Ex 4 - Pathology of the Thyroid/Parathyroid Flashcards
(25 cards)
Normal anatomy/function of thyroid gland
- 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
What does thyroid hormone effect?
- increases metabolism
- increases HR, contractility and CO, vasodilation
- enhances sympathetic nervous system activity
- important for normal development –> especially skeletal and nervous system
Primary hyperthyroidism
Defect of synthesis/ability to secrete TH
- lack of proper “ingredients” (i.e. a dietary issue)
- loss of transport mechanism
Hypothyroidism - most commonly affected
primary disease is most common in dogs
Destruction/loss of follicles
- Idiopathic collapse (atrophy)
- eventually replaced by adipose tissue
- Lymphocytic thyroiditis (immune mediated)
- degeneration can be secondary to amyloid infiltration
Hypothyroid related lesions
- Obesity + normal/decreased appetite
- Changes in mentation
- Skin changes
- Hypercholesterolemia
- -> long-term can results in fatal changes (atherosclerosis, hepatomegaly, glomerular/corneal lipidosis)
Hypothyroidism Pathogenesis
Decreased TH –> dec lipid breakdown –> hypercholesterolemia –> endothelial damage & inc permeability –> mobilization of MO –> atherosclerosis
*atherosclerosis of the cardiac or cerebral vessels can occur
Hypothyroidism - Skin Changes
- 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
Congenital hypothyroidism
Cretinism (severely stunted growth)
- mutation in thyroperoxidase enzyme
- -> unable to convert iodide to iodine
- -> unable to make TH
Goiter - Pathogenesis
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
Most common cause of Primary hyperthyroidism
Hyperplasia, neoplasia
*IA hormonal excess is uncommon
Hyperthyroidism - hyperplasia/neoplasia
- Nodular hyperplasia
- Adenoma (unilateral is most common –> gives rise to “thyroid slip”
- typically encapsulated
- compresses adjacent tissue
- Adenocarcinoma (less common)
Hyperthyroid related lesions
- 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
Hyperthyroidism - Clin Path
- High T4/T3
- Inc liver enzymes
- Low iCa++, hyperphosphatemia
- +/- azotemia
- -> inc GFR secondary to hyperthyroidism may mask underlying renal disease
Hyperthyroid - Dogs & Cats
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
Where are C-Cells located? what do they release? What are C-cell tumors?
- Located in between follicles of the thyroid
- Release calcitonin in response to hypercalcemia
- 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
What are the cells of the parathyroid gland?
Chief cells
- no follicles, uniform cell population, round to cuboidal cells, pale gray cytoplasm
*Secrete PTH
Parathyroid hormone
Secreted from chief cells in response to hypocalcemia (low iCa++)
*Goal is to increase Ca++ in the blood
How does PTH increase blood Ca++
- 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
Proliferative - Primary Hyperparathyroidism
Occurs most commonly in dogs
- keeshonds may have a genetic component
- adenomas more common > carcinomas
- unilateral most often
Secondary hyperparathyroidism - causes (3)
- Parathyroid hyperplasia –> a response to hypocalcemia
- Nutritional
- too little Ca++ or Vit D (hypocalcemia)
- too much P - Renal
- chronic renal failure –> dec GFR –> inc P –> dec iCa++ –> hyperparathyroidism
What is the main driver of hyperparathyroidism? what can result from this?
- **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
What is Periparturient hypocalcemia? what is the common name?
Milk Fever
Due to a high Ca++ pre-partum diet
Total inflow < total outflow of Ca++
What are the two kinds of hypoparathyroidism?
- Primary = immune mediated lymphocytic parathyroiditis
2. Secondary = chemical/toxic injury; parathyroid gland removal
