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Endocrine Literature Flashcards

1
Q

In dogs that are undergoing parathyroidectomy, what are pre-op factors that are associated with post-op hypoCa?

A

MULTIPLE factors! NOT PTH and iCa

			□ Hypo tCa: Old age, hx weakness, lack GI signs, high PTH, low CaXPhos
				® Hypo iCa: intact, low BW, high BUN, lack PU/PD
				® Linear Regression w/ age, BW, Ca x Phos, PTH, BUN
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2
Q

What happens with calcitonin in response to induced hyperCa (CaCl infusion) in cats?

A

VARIABLE calcitonin increased in response to hyperCa

Significant correlation in plasma calcitonin and calcitonin+ thyroid cells (IHC)

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3
Q

What was noted in dogs given Leventa?

A

Liquid l-T4: at 20 ug/kg PO q24hrs was god maintence supplementation in 50% dogs (5), minor change in 4 dogs, 1 dog needed q12hrs
§ CS of hypoT4 improved/resolved in all dogs after 4 wks

Rapid adsorption, T1/2: 11.8hrs

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4
Q

What are possible considerations for adult onset hypoT4 with goiter in cat?

A

Dietary iodine imbalance, chronic exposure to thyrotoxic substance, congenital form with late clinical presentation (similar in humans)

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5
Q

What is known about Tenterfield Terriers and hypoT4?

A

○ Congenital HypoT4 in Tenterfield Terriers
§ Goiters
§ Dysphormonogensis, thyroid peroxidase mutation (R593W)

Homooxygous (carriers can be tested for)

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6
Q

What effect does hypoT4 (induced) have on breeding?

A

Reversible periparturient mortality and low birth weights in offspring (compared to controls and tx hypoT4 dogs)
§ No diff: Interestrus interval, gestation duration, breeding behavior, or serum progesterone

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7
Q

What effect does hypoT4 (induced) have on peripheral neuropathyies?

A

Did NOT result in clinical or electrophysiologic evidence of peripheral neuropathy ( with EMG. Nerve conduction velocity, etc)
§ Did result in subclinical myopathy (histologic evidence of hypoT4 myopathy)

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8
Q

Name a breed that needs breed specific RR for thyroid hormones?

A

Sighthounds (salukis)

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9
Q

What effect does HypoT4 have on glucose metabolism?

A

Negative effect on glucose homeostasis = Insulin resistance
§ Overall glucose tolerance maintained by increased insulin secretion in hypoT4 dogs compared to controls
Possible factors: High serum Growth hormone, high IGF-1, increased abdominal fat in hypoT4 dogs

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10
Q

Can thyroid scintigraphy be diagnostic for hypoT4?

A

Uptake is useful test for thyroid function, BUT values may be nondiagnostic for hypoT4
§ Asymmetric uptake
§ Excess steroids may variably suppress technetium thyroidal uptake +/- thyroid hormones

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11
Q

What can be used in cats to differentiate euthyroidism from iatrogenic hypoT4?

A

○ Stimulation with recombinate human TSH (healthy, non-thyroidal illness, and iatrogenic hypoT4 after I131)
§ Differentiated euthyroidism from iatrogenic hypoT4 in cats
□ Baseline and post rhTSH lower than other controls
§ Thryoid/salivary gland uptake ratio (pertechnetate) differed from controls and iatrogenic hypoT4

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12
Q

What neurology condition has been noted to improve with thyroid supplementation?

A

○ HypoT4 polyneuropathy in dog (nerve bx) - Response to leveothyroxine = SLOW (6 months)
§ Recovery can occur if started before peripheral nerve fiver loss becomes severe

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13
Q

What is another name for TSH?

A

Thyrotropin

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14
Q

What is true regarding difference in MST bwtn azotemia in euthyroid vs iatrogenic hypoT4 cats?

A

§ No difference in MST btwn euthyroid azotemic and euthyroid non-azotemic cats (HUGE!!!!)
§ Iatrogenic hypoT4 contributed to the development of azotemia after tx
□ Larger portion of azotemia in hypoT4 significantly greater than euthyroid group
□ HyopT4 azotemic animals had worse survival (MST: 456 days) compared to HypoT4 nonazotemic (MST: 905 days)!!!
□ HypoT4 cats: 68% had low TT4 and increased TSH

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15
Q

In cats that were followed for 14 months, what were predictors of the them developing hyperT4?

A

§ Incidence: 7.4% (104 cats)
§ If became hyperT4: High ALP, higher prevalence of gioter at baseline compared to controls
§ Undetectable TSH (but NOT all cats with no TSH developed hyperT4)

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16
Q

What was seen in hyperT4 cats after 12 wks with novel lipophilic transdermal formulation of methimazole compared to oral carbimazole?

