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ACVIM Generals > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

From what structure does the anterior lobe of the pituitary develop?

A

Adenohypophysis (which develops from Rathke’s pouch)

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2
Q

From what structure does the posterior pituitary develop?

A

Neurohypophysis

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3
Q

The neurohypophysis is an extension of what?

A

The hypothalamus

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4
Q

T/F: The anterior pituitary is a collection of nerve endings that stores and releases hormones produced by the hypothalamus.

A

False: it’s the POSTERIOR pituitary that does this

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5
Q

What are the five cell types of the anterior pituitary?

A
  1. Corticotrophs
  2. Thyrotrophs
  3. Gonadotrophs
  4. Somatotropin’s
  5. Lactotrophs
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6
Q

What hormone from the hypothalamus stimulates corticotrophs and what does it cause them to release?

A

Corticotropin-releasing hormone (CRH) stimulates them to release adrenocorticotropic hormone (ACTH)

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7
Q

What hormone from the hypothalamus stimulates thyrorophs and what does it cause them to release?

A

Thyrotropin-releasing hormone (TRH) stimulates them to release thyroid-stimulating hormone (TSH)

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8
Q

What hormone from the hypothalamus stimulates gonadotrophs and what does it cause them to release?

A

Gonadotropin-releasing hormone (GnRH) stimulates them to release leuteinizing hormone (LH) and follicle stimulating hormone (FSH)

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9
Q

What hormone from the hypothalamus stimulates somatotrophs and what does it cause them to release?

A

Growth hormone-releasing hormone (GHRH) stimulates them to release growth hormone (GH)

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10
Q

What hormone from the hypothalamus stimulates lactotrophs and what does it cause them to release?

A

It’s unknown what acts on lactotrophs to stimulate release, but they secrete prolactin

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11
Q

What is the inhibitory hormone of somatotrophs?

A

Somatostatin (aka growth hormone inhibitory hormone). It is the same somatostatin that is found in the GIT, just located in the brain

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12
Q

What is the inhibitory hormone that acts on lactotrophs?

A

Prolactin inhibitory hormone (PIH)

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13
Q

Does the posterior pituitary produce hormones?

A

NO - it stores and releases hormones produced in the supraoptic and paraventricular nuclei of the hypothalamus

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14
Q

What hormone is produced by the supraoptic nuclei and what is its function?

A

Vasopressin/antidiuretic hormone (ADH) —> acts on V2 receptors in the collecting ducts of the nephron which results in insertion of aquaporin-2 channels for reabsorption of water

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15
Q

What hormone is produced by the paraventricular nuclei and what is its function?

A

Oxytocin —> causes uterine contraction, lactation, and promotes maternal nurturing behavior

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16
Q

Growth hormone is also known as what?

A

Somatotropin

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17
Q

What are the functions of growth hormone?

A
  1. Increase protein synthesis
  2. Increase mobilization of fatty acids from adipose tissue —> lipolysis and fatty acid oxidation (protein-sparing effect) during fasting
  3. Decreased utilization of glucose throughout the body
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18
Q

What molecule mediates most actions of growth hormone?

A

Insulin-like growth factors (IGFs) aka somatomedins

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19
Q

Where is IGF-1 predominantly made?

A

Liver —> will be produced in response to GH

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20
Q

Development of IGF-1 within the liver from the action of growth hormone is dependent on what?

A

Insulin

If you have a diabetic that has not been treated with insulin yet they could have falsely low IGF-1 levels just because there isn’t enough insulin in the portal vein

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21
Q

IGF-1 has inhibitory effects on GH production through what effects?

A
  1. Direct inhibition of GH
  2. Upregulation of somatostatin which will result in decreased GH production by the hypothalamus
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22
Q

What hormone will influence release of GH from the pituitary?

A

Ghrelin

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23
Q

GH predominates in the __ state

A

Fasting

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24
Q

GH has insulin __

A

Antagonism

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25
Q

Insulin-like activity INCREASES/DECREASES in response to IGF-1

A

Increases

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26
Q

What non-hormone factors stimulate growth hormone secretion?

