Parotid gland and hyperparathyroid, endocrine conditions

Question 1

Causes of parotid swelling: unilateral and bilateral

Answer 1

Unilateral
-Tumouir
-Blocked duct e.g. calculus

Bilateral:

Sjogrens
Mumps
TB
Alcoholism/liver cirrhosis
Diabetes
Sarcoidosis
Drugs (diuretics)

Question 2

What are the causes of unilateral parotid swelling?

Answer 2

Duct obstruction – salivary calculus, external ductal compression
Neoplasia – benign or malignant
Infective - mumps (although bilateral swelling is more common), parotitis

Question 3

What symptoms are associated with sialolisthiasis as a cause for unilateral parotid swelling?

Answer 3

Intense pain with an associated intermittent parotid swelling during mealtimes.
N.B. Symptoms can be re-produced with lemon juice.

Question 4

Are salivary calculi more common in the submandibular or parotid glands and why?

Answer 4

Submandibular glands.
{80% Submandibular, 18% parotid, 2% sublingual}

Submandibular sialolithiasis is more common because its saliva is more alkaline
-higher mucous content
-increased concentration of calcium and phosphate than `saliva of the parotid and sublingual glands.

Question 5

Do you know any ways in which parotid and submandibular calculi differ?

Answer 5

Parotid calculi tend to be multiple, smaller and 50% are within the gland

Submandibular calculi tend to be single, larger and intraductal

Question 6

What is the pathogenesis of salivary calculus formation?

Answer 6

-Saliva is rich in calcium.
-Salivary flow is slow and the intermittent stasis of flow predisposes to stones.
-Stones are mainly formed of calcium phosphate and hydroxyapatite

Question 7

What percentage of salivary calculi are radio-opaque?

Answer 7

80%

Question 8

What type of tumours are found in the parotid?

Answer 8

85% are benign – pleomorphic adenoma (70%) and Warthin’s tumour

15% are malignant - mucoepidermoid carcinoma and adenoid cystic carcinoma.

Question 9

Which worrying clinical sign may point towards malignancy in parotid tumours?

Answer 9

Ipsilateral facial nerve palsy. This is extremely uncommon in benign tumours.

Question 10

What are the post operative complications of parotidectomy?

Answer 10

VIIth nerve palsy
Frey’s Syndrome
Salivary fistula
Greater auricular nerve damage - numbness to earlobe

Question 11

What is Frey’s Syndrome?

Answer 11

-Gustatory sweating and facial flushing
-Caused by misdirected autonomic nerve regeneration
-Injury to auriculotemporal nerve, which then reattaches to sweat glands in skin rather than removed salivary gland
-Via sympathetic receptors
-Stimulation that normally causes salivation causes erythema and sweathing

Question 12

Where is parathyroid hormone produced and what does it do? Same question for calcitonin

Answer 12

-Secreted by chief cells of parathyroid glands
-Increases concentration of ca in blood
-Calcitonin (produced by parafollicular C cells) reduces calcium concentration in blood

Parathyroid hormone (PTH) is secreted by the chief cells of the parathyroid glands. It acts to
increase the concentration of calcium (Ca2+) in the blood, whereas calcitonin (a hormone
produced by the parafollicular cells (C cells) of the thyroid gland) acts to decrease calcium
concentration

Question 13

What are the causes of primary hyperparathyroidism?

Answer 13

85% are due to a single adenoma
< 1% are due to carcinoma (occasionally as part of MEN 1 and 2a syndrome)

Question 14

What are the causes of secondary hyperparathyroidism?

Answer 14

-Secondary hyperparathyroidism is the parathyroid glands’ response to hypocalcaemia,
-usually due to chronic renal failure:

Question 15

What is the mechanism behind secondary hyperparathyroidism?

Answer 15

-decreased levels conversion of 25 hydroxy-vitamin D to 1,25 dihydroxy-vitamin D in the kidneys.
-Reduced levels of active vitamin D therefore result in hypocalcaemia.

Question 16

What are the actions of 1,25 dihydroxy-vitamin D?

Answer 16

(1) increasing the uptake of calcium from the GI tract
(2) increasing the release of calcium from bone
(3) decreasing the renal excretion of calcium

Question 17

Describe tertiary hyperparathyroidism. What causes it?

Answer 17

-Chronic stimulation of the parathyroid glands by secondary hyperparathyroidism
-leads to disregulation and over activation of the parathyroid glan
- resulting in hypercalcaemia.

Renal transplant

Question 18

What are the clinical manifestations of hypercalcaemia?

Answer 18

Clinical manifestations of hypercalcaemia can be remembered with the following:
BONES: Bone pain
STONES: Renal
MOANS AND GROANS: Abdominal pain, constipation, acute pancreatitis and gallstones
THRONES: Polyuria i.e. sitting on the throne!
PSYCHIATRIC OVERTONES: Psychosis, depression

Question 19

Where are parathyroid glands found and what is their embryological origin?

Answer 19

The parathyroid glands, of which there are 4 (2 superior and 2 inferior), develop from the 3rd and 4th pharyngeal pouches and generally lie immediately posterior to the thyroid gland.

Question 20

Where can the parathyroid glands atypically be found?

Answer 20

As the thymus also develops from the 3rd pharyngeal pouch, occasionally the thymus may
drag the inferior glands down into the mediastinum

Question 21

What are frozen sections and why are these carried out during parathyroidectomy?

Answer 21

It is a pathological laboratory procedure to perform rapid microscopic analysis of a specimen

The reason for using frozen section during parathyroidectomy is to ensure that the surgeon
has actually removed parathyroid tissue as they are small and occasionally hard to recognise.

Question 22

What is the difference between primary, secondary and tertiary hyperparathyroidism?

Answer 22

Primary hyperparathyroidism: due to excess parathyroid hormone secretion from
parathyroid adenomas, hyperplasia, or carcinoma.

Secondary hyperparathyroidism: Increase in parathyroid hormone in response to low plasma
ionised calcium secondary to renal disease or malabsorption.

Tertiary hyperparathyroidism: development of autonomous hyperplastic parathyroid glands
in a patient with secondary hyperparathyroidism resulting in profound hypercalcaemia.

Question 23

What are the causes of hypoparathyroidism?

Answer 23

Post-thyroidectomy
Idiopathic (autoimmune)
After radioactive iodine therapy for Graves

Question 24

Which part of the adrenal gland secretes corticosteroids & mineralocorticoids, and which
secretes catecholamines?

Answer 24

Corticosteroids & mineralocorticoids: adrenal cortex
Catecholamines: adrenal medulla

Question 25

What is the difference between primary and secondary hyperaldosteronism?

Answer 25

Primary hyperaldosteronism: elevated aldosterone, suppressed renin levels.

Causes:
-aldosterone producing adenoma
-adrenal hyperplasia
-aldosterone producing adrenocortical carcinoma
-familial hyperaldosteronism

Secondary hyperaldosteronism: elevated aldosterone AND renin.

Causes
-renal vascular disease
-renin-secreting tumours
-liver cirrhosis