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12: Endocrine System > Chapter 121 Thyroid and Parathyroid Glands > Flashcards

Chapter 121 Thyroid and Parathyroid Glands Flashcards

1
Q

From what level are canine thyroid glands present (relative to tracheal rings)

A

1-8th tracheal ring

(R side 1-5, L side 3-8)

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2
Q

What is the (sometimes present) bridge of tissue between thyroid gland lobes called

A

Isthmus glandularis

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3
Q

What si the size of normal feline thyroid gland

A

10mm length

1-5mm wide

1-2mm thick

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4
Q

What structures is R thyroid gland in contact with?

A

Carotid sheta (i.e. internal jugular, common carotid, vagosympathetic trunk)

Trachea

Recurrent laryngeal n

N.B. Oesphagus of L so L thyroid not in contact with craotid sheath

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5
Q

What is the vascular supply to the thyroid gland

A

Cranial thyroid artery (first branch from common carotid)

Caudal thyroid artery (from brachiocephalic artery (N.B. caudal thyroid artery usually absent in cats)

Venous drainage via cranial and caudal thyroid veins into internal jugular)

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6
Q

Name an anatomic difference between blood supply of thyroids in dogs vs cats

A

Caudal tyroid artery not usually present in cats

Some dogs have an unpaired vessel near midline of trachea that received blood from middle segment of L thyroid gland

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7
Q

What LNs drain thyrids?

A

Drain cranially

Cranial and caudal deep cervical

Medial retropharyngeal

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8
Q

WHat is innervation to thyroid

A

Thyroid nerve

(Branch of cranial laryngeal nerve, bramch of vagus)

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9
Q

Briefly describe gross parathypid anatomy

A

4 glands in total,

one external gland and one internal gland on/in each thyroid lobe

External gland craniodorsal, internal gland caudally

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10
Q

Name 4 location sofr ectopic thyroid tissue

A

Ectopic thyroid: Base of tongue, cervical neck along trachea, thoracic inlet, mediastinum, heart base, along thoracic portion of descending aorta

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11
Q

What % of dogs have ectopic parathyroid tissue?

And what % of cats?

Clinically relevant as to do with likelyhood of needing long term post-op supplementation

A

30 - 50% of cats

3 - 6% of dogs

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12
Q

Describe the hormonal control of thyroid hormones

A

THR (thyroprophin releasing hormone) from hypothalamus

–> TSH (thyroid stimulating hormone aka Thyrotropin) from pituitary

–> thyroglobulin in thyroid follicle

–> thyroglobulin hydrolized into T4 and T3 from thyroid gland follicles

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13
Q

What thyroid hormone is major secretory product of thyroid?

And major hormon ein terms of biologic activity?

A

T4 secreted in graetest quantity

T3 has several times the biologic activity of T4 so is the major hormone in terms of biologic activity

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14
Q

Where is majority of canine T3 derviced from

A

60% derived from monodeiodination of T4 in peripheral tissues

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15
Q

How do majority of thyroid hormones travel round body?

A

Majority protein bound. Free thyroid hormones enter cell sthen protein-bound acts as a reserve, dissociating as free hormone enters cells

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16
Q

What part of thyroid hormone ‘feedback loop’ actually regulate the feedback?

A

Free (primarily T3) regulate pituitary feedback mechanism

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17
Q

Describe calcium homeostasis…

A
  • PTH is synthesized, stored, and secreted by chief cells of the parathyroid gland.
  • The effects of PTH are to increase calcium concentration and decrease phosphorus concentration in the blood. Calcium and phosphorus homeostasis, as it relates to PTH, takes place in three locations: the bones; kidneys; and, indirectly, intestine.
    • At the bone level, PTH causes calcium and phosphate resorption.
    • At the renal level, PTH causes a rapid decrease in the excretion of calcium and increase in the excretion of phosphorus. Because the overall effect of PTH is to decrease the serum concentration of phosphorus, renal excretion of phosphorus is greater than resorption of phosphorus from the bone.
    • PTH also increases formation of 1,25-dihydroxycholecalciferol (1,25-(OH)2-D3), also known as calcitriol, from vitamin D in the kidneys. Calcitriol increases absorption of calcium and phosphorus from the intestine. In this way, PTH has indirect effects on intestinal calcium and phosphate absorption.
  • Ionized calcium (Ca2+) is the physiologically active form of calcium and is regulated within a tight concentration range by the action of PTH. As such, secretion of PTH is regulated by serum ion calcium concentration. A high calcium concentration inhibits PTH secretion (negative-feedback homeostatic control), and a low concentration stimulates its production. PTH has a relatively short half-life, which has been reported to be 3 to 5 minutes in humans therefore, its effects are rapid.

i.e. net effect is to increase blood calcium, decrease phosphorous

  • Calcitonin is another hormone involved in the homeostasis of calcemia. It is produced by thyroid gland parafollicular cells, also known as C-cells. The primary function of calcitonin is to help prevent postprandial hypercalcemia in mammals. It acts by decreasing bone resorption but has no effect at the level of the kidneys or intestine.
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18
Q

What is function of calcitonin?

