Endocrine - pathology Flashcards

1
Q

In endocrine disease, what tends to cause the clinical signs?

A

The FUNCTIONAL effects of the altered hormone levels
Rather than physical effects of endocrine gland lesions - lots less common

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2
Q

What are the two mechanisms of increasing functional effects of hormones?

A

Hyperfunction - excess production of hormone
New source of hormone

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3
Q

What is primary hyperfunction?

A

Hormone secretion occurs independent of a stimulus
From a pathological change in the endocrine gland eg. hyperplastic or neoplastic cells
Causes autonomous secretion of excess hormone

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4
Q

What is secondary hyperfunction?

A

When the stimulus causing hyperfunction is outside the primary gland - extrinsic cause

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5
Q

What are some examples of secondary hyperfunction?

A

Functional lesion is on an endocrine gland producing excess stimulatory hormone
Or excess stimulation from negative feedback loops eg. from hypercalcaemia

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6
Q

What are two examples of a new source of hormones increasing functional effects of hormones on the body?

A

Exogenous - glucocorticoid administration
Endogenous - anal sac apocrine gland carcinoma producing PTHrp

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7
Q

What are two mechanisms that cause decreased functional effects of hormones on the body?

A

Hypofunction - insufficient production of hormone
Lack of response to a hormone

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8
Q

What causes primary hypofunction?

A

Impaired ability or lack of ability to produce hormone

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9
Q

What are two causes of congenital primary hypofunction?

A

Genetic mutation causing biochemical defect in hormone synthesis or activation
Developmental anomaly

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10
Q

What are 5 causes of acquired primary hypofunction?

A

Destruction of functional cells from -
Infections
Immune mediated disease
Treatments eg. radiotherapy, drugs
Vascular disease - infarcts
Neoplastic disease

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11
Q

What are two causes of secondary hypofunction?

A

Reduced stimulatory signal between endocrine glands causing subnormal hormone secretion
Or lack of substrate for hormone synthesis eg. nutritional deficiency

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12
Q

What causes lack of response to a hormone from the target tissue?

A

Primary disease
Or another disease condition in the body causing dysfunction to the target tissue

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13
Q

What are the main endocrine glands in the body?

A

Pituitary gland
Thyroids
Parathyroids
Adrenals
Pancreas

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14
Q

What hormones are produced in the adrenal gland (cortex)?

A

Mineralocorticoids - aldosterone
Glucocorticoids - cortisol
Sex steroids

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15
Q

What disease is hyperadrenocorticism known as?

A

Cushings syndrome

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16
Q

What is the endocrine pathway of cortisol?

A

Hypothalamus releases CRH
Acts on pituitary to release ACTH
Act on adrenals to release cortisol

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17
Q

What causes primary hyperadrenocorticism?

A

Functional tumour in the adrenal cortex

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18
Q

What are the consequences of primary hyperadrenocorticism?

A

Increased cortisol production
Negative feedback on hypothalamus/pituitary - decreased CRH/ACTH
Bilateral adrenal cortex atrophy

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19
Q

What are adrenal cortical tumours most common in? What type of tumour is most common?

A

Dogs - cortical adenomas

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20
Q

What tumour of the adrenal cortex doesnt cause hyperadrenocorticism but is a common incidental finding in older dogs/cats/horses?

A

Adrenal cortical nodular hyperplasia

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21
Q

What is secondary hyperadrenocorticism?

A

A functional pituitary tumour producing excess ACTH

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22
Q

What are the consequences of pituitary dependent secondary hyperadrenocorticism?

A

Increased cortisol
Bilateral HYPERTROPHY of the adrenal cortices

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23
Q

What is more common - primary or secondary pituitary dependent hyperadrenocorticism?

A

Secondary more common - 85% of cases are pituitary-dependent

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24
Q

What can cause iatrogenic hyperadrenocorticism?

