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117 Cards in this Set

  • Front
  • Back
Screening Test
a diagnostic test that aids in determining if there is a normal or abnormal endocrine function
Discriminatory Test
diagnostic test that can identify specific cause of abnormal endocrine function.
Sensitivity
tests for abnormal endocrine status. true positive and false negative
specificity
tests for normal endocrine status. true negative and false positive.
accuracy
true positive and true negative divided by the total. sensitivity and specificity combined.
Acidophil of adenohypophysis
GH (somatotroph) and PRL (lactotroph) both are acidophils, but GH is also eosinophil.
Chromophobe of adenohypophysis
ACTH (corticotroph cell)
Basophil of adenohypophysis
FSH and LH (gonadotroph) and TSH (thyrotroph) are all basophil.
What cell types make up the majority of the adenohypophysis?
Somatotroph (GH) makes up 45%.
Lactotroph (PRL) and corticotroph (ACTH) make up 20% each.... FSH, LH, TSH make up the rest.
What acts on GH?
GHRH is +
SS -
what acts on TSH?
TRH +
SS-
what acts on ACTH?
CRH +
Dopamine +
what acts on PRL?
Dopamine -
What acts on FSH?
GnRH +
Inhibin -
what acts on LH
GnRH +
Where is OT and ADH made
made and packaged in the hypothalamus but is released from the nerve endings of the neurohypophysis.
What composes the neurohypophysis
pars nervosa and neural stalk
what composes the adenohyophysis
pars tuberalis
pars distalis
pars intermedia
what is the drug otreotide?
it is a somatostatin agonist and inhibits GH (and TSH)
Two causes of juvenile panhypopituitarism.
craniopharyngioma: tumor of rathke's pouch (epithelial origin)

Empty Sella Syndrome: German Shepherds; cavity with a cyst compresses everything.. due to failure of differentiate of Rathke's Pouch.
Adult panhypopituitarism causes?
chromophobe adenoma (inactive)
and inactive pituitary carcinoma.
microadenoma's
functional and less than 1 cm
macroadenoma
functional and larger than 1 cm.
Acidophil adenoma
In the pars distalis
Hormone in excess is PRL.
Infertility; inappropriate lactation.
chromophobe adenoma
In the pars distalis
hyperfunction- ACTH in excess

Cushing's Disease.
Eosinophil Adenoma (acidophil too) Pars distalis.
Gigantism (juvenile)
Acromegaly (adult)
Diabetes Mellitus (adult).
Pars intermedia adenoma is most common type of pituitary tumor in ____ and 2nd most common in the ___
Horses, dogs.
Pars intermedia active tumor
Excessive ACTH leading to bilateral adrenocortical hyperplasia and cushing syndrome.
Neurohypophyseal Dysfunction
hypophyseal Diabetes insipidus - due to insufficient ADH. with PUPD. most common- treat with ADH injections
Nephrogenic diabetes insipidus-
ADH is normal but severe hormone resistance in the kidney (genetic cause!)
GH deficency causes what 3 things.
1) pituitary-dependant dwarfism
2) pituitary- indépendant dwarfism
3) GH- responsive alopecia
pituitary dependent dwarfism
zero or very low- GH and IGF-1.
Can be caused by:
1) empty sella syndrome (panhypopituitarism)
2)craniopharyngioma
3) Nonfunctional pituitary tumors
4) Idiopathic GH deficency (monotropic hypotituitarism)
Clinical signs of pituitary dwarfism?
proportional dwarfism, delayed eruption of permanent teeth, puppy coat, suppressed immune response, decreased visceral-organ size, delayed closure epiphyseal plate.
differential diagnosis- is diabetes mellitus and metabolic disease.
Pituitary- Independent dwarfism caused by?
Caused by :
1)hypothyroidism- need normal thyroid norman for GH gene transcription.
2) diabetes mellitus type 1 (IDDM)
3)cushingoidism- excessive cortisol suppresses GH secretion.
4) GH receptor deficiency- GH is elevated but IGF-1 is decreased. called Laron dwarfs.
Causes of endocrine dermatoses.
Most common to least.
hypothyroidism, cushingoidism, sex-steroid imbalance, diabetes mellitus, glucagonoma, GH responsive alocecia, hyperthyroidism.
GH responsive alopecia
unique to dogs, looks cushingoid-like. high in pomeranians.
endocrine testing for GH dysfunction.
use drug called Clonidine (alpha2 catecholaminergic agonist- stimulates GH).
Insulin can also stimulate GH. dopamine suppresses GH in acromegaly dogs.
High IGF-1 increases can mean hyper functioning.
Signs of Pituitary Independent dwarfism.
DISproportionate dwarfism!
primary hypothyroidism (lesion in thyroid)
skeletal displasia.
Clonidine (drug)
Stimulates GHRH and GH to test what is functional.
Dog increase GH etiology
progesterone from luteal phase --> mammary (hyperplasia)->ductile epithelium-> more GH

