Small Ani. Med- Endocrine 7

wilsbach's version from 2016-05-02 02:15

Hyperparathyroidism, Hypoparathyroidism, DI

Question Answer
explain the 3 main hormones responsible for Ca homeostasis?(1) parathormone- secreted by chief cells in the PTH gland, stimulated in response to low Ca++ (so inc Ca++) (2) Calcitonin- C cells in thyroid, lowers Ca++ if it's too high. (3) Vitamin D- Cholecalciferol (Dietary vitamin D3), or 25-hydroxycholcalciferol (liver), or *1,25 dihydroxycholecalciferol (Kidney) This last one is the ACTIVE vitamin D3 aka calcitriol (all inc Ca++ absorption from GI)
explain 1* vs 2* versus 3* hyperPARAthryroidismPRIMARY: most often benign adenoma of the parathyroid gland (hyperplasia rare). Similar to hypercalcemia of malignancy HHM (pseudohyperparathyroidism). SECONDARY: nutritional, renal, intestinal. TERITARY: Receptor abnormalities
if PTH is high and Ca is low... what is going on?2° Hyperparathyroidism-- Nutritional/Renal (either eating too much P and its binding up Ca++, or Kidney dz means not excreting P properly and it's binding up Ca)
if PTH is low and Ca is low... what is going on?1° Hypoparathyroidism
if PTH is high and Ca is high... what is going on?1° Hyperparathyroidism
if PTH is low and Ca is high... what is going on?Hypercalcemia of Malignancy
WHAT ARE THE REASONS FOR THERE TO BE HYPERCALCEMIA?GOSHDARNIT!!! G: granulomatous dz. O: Osteopathy/osteolytic disease S: spurious. H: hyperparathyroidism D: excess vitamin D. A: addisons R: renal dz N: NEOPLASIA. I: Idiopathic T: temperature- cats
what are the tumors most likely to cause hypercalcemia of malignancy? (3)****LYMPHOMA, analsac adenocarcinoma, multiple myeloma
CSs of hyperparathyroidismPU/PD (osmotic diuresis...can have Ca urolithiasis too), lethargy, incontinence, weakness/exercise intolerance, anorexia, mm wasting, vomiting, constipation, or NONE. Can def get urinary tract dz (Ca++ urolithaisis))
which type of Ca++ are you measuring for hyperParathyroidism?Always evaluate ionized Ca++, Non-hemolyzed non-lipemic sample
how can you dx hyperparathyroidism?First, you will see Elevated PTH (OR NORMAL) in the face of elevated Ca++ (even if PTH is normal, if the Ca++ is high, that is abnormal). (ALWAYS MEASURE IONIZED Ca++!!), on rads you will see osteopenia and urolithiasis, and if you US the neck you can often ID the affected glands (the other ones will be atrophied)
how do you tx hyperparathyroidism?Generally, you would surgically excise the tumor (and uroliths). but if they are not surgical candidates, you can medically manage them with bisphosphonates (osteoclasts munch on them instead of Ca++) or calcimimetics.
how should you post-op manage hyperparathyroid pts after you took out their parathyroid gland?YOU will make them hypocalcemic until the remaining parathyroids escape suppression!!! Therefore, monitor pt for hypocalcemia for Q2-4 hours, and MEASURE Ca++ and watch for BH changes and mm fasciculations (might look like they have an itchy face!) if they become hypopara, tx with calcium gluconate (monitor ECG!)
how do you prepare for sx of removal of hyperparathyroids?Initiate calcitriol (active vit D3) therapy the day of or one day before surgery. It can take 3-4 days to work so starting the day before sx is nice. After recovery monitor calcium and slowly decrease the calcitriol until they can maintain a normal calcium. You can also give Oral calcium supplementation as Calcium carbonate (tums)
iPTH (intact) is normal and Ca++ is high... what do you think?THAT IS NOT NORMAL. STILL HYPERPARA.