A

Glucocorticoid administration

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25
What are the consequences of glucocorticoid administration?
Reduced CRH and ADH Bilateral adrenal cortex atrophy
26
What are the similarities and differences in primary and secondary (pituitary dependent) hyperadrenocorticism?
Primary - adrenal cortical atrophy, decreased ACTH Secondary - adrenal cortical hypertrophy, increased ACTH
27
What is the name for hypoadrenocorticism?
Addisons disease
28
What occurs in primary hypoadrenocorticism?
Bilateral adrenocortical atrophy/destruction
29
What are 4 causes of primary hypoadrenocorticism?
Idiopathic Adrenal inflammation Vascular disease Metastatic tumour
30
What are the consequences of primary hypoadrenocorticism?
Reduced synthesis of mineralocorticoids - aldosterone Leads to disturbances in potassium, sodium and chloride - hyperkalaemia and hyponatremia
31
What are some causes of secondary hypoadrenocorticism?
Pituitary disease - uncommon Iatrogenic - withdrawal of glucocorticoid therapy
32
What tumour can you get in the adrenal medulla? (uncommon)
Pheochromocytoma
33
What hormones do pheochromocytomas affect?
Catecholamines - adrenaline and noradrenaline
34
Where can pheochromocytoma spread to?
Local invasion Metastatic spread via vena cava
35
What does insulin do?
Stimulates uptake of glucose into the tissues Suppresses hepatic glucose production - gluconeogenesis Stimulates glucose absorption from the GI tract
36
What are the two main mechanisms for diabetes mellitus?
Pancreatic beta cell hypofunction - insufficient insulin production (type 1) Insulin resistance - reduced response to insulin by target cells or antagonism of insulin (type 2)
37
What is type S diabetes mellitus?
Destruction of beta cells by exocrine pancreatic disease eg. pancreatitis Antagonism of insulin by other hormones/drugs
38
What is type 2 diabetes mellitus?
Complex multifactorial disease Involving inadequate insulin production AND resistance to insulin in tissues
39
What type of diabetes mellitus do dogs get?
Beta cell destruction - pancreatitis, pancreatic necrosis or immune mediated (type 1, type S) Insulin antagonism (type S)
40
What are some hormones that can cause insulin antagonism?
Progesterone - dioestrus, pregnancy Cortisol - hyperadrenocorticism, glucocorticoids Growth hormone
41
What type of diabetes mellitus do cats get?
Reduced insulin production and insulin resistance - type 2
42
What are the risk factors for cats getting diabetes mellitus?
Age Obesity Male Burmese breed
43
How does chronic hyperglycaemia cause diabetes mellitus (type 2)?
Chronic hyperglycaemia causes deterioration of beta cell function Reduces insulin secretion Initially reversible by progresses to irreversible injury
44
What can cause beta cell hyperfunction - excess insulin production?
Insulin secreting beta cell tumour - insulinoma
45
Are insulinomas benign or malignant?
Malignant - 90% of cases High risk of metastasis
46
What is the normal hypothalamic-pituitary-thyroid axis?
Hypothalamus releases TRH Pituitary releases TSH Thyroid gland releases T3 and T4
47
What causes primary hyperthyroidism?
Functional nodular hyperplasia or neoplasia In one or both thyroids
48
What are the consequences of primary hyperthyroidism?
Increased T3 and T4 Reduction in TRH/TSH
49
What tumours of the thyroid do cats get?
Multinodular hyperplasia Follicular adenoma
50
What tumours of the thyroid do dogs get?
Carcinomas - 90% Invasive and metastasise to lungs and lymph nodes But rarely cause hyperthyroidism
51
How does thyroid neoplasia differ between dogs and cats?
Cats more likely be benign or hyperplastic, but cause hyperthyroidism Dogs more likely to be malignant carcinoma, but not cause hyperthyroidism
52
What is primary hypothyroidism?
Destruction of thyroid follicular cells Causing insufficient production of thyroid hormones
53
