paratyroid sonz.pptx

8/10/2019 paratyroid sonz.pptx

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PARATHYROID

Oleh:

Radityo Budi Leksono (DIT)Pembimbing :

dr. P.M.T. Mangalindung O, Sp.B


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Historical background

In 1849, the curator of the London Zoological Gardens,Sir Richard Owen, provided the first accuratedescription of the normal parathyroid gland afterautopsy examination of an Indian rhinoceros

human parathyroids were not grossly andmicroscopically described until 1879 by Ivar Sandstrom,a medical student in Uppsala, Sweden. He suggestedthat these glands be named the glandulaeparathyroideae, lthough their function was not known

Calcium measurement became possible in 1909, andthe association between serum calcium levels and theparathyroid glands was established.


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Anatomy

The Parathyroid is one of our major endocrine system

Most patients have four parathyroid glands. The superior glands usuallyare dorsal to the RLN at the level of the cricoid cartilage, whereas theinferior parathyroid glands are located ventral to the nerve.

Normal parathyroid glands are gray andsemitransparent in newborns but appear goldenyellow to light brown in adults. Parathyroid colordepends on cellularity, fat content, and vascularity.They often are embedded in and sometimesdifficult to discern from surrounding fat.

Parathyroid glands measure up to 7 mm in size and

weigh approximately 40 to 50 mg each. Parathyroid glands usually derive their blood

supply from branches of the inferior thyroid artery,although branches from the superior thyroidartery supply at least 20% of upper glands.


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Anatomy There are four parathyroid glands, 2 in

the superior pole of the thyroid and 2in the inferior pole.

They are rich with vascularity

They has two types of cells:

Chief cells: Present in great

numbers, responsible of synthesizingthe parathyroid hormone (PTH)

Oksifil cells: Present in smallnumbers, function:?? (degenerationof chief cells?)

However, Parathyroid glands oftenvary in position.

Sometimes the superior gland can be foundparaesophageal or retroesophageal space.

Sometimes the superior gland may descendin the tracheoesophageal groove and cometo lie caudal to the inferior glands, or in thethymus, even in the mediastinum.


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Anatomy


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Physiology

Calcium homeostasis Calcium is the most abundant cation in human beings and has

several crucial functions. Extracellular calcium levels are10,000-fold higher than intracellular levels, and both aretightly controlled.

Extracellular calcium is important for excitationcontractioncoupling in muscle tissues, synaptic transmission in thenervous system, coagulation, and secretion of otherhormones.

The parathyroid cells rely on a G-protein-coupled membrane

receptor designated the calcium-sensing receptor (CASR), to

regulate PTH secretion by sensing extracellular calcium levels

PTH secretion also is stimulated by low levels of 1,25-

dihydroxy vitamin D, catecholamines, and hypomagnesemia.


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Physiology

Calcium Homeostasis PTH is synthesized in the

parathyroid gland as aprecursorhormone,preproparathyroidhormone, which is cleaved

first to proparathyroidhormone and then to the final84-amino-acid PTH.

Secreted PTH has a half-life of2 to 4 minutes. In the liver,

PTH is metabolized into theactive N-terminal componentand the relatively inactive C-terminal fraction


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Physiology

Calcium homeostasis The calcium-sensing receptor (CASR) is expressed on

the surface of the parathyroid cell and sensesfluctuations in the concentration of extracellularcalcium.

Increased PTH secretion leads to an increase inserum calcium levels by increasing bone resorptionand enhancing renal calcium reabsorption.

PTH also stimulates renal 1-Hydroxylase activity,

leading to an increase in 1,25-dihydroxy vitamin D,which also exerts a negative feedback on PTHsecretion


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Physiology

Calcium homeostasis PTH functions to regulate

calcium levels via its actions onthree target organs, the bone,kidney, and gut.

PTH increases the resorption

of bone by stimulatingosteoclasts and promotes therelease of calcium andphosphate into the circulation.

PTH and hypophosphatemia

also enhance 1-hydroxylationof 25-hydroxyvitamin D, which

is responsible for its indirect

effect of increasing intestinal

calcium absorption


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Physiology

Calcium homeostasis At the kidney, PTH acts to

limit calcium excretion at thedistal convoluted tubule viaan active transportmechanism.

