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VETM 425 Sys Path > Lecture 19: Endocrine 1 > Flashcards

Lecture 19: Endocrine 1 Flashcards

1
Q

List 7 endocrine organs of the body

A
  1. pituitary
  2. adrenal
  3. thyroid
  4. parathyroid
  5. pancreas (islets of langerhaans)
  6. aortic body (chemoreceptors)
  7. gonads
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2
Q

How does endocrine signalling work

A

Hormones are released into the bloos and act on distant cells

They cause biochemical changes that result in multisystemic effects
- abnormalities can cause lesions outside the endocrine system

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3
Q

Explain the steps of the HPA axis and how is it controlled

A
  1. release of releasing hormones from the hypothlamus
    - CRH/TRH/GnRH
  2. Anterior pituitary releases trophic hormones
    - ACTH/TSH/LH/FSH
  3. Specific target endocrine gland releases the product

The final product causes negative feedback on the hypothalamus and pituitary

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4
Q

What are 2 general categories of endocrine dysfunction

A

Hypo
- destruction or atrophy or immune mediated damage

Hyper
- proliferation either by a functional or non-functional hyperplasia, adenoma, or carcinoma

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5
Q

List the 7 mechanisms of disease/dysfunction of the endocrine system

A
  1. hypofunction (primary or secondary)
  2. hyperfunction (primary or secondary)
  3. hypersecretion of a hormone or analog
  4. dysfunction due to non response from target
  5. hyperactivity of non-endocrine organ
  6. dysfunction of hormone degradation
  7. iatrogenic
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6
Q

Compare the causes and lesion types common to primary and secondary hypofunction

A

primary hypofunction is usually due to a non-functional lesion in a gland
- reduced biochemical production
- failure to develop
- immune mediated destruction
- neoplasia

secondary is usually caused by a non-functional lesion in an organ higher up in the biochemical production cascade (ex. anterior pituitary or hypothalamus) = bilateral gland atrophy

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7
Q

Compare the causes and lesion types common to primary and secondary hyperfunction

A

primary is usually due to a functional lesion in the gland resulting in autonomous production of product
- ex. high cortisol production with low/no ACTH release

secondary is due to a lesion higher up in the biochemical production cascade
- resulting in bilaterally thickened glands (excess trophic stimulation)

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8
Q

Provide an example of endocrine dysfunction due to hypersecretion of a hormone/analog

A

hypercalcemia of malignancy

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9
Q

Provide an example of endocrine dysfunction due to non response of target

A

insulin resistance of diabetes mellitus

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10
Q

Provide an example of endocrine dysfunction due to hyperactivity of non-endocrine organs

A

renal or nutritional hyperparathyroidism

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11
Q

Provide an example of endocrine dysfunction due to iatrogenic causes

A

iatrogenic cushings

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12
Q

Where is the pituitary gland located

A

aka hypophysis

in the cranial vault of the spheniod
- sella turcica or hypophyseal fossa

dogs/cats/horses have an incomplete sella turcica

ruminants have a complete sella turcica

changes what structures are affected by a space occupying mass

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13
Q

What are the part of the pituitary gland

A

adenohypophysis
- pars distalis
-pars intermedia

neurohypophysis

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14
Q

What is the function of the pars distalis

A

Release trophic hormones under the control of the hypothalamus

acidophils - GN/PRL
basophils - TSH/FSH/LH
chromophobes - ACTH

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15
Q

What is the function of the pars intermedia

A

comprised on primarily melanotrophs that make propriomelanocrotin (POMC) that turns into MSH

dopamine will suppress

in dogs it also makes ACTH

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16
Q

What is the function of the posterior pituitary

A

makes oxytocin and ADH
the neurons extend into the hypothalamus

17
Q

What are 3 causes of hypopituitarism

A

aplasia and prolonged gestation

pituitary cysts

nonfunctional tumours

18
Q

In what animals is hypopituitarism in response to aplasia and prolonged gestation common in?

A

ruminants

19
Q

Why does hypopituitarism in response to aplasia and prolonged gestation occur? What are the clinical signs?

