Ex 4 - Pathology of the Thyroid/Parathyroid Flashcards Preview

742 - Biology of Disease III > Ex 4 - Pathology of the Thyroid/Parathyroid > Flashcards

Flashcards in Ex 4 - Pathology of the Thyroid/Parathyroid Deck (25):

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?

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


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?

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


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)

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


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?

1. Primary = immune mediated lymphocytic parathyroiditis

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


Vit D

1. Deficiency?
2. Toxicity?

1. Ricketts

2. Tissue mineralization