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Endocrinology Flashcards

1
Q

How affect propanolol to glucose levels?

A

Hypoglucemia
(reason: beta blocker –> epinephrine is an incretin)

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2
Q

How affect polycytemia to glucose levels?

A

Hypoglucemia

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3
Q

Which are the main causes of hypercholesterolemia?

A
  • Diabetes Mellitus (>50% cases)
  • Hypothyroidisim (>75% cases)
  • Cushing
  • Pancreatitis (30%)
  • Obesity (>25%)
  • Cholestasis
  • Nephrotic syndrome
  • Postprandial
  • Primary (dogs: Shnauzer Miniature, Beagle, Sheetland; cats: Burmese)
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4
Q

Which are the main consequences of hyperlipidemia?

A
  • Pancreatitis
  • Hepatobiliary diseases: vacuolar hepatopathy, lipidosis, mucocele
  • Insulin resistance
  • Ocular diseases
  • Neurologic disease: seizures
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5
Q

Which are the causes of reduced IGF1 levels in cats?

A
  • Real hyposomatotropism
  • False positives: liver disease, renal disease, newly diagnosed DM, lymphoma
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6
Q

Which is the prevalence of feline hypersomatotropism?

A

18-32%

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7
Q

Which is the PPV of a high IGF1 in a cat with hypersomatotropism?

A

95%

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8
Q

Why some cats with hypersomatotropism only treated with insuline can have hypoglycemic episodes?

A

Because the tumor mantains its pulsatile GH secretion –> when GH levels are low and high insulin doses are given, there is risk of hypoglycemia.

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9
Q

Which are the potential medical treatment for hypersomatotropism cats?

A
  • Pasireotide: somatostatin analogue
  • Cabergoline: dopamine D2 agonist (D2 R in the cat’s hypophyisis)

Remision rate ~85% with hypophysectomy (remission occurs ~1m after tt); ~25% with medical treatment; less predictable with radiotherapy

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10
Q

Which are the main differences between hypophysary and mammary GH?

A
  • Hypophysary:
    —- Pulsatile secretion
    —- Stimulated by: GHRH, Ghrelin
    —- Inhibited by: GHIH, mammary GH
  • Mammary:
    —- Non pulsatile secretion
    —- Stimulated by: progesterone
    —- No response to GHRH, GHIH, Ghrelin
    —- Its presence inhibit hypophysary GH secretion
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11
Q

Which are the causes of hypersomatotropism in dogs?

A
  • Pituitary adenoma
  • Progestins excess –> mammary hiperplasia –> mammary GH
  • Hypothyroidism
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12
Q

Which breed is predisposed to acromegaly in dogs?

A

German Shepherd

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13
Q

What is pegvisomant?

A

GH receptor antagonist

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14
Q

Which is the source of GH for canine dwarfism treatment?

A

Porcine

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15
Q

Which is the half life of ADH?

A

6min

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16
Q

Which is the heritance of primary DIN in Siberian Husky?

A

X-linked recessive trait

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17
Q

Which is the cause of low urea concentrations in diabetes insipidus?

A

Medullary washout

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18
Q

Which is the action mechanism of thiazide diuretics for DIN treatment?

A

Decrease Na absorption from distal tubules –> decreased blood volume –> decreased GFR –> increase in Na and water reabsorption from proximal tubules –> decreased water delivery to the distal tubule and decreased water loss

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19
Q

Which are the main causes of primary hyperparathyroidism in dogs?

A
  • Adenoma (85%)
  • Hyperplasia (8%)
  • Carcinoma (5%)

Unic gland > multiple gland (<10%)

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20
Q

Which are the main signs of primary hyperPTH in dogs?

A
  • Urinary signs (urolithiasis/UTI): calcium oxalate and calcium phosphate
  • PU/PD <10%
  • Reduced activity levels and hyporexia
  • GI: inappetence, constipation

Subtle signs, progressive.

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21
Q

Which is the cervical ultrasound interpretation in a primary hyperPTH?

A

It is a very sensible technique –> 90-95% of dogs have a parathyroid nodule detected.

