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Endocrine > Pathophysiology of endocrine tissues > Flashcards

Pathophysiology of endocrine tissues Flashcards

1
Q

Causes - primary endocrine hypofunction

A
  • cell destruction (abscess, granuloma, I-M damage)
  • embryonic tissue fails to form secreting tissue (cysts in pituitary causing lack of stiulating hormones causing lack fo growth generally and in specific tissues)
  • defective synthesis (congenital dyshormonogenic goitre in lambs) d/t defect in mRNA processing (hence no T3/T4 synthesis)
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2
Q

Describe secondary hypofunction

A
  • abnormal/reduced production of trophic hormones –> hypofunction of target endocrine organ
  • an inactive pituitary gland –> state of hypofunction and the arenal and thyroid glands and hypoplasia/ atrophy of the gonads
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3
Q

Describe primary hyperfunction

A
  • usually associated with tumours secreting an excessive amount of hormone (e.g. hyperthyroidism in old cats)
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4
Q

Describe secondary hyperfunction

A
  • excessive secretion of trophic hormone
  • causes inappropriate stimulation of target endocrine gland
  • e.g. ACTH-secreting pituitary adenomas causing hypertrophy and hyperplasia of the adrenal cortex and cushing’s disease
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5
Q

Outline hypothalamus

A
  • basal part of diencephalon
  • below thalaus
  • controls many automatic functions (appetite, HR)
  • important neuroendocrine centre
  • secretes many hormones (GnRH, GHRH, SS, TRH, DA, CRH)
  • BV portal system links to anterior pituitary gland
  • nerve fibres from PVN and SON nuclei of the hypothalamus pass directly to the posterior pituitary where hormones (oxytocin and vasopressin) are stored prior to secretion
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6
Q

Describe the anterior pituitary

A
  • ‘master gland’
  • controls funcitos of other endocrine glands
  • in the bony cavity (sella turcica) at base of skull
  • 5 main cells (gonadotroph, somatotroph, somatotroph, corticotroph, thyrotroph)
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7
Q

Describe the pituitary gland

A
  • rich blood suplly from hypophyseal portal system via pars tuberalis
  • 3 types of cells in pars distalis:
  • ACIDOPHILS = lactotrrophs, somatotrophs
  • BASOPHILS = thryotrophs and gonadotrophs, corticotrophs
  • CHROMOPHOBES
  • somatototrophs make up 40% cells
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8
Q

List pathology of pituitary gland

A
  1. Cysts
  2. addenoma - pars intermedia (dog and horse, functioning)
  3. adneoma - pars distalis, ACTH secreting
  4. adenoma - pars distalis: non-functioning
  5. other pituitary tumours including craniopharyngioma
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9
Q

What can POMC form?

A

Depends on where processed:

  • PARS INTERMEDIA: produces mainly MSH, CLIP and beta-endorphin
  • PARS DISTALIS: produces ACTH - excess cortisol
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10
Q

Describe pituitary cysts

A
  • d/t failure of differentitatttion or oropharyngeal ectoderm into hormone secreting cells of pars distalis
  • may compress pars nervosa and stalk of hypophysis
  • dog particularly affected (GSDs, spitz and toy pinschers)
  • suggested simple autosomal inheritance in GSDs
  • effects related to reduced trophic hormones:
  • DWARFISM (notice from 2 months, retained puppy coat –> bilateral alopecia with progressive hyperpigmentation, delay of closure of epiphyseal plates in long bones, delay of permanent dentition, hypoplasia of thyroid and adrenal glands, infantile external/internal genitalia, short lifespan)
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11
Q

Describe pituitary adenoma

A
  • horses > dogs
  • older animals
  • DOGS; usually result in moderate enlargement of gland so well demarcated from nearby tisue, hormonally active or inactive, active can cause cushing’s, larger adenomas may obliterate gland and cause hypopituitarism (reported mainly as DI)
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12
Q

Describe adenoma of the pars intermedia of the horse

A
  • large size
  • not in all cases of equine cushings
  • may compress pars nervosa and overlying thalamus
  • adenomas are multinodular, yellow/brown/white and firm
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13
Q

