Endocrine 1 – Thyroid Pathology Flashcards
1
Q
What is the ‘order’ of hormones to get thyroid hormones?
A
- TRH: hypothalamus
- TSH: pituitary
- T3 + T4: thyroid gland
o Amount will determine if need to make more or less
o If have adenoma in thyroid gland=does NOT care if being told to ‘shut down’
2
Q
Anatomy of thyroid
A
- Usually paired and similar size
- What to know how it compares to the trachea
o ~1/4 of width of trachea
3
Q
Microscopic anatomy of thyroid
A
- *look at colloid
- Relatively uniform in size
- C-cells: in clusters in between
- Normal=cuboidal/flat epithelium
- Activated=puffier and get ‘blebs’ (iodine being transferred across)
- Over stimulation=columnar and lots of blebs
- *usually see variants of all 3
4
Q
Microscopic anatomy of parathyroid
A
- partially embedded in thyroid (especially in cats)
5
Q
What does the cell need to create colloid?
A
- CHOs
- AAs
o If animal is undernourished=cannot produce thyroglobulin
o No T3+T4=no effects=no hair growth, so have hair loss (flame follicles) - *Iodine: brought across and added to thyroglobulin
6
Q
What are the effects of thyroid hormones?
A
- Normal development (brain) and growth
- **Increase metabolic rate
- Increase lipid metabolism
- Increase glucose metabolism
- Heart: rate, output, vasodilation
- Brain: alter mental state
- Reproductive system
7
Q
Increased lipid metabolism due to THs
A
- Mobilization of fat (lipolysis)
o Increased FAs in circulation
o Enhance oxidation of FAs in tissues
o Decreased concentration of cholesterol and TGs in circulation
8
Q
Increased glucose metabolism due to THs
A
- Increased glycolysis, gluconeogenesis, glucose absorption
- Increase action of insulin on peripheral tissue
9
Q
What is reverse T3?
A
- When T4 is converted to T3, but NOT biologically active
o **Protein starvation
o Liver and kidney disease
o Febrile illness
10
Q
Aplasia or hypoplasia:
A
- Rare
- *don’t even think about it
11
Q
**accessory thyroid tissue OR ectopic thyroid tissue
A
- Common in dogs
- Located anywhere from the larynx to diaphragm
o Most often in fat around the base of heart - 50% around intrapericardial aorta
- Differential diagnosis aortic base tumors
- *increase T3+T4=increased HR
- *likely need to remove it
12
Q
Thyroglossal duct cysts
A
- Ventral midline cervical region in dog
- Can become neoplastic
13
Q
Parathyroid cysts
A
- Bilaterally along trachea in CAT
14
Q
Hypothyroidism
A
- One of the MOST common endocrinopathies in large breed DOGS (Ex. golden and lab retrievers)
- Rare in cats and uncommon in other species
- 4-10 years of age
- No sex predilection
15
Q
If small thyroid gland
A
- Destroyed or was never there. So NO functional thyrocytes
o Thyroiditis
o Idiopathic follicular atrophy
o Agenesis
o *histo
16
Q
If big thyroid gland
A
- Continuously stimulated by TSH because hormones are NOT produced
o Goitrogenic compounds
o Iodine deficiency/excess
o Defect in biosynthesis of hormones
17
Q
What are some lesions of hypothyroidism?
A
- Metabolic changes
- Skin
- Reproductive: anestrus, lack of libido
- Joint pain
- Hypercholesterolemia: atherosclerosis, lipid infiltration in liver, kidney and cornea
- Anemia
18
Q
Metabolic changes with hypothyroidism
A
- *weight gain
- Cold intolerance
- Lethargy
19
Q
Skin changes with hypothyroidism
A
- Bilateral symmetrical thinning of hair coat
- Scaliness of coat
- Hyperpigmentation of skin
- Secondary pyoderma
- Myxedema
20
Q
What are the common causes of hypothyroidism?
A
- *Lymphocytic thyroiditis: inflammatory
- *idiopathic thyroid atrophy: degenerative
- Goiters
o Lambs + kids
21
Q
Lymphocytic (immune-mediated) thyroiditis
A
- Mostly in dogs
- Similar to Hashimoto’s disease in humans
o Autoantibodies to thyroglobulin, TSH receptor, etc.
22
Q
What is the gross appearance of lymphocytic thyroiditis?
