Small Ani. Med- Endocrine 2

wilsbach's version from 2016-05-01 05:23

HyperT continued

Question Answer
big risk with bilateral thyroid sx?hypoPARAthyroidism (if you get these on accident)
drug for hyperT?Methimazole (Tapazole is tradename but very common, worth knowing this one)
what supportive drugs can you give for hyperT?B-Blockers for cardiomyopathy, Treatment for renal failure if present
die useful for hyperT cats?HILLS Y/D diet. **told us to add this. important. IODINE DEFICIENT DIET. No iodine, no thyroid hormone. helps some cats. brings them to normal. can actually totally cure them. might cause goiter but its only aesthetically displeasing. can have hyper eu and hypothyroid goiters in cats.
explain MOA of methimazole/tapazoleBlocks hormone synthesis and release-- Prevents Iodine incorporation and inhibits coupling of DIT and MIT (dit-dit= T4, dit-mit=T3). Effects are reversible if you stop giving pill (so no perm hypo a risk), and effective in >99% of cases (gott pill cat daily tho)
If you are doing I-131 for the cat, why might you still do a tapazole trial (methimazole)bc you want them to be as healthy and stable as possible before going under anesthesia. Also assess how bad renal dz might be/ if its present
how do you recheck with methimazole/tapazole therapy?put them on it, recheck in 2wk. look for side effects, measure crt/USG. every 2-3 weeks for 3 months
whats up with Transdermal methimazole?Effective to begin with, but can change over time, because at first their metabolism is super high from the T4 but as the hyperT gets better, metabolism dec, might not absorb and process the ointment as well. Monitor tT4 and C/S. But remember: ointment in ear of cat. So owners need gloves!!
***once again- how do you dx hyperT in cats?TOTAL T4 (its free T4 in dogs with hypoT)
explain the two types of methimazole/tapazole side effects: Reversible and irreversible, what is going on. What do you do in each situationREVERSIBLE: anorexia, vomiting, lethargy. stop treatment for a few days then reinstate at lower dose. IRREVERSIBLE: facial excoriations, bleeding diathesis, hepatopathy, MG (myasthenia gravis), Cold agglutinin like disease (eartips will start to necrose). If irreversible signs-- will not tolerate Methimazole. Take them off it.
what weird sign can methimazole/tapazole tx cause which you should NOT confuse for what other dz?ANA+ which is intranuclear antibodies- which is how you check for lupus. so don't confuse with lupus if they're ANA+ bc it's just the methimazole
what is I-131 therapy?One shot once (SQ inj) radioactive iodine. Thyroid only place that concentrates iodine, so selectively destroys thyroid tissue. Automatically shunts to thyroid- and kills off specific overproducing cells (the active ones- bc actively concentrating iodine). The healthy tissue is preserved bc it is listening to the neg feedback from the hypothalamus/pituitary so very selective. CAUTION/RISKS: radioactive. Will need to put in isolation for like 13-14d depending on the state. Monitor behavior and appetite! Risk of unmasking renal dz and causing hypothyroidism tho. Monitor tT4!!
before you do I-131 therapy you should...DO A Methimazole/TAPAZOLE trial!! Give for at least one month. tT4 should be in lower 1/2 range. Make sure monitor with USG. You want to see if there is underlying CKD-- because if you tx with I-131, they have to be in isolation for like 2 weeks, but if tx with the I-131 unmasks the renal dz, that needs to be treated by cant be bc nobody can touch them. so the trial is to see how bad their CKD is and if they can survive quarantine. However this trial Does NOT guarantee absence of CKD. If you decide they can survive quarantine bc they have no CKD or its mild enough, then you can go through with I-131. BUT!!! MUST STOP METHIMAZOLE AT LEAST TWO WEEKS BEFORE I-131 BECAUSE THE I-131 TARGETS FUNCTIONING CELLS AND THE METHIMAZOLE STARTED MAKING THEIR THYROID BETTER-- so stop it, let it get back to just the bad cells functioning, and then do I-131
basic jist of how methimazole works?STOPS THYROID HORMONE SYNTHESIS by stopping iodine from being used AND the coupling of DIT and MIT to make T4 and T3
what is the main reason why a DOG might get hyperthyroid?Thyroid tumors! However, most are large,****nonfunctional, invasive, follicular carcinomas (90%) (hence, dogs basically never get hyperthyroid) There is a chance that there is a rare medullary carcinoma that releases calcitonin-- not only do these like to metastasize, are are very invasive around all the important neck structures, but they also BLEED LIKE CRAZY bc calcitonin dec Ca++ and Ca++ necessary for clotting!
Signalment and common presentation of a DOG with thyroid neoplasia?Middle aged to older, no sex predilection, boxers, beagles, and goldens. Basically the mass will bleed a ton with an FNA, and you will see dyspnea/dysphonia/dysphagia.
tx of canine thyroid neoplasia?sx removal, chemo, radiation, I-131 in some places. palliative relief usually achieved