Where is it produced?

A

Calcitonin is another hormone involved in the homeostasis of calcemia. The primary function of calcitonin is to help prevent postprandial hypercalcemia in mammals. It acts by decreasing bone resorption but has no effect at the level of the kidneys or intestine. i.e. works to lower calcium

Produced by thyroid gland parafollicular cells, also known as C-cells.

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19
Q

Where is PTH produced?

A

Chief cells of parathyroid glands

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20
Q

What is most common histo of felie hyperthyroidism

What % are due to carcinoma?

A

Adenomatous hyperplasia

4% due to carcinoma

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21
Q

List 5 factors used to distinguish benign vs malignant thyroid mass in cats

A
  • Degree of capsular and vascular invasion
  • Degree of local tissue invasion
  • Mitotic activity
  • Regional LN involvement
  • Distant mets
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22
Q

What % of cats have ectopic hyperfuntional tissue

A

9 - 23%

(therefore scintigraphy if unsure!)

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23
Q

What is it called when cats show ‘opposite’ signs to the usual hyperthyroid signs, but DO have hyperthyroidism

A

Apathetic hyperthyroidism

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24
Q

What systemic systems shoudl be checked with hyperT

A
  • Cardiac (HCM, arrythmia, gallop)
  • Hypertension (beta adrenergic activity)
  • Renal disease (i.e. always try medical first to ensure will cope - changes will occur within 4 weeks)
  • Hypokalaemia (?v/d/anorexia, PU, cathecholamine induced movement from extra- to intracellular space)
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25
Q

How is hyperT4 diagnosed

Ad if inconclusive

A
  • Total T4
  • Repeat a few weeks later
  • Otherwise check free T4, T3 suppression and TSH (Undetectable plasma concentration of TSH in cats has been shown to be highly prognostic for developing hyperthyroidism in the future.)
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26
Q

What radionucleotide is used for hyperT scintigraphy?

What is the advantage of the pertechnetate?

A

Technetium 99m pertechnetate

The pertechnetate ion is trapped by thyroidal iodide-concentrating mechanism but is not incorporated into organic thyroid hormone. Therefore, pertechnetate uptake reflects the trapping mechanism, but not function, of the gland. Antithyroid drugs (e.g., methimazole) do not affect the trapping mechanism of the thyroid pump; instead, they inhibit the organification of the iodine and coupling of iodotyrosyl groups. Therefore, pertechnetate still concentrates in the thyroid gland even after a cat has been made euthyroid with these drugs

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27
Q

Where does technetium 99m pertechnetate usually concentrate?

What ratio is used to assess degree of thyroid uptake

A
  • Thyroid glands
  • Salivary glands
  • Gastric mucosa

Normal uptake salivary glands:thyroids (size, shape and uptake intensity) = 1:1

In a hyperT cat all ‘normal’ thyroid tissue should be atrophied, so in that case any scintigraphy thyroid activity that shows up is ABNORMAL i.e. active adenomatous or cancerous tissue)

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28
Q

How does methimazole work?

A

Methimazole block synthesis of thyroid hormones by inhibiting organification of iodide and coupling of iodothyronines to form T4 and T3. Carbimazole is metabolized to methimazole and therefore has equivalent effects.

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29
Q

What is dose of methimazole?

How long should tx be given before sx?

And carbimazole?

What other pre-op med migth be necessary

A

Methimazole

  • 1.25-2.5 mg po bid
  • Treat for 4-6 weeks pre-op

Carbimazole

  • 10-15 mg sid
  • Tx for 10d pre-op

Beta blocker if severe tachycardia/SVT

Correct hypokalaemia

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30
Q

List 3 GA drugs that should be avoided in hyperT cats

A

KEtamine, halothane, atropine

(can induce arrythmia/tachycardia)

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31
Q

What is appearance of normal thyroid tissue vs abnormal?