A

once daily transfermal methimazole (novel lipophilic formulation) applied to pinnae was as effective and safe as carbimazole (PO q12hrs) to tx hyperT4 in cats
§ No difference in T4, BW, BP, HR, ALP/ALT, BUN, Creat, USG btwn groups
§ Serum methimazole correlated poorly with TT4 concentrations in BOTH groups

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17
Q

What was noted about the antioxidant status in hyperT4 cats?

What happened after I131 tx?

A

□ No difference in blood antioxidants (GSH, ascorbate, Vit E) comapred to controls
□ Urinary isoprostanes increased in hyperT4 compared to controls
® This may reflect reversible renal oxidative stress induced by hyperT4

Plasma free Vit A higher in hyperT4 compared to controls

		§ Both urinary isoprostanes and plasma free Vit A normalized with I131 tx
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18
Q

Is there an association btwn antioxidant status and idiosyncratic methimazole toxicosis in hyperT4 cats?

A

No!

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19
Q

When should T4 be measures after application of transdermal methimazole?

A

§ Timing of blood sampling does not seem to be critical to assess tx response
□ Methimazole prior to application was not significantly difference from any other time point
○ Transdermal methimazole (pluronic lecithin ogranogel) applied 2.5 mg q12hrs or 5 mg q24hrs
§ Sustained release was noted leading to prolonged suppression of T4 over 24 hours in both groups

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20
Q

What is known about RAAS activation and development of hypertension in hyperT4 cats?

A

○ RAAS Activation occurs in hyperT4 cats, BUT is NOT associated with development of hypertension
§ Plasma renin decreased after tx
§ Plasma aldosterone decreased after tx in normotensive group but did not change significantly in the hypertension-post tx group
□ Plasma aldosterone NOT influenced by changes in plasma renin in hyperT4 cats that developed hypertension after tx
® Possible RAAS dysfunction in these cats

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21
Q

What is true about the plasma amino acid profiles of hyperT4 cats?

A

○ Plasma amino acid profiles in hyperT4 cats and controls were similar
§ HyperT4 cats have significantly lower L-glutamine than controls
□ Lower: tryptophan, d-hydroxylysine
□ Higher: Cystine, citrulline, Amino butyric acid, L-asparagine, L-Alanine
§ Tyrosine, phenylalanine, iodine, and selenium NOT significantly different among with coat color or hyperT4
□ Light and dark cats OR cat w/hyperT4 or w/o hyperT4

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22
Q

Can NT-proBNP and cTNI be used to distingusih hypertrophy from hyperT4 from primary HCM in cats?

A

NO! ○ Neither NT-proBNP or cTNI distinguished hypertrophy associated with hyperT4 from primary HCM in cats
§ Both groups had higher biomarkers than controls (but not different)

HyperT4 cats (3 months after I131 tx) = Significantly lower plasma NT-proBNP and cTNI (ventricular wall thickness too)

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23
Q

What was seen with NT-proBNP and cTNI in cats with hyperT4 3 months after I131 tx?

A

HyperT4 cats (3 months after I131 tx) = Significantly lower plasma NT-proBNP and cTNI (ventricular wall thickness too)

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24
Q

After restoration of euthyroidism in cats with iatrogenic hypoT4 what happened to their creatinine?

A

§ Significant reduction in creatinine! (but also reduced BW, which could affect creat)

Significant increase in PCV, HR, ALP

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25
Q

What should be a consideration in a dog showing signs of hyperT4?

A

○ Dietary hyperT4 in dogs eating raw diet (BARF) or fed fresh/dried gullets
§ Elevated TT4 and low TSH in 12 dogs
□ CS in 6 dogs: Wt loss, aggression, tachycardia, panting, restlessness (6 dogs had no CS)
§ After diet change (8 dogs) - T4 normalized and CS resolved

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26
Q

Are baseline PTH and FGF-23 predictors of development of azotemic following tx in hyperT4 cats?

A

NO!
○ 270 hyperT4 cats (azotemic vs non-azotemic after tx): Baseline Elevated PTH, hyperphosphatemia, decreased FGF-23 and hypoCa noted
§ All parameters returned to RR with tx w/o azotemic CKD
§ After adjusting for creatinine: baseline PTH and FGF-23 were NOT predictors of development of azotemia following tx
§ Baseline FGF-23 was associated with all-cause mortality (may have some prognostic significance in hyperT4 cats)

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27
Q

How do PTH and calcitriol influence iCa in hyperT4 cats?

A

□ Thyroid hormones might influence iCa but NOT through PTH or calcitriol

	○ HypoCa (low iCa) seen in hyperT4 cats
		§ NOT associated with concurrent/unmasked CKD (higher iCa in these animals with hyperT4 than controls) or reduced calcitriol levels (higher calcitriol in hyperT4 than controls)
		§ Plasma T4 predictor of iCa after adjustment for PTH and calcitriol
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28
Q

In dogs with DM that were followed for 2 years, what vascular complications were seen?