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22
Q

Which are the main bisphosphonates available both PO and IV?

A
  • PO: clodronate, etidronate, alendronate
  • IV: pamidronate
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23
Q

Which are the perisurgical considerations in a hyperparathyroidism?

A

The other parathyroid glands are atrophied due to the hyperproduction of the affected gland –> once it is excised, hypocalcemia can occur.
It is reccommended to administer Ca and Vitamin D postsurgery or start 12-24h previous surgery in the cases with severe pre-surgery Ca (TCa>14 or iCa>1.8).

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24
Q

Which are the main differences between hyperPTH in dogs vs cats?

A

Cats use to have palpable nodules and PU/PD is not very common.

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25
Q

Which is the etiology of primary hypoPTH?

A

Idiopathic (immune-mediated etiology suspected)

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26
Q

Which breeds are predisposed to hypoPTH?

A

Miniature Shnauzer, Poodle, GSD, Terriers

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27
Q

Which is the main difference in hypoPTH clinical signs between dogs and cats?

A

Cats tends to be inappetent and lethargic more often than dogs.

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28
Q

Which are the different ways to supplement vitamin D?

A

Calcitriol:
- Active vitamine D
- Rapid action onset (1-4d)
- Quick toxicity resolution

Alfacalcidiol:
- Inactive vitamineD –> needs hepatic activation
- Onset of action similar than calcitriol

Ergocalciferol:
- Slower and longer T1/2 than calcitriol

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29
Q

Which is the most common neuroendocrine tumor in the dog?

A

Insulinoma

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30
Q

In which conditions gastrin can be elevated without gastrinoma (false positive)?

A

Kidney disease, liver disease, gastropathies and use of antiacid drugs

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31
Q

How can be gastrinoma confirmed?

A

Provocative test with secretin and calcium. In normal dogs post gastrin is reduced, but in gastrinoma dogs it is increased.

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32
Q

Which is the enzyme needed to convert norepinephrine to epinephrine?

A

Phenyletanolamine-N-methyltransferase (PNMT)

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33
Q

Which proportion of dogs with pheochromocytoma have systemic hypertension?

A

50%

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34
Q

Which is the interpretation of the laboratory diganostic tests for phreocomocytoma?

A

Can be evaluated:
- Epinephrine
- Norepinephrine
- Metanephrine
- Normetanephrine
NE and NME are more S than E and NE (due to the continuous/autonmous production and release), specially NME.
- NE or NME >x4, very specific of pheo
- NE or NME <x4, can be a false positive due to:
—- Treatment with phenoxibenzamyne
—- Steroids
Inhibin permits to distinguish (undetectable in pheo, detectable in hyperadrenoc).

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35
Q

Why alfa adrenergics antagonists must be added before beta antagonist in a pheocromocytoma?

A

Because when beta is blocked, the vasodilation secondary to beta adrenergics is lost and a hypertensive crisis can occur.

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36
Q

How is the abdominal US of pheo?

A

Adrenal mass, with the contralateral gland of normal dimensions.
In comparison with other adrenal masses, pheo tends to invade surrounding structures and vessels more often, and tends to be less mineralized.

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37
Q

Which are the main artefactual causes of hypercalcemia?

A
  • Juvenile dogs (high Ca and P)
  • Hyperlipidemia
  • Hyperproteinemia
  • Hemolysis
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38
Q

Which are the most common causes of hypercalcemia in cat?

A
  • AKI (13%)
  • Malignancy (10%)
  • Idiopathic (10%)
  • CKD (8%)
    –> renal diseases + malignancy + idiopathic
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39
Q

With which proteins is T4 and T3 united in circulation?

A

Globulins

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40
Q

Which hormones inhibit and increase TSH production?

A
  • Inhibit: dopamine, somatostatin, serotonin, glucocorticoids
  • Increase: TRH, prostaglandins, alpha adrenergic agonist
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41
Q

Which breeds are affected by each type of canine hypothyroidism?