A

Normal = pale tan flat

Abnormal = brown, reddish plump

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32
Q

List 4 thyroidectome techniques

A
  • Extracapsular
  • Intracapsular
  • Modified extracapsular
  • Modified intracapsula

Modified ones preferred these days (either fine). Basically means sharply dissecting around external parathyroid gland and leaving tht branch of cranial thyroid artery intact - either dissect from outside or from within capsule. End result is the same - thyroid, inernal parathyroid and majority of capsule removed while small piece of capsule overlying external pararthyroid and parathyroid itself remains

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33
Q

WHat is an alternative method if parathyroid artery damaged during dissection for thyroidectomy

How long does it take for funtion?

A

Parathyroid autotransplantation

Takes 7-21d to function.

Can stage ‘bilateral’ procedures

(Median duration of hypocalcaemia in cats undergoign bilateral thyroiparathyroidectomy = 71d!)

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34
Q

If hypocalcaemia a concern, how long should animal be hospitalised for

A

7 d

35
Q

List complications of thyroidectomy (6 points)

A
  • Haemorrhage
  • Laryngeal paralysis
  • Horner’s
  • Hypothyroidism
  • Hypoparathyroidism
  • Recurrence
36
Q

WHat % of cats undergoing bilateral thyroidectomy develop clinically significant hypocalcaemia

A

6%

(remeber - 30 - 50% have ectopic parathyroid tissue!)

37
Q

WHat are c/s of hypocalcaemia

A

Twitching, reslessness, muscle fasciculations, panting, weakness, tetant anorexia, convulsions

38
Q

How is hypocalcemia treated acutely?

And long term

In cats? and in dogs?

A

Acutely:

  • 1ml/kg 10% Calcium gluconate over 10-20 mins with ECG
  • Then CRI calcium gluconate 10 mg/kg/hr in cats (3 mg/kg/hr in dogs!)

Longer term:

  • Start Vitamin D (calcitriol) 0.02-0.03 ug/kg/d in cats for 4 d then reduce to 0.005 ug/kg/d
  • And calcium carbonate supplementation 1g/cat/day (50 mg/kg/day dog!)
39
Q

What is goal calcium level while on supplementation

A

iCa 0.9 - 1.2 mmol/L

i.e lower end of normal to try to stimulate endogenour parathyroid tissue

40
Q

When is vit D/calcium supplemtntation stopped in cats after bilateral thyrpidectomy

A

21d if autotransplantation of parathyroid performed

3 months if no autotransplantation

41
Q

How is overactive ectopic thyroid tissue treated

A

radioactive iodine (I131)

42
Q

List some s/e of methimazole

A

Leukopaenia, thrombocytopaenia, eosinophilia, lymphocytosis, hepatotoxicity,

43
Q

List 3 non-sx tx options for hyperT

A

Medication (methimazole/carbimazole)

Iodine restricted diet (75 - 90% success)

Radioactive iodine therspy (I131)

44
Q

How does pre-treatment with methimazole affect scintigraphy?

and radioactive iodine?

A

Doesnt

Doesnt

45
Q

How does radioactive iodine tratment differ for thyroid carcinoma?

A

higher doses necessary

46
Q

WHat % of clinically detected canine thyroid tumours are malignant?

What % are functional?

What % bilateral

A

90% malignant

10 - 30% functional

25-50% bilateral

47
Q

How are thyroid tumours of follicular cell origin classified in dogs?

Which are most common

A

Papillary

Compact (most common)

Follicular (most common)

Anaplastic

48
Q

What doe functional thyroid tumour in dog mean re prognosis

A

If functional almost always associated with malignancy

49
Q

What dog breds are prone to thyroid tumours

A

Golden ret

Husky

Beagle

50
Q

How does iodonated contrast material affect scintigraphy and radioactive iodine treatment

A

Inhibits uptake so leave 4-6 weeks after CT contrast before scintigraphy or iodine tx.

51
Q

What modailty can be used to asses canine patient for radioactive iodine treatment

A

scintigraphy - doesnt exactly correlate but give an idea re dose of I131 necessary

52
Q

What is use of cytology for suspect thyroid mass

A

CAn say whetehr thyroid origin or not but probs cant say if malignant or benign

53
Q

What bloods should be run in canine thyroid tumour

A

Usual

Total T4

free T4

TSH

Coags

Blood type

Cross match

54
Q

What is meant by a ‘freely movable” thyroid mass

Whtat is significance of a canine thyroid tumour being freely movable?

