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Endocrine > Pathophysiology of Endocrine tissues > Flashcards

Pathophysiology of Endocrine tissues Flashcards

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
Q

pars intermedia

A 
2 types of cell in dog
secrets adrenocorticotrophin (ACTH)
26
Q

what is the pituitary gland also known as

A

hypophysis

27
Q

pituitary cysts - cause

A

failure of differentiation of the oropharyngeal ectoderm into hormone secreting cells of the pars distalis
can compress pars nervosa + pituitary
dog particularly affected

28
Q

pituitary cysts - effects

A

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
Q

pituitary adenoma of the pars intermedia - dog

A

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
Q

pituitary adenoma of the pars intermedia - horse

A

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
Q

ACTH secreting adenoma – dog

A

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
Q

ACTH secreting adenoma – dog - micro

A

nests or groups of chromophobe cells
a fine connective tissue stroma
no secretory granules seen in light microscopy
stain shows ACTH in cells

33
Q

ACTH secreting adenoma - effects

A

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
Q

central diabetes insipidus (DI)

A

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
Q

adrenal gland

A

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
Q

main actions of glucocorticoids

A

Most actions of cortisol aimed at dealing with stressful events - trauma (physical or emotional), starvation or infection.

37
Q

main actions of mineralcorticoids

A

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
Q

Pathology of the Adrenal Cortex - General changes

A

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
Q

Hyperadrenocorticism - causes

A 
excessive glucocorticoids 
adrenal gland tumour. 
Increased ACTH. 
Increased CRH. 
Exogenous corticosteroid treatment
40
Q

canine cushings syndrome - clinical signs

A

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
Q

canine cushings syndrome

A

Probably the most common endocrine disorder in dogs, particularly in poodles, boxers and dachshunds
80% of cases caused by pituitary tumour.

42
Q

Adrenocortical hyperplasia - Nodular hyperplasia

A

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
Q

Adrenocortical hyperplasia - Diffuse hyperplasia

A

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
Q

Adrenocortical adenoma

A

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
Q

Primary hypoadrenocorticism

A

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
Q

Primary hypoadrenocorticism - causes

A

Destruction of adrenals
idiopathic bilateral adrenocortical atrophy (upto 1/10th normal thickness )
Autoimmune reaction or inflammatory disease.

47
Q

Primary hypoadrenocorticism - pathogenesis

A

effects due mainly to lack of mineralocorticoid

48
Q

Primary hypoadrenocorticism - effects

A

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
Q

thyroid - histological structure

A

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
Q

Control of thyroid secretions by hypothalamic-pituitary axis

A

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
Q

Actions of thyroid hormones

A

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
Q

goitre

A

a loose term denoting a non-neoplastic and non-inflammatory enlargement of the thyroid
not common now due to supplementation

53
Q

goitre - causes

A

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
Q

goitre - micro

A

diffuse hyperplasia of follicles

55
Q

hyperthyroidism - caused by

A

Overactivity of thyroid gland (thyroid gland hyperplasia and thyroid adenomas)
50% caused by autoimmune response

56
Q

hyperthyroidism - symptoms

A 
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
Q

hyperthyroidism - micro

A

hyperplastic follicles with a variable amount of colloid (often very little).
The lining of the follicles can be monolayer or stratified

58
Q

hyperthyroidism - appearance of the thyroid

A

Multifocal nodular hyperplasia – in older dogs, cats and horses
no capsule and no compression of the adjacent gland.

59
Q

Hypothyroidism - Idiopathic atrophy

A

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
Q

Hypothyroidism - Immune-mediated thyroiditis

A

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
Q

Hypothyroidism - signs

A

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
Q

tests for diagnosing thyroid disease

A 
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.

Endocrine (7 decks)

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