why is halitosis with missing teeth a big sign?Bc hyperpara is absorbing bone from alveolus around teeth, and this can cause bad breath
what is happening in Renal Secondary Hyperparathyroidism?There is Chronic Kidney Disease and Low calcium triggers elevated PTH--> Demineralized bone
tx for Renal Secondary Hyperparathyroidism?Treat CKD, Ensure normal Ca++/Phos product (should be <70) and you can do CALCITRIOL therapy-- If Phosphorus is <6
2 types of nutritional secondary hyperparathyroidism? explain them/their CSs and txINTESTINAL: Intestinal malabsorption because Fat malabsorption (need fat for vitamin D, need vitamin D to absorb Ca++), can see diarrhea. Correct/tx underlying dz. can consider calcitriol. DIETARY: Inappropriate Ca++/Phos ratio in diet: Low Ca++, low vitamin D, high P. c/s lameness, loose teeth, swollen maxilla. Pathologic fractures
Main reason for Hypoparathyroidism? signalment? Immune mediated destruction of parathyroids= Lymphocytic parathyroiditis. Can be any age, but immune mediated tends to be middle aged (5 years). No obvious breed or sex predilection- maybe small breeds.
CSs of hyPOparathyroidismrelated to HYPOcalcemia!! will see: Muscle fasciculation and cramps, seizures, Itchiness, pawing at the face, cataracts, Diaphragm contractions concurrent with heartbeat (thumps)
how do you dx and tx hyPOparathyroidism?Dx: Decreased total and ionized Ca++ (Total Ca++ < 6.5 mg/dL). Inc phosphorous. Decreased iPTH. TX: IV calcium for emergency stabilization. Oral Calcitriol, Oral Calcium supplements if needed (tums)
what is diabetes insipidus? what are the two kinds?there is primary Central (Decrease in ADH/vasopressin) and Nephrogenic (dec in receptors for ADH)
explain primary central diabetes insipidus. Age distribution?there is a dec in ADH being produced- this can be congenital or acquired, bimodal age distribution of <2yr versus >6yr depending on is congenital or acquired. It can totally be 2* to a pituitary tumor for the acquired.
explain nephrogenic diabetes insipiduscongenital lack of ADH receptors, extremely rare
CSs of diabetes insipidus? PU/PD, Incontinence (Due to large amount of urine), +/- neuro signs if the pituitary tumor is being an ass
minimum database signs of diabetes insipidus?+/- polycythemia, +/- azotemia, +/- hypernatremia, USG 1.001-1.012 (SUPER DILUTE). If acquired consider CT or MRI (tumor)
one way to start to dx diabetes insipitus is?Quantify water intake! > 100 ml/kg/day
before you dx DI you much RO every other PUPD dz your final 3 R/Os will be....and what will you do then?Final 3 rule outs will include CDI, NDI, or psychogenic polydipsia. Then and only then…and after you discuss the case with an internist, you can do: DDAVP response test (synth vasopressin/ADH hormone.) and MAYBE Consider Water Deprivation test
does hypothyroidism cause PUPD?NO!!! basically everything else does tho
explain the DDAVP Response Test and the resultsMeasure water intake for 2-3 days, Catch urine at same time every day, then treat with DDAVP for 5-7 days (synth ADH), Monitor water intake and urine on days 5-7. IF there is a Dramatic decrease in H2O intake and >50% increase in USG, this is consistent with CDI or PP(psychogenic polydipsia) (ADH is made for you to retain water. So if the problem was they had no ADH and then you gave them ADH, they would pee less so the USG would inc.). If there is no response, it's nephrogenic DI (no receptors, so doesnt matter if you give ADH, they still wont conserve water)
things to know about tests/dx of DI is...that it doesnt matter how you officially dx it.. in the end theyre just gonna drink more water and pee more.
explain the water deprivation test and the resultsYOU CAN KILL A DOG WITH THIS TEST. NEVER do on a dehydrated dog!! You MUST rule out all other causes of PU/PD first!!! Modified protocol is safer: Slowly decrease water available over 3 days as an in-hospital test. Weight, USG, creatinine, PE every hour, Until 5% dehydrated, USG > 1.030, azotemic. 5% dehydrated is the endpoint- if they are 5% dehydrated and havent concentrated their urine, it is CDI. If they concentrate, its psychogenic polydipsia.