A

Moves >1cm in all planes

More amenable to surgical excison

55
Q

What additonal complication has been reported i dogs undergoing thyrpidectomy (vs cats)

A

Megaoesophagus with vagal nerve injury

56
Q

What is levothyroxine dose

A

0.02 mg/kg bid

57
Q

What % of dogs undergoing bilateral lobe thyroidectomy become hypothyroid?

A

40%

(weirdly low…)

58
Q

List 3 factors associated with outcome in dogs with thyroid tumour

What factors are associated with local invasiveness?

A

Outcome:

  • Size
    • 23 cm2 14% mets
    • 23-100 cm2 74% mets
    • >100 cm2 100% mets
  • Mobility
  • Stage of disease

Local invasiveness:

  • tumour diameter
  • tumour volume
  • tumour fixation
  • ectopic location
  • follicular cell origin
59
Q

What is a tx option for non-resectable canine thyroid tumours

A
  • Radioactive iodine (n.b. tumour doesnt need to be functional). MST 840d
  • Radiation (48 Gy (4 Gy/fraction). MSt 24 months
  • Chemo (improved survival not reported)
60
Q

What part of hyoid is most commonly affected by ectopic thyroid tumour?

A

Basihyoid

61
Q

How is ectopic thyroid tumour affecting hyoid treated? Describe technique

A

The dog is placed in dorsal recumbency. A towel is placed under the neck to slightly elevate the cervical area. A ventral midline cervical approach is performed over the mass between the paired sternohyoid muscles. A marginal excision of the mass is performed, using a combination of sharp and blunt dissection to isolate the mass from surrounding structures, leaving its attachment to the hyoid apparatus. Care is taken not to damage the trachea, larynx, esophagus, or oropharyngeal mucosa, although theoretically, excision of part of the oropharyngeal mucosa and repair is possible. Identification and preservation of the hypoglossal and recurrent laryngeal nerves is attempted, but any branches incorporated into the tumor parenchyma are sharply transected. Surrounding musculature involved with the tumor is sharply transected approximately 1 to 2 mm from the mass, including various portions of the mylohyoid, geniohyoid, stylohyoid, genioglossus, styloglossus, hyoglossus, and thyrohyoid muscles, as well as the root of the tongue. Finally, the thyrohyoid and ceratohyoid or epihyoid bones (depending on the degree of hyoid apparatus involvement) are sharply transected bilaterally, allowing en bloc removal of the mass. The ipsilateral cut ends of the thyrohyoid and ceratohyoid or epihyoid bones (depending on which was cut in the preceding step) are sutured together with nonabsorbable suture in a simple interrupted pattern. Muscle, subcutaneous tissue, and skin closures are performed in a routine manner.

Placement of hyoid apparatus-stabilizing, nonabsorbable sutures that connect the cut ends of the epihyoid or ceratohyoid bones (depending on the amount of hyoid apparatus resected) to their ipsilateral thyrohyoid counterparts has been performed to potentially improve postoperative laryngeal and pharyngeal function. The hyoid apparatus provides a skeletal scaffold, supporting the tongue and upper vocal tract and larynx, and allows for purposeful tongue movements during chewing, swallowing, and vocalization. Although not specifically evaluated, creation of discontinuity in the canine hyoid apparatus via excision of the basihyoid bone and variable portions of the thyrohyoid, epihyoid, and ceratohyoid bones would be expected to have negative consequences for these functions. Placement of hyoid apparatus–stabilizing sutures is an attempt to ameliorate these potentially negative consequences; however, the necessity of such suture placement is unknown.

62
Q

How is canine hypothyroidism classified/

A

Primary = lack of T3 and T4

Secondary = lack of TSH

Tertiary = lack of TRH

63
Q

How does T4 differ in sighthounds

A

Thet have lower free and total T4

64
Q

How does hypothyroidism affect surgical patient?

A

Reduced cardiac output (decreased cardiac contractility, reduced intravascular volume, increase vascular resistance)

Therefore preferable to treat for 6-8 weeks before sx

65
Q

What is primary hyperparathyroidism?

And 2 examples of secondary

A

Primary = excretion of PTH by autonomously functioning parathyroid chief cells

Secondary = as a result of renal disease (low calcium or high phosphorus –> PTH secretion) or nutritional (low CA or high phos in diet –> PTH)

66
Q

What breed is at highest risk of primary hyperparathyroidism?

What is the OR for this breed

A

Keeshond (autosomal dominant - can do a gene test)

OR 50.7

67
Q

What % of paratyroid masses are carcinoma?

