Lecture 19: Endocrine 1 Flashcards
List 7 endocrine organs of the body
- pituitary
- adrenal
- thyroid
- parathyroid
- pancreas (islets of langerhaans)
- aortic body (chemoreceptors)
- gonads
How does endocrine signalling work
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
Explain the steps of the HPA axis and how is it controlled
- release of releasing hormones from the hypothlamus
- CRH/TRH/GnRH - Anterior pituitary releases trophic hormones
- ACTH/TSH/LH/FSH - Specific target endocrine gland releases the product
The final product causes negative feedback on the hypothalamus and pituitary
What are 2 general categories of endocrine dysfunction
Hypo
- destruction or atrophy or immune mediated damage
Hyper
- proliferation either by a functional or non-functional hyperplasia, adenoma, or carcinoma
List the 7 mechanisms of disease/dysfunction of the endocrine system
- hypofunction (primary or secondary)
- hyperfunction (primary or secondary)
- hypersecretion of a hormone or analog
- dysfunction due to non response from target
- hyperactivity of non-endocrine organ
- dysfunction of hormone degradation
- iatrogenic
Compare the causes and lesion types common to primary and secondary hypofunction
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
Compare the causes and lesion types common to primary and secondary hyperfunction
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)
Provide an example of endocrine dysfunction due to hypersecretion of a hormone/analog
hypercalcemia of malignancy
Provide an example of endocrine dysfunction due to non response of target
insulin resistance of diabetes mellitus
Provide an example of endocrine dysfunction due to hyperactivity of non-endocrine organs
renal or nutritional hyperparathyroidism
Provide an example of endocrine dysfunction due to iatrogenic causes
iatrogenic cushings
Where is the pituitary gland located? What are anatomical species differences?
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
What are the part of the pituitary gland
adenohypophysis
- pars distalis
-pars intermedia
neurohypophysis
What is the function of the pars distalis
Release trophic hormones under the control of the hypothalamus
acidophils - GN/PRL
basophils - TSH/FSH/LH
chromophobes - ACTH
What is the function of the pars intermedia
comprised on primarily melanotrophs that make propriomelanocrotin (POMC) that turns into MSH
dopamine will suppress
in dogs it also makes ACTH
What is the function of the posterior pituitary
makes oxytocin and ADH
the neurons extend into the hypothalamus
What are 3 causes of hypopituitarism
aplasia and prolonged gestation
pituitary cysts
nonfunctional tumours
In what animals is hypopituitarism in response to aplasia and prolonged gestation common in?
ruminants
Why does aplasia and prolonged gestation occur in response to hypopituitarism? What are the clinical signs?
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
What are pituitary cysts and what common disease are they related to?
they are formed by the failure of the oropharyngeal ectoderm of rathke’s pouch to develop
causes juvenile panhypopituitarism
What animal is juvenile panhypopituitarism common in? What are the main clinical signs?
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
What is the mechanism of disease of pituitary cysts?
secondary hypofunction
What are the common characteristics of nonfunctional tumors causing hypopituitarism?
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
What are the clinical signs of hypopituitarism due to a nonfunctional tumor?
hypothyroidism
hypoadrenocorticism
gonadal atrophy
CNS compression leading to
- ataxia
- paresis
- blindness
- diabetes insipidus (no ADH)
List 3 types of functional tumors causing hyperpituitarism
corticotroph adenoma
pituitary pars intermedia dysfunction
somatotroph adenoma
What are the consequences of corticotroph adenomas? What species are they most common in?
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
What do the adrenal glands look like when a corticotroph adenoma is present? What mechanism is used?
bilaterally diffuse adrenocortical hyperplasia
secondary hyperfunction
What is the typical signalment of an animal with pituitary pars intermedia dysfunction?
> 15yo horse
(most common equine endocrine disorder)
What is the pathogenesis of pituitary pars intermedia dysfunction?
It is an age related change
reduced number of dopamine neurons
- causes melanotroph hyperplasia
excessive POMC production and ACTH
What are the clinical signs of pituitary pars intermedia dysfunction?
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)
What is the common signalment of an animal affected by somatotroph adenomas
cats with diabetes mellitus
What is the pathogenesis of somatotroph adenomas?
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
What are the clinical signs of somatotroph adenomas
acromegaly
- broad face
- club shaped paws
- plantigrade stance
What is the mechanism of dysfunction of somatotroph adenomas
failure of target cells to respond
What is the primary disorder affecting the posterior pituitary
diabetes insipidus
What are the 2 types of diabetes insipidus and how do you differentiate them?
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
