of gravity and the action of swallowingand variations in intrathoracic pressure


12/121

Parathyroid Anatomy

Eighty percent of the superior parathyroid glands are found at thecricothyroid junction approximately 1 cm cranial to thejuxtaposition of the recurrent laryngeal nerve and the inferiorthyroid artery.

The superior parathyroids, which are intimately associated with the

posterior capsule of the superior thyroid pole, are usually coveredby an extension of the pretracheal fascia that envelopes the thyroidgland and connects it to the hypopharynx and esophagus and thecarotid sheath.

The relationship of these superior parathyroid glands with thepretracheal fascia is such that the glands themselves are allowed

freedom of movement under this pseudocapsule. This feature discriminates parathyroid glands from thyroid nodules,

which cannot move freely because they are enveloped by the truecapsule of the thyroid gland


13/121

Parathyroid Anatomy

Normal superior parathyroid glands may be

found in the retroesophageal or

paraesophageal space in approximately 1% of

all instances.

These spaces represent sites where enlarged

superior parathyroid glands potentially

descend to the superior and posteriormediastinum.


14/121

Parathyroid Anatomy

The inferior parathyroid glands tend to have a morevariable location. Greater than 50% of the inferiorparathyroid glands are situated neighboring the lowerpole of the thyroid gland.

Twenty-eight percent of the inferior parathyroids arefound within the thyrothymic ligament or within theanterior superior mediastinal thymic gland.

The migratory pattern of inferior parathyroid glands

tends to follow a pathway into the anterior superiormediastinum, where one third of all missedparathyroid tumors may be found.


15/121

Parathyroid Anatomy

The incidence of intrathyroidal parathyroid

glands is controversial.

Wang considered the superior parathyroid

gland the most likely to be intrathyroidal

primarily because of the close embryologic

relationship of the primordium of the superior

parathyroid gland with the lateral complex ofthe thyroid.


16/121

Parathyroid Anatomy

The overall incidence of intrathyroidal

parathyroid glands ranges from approximately

0.5% to 3% as reported in the literature


17/121


18/121

Parathyroid glands that are located in loose connectivetissue generally are more characteristically oval-shaped, bean-shaped, or teardrop-shaped.

The color of normal parathyroid glands ranges from

yellowish brown to reddish brown. Generally, the color may depend on the amount of

stromal fat, oxyphil cell concentration, and degree ofvascularity

Normal glands tend to be more reddish brown or rust-colored in younger patients, whereas older individualshave parathyroid glands of a more yellow-brown ortobacco color.


19/121


20/121

Enlarged hyperfunctional parathyroid glands

have a color variation from dark brown to light

yellow.

Enlarged glands occurring in either secondary

or tertiary hyperparathyroidism may have a

lighter gray tone to the coloration.

Parathyroid carcinoma can also show a

mottled gray-to-white surface appearance


21/121

Normal parathyroid glands most commonly are

supplied by a single dominant artery (80%).

The length of the dominant artery supplying the

parathyroid gland may vary from 1 to 40 mm.

In most instances, the superior and inferior

parathyroid glands derive their dominant arterial

blood supply from the inferior thyroid artery.


22/121

Abundant arterial anastomoses exist between theparathyroid glands and include anastomoses withthyroid arteries and dominant arteries of the larynx,pharynx, esophagus, and trachea.

Of the superior parathyroid glands, 20% or more maybe vascularized solely by the superior thyroid artery.

10% of the inferior parathyroid glands derived theirdominant arterial supply from a branch of the superior

thyroid artery. In most of these instances, the inferiorthyroid artery was noted to be absent.


23/121

The venous drainage distribution of theparathyroid glands generally runs parallel tothe arterial vessels and drains via the

neighboring thyroid venous tributaries intothe internal jugular system.

Similarly, lymphatics from the parathyroidglands drain with the lymphatics of thethyroid gland into the paratracheal and deepcervical lymphatic basins.


