Pathophysiology of Endocrine tissues Flashcards

(62 cards)

1
Q

hypothalamus - releasing hormones

A

GHRH, CRH, TRH, GnRH, vasopressin

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2
Q

hypothalamus - inhibiting hormones

A

somatostatin, dopamine

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3
Q

pituitary gland - secretions

A

growth hormone, prolactin, oxytocin, vassopressin, ACTH, TSH, MSH (melanocyte), FSH, LH

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4
Q

thyroid gland - secretions

A

thyroid hormones

calcitonin

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5
Q

parathyroid gland - secretions

A

parathyroid hormone

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6
Q

adrenal gland - secretions

A

cortisol, aldosterone, adrenal androgens, epinephrine, norepinephrine

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7
Q

pancreas - secretions

A

insulin

glucagon

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8
Q

testes - secretions

A

testosterone

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9
Q

ovaries - secretions

A

estrogen

progesterone

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10
Q

4 groups of hormones

A

Protein and peptide hormones
steroid hormones
hormones derived from tyrosine or tryptophan
eicosanoids

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11
Q

do steroid hormones show species differences?

A

no

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12
Q

which are lipid soluble

A

steroids, catecholamines, thyroid hormones

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13
Q

classification of endocrine disease

A

Primary hypofunction
Secondary hypofunction
Primary hyperfunction
Secondary hyperfunction

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14
Q

other types of endocrine disease

A

Failure of target cell response
Endocrine disease secondary to diseases of other organs
Failure of foetal endocrine function
Iatrogenic syndrome of hormone excess

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15
Q

primary hypofunction - causes

A

destruction of the cells - abscess, granuloma, immune mediated damage
embryonic tissue fails to form secreting tissue e.g. cysts
in pituitary – lack of stimulating hormones
defective synthesis

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16
Q

secondary hypofunction

A

abnormal (or lack of) production of trophic hormones

hypofunction of a target endocrine organ

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17
Q

primary hyperfunction

A

is usually associated with tumours secreting an excessive amount of the hormone

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18
Q

Secondary hyperfunction

A

excessive secretion of a trophic hormone

results inappropriate stimulation of the target endocrine gland

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19
Q

hypothalamus

A

basal part of the diencephelon lying below the thalamus
controls many automatic functions e.g. appetite, heart rate, etc.
important neuorendocrine centre which secretes many hormones

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20
Q

anterior pituitary - 5 cell types

A
gonadotroph 
lactotroph 
somatotroph 
corticotroph 
thyrotroph
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21
Q

posterior pituitary

A

only stores hormones - doesn’t secrete any
oxytocin
vassopressin

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22
Q

Pathology of the Pituitary Gland

A

Cysts
Adenoma – pars intermedia: dog and horse (functioning)
Adenoma – pars distalis: ACTH secreting
Adenoma – pars distalis: non-functioning
Other Pituitary Tumours including craniopharyngioma

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23
Q

4 parts of the pituitary gland

A

pars tuberalis
pars distalis
pars intermedia
pars nervosa

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24
Q

pars distalis - 3 cell types

A

acidophils (lactotrophs, somatotrophs)
basophils (corticotrophs, thyrotrophs and gonadotrophs)
chromophobes

