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Endocrinology > Lect 4. - Parathyroid > Flashcards

Lect 4. - Parathyroid Flashcards

1
Q

the parathyroid glands produce?

A

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

(calcitonin comes from thyroid gland C cells)

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2
Q

Describe the parathyroid glands

A

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

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3
Q

Calcitonin is

A

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

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4
Q

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

A

parathyroidhormone(PTH)
calcitonin(CT)
vitaminD

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5
Q

Synthesisandreleaseofthe calciotropic hormonesaremainlytriggeredby

A

variationsinplasmacalciumconcentration.

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6
Q

Thelocationoftheparathyroidglands.

A

Thecranialor»external«parathyroids arelooselyattachedtothethyroidcapsule.

Thecaudalor»internal«parathyroids aresubcapsularandusually
embeddedinthyroidtissue.

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7
Q

Themajorcelloftheparathyroids is

A

thechiefcell.

The chief cells synthesize, store, and
secrete PTH.

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8
Q

Parathyroid hormone (PTH)is synthesized andsecreted inresponse to

A

hypocalcaemia

low blood levels ofcalcitriol (vitamin D3)

Anincreaseinplasmaphosphorusconcentration

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9
Q

Parathyroid hormone function (3)

A

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.

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10
Q

Increases in extracellular [Ca2+]
inhibit

A

PTH secretion.

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

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11
Q

themostimportantdeterminantof PTHsecretion is the

A

thefractionofionizedcalcium in the blood

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12
Q

PTHcirculatesinplasma how

A

freelyinplasma, not bound

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

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13
Q

Inadditiontotheionizedcalciumconcentration what substacnes havesignificantrolesinregulatingPTHsecretion?

A

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

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14
Q

1,25‐dihydroxyvitaminDor calcitriol is releasedby

A

renalproximal‐tubulecells

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15
Q

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

A

osteocytes.

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16
Q

1,25‐dihydroxyvitaminDor

A

calcitriol

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17
Q

spontaneoushypoparathyroidismisrare in what species

A

dog and cat

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18
Q

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

A

youngadults(onetofouryearsofage).

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19
Q

Hypoparathyroidism presenting signs and symptoms are directly attributable to

A

thedecreasedconcentrationofextracellularionizedcalcium.

Therateofdecreaseintheplasmacalciumconcentrationisanimportantdeterminantinthedevelopmentofneuromuscular
manifestations.

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20
Q

Intheabsenceofrenalfailure,thediagnosisofhypoparathyroidismis
virtuallycertainif what are found

A

if hypocalcemiaandhyperphosphatemiaarefound.

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21
Q

After hypocalcemia and hyperphosphatemia, thediagnosisof hypoparathyroidism maybefurthersupportedby

A

measurementoftheplasmaPTHconcentration.

AninappropriatelylowplasmaPTHconcentrationwhilethereishypocalcemia
confirmsthediagnosis,providedthattheassayusedissensitiveenoughto
measureplasmaPTHinhealthyanimals.

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22
Q

Emergencytreatmentofhypocalcemic tetany,requires

A

slow(5–10min)
intravenousinjectionofcalcium.

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23
Q

Oralmaintenancetherapyof hypoparathyroridism comprisessupplementationwith

A

avitaminDcompoundandcalciumlactateorcarbonate.

Hypercalcemiamaybesuggestedbypolyuriaandwhenconfirmedby
measurementsofplasmacalcium,supplementationshouldbestoppedtominimizetheriskofrenalinsufficiencyduetonephrocalcinosis.

24
Q

Hyperparathyroidismcanbe classed as (2)

A

primaryorsecondary

25
Q

Primaryhyperparathyroidismis

A

thestateofautonomoushypersecretionofPTH,mostcommonlybyanadenomaofthechiefcells of the PTgland.

26
Q

Secondaryhyperparathyroidismis

A

anadaptiveincreaseinPTHsecretion,unrelatedtointrinsicdiseaseoftheparathyroids.

theincreasedPTHsecretionistheresultofchronicdecreasesintheconcentrationofionizedcalciuminplasma.

27
Q

there are onlytwo conditionsinwhichsecondaryhyperparathyroidismproducesclinically
significantmanifestations:

A
  • chronicrenalfailure
  • calciumdeficiencyduringgrowth
28
Q

Primaryhyperparathyroidismisrare; it can be due to either…

A

atumour (mostlyadenomasinolderanimals,particularlydogs)ortheremaybeprimaryhyperplasia.

29
Q

Primaryhyperparathyroidismleadsto
what blood dyscrasias?

A

hypercalcaemia/hypophosphatemia;

plus renalcalculiandmetabolic
effects;because calciuminfluxisinvolvedincellularactivityinmanytissues.

30
Q

Primaryhyperparathyroidismisanuncommondiseaseof what age group

A

olderdogs(≥6years)andthereisnopronouncedsexpredilection.

31
Q

Primaryhyperparathyroidism incatsisevenlessfrequent than in dogs,andoccursinthesameage
range (6+ years),possiblywithapredilectionfor

A

femalesandSiamesecats.

