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ECVIM Certifier > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Percentage of lymphocytic thyroiditis?

A

> 50 %

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2
Q

Percentage TGAA?
T4?
T3?

A

50 %
15 %
30 %

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3
Q

What breeds predisposed TGAA?

A

Beagle, borzoi (inherited)

GRet, Gt Dane, Irish setter, Doberman, OES

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4
Q

What ECG changes hypothyroidism?

A

Bradycardia, low QRS voltage, low P wave amplitude, inverted T waves
1st/2nd degree AV block

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5
Q

How many TGAA pos dogs get decreased T4/signs hypothyroidism in a year?

A

20 % decreased T4, 5 % signs, 15 % TGAA negative

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6
Q

What mutations cause congenital hypothyroidism? What breeds?

Genetic tests?

A

Nonsense TPO mutation, autosomal recessive, toy fox and rat terriers
Missense TPO mutation, autosomal recessive, Tenterfield terrier

Genetic tests available for both. Both goitre.

Also Spanish water dog/papillon

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7
Q

Sensitivity and specificity of T4?

A

89 - 100/73 - 82

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8
Q

T3?

A

10/poor

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9
Q

Free T4?

A

80 - 98/93-94 most accurate

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10
Q

TSH?

A

58-87/82-100

Normal up to 30 % hT4 dogs

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11
Q

TGAA?

A

91-100/94-100

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12
Q

T4 + TSH?

A

63 - 67/98-100

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13
Q

FT4 + TSH

A

74/98

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14
Q

What breeds have decreased T4?

A

Greyhound, Basenji, Sloughi, Saluki, Whippet

Small number Scottish deerhound, dogue de Bordeaux and giant schnauzer

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15
Q

Decreased T3?

A

Saluki, Irish Wolfhound

NORMAL in greyhounds

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16
Q

Decreased free t4?

A

Greyhound, Sloughi, Saluki, Irish wolfhound

NORMAL whippet

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17
Q

What changes T4 to T3?

A

5’deiodinase

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18
Q

What happens to TSH and GH after TRH stim in hT4 dogs?

A

Increase GH more and TSH less than healthy

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19
Q

Why are human thyroid supplements inappropriate for dogs?

A

Too much T3

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20
Q

When should thyroid supplementation starting dose be decreased?

A

Underlying heart disease, decrease 25 - 50 %

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21
Q

What drugs decrease T4?
cTSH?
Free T4?

A

T4 - Prednisolone, phenobarbital, TMPS, aspirin, clomipramine

cTSH - prednisolone, phenobarbital (may also increase)
TMPS increases TSH

FT4 - prednisolone, phenobarbital, TMPS, aspirin, clomipramine

No effect on anything - NSAIDs (ketoprofen decrease T4?), propranolol, KBr

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22
Q

What is Schmidt’s syndrome?

A

Polyglandular endocrinopathy type 2 - hypoadrenocorticism with hT4 and/or DM

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23
Q

Skin histopathology hT4?

A

Telogen preedominance, dermal thickening, erector pili vacuolation

UNCOMMON - atrophic/dystrophic follicles

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24
Q

Myopathy in hypothyroidism?

A

Increased T1 decreased T2 fibres, nemaline rod inclusion, myofiber degeneration

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25
Q

When will congenital hT4 be apparent by?

A

8w

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26
Q

Mechanism bradycardia hT4?

A

Decreased beta receptor number/function
Decreased sarcolemmal ATPase
Decreased Na K ATPase

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27
Q

Mechanism hyponatraemia hT4?

A

Aldosterone pumps require T4

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28
Q

Renal effects of hyperthyroidism?

A

Decreased TPR, decreased effective arterial filling volume, stimulation RAAS.
Sodium absorption, increased plasma volume, increased CO.
Increased chloride resorption PCT, increased tubuloglomerular feedback as decreased tubular chloride - inc GFR.

Impaired renal natriuretic peptide response.

Increased glomerular capillary hydrostatic pressure.

Increased plasma volume and decreased sodium excretion.

Increased tubular phosphate absorption.

Downregulate aquaporin, increase Na/K ATPase

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29
Q

Bilateral disease hyperthyroid cats?

A

> 66 %

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30
Q

Possible mechanisms for hyperthyroid renal injury?

A

Hyperphosphataemia, glomerular hyperfiltration, proteinuria

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31
Q

Ectopic thyroid tissue in hyperthyroidism?

A

4 - 20 %

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32
Q

Risk factors for hyperthyroidism

A

Non pure breed, canned food, cat litter, flea control, long hair, female

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33
Q

Tachycardia in hyperthyroidism?

A

Thyroid hormone positive chronotrope, increase myocardial beta receptors, decrease AV conduction time, positive inotrope

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34
Q

Predictors of azotaemia post-I131?

A

GFR, SDMA

NOT proteinuria, creatinine, USG, cystatin C

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35
Q

T/F: Cats with hyperthyroidism have a higher prevalence of subclinical bacteriuria

A

False

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36
Q

Cystatin C in HT4?

A

Increased in serum versus FIV cats and increased in urine versus healthy cats

No difference azotaemic and didn’t change with treatment

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37
Q

T4/TSH association with mortality in cats?