Classification - endocrine dz

A
  • primary / secondary hypofunction
  • primary/ secondary hyperfunction
    OTHERS:
  • failure of target cell response
  • endocrine dz secondary to dz of other organs
  • failure of foetal endocrine function
  • iatrogenic syndrome of hormone excess
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14
Q

Outline ACTH-secreting adenoma in DOGS

A
  • from pars distalis or pars intermedia
  • adult/aged dogs
  • Boxers, Boston Terriers, Dachshunds
  • excess secretion of ACTH results in bilateral enlargement of adrenal cortex and Cushing’s/hyperadrenocorticism
  • adrenals: yellow or orange coloured nodules of variable size often compressing corticomedullary junction
  • similar nodules can be found in fat around gland
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15
Q

Microscopy - ACTH secreting adenoma

A
  • nests or groups of chromophobe cells
  • fine CT stroma
  • no scretory granules seen in light microscopy
  • EM demonstrates granules containing homrone
  • immunocytochemical staining will show ACTH within cells
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16
Q

Effects of excess GC on body (d/t ACTH secreting adenoma)

A
  • gluconeogenesis
  • lipolysis
  • protein catabolism
  • anti-inflammatory actions
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17
Q

CS - GC excess

A
  • gradual enlargement of abdomen
  • mm wasting (head, legs)
  • enlarged liver
  • bilateral alopecia, thin skin with mineralisation, hyperpigmentation
  • thick pads of fat around neck and shoulders
  • poor wound healing
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18
Q

What is the pars nervosa?

A

posterior pituitary

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19
Q

Function - posterior pituitary

A
  • secretes OT and AVP
  • synthesised by nerve cell bodies within hypothalamic nuclei (SON and PVN)
  • transported by axons to terminals within posterior pituitary
  • half life of 5 minutes
  • acts through GPCRs
  • circulates at v low levels
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20
Q

Name a dz of neurohypophysis

A

CDI

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21
Q

Outline CDI

A
  • inadequate production/release of ADH
  • d/t obliteration or compression of pars nervosa by expaning cyst or by pituitary tumour
  • compression of hypothalamus can also cause neuronal dysfunction and inadequate ADH production
  • PUPD and hypotonic urine
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22
Q

Dx - CDI

A
  • water deprivationt test AND assessment of response to exogenous ADH
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23
Q

What is nephrogenic DI?

A
  • unrelated to pituitary dz

- inability of epithelium in CD to utilise ADH

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24
Q

What are the 2 parts of the adrenal?

A
  • OUTER CORTEX: secretes GCs, MCs and small amount of sex steroids. 90% of gland
  • INNER MEDULLA: secretes catchecholamines (adrenaline and noradrenaline)
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25
Q

What are the parts of the cortex?

A
  • ZG: outermost, MC (aldosterone)
  • ZF: 70% gland, cortisol
  • ZR: adrenal androgens
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26
Q

Name the 2 adrenal androgens produced by ZR

A
  • dehydroepiandrosterone

- androstenedione

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27
Q

Which animal converts oestradiol to estrone?

A

ferrets

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28
Q

Actions - GCs

A
  • most actions aimed at dealing with stressful events such as trauma (physical, emotional), starvation or infection
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29
Q

Actions - MCs

A
  • essential for life
  • regulated by RAAS and plasma levels of Na and K
  • conservation of body Na by stimulating resorption of Na in kidney in exchange for K
30
Q

PAthology of adrenal cortex - general

A
  • accessory adrenocortical tissue (dogs, rodents, rabbits)
  • mineralisation (adult cats and monkeys)
  • amyloidosis (old rats, mice, monkeys)
  • adrenalitis: abscesses and other disseminated dz (e.g. toxoplasmosis and TB)
31
Q

Define adrenalitis

A

inflammation of one or both adrenal glands (causing it to be non-functional)

32
Q

Causes - cushings/ hyperadrenocorticism

A
  • adrenal gland tumour
  • increased ACTH
  • increased CRH
  • exogenous corticosteroid tx
33
Q

Outline canine Cushing’s syndrome (breeds, cause, CS)