What are the main causes of primary hypothyroidism in dogs?
Lymphocytic thyroiditis - autoantibodies in inflammatory cell infiltrate causing degeneration of thyroid follicular cells Idiopathic follicular atrophy
54
What are 2 less common causes of hypothyroidism in dogs?
Destruction of thyroid glands by neoplasms Secondary hypothyroidism from pituitary lesion - insufficient release of TSH
55
What is the main species affected by hypothyroidism?
Dogs
56
What cells produce PTH?
Chief cells in the parathyroid gland
57
What are the methods of action of PTH?
Increases calcium reabsorption in bones, GI tract and kidneys Decreases phosphorus reabsorption in the kidneys Activates calcitriol (vitamin D) synthesis
58
What has suppressive regulatory action on PTH production?
Calcitriol Increased blood Ca
59
What causes primary hyperparathyroidism?
Functional chief cell adenoma Or nodular hyperplasia
60
What are the consequences of primary hyperparathyroidism on the parathyroid glands?
Atrophy - reduced PTH secretion from normal chief cells
61
What is humoral hypercalcaemia of malignancy?
Neoplasia producing parathyroid hormone related protein (PTHrp)
62
What are some tumours that produce PTHrp?
Anal sac apocrine gland carcinoma Multiple myeloma Lymphoma
63
What is renal secondary hyperparathyroidism?
Where renal disease causes hyperphosphataemia This reduces calcitriol synthesis - less regulation on PTH It also decreases blood calcium by reducing Ca uptake in GI tract Increased PTH produced to compensate causes Ca resorption from bones
64
What is nutritional secondary hyperparathyroidism?
Dietary calcium:phosphate imbalance And vitamin D deficiency Increased PTH to compensate for low Ca - Ca resorption from bones
65
What bone condition occurs due to nutritional/renal secondary hyperparathyroidism?
Fibrous osteodystrophy - Ca resorption causes bone to be replaced with fibrous tissue
66
What animals are susceptible to nutritional secondary hyperparathyroidism?
Horses fed mostly grain and bran Pig on unsupplemented rations Dogs fed only meat or offal
67
To summarise what are the causes of hyperparathyroidism?
Primary - functional tumour/nodular hyperplasia Secondary - chronic renal disease, nutritional imbalance PTHrp - neoplastic disease
68
What is cushings called in horses?
Pituitary pars intermedia dysfunction (PPID)
69
What is pituitary pars intermedia dysfunction (PPID)?
Age related degeneration of the inhibitory dopaminergic neurones that regulate pars intermedia activity between the hypothalamus and the pituitary Causing excess secretion of pars intermedia hormones and hyperplasia adenoma formation Adenoma can compress pituitary and hypothalamus
70
What are the clinical manifestations of pituitary pars intermedia dysfunction (PPID)
Sweating Fail to shed hair Muscle weakness Increased appetite PUPD Laminitis Lethargy
71
What is diabetes insipidus?
Inability of the kidneys to concentrate urine due to loss of functional effects of ADH
72
What are the two mechanisms of diabetes insipidus?
Insufficient ADH production or release from hypothalamus/pituitary (central diabetes insipidus) Renal tubules insensitive to ADH (nephrogenic diabetes insipidus)
73
What can cause central diabetes insipidus?
Injury/destruction of hypothalamus or pituitary - insufficient ADH production eg. trauma, neoplasm, inflammatory disease
74
What can cause nephrogenic diabetes insipidus?
Primary - rare congenital diseases eg. mutation of ADH receptor Secondary - diseases eg. pyometra, pyelonephritis, hyperadrenocorticism
75
What is acromegaly?
Growth hormone secretion by a functional pituitary tumour - usually adenoma
76
What species does acromegaly usually affect?
Cats
77
What are the consequences of acromegaly?
Broader face Feet enlargement Liver and kidney enlargement Growth hormone has insulin antagonistic effects - can cause symptoms of diabetes mellitus