A
  1. Decrease BG
  2. Decreased FFA
  3. Increased amino acids
  4. Starvation, fasting, protein deficiency
  5. Trauma, stress, excitement
  6. Exercise
  7. Testosterone, estrogen
  8. Deep sleep (stages II, IV)

Remember hormones are GHRH and ghrelin

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27
Q

What non-hormone factors inhibit GH secretion?

A
  1. Increased BG
  2. Increased FFA
  3. Aging
  4. Obesity

Remember hormones are GHIH (somatostatin) and Somatomedins (IGFs)

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28
Q

Pituitary dwarfism is also known as

A

Congenital hyposomatotropism

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29
Q

What dog breeds are typically associated with pituitary dwarfism?

A

GSDs, Karelian bear dogs, saaroloos wolfhound, Czechoslovakian wolf dog

**Rare in cats

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30
Q

What mutation is associated with pituitary dwarfism and how is it inherited?

A

LHX3 mutation, autosomal recessive

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31
Q

What is the pathophysiology of pituitary dwarfism?

A

Pituitary cysts or pituitary hypoplasia —> unclear if the cysts cause the hypoplasia or are a consequence of it

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32
Q

In GSDs with pituitary dwarfism, what hormone abnormalities might you find on screening tests?

A

Combined GH, TSH, and prolactin deficiency

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33
Q

What age do pituitary dwarfism patients typically present?

A

3-5 months of age

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34
Q

What are common musculoskeletal clinical signs associated with pituitary dwarfism?

A

Musculoskeletal:
- Proportionate growth failure (unlike congenital hypothyroidism where short legs and big head)
- Pointed nose/fox like facial features
- Delayed closure of growth plates
- Delayed dental eruption

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35
Q

What are common dermatologic clinical signs associated with pituitary dwarfism?

A

Dermatological:
- Soft woolly hair coat
- Lack of guard hairs
- Hair loss (areas of wear - collar, sitting)
- Hyperpigmented, scaly, thin wrinkled skin
- Papules, pyoderma, comedones

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36
Q

What are common reproductive clinical signs associated with pituitary dwarfism?

A
  • Cryptorchidism
  • Testicular atrophy
  • Persistent anestrus
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37
Q

What CBC and chem findings might you find with pituitary dwarfism?

A

**Often normal, but may see
CBC: mild anemia due to hypothyroidism

Chem: hypophosphatemia (b/c of changes happening at bone), hypoalbuminemia, azotemia (develops over time)

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38
Q

How is pituitary dwarfism diagnosed?

A

Genetic testing for LHX2 —> if positive, no further testing needed

Growth hormone stimulation test —> GH measurement after stimulation with GHRH, colonizing, xylazine, ghrelin DIFFICULT TO PERFORM

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39
Q

How is pituitary dwarfism treated in dogs?

A
  1. Human-recombinant, porcine, ovine, or bovine GH supplementation (usually porcine b/c it’s the most genetically similar)
  2. Progesterone —> induces GH synthesis in the mammary gland

No protocols described in cats

Response: Often see regrowth of secondary hair, some dogs may develop a full hair coat. May see linear growth determined by status of growth plates at time of therapy (although typically very little improvement).

Risk of treatment leading to DM b/c of progesterone

Prognosis: guarded even with treatment; dogs usually euthanized by 3-5y of age if not treated

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40
Q

Hypersomatotropism is also known as

A

Acromegaly

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41
Q

What is the typical signalment of an acromegalic patient?

A

Feline
~10y
Male (88%)&raquo_space;> female
DSH > DLH

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42
Q

What is the pathophysiology of acromegaly in CATS?

A

GH-producing acidophil pituitary adenoma —> produces too much GH —> increased IGF-1 levels resulting in proliferation of bone, cartilage, soft tissues, and and increased size of organs

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43
Q

Despite increased IGF-1 levels, acromegalic cats are typically still insulin resistant. Why?

A

The increased IGF-1 levels are unable to counteract insulin-resistance induced by excessive GH concentrations —> the GH is too excessive they can’t convert enough GH to IGF-1

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44
Q

What are common clinical signs of acromegaly in cats

A

Think DM signs: PU/PD, plantigrade stance, polyphagia (from DM and the excessive production of GH)

Also broadening of head, prognathia inferior, widening of interdental spaces, respiratory stridor +/- distress (due to increased/thickening of oropharyngeal tissue), CNS signs

WEIGHT PATTERNS ARE HUGE CLUE
Typically these cats will lose weight due to the secondary DM but stabilize with super high doses of insulin and then actually gain weight which doesn’t usually happen in uncontrolled diabetics

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45
Q

At what dose of insulin should you start questioning if a cat has acromegaly?