24/121


25/121

The parathyroid glands are enveloped in their

own thin collagenous connective tissue

capsule. This capsule extends septa into the

gland, which separate the parenchyma intoelongated chords or clusters of functional

secretory cells. Blood vessels, lymphatics, and

nerves travel along the septa to reach theinterior of the gland


26/121

The major functional parenchymal cells of theparathyroid glands are the chief cells, which areslightly eosinophilic staining and measure 5 to 8

in diameter. These granules contain PTH, which is synthesized

from a precursor of prepro-PTH. With increasingage, the secretory cells of the parathyroid glands

may be replaced by adipose cells, which maymake up 50% to 60% of the gland in olderindividuals.


27/121

The second cell type making up parathyroid

glandular parenchyma is the oxyphil cell.

Although their function is unknown, it is believed

that oxyphil cells and a third cell type, sometimesdescribed as intermediate cells, may represent

inactive phases of a single cell type

Oxyphil cells are less numerous, are larger (6 to10 millimicrons in diameter), and stain more

deeply with eosin than chief cells.


28/121

Parathyroid Gland Physiology


29/121

Calcium Homeostasis

Produce parathyroid hormone which

maintains extracellular fluid calcium level on a

normal range

It acts on bones, kidneys and intestines


30/121

Acts directly on bones which promotes

calcium resorption, produces remodelling

effect of osteoclast and osteoblast activity.

Acts directly on kidneys promotes calcium

reabsorption and decrease tubular

reabsorption of phosphorus

Increase synthesis of 1,25 dihydroxyvitamin D,

increase gastrointestinal calcium absorption


31/121

Bone

osteoblasts have receptor proteins for binding

PTH

PTH activate the calcium pump, causing rapid

removal of calcium phosphate salts amorphousbone crystals that lie near the cells.

PTH stimulate by increasing calcium permeability

of the bone fluid of the osteocytic membrane,allowing calcium ions to diffuse into the

membrane cells from the bone fluid


32/121

Kidneys

PTH also increases renal tubular reabsorption

of calcium at the same time that it diminishes

phosphate reabsorption

increased calcium absorption occurs mainly in

the late distal tubules, the collecting tubules


33/121


34/121

Vitamin D in promotes bone calcification

One of the ways in which it does this is to

increase calcium and phosphate absorption

from the intestines


35/121

effect of PTH is mediated by the cyclic

adenosine monophosphate (cAMP) second

messenger mechanism

the concentration of cAMP increases in the

target cells


36/121

Calcium most potent regulator of parathyroid

hormone secretion

ECF Calcium controls PTH secretions by

interaction of with calcium sensor, GPCR

Receptors are present in parathyroid glands

and calcitonin producing cells of thyroid gland


37/121

Negative feedback control

parathyroid glands have calcium-binding

surface receptors that are the same as the

receptors found on calcitonin-secreting cells of

the thyroid and on the calcium-absorbing cellsof the kidneys

Ca binding to the receptors depresses the

release of PTH


38/121

slightest decrease in calcium ion

concentration in the extracellular fluid causes

the parathyroid glands to increase their rate of

secretion within minutes

conditions that increase the calcium ion

concentration above normal cause decreased

activity and reduced size of the parathyroidglands


39/121

excess quantities of calcium in the diet

increased vitamin D in the diet

Bone absorption caused by factors other than

PTH


40/121

Blood Ca2+ is low, receptors on parathyroidcells are activated, and PTH is produced

high calcium concentration inhibits the

secretion of preformed PTH from storagegranules in the parathyroids

calcitonin, which is produced in parafollicularcells (C cells) of the thyroid gland, works inopposition to PTH and acts to decrease bloodcalcium concentration


41/121

Calcitonin

peptide hormone secreted by the thyroid

gland, tends to decrease plasma calcium

concentration and, effects opposite to those

of PTH

primary stimulus for calcitonin secretion is

increased plasma calcium ion concentration


42/121

immediate effect is to decrease the absorptive

activities of the osteoclasts and possibly the

osteolytic effect of the osteocytic membrane

throughout the bone

decrease the formation of new osteoclasts

minor effects on calcium handling in the

kidney tubules and the intestines


43/121


44/121


45/121

DISEASE ENTITIES AND CLINICALPRESENTATION FOR PTG DISEASES


46/121

Outline

Hyperparathyroidism

Primary

Secondary

Tertiary

Hypercalcemic Crisis

Hypoparathyroidsm

Inherited Parathyroid Disease


47/121

Hyperparathyroidism

Incidence increased after the introduction of

routine serum calcium assessment (1970s)