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25
pars intermedia
``` 2 types of cell in dog secrets adrenocorticotrophin (ACTH) ```
26
what is the pituitary gland also known as
hypophysis
27
pituitary cysts - cause
failure of differentiation of the oropharyngeal ectoderm into hormone secreting cells of the pars distalis can compress pars nervosa + pituitary dog particularly affected
28
pituitary cysts - effects
dwarfism retention of puppy coat - bilateral alopecia with progressive hyperpigmentation delay of closure of epiphyseal plates in long bones delay of permanent dentition hypoplasia of the thyroid and adrenal glands infantile external/internal genitalia life span short for the most severely affected
29
pituitary adenoma of the pars intermedia - dog
usually moderate enlargement of the gland - well demarcated from nearby tissue can be hormonally inactive or active active adenomas produce ACTH - Cushing’s disease (hyperadrenocorticism) larger adenomas may obliterate the gland and cause hypopituitarism, reported mainly as Diabetes insipidus
30
pituitary adenoma of the pars intermedia - horse
tends to attain large size but not in all cases of Cushing’s disease in horses may compress the pars nervosa + overlying thalamus multinodular, yellow/brown/white and firm Plasma cortisol levels are normal or slightly raised due to different metabolism of precursor in pars intermedia (produces mainly MSH, CLIP, and β-endorphin) in pars distalis (produces ACTH – excess cortisol)
31
ACTH secreting adenoma – dog
from pars distalis excess secretion of ACTH bilateral enlargement of the adrenal cortex and in Cushing’s disease (hyperadrenocorticism) adrenals show yellowish/orange nodules of variable size often compressing the corticomedullary junction similar nodules can be found in the fat around the gland
32
ACTH secreting adenoma – dog - micro
nests or groups of chromophobe cells a fine connective tissue stroma no secretory granules seen in light microscopy stain shows ACTH in cells
33
ACTH secreting adenoma - effects
effects related to excess glucocorticoids released from the hyperplastic adrenal cortices gluconeogenesis, lipolysis, protein catabolism, anti-infl actions gradual enlargement of abdomen muscle wasting (head and legs) and enlarged liver bilateral alopecia, thin skin with mineralisation, hyperpigmentation thick pads of fat around neck and shoulders poor wound healing
34
central diabetes insipidus (DI)
result of inadequate production or release of antidiuretic hormone (ADH) caused by obliteration/compression of pars nervosa by an expanding cyst/pituitary tumour compression of the hypothalamus can cause neuronal dysfunction and inadequate production of ADH characterized by marked polydipsia and polyuria, and hypotonic urine diagnosis requires water deprivation test and assessment of response to exogenous ADH
35
adrenal gland
structurally and functionally two endocrine glands in one. outer cortex secretes glucocorticoids, mineralocorticoids and a small amount of sex steroids. inner medulla secretes the catecholamines adrenaline and noradrenaline
36
main actions of glucocorticoids
Most actions of cortisol aimed at dealing with stressful events - trauma (physical or emotional), starvation or infection.
37
main actions of mineralcorticoids
e.g. aldosterone Regulated by renin-angiotensin system and by plasma levels of sodium and potassium. Conservation of body sodium by stimulating resorption of sodium in the kidney in exchange for potassium
38
Pathology of the Adrenal Cortex - General changes
Accessory adrenocortical tissue seen in dogs, rodents and rabbits Mineralization: calcification of the adrenals in adult cats + monkeys Amyloidosis – old rats, mice and monkeys Adrenalitis – abscesses and other disseminated disease e.g. Toxoplasmosis and tuberculosis
39
Hyperadrenocorticism - causes
``` excessive glucocorticoids adrenal gland tumour. Increased ACTH. Increased CRH. Exogenous corticosteroid treatment ```
40
canine cushings syndrome - clinical signs
Pot bellied abdomen due to hepatomegaly and abdominal muscle weakness. Polyuria/polydipsia - excess urinating and drinking of water. Muscle wasting over the head, shoulders, thighs and pelvis. Polyphagia - excess appetite
41
canine cushings syndrome
Probably the most common endocrine disorder in dogs, particularly in poodles, boxers and dachshunds 80% of cases caused by pituitary tumour.
42
Adrenocortical hyperplasia - Nodular hyperplasia
yellowish, spherical nodules (1-2cm) in the cortex older dogs, cats and horses (similar nodules can be found in the spleen, liver and pancreas). Micro - resemble the zonae glomerulosa or fasciculata
43
Adrenocortical hyperplasia - Diffuse hyperplasia