A

Decreased predicts 30 d mortality

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38
Q

How much feline TSH does canine assay detect?

A

40 %

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39
Q

Sensitivity T4/free T4 for HT4?

A

91/98

fT4 low specificity - increased 12 % NTI

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40
Q

Side effects thyroperoxidase inhibitors?

A

GI upset (less transdermal methimazole), hepatopathy (necrosis/degeneration/glutathione depletion), bleeding diathesis (inh vit K epoxide reductase?), cytopenia, facial excoriation, myasthenia graves

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41
Q

Negative prognostic indictors HT4 cat?

A 
Azotaemic pre-treatment (NOT POST)
Hypothyroid and azotaemic after therapy
Older
Hypertensive
Proteinuric
Male
Methimazole vs I131 tx
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42
Q

Post-I131 hypothyroidism?

A

Usually return to normal 3 months.
Increased risk hypothyroidism if bilateral/previous medical management/medical management close to I131
5 - 83 % depending on classification
57 % azotaemic (more than euthyroid) - will resolve azotaemia in 50 % if supplement
TSH most specific and sens.

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43
Q

Efficacy methimazole?

A

90 % if use BID, 54 % SID

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44
Q

Post-treatment azotaemia prevalence?

A

15 - 20 %

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45
Q

Methimazole effect on technetium scanning?

A

None - no effect iodine uptake

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46
Q

Association between methimazole and I131 efficacy?

A

None

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47
Q

Beta blockers in HT4?

A

Decrease T4 - T3 conversion
Propanolol non-selective (bronchospasm)
Atenolol B1 selective

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48
Q

Half life of radio iodine?

A

8 days

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49
Q

Can you use Y/D in cats with renal disease?

A

Might be ok - controlled phosphorous and sodium, high quality protein, supplemented with omega 3

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50
Q

Response to diet HT4?

A

90 % euthyroid

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51
Q

Mechanism of action of I131?

A

Beta particles damage hyper functional thyroid tissue (80 %) - gamma other 20 %

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52
Q

Most sensitive diagnostic for hyperthyroidism?

A

Pertechnate scan

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53
Q

Levothyroxine dosing hypothyroid cats?

A

Twice daily, short T4 half life

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54
Q

Lipid changes in canine hypothyroidism?

A

Increased cholesterol/triglyceride (75 %), decreased LDL receptors, decreased cholesterol-rich LDL entry into liver for clearance

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55
Q

Altered initial management of concurrent hypothyroidism and DM?

A

Slow intro levothyroxine 25 % dose at first as insulin requirements will decrease (improvement of receptor and post receptor factors)

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56
Q

Insulin action on adipocytes?

A

Inhibit hormone sensitive lipase and stimulates lipoprotein lipase

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57
Q

Glargine insulin characteristics?

A

Asparagine replaced with glycine, two arginine additions.

Microprecipitates at neutral pH, soluble pH 4

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58
Q

Detemir characteristics?

A

Myristic acid replaces threonine

Binds to albumin to prolong metabolism

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59
Q

Factors increasing/decreasing fructosamine?

A

Increase: hyperproteinaemia, hypothyroidism.
Decrease: azotaemia, haemolysis, hyperlipidemia, hyperthyroidism

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60
Q

DoA insulin dog?

A 
Lente 8 - 14
NPH 4 - 10
PZI 10 - 16
Glargine 8 - 16
Detemir 8 - 16 - much more potent
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61
Q

Number of HAC dogs with DM?

A

8 %, 40 % increase glucose

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62
Q

UTI prevalence in canine DM?

A

50 %

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63
Q

Histopath diabetic neuropathy?

A

Segmental demyelination, axonal degeneration

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64
Q

Diabetic renal changes in dogs?

A

Membranous glomerulonephropathy

Increased UPCR/albuminuria in 50 %

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65
Q

Factors impacting PBGM

A

Haematocrit, hypotension, hypoxia, triglycerides

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66
Q

Factors increasing the probability of DM remission in cats?

A

Protocol, shorter time since diagnosis, steroid administration, high protein low carb diet, longer acting insulins, tight control, older animal.

Less likely - plantigrade stance, increased insulin dose for glycemic control, increased cholesterol

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67
Q

GH and IGF1 effects?

A

GH catabolic - insulin resistance, carbohydrate intolerance, hyperglycaemia, DM

IGF-1 - anabolic

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68
Q

Risk factors feline DM?

A

Male, Burmese (incomplete penetrant autosomal dominant), obesity, diabetogenic drugs, high fat/high carb diet, Maine Coone, Russian blue, Siamese

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69
Q

What polymorphism do obese cats with DM have?

A

Melanocortin 4 receptor

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70
Q

Mechanisms of beta cell toxicity feline DM?

A

Misfolded amyloid deposition and cytokine infiltration.
ROS generation and apoptosis.
ER stress, misfolded protein, apoptosis.
Hexosamine biosynthetic pathway and glucose flux
Overabundant nutrient supply (glucolipotoxicity)
Advanced glucosylation end products
Inflammation
Dedifferentiation and death

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71
Q

How many cats are in DKA at DM diagnosis?

A

12 - 37 %

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72
Q

How many DM cats have hypersomatotropism?

A

25 - 30 %

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73
Q

SDMA in feline DM?