Common among women, usually beyond

menopause

Every woman has a 1% risk of experiencing

primary hyperparathyroidism during her lifetime


48/121

Hyperparathyroidism

Classification Definition

Primary Autonomous secretion

Secondary Response to normal regulatory

stimuli

Tertiary Refractory secondary HPT with

hypercalcemia


49/121

Clinical Manifestations

Classic Pentad:

Kidney stones

Painful bones

Abdominal groans

Psychic moans

Fatigue overtones


50/121


Two populations may be identified:

Disease progresses insidiously over several years

and eventually manifests as renal colic

Symptoms manifest over a considerably shortertime with marked elevations in serum calcium

leading to weight loss, acute gastrointestinal

symptoms, anorexia, bone pain, and occasionally

pathologic fracture


51/121


52/121


Minimally symptomatic

Non-specific complaints

Emotional complaints

Muscular fatigue

Constipation

Bone and joint pain

Asymptomatic renal calculi

Decreased bone mineral density

Eliminated by parathyroidectomy


53/121


Kidney and Urinary Tract

Nephrolithiasis or nephrocalcinosis

Majority: Calcium oxalate

Calcium phosphate

S/Sx:

Renal Colic

Hematuria

Pyuria

Metabolic acidosis


54/121


Skeletal System Osteitis Fibrosis Cystica (now rare,


55/121


Neuromuscular System

Proximal muscle weakness

Progressive fatigue and malaise

EMG changes with atrophy of the skeletal muscle

on biopsy specimens


56/121


Neurologic

Spectrum: from anxiety and mild emotional

disturbance to frank psychosis

Depression, nervousness, and cognitivedysfunction in primary hyperparathyroidism

Cerebral dysfunction is more common in elderly

patients with an underlying mild cognitive

abnormality exposed to hypercalcemia

Others: deafness, dysphagia, dysosmia, and

dysesthesia


57/121


Gastrointestinal

Peptic Ulcer Disease

Hypercalcemia Gastrin Gastric acid

secretion Pacreatitis

Cholelithiasis

biliary calcium calicium bilirubinate stones

Sluggish bowels or constipation in asymptomatic


58/121


Cardiovascular

Hypertension


59/121

Primary Hyperparathyroidism

Third most common endocrine disorder

Results from a hyperfunction of the

parathyroid glands

Generalized disorder of calcium, phosphate,

and bone metabolism


60/121


Causes

Hyperplasia

Adenoma, lipoadenoma

Carcinoma

Primary

Multiple Endocrine Neoplasia [MEN] Type 1

Multiple Endocrine Neoplasia [MEN] Type 2a Lithium therapy


61/121



62/121

Secondary Hyperparathyroidism

Refers to the excessive secretion of PTH by

the parathyroid glands in response

tohypocalcemia and associated hypertrophy

of the glands

Especially seen in patients with chronic renal

failure


63/121

Secondary Hyperparathyroidism


64/121

Tertiary Hyperparathyroidism

Long standing renal failure s/p renaltransplant

Autonomous parathyroid gland function andtertiary HPT.

Can cause problems similar to primaryhyperparathyroidism


65/121

Summary


66/121


Hypercalcemia may decompensate from a

more or less chronic status into a critical and

life-threatening condition

Majority of cause: Primary HPT


67/121



68/121

Other Causes of Hypercalcemia

Benign Tumors Parathyroid hormoneresecreting ovarian

dermoid cyst or uterine fibroid

Endocrine Disease Thyrotoxicosis

Pheochromocytoma

Addisons disease

Islet cell pancreatic tumors

VIPoma


69/121


Granulomatous Disorders Sarcoidosis

Wegeners granulomatosis

Berylliosis

Silicone-induced and paraffin-induced granulomatosis

Eosinophilic granuloma

Tuberculosis (focal, disseminated, Mycobacterium aviumcomplex in AIDS)