Hyperadrenocorticism (CUSHINGS)

Question Answer
remember anatomy of adrenal gland and the things the different anatomical locations doMEDULLA: basically a modified postganglionic sympathetic neuron. Releases catecholamines (epinephrine, norepi). Then there is the cortex. From outermost layer to innermost, its "GFR" for glomerulosa, fasciculata, reticularis.... and "the deeper you go the sweeter it gets-- salt, sugar, sex" for mineralocorticoids, glucocorticoids, and sex hormones
what do mineralocorticoids do? (what is main one, what layer?)Layer glomerulosa. Main one is Aldosterone! balance salt and water in the body, balance electrolytes, extracellular fluid volume.
what do glucocorticoids do? (what is main one, what layer?) Layer fasciculata. Main one is cortisol. Deal with energy production, protein, fat, and glucose metabolism (catabolic hormone!) is tied in with stress.
what do androgens do? (what is main one, what layer?)Layer reticularis. Main one is DHEA, responsible for secondary sex characteristics.
explain the HPA axishypothalamus secretes peptide hormone Corticotropin-releasing hormone (CRH) in reaction to stress. The CRH stimulates the ANTERIOR pituitary to release the peptide hormone Adrenocorticotropic hormone (ACTH), a trophic (meaning "stimulates another gland") hormone which in turn stimulates the adrenal gland to release cortisol, which in turn has metabolic effects as well as neg feedback on the hypothalamus and ANTERIOR pituitary and ideally on the stress.
how common is hyperadrenocorticism?****MOST COMMON ENDOCRINOPATHY OF DOGS
what is there an overproduction of in cushing's?GLUCOCORTICOIDS (mineralcorts mostly controlled with RAAS)
all breeds can get cushing's, what breeds are overrepresented tho?poodles, dachshunds, and bostons!!
average age of cushings dog? Sex predilection?8yo, no sex predilection but Females more prone to adrenal tumors than males (so they are more likely to get primary form)
1* vs 2* hyperA?Primary is ADRENAL TUMOR. Secondary is PITUITARY TUMOR.
which type of hyperA is more common?PITUITARY DEPENDANT IS MORE COMMON (brain tumors are the main one....bummer) aka 2* hyperA
if you're looking at the adrenal glands-- how do they look diff between 1* (adrenal tumor) and 2* (pituitary dependant)?1*= one is HUGE, other is super small or invisible because its responding to neg feedback from functioning brain. 2* both are big/plump
where (in the pit) are pituitary dependant hyperA tumors usually? what kinda tumors are they?80% in the ANTERIOR LOBe (makes sense bc thats what CRH stims) they are micro or macro adenomas
how common is adrenal tumors as cause of cushing's? are they malig or benign?only 15% of cases. 50/50 malig vs benign. FEMALES MORE PRONE TO PITUITARY TUMORS
how common is iatrogenic cushing's?50% of cases!!
so...breakdown of most common causes of cushings50% is iatrogenic. other 50% is tumors. Of the tumors, 85% is anterior pituitary micro/macroadenomas, and 15% is adrenal tumors, of which more females get
*CS of hyperA?PU/PD, Polyphagia, Panting, Pendulous abdomen, Proteinuria, Bilateral alopecia, Thin skin, Hyperpigmentation, Hepatomegaly, Calcinosis cutis (<-- can appear after steroid cessation in iatrogenic Cushings)
what does CBC/Chem/US look like with cushings?CBC: Stress leukogram (ITS STEROIDS!!!!!), Thrombocytosis (cortisol affects antithrombin). CHEM: inc glucose, ALT, cholesterol, *ALP (Steroid induced isoenzyme-- or from liver if steroid hepatopathy). UA: Dilute urine, proteinuria
***which enzyme has a steroid induced isoenzyme?ALP!!