Endocrine and metabolic disease.

Question 1

What important hormones that control the adenohypophysis are released by the hypothalamus?

Answer 1

1) Corticotrophin- releasing hormone (CRH).
2) Thyrotropin-releasing hormone (TRH).
3) Growth hormone-releasing hormone (GHRH).
4) Somatostatin (growth hormone-inhibiting hormone).
5) Gonadotropin-releasing hormone (GnRH).
6) Dopamine (the major prolactin-inhibiting factor).

Question 2

Under light microscopy what three cell types make up the adenohypophysis?

Answer 2

1) Acidophils.
2) Basophils.
3) Chromophobes.

Question 3

What hormones do acidophils in the adenohypophysis produce? (light microscopy).

Answer 3

1) Growth hormone (GH).

2) Prolactin.

Question 4

What hormones do basophils in the adenohypophysis produce? (light microscopy).

Answer 4

1) Follicle-stimulating hormones (FSH).
2) Luteinizing hormone (LH)
3) Thyrotropin (TSH).
4) Beta-lipotropin.
5) Corticotrophin.

Question 5

What hormones do Chromophobes in the adenohypophysis produce? (light microscopy).

Answer 5

1) Beta-lipotropin.

2) Corticotrophin.

Question 6

Under electron microscopy what cell types make up the adenohypophysis?

Answer 6

1) Thryotrophs (TSH).
2) Corticotrophs (Proopiomelanocortin POMC cleaved into B-LPH, A-MSH +others).
3) Gonadotrophs (FSH + LH).
4) Somatotrophs (GH).
5) Mammotrophs (Prolactin).

Question 7

What three factors determine the secretory rates of endocrine glands (in general)?

Answer 7

1) Humoral feedback loops.
2) Neurological stimulation or suppression.
3) Genetic influence.

Question 8

How do hormones (peptide, steroid, thyroid) initiate their actions?

Answer 8

1) Peptide (TSH, FSH, LH, TRH): active the cell membrane enzyme adenylcylase and the cyclic adenosine monophosphate (cAMP) system.
2) Steroid (glucocorticoids + sex hormones): pass through target cell membranes and bind to cytoplasmic receptors. Resultant steroid-receptor complex binds to nuclear chromatin receptors to initiate activity.
3) Thyroid hormones: pass into target cell cytoplasm to the nucleus where they bind chromatin receptors and initiate activity.

Question 9

What inhibits TSH release?

Answer 9

1) Hypothalamic somatostatin.
2) Thyroid hormones.
3) Glucocorticoids.
4) Dopamine.
5) Stress.

Question 10

What does TRH simulate the release of?

Answer 10

1) Prolactin.

2) TSH.

Question 11

What enhances TRH secretion?

Answer 11

1) Norepinephrine.
2) Histamine.
3) Serotonin.
4) Dopamine.

Question 12

Which hair follicle stage does Thyroid hormones initiate?

Answer 12

Anagen

Question 13

What role does T3 play in wound healing?

Answer 13

T3 is necessary for keratinocyte proliferation by stimulating wound-healing keratin genes.

Question 14

What are the two acquired forms of canine hypothyroidism?

Answer 14

1) Lymphocytic thyroiditis.

2) idiopathic thyroid necrosis and atrophy.

Question 15

What is responsible for the ‘tragic’ facial expression in hypothyroid dogs?

Answer 15

Myxoedema- mucin accumulation.

Question 16

What cutaneous histopathological changes are seen in hypothyroid dogs?

Answer 16

Non-diagnostic changes consistent with an endocrinopathy include: orthokeratotic hyperkeratosis, epidermal melanosis, follicular keratosis, follicular dilation, follicular atrophy, telogenization of hair follicles, excessive trichilemmal keratinization and sebaceous gland atrophy. Highly suggestive findings include: vacuolated hypertrophied arrector pili muscles, increased dermal mucin and a thick dermis.

Question 17

How do glucocorticoids decrease TT4 and fT4?

Answer 17

By decreasing protein binding, decreasing conversion of t4 to T3 and decreasing TSH binding by the pituitary.

Question 18

How to potentiated sulphonamides decrease T4 concentration?

Answer 18

By inhibiting iodine conversion, binding to thyroglobulin and coupling iodotyrosines resulting in thyroid gland hyperplasia.
Effects can occur as little as 2 weeks after starting therapy and can take 3 weeks or longer to reverse after discontinuation of the drug.

Question 19

What are the three parts of the adrenal cortex?

Answer 19

1) Zona glomerulosa.
2) Fasciculata.
3) Reticularis.

Question 20

Where are endogenous glucocorticoids produced?

Answer 20

Zona fasciculata in the adrenal cortex.

Question 21

What are glucocorticoids primary bound to?

Answer 21

80% Globulin, 10% albumin, other 10% is metabolically active.

Question 22

In what way do the protein catabolic, anti-enzymatic and anti-mitotic effects of glucocorticoids manifest in the skin of dogs and cats?

Answer 22

1) Epidermis becomes thinned + hyperkeratotic. (2ndry to suppression of DNA synthesis, decreased mitosis and keratinization abnormalities).
2) Basement membrane zone becomes thinned and disrupted.
3) pilosebaceous atrophy becomes pronounced.
4) Dermis becomes thinned and dermal vasculature becomes fragile (inhibition of fibroblast proliferation, collagen and ground substance production).
5) Wound healing is delayed.

Question 23

What percentage of dogs have pituitary dependant hypercortisolism?

Answer 23

80-85%

Question 24

What % of pituitary tumours are functional in pituitary dependant hypercortisolism?

Answer 24

90% and large tumours cause neurologic signs in over 50% of patients.

Question 25

Where in the pituitary is a macro/micro adenoma found?

Answer 25

Pars distalis ( up to 30% be found in pars intermedia)

Question 26

Where in the adrenal cortex is hyperplasia seen secondary to PDH?

Answer 26

Zona fasciculata and zona reticularis.

Question 27

Where are oestrogens produced?

Answer 27

Ovarian follicles, zona reticularis of the adrenal cortex, and Sertoli and interstitial cells of the testicles. They may also be made by peripheral aromatization of androgens.

Question 28

Where are androgens produced?

Answer 28

Interstitial cells of the testicle, zona reticularis of the adrenal cortex and through peripheral conversion of other sex steroids.

Question 29

What are the typical clinical signs seen with sex hormone dermatosis?

Answer 29

Absence of systemic signs and presence of truncal alopecia which may be generalised or regionalised.