also remember ^GH=^IGF-1
growth in foetal animal.
Insulin and IGF-2 are determinants of foetal growth.
important factors in prepubertal growth.
GH, IGF-1 and thyroid hormones (so GH gene transcribed).
Giantism causes
excessive GH. Often accompanied with hypogonadism- leaving the epiphyseal open longer.
less common than dwarfism.
most likely caused by adenohypophyseal adenoma.
Acromegaly Causes/ Clinical Signs
Excessive GH postpubertal.
eosinophilic adenoma- secret GH. progesterone can secrete GH in the bitch mammary gland.

Clinical Signs- associated with local appositional growth of bone and connective tissue in the face and paws (enlarged)
everything megaly, prognathism, fast growing toenails.. lethargy.
GH-induced diabetes mellitus
Excessive GH can produce mild to moderate diabetes...
also induces insulin resistance.
creates right-ward shift. and makes hepatic glucose production too high.
GH hypersecretion in dogs with injectable progesterone.
with doses of progesterone. progestins... can cause acromegaly, diabetes, mammory tumors etc...
Drugs like MPA and ovaban that produces GH hyper secretion.
Pituitary independent dwarfism- could also be called
primary hypothyroidism- lesion in thyroid. also disproportionate.
IGF-1
comes from the liver when stimulated by GH. without IGF-1 there is no growth!!
Laron Dwarfism
have very high GH but a problem with GH Rc in the liver so low IGF-1
drug xylazine/clonidine
it affect presynaptic membrane from releasing NE and should increase GH

clonidine acts on alpha 2 rc to increase GH secretion
GH affects on the body.
besides for growing, it helps with protein synthesis, lipolysis, Hepatic glucose production..
drug octreotide
somatostatin agonist
drug pegvisomant/ somavert®
rhGH-PEG
antagonist to GH
what part of the pituitary does ACTH come from?
pars intermedia. Causes Cushingoidism!!
3 things needed for water transport in the kidney.
1) osmotic conc gradient. most important!!!
2) water channels on both sides of cell ( always in BsL but changes in apical)
3) tight junctions
Define: renal medullary solute washout-

obligate solute load
The loss of some Na and /or urea from the medullary interstitium. gradient in not normal- produce more urine= polyuria.

what must be urinated out everyday.
What parts of the kidney can absorb ( leave tubule and enter blood) water without ADH?
PCT and thin descending limb
function of distal convoluted tubule!
it puts Na, Cl, Ca and electrolytes into the blood (absorption) in absence of H2O absorption (no water leaving)

