Endocrine Path Flashcards
1
Q
How do thyroid and steroid hormones differ from other endocrine?
A
Lipid soluble so act on intracellular receptor cf. PGs, catecholamines etc. Which act on membrane receptors and exert actions quickly
2
Q
How may endocrine diseases be classified?
A
> 1* hypo function > 2* hypo function - lack of stimulation > 1* hyper function > 2* hyper function - excessive stimulation > other dz - failure target cell response - endocrine dz 2* to other organ dz - failure foetal endocrine function - iatrogenic syndrome of hormone excess (external administration)
3
Q
Causes of 1* hypo function and eg. Of effects?
A
- destruction of cells (abscess, granulomatous, immune mediated)
- embreyonic tissue fails to form secreting tissue (cysts in the pituitary -> lack of stimulating hormones)
- can cause lack of general growth and of specific tissue eg. gonads (2* hypofunction)
- defective synthesis eg. some lambs cannot make thyroglobulin -> congenital dyshormonogenic goitre d/t defect in mRNA processing
4
Q
Causes of 2* hypo function
A
- abnormal (or lack of) production of tropic hormones
- hypofunction of target endocrine organ
- eg. Inactive pituitary –> hypo function adrenal and thyroids, hypoplasia/atrophy of the gonads
5
Q
Causes of 1* hyper function. Eg?
A
- commonly tumour secreting excessive hormones
- hyperthyroid cats (pathogenesis differs to human Graves, hypofunction of thyroid -> ^TSH -> ^ gland size -> autonomous activity cf. Graves autoAb against TSH-R)
6
Q
Causes of 2* hyper function
A
- excessive secretion of a trophic hormone -> inappropriate stimulation of target endocrine organ
- eg. ACTH secreting pituitary adenomas -> hyper trophy and hyperplasia of adrenal cortex (Cushings, ^ cortisol; aldosterone less of a problem as controlled by RAAS)
7
Q
Where is the Hypothalamus ? Function?
A
- basal diecephalon below the thalamus
- autonomic function (apetite, heart rate)
- important neuroendocrine also (secretes hormones)
8
Q
How are the hypothalamus and pituitary linked?
A
> anterior
- vascular portal system via pars tuberalis
- no direct neuronal connection to hypothalamus
posterior
- neuronal fibres from paraventricular (PVN) and supraoptic (SON) nuclei of hypothalamus pass directly to posterior pituitary
- OT and ADH stored here prior to secretion
9
Q
Functions of the anterior pituitary?
A
- Master gland
- controls other endocrine organs (gonads, thyroid, adrenal cortex etc.)
10
Q
Where is the anterior pituitary situated?
A
- sella turcica base of skull
11
Q
- 5 cell types of the anterior pituitary
A
- gonadotroph
- lactotroph
- somatotroph
- corticotroph
- thyrotroph
12
Q
anterior pituitary : Three Types of cells in the pars distlais and how they can be identified histologically. How many types of cells in pars intermedia?
A
~ pars distlais ~ > acidophils - lactotrophs - somatotrophs > basophils - thyrotrophs - gonadotrophs > chromophobes - corticotrophs (or baso) ~ pars intermedialis ~ - 2 types in dog - 1 makes ACTH
13
Q
Which hormones are secreted from the anterior and posterior pituitary
A
> ## anteriorposterior
14
Q
5 main pathologies of the pituitary gland
A
- Cysts
- esp dogs - Adenoma
- pars intermedia, functioning
- dog and horse - Adenoma
- pars distalis
- ACTH secreting - Adenoma
- pars distalis non functioning - Other pituitary tumours
- including craniopharyngioma
15
Q
Pathology of pituitary cysts
A
- d/t failure of differentiation of oropharyngeal ectoderm into hormone secreting cells of pars distalis
- may compress pars nervosa and stalk of hypophysis -> especially affects the dog
- esp GSDs, Spitz, Toy Pinschers
- inherited in GSDs
16
Q
Effects of pituitary cysts
A
- d/t v trophic hormones > dwarfism - noticable @ 2mo - v growth, retention of puppy coat -> bilateral alopecia and progressive hyperpigmentation - delayed closure of epiphyseal plates in long bones - delayed permenant dentiition - hypoplasia thyroid and adrenals - infantile gneitalia - life span short if severely affected
17
Q
Which animals are affected by pituitary adenoma of the pars intermedia
A
- horses mainly (less common dogs)
- older animals
18
Q
Pituitary adenoma dogs
A
- usually -> mod enlargemetn of gland, well demarcated from surrounding tissue
- may be hormonally active/inactive (if active -> ACTH production and Cushings
- larger tumours may obliterate gland causing hypopituitarism: seen mainly as diabetes insipidus
19
Q
Details of pars intermedia pituitary adenoma in the horse
A
- tumour often large size but not always in Cushings
- may compress pars nervosa and overlying thalamus
- adenomas are multinodular, yellow/brown/white and firm
- plasma cortisol levels normal/slightly raised d/t diffferent metablism of precursor (Pro-OMC)
> in pars intermedia (produces mainly MSH, CLIP, B-endorphin)
> in pars distalis (produces ACTH - excess cortisol)
20
Q
Why is size of pituitary adenoma of pars intermedia not necessary related to ACTH levels?
A
- depends which molecules are produced - not necessarily lots of ACTH produced
- cf. pars distalis where lots of ACTH -> lots of cortisol produced
21
Q
Where do ACTH secreting adenomas in the dog arise from? Common? Breed pdf?
