Endocrine Regulation Flashcards
major hormone-producing organs
hypothalamus
pituitary
thyroid
parathyroid
adrenals
pancreas
muscle
kidneys
adipose
liver
GIT
what hormone do muscles release
myokines
major functions of hormones
metabolism
blood sugar regulation
fluid balance
homeostasis
electrolyte balance
steroid hormone action vs AA hormone regulation
steroid hormones enter the cell and binds to receptor in nucleus
AA hormones cant enter cell and bind to a receptor on the cell membrane which activates proteins within the cell to carry the signal to the nucleus
central nervous system
located in brain and spinal cord to respond to sensory information
peripheral nervous system
extends from CNS and carries message from CNS throughout the body
what nervous cells make up the PNS
nerves
ganglia
enteric nervous system
nervous system withing the GIT
where is the area for appetite control located in the brain
arcuate nucleus
how do POMC and CART impact appetite
they release melanocyte stimulating hormone to decrease food intake
how do AgRP and NYP affect appetite
they increase food intake
feedback from organs that cause decrease in food intake
(name the organ and what it releases)
SI: CCK, GLP
LI: OXM, PYY
pancreas: insulin
fat: leptin
feedback from organs that cause increase in food intake
(name the organ and what it releases)
SI: motlin
stomach: ghrelin
two major hormones in the stomach
gastrin
somatostatin
actions of gastrin in the stomach
-produce G-cells in pyloric region
-released by nutrient sensing protein
-stimulate HCl secretion
action of somatostatin in the stomach
inhibit gastrin secretion
what 3 ways can HCL secretion be stimulated
-G cell–>gastrin
-ECL cell–>histamine
-histamine or gastrin acts on parietal cell
functions of insulin throughout the body
-glucose uptake and utilization
-increase lipogenesis
-decrease glucose output from liver
how does eating vs fasting affect glucagon and insulin levels
inversely
fasting: increase glucagon, decrease insulin
feeding: decrease glucagon, increase insulin
what adrenal cortex zone is responsible for glucocorticoid production
zona fascuculata
what are the catecholamines
epinephrine
norepinephrine
function of catecholamines
BG homeostasis
nutrient mobilization
function of glucocorticoids(cortisol)
catabolic hormones
stimulate substrate utilization
affect insulin levels
dexamethasone treatment possible issues
causes insulin levels to rise, can be an issue if given to horses with already high insulin
pituitary hormones
growth hormone
thyroid stimulating hormone
thyroid hormones
thyroxine(T4)
T3
function of T3
regulate all bodily cells by deciding how much energy they expend
how is T4 activated to T3
de-ionized in liver, kidneys, muscle, and fat
equine endocrine diseases
hypothyroidism
insulin dysregulation
equine metabolic syndrome
PPID
hypothyroidism definition and traits
-inability of thyroid gland to produce thyroid hormone when stimulated
-very rare in adult horses
what is the issue with diagnosing on a single “point in time” sample? what disease is most over diagnosed through it?
-other factors could cause temporary inflation and do not provide accurate information
-hypothyroidism is most over diagnosed
what is the only way hypothyroidism should be diagnosed
thyroid function test
what thyroid issue is rare unless iatrogenic
hyperthyroidism
what is a common treatment for thyroid issues? what are drawbacks of this treatment?
Thyro-l
-it can provide energy but will often decrease cardiac output
clinical signs of hyperthyroidism
weight loss
hyperexcitability
polyphagia
tachycardia
polydisia
goiter definition and main issue
enlarged thyroid gland
-swelling occludes trachea and esophagus
why does ID and EMS increase risk of laminitis
high insulin in blood binds to insulin receptors in laminae, causing them to inflame
T/F ID horses have greater seasonal insulin level fluctuation than NID horses
TRUE
when is a good time to turn out ID horses
when sugar in grass is low
(2am-7am)
what is the proposed insulin threshold for laminitis
200 ulU/mL
ways to prevent laminitis(particularly in ID horses)
-<.10 g NSC/kg BW in concentrate feeds per meal
T/F all ID horses will be fat
FALSE. they wont be fat if they dont also have EMS
what human disease is most similar to PPID
parkinsons
what age does PPID generally present
greater than 15 years old
what percent of senior horses have PPID
30%
what damages dopamine related neurons and induces PPID
pars intermedia hyperplasia
how to test for PPID
inject TRH and test ACTH response
what is often given to treat PPID
pergolide
secondary complications of PPID
loss of topline muscle
chronic laminitis