A

Decreased cf healthy cats

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74
Q

Risk factors for relapse after DM remission in cats?

A

30 - 80 % remission, 25 - 30 % relapse, < 25 % second remission
Impaired fasting glucose/impaired glucose tolerance, obesity, use of steroids.

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75
Q

Why might lente insulin have a very short duration of action in cats?

A

Shorter duration of action anyway, glucose very high, rapid drop, counter-reg hormones (glucagon cortisol epinephrine)

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76
Q

When should insulin be stopped in a cat with DM?

A

Preinsulin blood glucose consistently < 10, nadir 4 - 7 and 0.5 IU once daily for two weeks

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77
Q

Mechanism of action of glipizide? Drug class? DM cat response?

A

Stimulates potassium channel on beta cell therefore increases insulin secretion

Sulfonylurea

< 20 % remission, improvement 30 %

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78
Q

Acarbose DM?

A

Inhibit brush border disacharidase

Alpha glucosidase inhibitor

Similar to low carb diet for glucose lowering post prandial but only if 1/2 meals per day

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79
Q

Risk of CKD in DM cats?

A

44 % (versus 11 % without DM)

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80
Q

UTI in DM cats?

A

12 - 13%

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81
Q

Renal changes DM cats?

A

50 % glomerular changes, 33 % tubulointerstitial, 70 % increase UPCR/albuminuria

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82
Q

Negative prognostic indicators for feline DKA?

A

Azotaemia, hyperbilirubinemia

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83
Q

Changes in IGF1 in DM cats?

A

IGF1 predicts remission (increased) at 2w. Ternary complex (acid labile complex) and IGFB3 increased in cats achieving remission.

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84
Q

Lispro versus soluble insulin for feline DKA?

A

One study found quicker time to BG <13, other no diff.

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85
Q

Carbohydrate content for DM cats?

A

< 12 %

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86
Q

Mechanism/drug class/response nateglinide?

A

Stim potassium channel beta cells (different site cf sulfonylureas)

Meglitinide

Faster action/shorter duration cf sulfonylurea, renal excretion

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87
Q

Metformin?

A

Insulin sensitiser

Biguanide

One case report good glycemic control

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88
Q

Chromium/vandium

A

Chromium = insulin function cofactor
Vandium glycemic control, bypass insulin receptor to activate glucose metabolism in the cell - can help with receptor problems

Trace elements

Chromium increase glucose tolerance, vandium improved clin signs, PZI req, BG and fructosamine

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89
Q

Frequency of hypoglycaemia/rebound hyperglycaemia?

A

Common hypoglycaemia with 25 % rebound hyperglycaemia, however insulin resistance rare. No diff PZI/glargine

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90
Q

DoA insulin cat?

A

Lente 8 - 10 (nadir 3 - 6)
PZI 9 - 24 (nadir biphasic 1st 5 - 7)
Glargine 6 - 24 (nadir 10 - 24)
Detemir 9 - 14, more potent

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91
Q

Mechanism exenatide?

A

GLP1 agonist - remission 40 % good control 89 % cats DM versus placebo, no weight gain, decreased glycemic variability

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92
Q

PZI versus lente cat?

A

Longer duration of action, transition from lente better QoL and control

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93
Q

When is IGF-1 produced?

A

GH stimulation, in the liver, with sufficient portal insulin concentrations

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94
Q

Cause of feline hypersomatoptropism?

A

Pituitary acidophil adenoma or acidophil hyperplasia (latter = minority). Anterior pituitary.

Some produce other pituitary hormones.

Cause - organohalogenated contaminants eg polybrominated diphenyl ethers. AIP protein mutation.

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95
Q

Sex bias feline hypersomatoropism?

A

Male

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96
Q

Breed bias?

A

DSH

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97
Q

Phosphate in hypersomatotropism?

A

Increased - increased tubular absorption

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98
Q

T/F - hypersomatotopism and DM cats have increased prevalence azotaemia

A

False

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99
Q

GH sens/spec for hypersomatotropism?

A

> 10 84/95 - feline assay

Above RI 100 %

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100
Q

Prevalence CNS signs hypersomatotropism?

A

10 - 15 %

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101
Q

What does IGF1 do to somatostatin?

A

Increases - which inhibits insulin release

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102
Q

IGF-1 performance for feline hypersomatotropism?

A

84 - 100 % sens, 88 - 92 % spec. PPV 95 %.
False neg untreated DM, malnutrition, hepatic/renal failure, hypothyroidism

Decreases after hypophysectomy and pasireotide, not XRT

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103
Q

What does ghrelin do to GH? What happens in hypersomatotropism?

A

Stimulates secretion. Is decreased in hypersomatotropism.

104
Q

N-terminal type 3 procollagen polypeptide (PIIIP) in hypersomatotropism?

A

Increased versus DM cats alone, > 10 87/100 sens/spec. Decreases with hypophysectomy not XRT.

105
Q

Pasireotide mechanism of action? Response in hypersomatotropism cats?

A 
Somatostain analogue (1/2/3/5)
Decrease IGF1, insulin requirement, no change fructosamine. 21 % remission. Hypoglycaemia/polyphagia
106
Q

Hypophysectomy response hypersomatotropism?