A
  • most common endocrine disorder in dogs
  • poodles, boxers, dachshunds
  • 80% cases caused by pituitary tumour
  • pot bellied abdomen to point dog might look pregnant (d/t hepatomegaly and abdominal mm weakness)
  • PU/PD: excess urinating and drinking of water
  • mm wasting (head, shoulders, thigh, pelvis)
  • Polyphagia
34
Q

2 types of adrenocortical hyperplasia

A

nodular and diffuse

35
Q

Describe nodular adrenocortical hyperplasia

A
  • yellowish, spherical nodules (1-2cm) in cortex
  • older dogs, cats, horses (similar nodules can be found in liver, spleen, pancreas)
  • MICRO: resemble the ZG or ZF
36
Q

Describe diffuse adrenocortical hyperplasia

A
  • usually d/t ACTH secreting pituitary tumours, can be idiopathic
  • cortices uniformly enlarged
  • excess cortisol produced
  • MICRO: hypertrophy and hyperplasia of ZF and ZR, cells often vacuolated
37
Q

Ddx - nodular adrenocortical hyperplasia

A

adrenocortical (difficult, latter tend to be encapsulated, compressive and solitary)

38
Q

Appearance - adrenocortical adenoma of old dogs

A
  • single pale yellow/red nodule
  • partially/completeley encapsulated
  • adjacent parenchyma compressed
  • sometimes appears in both glands
39
Q

Microscopy - adrenocortical adenoma of old dogs

A
  • well-differentiated cells resembling ZF and ZR
  • cells vacuolated and are divided by a fibrovascular stroma
  • capsule dividing it from normal adrenocortical tissue is on left
40
Q

What is primary hypoadrenocorticism

A

= addison’s disease

  • deficiency of both GC and MC
  • relatively common but under-diagnosed
41
Q

Causes - hypoadrenocorticism

A
  • adrenal destruction
  • idiopathic bilateral adrenocortical atrophy
  • all 3 layers of cortex affected
  • young adults mainly
  • autoimmune reaction or inflammatory dz
42
Q

Pathogenesis - hypoadrenocorticism

A

effects due mainly to lack of MC (aldosterone which promotes retention of Na and Cl and secretion of K through kidney)

43
Q

Effects - hypoadrenocorticism

A
  • increased Na and Cl excretion (and water): haemoconcentration and dehydration
  • increased K in blood –> bradycardia and shutdown
  • generalised tissue underperfusion (vomiting and diarrhoea)
  • reduction of GCs (susceptible to stressful situations)
44
Q

What does thyroid secretion

A
  • thyroxine (T4)
  • tri-iodothyronine (T3)
  • calcitonin
45
Q

Histology - thyroid

A
  • 2 iodine containing hormones
  • T4 and T3 are attached to thyroglobulin and stored in colloid material
  • C cells (parafollicular cells) secrete calcitonin, which is involved in regulation of plasma Ca levels
  • nerves control BS to thyroid
46
Q

Outline control of thyroid secretions

A
  • TRH from hypothalamus stimulates anterior pituitary to release TSH which acts on thyroid to increase T4/T3.
  • T3 is most potent thyroid hormone and target tissues contain a deiodinase enzyme (DI) to convert T4 to T3
  • pituitary also expresses diodinase to convert T4 to T3 to facilitate negative feedback
47
Q

Actions - thyroid

A
  • T3 most potent –> nuclear receptors –> transcription of a wide variety of genes
  • increased heat production (calorigenesis) by increasing basal metabolic rate
  • increased CO
  • altered metabolism
48
Q

Outline thyroid hormone synthesis

A
  1. iodide trapping
  2. tyrosine iodination and coupling
  3. retrieval
49
Q

Outline broady thyroid dz

A
  • many spp
  • major effects on growth and maturation
  • required for proper development of skeleton and nervous system
50
Q

Define goitre

A

non-neoplastic and non-inflammatory enlargement of thyroid (now uncommon d/t supplementation)

51
Q

Causes - goitre

A
  • different causes ID:
  • genetic enzyme defect
  • iodine deficiency
  • iodine excess
  • goitrogenic substances
52
Q

How may a genetic enzyme defect cause goitre?

