Lect 4. - Parathyroid

Question 1

the parathyroid glands produce?

Answer 1

parathyroid hormone, which increases levels of calcium in the blood.

(calcitonin comes from thyroid gland C cells)

Question 2

Describe the parathyroid glands

Answer 2

The parathyroid glands are small pea-sized glands located in the neck just behind the butterfly-shaped thyroid gland.

Question 3

Calcitonin is

Answer 3

a hormone that is produced and released by the C-cells of the thyroid gland.

Question 4

Inconditionsinwhichcalciumhomeostasisisunderstress(suchasrapidgrowth,over‐ orundersupplementation,orpregnancyandlactation)calciummetabolismisregulatedbythecalciotropichormones: (3)

Answer 4

parathyroidhormone(PTH)
calcitonin(CT)
vitaminD

Question 5

Synthesisandreleaseofthe calciotropic hormonesaremainlytriggeredby

Answer 5

variationsinplasmacalciumconcentration.

Question 6

Thelocationoftheparathyroidglands.

Answer 6

Thecranialor»external«parathyroids arelooselyattachedtothethyroidcapsule.

Thecaudalor»internal«parathyroids aresubcapsularandusually
embeddedinthyroidtissue.

Question 7

Themajorcelloftheparathyroids is

Answer 7

thechiefcell.

The chief cells synthesize, store, and
secrete PTH.

Question 8

Parathyroid hormone (PTH)is synthesized andsecreted inresponse to

Answer 8

hypocalcaemia

low blood levels ofcalcitriol (vitamin D3)

Anincreaseinplasmaphosphorusconcentration

Question 9

Parathyroid hormone function (3)

Answer 9

The parathyroid hormone stimulates the following functions:

Release of calcium by bones into the bloodstream.

Absorption of calcium from food by the intestines.

Conservation of calcium by the kidneys.

Question 10

Increases in extracellular [Ca2+]
inhibit

Answer 10

PTH secretion.

Increased [Ca2+] also inhibits PTH synthesis. Thus, increased levels of plasma Ca2+ lower PTH
release and therefore tend to lower plasma [Ca2+].

Question 11

themostimportantdeterminantof PTHsecretion is the

Answer 11

thefractionofionizedcalcium in the blood

Question 12

PTHcirculatesinplasma how

Answer 12

freelyinplasma, not bound

thus, PTHisrapidlymetabolized. Thehalf‐lifeof1‐84PTHis~4minutes.

Question 13

Inadditiontotheionizedcalciumconcentration what substacnes havesignificantrolesinregulatingPTHsecretion?

Answer 13

calcitriol(1,25‐(OH)2D;ametaboliteofvitaminD)andphosphate both also play significant roles in regulating pTH secretionn.

Question 14

1,25‐dihydroxyvitaminDor calcitriol is releasedby

Answer 14

renalproximal‐tubulecells

Question 15

Plasma Ca2+ concentration feeds back on the parathyroid glands, whereas plasma inorganic phosphate (Pi) concentration feeds back on

Answer 15

osteocytes.

Question 16

1,25‐dihydroxyvitaminDor

Answer 16

calcitriol

Question 17

spontaneoushypoparathyroidismisrare in what species

Answer 17

dog and cat

Question 18

spontaneous hypoparathyroidism may occur at almost any age but the occurrence appears to be highest in

Answer 18

youngadults(onetofouryearsofage).

Question 19

Hypoparathyroidism presenting signs and symptoms are directly attributable to

Answer 19

thedecreasedconcentrationofextracellularionizedcalcium.

Therateofdecreaseintheplasmacalciumconcentrationisanimportantdeterminantinthedevelopmentofneuromuscular
manifestations.

Question 20

Intheabsenceofrenalfailure,thediagnosisofhypoparathyroidismis
virtuallycertainif what are found

Answer 20

if hypocalcemiaandhyperphosphatemiaarefound.

Question 21

After hypocalcemia and hyperphosphatemia, thediagnosisof hypoparathyroidism maybefurthersupportedby

Answer 21

measurementoftheplasmaPTHconcentration.

AninappropriatelylowplasmaPTHconcentrationwhilethereishypocalcemia
confirmsthediagnosis,providedthattheassayusedissensitiveenoughto
measureplasmaPTHinhealthyanimals.

