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Endocrine > Endocrine Path > Flashcards

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

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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)
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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
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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
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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)
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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)
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7
Q

Where is the Hypothalamus ? Function?

A
  • basal diecephalon below the thalamus
  • autonomic function (apetite, heart rate)
  • important neuroendocrine also (secretes hormones)
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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

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9
Q

Functions of the anterior pituitary?

A
  • Master gland

- controls other endocrine organs (gonads, thyroid, adrenal cortex etc.)

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10
Q

Where is the anterior pituitary situated?

A
  • sella turcica base of skull
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11
Q
  • 5 cell types of the anterior pituitary
A
  • gonadotroph
  • lactotroph
  • somatotroph
  • corticotroph
  • thyrotroph
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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
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13
Q

Which hormones are secreted from the anterior and posterior pituitary

A

> ## anteriorposterior

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14
Q

5 main pathologies of the pituitary gland

A
  1. Cysts
    - esp dogs
  2. Adenoma
    - pars intermedia, functioning
    - dog and horse
  3. Adenoma
    - pars distalis
    - ACTH secreting
  4. Adenoma
    - pars distalis non functioning
  5. Other pituitary tumours
    - including craniopharyngioma
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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
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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
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17
Q

Which animals are affected by pituitary adenoma of the pars intermedia

A
  • horses mainly (less common dogs)

- older animals

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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
Q

What is the pars nervosa and what does it produce? How do these act?

A
  • 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
Q

Outline pathology of central diabetes insipidus

A
  • 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
Q

What is the adrenal gland comprised of? Which sections secrete what?

A

> medulla
- catecholamines (adrenaline, noradrenaline)
cortex
- steroids
( zona glomerulosa outside: MC aldosterone)
( zona fasiculata middle: GCs cortisol)
(zona reticularis inner: adrenal androgens small amount)

28
Q

What is the cortex divided into

A
  • See previous
29
Q

Which species produces oestrogen in the adrenal?

A

Ferrets only species

30
Q

Main actions of GCs

A
  • eg. cortisol

- dealing with stress (physical or emotional), starvation or infection

31
Q

Main actions of MCs?

A
  • 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
Q

General pathological changes of the adrenal gland

A
  • 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
Q

Causes of hyperadrenocorticism (Cushings)

A

> excess GCs (dogs and horses)

  • adrenal gland tumour
  • ^ ACTH
  • ^ CRH
  • exogenous corticosteroid tx
34
Q

Most common endocrine disorder of dogs is? Clinical signs? Breed pdf?

A

> 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
Q

comonest cause of Canine Cushings

A
  • pituitary tumour
36
Q

How do GCs affect kidney function?

A
  • antagonise ADH-R -> nephrogenic DI
37
Q

Adrenocorical hyperplasia types

A

> 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
Q

Path and histo of adrenocorticol adenoma. Ddx?

A

> 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
Q

Hypoadrenocorticism common?

A

> deficiency of GC and MC

- relatively common and under diagnosed

40
Q

Causes of Addisons - pathophysiology?

A
  • 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
Q

Effects of Addisons

A
  • ^ 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
Q

Histo changes with Hypoadrenocorticism

A
  • medulla increases in size , cortex decreases in size
43
Q

How does cushings differ in horses and dogs?

A

Dogs hair loss, horses curly coat

44
Q

Other slides on thyroid look

A

Endocrine (16 decks)

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