32
Q

Primaryhyperparathyroidismcan be divided into 3 rough categoriesorstagesofpresentation:

A
  1. mild - no clinical signs. hypercalcemia is an incidental finding in routine bloods.
  2. form - polyuria fromdecreasedvasopressin‐
    regulatedexpressionofaquaporinsinthekidneycollectingducts.
  3. most common form - surplus of nonspecific clinical signs. weakness and lethargy.
33
Q

Themainprobleminthedifferentialdiagnosisofprimaryhyperparathyroidismis

A

distinguishingitfromotherconditions
associatedwithhypercalcemiaandspecificallyhypercalcemiaof malignancy.

34
Q

Hypercalcemia of malignancy is

A

a common finding typically in patients with advanced stage cancers.

35
Q

Othercausesofhypercalcemiacan be e.g. (3)

A

hypervitaminosisD,
acute renalfailure,and
primaryhypoadrenocorticism

36
Q

Moderatehypercalcemiawithnoobviousidentifiablecauseisseenregularlyin

A

cats.

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

37
Q

idiopathichypercalcemiaincatsmaybeassociatedwith what type of urolithiasis?

A

calciumoxalateurolithiasis.

38
Q

Thepresenceofhypercalcemiaisestablishedwhen

A

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.

39
Q

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

A

hypercalcemia of malignancy

40
Q

Definitedifferentiationbetweenparathyroidandnonparathyroid causesof
hypercalcemiamayrelyon

A

measurementofplasmaPTHconcentration.

Intheabsenceofrenalfailure,anelevatedPTHlevelconfirmsthediagnosisofprimaryhyperparathyroidism.

Aseriousdiagnosticproblemmayarisewhenitissuspectedthatprimary
hyperparathyroidismiscomplicatedbyrenalfailure.

41
Q

PlasmaPTHconcentrationwithinthereferencerange,occurringin
approximately70%ofdogswithprimaryhyperparathyroidism,also
confirmsthediagnosis,asinhypercalcemiaofnonparathyroid originPTH
concentrationsshouldbelowasaresultof

A

theinhibitoryeffectofthehigh
plasmacalciumconcentrationonPTHrelease.

42
Q

treatment of choice for hyperparathyroidism?

A

surgical resection of abnormal parathyroid tissue

43
Q

Secondary hyperparathyroidism is more common than primary.

Give 2 Examples of secondary

A

Nuritional secondary hyperparathyroidism

Renalsecondary hyperparathyroidism

44
Q

Nuritional secondary hyperparathyroidism is usually aresult ofadiet containing

A

excess phosphate (inmeat or cereal)

and/or vitamin D3deficiency may also lead to secondary hyperparathyroidism and hypocalcaemia andfinally to skeletal disease

45
Q

Renalsecondary hyperparathyroidism occurs inwhat situation and due to what?

A

chronic intrinsic renal disease (congenital or acquired)due to failure ofphosphate excretion.

Additionally there may be reduced activation ofVitD3inthe diseased kidneys taht then reduces gut absorption ofcalcium leading to hyperparathyroidism as the body attempts to return homeostasis.

46
Q

hyperostotic osteodystrophy

A

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.

47
Q

Themainstimuli inthe
pathogenesisofsecondary
hyperparathyroidismduetochronic
renalinsufficiency

A

1)renalretentionofphosphate,which
causesprecipitationofcalciuminsoft
tissues

(2)decreasedproductionof1,25‐(OH)2D/ calcitriol

= all equal too little calcium which triggers more and more PTH

48
Q

clinical presentation of Renalsecondaryhyperparathyroidism

A

classicsignsofrenalinsufficiency:
* Anorexia
* Vomiting
* Polydipsia
* Polyuria
* Depression

Insomecasesthesefeaturesmaybemildoronlyintermittent.

Theskeletalchangesrangefrommildtosevereformsoffibrousosteodystrophy (loss of teeth).

49
Q

Whenrenalinsufficiencydevelopsbeforematurationoftheskeleton
therepairbyproliferationofconnectivetissuemayexceedtherateof
boneresorption.Thisresultsin

A

anincreaseinbonevolumeandfacial
swelling.

50
Q

Treatment of Renalsecondaryhyperparathyroidism

A

restrictionofdietaryphosphorus

Administeringaluminumcontainingantacidsthatpreventphosphateabsorption.

IncasesinwhichthereisatendencytohypocalcemiathisapproachmaybeextendedbysupplementationwithcalciumandvitaminDsterols.

51
Q

what is allmeatsyndrome

A

seeninanimalsfedanunbalancedfoodmainlybasedonmeatormeatby‐products.

Ifinsufficientcalciumisavailableinthefood,thecalciumconcentrationinplasmawilltendtodecrease,initiatingnutritional secondary hyperparathyroidism.

52
Q

Clinicalmanifestations of nutritional secondary hyperparathyroidism.

A

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.

53
Q

Secretionofcalcitoninisstimulated
by?
And inhibited by?

A

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

54
Q

Themainroleofcalcitoninisto

A

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).

55
Q

Calcitoninincreasestheurinaryexcretionof

A

Ca2+,PO43−,Na+,andK+and
reducestheexcretionofMg2+.

56
Q

DiseaseStatesofCalcitonin

A

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.

Endocrinology (16 decks)

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