A

§ 55% systolic hypertension, 64% diastolic hypertension
§ 73% Microalbuminuria, 55% Increased UPC
§ 20% Retinopathy
□ No significant different of time since dx of DM or glycemic control for abnormalities (no significant association btwn the abnormalities either)

Except for proteinuria (substantial in some cases) - Clinically deleterious diabetic vascular complications were NOT seen in dogs in the study

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29
Q

Based on a DIAQoL-pet, in DM dogs, how many owners reported the DM negatively impacted QOL?

A

84%

		§ Areas negatively impacting dogs/owner QOL:
			□ Worry, difficulties leaving dog w.family/friends, worry vision, boarding difficulties, worry hypoglycemia, social life, future care
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30
Q

What is known about PZI in dogs?

A

○ Protamine zinc recombinant human insulin (PZI) is an alternative in DM dogs (17 dogs)
§ Nadir: About 10 hrs
§ Over 60 days: Significant decreased in 10 hr BG and fructosamine
□ Improvement in PU/PD (14), BW stable/increased (16)
§ Adverse event: Hypoglycemia

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31
Q

What is true regarding DM in Elkhounds?

A

• DM in Elkhounds develops during diestrus and pregnancy (11% at dx)
○ Higher GH and lower progesterone compared to age matched controls
○ Immediate OHE (46%) improved prognosis for remission of DM
§ Lower remission if high BG at dx and long time (wks) til sx

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32
Q

How does glucosamine affect fructosamine in dogs?

A

• No significant change in serum fructosamine in healthy dogs (21 days) of glucosamine-chondroitin sulfate compared to placebo
○ Did not affect glycemic control or result in DM

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33
Q

What are conditions in dogs that result in hyperfructosaminemia?

A 
DM
Obesity
HypoT4
Monocolonal IgA Gammopathy
Dietrus/Pregnancy

Drugs (cyclosporine, prednisolone)

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34
Q

What are conditions in cats that result in hypofructosaminemia?

A

Hyperproteinemia

HyperT4

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35
Q

What are conditions in dogs that result in hypofructosaminemia?

A 
Hypoalbuminemia
Insulinomas
Azotemia
Hyperlipidemia (high TG and cholesterol)
Metabolic epidermal necrosis secondary to alpha cell pancreatic tumors

Infections (Angiostrongylus vasorum and Leishmaniasis)

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36
Q

What is known about glargine in dogs?

A

○ Glargine Use in Dogs (gave dose of 0.5U/kg SQ q12hrs)
§ All dogs (10) well regulated within 38+/- 14 days
§ Mean glargine dose: 0.5 +/- 0.15U/kg
§ When fed a high fiber (insoluble) - Glargine resulted in peakless insulin that does not induce a distinct BG nadir
□ Min BG: 163 within 2 hrs of administration

Max BG: 230 within 12 hrs of administration

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37
Q

What has a relevant impact on glucose readings with glucometers?

A

○ HCT had a relevant impact on correlation btwn whole blood (glucometeres) and plasma (analyzers) in dogs
§ Glucometers (vet) more closely correlated with glucose when HCT was within or above RR

Glucometers (human) more closely approximated glucose in anemic dogs

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38
Q

What should not be used to measure BG on a dog under anesthesia?

A

○ Continuous Glucose Monitoring System should NOT be used to monitor BG in a dog under anesthesia
§ CGMS significantly different BG from glucometer during anesthesia
□ Differed by >20% on 42.9% of the paired measurements

Hypoglycemia 19.8% on CGMS by only once was detect by glucometer

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39
Q

What is the Glucagon Stimulation test?

A

Alternative to glucose tolerance test - Assess Residual B cell function in hyperglycemic peoplas, used to identify ACTH and GH def

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40
Q

What could be used in an ER situation of hypoglycemia at home?

A

SQ Glucagon (1 mg)

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41
Q

Can SQ glucagon do used in dogs to dx corticotrophic insufficiecny?

A

□ SQ glucagon did NOT increase cortisol or ACTH concentrations during study (Little use in suspected Corticotrophic insufficiency!!)

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42
Q

What is an alternative to regular insulin in DKA dogs?

A

○ Lispro insulin as CRI (0.09U/kg/hr) vs regular insulin CRI for DKA dogs
§ Lispro was safe and just as effective (12 dogs)
□ Biochemical resolution of DKA with lispro was significantly shorter (26h) compared to 61hr in dogs with regular insulin

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43
Q

What is an alternative to regular insulin in DKA dogs?

A

○ Lispro insulin as CRI (0.09U/kg/hr) vs regular insulin CRI for DKA dogs
§ Lispro was safe and just as effective (12 dogs)
□ Biochemical resolution of DKA with lispro was significantly shorter (26h) compared to 61hr in dogs with
regular insulin

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44
Q

What lifestyle risk factor is associated with progesterone related DM in Elkhounds?