A
- arises from pars distalis or pars intermedia
- more commonly causes Cushings in the dog (cf. horse where may not necessarily become cushingoid)
- not uncommon in older dogs
- Boxer, boston terrier, daschaund over-represented
22
Q
What is seen pathologically with pituitary adenoma in the dog?
A
- excess secretion ACTH -> bilateral enlargement adrenal cortex and Cushings
- adrenals yellowish/orange colored nodules, variable size, compress corticomedullary junction
- similar nodules in fat surrounding gland
- micro: nests/groups chromatophobe cells
- fine connective tissue stroma
- no secretory granules in light microscopy
> IHC ACTH staining in cells
> electron microscopy shows granules containing hormone
23
Q
What causes the effects on the animals of Pituitary adenoma ?
A
- excess GCs from hyperplastic adrenal cortices
- gluconeogenesis, lipolysis, protein catabolism, anti-inflam options
24
Q
Effects on the animal of pituitary adenoma
A
- gradual enlargement abdo
- muscle wasting (head and legs)
- enlarged liver
- bilateral alopecia , thin skin with mineralisation, hyperpigmentation
- fat pads neck and shoulders
- poor wound healing
25
What is the pars nervosa and what does it produce? How do these act?
- posterior pituitary
- OT and ADH (not produced here, produced in nerve cell bodies within hypothalamic nuclei, just secreted post pit)
- circulate at very low levels
- half life ~5mins
- acts though G-protein linked plasma membrane receptors
26
Outline pathology of central diabetes insipidus
- inadequate prouction/release of ADH
- d/t obliteration/compression pars nervosa by cyst or tumour
- compression of hypothalamus can also cause neuronal dysfunction and inadequate production ADH
- PUPD, hypotonic urine
- dx by water deprivation test and respnse to exogenous ADH
27
What is the adrenal gland comprised of? Which sections secrete what?
> medulla
- catecholamines (adrenaline, noradrenaline)
> cortex
- steroids
( zona glomerulosa outside: MC aldosterone)
( zona fasiculata middle: GCs cortisol)
(zona reticularis inner: adrenal androgens small amount)
28
What is the cortex divided into
- See previous
29
Which species produces oestrogen in the adrenal?
Ferrets only species
30
Main actions of GCs
- eg. cortisol
| - dealing with stress (physical or emotional), starvation or infection
31
Main actions of MCs?
- eg. adosterone
- essential for life
- regulated by RAAS and plasma levels of sodium/potassium
- conservation body sodium by stim resorption sodium in kidney in exchange for potassium
32
General pathological changes of the adrenal gland
- accessory adrenocortical tissue seen in dogs, rodents, rabbits
- mineralisation: calcification of adrenals in adult cats and monkeys
- amyloidosis old rats, mice and monkeys
- adrenalitis (abscesses and other disseminated dz eg. toxoplasmosis and TB)
33
Causes of hyperadrenocorticism (Cushings)
> excess GCs (dogs and horses)
- adrenal gland tumour
- ^ ACTH
- ^ CRH
- exogenous corticosteroid tx
34
Most common endocrine disorder of dogs is? Clinical signs? Breed pdf?
> Canine Cushings Syndrome
- esp poodles, boxers and dachshunds
- 80% cases caused by pituitary tumour
- pot bellied abdomen may look preg d/t hepatomegaly and abdo muscle weakness
- PUPD (excess GC antagonises ADH-R -> nephrogenic DI)
- muscle wastage over head, shoulders, thighs and pelvis
- polyphagia
35
comonest cause of Canine Cushings
- pituitary tumour
36
How do GCs affect kidney function?
- antagonise ADH-R -> nephrogenic DI
37
Adrenocorical hyperplasia types
> nodular hyperplasia
- yellowish spherical nodules (1-2cm) in cortex
- older dogs, cats and horses (similar found in spleen, liver and pancreas)
- micro: resemble zona glomerulosa
> diffuse hyperplasia
- usually casued by ACTH secreting pit tumours, can be idiopathic
- cortices uniformly enlarged
- excess cortisol produced -> Cushings
- micro: hypertrophy and hyperplasia of zona fasciculaa and reticularis
- cells vacuolated (rich in lipids)
38
Path and histo of adrenocorticol adenoma. Ddx?
> seen old dogs occasionally
- appears as single pale yellow/red nodule
- partially/completely encapsulated
- adjacent parenchyma compressed
- sometimes bilateral
> micro:
- well diff cells resembling zona fasiculata/reticularis
- vacuolated and divided by fibrovascular stroma
- capsule divides from normal adrenocortical tissue
> ddx nodular hyperplasia: difficult, but adenoma more encapsulated, compressive and solitary
39
Hypoadrenocorticism common?
> deficiency of GC and MC
| - relatively common and under diagnosed
40
Causes of Addisons - pathophysiology?
- destruction of adrenals
- idiopathic bilateral adrenocortical atrophy (1/10 normal thicknesss)
- all 3 layers of cortex affected
- young adults mainly affected
- autoimmune or inflam disease
> effects mainly d/t lack of MC (aldosterone) -> PUPD
41
Effects of Addisons
- ^ excretion Na Cl and Water -> Haemoconcentration and dehydration
- ^ blood K+ -> bradycardia and cardiac arrest
- generalised tissue underperfusion -> VD+
- v GC increases suscpetibility to stressful situations
42
Histo changes with Hypoadrenocorticism
- medulla increases in size , cortex decreases in size
43
How does cushings differ in horses and dogs?
Dogs hair loss, horses curly coat
44
Other slides on thyroid look
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