Histoplasmosis

Coccidioidomycosis

Candidiasis

Leprosy

Cat-scratch disease


70/121


Drugs Vitamin D excess (oral or topical)

Vitamin A excess

Thiazide diuretics

Lithium Estrogens and antiestrogens

Androgens

Aminophylline, theophylline

Ganciclovir

Recombinant growth hormone treatment of AIDS patients

Foscarnet

8-Chloro-cyclic adenosine monophosphate


71/121


Miscellaneous Familial hypocalciuric hypercalcemia

Immobilization with or without Pagets disease of bone

End-stage liver failure

Total parenteral nutrition

Milk-alkali syndrome

Hypophosphatasia

Systemic lupus erythematosus

Juvenile rheumatoid arthritis

Recent hepatitis B vaccination

Gauchers disease with acute pneumonia

Aluminum intoxication (long-term hemodialysis)

Manganese intoxication

Primary oxalosis


72/121

Hypercalcemia of Malignancy


73/121

Hypoparathyroidism

Deficient secretion of PTH which manifests

itself biochemically by hypocalcemia,

hyperphospatemia diminished or absent

circulating iPTH and clinically the symptoms ofneuromuscular hyperactivity


74/121

Hypoparathyroidism

Causes

Surgical hypoparathyroidism (most common)

Idiopathic hypoparathyroidism

Functional hypoparathyroidism(hypomagnesemia)


75/121

Clinical Features

Neuromuscular The rate of decrease in serum

calcium is the major determinantfor the development of

neuromuscular complications When nerves are exposed to low

levels of calcium they showabnormal neuronal function

which may include decreasethreshold of excitation, repetitiveresponse to a single stimulus andrarely continuous activity


76/121

Clinical Features

Neuromuscular Parathesia

Tetany

Hyperventilation

Adrenergic symptoms Convulsion (More common in young

people and it can take the form ofeither generalized tetany followed byprolonged tonic spasms or the typicalepileptiform seizures.)

Signs of latent tetany Chvostek sign

Trousseau sign

Extrapyramidal signs (due to basalganglia calcification)


77/121

Clinical Features


78/121

Clinical Features

l l


79/121

Clinical Features

Other

1. Posterio lenticular cataract

2. Cardiac manifestation:

1. Prolonged QT interval in theECG

2. Resistance to digitalis

3. Hypotension

4. Refractory heart failure with

cardiomegally can occur.

l l


80/121

Clinical Features

Other3. Dental Manifestation

Abnormal enamel formationwith delayed or absent dental

eruption and defective dentalroot formation.

4. Malabsorption syndrome

Presumably secondary to

decreased calcium level andmay lead to steatorrhoea withlong standing untreateddisease.

Pseudohypoparathysoidism and


81/121


Pseudopseudohypoparathyroidism

Rare familial disorders with target tissue

resistance to PTH. There is hypocalcaemia,

hyperphosphataemia, with increasedparathyroid gland function. There is also a

variety of congenital defects in the growth

and development of skeleton including: Short statue

Short metacarpal and metatarsal bones



82/121


Pseudopseudohypoparathyroidism

In pseudopseudohypoparathyroidism they

have the developmental defects without the

biochemical abnormalities

O h C f H l i


83/121

Other Causes of Hypocalcemia

Dietary deficiency of vitamin D or calcium

Decreased intestinal absorption of vitamin Dor calcium due to primary small bowel

disease, short bowel syndrome, and post-gastrectomy syndrome.

Drugs that cause rickets or osteomalacia suchas phenytoin, phenobarbital, cholestyramine,

and laxative.


84/121

Diagnosis of

Hyperparathyroidism


85/121

Diagnosis of hyperparathyroidism is basedupon 2 laboratory tests: serum calcium, and

serum parathyroid hormone.