A

Increased odds if overweight (owner perceived), diet not factor once controlling for BCS

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45
Q

What is known about Streptozotocin in sinulinoma dogs given q14 days?

A

• Streptozotocin in dogs with insulinoma (19): Given q2weeks (with saline diuresis and anti-emetics)
○ No myleosuppression noted
○ Mild to moderate GI toxicity
○ DM in 8 dogs (6 of which euthanized)
○ 2 nephrotoxicity (Fanconi syndrome and nephrogenic DI)
○ Increased ALT 6
○ Median progression free survival: 196 days and MST 308 days

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46
Q

Can the CGMS be used in cats?

A

YES! ○ Guardian REAL (continuous glucose monitoring device) is clinically accurate in cats with hyperglycemia (96.1%), euglycemia (100%) but slightly less accurate at low BG (91%)
§ Paired readings had good concordance 95.7%
§ Median delay after IV glucose to interstitial glucose = 11.4 mins

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47
Q

How do glaragine and detemir differ in healthy cats?

A

Onset of Action: 1.8 hrs detemir and 1.3 hr glaragine

	○ Some had relatively flat curves, others had peaked curves
	○ Shorter duration of action than in humans = Useful for q24hrs in some cats
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48
Q

What are the predictors of clinical remission in cats with DM?

A

Age, BW, Cholesterol, Glucose

50% (45/90): Remission
§ Achieved remission: median 48 days
§ Remission Duration: median 114 days (died) and 151 days (alive)
§ Remission more likely: Higher Age
§ Remission less likely: Increased cholesterol
§ Longer remission with higher BW
§ Shorter remission with higher BG

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49
Q

What is known about the arginine stimulation test in predicting clinical remission in cats with DM?

A

○ Arginine Stimulation Test (IV arginine to assess residual insulin and glucagon secretion) CANNOT predict remission in DM cats
§ 41% (7/17) went into remission
§ BG significantly lower in cats with remission (389 vs 506) - Lots of overlap!!!

Higher AUC of glucagon-to-insulin ratio in cats with remission - Large overlap btwn groups

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50
Q

Which diet resulted in a high postprandial glycemia in healthy cats?

A

Diet high in carbs compared to high fat vs high protein diets (5 weeks in healthy cats)

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51
Q

Which polymorphism has been associated with DM and overweight DSH?

A

Melanocortin 4 receptor (MC4R:C.92C>T)

	○ Similar to humans: MC4R associated with obesity and DM (role in energy balance and appetite regulation)
	○ No difference in nondiabetic overweight and lean cats
	○ Overweight diabetics: 55% homozygous for allele compared to 33% lean diabetics and 30% nondiabetics
		§ Significant difference btwn overweight DM and non-DM cats
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52
Q

What is the glucose status of cats with DM in remission?

A

§ 21 cats in remission: 19% Impaired fasting glucose; 76% impaired glucose tolerance = Considered “Prediabetic”

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53
Q

What are predictors of relapse from remission in DM cats?

A

§ Predictors of relapse: Severe glucose intolerance (>5hrs to return to BG 135)
§ Need ongoing glucose monitoring in cats in remission

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54
Q

Based on Randomized, prospective study (30 newly DM cats), what results in decreased insulin requirements in the following 6 months?

A

IV insulin for 6 days (tight glycemic control - 90-180) compared to standard glargine dosing

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55
Q

In newly diagnosed cats with DM what is the prognosis and what is associated with a shorter survival?

A

• In 114 newly dx DM cats: Median survival 516 days (1-3,486 days) = Far to good prognosis
○ Lived longer than 3 months (70%), 6 months (64%), 24 months (46%)
○ Significantly shorter survival time in cats with higher creatinine at dx
§ Hazard of dying 5% greater for each 10ug/dl increased in creatinine
○ DKA was NOT associated with survival time (NOT considered unfavorable)

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56
Q

What is wrong with compounded PZI?

A

• Comparison of commercially manufactured PZI (112 vials) vs compounded PZI (12 pharmacies, 8 vials from each)
○ All commercial PZI met USP specifications
○ Only 1 compounded PZI met USP specifications!!!
§ Endotoxin, not enough zinc, different concentrations!!
○ DO NOT USE COMPOUNDED PZI

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57
Q

In non-diabetic cats what is associated with increased BCS?

A

Increased BCS (obesity measure) associated with increased in circulating Islet Amyloid Polypeptide (IAPP) and insulin in NON-DM cats

58
Q

What is known about the mean plasma IAPP in DKA cats?

A

Mean IAPP significantly reduced in DKA cats compared to non-DM cats (BCS 6-8) and DM (Not DKA) cats

Islet Amyloid Polypeptide

59
Q

What is known about IGF-1 and lymphoma?