A

When you get above 2 units/kg q12h

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46
Q

What organs typically become enlarged in acromegalic cats?

A

Heart
Kidneys
Spleen
Pancreas
Adrenals
Thyroid

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47
Q

What percentage of cats with acromegaly can have neurologic signs?

A

10-15%

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48
Q

What abnormalities might you see on CBC in an acromegalic cat?

A

Relative erythrocytosis due to dehydration

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49
Q

What abnormalities may you see on chemistry panel in an acromegalic cat?

A
  • Hyperglycemia
  • Hyperproteinemia (due to dehydration)
  • Mild increases in ALT and ALP activity (due to mobilization of fats and sugars that cause hepatocytes to swell —> vacuolar change)
  • Hyponatremia b/c glucose pulls more water into vascular space to dilute out sodium
  • Hyperphosphatemia without azotemia (GH/IGF-1 mediates increased renal tubular absorption of phosphorus; will look like decreased GFR without azotemia)
  • Azotemia (50% of acromegalic cats develop CKD within 8-36m of diagnosis; mechanism not fully understood but may be due to glucosuria causing glomerulopathy)
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50
Q

What abnormalities might you see on a UA with an acromegalic cat?

A
  • Glucosuria
  • Proteinuria (when azotemia present)
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51
Q

When should you consider testing for acromegaly?

A

Cats with difficult to regulate DM in which other common concurrent problems (stomatitis/gingivitis/UTIs, corticosteroid administration) have been eliminated

Remember >2U/kg of insulin q12h

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52
Q

What is the diagnostic test of choice for acromegaly?

A

IGF-1 measurement

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53
Q

Why is IGF-1 measurement preferred for diagnosis of acromegaly in cats?

A
  • Reflects 24h GH secretion
  • Is not secreted in pulses (unlike GH) so single random sampling is sufficient
  • Structure is conserved across species, so more assay availability (unlike GH)
  • Stable, so serum sample can be sent by regular mail (GH cannot)
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54
Q

What concurrent disease can decrease IGF-1 making interpretation of the assay difficult if acromegaly is of concern?

A
  • Malnutrition
  • Liver failure
  • Renal failure
  • Hypothyroidism
  • Poorly controlled DM
  • Oral estrogen intake
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55
Q

Why might IGF-1 be normal when assessed prior to starting insulin therapy in acromegalic diabetic cats?

A

Remember IGF-1 is produced because of insulin in the portal vein —> in cats with diabetes, it may be low because there is not enough insulin available to stimulate IGF-1 production

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56
Q

If IGF-1 is normal in a cat you suspect has acromegaly and you have not yet started insulin, when should you recheck?

A

6-8 weeks after insulin therapy is initiated

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57
Q

What is the “gray zone” for IGF-1 testing?

A

800-1000ng/mL - if in this range and suspicion for acromegaly is high, consider pituitary imaging

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58
Q

What are goals of treatment of acromegaly?

A

Two goals:
1. Treat acromegaly (sx, SRT)
2. Treat concurrent DM

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59
Q

T/F: Pituitary surgery is the gold standard for treatment of acromegaly

A

TRUE - but technically demanding, one study showed remission of DM in a cat 3 weeks after surgery

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60
Q

What medications are used to decrease GH secretion?

A

Somatostatin analogs (octreotide, lanreotide, pasireotide)

Also dopamine agonist L-deprenyl

All showed very little effect EXCEPT pasireotide

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61
Q

A 2017 study (Gostelow et al, JVIM) showed which somatostatin analong to be most effective in treatment of acromegaly?

A

Pasireotide

A 2017 study (Gostelow et al, JVIM) showed long-acting pasireotide induced diabetic remission in 3/8 cats

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62
Q

SRT shows improvement in symptoms and improved control of DM in what percentage of cats?