usually caused by ACTH secreting pituitary tumours, but can be idiopathic cortices are uniformly enlarged excess cortisol produced – Cushing’s disease Micro - hypertrophy and hyperplasia of the zonae fasciculata and reticularis, cells are often vacuolated (rich in lipids)
44
Adrenocortical adenoma
old dogs occasionally appears as a single pale yellow/red nodule partially or completely encapsulated adjacent parenchyma is compressed sometimes appears in both glands may be differentiated from nodular hyperplasia because they tend to be encapsulated, compressive and solitary
45
Primary hypoadrenocorticism
Addison's disease results in deficiency of both glucocorticoids and mineralocorticoids, relatively common and under diagnosed – disease young adults mainly affected all three layers of cortex affected
46
Primary hypoadrenocorticism - causes
Destruction of adrenals idiopathic bilateral adrenocortical atrophy (upto 1/10th normal thickness ) Autoimmune reaction or inflammatory disease.
47
Primary hypoadrenocorticism - pathogenesis
effects due mainly to lack of mineralocorticoid
48
Primary hypoadrenocorticism - effects
Increased excretion of Na+ and Cl- (and water) haemoconcentration & dehydration Increased K+ in the blood – slows the heart (bradycardia) and shutdown Generalised tissue underperfusion – vomiting and diarrhoea Reduction of glucocorticoids – susceptible to stressful situations
49
thyroid - histological structure
The two iodine-containing hormones attached to thyroglobulin and stored in the colloid material. The C cells (parafollicular cells) secrete calcitonin, which is involved in regulation of plasma Ca2+ levels. The nerves control the blood supply to the thyroid.
50
Control of thyroid secretions by hypothalamic-pituitary axis
TRH from hypothalamus - TSH from anterior pituitary which acts upon the thyroid to increase T4/T3secretion. T3 is the most potent thyroid hormone - target tissues that contain a deiodinase enzyme (DI) to convert T4 to T3. The pituitary also expresses deiodinase to convert T4 to T3 to facilitate -ve feedback.
51
Actions of thyroid hormones
Increased heat production(calorigenesis) by increasing the basal metabolic rate. Increased cardiac output. Alterations in metabolism. effects on growth and maturation. Required for proper development of skeleton and nervous system lack early in development can cause mental retardation
52
goitre
a loose term denoting a non-neoplastic and non-inflammatory enlargement of the thyroid not common now due to supplementation
53
goitre - causes
genetic enzymatic defect leading to an inability to produce T3 orT4 iodine deficiency – foals, pigs, lambs and goats: calves seem more resistant to the effects of low iodine iodine excess – interferes with one or more steps in thyroxine synthesis goitrogenic substances - interfere with the synthesis of T3 , T4 , - Brassica plants and certain sulphonamides
54
goitre - micro
diffuse hyperplasia of follicles
55
hyperthyroidism - caused by
Overactivity of thyroid gland (thyroid gland hyperplasia and thyroid adenomas) 50% caused by autoimmune response
56
hyperthyroidism - symptoms
``` Weight loss Sweating PU/PD (incr glomerular filtration rate) Tremor Possibly a goitre Agitated and nervous Fast heart rate and atrial fibrillation. Muscle weakness Rapid growth rate and bone maturation in children Staring eyes. Infertility and lack of cyclicity ```
57
hyperthyroidism - micro
hyperplastic follicles with a variable amount of colloid (often very little). The lining of the follicles can be monolayer or stratified
58
hyperthyroidism - appearance of the thyroid
Multifocal nodular hyperplasia – in older dogs, cats and horses no capsule and no compression of the adjacent gland.
59
Hypothyroidism - Idiopathic atrophy
mainly larger breeds of dogs severe cases show signs of hypothyroidism blood assays show low levels of T3 and T4 Micro – atrophy of thyroid follicles (reduced in number and size), prominent connective tissue and fat cells
60
Hypothyroidism - Immune-mediated thyroiditis
caused by binding of autoantibodies to thyroglobulin can lead to hypothyroidism some may be inherited Micro – infiltration of lymphocytes, plasma cells and macrophages, degeneration of follicular cells
61
Hypothyroidism - signs
almost all due to a reduction in basal rate of metabolism weight gain and sluggishness scaly skin (hyperkeratosis), seborrhoea,hyperpigmentation and alopecia infertility incr cholesterol in the blood – can cause atherosclerosis of vessels lipid accumulation in liver, renal glomeruli (renal disease) and eye (cornea) bradycardia
62
tests for diagnosing thyroid disease
``` total thyroxine (TT4), free T4 (fT4), endogenous canine thyroid stimulating hormone (cTSH), also - total 3,5,3’-tri-idothyronine (TT3), TSH response test, TRH response test, T4 and T3 autoantibodies, antithyroglobulin antibodies, nuclear scintigraphy, and thyroid gland biopsy. ```