what is DDAVP?Structurally similar to ADH/VP, More antidiuretic effect that pressor effect. Can use as the response test for dx of CSI/PP vs NDI, or if it IS central, can use as tx (can give intranasal or intraconjunctival if you sterilize the nasal drops)
primary vs secondary nephrogenic DI?remember nephrogenic is no receptors/aren't working. Primary is a congenital lack of receptors (super rare and congenital), secondary is PUPD ignoring ADH because of some other dz going on (sthing affecting receptors ability to respond)- theyre there but not responding as well as they should)
how do you tx primary nephrogenic diabetes insipidus?This sounds weird but...THIAZIDE DIURETICS! This is bc it Inhibits Na+ reabsorption in ascending loop of Henle--> Feedback will increase proximal Na+ and H20 absorption (so they will be PUPD...but not as much). Also give a low salt diet. Just make sure the dog never runs out of water basically
If they have Central diabetes insipidus, what will... initial USG be? 5% dehydrated USG be? Post-ADH USG be?initial: <1.006. 5%: <1.006. Post ADH: >1.018
If they have PARTIAL central diabetes insipidus, what will... initial USG be? 5% dehydrated USG be? Post-ADH USG be?initial: <1.006. 5%: 1.008-1.020 Post ADH: Inc 10-50%
If they have nephrogenic diabetes insipidus, what will... initial USG be? 5% dehydrated USG be? Post-ADH USG be? initial: <1.006. 5%: <1.006. Post ADH: <1.006.
If they have psychogenic polydipsia, what will... initial USG be? 5% dehydrated USG be? Post-ADH USG be?initial: 1.002-1.020. 5: >1.030. postADH: N/A
what is Syndrome of Inappropriate ADH release? (SIADH)basically the opposite of DI-- TOO MUCH ADH is being released. This leads to severe hyponatremia With natriuresis (bc no aldosterone to say to save it, and its diluted). Basically leads to water intoxication in the face of Normal renal and adrenal function
CSs of SIADH?since its water intox from too much ADH leading to hyponatremia both in terms of dilution and not saving it in the kidneys, you will see: vomiting, agitation, seizures
possible causes of SIADH? tx?drugs, encephalitis, neoplasia, Intrathoracic masses (Decreases preload). TX: treat primary dz, restrict water, furosemide
what does growth hormone do?Has both catabolic and anabolic actions. CATABOLIC: it is ANTI-INSULIN-- stimulates gluconeogenesis, promotes lipolysis, Hyperglycemia and ketogenesis. ANABOLIC EFFECTS: anabolic effects work Via IGF-1 (Insulin-like growth factor 1) which is the growth factor from the liver, which is basically what makes the difference between a mini and a standard poodle ( Body size proportionate to IGF-1 levels). Stimulates protein synthesis and growth promotion
Growth Hormone Deficiency: 2 ways this happens/a little about them?(1) CONGENITAL: Retained Rathke’s pouch (cyst under brain-- can keep growing and squish brain) (2) DWARFISM: Primarily German Shepherds ( Has been reported in cats). No sex predilection. signs appear at 2-3mo. Dx via basal IGF-1, thyroid testing, Open epiphysis in older dogs
how do you tx GH deficiency?you can give hGH (might end up with Ab formation tho). Will usually only live 3-4yr tho bc cyst keeps growing
what usually causes acromegaly for cats? dogs? what dz is 100% concurrent and why?CATS: It's usually OLDER CATS AND ALMOST ALWAYS MALES. It is a GH secreting tumor (90% macroadenoma) and there will be 100% concurrent rate of DM (bc GH is antiinsulin)..... DOGS: Older, INTACT FEMALES (more common in EU), GH synthesis in mammary tissue
CSs of acromegaly? Conformational alterations: BIG heads, big interdental spaces, prognathism. Also GAINING WEIGHT IN THE FACE OF DM (this is either acromegaly or hyperA...basically is it andre the giant or a skinless cat). There will be a Inspiratory stridor (inc soft tissue in throat), or it's a female intact dog.
dx of acromegaly?CT/MRI (look for macroadenoma in anterior pit. gland) or check IGF-1 levels (Conflicting evidence... Can take a while for levels to fall)
tx for acromegaly?In the case of the intact female dog who's synthesizing GH in her mammary tissue....spay her. For the pituitary dz, RADIATION THERAPY is the best choice bc of its difficult location, but there is a variable response (Will recur in 12-24 months). possible Surgery but need specialist. PROG: MST 4-60 months, short term guarded to good, long term poor but QOL better