A

the fetus stimulates birth through the HPA axis and if the pituitary is small = won’t stimulate

may be caused by veratrum californicum (skunk cabbage) ingestion when the animal is less than 14d gestation

It causes
- neural tube defects
- craniofacial defects (cyclopia - one eye and one orbit)
- aplasia and malformed adenohypophysis

20
Q

What are pituitary cysts and what common disease are they related to?

A

they are formed by the failure of the oropharyngeal ectoderm of rathke’s pouch to develop

causes juvenile panhypopituitarism

21
Q

What animal is juvenile panhypopituitarism common in? What are the main clinical signs?

A

autosomal recessive conditon in GSD

reduced growth/retained puppy coat due to low GH

hypoadrenocorticism bc low ACTH

hypothyroidism due to low TSH

sterility/infertile because low FSH/LH

22
Q

What is the mechanism of disease of pituitary cysts?

A

secondary hypofunction

23
Q

What are the common characteristics of nonfunctional tumors causing hypopituitarism?

A

this is the most common cause of hypopituitarism
- secondary hypofunction

can be large because they are nonfunction - clinical signs not noticed until later

adenoma > carcinoma

affect older cats and dogs

24
Q

What are the clinical signs of hypopituitarism due to a nonfunctional tumor?

A

hypothyroidism
hypoadrenocorticism
gonadal atrophy
CNS compression leading to
- ataxia
- paresis
- blindness
- diabetes insipidus (no ADH)

25
Q

List 3 types of functional tumors causing hyperpituitarism

A

corticotroph adenoma

pituitary pars intermedia dysfunction

somatotroph adenoma

26
Q

What are the consequences of corticotroph adenomas? What species are they most common in?

A

They secrete ACTH and thus cause cushings

occur mainly in dogs but also in cats
- dogs can have this occur in the pars distalis or intermedia

27
Q

What do the adrenal glands look like when a corticotroph adenoma is present? What mechanism is used?

A

bilaterally diffuse adrenocortical hyperplasia

secondary hyperfunction

28
Q

What is the typical signalment of an animal with pituitary pars intermedia dysfunction?

A

> 15yo horse

(most common equine endocrine disorder)

29
Q

What is the pathogenesis of pituitary pars intermedia dysfunction?

A

It is an age related change

reduced number of dopamine neurons
- causes melanotroph hyperplasia

excessive POMC production and ACTH

30
Q

What are the clinical signs of pituitary pars intermedia dysfunction?

A

hypertrichosis
- pathogneumonic
- due to hypothalamus dysfunction

recurrent infection

PU/PD (no ADH)

weight loss

increased sweating
- hypothalamus/temp regulation dysfunction

laminitis
- not directly due to PPID

CNS signs

use the clinical signs to make a diagnosis
- can use ACTH levels but not always accurate because there is seasonal variation (higher levels in fall than spring)

31
Q

What is the common signalment of an animal affected by somatotroph adenomas

A

cats with diabetes mellitus

32
Q

What is the pathogenesis of somatotroph adenomas?

A

cause excess GH release

cause increase in insulin like growth factor 1 in liver

results in
- excess deposition of soft tissue and bone (acromegaly)
- insulin resistant diabetes mellitus

33
Q

What are the clinical signs of somatotroph adenomas

A

acromegaly
- broad face
- club shaped paws
- plantigrade stance

34
Q

What is the mechanism of dysfunction of somatotroph adenomas

A

failure of target cells to respond

35
Q

What is the primary disorder affecting the posterior pituitary

A

diabetes insipidus

36
Q

What are the 2 types of diabetes insipidus and how do you differentiate them?

A

hypophyseal/central: caused by a primary hypofunction (space occupying mass) resulting in low ADH

nephrogenic: caused by a decreased response of target cells. Kidney cells are non-responsive to ADH

Both result in an inability to make/concentrate urine

can differentiate via
- water deprivation test: if still dilute = you know it is DI

  • exogenous ADH - if no response = nephrogenic

VETM 425 Sys Path (21 decks)

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