Other Tests


86/121

Laboratory Rationale

Albumin the level of total serum calcium is directly

proportional to serum albumin

Alkaline Phosphatase if elevated prior to parathyroidectomy, these

patients are more likely to require calcium

supplementation post-operatively

Phosphorus Normally low; if high suspect renal failure or

high intake

Chloride Normally elevated; because PTH decreasesthe renal resorption of bicarbonate, resulting

in increased renal resorption of chloride; a

chloride:phosphorous ratio >33 suggests

hyperparathyroidism

BUN and Creatinine To assess renal function

24-hour urine calcium High in the majority of hyperparathyroidism

cases

Bone Densomitry A Z-score of 2 is considered indicative of

clinically significant HPT in an otherwise

asymptomatic patient.

Localization Studies and Their


87/121

Application Localization studies has permitted surgeons to

employ more limited procedures in neck

exploration, while achieving the same, or

improved, surgical outcomes Operationally classified as preoperative

(invasive or non invasive)or intraoperative


88/121

Non Invasive Preoperative

Localization1. Pertechnetate Thallous Chloride Imaging

2. Technetium 99m Sestamibi Scintigraphy

3. Technetium 99m Sestamibi with SPECT

4. CT- Sestamibi Fusion5. Ultrasonography

6. Compiuted Tomography

7. MRI

1. Pertechnetate Thallous Chloride


89/121

Imaging This technique requires prolonged patient

immobilization

Sensitivity: 27-82%

Widespread availability, minimal irradiation,

and low risk

2. Technetium 99m Sestamibi


90/121

Scintigraphy Late phase is preferable for detecting PT

adenomas because the thyroid and thyroid

nodules clear of uptake is faster than do

parathyroid neoplasms No need to immobilize the patient between

images

100% sensitivity, 90% specificity

3. Technetium 99m Sestamibi with


91/121

SPECT It uses a camera collimator that rotates 360

around the patient in the axial plane

Portrays a 3D image as the sequence

progresses from the mandible to thorax

Images appear to have a higher resolution

4 CT S t ibi F i


92/121

4. CT Sestamibi Fusion It is a combined imaging modality whereby

anatomic and physiologic images are

combined to create a single image providing

concise anatomic localization of physilogicallyhyperactive parathyroid tissue

5 Ultrasonography


93/121

5. Ultrasonography Easy to perform, well tolerated by the patient,

does not require radiotracer, rapid and at low

cost.

Sensitivity depends on the ultrasonographers

experience, frequency of transducer,

resolution of image, parathyroid gland size

CT vs MRI


94/121

CT vs. MRIMRIComputed Tomography

More sensitive (50-80%)Less sensitiveexpensive

Non exposure to radiationExposure to radiationDoes not require contrast materialRequires administration of a contrast

materialNo interference from surgical clips left in

the neck after initial explorationWith interference from surgical clipsUseful for ectopic parathyroid glandsUseful for ectopic parathyroid glandsOffer limited application in preoplocalizationOffer limited application in preoplocalization


95/121

Invasive Preoperative

Localization

1. Parathyroid Arteriography

2. Selective Venous Sampling for PTH

3. USG guided Fine Needle

aspiration

1 Parathyroid Arteriography


96/121

1. Parathyroid Arteriography Includes examination of both thyrocervical

trunks, the int. mammary arteries, and

carotids

60% sensitivity

2 Selective Venous Sampling for PTH


97/121

2. Selective Venous Sampling for PTH Angiography is performed to outline the

venous drainage, facilitating sampling for PTH

assay

Expensive and technically difficult

Generally believed to be the most sensitivity

lateralizing about 80% of the parathyroid

tumors

3. Ultrasound Guided Fine Needle


98/121

Aspiration May provide for direct cytologic exam

May facilitate the use of a bioassay of the

aspirate to determine PTH level

When the aspirate is positive for PTH, it confirmsthe presence of parathyroid tissue within the

enlarged gland


99/121

Surgical Management of

Hyperparathyroidism


100/121

Medical surveillance vs. Surgical treatment If severe hypercalcemia (>11.5mg/dl) is present,

surgery is mandatory

According to NIH, patients


101/121

Asymptomatic Hyperparathyroidism Defined as documented HPT without signs or

symptoms attributable to the disease

2000 Guidelines for Parathyroid


102/121

Surgery in Asymptomatic Primary HPT

Measurement 2000 Guidelines

Serum Ca >1.0 mg/dl above normal

24-h urine Ca >400mg/dl

Creatinine Clearance Reduced by 30%

Bone Mineral Density T score


103/121

Parathyroidectomy Technique

1 Anesthesia and Preparation


104/121

1. Anesthesia and Preparation General anesthesia with endotracheal

intubation

The patients neck should be hyperextended

dorsally to provide optimal access to the neck

The table may be adjusted in the reverse

Trendelenburg position to decrease venous

congestion around the thyroid bed and centralneck.