A

Lower IGF-1 in cats with lymphoma regardless of the method used

60
Q

In DKA patients when was the CGMS more accurate?

A

When the patient was more hydrated

61
Q

What is an alternative for regular insulin in DKA patients?

A

IM Glargine (q2+hrs) administered with SQ glargine (q12hrs)

62
Q

What was the remission rate of detemir in cats with DM?

A

• Use of detemir in 18 DM cats
○ Overall remission 67% (81% if on detemir first, 67% if 6 months after dx)
○ No significant difference in outcome compared to glargine (online)
§ But Detemir group: Slightly older, more CKD, lower max detemir dose (all likely interreleated factors)

63
Q

What is a more sen, spec, and accurate measure of urine glucose in cats?

A

Purina Glucotest (litter additive) compared to Bayer Multistix, BUT not up to 8hrs (which they claim)

64
Q

What is known about multiple endocrine disease in cats?

A

• Multiple Endocrine Disorders in cats is uncommon (15 cats)
○ Most common: DM and hyperT4 (5)
§ DM + HAC (11), Central DI + DM (1), HyperT4 +HyperPTH (1)
§ DSH, Mean age: 10.3 yrs

25.7 months elapsed btwn dx of first and second endocrine dz

65
Q

In acutely sick cats, what can be used to determine if they have DM or not?

A

• Beta-hydroxybutyrate (plasma) as a marker of DM in acutely sick cats is useful to distinguish from nonDM sick cats
○ Cut off: 0.58mmol/L B-OHB (sensitive and specific test)

Diabetic cats had significantly higher B-OHB values (1.47 vs 0.07)

66
Q

What are the major adipokines?

A

Leptin
Adiponectin
RAAS
Resistin

67
Q

What is leptin?

A 
If regulated = STOP eating
If dysregulated = " Good" leptin ignored and "BAD" leptin occur
	• Pro-inflammatory
	• Insulin Resistance
	• Atherosclerosis
	• Hypertension……
68
Q

What is adiponectin?

A

Marker of appropriate BMI
Good!! = Anti-inflammatory, increased insulin sensitivity, vasodilatory
Obesity = Decreased!

69
Q

How are RAAS and obesity related?

A

Obesity results in increased RAS = Secondary inflammation and hypertension

70
Q

What is the cross-talk btwn the adipokines?

A

Leptin stimulates angiotensin II; angiontensin II decreased adiponectin; RAS antagonism = increased adiponectin

71
Q

In what heart disease had adiponectin been increased?

A

DCM

72
Q

What has plasma adpionectin been negatively correlated with in dogs?

A

Older and neutered animals have lower adiponectin

73
Q

What is known about adipokines and feline hepatic lipidosis?

A

§ Alterations in adipokines are seen with HL
□ Increased adiponectin - Related to liver dz
® Adiponectin HIGHER in overweight cats with HL (4.5ug/ml), HL/concurrent dz (4.4ug/ml), other liver dz (1.5ug/ml) compared to healthy controls (1.5ug/ml)
® Adiponectin correlated with ALT
□ Increased Leptin - Related specially to HL
® Leptin HIGHER in cats with HL (9.8 ng/ml) or HL/concurrent dz (10.7ng/ml) compared to healthy controls (4.9 ng/ml)
◊ Cats with other liver dz (4.9 ng/ml) were similar to healthy cats
® Leptin correlated with ALP

74
Q

Which adipokine is specific for feline hepatic lipidosis?

A

Increased Leptin

75
Q

Which LEs are the adipokines correlated with in feline hepatic lipidosis?

A

Adiponectin correlated with ALT

Leptin correlated with ALP

76
Q

What has been shown in dogs in CHF with leptin?

A

§ CHF dogs significantly HIGHER leptin than controls

77
Q

What is known about myocaridal leptin in heart dz dogs?

A

§ Myocardial leptin significantly HIGHER in acquired and LOWER in congenital heart disease compared to controls
§ Dogs in FH stage D higher myocardial leptin than dogs in Stage C3 and B
§ Difference in myocardial region = Higher leptin in atria compared to ventricles in heart dz dogs

Females with heart dz HIGHER leptin than males

78
Q

What significantly increase circulating adiponectin in healthy non obese dogs?

A

Fish oil supplementation

79
Q

How was salivary cortisol correlated with salivary cortisol?

A

○ Salivary cortisol correlation with plasma cortisol (it was higher dogs with hypercortisolism compared to controls), not affected by time of day or location of collection
§ BUT hard to collect enough saliva for test (failed in 88/326 controls and 15/30 hypercortisol dogs)

80
Q

When using AUS and there is equivoval adrenal asymmetry, what is the cut off for the smaller adrenal gland for ACTH independent (adrenal mass)?

