Ex 4 - Pathology of the Thyroid/Parathyroid

Question 1

Normal anatomy/function of thyroid gland

Answer 1

• glandular tissue made up of follicles
• follicles filled with colloid
• cuboidal to columnar epithelial cells - depending on level of activity
• Iodine from blood –> oxidized to iodine in colloid by thyroperoxidase
• tyrosine from blood moves into cells to make thyroglobulin –> excreted into colloid
• thyroglobulin + !2 –> T3 & T4 in colloid

Question 2

What does thyroid hormone effect?

Answer 2

1. increases metabolism
2. increases HR, contractility and CO, vasodilation
3. enhances sympathetic nervous system activity
4. important for normal development –> especially skeletal and nervous system

Question 3

Primary hyperthyroidism

Answer 3

Defect of synthesis/ability to secrete TH

• lack of proper “ingredients” (i.e. a dietary issue)
• loss of transport mechanism

Question 4

Hypothyroidism - most commonly affected

Answer 4

primary disease is most common in dogs

Question 5

Destruction/loss of follicles

Answer 5

• Idiopathic collapse (atrophy)
• eventually replaced by adipose tissue
• Lymphocytic thyroiditis (immune mediated)
• degeneration can be secondary to amyloid infiltration

Question 6

Hypothyroid related lesions

Answer 6

• Obesity + normal/decreased appetite
• Changes in mentation
• Skin changes
• Hypercholesterolemia
• -> long-term can results in fatal changes (atherosclerosis, hepatomegaly, glomerular/corneal lipidosis)

Question 7

Hypothyroidism Pathogenesis

Answer 7

Decreased TH –> dec lipid breakdown –> hypercholesterolemia –> endothelial damage & inc permeability –> mobilization of MO –> atherosclerosis

*atherosclerosis of the cardiac or cerebral vessels can occur

Question 8

Hypothyroidism - Skin Changes

Answer 8

• symmetrical alopecia
• hyperpigmentation
• epidermal/dermal atrophy
• Myxedema (“tragic” expression)

TH is important for maintaining normal hair cycles –> cells remain in telogen state (resting state) –> progressive alopecia, more prone to secondary skin dz

Question 9

Congenital hypothyroidism

Answer 9

Cretinism (severely stunted growth)

• mutation in thyroperoxidase enzyme
• -> unable to convert iodide to iodine
• -> unable to make TH

Question 10

Goiter - Pathogenesis

Answer 10

Follicular cells can’t make T3/T4 –> pituitary increases the release of TSH –> thyroid hyperplasia/hypertrophy

Inadequate thyroxidase synthesis

• iodine deficient diets
• goitrogenic compounds
• excess dietary iodide
• genetic defect in enzymes or thyroglobulin

Question 11

Most common cause of Primary hyperthyroidism

Answer 11

Hyperplasia, neoplasia

*IA hormonal excess is uncommon

Question 12

Hyperthyroidism - hyperplasia/neoplasia

Answer 12

• Nodular hyperplasia
• Adenoma (unilateral is most common –> gives rise to “thyroid slip”
• • typically encapsulated
• • compresses adjacent tissue
• Adenocarcinoma (less common)

Question 13

Hyperthyroid related lesions

Answer 13

• weight loss w/increased appetite (inc basal metabolic rate)
• PU/PD, inc GFR
• Excitability, poor grooming
• tachycardia, hypertension, cardiac hypertrophy, detached retina
• thromboembolism (saddle thrombus)
• V/D +/- bulky stool

Question 14

Hyperthyroidism - Clin Path

Answer 14

• High T4/T3
• Inc liver enzymes
• Low iCa++, hyperphosphatemia
• +/- azotemia
• -> inc GFR secondary to hyperthyroidism may mask underlying renal disease

Question 15

Hyperthyroid - Dogs & Cats

Answer 15

Cats: follicular adenoma –> functional

Dogs: follicular carcinoma –> usually non-functional

• enterohepatic clearance of thyroid hormone is very rapid –> this is why we don’t see hyperthyroid dogs often
• Fixed, locally invasive
• Mets to lungs occur

Question 16

Where are C-Cells located? what do they release? What are C-cell tumors?

Answer 16

1. Located in between follicles of the thyroid
2. Release calcitonin in response to hypercalcemia
3. C-cell tumors occur in bulls
   * assoc’d with Ca++ rich diet
   * multiple endocrine neoplasia (MEN) syndrome –> pheochromocytoma and pituitary adenomas
   * C-cell tumors can either be adenomas or carcinomas
   - carcinomas metastatsize to cervical LNs

Question 17

What are the cells of the parathyroid gland?

Answer 17

Chief cells
- no follicles, uniform cell population, round to cuboidal cells, pale gray cytoplasm

*Secrete PTH

Question 18

Parathyroid hormone

Answer 18

Secreted from chief cells in response to hypocalcemia (low iCa++)

*Goal is to increase Ca++ in the blood

Question 19

How does PTH increase blood Ca++

Answer 19

• Efflux of Ca++ and P from bone
• Dec loss of Ca++ in urine (increased loss of P in urine –> PTH puts the P in pee)
• -> increased Vit D synthesis
• Enhanced absorption of Ca++ and P from the gut

Question 20

Proliferative - Primary Hyperparathyroidism

Answer 20

Occurs most commonly in dogs

• keeshonds may have a genetic component
• adenomas more common > carcinomas
• unilateral most often

Question 21

Secondary hyperparathyroidism - causes (3)

Answer 21

1. Parathyroid hyperplasia –> a response to hypocalcemia
2. Nutritional
   - too little Ca++ or Vit D (hypocalcemia)
   - too much P
3. Renal
   - chronic renal failure –> dec GFR –> inc P –> dec iCa++ –> hyperparathyroidism

Question 22

What is the main driver of hyperparathyroidism? what can result from this?

Answer 22

• **Hypocalcemia is THE driver for hyperparathyroidism!!
• anything that causes secondary hyperparathyroidism can cause fibrous osteodystrophy
• • inc osteoclastic bone resorption, thin cortex, and fibrous proliferation

NB: if the product of Ca x P > 60, tissues are at risk for mineralization

Question 23

What is Periparturient hypocalcemia? what is the common name?

Answer 23

Milk Fever

Due to a high Ca++ pre-partum diet

Total inflow < total outflow of Ca++

Question 24

What are the two kinds of hypoparathyroidism?

Answer 24

1. Primary = immune mediated lymphocytic parathyroiditis

2. Secondary = chemical/toxic injury; parathyroid gland removal

Question 25

Vit D

1. Deficiency?
2. Toxicity?

Answer 25

1. Ricketts

2. Tissue mineralization