A

Decrease (normalise) IGF1, P3P, fructosamine and insulin dose. Remission 85 %. 10 % period mort.

Contraindication large tumour/concurrent disease.

Transient CD permanent hAC.

107
Q

XRT for hypersomatotropism?

A

Reduce size and secretory capacity of tumour. Ghrelin increases, no normalisation P3P/IGF1. Sig decrease fructosamine/insulin req. 95 % decrease insulin dose. 32 % remission (permanent 62 %). 9m to lowest dose insulin. 15 % hT4. MST 1000d.

HS might progress despite DM improvement.

108
Q

Does perivascular administration of ACTH on ACTH stim for healthy dogs or those receiving trilostane for PDH?

A

No sig diff versus IV

109
Q

Possible aetiologies for ‘occult/atypical’ HAC?

A

Increased adrenal production of 17OHP due to partial 21 hydroxylase deficiency.

For - some studies all dogs with HAC inc 17OHP

Against - only female poms have inc 17OHP. Sex hormones (many) only increased 73 % alopecia X, progesterone most common 37 %. No 21 hydroxylase gene mutation identified. No HAC in oestrus/diestrus (60 - 90d). Only hair changes not other signs. 17OHP low spec (neoplasia, phaeo, nonfunc AT)

Progesterone binds cortisol receptor and increases free cortisol?

Against - ACTH not suppressed, higher in the poms

Alopecia X - some animals respond to trilostane/mitotane however inconsistent, also respond melatonin, sex hormones remain increased in many

110
Q

Mitotane mechanism of action? Response canine ADH/PDH?

A

Adrenocorticolytic, fasciculate/reticularis with selective, gomerulosa with non-selective. Inhibit CYPIIA1 (cP460 side chain cholesterol cleavage), inhibit sterol-o-transferase I (SOAT-1 - inhibit cholesterol - cholesterol Esthers), inhibit CYPIIB1 (11beta hydroxylase). Increase CYP3A4 (cortisol clearance).

FAT MST 100 - 476, no sig diff trilostane

PDH - MST 700 d

50 - 60 % relapse, less with non selective protocol

111
Q

Trilostane mechanism of action? Response canine ADH/PDH?

A

Competitive inhibitor 3betahydroxysteroid dehydrogenase (maybe 11 beta hydroxylase too) - decrease pregnenolone/17alphapregnenolone conversion to progesterone/17OHP, DHEA to androstenedione, 11deoxycorticosteroine to corticosterone, 18-hydroxycorticosterone and aldosterone, and 11deoxycortisol to cortisol.

Effective 75 % PDH, MST longer BID
MST FAT 300 - 500 d. Not sig diff mitotane.

112
Q

Concurrent trilostane and spironolactone?

A

Potentiates spironolactone

113
Q

What causes adrenal necrosis?

A

Oversecretion of ACTH

114
Q

Ketoconazole mechanism of action? Canine response?

A

Inhibit CYPIIA1 (p450 cholesterol side chain cleavage), 17 alpha hydroxylase (CYP17 - pregnenolone to 17alphaOHpregnenolone and progesterone to 17OHP), 17,20lyase (CYP17 17OHpregnenolone to DHEA and 17OHprogesterone to androstenedione) and CYPIIBI (11deoxycorticosterone down to aldosterone and 11deoxycortisol to cortisol)

50 - 75% respond

115
Q

Selegiline mechanism of action? Canine response?

A

Selective irreversible MAO B inhibitor - increase dopamine decrease ACTH.

80 % clin imp no ACTH stim change

116
Q

Cabergoline mechanism? Response canine?

A

Dopamine 2 receptor agonist, decrease ACTH.

40-60% response with decrease in ACTH, cortisol, alphaMSH, pit size and imp clin signs. Most effective small tumour. Longer survival cf ketoconazole.

117
Q

Retinoic acid?

A

Decreased transcription factor binding and POMC expression, decrease ACTH, decrease cell proliferation and induce apoptosis.

Clin imp 80 % with decreased pit size, ACTH and cortisol. Synergy with cabergoline.

118
Q

Pasireotide?

A

Somatostatin analogue (1,2,3,5). Problem - SST 2 dominates canine pituitary.

119
Q

Melanocortin 2 receptor antagonist?

A

MC2R - adrenal ACTH receptor

120
Q

Abitaterone acetate?

A

Selective CYP17 (17alphahydroxylase) inhibitor

121
Q

Steryl-o-acyl transferase inhibitors

A

Increase free cholesterol (no cleavage to cholesterol esters) - cytotoxic

122
Q

Most common place for ACTH secreting tumour?

A

Pars distalis anterior pituitary

123
Q

Hypothalamic and pituitary theories of PDH?

A

Increased CRH/vasopressin with glucocorticoid receptor defects and dopaminergic neurodegeneration, or somatic corticotroph mutation (latter more likely as CRH decreased in HAC and adenomas are monoclonal)

124
Q

When to suspect malignant adrenal tumour?

A

> 2cm or invasion

125
Q

Bilateral tumours in canine FAT HAC?

A

Up to 14 %

126
Q

Prevalence hypertension in canine HAC?

A

40 - 90 %, one study all dogs with increased platelets had increased BP, no diff PDH/FAT, DM lowered and hypokalaemia increased risk of hypertension

127
Q

Sensitivity and specificity of adrenal function tests for HAC in dogs?