A
  • CENTRAL:
    —- CONGENITAL: Shnauzer
    —- ACQUIRED
  • THYROID:
    —- CONGENITAL: Toy Fox, Rat Terrier; Tenterfield Terrier, Spanish Water Dog, Papillon
    —- ACQUIRED: English Setter, Golden/Labrador R, Cocker Spaniel, Rhodesian Ridgeback, Boxer, Beagle, Shnauzer
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42
Q

Which are the stages of lymphocytic thyroiditis?

A
  • Silent: N T3/T4, N TSH, H TgAA
  • Subclinical: N T3/T4, H TSH, H TgAA
  • Clinical:
    —- L T3/T4, H TSH, H TgAA
    —- L T3/T4, H TSH, H TgAA

20% of TgAA positive euthyroid dogs develop hormonal evidence of thyroid disfunction within a year of testing, but only 5% become clinically hypothyroid.

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43
Q

Which are the most common type of autoantibodies in hypoT4?

A

Anti thyroglobulin antibodies

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44
Q

Which are the suggested reproductive disorders associated to hypothyroidism?

A
  • Female: parturient problems, reduced fertility, reduced birth weights
  • Male: no effect
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45
Q

Which is the effect of breed on thyroid hormones evaluation?

A
  • Reduced TT4:
    —- Greyhounds
    —- Whippet
    —- Salukis
    —- Basenji
    —- Dogue de Bourdeaux
    —- Irish Wolfhound
  • Reduced fT4:
    —- Greyhound
    —- Salukis
    —- Irish Wolfhound
  • Reduced T3:
    —- Salukis
    —- Irish Wolfhound
    –> Greyhound has normal T3
  • TSH: not affected by breed
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46
Q

How much time is reccommended to wait until drug administration (included thyroxine) and thyroid panel evaluation?

A

6w

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47
Q

Which is the most accurate single test for diagnosing hypothyroidism?

A

fT4

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48
Q

Which are the S/E of every hypothyroidism test?

A
  • T4: S 89-100%, E 73-82%
  • fT4: S 80-98%, E 78-94%
  • TSH: S 58-87%, E 82-100%
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49
Q

How is TSH stimulation test performed and interpreted in a hypothyroid dog?

A
  • Pre blood sample
  • Administration of TSH
  • Post 6h blood sample
    —- Post <1.3 (PPV 95%)
    —- Post >1.7 (NPV 100%)
    —- Post 1.3-1.7 suggestive of hypoth
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50
Q

Which are the objectives of hypoT4 treatment in the thyroid tests?

A
  • If levothyroxine once daily: T4 at 4-6h ~4mcg/dl
  • If levothyroxine twice daily: T4 at the high end or just above the RR 4-6h post
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51
Q

Which is the relation between visfatin and betatrophin and hypothyroidism?

A

Both are adipokines
- Visfatin: hypothyroid < healthy; hypoT4 tt produce an increase
- Betatrophin: lean hypothyroid < obese hypothyroid; hypoT4 tt produce a reduction

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52
Q

Which cat breed is predisposed to congenital hypothyroidism?

A

Abyssinian

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53
Q

Which is the most efficient way to diagnose feline hypothyroidism?

A

Combining TT4 + cTSH. When results are equivocal, further diagnostic tests such as TSHst or scintigraphy

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54
Q

Which is the scintigraphy interpretation in a feline hypothyroidism? Which ions are used?

A

Tecnetium 99 and Iode 123.
The expected finsing in an adult-onset hypoT4 is a reduction or absence of uptake of 99Tc.
In a congenital hypoT4, in cases of dysmorphogenesis, an absence of I123 uptake is expected. But uptake will be normal in cases of dyshormogenesis, but organification is defficient and abnormal discharge of I123 is observed after administration of perchlorate.

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55
Q

Which is the prevalence of feline hyperT4?

A

6-10%

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56
Q

Which is the etiology of feline hyperthyroidism?

A

There is an increased TSH stimulation (due to a more receptive thyroid gland) –> thyroid hyperplasia.
- > 50% bilateral
- 1-2% carcinoma

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57
Q

Which are the main signs of feline hyperT4?

A
  • Weight loss (88%) > polyphagia > V > PU/PD > hyperactivity
  • Less common but also possible: apathetic hyperT4
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58
Q

Which is the relevance of a palpable goiter?