A

Improvement of symptoms in 2/3 of cats

Improved control of DM in 50-92% of cats

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63
Q

What is prognosis for acromegaly with and without treatment?

A

Guarded to poor if not treated (months)

If they have pituitary surgery or SRT - favorable outcomes, MST 25m

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64
Q

What is the etiology of acromegaly in DOGS?

A

Almost always induced by endogenous or exogenous progestogens giving rise to GH hypersecretion from the mammary gland

AKA they’re either getting progesterone or have a progesterone-secreting tumor in the mammary glands

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65
Q

What breeds of dogs are predisposed to acromegaly?

A

Swedish and Norwegian Elkhounds
Border collies
Beagles

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66
Q

T/F: GH-producing tumors in the pituitary gland of dogs resulting in acromegaly are very common

A

FALSE - very rare, opposite of cats

Somatotrophic adenoma only described in 2 dogs

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67
Q

What is the treatment for acromegaly in dogs?

A

If diestrus-associated acromegaly in intact females: OHE

If due to exogenous progesterone - stop giving them

If a mass producing progesterone - remove the mass

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68
Q

What are the three zones of the adrenal cortex and what do they produce?

A
  1. Zona glomerulosa - mineralocorticoids (aldosterone)
  2. Zona fasciculata - glucocortocoids (cortisol)
  3. Zona reticularis - sex hormones (progesterone, estrogens, androgens)

“The deeper you go the better it gets”

Salt —> sugar —> sex

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69
Q

All hormones produced by the adrenal cortex are derived from what molecule?

A

Cholesterol

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70
Q

Conversion of cholesterol to aldosterone is regulated by what enzyme?

A

Aldosterone synthase

Zona glomerulosa is rich in aldosterone synthase

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71
Q

Conversion of cholesterol to glucocorticoids (cortisol) and sex hormones is regulated by what enzyme?

A

17a hydroxylase Aka cholesterol desmolase

Zona faciculata and reticularis are both rich in this enzyme (inhibitors of this enzyme exist in people)

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72
Q

T/F: Trilostane is a 17a hydroxylase inhibitor

A

FALSE - it’s a competitive inhibitor of 3beta-hydroxysteroid dehydrogenase

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73
Q

What is the half life of corticotropin-releasing hormone (CRH) in plasma?

A

~60 minutes

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74
Q

CRH produced in the __ is released by the __ and acts on __ in the __. This stimulates release of __ which stimulates secretion of __ from the adrenal gland.

A

CRH produced in the PARAVENTRICULAR NUCLEI is released by the HYPOTHALAMUS and acts on CORTICOTROPHS in the ANTERIOR PITUITARY. This stimulates release of ACTH which stimulates secretion of GLUCOCORTICOIDS from the adrenal gland.

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75
Q

Adrenocorticotropic hormone (ACTH) is derived from what?

A

POMC - proopiomelanocortin

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76
Q

What is the half life of ACTH in plasma?

A

~10min

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77
Q

T/F: ACTH causes some secretion of mineralocorticoids and sex hormones, but to a lesser extent than glucocorticoids

A

True

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78
Q

What hormone provides negative feedback on the hypothalamic-pituitary-adrenal axis?

A

Cortisol

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79
Q

Why does elevated cortisol result in elevated blood glucose?

A

Causes increase in gluconeogenesis and decrease in insulin responsiveness and production, and decreases glucose utilization b/c there’s less insulin in circulation

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80
Q

What are the five effects of cortisol?

A
  1. Increased blood glucose
  2. Decreased insulin sensitivity
  3. Increased protein mobilization
  4. Increased mobilization of fat
  5. Decreased inflammation and immune system function
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81
Q

How does cortisol cause increased protein mobilization?

A

Decrease in cellular proteins while increasing production of proteins from liver and in plasma

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82
Q

How does increased cortisol decrease inflammation and immune system function?

A
  1. Decreases expression of adherence molecules on sides of blood vessels —> less migration of WBCs into interstitium
  2. Decreases permeability of capillaries —> less diapedesis
  3. Decreases lymphocyte production —> lymphopenia on stress leukogram
  4. Increases lysosome stabilization w/in phagocytes —> less able to fight off pathogens
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83
Q

What does the SMILED acronym for a stress leukogram mean?