Due to NaCl cotransporters
ECaC
function of vasa recta in kidney
AKA- counter current exchange
maintains hypertonicity of medullary interstitium.
list the osmoality of the interstitial of the kidney
near the cortical medullary junction- 500
outer medulla- 700
inner medulla- 1200
how much of the blood flow does the cortex of the kidney receive?
90-95% of blood flow to kidney.
does renal medullary solute washout increase or decrease with increase bloodflow?
increase!
Where does ADH affect in the kidney?
the distal tubule, cortical collection tubule (primary site) and medullary collecting duct.
what hormone regulates Na reabsorption and K and H secretion in the distal tubule. In the principal cells!!
aldosterone. in the cortical collecting duct. (and maybe the outer medullary collecting duct.)
what do intercalated cells do of the cortical collecting ducts?
secretion of H in exchange for K and HCO3-.
what parts of the kidney are impermeable to urea.
the cortical collecting tubule and distal tubule is impermeable to urea regardless of ADH.
if urea was to be reabsorbed-- where would it occur in the kidney?
the medullary collecting duct. only in the presence of ADH.
causes of PUPD!
renal failure, diabetes mellitus, hyperthyroid, diabetes insipidus, other hormones.
what diseases are found with hyposthenuric (usg ≤ 1.070)?
cushingoidism, hypercalcemia, ADH ( central and nephrogenic diabetes insipidus)
isosthenuric polyuria (usg ~1.010) is found in what diseases?
osmotic diuresis
cushingoidism
partial CDI (central diabetes insipidus)
hypersthenuric polyuria (USG ≥ 1.030) is found in what?
uncommon but found with diabetes mellitus
Causes of Polyuria?!
1. lack of ADH (central diabetes insipidus)
2. ineffective ADH (genetic/ nephrogenic diabetes insipidus)
3. tubule solute load
glucose, mannitol, diuretics (increase Na in collecting tubule)
4. renal medullary solute washout
diseases causing osmotic disuresis.
diabetes mellitus (glucose)
addisonism (Na)
postobstructive diuresis (BUN)
causes of acquired nephrogenic diabetes insipidus.
cushingoidism, chronic renal failure, pyometra, pyelonephritis, hyperthyroidism, hypercalcemia, hypokalemia, hepatic failure.
diagnosis Diabetes insipidus
1. water deprivation tells normal from abnormal in ability to concentrate urine.
2. ADH stimulation test- tells nephrogenic vs central DI.
constitutively permeable
semipermeable to water molecules if the basilateral and apical membranes contain constitutive water channels called aquaporin 1 (AQ1) channels
Verney’s receptors
specialized nerve cell bodies are located in a region of the anterior hypothalamus called the organum vasculosum terminalis (OVLT) and the subfornical organ (SFO).
neurophysin I
helps package OT and ADH to go through the axon tobe release from the neurophysis
what makes tight junctions impermeable
claudin and occludin proteins in the tight junction physically impair the movement of water
AQ3 AQ4
constitutively in the basilateral membrane of principal cells of the collecting duct. not ADH dependent.
Bulk-reabsorption segments
proximal convoluted and straight segments
Diluting segments of the kidney
TAL with some contribution from the distal convoluted tubule and aldosterone target cells (principal cells) in the cortical collecting and outer medullary collecting ducts
Electrolyte balance segment of kidney
effects of aldosterone and PTH in distal tubule and collecting ducts
Concentrating segments of kidney
cortical collecting duct (CCD), outer medullary collecting duct (OMCD), and inner medullary collecting duct (IMCD) of the nephron
solvent drag in proximal tubule of nephron.
responsible for most of the passive, paracellular route of absorption of chloride, calcium and potassium in the proximal tubule
how does water leave the proximal tubule if it is iso-osmotic with the interstitium of kidney.
The active and passive transport of solutes (electrolytes, glucose, and amino acids) establishes a microenvironment of hyperosmolarity within the lateral intercellular spaces of the proximal tubule which drives both the transcellular and paracellular absorption of water.
what transporter is responsible for reabsorption of glucose back into blood in the nephron.
apical glucose transporters (SGLUT) are only found in the proximal tubule. its a Na-glu cotransporter.
what transporter is found in the thick ascending limb of the kidney?
Na-2Cl-K which reabsorbs about 25% of the solutes back into the blood
What transporters are found in the distal tubule of the nephron?
(1) Thiazide-sensitive Na-Cl cotransporters in DCT.
(2) Aldosterone-responsive Na channels known as ENaC.
(3) PTH-responsive calcium channels (ECaC) are also found in these segments. Parathyroid hormone stimulation increases calcium reabsorption by distal tubule ECaC whilst decreasing phosphate reabsorption in the proximal tubule.
how do you calculate solute load?
Solute load is calculated as plasma concentration of a solute (e.g. Na or glucose) and the plasma filtration rate (GFR).
what creates Hyperosmolarity of the medullary interstitium
The countercurrent multiplier system of the Loop of Henle and the countercurrent exchange system of the vasa recta are critical determinants of the medullary hyperosmolarity.
the major osmolytes in the medullary interstitium
Sodium (and chloride) along with urea
drug Furosemide
example of diuretic drug. extended use decreases the medulla interstitium osmolality.
how can water leave the cortical collecting ducts if the interstitum of the cortex is iso-osmotic.
water reabsorption across the cortical collecting duct epithelium into the iso-osmotic cortical interstitium requires a hypoosmotic tubule fluid and ADH stimualtion of the cortical duct epithelium
function of vasa recta.
The vasa recta maintains the hyperosmolarity of the interstitium by recycling/trapping Na and urea within the medulla and by removing water that is reabsorbed from the DTL of the Loop and the collecting ducts
what part of the kidney receive the most blood?
cortex. it gets about 95%.
medulla gets 2% because it needs slow blood flow to maintain hyperosmolality.
at what rate does one become clinically polyuric?
Animals may be considered clinically polyuric if urine volume exceeds an average 50 mL/kg/d.
normal is 20mL/kg/d.
at what rate does one become clinically polydipsic?
Animals may be considered polydipsic if their fluid intake exceeds 100 mL/kg/d.
50 mL/kg/d is normal
Do urine osmolarity and USG change in parallel?
10 molecules might affect USG more than osmolarity if the molecules are big.
osmotic diuresis definition.
a diuresis caused by presence of greater than normal amounts of osmotically active solute(s) in the tubule fluid that increase tubule flow and dissipate the osmotic gradient between the hyperosmotic interstitium and the tubule fluid. ADH secretion and ADH receptor number in collecting duct epithelia are normal in osmotic diuresis.
what can the water deprivation test not discriminate between and when should you stop the test.
The water-deprivation test cannot distinguish if the animal has CDI or gNDI