A

80% of cats with hyperT4 have a palpable goiter. But normal cats can also have a palpable goiter.
Goiter of hyperT4 tends to be bigger than healthy cats, but there is no relationship between the size of the goiter and the T4 level in hyperT4 cats.

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59
Q

Which is the hemostatic status of feline hyperT4?

A

It is suspected that there is a hypercoagulable status due to:
- Increased fibrinogen levels
- Increased vWF levels
Improves with the treatment (fibrinogen increase early with I131 tt due to a secondary thyroiditis, but in few days decrease).

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60
Q

Which situations can be found when performing thyroid tests in a suspected hyperT4 cat?

A
  • Normal
  • Overt hyperthyroid: T4 and fT4 H, TSH L
  • Occult hyperthyroid: T4 N, fT4 H, TSH L
  • Subclinical hyperthyroid: T4 and fT4 N, TSH L
  • Non thyroidal illness
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61
Q

Which are the most common diseases affecting thyroid evaluation in cats?

A
  • Diabetes mellitus
  • Hepatic and renal diseases
  • Neoplasia
  • Cardiac diseases
  • Inflammatory GI/resp diseases
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62
Q

Which is the difference between fT4 in dogs and cats?

A

It is less useful in cats because it has a larger variability between cats, and some healthy/non-thyroidal cats can have fT4 above the RR

63
Q

Which are the most useful dinamic tests in canine hypoT4 and feline hyperT4?

A
  • Canine hypoT4:
    —- TSH stimulation test
    —- TRH stimulation test: not used
  • Feline hyperT4:
    —- T3 supression test
    —- TRH stimulation test: not used
64
Q

Which are the drugs used for medical hyperT4 treatment and the related adverse effects?

A

Methimazole and carbimazol (prodrug)
Propilthiouracil is not used due to hemolytic anemia.

Adverse effects:
- Severe, uncommon (only methimazole, TD > PO): thrombocytopenia, bleeding without thrombocytopenia, hepatopathy, agranulocytosis –> the drug must be stopped.
- Mild, common (carbimazole > methimazole): GI signs, facial excoriations, leukopenia with eosinophilia and lymphocitosis) –> the drug doesn’t need to be stopped.

65
Q

Which are the main characteristics of radioiodine tt?

A
  • Rapid response: in general TT4 in range/below range in 2-3w
  • Can continue decreasing until 6m
  • Post tt hypothyroidism in ~20%
  • Post tt hyperthyroidism in <5% (100% of cats with TT4 > 11.6 at 2-3w will remain hyperT4)
66
Q

Which are the predictors of hyper/hypoT4 in a cat under radioiodine tt?

A
  • HyperT4: younger, more severe clinical signs, less I131 uptake
  • HypoT4: adult, female, detectable TSH, bilateral, less severe clinical signs, more I131 uptake
    –> T4 prett is not a predictor.
67
Q

Which is the main cause of canine hyperT4?

A

Thyroid neoplasia: carcinoma (productive <10%) > adenoma (non productive)
- Folicular (70%): follicular cells
- Medullar (30%): parafollicular cells (calcitonin productors)

68
Q

Which is the main adverse effect of radioactive iodine treatment for canine hyperthyroidism?

A

Irreversible bone marrow supression

(neoplasic thyroid cells also take I131 but in lower levels than normal cells)

69
Q

Which is the rate of metastases in insulinoma?

70
Q

Which type of thyroid carcinoma have a poorer prognosis?

A

Those with metastases and of parafollicular cells

71
Q

Which proportion of dogs with insulinoma have seizures?

72
Q

Which are the causes of insulinoma clinical signs?

A
  • Effect of hypoglycemia on the central nervous system
  • Hypoglycemia-induced release of catecholamines
73
Q

Which proportion of dogs with insulinoma have a pancreatic mass detected by US?

A

56%
(has both false positive and false negatives)

74
Q

In an acute hypoglycemic crisis due to insulinoma, which is the treatment of choice?