A

5%

68
Q

Describe the pathophysiology of increased urinary calcium with increased PTH (which usually functions to absorb/excrete less calcium form kidney)

A
  • At the kidney level, increased PTH initially stimulates excessive renal Ca2+ resorption, resulting in decreased urine excretion. As hypercalcemia worsens (serum calcium >3.5 mmol/L), renal tubular mechanisms for reabsorbing calcium become overwhelmed, and the kidney starts to excrete excessive amounts of Ca2+ despite the presence of PTH.
  • Hypercalciuria increases the risk for urolithiasis and urinary tract infections.
  • Hypercalcemia also leads to polyuria and polydipsia from an inability of the kidneys to respond normally to antidiuretic hormone, resulting in diabetes insipidus.
69
Q

Describe two mechanisms by which hypercalcaemia can lead to reduced renal function

A
  • Hypercalcemia can decrease renal function by two means. When the calcium phosphorus product (Ca × P) is greater than 60 to 80 mg/dL, soft tissues (including the kidney) can calcify, affecting function.
  • Second, hypercalcemia also induces renal vasoconstriction and decreases renal blood flow
70
Q

What are most common clinical signs of hypercalcaemia

A
  • urolithiasis
  • UTI
71
Q

What tests are performed to confirm primary hyperparathyroidism

A
  • iCa
  • PTH
  • PTH-rp
  • (+- Vit D)
  • Usual bloods
  • Imaging of nodule - US good
72
Q

List 8 ddx for hypercalcaemia

A

HARDIONS

Hyperpararthyroidism

Addisons

Renal

D Vitamin D

Infectious/idiopathic

Osteolysis

Neoplasia

Spurious/supplementation

73
Q

Comment on the levels of PTH, PTH-rp, iCA, and Vit D in the following conditions

  • Primary hyperparathyroidism
  • Lymphoma or AGASAC
  • CKD
  • Hypervitaminosis D
A

N.B. CKD –> high PTH and PTH-rp - remember this

74
Q

How is primary hyperparathyroidism distinguished from secondary renal

A

With secondary renal would expect:

  • Azotaemia
  • Low iCa
  • High PTH-rp as well as high PTH
  • Low Vitamin D (produced by kidney)
75
Q

List 4 neoplasias that produce PTH-rp

A

Lymphoma

AGASAC

Carcinomas (lung, mammary, nasal, pancreas, thymus, thyroid)

Melanoma

76
Q

WHat size parathyroid nodule can be detected on US

How does it appear

A

0.5cm

Hypo echoic compared to surrounding parenchyma, well demarcated, round-oval

77
Q

How is hypercalcaemia managed?

A

0.9% NaCL at 5 ml/kg/hr

If needs be frusemide

If still needs be Glucocorticoids (promote calciuresis)

If STILL Calcitonins or bisphosphonates

78
Q

How can parathyroid nodule location be helped intraop?

A
  • Intr-op PTH measurement (wait at least 10 mins, look for >50% drop. Not v reliable)
  • Methylene blue at 3 mg/kg but –> renal failure so not recommended
  • Indocyanine green near infrared fluoroescence (experimental)

basically none are great or of practical use

If cant find nodule, excise anything suspiscious looking. Consider removing one thyroid/parathyroid complex… - re-assses in a few weeks.

79
Q

List 3 methods for external parathyroid removal

A

Sharp dissection

Partial thyroidectomy (i.e. hald of one lobe)

‘Whole’ parathyroidectomy

80
Q

How is internal parathyroidectomy performed

A

Partial thyroidectomy

81
Q

What should be done morning of parathyroidectomy sx

A

Give calcitriol

20-30 ng/kg in dogs.

Cont bid for 2 days then reduce dose by 10% q4d

82
Q

WHen shoudl hypocalcaemia be treated

A

If clinical signs or if iCa <0.95 mmol/L

83
Q

List 3 possible causes for failure of resolution after parathyroidectomy for primary hyperparathyroidism

A
  • Incompletely excised functional nodule
  • Multiglandular diease
  • Ectopic parathyroid tissue
  • Malignant disease with functional mets
84
Q

What non-sx procedure has been reported for management of functional parathyroid masses in dogs

A
  • Percutaneous US guided intralesional ethanol (72% success)
  • Percutaneous US guided heat ablation (90% success)

Complications = coughing, change in bark, (heat ablation only) Horner’s

12: Endocrine System (2 decks)

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