Question 22

Emergencytreatmentofhypocalcemic tetany,requires

Answer 22

slow(5–10min)
intravenousinjectionofcalcium.

Question 23

Oralmaintenancetherapyof hypoparathyroridism comprisessupplementationwith

Answer 23

avitaminDcompoundandcalciumlactateorcarbonate.

Hypercalcemiamaybesuggestedbypolyuriaandwhenconfirmedby
measurementsofplasmacalcium,supplementationshouldbestoppedtominimizetheriskofrenalinsufficiencyduetonephrocalcinosis.

Question 24

Hyperparathyroidismcanbe classed as (2)

Answer 24

primaryorsecondary

Question 25

Primary hyperparathyroidism is

Answer 25

 the state of autonomous hypersecretion of PTH, most commonly by an adenoma of the chief cells of the PTgland.

Question 26

Secondary hyperparathyroidism is

Answer 26

an adaptive increase in PTH secretion, unrelated to intrinsic disease of the parathyroids. the increased PTH secretion is the result of chronic decreases in the concentration of ionized calcium in plasma.

Question 27

there are only two conditions in which secondary hyperparathyroidism produces clinically  significant manifestations:

Answer 27

* chronic renal failure  * calcium deficiency during growth

Question 28

Primary hyperparathyroidism is rare; it can be due to either...

Answer 28

a tumour (mostly adenomas in older animals, particularly dogs) or there may be primary hyperplasia. 

Question 29

Primary hyperparathyroidism leads to  what blood dyscrasias?

Answer 29

hypercalcaemia/hypophosphatemia;  plus renal calculi and metabolic  effects; because calcium influx is involved in cellular activity in many tissues. 

Question 30

Primary hyperparathyroidism is an uncommon disease of what age group

Answer 30

older dogs (≥ 6 years) and there is no pronounced sex predilection.

Question 31

Primary hyperparathyroidism in cats is even less frequent than in dogs, and occurs in the same age  range (6+ years), possibly with a predilection for

Answer 31

 females and Siamese cats.

Question 32

Primary hyperparathyroidism can be divided into 3 rough categories or stages of presentation:

Answer 32

1. mild - no clinical signs. hypercalcemia is an incidental finding in routine bloods. 2. form - polyuria from decreased vasopressin‐ regulated expression of aquaporins in the kidney collecting ducts. 3. most common form - surplus of nonspecific clinical signs. weakness and lethargy.

Question 33

The main problem in the differential diagnosis of primary hyperparathyroidism is

Answer 33

distinguishing it from other conditions  associated with hypercalcemia and specifically hypercalcemia of malignancy.

Question 34

Hypercalcemia of malignancy is

Answer 34

a common finding typically in patients with advanced stage cancers.

Question 35

Other causes of hypercalcemia can be e.g. (3)

Answer 35

hypervitaminosis D,  acute renal failure, and  primary hypoadrenocorticism

Question 36

Moderate hypercalcemia with no obvious identifiable cause is seen regularly in

Answer 36

cats. Longhaired cats seem to be predisposed and diet history may reveal that acidifying diets have been fed.

Question 37

idiopathic hypercalcemia in cats may be associated with what type of urolithiasis?

Answer 37

calcium oxalate urolithiasis.

Question 38

The presence of hypercalcemia is established when

Answer 38

3 measurements of total and ionized plasma Ca2+ concentration reveal values exceeding the reference range. This, in combination with normo‐ or hypophosphatemia and the appropriate signs, may give rise to the suspicion of primary hyperparathyroidism.

Question 39

what type of hypercalcemia is more common than hypercalcemia of PTorigin?

Answer 39

hypercalcemia of malignancy

Question 40

Definite differentiation between parathyroid and nonparathyroid causes of  hypercalcemia may rely on

Answer 40

measurement of plasma PTH concentration. In the absence of renal failure, an elevated PTH level confirms the diagnosis of primary hyperparathyroidism. A serious diagnostic problem may arise when it is suspected that primary  hyperparathyroidism is complicated by renal failure.