A
  • Glucose supplementation (give as less glucose as possible to avoid rebound hypogycemia)
  • If no response to dextrose supplementation:
    —- Dexamethasone
    —- Somatostatin analogue
    —- Glucagon: it also increases insulin secretion –> important monitoring to rebound hypogycemia
75
Q

Which proportion of dogs that received surgical treatment for insulinoma develop diabetes mellitus?

A

10%
(There is no markers that permit to predict it)

76
Q

Which is the action mechanism of streptozocina?

A

Destruction of pancreatic beta cells (both in pancreas and methastases)
Nephrotoxic!

77
Q

Which is the action mechanism of diazoxide?

A

Normal conditions: high glucose –> enter the beta cell by GLUT2 receptors –> glucose is used to produce ATP –> closure of ATP-dependent K receptors –> depolarization of the cell –> opening of voltage-dependent Ca receptors –> exocytosis insulin

Dizoxide:
- Inhibit K R closure –> no depolarization –> no insulin exocytosis
- Increase gluconeogenesi
- Increase glucogenolysis
- Reduce glucose uptake by cells

78
Q

Which are the prognosis factors of insulinoma?

A

Markers of prognosis:
- Persistent postCx hypoglucemia have a poorer prognosis, whereas hyperglycemia or normoglycemia have a better prognosis
- Tumor size and mitotic index
- Stage: Stage I have a longer survival time in comparison with II and III
- No associated with prognosis: age, sex, BW, clinical signs and duration, US pancreatic mass, blood glucose or insulin concentration

79
Q

Which are the most common tumors producing an adrenal metastases?

A

Mammary, pulmonary, prostatic, gastric and pancreatic carcinoma and melanoma

80
Q

Which is the proportion of every adrenal tumor?

A
  • Cortical: 75%
  • Medular: 25%
  • Bening: 75%
  • Malign: 25%
81
Q

Which is the incidence of incidentaloma in dogs?

82
Q

Which is the etiology of an hyperaldosteronism in cats?

A
  • Primary hyperaldosteronism:
    —- Tumor related PHA (carcinoma > adenoma):
    —- Non-tumor related PHA:
    ——– Associated with CKD
    ——– Non-associated with CKD (idiopathic hyperplasia)
  • Secondary hyperaldosteronism: CKD, cardiac disease
83
Q

Which other hormones can be produced in a hyperaldosteronism?

A

Corticosterone and progesterone.
Signs ~ glucocorticoids –> axis supression –> reduce cortisol levels and adrenal mass

84
Q

Which proportion of cats with hyperaldosteronism have hyperstension?

85
Q

Is it common to fins hyperNa in a hyperaldosteronism?

A

No, due to aldosterone escape phenomenon.

86
Q

How are the renin levels in a primary and secondary hyperaldosteronism?

A
  • Secondary: increased
  • Primary: Within range or reduced
87
Q

How is the S and E of aldosterone in a primary hyperaldosteronism?

A
  • High S (90%, not 100%): because in some early cases or non-tumor related PHT aldosterone levels can be in range.
  • Low E because it cannot distinguish between primary/secodnary hyperaldosteronism
88
Q

Which are the main hormones produced by a sexual adrenal tumour?

A
  • 17OH progesterone –> bind to glucocorticoid receptor and also displace cortisol from its binding proteins –> increase serum cortisol –> signs of hypercortisolism + axis supression(contralateral gland atrophy)
  • Estradiol (signs of feminization)
  • Androstenidione (signs of masculinization)
89
Q

Which is the nature of most sexual adrenal tumors?

90
Q

Which are the reasons a hyperT4 cause an increase in GFR?

A
  • Vasodilation
  • RAAS activation
  • SNs activation
91
Q

Which is the relationship between creatinine, SDMA and GFR in a hyperthyroid cat?

A

In a hyperT4 cat, SDMA-creatinine and SDMA-GFR are not well correlated –> not used SDMA as the only biomarker to evaluate renal function in a hyperT4 cat.

SDMA is specific but insensitive to predict post tt CKD development (high probability to develop CKD if it is increased, but cannot discard if it is low). Once treated, there is no relationship between the changes in creatinine/GFR and SDMA.