A

Segs, monos increased
Lymphs, eos decreased

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84
Q

Do the majority of dogs have adrenal or pituitary dependent hyperadrenocorticism?

A

Pituitary-dependent (PDH) —> 85% have pituitary tumors

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85
Q

What percentage of dogs with hyperadrenocorticism have adrenal tumors?

A

15%

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86
Q

Iatrogenic hyperadrenocorticism result from?

A

Exogenous steroid administration

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87
Q

Bilaterally adrenomegaly is associated with ADH or PDH?

A

PDH - increased ACTH stimulation from pituitary acts on both adrenals

Negative feedback loop from cortisol doesn’t work

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88
Q

Unilateral adrenomegaly with atrophy of the contralateral adrenal gland is consistent with ADH/PDH?

A

ADH

Negative feedback loop from cortisol still works and you get decreased ACTH production to act on the unaffected adrenal gland

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89
Q

Canine Pituitary tumors are commonly adenoma or carcinomas?

A

Adenomas (carcinomas are rare)

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90
Q

Are most pituitary adenomas more commonly micro or macro and what is the size cutoff?

A

Most commonly microadenomas (<10mm)

Macroadenoma = >10mm

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91
Q

What percentage of dogs at diagnosis of a pituitary adenoma have a tumor <3mm?

A

21-48%

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92
Q

Adrenal tumors are commonly UNILATERAL/BILATERAL

A

Unilateral

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93
Q

Adrenal tumors > ___cm are more likely to be carcinomas

A

> 2cm

Also those that are invading regional vasculature

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94
Q

What is the common signalment of patients with hyperadrenocorticism?

A

Dogs
Middle aged to older (>= 89% older than 6y)
Poodles, Dachshunds, terriers, Beagles, GSDs, Labs

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95
Q

ADH/PDH tends to occur more in smaller dogs, and ADH/PDH tends to occur more in larger dogs

A

PDH in smaller dogs
ADH in larger dogs

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96
Q

What breeds are more commonly associated with PDH?

A

Poodles
Dachshunds
Terriers
Beagles

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97
Q

What breeds are more commonly associated with ADH?

A

Poodles
GSDs
Dachshunds
Labradors

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98
Q

How does hyperadrenocorticism result in polyuria?

A

Increased cortisol inhibits ADH’s action on V2 receptors leading to secondary nephrogenic diabetes insipidus, so you get polyuria

USG is <1.015, often less than 1.008

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99
Q

Why do dogs with hyperadrenocorticism get muscle wasting?

A

Cortisol causes protein catabolism

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100
Q

Why does calcinosis cutis develop with hyperadrenocorticism?

A

Cortisol causes secondary hyperparathyroidism (90% of dogs with HAC have high PTH) —> leads to Ca & Phos deposition

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101
Q

Why do dogs with HAC get hepatomegaly?

A

Cortisol causes increased protein, fat, and glucose mobilization —> vacuolar hepatopathy —> hepatomegaly

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102
Q

Why do dogs with HAC get a “pot bellied” appearance

A

Hepatomegaly, weakened abdominal muscles, abdominal fat accumulation, enlarged bladder from polyuria all contribute

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103
Q

Why do dogs with HAC have increased panting?

A

Weakened respiratory muscles, hepatomegaly, and decreased lung compliance (from pulmonary/bronchial mineralization) all contribute

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104
Q

What CBC changes may you see in dogs with HAC?

A
  1. “Stress Leukogram” - SMILED
    - Neutrophilia and monocytosis from steroid-enhanced demargination
    - Lymphopenia from steroid-induced lymphocytes
    - Eosinopenia from bone marrow sequestration of eosinophils
  2. Mild polycythemia - cortisol tells BM to make more RBCs
  3. Thrombocytosis (75-80% of dogs) - cortisol tells BM to make more platelets
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105
Q

What chemistry changes can be seen with HAC?

A
  1. Liver enzyme changes
    - ALP&raquo_space;> ALT (80-90%) due to corticosteroid induced ALP (cALP) coming from bile canilicular membranes of hepatocytes
    - Mild ALT increase (<500U/L) b/c of swelling of hepatocytes from the vacuolar hepatopathy
  2. Hypercholesterolemia and hypertriglyceridemia b/c cortisol results in lipolysis
    - Results in lipemia
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106
Q

What UA changes might you see in a dog with HAC?