A

○ Cases with equivoval adrenal asymmetry a maximal dorsoventral thickness of smaller adrenal gland ≤ 5 mm was the cut off for ACTH independent HAC (adrenal tumor) with ultrasound diagnosis

81
Q

What was the difference in MST for dogs with adrenal tumors (HAC) treated with trilostane vs mitotane?

A

○ 37 dogs with adrenal tumors (8 had mets) = No significant difference in MST btwn trilostane (13: MST: 353 days) compared to mitotane (22: MST: 102 days) treated dogs
§ Significantly lower probability of survival for dogs with metatstaic disease regardless of tx

82
Q

Can CT be used to differentiate types of HAC?

A

○ Using CT (cross-sectional measurements of adrenal glands) is of little use to differentiate HAC in dogs = LOTS OF overlap

Maximal adrenal diameter ratio >2.08 highly suggestive of Adrenal dependent cushings

83
Q

What has been demonstrated in PDH dogs regarding renal function after tx?

A

○ 19 PDH dogs (tx with trilostane or sx) - Decreased GFR (creatinine and iohxol clearance) and persistent proteinuria (5/3 dogs at 12 months post tx) - Need to consider renal changes in PDH patients
§ Serum creat/BUN did increased post-tx but within RR
§ Decreased in UPC, urine albumin, IgG, and RBP post tx (no change in NAG)

84
Q

Is there a difference in dogs trilostane in PDH dogs by mg/kg or total daily dose?

A

○ 70 dogs with PDH (tx with trilostane for 6 months and doing well per owners)
§ No significant difference in dose in mg/kg vs total amount trilostane required daily to control CS, EXCEPT in dogs >30 kg

Dogs >30kg (and possibly >15 kg) - Might require smaller amounts of trilostane per dose or per day than those weighing less to control PDH associated CS

85
Q

Which two sex hormones are also be elevated post-ACTH stim in HAC dogs?

A

○ Serum progesterone and 17-hydroxyprogesterone (post-ACTH stim) were useful to dx HAC = BUT NOT more sensitive or specific than cortisol

86
Q

What was found with low dose q12 dosing of trilostane compared to high dose q24 hrs?

A

○ 16 PDH dogs (tx with low dose trilostane (0.78 mg/kg q12hrs) compared to high dose trilostane (30 mg/dog q24hrs) = Dogs were

87
Q

Can ACTH stimulation be replaced with baseline cortisol, eACTH, or cortisol/ACTH ratio in dogs on trilostane?

A

NO!
○ Monitoring trilostane tx with ACTH stim CANNOT be replaced with baseline cortisol, eACTH, or cortisol/ACTH ratio (40 dogs with PDH on trilostane)
§ Baseline cortisol >4.4ug/dl was reliable dx of inadequate controls (BUT only in 12%)
§ No difference in eACTH btwn groups

LOTS of overlap with cortisol/ACTh ratio (inadequate if >15, but this only in 4% tests)

88
Q

Can hair cortisol be used to diagnose HAC?

A

○ Hair cortisol concentrations were higher in dogs with HAC compared to sick control dogs, and control dogs = BUT LOTS of overlap
§ Cut off for HAC: 1.93 pg/mg (91% sen; 61% spec)

89
Q

Are there any clin path changes that will predict hypercoagubility in dogs with HAC?

A

NO!
○ Majority of dogs (88.2%) had hypercoagulable tendency (abnormalities in one assay did not predict abnormalities in others)
§ Not affected by duration of CS, comorbid conditions, or any clinpath changes

90
Q

How does the hypercoagubility in dogs with HAC change after tx with trilostane?

A

○ 19 dogs with PDH treated with trilostane (kaolin acitvated TEG-platelet mapping, protrhombin time, aPTT, fibrinogen, and antithrombin activity before and after tx, 3 and 6 months)
§ Increased alpha-angle and MA (evidence of hypercoagulbility) before and AFTER tx
§ Platelet count and fibrinogen increased at all time points
§ No change in antithrombin activity (hypercoagubility in HAC NOT related to AT def)

91
Q

Is the hypercoagbulity in HAC dogs related to antithombin def?

A

NO!

92
Q

What mutation may play a role in cortisol secretion in adrenal tumors in dogs?

A

○ 44 adrenal tumors (14 adenomas and 30 carcinomas) - Activation of cAMP signaling (G protein alpha subunit - GNAS) found in 1/3 cortisol secreting adrenal tumors in dogs - May play a role in cortisol secretion

93
Q

What was the potential positive impact of giving PDH dogs trilostane q12hrs instead of q24hrs?

A

○ Randomized study comparing PDH dogs with q12hrs vs q24hrs trilostane
§ Q12hrs trilostane might increase #dogs with good clinical response compared to q24hrs
§ NO significant difference in mean post-ACTH cortisol btwn groups
§ Baseline cortisol higher in q24hrs compared to q12hrs at 6 months
§ No difference in adverse events with either protocol

94
Q

What effects did trilostane have on cortisol, eACTH, aldosterone, Na, K, iCa, and renin?