A

ACTH stim: 0 - 95/59-95, less sens FAT
LDDST: NB increased dose polyethylene glycol vs sodium phosphate - 85-100/44 - 95, highest sensitivity for FAT
UCCR - 75 - 100, 21 - 100, 90 % chance PDH if > 100. Increased by hospitalisation

128
Q

Differentiate PDH and FAT?

A

> 50 % suppression at 4 or 8 hours, complete suppression at 4h then loss of suppression,

Partial, escape, inverse. In order from highest to lowest PPV.

HDDST - 65 % PDH suppress, less likely if large tumour (only get extra info 10 %)

eACTH - not perfect, overlap and misclassification

129
Q

Abdominal ultrasonography in canine HAC?

A

25 % PDH normal adrenals, highly sens/spec for identify adrenal tumour, find mets

130
Q

Skull CT in canine PDH?

A

Abnormal around half.

131
Q

Neuro signs canine PDH?

A

Develop approx 10 - 25 %, > 6m later usually

132
Q

Mechanism gall bladder mucocoele in canine HAC?

A

Increased unconjugated bile acids, increased leptin? No difference cholecystokinin concentrations.

133
Q

UTI in canine HAC?

A

10 - 50 %, urinary tract signs < 5 %, active sediment around half

134
Q

Ectopic/food associated HAC?

A

Ectopic 2 x GSD, 1 x Dachs - neoplastic

Food-dependent - GIP receptor zona fasciculata - vizsla. Octreotide blocks.

135
Q

Trilostane canine HAC ACTH goals?

A

41 - 150 post ACTH
Trough ACTH post 55 - 280
Pre-pill cortisol 40 - 139
Post-pill cortisol < 40

136
Q

Hypophysectomy outcome in canine HAC?

A

Survival > 85 % one year, recurrence 27 % (median 500d), MST 2y, most relapse free one year.

Negative factors - large tumour, old, high eACTH, extension into cavernous sinus and circle of willis or past inter thalamic adhesion, increased pituitary transforming gene 1

Recurrence - large tumour, thicken sphenoid, high UCCR, high alpha MSH

137
Q

XRT canine HAC?

A

More rapid imp neuro cf HAC. MST 500 d, less clinical improvement cf hypophysectomy.

Worse outcome - macro tumour > 2cm/neuro signs

138
Q

Adrenalectomy canine FAT HAC?

A

MST 700 - 900 d. Recurrence 30 %

Negative px - tumour > 5cm/mets

Increased mortality if thrombus (past hepatic hilus) but no decreased survival time if no periop death.

139
Q

Genetic predisposition hAC dog?

A

Standard poodle, leonberger, bearded collie, NSDTR, Portuguese water spaniel, Gt dane, , Rottweilers, wheaten terrier, westies

Female 2x risk

140
Q

What adrenal enzyme are antibodies directed at in canine hAC?

A

21betahydroxylase

141
Q

hAC inheritance?

A

Autosomal recessive standard poodle and Portuguese water dog

142
Q

Why might atypical hAC develop?

A

Less 21 beta hydroxylase in zona glomerulosa, relatively spared?

143
Q

ECG in hyperkalaemia?

A

Bradycardia, decreased P waves, spiked T waves, wide QRS, increased PR/decreased QT interval. Potassium can’t move out of cardiomyocytes in phase 3 depolarisation

144
Q

T/F - a dog with hAC is less sensitive to insulin?

A

False - more sensitive, no steroid

145
Q

NA:K ratio to aim for with DOCP therapy?

146
Q

TSH in hAC dogs?

A

Increases female dogs, with normalisation after manage hAC

147
Q

What makes up juxtaglomerular apparatus?

A

Afferent arterioles macula densa distal tubule

148
Q

What stimulates renin secretion?

A

Decrease in afferent perfusion pressure, decreased sodium in glomerular filtrate, sympathetic neutron activity after cardiac baroreceptor stimulation

149
Q

What effects does ATII have?

A

Vasoconstriction, promote tubular sodium reabsorption, , stimulate aldosterone release

150
Q

Aldosterone effects?

A

Promote sodium reabsorption in exchange for potassium and H+ - salivary glands, renal tubule, colon

Promotion of calcium, magnesium and phosphate loss (? secondary PTH?)

151
Q

Hypokalaemic polymyopathy in hyperaldosteronism?

A

Less common in adrenal hyperplasia (arterial hypertension more common those)

152
Q

Concurrent hormone secretion in feline hyperaldosteronism?

A

Progesterone - thin skin PUPD DM

Might also have increased corticosterone

153
Q

Proportion of azotaemic primary hyperaldosteronism cats?

A

50 %, usually not hyperphosphataemic

154
Q

What factors have been shown not to impact likelihood of haemorrhage for hyperaldosteronism adrenalectomy in cats?

A

Benign/malignant, presence of tumour extension, hypertension

155
Q

Best confirmatory test for feline primary hyperaldosteronism?

A

Fludricortisone suppression of urine aldosterone:creatinine ratio - consistently suppresses in normal cats.

156
Q

When does hypokalaemic myopathy occur?

157
Q

Percentage of cats with primary hyperaldosteronism and hypertension?