PTH also inhibits phosphatereabsorption (at the Proximalconvoluted tubule) andbicarbonate reabsorption.


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Hyperparathyroidism

Hyperfunction of the parathyroid glands may be classified asprimary, secondary, or tertiary.

PHPT arises from increased PTH production from abnormalparathyroid glands and results from a disturbance of normalfeedback control exerted by serum calcium.

Elevated PTH levels may also occur as a compensatory response tohypocalcemic states resulting from chronic renal failure or GImalabsorption of calcium.

Secondary HPT can be reversed by correction of the underlyingproblem (e.g., kidney transplantation for chronic renal failure).

However, chronically stimulated glands may occasionally becomeautonomous, resulting in persistence or recurrence ofhypercalcemia after successful renal transplantation, resulting intertiary HPT


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Primary Hyperparathyroidism PHPT is a common disorder, affecting 100,000 individuals annually in the United

States. PHPT occurs in 0.1% to 0.3% of the general population and is morecommon in women (1:500) than in men (1:2000).

Increased PTH production leads to hypercalcemia via increased GI absorption ofcalcium, increased production of vitamin D3, and reduced renal calcium clearance.

PHPT is characterized by increased parathyroid cell proliferation and PTH secretionthat is independent of calcium level

Etiology : The exact cause of PHPT is unknown, although exposure to low-dosetherapeutic ionizing radiation and familial predisposition account for some cases.Various diets and intermittent exposure to sunshine may also be related.

Other causes include renal leak of calcium and declining renal function with age aswell as alteration in the sensitivity of parathyroid glands to suppression by calcium.

Clinical Manifestations : Patients with PHPT formerly presented with the classicpentad of symptoms (i.e., kidney stones, painful bones, abdominal groans, psychic

moans, and fatigue overtones). They are more likely to be minimally symptomatic or asymptomatic. Currently,

most patients present with weakness, fatigue, polydipsia, polyuria, nocturia, boneand joint pain, constipation, decreased appetite, nausea, heartburn, pruritus,depression, and memory loss

These symptoms and signs improve in most, but certainly not all, patients afterparathyroidectomy.


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Primary Hyperparathyroidism

Complications of PHPT are :

Renal disease : Approximately 80% of patients with PHPT havesome degree of renal dysfunction or symptoms. Kidney stones werepreviously reported in up to 80% of patients but now occur in about20% to 25%.

Bone disease : osteopenia, osteoporosis, and osteitis fibrosa cystica,is found in about 15% of patients with PHPT.

Gastrointestinal Complications : PHPT has been associated withpeptic ulcer disease, pancreatitis, and cholelithiasis

Neuropsychiatric Complications : Severe hypercalcemia may lead to

various neuropsychiatric manifestations such as florid psychosis,obtundation, or coma. Other findings such as depression, anxiety,and fatigue are more commonly observed in patients with only mildhypercalcemia


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Hypoparathyroidism

Hypocalcemia can be the result of a multitude of conditions, which are listed inTable 38-14.

The parathyroid glands may be congenitally absent in DiGeorge syndrome, whichalso is characterized by lack of thymic development and, therefore, a thymus-dependent lymphoid system

By far, the most common cause of hypoparathyroidism is thyroid surgery,

particularly total thyroidectomy with a concomitant central neck dissection.Patients often develop transient hypocalcemia due to ischemia of the parathyroidglands, permanent hypoparathyroidism is rare.

Hypoparathyroidism also may occur after parathyroid surgery. Acute hypocalcemiaresults in decreased ionized calcium and increased neuromuscular excitability.

Patients initially develop circumoral and fingertip numbness and tingling. Mentalsymptoms include anxiety, confusion, and depression.

Physical examination reveals positive Chvostekssign (contraction of facial muscleselicited by tapping on the facial nerve anterior to the ear) and Trousseaus sign(carpopedal spasm that is elicited by occluding blood flow to the forearm with ablood pressure cuff for 23 minutes). Tetany, which is characterized by tonic-clonicseizures, carpopedal spasm, and laryngeal stridor, may prove fatal and should beavoided.


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paratyroid sonz.pptx