92
Q

Which breed is predisposed to canine DM? And which is less represented?

A

+ Keeshonden
- Bóxer

93
Q

What is a Honeymoon period in canine DM?

A

In a newly diagnosed DM dog, excellent glycemic control in response to small doses of insulin due to residual beta cell function. Whin time, insulin doses needs to be increased.

94
Q

Which is the effect of glucose on urine?

A

1 g of protein or glucose –> increase 0.004 USG –>+4 gluc = increase 0.01
DM Typical USG>1025

95
Q

Which is the glucose objective in a diabetic treated dog?

96
Q

How to administer food in a dog not anxious with food?
And in dogs with once daily insulin?

A
  • Admnister the food two daily with the insulin injections, but keeping the restant food all day.
  • To give the 50% of food with insulin and the rest at 8h post insulin
97
Q

Which are the effects of exercise on DM?

A

Physical activity decrease glucose concentrations by increasing the absorption of insulin from its injection site, increasing blood flow and insulin delivery to exercising muscles, stimulates translocation of glucose transporters in muscle cells, and increasing glucose disposal despite basal insulin concentrations

98
Q

Which is the difference between bolus insulin in dogs and cats?

A
  • Dogs: more rapid peak (30min), of higher magnitude and less duration (6-9h)
  • Cat: slower peak (1-8h), less magnitude and more duration (6->12h)
99
Q

Which are the insulin suspensions?

A
  • Lente: +Zn
  • NPH: + protamine
  • ProZinc: + Protamine and Zn
100
Q

Which are the causes of reductions / increases of FSA?

A
  • Reduction: hypoglycemia, hypoproteinemia, hypoalbuminemia, azotemia, hyperlipidemia, hemolysis
  • Increase: hyperproteinemia, hypothyroidism
101
Q

Which are the results of FSA in DM monitoring?

A
  • 350-450; good glycemic control
  • 450-550: moderate glycemic control
  • > 450: poor glycemic control
  • <350: hypoglycemia
102
Q

Which type of neoplasia is more common as a cause of insulin resistance?

103
Q

Which cat breeds are overrepresented in feline DM?

A

Main Coon, Burmese, Siamese, Russian Blue

104
Q

Which diabetic states can be distinguished in cats?

A
  • PreDM: 120-180
  • Subclinical DM: 180-250
  • Overt DM: >250
105
Q

Which is the prevalence of DKA at diagnosis in cats?

106
Q

Which are the percentages of remission in DM cats?

A

60% of newly DM cats enter in remission, most of them in the first 3m of treatment.
Remission cats are considered preDM, and a 30% relapse and need insulin again. <25% of newly relapse cats enter in a new remission.

107
Q

Which is the best way to monitor a cat with DM?

A

With blood glucose evaluation (because signs are very insensitive and FSA can be variable among labs)

108
Q

Which is the action mechanism of bexagliflozin for feline DM?

A

It is a renal Na-glucose-cotransporter inhibitor 2 –> 50% of filtered glucose is excreted by urine and the other 50% is reabsorbed by SGT1.
It permits to control DM in 84% of cases.
10% severe complicatios: euglycemic ketoacidosis

109
Q

Which proportion of DM cats have concurrent pancreatitis?

110
Q

Which proportion of HAC cats have DM at diagnosis?

111
Q

Which is the relationship between DM and renal disease?

A

DM can produce a glomerulopathy

112
Q

Whics is special for brain cells among their energy metabolism?

A

They don’t need insuline to glucose uptake.
They cannot use fatty acids for energy but can utilize ketones.

113
Q

Which is the main difference between DKA and HHS into the pathophiologic point of view?

A

In HHS ketone bodies production is minimal or absent because these patients possess enough insulin to limit lipolysis but not enough to counter hyperglycemia (–> HHS sever hyperglycemia with sOsm >320)

114
Q

How are the electrolytes in a DKA?

A

Theu use to be low, except K at early phases than can be increased (due to acidosis and insulin defficit, moving K to extracellular space).