158
Q

What predicts survival in adrenalectomy with feline primary hyperaldosteronism?

A

Long GA decreases survival

No sig diff adenoma versus carcinoma (although adenoma numerically longer MST).

Can also get long survival medical management (900d vs 1200 surg)

159
Q

Feline CKD - prevalence of increased calcium?

A

Ionised 30 % total 10 - 15 %

160
Q

When would total calcium and ionised not agree?

A

Renal/neoplasia

161
Q

Risk factors idiopathic feline hypercalcaemia?

A

Long haired overrepresented, mean age 9y

162
Q

T/F: PUPD is common in cats with hypercalcaemia

A

False - still can concentrate urine

163
Q

Management of feline idiopathic hypercalcaemia?

A

Diet (high fibre? controversial, acidifying in general and more calcium added to offset the decreased gi transit time, CKD diets less acidifying and calcium/phos restricted but could inc vit d production due to phos restrict. canned diets more calcium restricted. diet for caox stones?)Evidence high fib and caox diet
Alendronate
Prednisolone

Therapy perhaps not required if < 0,25 above upper end of RI and no renal complications, clinical signs or stones

164
Q

Bisphosphonate mechanism of action?

A

Reduce activity and number of osteoclasts binding hydroxyapatite, Prevent bone breakdown..

Can be nephrotoxic. Oesophageal necrosis (alendronate sodium > free acid in presence of gastric juice). Jaw necrosis (high basal turnover rate, prone to necrosis bone matrix - more common if chronic admin. Zolendronate > alendronate. Dog reports not cats.).

Absorption decreased by food.

165
Q

How might steroids decrease calcium?

A

Decreased intestinal absorption, tubular absorption and skeletal mobilisation

166
Q

Magnesium in critical illness?

A

Common, with hypoK and hypoNa, longer hosp

167
Q

Purpose of Mg?

A 
Metabolism/synth of CHO, lipid, protein, nucleic acid
Oxphos/anaerobic glycolysis
Neuromuscular, cardio
Signal transduction
Intracell K/Ca conc
Immunological function
168
Q

Mg complexes with?

A

Phosphate compounds - imp cellular phosphorylation

ATP must complex with Mg for activity

169
Q

Where does Mg live?

A

99 % intracell - 70 % bone rest other tissue,.

Extracell - ionised 60 %, 25 % protein bound, 15 % complexed - less protein bound than albumin

170
Q

Where is most dietary Mg absorbed?

A

Ileum - only crosses if ionised

171
Q

What makes Mg translocate to cells?

A

Insulin, catecholamine, amino acids

FAs, citrate, can chelate Mg. Can be sequestered in saponified fat.

172
Q

Mg assoc arrhythmias?

A

Vtach/fib, SVT, AFib, prolong PR/widen QRS/peak T

173
Q

Pumps impaired by hypoMg?

A

NaKATPase, NaK, Na/K-chloride, Ca ATPase - extracell K accum and loss, urine Na loss, Ca loss, phosphate loss, impaired PTH function

174
Q

Divalent cation conversion?

A

2mEq/l = 1mmol/l=2.48mg/dL

175
Q

Mg dose in azotaemia?

A

Excreted by kidney - reduce dose by 50 %

176
Q

Mg supp cardiac SEs?

A

AV block/bundle branch block

177
Q

What Mg salt to use?

A

Sulfate can chelate Ca, use chloride

178
Q

Mechanism for excreting/increasing absorption of K other than renal?

A

Colon if renal compromised

179
Q

What does hypokalaemia due to cell membranes?

A

Hypopolarise - weakness and ileus

180
Q

Cardiac effects hypoK?

A

Prolong AP, increase automaticity, prolong ventricular repol - atrial/vent arrhythmia

Increase P decrease T wide QRS refractory class I antiarrthythmics and exacerbate digitalis cardiotox

181
Q

Breed associated hyperlipidemia?

A

Mostly triglyceride - mini schnauz

Chol and/or trig - beagle

Mostly Chol - sheltie

Chol - doberman, rotate, briard, rough collie, pyrenees mountain dog, cats

Postprandial increase trig Burmese

Hyperchylomicronemia cat lipoprotein lipase deficiency

182
Q

Manifestations of hyperlipidemia?

A

Mostly trig directed but atheroclerosis, arcus lipids and mucocoele chol also

183
Q

Evidence for manifestations of hyperlipidemia?

A

Pancreatitis - mini schnauzers with hypertrig increased prevalence pancreatitis, increased trig in mini schnauz with pancreatitis, hyperlip mini schnauzers increased PL.

Hepatic dz (vac hep/steatitis) - increased hepatic enzymes in hyperlip mini schnauzers

GBM seen in breeds predisposed to hyperlip, hyperlip more common in GBM

30 % hyper trig mini schnauz had insulin resistance

Proteinuria documented in hyper trig minio schnauz

184
Q

When to implement dietary management for hyper trig? Goals?

A

2.2, if severe aim < 4,5 to prevent glomerular damage

Diet in mini schnauz decreased < 5.6 in all, normal 30 %

185
Q

Mechanism omega 3 in hyperlipidemia?

A

Eicosapentaenoic acid and docosahexaenoic acid.

