how does ketoconazole work as an anti-hyperA? SEs? Why use this?
antifungal that inhibits numerous steps in steroid biosynth. It has reversible side effects (Anorexia, V/D, enzyme elevations, icterus). Generally this is just used for pts who can't handle mitotane or trilostane. It can also be used presx for AT patients to stabilize. It is not as effective as mito or trilo though, and can have bad effects on the liver
how does Selegilene work as an anti hyperA?
Increases dopamine from the hypothalamus to the intermediate lobe and Dec ACTH release. But...most tumors are in the anterior lobe :( so this only works on animals with intermediate lobe tumors. It also might not completely stop clinical signs (not very clinically successful). If mild can give it a shot but still might need to try another protocol
when is radiation therapy indicated?
indicated if there are neuro signs present (shrinks the tumor)- do CT to eval before radiation. you basically have a 1/3 change of either getting worse, improving short term, or improving long term. The therapy might change size or CSs of the tumor. Radiation should be done in conjunction with medical mgmt
Adrenocortical tumors: how many malig/benign? What signs do you see? What are your tx options?
50/50 malig/benign. can cause Glucocorticoid excess, Mineralocorticoid excess (THINK CATS- THIS IS CONN'S SYNDROME), or Sex Hormone excess (Feminization-- common in ferrets.) You can attempt sx removal (caution: often invade the vena cava) or can try mitotane (HIGH HIGH dose= more side effects)
What does FELINE HyperA present like? what other concurrent dz is common with this?
feline version is rare. Often presents with dm. They will be PU/PD WITH MARKEDLY THIN SKIN (think of ripping off their skin from just gently scruffing them) and you can see alopecia of the ears. There will be Hypercortisolism, Hyperprogesteronism, Hypertestosteronism, hyperaldosteronism (all the things)
what is the way to tell if a cat is a hyperA?
They are basically an insulin resistant diabetic WITHOUT acromegaly (remember cortisol is anti-insulin)
what will be diff in a hyperA CATS serum chem from a dogs?
They will NOT have elevated ALP
how do you dx a hyperA cat?
do a ACTH stimulation test (diff dose from dog), can do abd rads/US
how do you tx hyperA cat?
Adrenalectomy--> if you do this, be very careful with their insulin dose if they are diabetic, because once you cut it out, their insulin resistance dec, so you can't just keep giving them the same dose or you might make them hypoglycemic
Both Mineralocorticoid and Glucocorticoid deficiencies.
is it more common in hypOa to have only mineralcort deficiency, only glucocort deficiency, or both?
MOST COMMON IS BOTH- if only GC is missing that's atypical. (if only gluco deficiency- wont have electrolyte abnormalities. they are hard to dx. if cant find anything wrong- think atypical addisonian.)
The most common signalment of a hypOa
Dogs, young (4yr), females (3x more likely), Danes, WHWT, Bearded collies, Poodles, Bassets (in cats it is extremely rare, they are young with no sex predilection)
The most common signalment of a hypOa for NAVLE
YOUNG FEMALE POODLE that looks like she has renal dz
if you have 2* addisons, is it typical, atypical, or both?
can only be atypical (aka only glucocort deficiency) because the pituitary releases ACTH which has to do with glucocorts, but the RAAS is what is controlling the mineralcorts
explain 1* vs 2* addisons
1*= dz of adrenal gland. can be typical or atypical. 2*= dz of pituitary (it doesnt have or isnt releasing ACTH)
explain what can cause typical and what can cause atypical IATROGENIC addisons
(1) TYPICAL: can be caused by mitotane or trilostane (either one can knock out the glom and the fasciculata layers) (2) ATYPICAL: steroids, mitotane, trilostane, ketoconazole
GI/appetite for addison's vs cushings
cushings the are STARVING!!! addisons they have no appetite and might be V/D
**CHRONIC CSs of addison's? (not a crisis)
*****WAXING AND WANING V/D, VD, anorexia, lethargy, weakness, weight loss..... "the great pretender" (Any to no clinical signs possible)
**ACUTE CSs of addison's? (crisis)
sudden severe collapse, SHOCK (hypovolemic-- losing so much blood and water from V/D), severe bloody diarrhea, any hx of the chronic signs, bradycardia (bc K+ is high), dehydration, abd pain
*****what will CBC/Chem/UA look like?
CBC: NO STRESS LEUKOGRAM, EVEN IF SICK (they have no effin steroids!!), might be anemic after fluid replacement (bc bloody diarrhea). CHEM: PRERENAL azotemia (Dehydrated from the V/D), hypOnatremia (no aldosterone to save it), hypERkalemia (no aldosterone to stim its excretion), hypERcalcemic (prolly not peeing this out either). UA: will be LESS THAN 1.030 due to medullary washout (looks like a renal dog that doesn't quite fit renal dz)
what should you know about hypOa and using the Na:K ratio?
it is NOT diagnostic OR pathgnomonic...however, it can be a classic sign if it is off. This ratio being off only occurs with a mineralcort deficiency. Normal Na:K is 27:1 up to 40:1......if it is LESS THAN 27:1 (meaning there is more K) this is suggestive and you should perform a ACTH stim test
DDxs to consier with addisons?