A

inability to produce T3 or T4 (congenital dyshormogenetic goitre in certain breeds of sheep - weak and rough, sparse coats, most die quickly)

53
Q

Describe I2 deficiency as cause of goitre

A
  • foals, pigs, lambs, goats
  • calves seem more resistant to effects of low I2
  • in humans, I2 deficiency is thought to be biggest preventable cause of brain damage globally
54
Q

Describe I2 excess as cause of goitre

A
  • interferes with one or more steps in thyroxine synthesis

- foals from dams fed dried seawed

55
Q

Outline goitrogenic substances as cause of goitre

A
  • interfere with T3 and T4 syntehsis

- brassica plants, certain sulphonamides

56
Q

Microscopic appearance - goitre

A
  • diffuse hyperplasia of follicles
  • when goitre can be tx (e.g. I2 deficiency) or I2 leels increase in feed, T3 and T4 can return to normal and hyperplasia ceases
  • rate of colloid excreted eventually slows down and follicular cells become flat (less active)
  • the unused colloid becomes prominent (= involuted colloid goitre)
57
Q

Causes - hyperthyroidism

A
  • OVERACTIVITY: thyroid gland hyperplasia and thyroid adenomas (commonest cause - older cats)
  • AUTOIMMUNE RESPONSE (50%, Graves’s disease)
58
Q

CS - hyperthyroidism

A
  • wt loss
  • sweating
  • tremor
    +/- goitre
  • agitated and nervous
  • fast HR and AF
  • mm weakness
  • rapid growth rate and maturation (young)
  • starting eyes
  • V/D
  • increased water consumption
59
Q

Cause - wt loss with hyperthyroidism

A

increased protein catabolism –> negative nitrogen balance

60
Q

Cause - polyphagia - hyperthyroidism

A
  • unknown

- response to increased caloric utilisation?

61
Q

Cause - umkempt coat/ hair loss in hyperthyroidism

A
  • heat intolerance?
62
Q

Cause GIT upset - hyperthyroidism

A
  • stimulation of CRTZ by thyroid hormone

- hypermobility

63
Q

Cause nervousness/ hyperactive / increased vocalisation in hyperthyroidism

A

stimulation of adrenergic activity of nervous system

64
Q

Cause - decreased appetite - hyperthyroidism

A
  • psychological depression
  • CV dz
  • thiamine deficiency
65
Q

Cause - weakness/lethargy in hyperthyroidism

A
  • catabolic state
  • hypokalaemia
  • thiamine deficiency
66
Q

Cause - dyspnoea in hyperthyroidism

A
  • respiratory mm weakness

- increased CO2 production

67
Q

Describe multifocal nodular hyperplasia - hyperthyroidism

A
  • older dogs, cats, horses
  • NO capsule
  • NO compression of adjacent gland
  • MICRO: hyperplastic follicles with variable amount of colloid (often little). The lining of follicles can be monolayer or stratified
  • In cats, these nodules can be hormonally active and cause hyperthyroidism
68
Q

Causes - hypothyroidism

A
  • IDIOPATHIC ATROPHY
  • I-M THYROIDITIS
  • Less commonly: bilateral non-functioning thyroid tumours, severe iodine deficiency and destructive lesions in the pituitary gland
69
Q

Describe idiopathic atrophy of thyroid gland –> hypothyroidism

A
  • larger breed dogs
  • severe cases show signs of hypothyroidism
  • blood assays show levels of T3 and T4
  • MICRO: atrophy of thyroid follicles (reduced #, size), prominent CT and fat cells
70
Q

Describe I-M thyroiditis –> hypothyroidism

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
71
Q

CS - hypothyroidism

A
  • almost all d/t recution in basal rate of metabolism and include:
  • wt gain
  • sluggishness
  • bradycardia
72
Q

Dx - hypothyroidism. What is recommended routinely?

A

TESTS available include (*recommended routinely)

  • TT4
  • total 3,5,3’-tri-idothyronine (TT3)
  • fT4 by dialysis
  • endogenous canine TSH (cTSH)
  • TSH response test
  • TRH response test
  • T4 and T3 autoantibodies
  • antithyroglobulin Abs
  • nuclear scintigraphy
  • thyroid gland biopsy

Endocrine (11 decks)

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