(1) the USG attains 1.025, (2) when the animal becomes dehydrated as shown by loss of 5% of its body weight, or (3) when the BUN becomes abnormally elevated regardless of USG or body weight loss.
how does Cushing's affect kidney function?
it creates resistance to ADH stimulation- and decreases the amount of ADH produced from the pituitary. Also increases GFR by increasing bloodflow to medulla- causing washout. Also causes osmotic diuressis by too much solute in tubule.
how does hyperthyroidism affect kidney function?
high thyroid hormones -> increased renal blood flow. leads to medullary washout. Also reduces the ADH made and cause resistance.
How does hypokalemia and hypercalcemia affect kidney function?
cause cellular resistance to ADH. can hinder solutes getting into the interstitum of the medulla.
hepatic insufficiency affects renal function how?
impaired production of urea- so hypertonicity of the renal medulla.
how does chronic renal failure affect kidney function?
with loss of nephrons- blood flow is increased to the remaining nephrons. eventually, with enough nephrons lost... you get medullary washout from increased blood flow.
What preforms the extra thyroidal conversion of t4 to t3?
the plasma membrane bound 5´-deiodinase (type 1 deiodinase; D1) in hepatocytes.
how much of serum T3 come directly from they thyroid?
40%.. rest is extra thyroidal like in the liver.
describe the nuclear transcription factors for T4 and T3?
Ligand-occupied thyroid receptors bind to specific DNA regions known as thyroid hormone-response elements (TRE).
d. Induction, rarely repression, of target genes that code for hormones, metabolic enzymes, structural proteins and other products
Does t3 or t4 or both bind to mitochondrial receptors.
t3 only.
. A positive test result for Tg·Ab suggests...?
. A positive test result for Tg·Ab suggests an ongoing lymphocytic thyroiditis,
type1 5' deiodinase activity is decreased by what?
fasting, diabetes mellitus, fetus, glucocorticoids, nonthyroidal illness (euthryoidal sick syndrome)
Eurthyroidal sick syndrom define
hypothyroid animals that are sick with normal thyroid function.
caused by: decreased production, decreased plasma-protein binding so increased degradation, reduced extra thyroidal production of t3
type 1 5' deiodinase does what
turns t4->t3 and rt3->t2
Grave's disease
when Ab against the TSH Rc stimulate the receptor to produce a hyperactive thyroid gland.
trophoprivic hypothyroidism
insufficient stimulation of thyroid gland.
thyroprivic hypothroidism
means primary hypothyroidism.
dishormonogenesis
idiopathic hypothyroidism- atrophy/ immune mediated attack.
lymphocytic thyroiditis becomes idiopathic if chronic.
goitrogenic hypothyroidism due to drugs.
the most dangerous consequence of severe hypothyroidism
myxoedema coma- caused from poor degradation of collagen that is deposit into the skin- causing edema and dry skin and poor hair coat.