2 Exploration of the neck


105/121

2. Exploration of the neck A low transverse cervical incision (Kocher) is

designed two finger breadths above the

suprasternal notch

In any event, the incision should not extendbeyond the SCM muscles

Depending on the surgical preference, the

usual trend is to identify the inferior glandsinitially (larger and more anterior)


106/121

Most PTG have a light brown or tobacco color PTG have a freedom of mobility

Lymph nodes are more firm, translucent white

gray Parathyroid adenomas appear rust red or beefy

red in situ, mottled

Hyperplastic glands appear darker than adenoma

After abnormal gland is removed, it is sent forpathologic analysis

3 Closure of the Incision


107/121

3. Closure of the Incision Operative field is irrigated with warm saline

solution and inspected for adequate

hemostasis

An occlusive dressing is placed to prevent fluidcollection under the incision.

Post operative Care


108/121

Post operative Care Successful parathyroid exploration with removal

of a solitary adenoma results in a decrease intotal serum calcium level, which usually reaches anadir at approximately 48 hours after the

operation. Normocalcemia at 6 months postop is the usual

standard assessment for surgical success.

Total serum calcium level and intact PTH levelshould be assessed at 1 month and 6 monthspostoperatively.


109/121

Medical Management of

Hyperparathyroidism


110/121

Symptom complex, age, overall medicalcondition and health status

Hypercalcemia

Hydration by loop diuretics

Meds that reduce osteoclastic bone resorption:

bisphosphonates, calcitonin, plicamycin

Enhancement of urinary calcium excretion isthe initial approach for Ca>12mg/dl


111/121

Diagnosis of Hypoparathyroidism

Types of Hypoparathyroidism


112/121

Laboratory ResultsPrimary Hypoparathyroidism Low PTH, Low Ca

Secondary Hypoparathyroidism Low PTH, High Ca

Pseudohypoparathyroidism High PTH, Low Ca

Types of Hypoparathyroidism


113/121

Laboratory Tests RationaleMeasurement of ionized calcium

concentration in the plasma

It is the ideal measurement

Albumin Hypoalbuminemia causes a drop in total

calcium concentration

Serum 25-hydroxy vitamin D to exclude vitamin D deficiency as a causeof hypocalcemia

Serum Magnesium Hypomagnesemia may cause PTH

deficiency and subsequent hypocalcemia.

Exclude it in any patient with primary

hypoparathyroidism.

Serum Phosphorus PTH is a phosphaturic hormone. In its

absence, phosphorus levels in the blood

rise.

Physical Examination


114/121

Physical Examination

Chvosteks(Weisss) and Trousseaus signsindicate latent tetany.


115/121


116/121

A grading system exists for Chvosteks sign: Grade I=twitching of lip at angle of mouth (8% of

normals)

Grade II=Grade I with twitching of ala nasi

Grade III=Grade II with twitching of lateral angle of

eye

Grade IV=twitching of all facial muscles


117/121


118/121

Management of

Hypoparathyroidism

Medical Care


119/121

Medical Care

Currently, treatment of patients withhypoparathyroidism involves correcting the

hypocalcemia by administering calcium and

vitamin D.

Surgical Care


120/121

Surgical Care

Patients may be treated with anautotransplant of a segment of parathyroid

gland to prevent hypoparathyroidism.

This autotransplant is usually placedsubcutaneously in the forearm or in the neck.


121/121

THANK YOU!

Date post:	14-Apr-2018
Category:	Documents
Upload:	ezekiel-arteta
View:	234 times
Download:	0 times

Disorders of the Parathyroid Gland

Documents