Decrease lipogenesis, increase beta oxidation, activate lipoprotein lipase

186
Q

Mechanism fibrates in hyperlipidaemia?

A

Weak agonist peroxisome proliferator activated receptor a (PPARalpha) which reg lipid and lipoprotein synth and catabolism.

Suppress FA synth, stim FA oxidation, activate lipoprotein lipase, inhibit diacylglycerol acyltransferase (convert diglyc to trigs). Increase hepatic VLDL/LDL update.

Gemfibrozil, only trig.

Urolithiasis? Liver?

187
Q

Niacin mechanism hyperlip?

A

Inhibits hormone sensitive lipase and diacylglycerol transferase. Decreased trig biosynth

NB DM (inc BG). Monitor hepatic enzymes.

188
Q

Statins in hyperlip?

A

BetaOHbetamethylglutarylCoA (HMGCoA) reductase inhibitor - blocks rate limiting step for cholesterol biosynthesis.

Atorvastatin.

Only chol. NG hepatic steatosis. Fibrates increase statin tox.

189
Q

Mutation in what breed causes hyperparathyroidism?

A

Autosomal dominant mutation Keeshond. Tumour suppressor gene?

190
Q

Prevalence of calcium oxalate calculi in dogs with primary hyperparathyroidism?

A

30 % (most asymptomatic, same with UTI which is present as frequently)

191
Q

Renal disease risk in primary hyperparathyroidism?

A

Don’t seem to be at increased risk

192
Q

Primary hyperparathyroidism recurrence rate?

A

10 %, more in Keeshond

193
Q

Distribution of histopathology in primary hyperparathyroidism?

A

87 % solitary adenoma, 8 % hyperplasia, 5 % carcinoma

90 % single gland

194
Q

What assay should be used to measure PTH?

A

Whole or intact so no fragment cross reaction

195
Q

How many primary hyperparathyroidism dogs have a nodule on cervical US?

196
Q

Management options for primary hyperparathyroidism? Success?

A

Surgery (up to 3 glands at a time) - 94 % efficacy

Percutaneous heat/ethanol ablation - both around 90 %

197
Q

Risk factors for post op hypocalcaemia after primary hyperparathyroidism?

A

> 1 gland removal, total/ionised calcium > 3.5/1.8

Very high PTH/bone ALP

One study found positive correlation of calcium pre and post op, another found increased likelihood post op Ca <1 if pre op was > 1.72

198
Q

How is vitamin D2/3 transported from intestine?

A

Digestive enzymes, chylomicrons, bile acids, transcalciferon, vit D binding protein

199
Q

Advantages of subcutaneous DDAVP?

A

More efficacious, longer duration of action, decreased cost as smaller dose, compliance

200
Q

What supports a diagnosis of CDI during a DDAVP trial?

A

> 50 % decrease in water intake

201
Q

How often does CDI develop after hypophysectomy in dogs and how often is it permanent?

A

50 %, 40 %

202
Q

What breeds have congenital CDI described?

A

Afghan, GSHP, schnauzer

203
Q

What breeds have primary NDI described?

A

Husky (X linked V2 receptor mutation)

204
Q

What do V2, V1A and V1B ADH receptors do?

A

V2 = increase aquaporin/coag changes, V1A systemic vasoconstriction renal /CNS vasodilation/platelet activation/glycogenolysis, V1B ACTH catecholamine and insulin release

205
Q

When should a water deprivation test be stopped?

A

Na > 165, 3 - 5 % BW loss, osmolality > 350, USG > 1.025 - 1.030 (dog) 1.035 (cat)

Problems with water deprivation test - partial CDI might respond to dehydration, NDI might respond to high dose DDAVP

206
Q

Mechanism of action of chlorpropamide in partial CDI?

A

Unmask constitutive receptor signalling and increase ADH receptors

207
Q

What drugs potentiate ADH action?

A

Aspirin/thiazides, may cause SIADH

208
Q

Diabetic neuropathy nerve changes?

A

Splitting/ballooning myelin and demyelination, Schwann cell injury.

Axonal degeneration only in severe

209
Q

UTI in diabetic cats?

210
Q

Definition of hyperosmolar hyperglycaemic DM?

A

Glucose > 30 Osm > 350

211
Q

Pathophys DKA?

A

No HSL inhibition, no lipoprotein lipase stim, increased FA production, hepatic ketogenesis (decreased malonyl CoA stimulation and therefore increased translocation of carnitine by carnitine palmitoyl transferase). Citric acid cycle overwhelmed.

212
Q

Cats - CKD and CHF more common which DM complication?

A

HHS, Panc/heptic dz less common

213
Q

When is acetoacetate transformed into betahydroxybutyrate?

A

In presence of hydrogen ions.

214
Q

When should a pituitary mass in PDH dogs have additional management?

215
Q

ECG changes in hypocalcaemia?

A

Prolonged QT interval, tachyarrhythmia

216
Q

Proportion of animals with MG change in primary hypoparathyroidism?

A

75 % low - causes functional decrease in PTH activity

217
Q

ECG changes to monitor for during calcium supplementation?

A

Short QT/bradycardia/VPC/ST elevation

218
Q

Why is calcium carbonate useful in primary hypoparathyroidism?