RENAL DZ (ARF, obstruction, uroabd), hepatic failure, severe GI dz, severe acidosis, CHF, massive tissue destruction, primary polydipsia, 3rd spacing (pleural effusions), WHIPWORMS
what will addisons look like on rads?
microcardia, hypocirculation, eso dilation
*what will ECG look like with addisons?
remember-- no aldosterone-- saving K instead of Na-- so hyperkalemia ECG= BRADYCARDIA, absent P's, tented T's, prolonged QRS
3 tests you can use to diagnose addisons?
(1) ACTH stim: baseline cortisol is important! (2) Endogenous ACTH conc (helps differentiate 1* vs 2*, atypical) (3) aldosterone levels (not necessary most of the time)
explain ACTH stim and how you can dx addisons with it
Eval baseline cortisol. Give exogenous synthetic ACTH. Wait an hour, measure cortisol again. If it's hypo, it will be <14mmol/L for both pre and post
what is a mineralcorticoid/glucocorticoid suppliment you can give for addisons?
fludrocortisone (can do Mc and Gc but half will still need additional pred)
what is a mineralcort ONLY suppliment you can give for addisons?
DOCP (desoxycorticosterone pivalate) (based on Na/K levels)
how do you tx CHRONIC addisons?
fluids if necessary, ORAL steroids (pred daily, 2-10x the dose if there is a stressful event), fludrocortisone, DOCP (desoxycorticosterone pivalate)
how do you tx addisonian acute crisis?
ER!!! Give IV fluids (NaCl), IV dexmethasone, oral fludrocortisone, GI protectants. When stable, reassess and switch to maintenance protocol
What can happen if you suddenly put them through an acute glucocorticoid withdrawal? (iatrogenic cushing's with rapid steroid withdrawal)
the exogenous steroids have been neg feedbacking, so the pituitary is off and the adrenals are small. The sudden withdrawl can lead to SECONDARY hypoA. (secondary=prob with pituitary. it has been inhibited for forever)
what will 2* hypOa look like? what will ACTH stim be like? what will endogenous ACTH be like?
NORMAL ELECTROLYTES (2*= pituitary prob and pituitary mostly only works with glucocorts), ACTH stim will show no response (adrenals atrophied), low endogenous ACTH conc (pituitary not making it)
how do you tx 2* hypOa?
replace glucocorts!! If you are trying to reverse iatrogenic cushings, you need to SLOWLY reduce the steroid levels!! (severe cases can take up to 4-6mo to withdrawal)-- supportive care with wound management
what is a pheochromocytoma? Who usually gets them?
This is a tumor of the MEDULLA of the adrenal gland. Often older dogs and often incidental/associated with other tumors.
what is the problem(s) pheochromocytoma causes?
excessive catecholamine release!! bc its a tumor of the medulla! so: (1) Excessive epinephrine: elevated glucose, secondary DM. (2) Excessive norepi: hypertension, retinal hge, splenic contraction leading to inc RBCs
how can you dx a pheochromocytoma?
repeated BP measurements, abd radiography and US, venography, CT
tx for pheochromocytoma?
adrenalectomy-- but it's risky!! MONITOR BP!! might have to pharmacologically manipulate BP. IF BILAT will have to tx for hypOa
which cells secrete insulin/ what does insulin do?
BETA CELLS (betas make you Big bc insulin helps you store fat), so insulin in anabolic (storage hormone), moves glucose into cells, promotes glycogenesis, promotes lipogenesis, promotes protein synth, and nucleic acid synth
explain the types of DM
(1) SPONTANEOUS: (a) type 1: IDDM/juvenile... this is most dogs. (b) type 2: NIDDM/adult....this is most fat cats. (2) SECONDARY: happens because of insulin antagonists-- in the case of ACROMEGALY
most cats get _ DM, most dogs are _
CATS= TYPE 2. DOGS=TYPE 1
signalment of dog with DM? What might be the FIRST SIGN you see?
all breeds can get it (dachshunds and poodles), middle aged to older. females up to 4x likely. CATARACTS might be the initial sign
signalment of cat with DM? what might be the FIRST SIGN you see?
all breeds, middle aged to older, MALES slightly more represented.peripheral neuropathy might be initial sign which is shown by a plantigrade stance
pathophys of DM.... for dogs?
Usually due to chronic pancreatic inflammation (dogs love pancreatitis), pancreatic atrophy OR can be immune mediated destruction of the B cells. Might also get TRANSIENT DM from pregnancy or diestrus
what are two situations of transient DM and why does it happen?
dog thing- with pregnancy/diestrus it's because progesterone can sometimes cause it, or the growth hormone secreted from the mammary glands
what are the anti-insulin hormones?
Glucocorticoids, progesterone, growth hormone (hence acromegaly ppl get DM), epinephrine (want glucose in blood for running away), and glucagon (just the opposite hormone)
weight loss in the face of inc intake, polyphagia, PU/PD, CATARACTS in dogs (can happen quickly)
explain the CSs of the ketoacidotic/non-ketotic hyperosmolar DM pt
see weight loss, PU/PD, dehydration, labored breathing*, lethargy/collapse/stupor*, and for the NON-KETOTIC HYPEROSMOLAR: you will see DEC GFR, and Blood glucose is really high chronically which causes idiogenic osmoles to form to make sure the cells have enough draw to still get fluid-- caution on brain edema when rehydrating them
thing you need to worry about with non-ketotic hyperosmolar DM
so hyperosmolar that act like salt poioning in a pig. so all probs wirh hyperosmola. brains get idiogenic osmoles to equilibrate. if you throw fluids at them, look out for cerebral edema.
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