Question 41

Plasma PTH concentration within the reference range, occurring in  approximately 70 % of dogs with primary hyperparathyroidism, also  confirms the diagnosis, as in hypercalcemia of nonparathyroid origin PTH  concentrations should be low as a result of 

Answer 41

the inhibitory effect of the high  plasma calcium concentration on PTH release. 

Question 42

treatment of choice for hyperparathyroidism?

Answer 42

surgical resection of abnormal parathyroid tissue

Question 43

Secondary hyperparathyroidism is more common than primary. Give 2 Examples of secondary

Answer 43

Nuritional secondary hyperparathyroidism Renal secondary hyperparathyroidism

Question 44

Nuritional secondary hyperparathyroidism is usually a result of a diet containing

Answer 44

excess phosphate (in meat or cereal) and/or vitamin D3 deficiency may also lead to secondary hyperparathyroidism and hypocalcaemia and finally to skeletal disease

Question 45

Renal secondary hyperparathyroidism occurs in what situation and due to what?

Answer 45

chronic intrinsic renal disease (congenital or acquired) due to failure of phosphate excretion. Additionally there may be reduced activation of VitD3 in the diseased kidneys taht then reduces gut absorption of calcium leading to hyperparathyroidism as the body attempts to return homeostasis.

Question 46

hyperostotic osteodystrophy

Answer 46

Mineral is removed from the skeleton and replaced by immature fibrous connective tissue. Fibrous osteodystrophy is generalized throughout the skeleton but is accentuated in local areas such as the cancellous bone of the skull. Bones of the skull are markedly thinned by the increased resorption and have a characteristic “moth-eaten” appearance radiographically. In advanced cases, the mandible can be twisted gently due to loss of osteoid and severe fibrous osteodystrophy—hence the name “rubber jaw” syndrome.

Question 47

The main stimuli in the  pathogenesis of secondary  hyperparathyroidism due to chronic  renal insufficiency

Answer 47

1) renal retention of phosphate, which  causes precipitation of calcium in soft  tissues (2) decreased production of 1,25‐(OH)2D/ calcitriol = all equal too little calcium which triggers more and more PTH

Question 48

clinical presentation of Renal secondary hyperparathyroidism

Answer 48

classic signs of renal insufficiency: * Anorexia * Vomiting * Polydipsia * Polyuria  * Depression  In some cases these features may be mild or only intermittent. The skeletal changes range from mild to severe forms of fibrous osteodystrophy (loss of teeth).

Question 49

When renal insufficiency develops before maturation of the skeleton  the repair by proliferation of connective tissue may exceed the rate of  bone resorption. This results in 

Answer 49

an increase in bone volume and facial  swelling. 

Question 50

Treatment of Renal secondary hyperparathyroidism

Answer 50

restriction of dietary phosphorus Administering aluminum containing antacids that prevent phosphate absorption. In cases in which there is a tendency to hypocalcemia this approach may be extended by supplementation with calcium and vitamin D sterols.

Question 51

what is all meat syndrome

Answer 51

seen in animals fed an unbalanced food mainly based on meat or meat by‐products. If insufficient calcium is available in the food, the calcium concentration in plasma will tend to decrease, initiating nutritional secondary hyperparathyroidism.

Question 52

Clinical manifestations of nutritional secondary hyperparathyroidism.

Answer 52

In growing dogs, especially of the larger breeds, and cats a substantial amount of calcium is laid down as calcium phosphates in newly‐formed osteoid and cartilage. Compression fractures, partial thickness fractures and deformed skeletal protuberances.

Question 53

Secretion of calcitonin is stimulated  by? And inhibited by?

Answer 53

high serum [Ca2+] and is inhibited by normal or low serum [Ca2+]

Question 54

The main role of calcitonin is to

Answer 54

inhibit bone resorption, which reduces liberation of the calcium and phosphate, thereby indirectly lowering serum Ca2+ levels. It also prevents acute hypercalcemia due to dietary intake postprandially (after eating).

Question 55

Calcitonin increases the urinary excretion of 

Answer 55

Ca2+, PO43−, Na+, and K+ and  reduces the excretion of Mg2+.

Question 56

Disease States of Calcitonin

Answer 56

A large number of diseases are associated with abnormally increased or decreased levels of calcitonin, but pathologic effects of abnormal calcitonin secretion per se are not generally recognized.