A
- Multifocal to diffuse infiltrates of lymphocytes, plasma cells and macrophages
o Lateral replacement fiborisis - Slightly enlarged, normal size or smaller
- Pale
23
Q
idiopathic follicular atrophy
A
- primary degenerative disease of thyrocytes
- replacement of gland by adipose tissue
- not associated with inflammation
- decreased TSH stimulation=distinct from follicular atrophy
- **small and pale
24
Q
Thyroid hyperplasia: Goiter
A
- Mostly in goats and sheep at birth (sometimes dairy cattle)
o Abortion or slow growth rate with lethargy and abnormal mentation - Non-neoplastic, non-inflammatory enlargement due to increased TSH secretion
o Resulting from inadequate thyroxine synthesis and decreasd blood levels T4 and T3
25
Q
Goiters: 4 major pathologic mechanisms
A
- Iodine deficient diet
- Excess dietary iodine
- Goitrogenic compounds interfering within thyroxingenesis
- Genetic enzyme defects in hormone synthesis
26
Q
Goiters: 3 morphologic types of goiter in animals
A
- Diffuse hyperplastic goiter
- Colloid goiter
- Congenital dyshormongenetic goiter (inherited goiter)
*all enlarged, NO gross differences, different underlying causes
>often see mandibular prognathism
27
Q
Diffuse hyperplastic goiter
A
- More common in young animals born to dams on iodine deficient diet or excess iodide OR dams fed goitrogenic substances
- Marked enlargement due to follicular cell hyperplasia within irregular follicles
28
Q
Colloid goiter
A
- Represents involutionary phase of hyperplastic goiter
- Has macrofollicles with densely eosinophilic colloid
o Less vascularized than diffuse hyperplastic goiter
29
Q
Thyroid hyperplasia/musculoskeletal syndrome: horses
A
- Hyperplastic goiters
- Mandibular prognathia
- **Flexural deformity
- Ruptured tendons on the common digital extensor muscles
- Delayed ossification of carpal bones
- *euthanized
30
Q
Hyperthyroidism in cats
A
- COMMON in CATS
- Middle aged and old cats (mean age 12 years old, start monitoring at 10)
- No breed or sex predilection
- *discrete adenomas or multifocal nodular hyperplasia
- Carcinomas are UNCOMMON in cats
31
Q
Metabolic lesions with hyperthyroidism
A
- Hyperactivity
- Weight loss
- PU/PD/PP
32
Q
Skin lesions with hyperthyroidism
A
- Rough hair coat
- May be cervical swelling, coughing and dyspnea due to enlarged gland
33
Q
*Heart lesions with hyperthyroidism (untreated)
A
- Left ventricular hypertrophy in cats (can progress to HCM)
- Tachycardia
- Murmur
- 10-15% of cats present with overt congestive heart failure
34
Q
What should you expect to see in a horses thyroid gland?
A
- Cysts=do NOT mean anything
35
Q
Hyperthyroidism in dogs
A
- Rare
- Middle to older dogs
- Clinical findings similar to cats
- Discretn ademoms or hyperplastic nodules=NOT common
- **THYROID FOLLICULAR CELL CARCINOMAS
36
Q
Thyroid carcinomas in dogs
A
- Follicular cell adenocarcinoma
- May or may not be functional
- Highly aggressive and invasive
o Outgrows blood supply=get central necrosis - Umbilicated appearance
- *NOT GOOD=hard to treat or excise
37
Q
Parafollicular cells (C cells)
A
- found between follicles and are derived from NEURAL CREST CELLS
- *secretory granules contain calcitonin (emergency hormone)
o Protects against hypercalcemia by
Inhibiting bone resorption
Diuresis of Ca2+
38
Q
PTH level
A
- Controlled by direct feedback control system based on [Ca/P] in blood
- Protects against hypocalcemia
39
Q
How does PTH protect against hypocalcemia?
A
- Increases intestinal absorption of Ca (with VitD3)
- Stimulating bone resorption of calcium
- Enhances renal tubular reabsorption of Ca
40
Q
Hypoparathyroidism: causes
A
- Lymphocytic parathyroiditis: rare in adult dogs (smaller breeds, immune-mediated)
- Parturient paresis (milk fever)
- Destruction by neoplasms, accidental or long-term hypercalcemia from ingestion of carcinogenic plants (Cestrum diurnum)
41
Q
Parturient Paresis (Milk Fever)
A
- Cows fed a high calcium diet before parturition
- Onset of lactation is delayed response to parathyroids to sudden significant calcium loss in milk
- Develop hypocalcaemia, hypophosphatemia and paresis with onset of lactation
42
Q
Hyperparathyroidism: primary
A
- Parathyroid adenomas or carcinomas
- Functional tumors: produce excess PTH in spite of negative feedback by increased blood calcium
o See atrophy of other parathyroid glands
43
Q
What are the clinical signs of primary hyperparathyroidism?
A
- Hypercalcemia
- PU/PD
- Weakening of bones: fibrous osteodystrophy
44
Q
What are examples of secondary hyperparathyroidism?
A
- to nutritional imbalances
- *to renal disease
- **prolonged hypercalcemia leads to various things
45
Q
What will prolonged hypercalcemia with nutritional and renal causes of secondary hyperparathyroidism lead to?
A
- Hypertrophy and hyperplasia of chief cells=bilateral enlargement of parathyroids
- Excess PTH causes excessive bone resorption and marked proliferation of fibroblasts and unmineralized osteoid throughout the body
o *fibrous osteodystrophy: ‘big head’ in horses and ‘rubber jaws’ in dogs & cats
46
Q
Humoral hypercalcemia of malignancy=pseudohyperparathyroidism
A
- Paraneoplastic syndrome
- PTH related protein which mimics action of PTH
- Cause hypercalcemia and hypophosphatemia
- *adenocarcinoma of apocrine glands of anal sac (mainly dogs)
- *Lymphosarcoma (in dogs and cats)
47
Q
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