115
Q

How to calculate corrected Na

A

Corrected Na = 1.6 x ((glucose -100)/100) + mesured Na

116
Q

Which ketone bodies contribute to acidosis?

A

Betahidroxibutirat and acetoacetate, because both dissociate to H+.
In contrast, acetone doesn’t contribute to acidosis because it doesn’t dissociate.

117
Q

Which is the expected velocity of glucose reduction in a DKA/HHS treatment?

118
Q

Which molecules stimulates/inhibits CRH production?

A
  • Stimulate: IL1, IL6 and TNF alpha, leptin, dopamine, vasopresin, ATII
  • Inhibition: glucocorticoids, somatostatin
119
Q

Which are the adrenal cortex layers?

A
  • Glomerulosa: presence of aldosterone synthase and defycit of 17alfa hydroxylase –> synthesis aldosterone
  • Reticulada and fasiculata: presence of 17alfa hydroxylase –> synthesis of cortisol and sexual hormones
120
Q

Which is the distribution of PDH?

A
  • Pars distalis: 70%
  • PArs intermedia: 30%
121
Q

Which proportion of HAC dogs have DM?

122
Q

Which proportion of dogs with HAC have HTS?

A

More or less 80% dogs with HAC have HTS, and of them, 50% is a severe HTS. 30% of non HTS dogs develop HTS during the course of the disease.
No response completely to tt in all dogs.

123
Q

Which are risk factors for the development of HTS in dogs with HAC?

A
  • Thrombocytosis
  • Hypokalemia
  • Proteinuria
124
Q

How are the leptin and insulin concentrations in dogs with HAC?

A

Both are increased and improves with tt

125
Q

How is Ca and P in HAC?

A

Ca normal, P high.
FGF23 low. PTH high.

126
Q

Which is the most common LDDST pattern in HAC dogs?

A

Lack of supression

127
Q

Which are the possible LDDST patterns and their predictive values?

A
  • Complete supression: cortisol at 4/8h <cutoff –> no Cushing (96% NPV)
  • Lack of supression: cortisol at 4/8h > cutoff and >50% basal cortisol concentration –> Cushing (94% PPV)(cannot distinguish PDH or FAT)
  • Escape: 4h < cutoff but 8h > cutoff –> possible PDH (PPV 40%)
  • Inverse: 4h > cutoff but 8h > cutoff –> possible PDH (PPV 40%)
  • Partial supression: 4/8h > cutoff but either <50% basal cortisol concentration
128
Q

How is haptoglobin modified by HAC treatment?

A

It is increased prett and with tt the levels reduced. Those animals with well controlled HAC have a lower Hp, whereas animals with bad controlled HAC have higher Hp

129
Q

Characteristics of trilostane-induced adrenocortical necrosis

A
  • Occur in 25% of dogs, and of them, 25% will remain permanent
  • Reduced production of glucocorticoids +/- mineralocorticoids (most affected layer is fasciculada)
  • Most cases are PDH
  • The duration and doses of trilostane don’t affect
  • Unknown etiology: necrosis 2ary to high ACTH due to low cortisol levels, idiosincratic reaction, trilostane toxicity
  • Abdominal US: reduced adrenals
  • USe to be associated with a concomitant disease (specially infectious disease)
130
Q

Which is the prepill or postACTH cortisol objective in a wel controlled HAC?

131
Q

Which is the most electrolytic disturbance secondary to hypophisectomy?

A

Hypernatremia

132
Q

Which alternative drugs to trilostane for HAC exist?

A
  • Mitotane
  • Cabergoline and silegiline = dopamine agonist
  • Retinoic acid
  • Ketoconazole
133
Q

Which are the main causes of feline HAC?

A

The same than dogs: iatrogenic, pituitary (85%) and adrenal (15%)

134
Q

Which are the most common concomitants diseases in cats with HAC?

A
  • Diabetes mellitus (80%) (in contrast to dogs 5-10%)
  • CKD

Hypertension only in 20% (in contrast to dogs 80%)

135
Q

Which is the most common disease causing false positive in the endocrine tests for feline HAC?