A

○ 9 dogs with PDH tx with trilostane for 30 days (looked at 24 hr effects on cortisol, eACTH, aldosterone, Na, K, iCa, and renin)
§ Trilostane did not cause clinically relevant changes in aldosterone or K
□ Increase in aldosterone 16-20hrs and decreased K at 0.5-2 hrs
§ Optimal time for ACTH stim is 2-4 hours after trilostane (need to establish how to interpret) - Cortisol significantly decreased at 2-4 hrs

95
Q

Which adipokine was upregulated in PDH dogs compared to BCS matched controls?

A

○ 15 PDH obese dogs compared to BCS matched control dogs to check adipokines
§ Serum leptin (linear with cortisol) and insulin significantly higher in PDH compared to controls
□ Decreased in leptin and insulin after trilostane tx (9 dogs)
§ No difference in adpionectin, resistin, TNFa, IL-1B, IL-6, IL-10, IL-18

96
Q

What is the aldosterone secretory reserve in dogs with PDH tx with trilostane and mitotane?

A

○ Decreased aldosterone secretory reserve (based on post-ACTH aldosterone) is a sequela to tx with mitotane and trilostane in PDH dogs (more common with mitotane, 78% compared to 49% in trilostane)
§ Decreased aldosterone reserve cannot predict the serum electrolytes
§ Need to check at 30 and 60 mins post (to identify more cases)

Aldosterone should be measures in tx PDH dogs showing CS of hypoadrenocorticism

97
Q

What was a negative prognostic indicator in adrenal tumor dogs?

A

Weakness at presentation has a worse prognosis

98
Q

Was there a difference in post-ACTH cortisol in stims performed 2 hr post pill vs 4 hrs?

A

○ 21 dogs treated with trilostane for at least 30 days (ACTH stim performed 2 hr and 4 hr post pill)
§ Significant difference in postACTH stim performed at 2 hrs vs 4 hrs post pill (2 hr post pill had significantly lower post-cortisol)
§ Need to perform ACTH stim in patient around the same time every time

99
Q

Can Spec cPL and SNAP tests be used in dogs with HAC?

A

• 20 dogs with HAC and no evidence of pancreatitis - Higher Spec cPL (491.1ug/l vs 75.2ug/L) and more + SNAP (55% vs 6%) results than healthy dogs
○ Need to be careful about using these tests in dogs with HAC to avoid false diagnosis with concurrent pancreatitis

100
Q

Do dexSP and synthetic ACTH affect eACTH results?

A

YES! ○ Dexamethasone and synthetic ACTH (given IV) can significantly and transiently reduce eACTH in healthy dogs
§ A 2 hr wash out is NOT enough time = Need to consider before or >8hrs after ACTH stim AND before or >12 hrs after LDDST for collection of eACTH

101
Q

In dogs with diabetes and HAC was there a change in insulin needs or fructosamine after trilostane?

A

○ Insulin requirements and fructosamine did NOT consistently decreased during trilostane tx in dogs with HAC and diabetes

102
Q

Can acute phase proteins be used to monitor tx with trilostane?

A

NO
○ No benefit to checking acute phase proteins for management of HAC with trilostane compared to ACTH stim
§ Significant reduction in haptoglobulin, ALP, cholesterol, and serum amyloid A after control of HAC
§ Only haptoglobulin, cholesterol, and ALP were moderately informative (Sen/Spec >70) for dz control

SAA and C-reactive protein were NOT helpful at all

103
Q

What urinary metabolite could be used to determine HAC from PHEO?

A

• High concentration of urinary normetanephrine (4X normal upper RR) = Highly suggestive of PHEO
○ Dogs with HAC also have significantly higher urinary epinephrine, norepinephrine, normetanephrine to creatinine ratios compared to healthy dogs

104
Q

How can inhibin be used to diagnose a PHEO?

A

• Adrenocortical tumors = Make inhibin; PHEO = NO inhibin
○ Adrenocortical tumors and PDH dogs had increased inhibin
○ Undetectale inhibin (in neuter dog) = HIGHLY suggestive of PHEO (sen 100%, spec 88.9%, accuracy 93.6%)
§ NOTE intact animals have significant higher inhibins than neutered (inhibin made in gonads) - Can only be used in neutered animals

105
Q

Since hypoT4 results in insulin resistance, how dog hypoT4 dogs maintain glucose tolerance?

A

Increased insulin secretion

106
Q

How does y/d diet work?

A

Iodine restricted diet that can normalize TT4 and improve CS in hyperT4 within 4 weeks

107
Q

What acquired immune mediated has been noted in hyperT4 cats treated with methimazole?

A

Myasthenia gravis

108
Q

How many hyperT4 cats become azotemic?