A

Carbonate binds intestinal phosphate, stim endogenous calcitriol production

219
Q

Problems with ergocalciferol?

A

Long time to saturate (very fat soluble), long half life, minimal vit D receptor affinity. But is cheap.

220
Q

Calcitriol mechanism of action?

A

Programs undifferentiated enterocytes to increase intestinal calcium transport (twice daily is useful)

221
Q

Thiazide diuretic and calcium?

A

Decrease calciuresis

222
Q

Histopath neuro changes from prolonged hypoglycaemia?

A

Necrosis in cerebral cortex

Also cerebral oedema

223
Q

% mets in insulinoma?

224
Q

Streptozoocin mechanism of action?

A

Selective beta cell destruction.

NB nephrotox

225
Q

Where is diazoxide metabolised?

226
Q

What diuretics enhance diazoxide action?

227
Q

Ki67 in insulinoma?

A

Index prognostic - positive have shorter symptom free interval

228
Q

What osmolality would you expect in SIADH?

A

Low - < 275

229
Q

What gene mutation causes congenital hyposomatotropism in dogs?

A

LHX3, autosomal recessive, GSD, sarloos wolfdog, czechoslocakian wolfdog, Karelian bear dog

230
Q

What tests could diagnose canine hypersomatotorpism?

A

Measure GH, measure IGF1, GHRH/somatostatin/glucose suppression tests

231
Q

What tests could diagnose canine hyposomatotropism?

A

IGF1, GHRH/clonidine/xylazine/ghrelin stim, genetic test

232
Q

What concurrent hormone deficiencies might be present with hyposomatotropism in dogs (congenital)?

A

TSH, prolactin, gonadotropin (rare ACTH)

233
Q

How might you treat congenital hyposomatotropism?

A

Porcine GH, medroxyprogesterone

234
Q

What impact does lack of GH have on kidneys?

A

Poor glomerular development, get azotaemia

235
Q

How many cats with HAC have detectable pituitary masses?

236
Q

How many cats with HAC are hypertensive?

237
Q

How to diagnose feline HAC?

A

LDDST (but with 0.1mg/kg) 10 - 20% normal cats don’t suppress with reg dose. This can distinguish HAC from DM..

ACTH has poor sensitivity and affected by HT4

UCCR poor spec

238
Q

How to differentiate feline PDH from FAT?

A

LDDST: escape or partial (4 or 8)

HDDST

UCCR LDDST combo(> 50 % PDH suppress)

AUS (93 % sens)

eACTH (not affected by DM or hypersomato) - 73 % sens PDH

239
Q

Management of feline HAC?

A

Medical MST 617 d, 36 % will have decreased insulin requirements

Mitotane MST 2 - 63m

Metyrapone (11 betahydroxylase inhibitor)

Adrenalectomy (high mort - 50 - 70 % survival > 1y)

XRT - MST 17m, imp neuro, HAC and DM

240
Q

T/F: measurement of urine aldosterone is useful to diagnose hyperaldosteronism in dogs?

A

False - no aldosterone and no aldosterone-18-glucuronide

Measure aldosterone

241
Q

What catecholamine requires steroids?

A

Epinephrine - cortisol in adrenal venous effluent stimulates PNMT

242
Q

What might cause a false positive normetanephrine in a dog?

A

HAC - use 4x upper RI to dx phaeochromocytoma

243
Q

T/F: phaeochromocytomas are often mineralised

A

False, usually not

244
Q

What positive stain is found in pheochromocytoma?

A

Chromogranin A

Only mets distinguish malignancy

245
Q

MST phaeo post adrenalectomy?

246
Q

How to diagnose zollinger Ellison syndrome?

A

Gastrinoma. Increased gastrin decreased gastric pH. Calcium/secretin stim.

247
Q

What amino acids might be decreased with glucagonoma?

A

Arginine, lysine, histidine

248
Q

What breeds of cats have congenital hypothyroidism described?

A

Abyssinian and DSH - dysmorphogenesis, autosomal recessive

249
Q

What skeletal changes are identified in congenital hypothyroidism?

A

Epiphyseal dysgenesis in the vertebral bodies and long bones

250
Q

How many canine thyroid masses are carcinomas? Follicular?

A

90 % (size not predictor)

70 % (thyroglobulin staining), remainder medullary ?(calcitonin)

251
Q

How many beagles with thyroiditis get thyroid neoplasia?

252
Q

How many thyroid neoplasia in dogs are productive?

253
Q

What predicts malignancy in thyroid neoplasia dog?

A

Capsular invasion

254
Q

Management of canine thyroid neoplasia?

A

Surgery MST 3y (similar bilateral)

RT - variable but can be years PFI, max tumour reduction at 8 - 22m 50 % die of metastatic disease

Chemo - cisplatin MST 11m

I131 - stage 2 - 4, 12 - 34m MST, longer if combine with surgery

255
Q

Sensitivity of imaging for insulinoma?

A

AUS 56 % CT 71 %

256
Q

Negative prognostic factors for insulinoma?

A

Post op hypoglycaemia, stage II/IIIM, lack of addition of pred, postop pancreatitis

Diazoxide less MST

257
Q

What percentage of dogs with insulinoma will be normoglycemic at 14m?

A

50 % stage I, 20 % stage 2/3

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