Pathophysiology of Endocrine Tissues Flashcards

1
Q

What is autocrine and give an example of where in the body this is used..

A

Cells that have receptors for their own secreted factors e.g. liver regeneration

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2
Q

What is paracrine and give an example of where in the body this is used.

A

Cells respond to secretions of nearby cells e.g. wound healing

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3
Q

What is endocrine and give and example of where this is used in the body..

A

Cells responding to factors (hormones) produced by distant cells e.g. insulin

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4
Q

What hormones are secreted from the anterior pituitary?

A
GH
TSH
ACTH
FSH
LH
Prolactin
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5
Q

Give examples of hormones produced by the posterior pituitary..

A

ADH

Oxytocin

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6
Q

Name the three parts to the anterior pituitary…

A

Pars tuberalis
Pars intermedia
Pars distalis

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7
Q

Explain pituitary dwarfism..

A

Pituitary cyst(s) causing deficiency in GH. Seen in GSD.

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8
Q

Describe pituitary neoplasms..

A

Often adenomas and therefore benign. Some can be non-secretory, space occupying lesions but some are endocrinologically active.

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9
Q

What is central diabetes insipidus?

A

ADH deficiency, which may be caused by compression of a space occupying lesion

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10
Q

Where would you typically find pituitary adenomas in the dog?

A

In the pars distalis/intermedia

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11
Q

Give a clinical sign of a pituitary adenoma in the dog..

A

Dysregulation of ACTH leads to pituitary dependent hyperadrenocorticism

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12
Q

How does a pituitary adenoma differ in the cat vs the dog?

A

Pituitary adenomas in the cat is more likely to see dysregulation of GH and thus acromegaly and type II diabetes, where as in the dog ACTH is the main dyregulated hormone.

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13
Q

Pituarity adenoma is the horse is usually seen in which area?

A

Pars intermedia

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14
Q

What are the clinical signs of PPID in the horse?

A

Associated with ACTH/MSH release so Cushing’s disease and thick matted hair. Space occupying lesions may also be present (behaviour, appetite, hyperthermia)

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15
Q

What does the thyroid gland respond to and what does it produce?

A

Responds to TSH from the pituitary
Thyroxine (T4)
Triiodothyronine (T3)
Calcitonin

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16
Q

What is lympocytic thyroiditis?

A

An immune-mediated destruction of the thyroid tissue leading to thyroid atrophy

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17
Q

What are the clinical features of hypothyroidism?

A

Lethargy/weight gain
Bilateral symmetrical alopecia
Hyperpigmentation
Scrufy coat

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18
Q

What are TgAAs?

A

Thyroglobulin autoantibodies that are produced as a secondary response to thyroid follicle damage

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19
Q

What is goitre?

A

A non-inflammatory/non-neoplastic enlargement of the thyroid

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20
Q

What typically causes goitre?

A

Deficiency in dietary iodine

21
Q

Why does iodine deficiency produce goitre?

A

Iodine is used to create T4. Thus low T4 and high TSH create an unproductive thyroid hyperplasia

22
Q

What are the neoplasias of the thyroid gland?

A

Thyroid adenoma
Thyroid car income
Thyroid C cell neoplasia

23
Q

When do we typically see a thyroid C cell neoplasm?

A

Seen in older bulls on a calcium-rich diet

24
Q

What cells in the parathyroid produce PTH?

A

Chief cells

25
Q

Chief cells in the parathyroid respond to..

A

Low Ca2+

26
Q

What does PTH release cause?

A

Release of calcium and PO4 from bone and calcium resorption and PO4 excretion by the kidney

27
Q

What is hypoparathyroidism and how is it caused?

A

PTH deficiency and hypocalcaemia via immunmediated destruction or inadvertent damage during surgery

28
Q

What is the clinical sign of hypocalcaemia?

A

Muscle tremors

29
Q

What is primary hyperparathyroidism?

A

Hypercalcaemia due to high PTH via a primary tumour

30
Q

How is secondary nutritional hyperparathyroidism caused?

A

Low calcium and high phosphate in the diet

31
Q

What is typically seen in nutritional hyperparathyroidism?

A

Fibrous oestodystrophy
(All meat diets in dogs/cats. Bran fed horses and reptiles)
Calcification of soft tissues

32
Q

What is hypercalaemia of malignancy?

A

Hypercalaemia associated with tumour production of PTHrp, typically seen in T cell lymphoma, myeloma and anal gland adenocarinomas

33
Q

What is Addison’s disease?

A

Hypoadenocorticism

34
Q

What causes hypoadenocorticism?

A

Lymphocytic adrenalitis that causes atrophy of the adrenal glands. Patients are usually deficient in both cortisol and aldosterone

35
Q

What are the predisposing factors to canine Addison’s disease?

A

Young to middle aged dogs
Female
Breed: Portuguese Water Dog, Poodle, Bearded Collie

36
Q

What are the acute symptoms of Addison’s?

A

Collapse, hypovolaemic shock, bradycardia, vomiting, diarrhoea

37
Q

What are the chronic symptoms of Addison’s disease?

A

Waxing and waning anorexia/lethargy/weakness. Intermittent V/D. PU/PD

38
Q

What are the two types of hyperadrenocorticism?

A

Pituitary-dependent hyperadrenocorticism

Adrenal-dependent hyperadrenocorticism

39
Q

What are the clinical features of hyperadrenocorticism?

A

PU/PD
Bilateral symmetrical alopecia, thin skin, hyperpigemnation, calcinosis cutis
Pendulous abdomen
Poor wound healing

40
Q

What is a phaeochromocytoma?

A

A tumour of catecholamine-producing cells in the adrenal medulla

41
Q

What are the clinical signs of a phaeochromocytoma?

A

Tachycardia, sweating and abdominal pain

42
Q

What is the basic pathogenesis of diabetes mellitus?

A

Persistent hyperglycaemia due to:
a. Failure of insulin production
I.e problem with pancreatic beta cells

b. Failure of insulin action
I.e problem with insulin activity in tissues

43
Q

What type of diabetes typically affects dogs and cats respectively?

A

Dogs: Type I
Cats: Type II

44
Q

What is equine metabolic syndrome?

A

An endocrinopathy linked to insulin resistance and obesity

45
Q

What does equine metabolic syndrome predispose to?

A

Laminitis

46
Q

What is insulinoma?

A

A tumour often seen in older dogs and ferrets which causes hyperinulinaemia and hypoglycaemia

47
Q

What are the clinical signs of an insulinoma?

A

Weakness, ataxia, twitching, seizures particularly on exercise

48
Q

What physiological things does insulin do in the body?

A

Increase in peripheral glucose uptake
Decrease muscle catabolism and thus hepatic gluconeogenesis
Increase intracellular K flux
Decrease peripheral lipolysis and ketone bodies while increasing lipogenesis