A

15%
Increased survival with increased USG and increased PCV

Decreased survival with increased UPC, age, and hypertension

109
Q

How many cats that undergo I131 will become hypoT4 and how many will develop azotemia?

A

40% become hypoT4

40% become azotemic (50% hypoT4 vs 33% euthyroid)

110
Q

Was DKA associated with decreased survival time in cats?

A

No! Not consider unfavorable

111
Q

What can be used to distinguished non DM sick cats from DM sick cats?

A

Beta hydroxybutyrate
Non DM 0.58
DM cats much higher 1.47 vs 0.07

112
Q

Do thrombi within pancreaticoduodensl vein affect prognosis for animals with insulinoma?

A

No!

113
Q

What is the difference in Hyperlipidemia in mini schnauzers with and without pancreatitis?

A

If hx panc= 5 x more likely to have hyperTG 71% vs no hx panc 33%
And 15x more likely to have moderate to severe hyperTG > 500

114
Q

Was there a difference in serum TG during and after pancreatitis in schnauzers?

A

No! Serum TG were not different during pancreatitis and after the episode

115
Q

What was noted in mini schnauzers with no CS?

A

Insulin resistance

116
Q

In overweight and obese dogs with peak postprandial TG > 442 where more likely to have what?

A

More likely to have cPLI> 400 but did not develop clinical pancreatitis

117
Q

In healthy dogs did fasting TG accurately predict peak concentration?

A

No, peak samples at 2,5,6 hours after meal is ideal

118
Q

How long should food be withdrew prior to TG?

A

May need to be greater than 12 hrs. In some heathy dogs at 12 hrs there TG was still elevated

119
Q

What happens in kittens with server Hyperlipidemia?

A

MODS and severe anemia

120
Q

What is primary hyperchylomicronemia?

A

Primary inherited LPL deficiency

121
Q

For pheochromocytomas what pretreatment helped to decrease mortality in dogs undergoing sx?

A

Alpha blockage with phenooxybenzamine

122
Q

Why should a beta blocker not be given to a patient with pheo until after alpha blockade?

A

To avoid hypertension

123
Q

What can a baseline cortisol of > 1.3 tell you?

A

Rule out over suppression

124
Q

What can a baseline cortisol of

A

Can rule out under control in 88% dogs

125
Q

What in the Urine can diff cushings from pheo?

A

Urine normetanephrine 4times normal = pheo

126
Q

What can be used in addisonian to monitor mineralocorticoid tx?

A

Plasma renin
Increased in dogs with addisons and decreased and normalized with tax with DOCP
Fluoro cortisone not as predictable

Sodium higher and potassium lower in DOCP compared to Florine’s

127
Q

What can be used to diagnose primary hypoadrenocortism?

A

ACTH stim

Cortisol:eACTH ratio (

128
Q

What is low in dogs with primary hypoadrenocortism even with normal electrolytes?

A

Aldosterone (and cortisol) are LOW even without electrolyte abnormalities
Suggesting that normal sodium and potassium do not mean normal function to zone glomerulosa

129
Q

What had hyperphosphatasemia in scotties been associated with?

A

Higher steroid isoenzyme of ALP
ALP that correlated with cortisol and androstenedione after ACTH stim
Suggestive of hyperadernocorticism w/o CS of cushings

130
Q

With adrenal tumors what are poor prognostic indicators?

A

> 5 cm
Mets
Vein thrombosis

131
Q

For cats with HAC what is the recommended testing and treatment?

A

Screening LDDST
Diff AUS good in 93%
Tx trilostane

132
Q

What are the chief complaints with feline HAC?

A

Unregulated DM and derm issues

133
Q

Does insulin requirement decreased with HAC tx in cats?

A

Yes decreased by 36% in cats to with trilostane

134
Q

How can ACTH precursors be using in cats with HAC?

A

POMC and pro ACTH >100 pmol/ l in cats is suggestive of HAC

135
Q

Can low dose cosyntropin 5ug/kg be used in cats for ACTH stim?

A

Yes it did just as well as the 125ug/cat

136
Q

Can PDH HAC cats have adrenals in rr?

A

Yes!

137
Q

Was UCCR increased in hyperT4 cats?

A

No but higher before and after ACTH stim cortisols

138
Q

Can the human ELISA for IGF-1 be used in cats?

A

Yes!

139
Q

Do cats with acromegaly have cardiac changes?

A

Yes they have structural and functions changes

140
Q

Which mutation is seen in sarrloos and Czech wolf dogs and GSD with pituitary dwarfism?

A

LHX3 mutation

141
Q

What type of hypertension can cats have?

A

Similar to black people

Low renin and high aldosterone

142
Q

When you have a middle aged cat with hypokalemia poly myopathy and systemic hypertension you should consider which disease?

A

Primary hyperaldosteronism
Did great with unilateral adrenalectomy none required medical management
MST 1297 days

Endocrine (4 decks)

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