big boned
what controls and promotes GIT absorption of calcium?
What does FSH do to sertoli cells? (what are some things that get upregulated or produced?)
what is upregulation of aromatase, growth factors, and androgen binding proteins
how much blood can you pull from a bird?
what is 1% of BW in grams (ex: 400 g bird -> can draw 4 mL)
what does iodine get conjugated with in the thyroid
what is thyroglobulin (has tyrosines on it)
what is zona fasciculata
what is hypocalcemia and activates vitamin D in kidney, promote bone resorption, and promote calcium reabsorption in kidney (to increase Ca2+)
which species are long day breeders vs. short day? What hormone controls the estrus cycle?
long day - horse and cats (increased melatonin -> stimulates estrus)
short day - sheep and goats (decreased melatonin -> stimulates estrus)
what are the fused thoracic vertebrae and fused lumbar vertebrae called in birds?
what is notarium and synsacrum
what are T3 and T4 bound to when circulating
what is TBG (thyroid binding globulin) and albumin
when doing an ACTH stim test, you see increased cortisol. where is the lesion
what is pituitary gland tumor
because giving synthetic ACTH should stimulate the adrenal gland to produce more cortisol if functioning. If pituitary lesion, then should see more cortisol. If adrenal gland lesion, then should see no change in cortisol level.
what hormone responds to hypercalcemia? what type of hormone and where does it come from?
estrus cycle and which hormone is dominant in each stage? what molecule regulates reproductive cycling as a whole?
1. proestrus - developing E
2. estrus - peak E and ovulation
3. metestrus - developing P
4. diestrus - peak P
kisspeptin regulates GnRH secretion which regulates reproductive cycles
what are the wing and tail flight feathers called? how many primary flight feathers on wing?
what is femiges (wing) and retricles (tail)? and 10 primary femiges
functions of T3
what is increase energy mobilization, Na/K pump expression (thermoregulation), and beta-adrenergic receptors to increase cardiac output?
cortisol functions
what is fat metabolism by upregulating HSL, increase gluconeogenesis enzymes, increase protein catabolism, immune function (acute: enhance, chronic: suppress), and promote insulin secretion (to downregulate HSL)
what are the functions of calcitriol in the GIT?
what hormone controls parturition and what does it do?
where are the air sacs located in the bird? which ones are not connected to the main respiratory system?
what is cervicocephalic, clavicular (1), cranial thoracic, caudal thoracic, and abdominal (all are paired except clavicular)
cervicocephalic is not connected to resp. system
respiratory vs. metabolic acid/base disturbance is caused by alterations to what parameters?
what is respiratory - altered PCO2
metabolic - anything else but usually altered HCO3-
you do the high dose dex suppression test (HDDS) and see no change in cortisol levels. what does this tell you about where the lesion is?
what is adrenal tumor (or ectopic tumor but this is very rare)
no changes to cortisol after high dose dex means that adrenal is ignoring regulatory hormones (ACTH ) and is just pumping out cortisol for fun.
signs of hypercalcemia vs. hypocalcemia?
what is hypercalcemia: weakness and CNS depression
hypocalcemia: stiffness and tremors
how is lactation controlled? what are the hormones and what does each do?
oxytocin (from PP) promotes milk let-down
dopamine inhibits lactotrophs (in AP) from releasing prolactin (which stimulates milk production)
list the coelomic cavities in birds.
then list the 4 main compartments food travels through when eating
what is intestinal peritoneal cavity, L/R pleural cavities, L/R dorsal hepatic, L/R ventral hepatic, and pericardial cavities (8 cavities in total)
what is crop, proventriculus, ventriculus, ceca
during metabolic acidosis, what happens in kidneys to produce acidic urine?
what is increased production of HCO3- and H+ (bc acidic) in PCT of kidney that leads to HCO3 being retained while H+ gets actively secreted and excreted
you do a low dose dexamethasone suppression test (LDDS) on a patient you suspect has hyperadrenocorticism. You get the results back and see no change in cortisol level. what do you do next and what does this result mean?
what is high dose dex suppression test?
LDDS results being no change means that the dexamethasone was not successful in inhibiting pituitary and hypothalamus from pumping out ACTH and CRH (negative feedback loop) so cortisol is still being produced by adrenals.