Endocrine and metabolic disease. Flashcards
What important hormones that control the adenohypophysis are released by the hypothalamus?
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).
Under light microscopy what three cell types make up the adenohypophysis?
1) Acidophils.
2) Basophils.
3) Chromophobes.
What hormones do acidophils in the adenohypophysis produce? (light microscopy).
1) Growth hormone (GH).
2) Prolactin.
What hormones do basophils in the adenohypophysis produce? (light microscopy).
1) Follicle-stimulating hormones (FSH).
2) Luteinizing hormone (LH)
3) Thyrotropin (TSH).
4) Beta-lipotropin.
5) Corticotrophin.
What hormones do Chromophobes in the adenohypophysis produce? (light microscopy).
1) Beta-lipotropin.
2) Corticotrophin.
Under electron microscopy what cell types make up the adenohypophysis?
1) Thryotrophs (TSH).
2) Corticotrophs (Proopiomelanocortin POMC cleaved into B-LPH, A-MSH +others).
3) Gonadotrophs (FSH + LH).
4) Somatotrophs (GH).
5) Mammotrophs (Prolactin).
What three factors determine the secretory rates of endocrine glands (in general)?
1) Humoral feedback loops.
2) Neurological stimulation or suppression.
3) Genetic influence.
How do hormones (peptide, steroid, thyroid) initiate their actions?
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.
What inhibits TSH release?
1) Hypothalamic somatostatin.
2) Thyroid hormones.
3) Glucocorticoids.
4) Dopamine.
5) Stress.
What does TRH simulate the release of?
1) Prolactin.
2) TSH.
What enhances TRH secretion?
1) Norepinephrine.
2) Histamine.
3) Serotonin.
4) Dopamine.
Which hair follicle stage does Thyroid hormones initiate?
Anagen
What role does T3 play in wound healing?
T3 is necessary for keratinocyte proliferation by stimulating wound-healing keratin genes.
What are the two acquired forms of canine hypothyroidism?
1) Lymphocytic thyroiditis.
2) idiopathic thyroid necrosis and atrophy.
What is responsible for the ‘tragic’ facial expression in hypothyroid dogs?
Myxoedema- mucin accumulation.
What cutaneous histopathological changes are seen in hypothyroid dogs?
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.
How do glucocorticoids decrease TT4 and fT4?
By decreasing protein binding, decreasing conversion of t4 to T3 and decreasing TSH binding by the pituitary.
How to potentiated sulphonamides decrease T4 concentration?
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.
What are the three parts of the adrenal cortex?
1) Zona glomerulosa.
2) Fasciculata.
3) Reticularis.
Where are endogenous glucocorticoids produced?
Zona fasciculata in the adrenal cortex.
What are glucocorticoids primary bound to?
80% Globulin, 10% albumin, other 10% is metabolically active.
In what way do the protein catabolic, anti-enzymatic and anti-mitotic effects of glucocorticoids manifest in the skin of dogs and cats?
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.
What percentage of dogs have pituitary dependant hypercortisolism?
80-85%
What % of pituitary tumours are functional in pituitary dependant hypercortisolism?
90% and large tumours cause neurologic signs in over 50% of patients.