A

Hyperthyroidism

136
Q

Which is the interpretation of endocrine tests to diagnose a feline HAC?

A
  • UCCR: same interpretation as dogs
  • ACTHst:
    —- Specificity can be affected by hyperthyroidism, that increase post cortisol levels
    —- Sensitivity can be affected because cats use to have lower cortisol levels
  • Dexamethasone supression test:
    —- Start with 0.1mg/kg dexa (because cats are more resistant to the dexa supression)
    ——– High specificity –> no supression = Cushing
    ——– Low sensitivity because due to the high doses administered, some PDH cab supressed –> if we suspect a lot HAC, perform supression with 0.01.
    —- 0.01mg/kg dexa:
    ——– Low specificity due to the low doses
    ——– High sensitivity
137
Q

Which is the reason of skin fragility in feline HAC?

A

Glucocorticoid excess –> supression of fibroblast activity

138
Q

In which proportion of cases with hypoadrenocorticism the Na/K ratio is altered?

139
Q

In which proportion of cases with hypoadrenocorticism the glucose is low?

140
Q

Which are the hypothesis of a high calcium in Addison?

A

Deficit glucocorticoids –> no calcium excreted by urine.
Acidemia contributes to an increase in iCa as an excess of positively charged hydrogen ions compete for albumin binding and displace positively charged Ca ions.

141
Q

How is the additive index in an Addison?

A

Low (it depends of transtubular K gradient and sNa, and both are low)

142
Q

Which is the prevalence of Addison dogs with hypercalcemia?

A

35%
- tCa: typical Addison, higher creatinine and higher albumin –> due to DH?
- iCa: younger, lower K –> RAAS activation due to secondary renal disease?

143
Q

Which test can be used to diagnose Addison in cases of non disponible synthetic ACTH?

A
  • Cortisol:eACTH ratio (low in Addison)
  • UCCR: <1.4 100% S and 97% E
144
Q

If a dog has received prednisone, how many hours we have to wait until performing ACTH st?

145
Q

Which are the main characteristics of feline hypoadrenocorticism?

A
  • Clinical and clinicopathological features similar to dogs
  • Predisposition in British Shorthair
  • K tend to be lower than dogs
  • Slower response to treatment than in dogs
  • Needs higher doses of DOCP (2.2) and steroids (0.3)
  • Can be caused by an adrenal infiltration –> poorer prognosis (but excellent if it is an idiopathic disease)
146
Q

How are Ca, P, PTH and vitamin D in 2ary hyperPTH and rickets?

A
  • Secondary hyperPTH: PTH increased, vitamin D increased, Ca normal/low, P low
  • Rickets: PTH increased, vitamin D low, Ca and P normal/low
147
Q

Which prevalence of hyperT4 cats have HTS?

148
Q

Which vitamin D disorders in dogs and cats can we found?

A
  • Congenital:
    —- Vitamin D dependent rickets type 1A
    —- Vitamin D dependent rickets type 1B
    —- Vitamin D dependent rickets type 2A
  • Acquired:
    —- Deficyt:
    ——– PLE
    ——– IPE
    ——– Acute pancreatitis
    ——– Liver diseases
    ——– Renal diseases
    —- Excess:
    ——– Endogenous: granulomatous diseases, immunemediated diseases
    ——– Exogenous: high vit D diet, drugs and toxics
149
Q

Which are the causes of low IGF1 in cats?

A
  • Real hyposomatotropism
  • False positives: liver disease, renal disease, newly diagnosed DM, lymphoma
150
Q

Whichs is the prevalence of cats with hypersomatotropism without DM?

151
Q

Which is the evolution of dogs with positive TgAA?

A

20% of dogs with positive TgAA will develop analytic abnormalities compatible with hypoT4, but only 5% will develop clinical signs

152
Q

Which factors are associated with DM remission?

A
  • Low CH diet
  • Long acting insulin
  • Higher age
  • Lower maximum dose of insulin
  • Early institution of tight glycemic control
  • Recent corticoisteroid administration
  • Absence of neuropathy
  • Lower mean blood glucose
  • Lower cholesterol concentrations

Certifying Examination (10 decks)

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