A
  1. Hyposthenuria to isosthenuria - USG <1.020 but often <1.008
  2. Proteinuria - occurs in >50% of dogs with HAC
    - Usually UPC <5, and they never get secondary hypoalbuminemia
    - Glomerulosclerosis, glucocorticoid-induced glomerular hypertension
  3. UTIs - found in 50% of dogs with hyperadrenocorticism, but <5% have clinical signs of infection (relates to decreased diapedesis of WBCs)
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107
Q

What changes to pre- and post-bile acids may you see with HAC?

A

May be mildly increased, occurs in about 30% of dogs with HAC

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108
Q

T/F: 55% of HAC dogs without pancreatitis can have positive SNAP cPLs

A

True

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109
Q

cPLI has been shown to be HIGHER/LOWER In dogs with HAC who do not have pancreatitis

A

HIGHER

Basically don’t assume they have active panc if you’re suspicious of HAC

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110
Q

Why do dogs with HAC often have a secondary hypothyroidism?

A

Cortisol alters thyroid hormone binding to plasma proteins, metabolizes thyroid hormone and decreases peripheral deionization of T4 and T3

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111
Q

What percentage of dogs with HAC have hypertension, and what is the proposed mechanism?

A

31-86%

Etiology is unclear but thought to result from increased sensitivity to norepinephrine

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112
Q

What potential complication of HAC is the primary driver for treatment?

A

Development to PTEs

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113
Q

T/F: A urine cortisol:creat ratio can diagnose Cushings

A

NO - used to think it would help rule it out, but even that is not as sensitive

Sensitivity used to be 99%, new study showed 75%
Low specificity

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114
Q

What test is the only way to diagnose iatrogenic Cushings?

A

ACTH stim test (dog will have PU/PD and ALP, but ACTH stim looks like Addisonian)

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115
Q

What is Cortrosyn?

A

ACTH

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116
Q

What is the cutoff for an “exaggerated” response on a post sample of the ACTH stim test that would indicate Cushings disease?

A

<22ug/dL

Post-ACTH values:
Normal: <18ug/dL
Grey zone: 18-22ug/dL **if the patient has clinical signs and falls in this value, either do a LDDST or new guidelines say ok to assume they’re Cushinoid
Exaggerated: >22ug/dL

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117
Q

Steps for interpreting LDDST

A
  1. Look at 8h mark to determine who is Cushinoid - if cortisol is >1.4ug/dL, they’re Cushinoid
  2. Look at 4h mark - if they suppress <1.4ug/dL, it’s definitely pituitary dependent OR if 4 or 8h is <50% of baseline, it’s PDH

Remember adrenal dependent is overproduction of ACTH and negative feedback is not intact, so they don’t care if you give more cortisol

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118
Q

T/F: You can use a high dose dex suppression test to determine if a dog has HAC or not

A

NO - it is a differentiating test - it will NOT tell you if a dog has Cushing’s or not, must do a LDDST prior for this

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119
Q

How much more dexamethasone are you giving with a HDDST vs. LDDST?

A

10x

120
Q

How to interpret HDDST?

A
  1. If 8h sample is <1.4mg/dL (or lab cutoff) = PDH
  2. If 4h sample <1.4mg/dL (or lab cutoff) = PDH
  3. If 4h or 8h sample is <50% of baseline = PDH

If none of the above are met = PDH or ADH —> imaging or eACTH

121
Q

Treatment of ADH?

A

Adrenalectomy, especially if tumor >2cm

122
Q

Treatment for PDH?

A

Surgery - hypophysectomy especially for pituitary macroadenomas

RT can be considered

Medical management - trilostane, mitotane, ketoconazole

123
Q

How long after starting a dog on trilostane or after changing a dose should you check an ACTH stim test?

A

10-14 days

test 4-6h post pill

124
Q

What is the difference between mitotane and trilostane

A

Trilostane effects are reversible, mitotane is not

125
Q

What is the MOA of mitotane?

A

It’s adrenocorticolytic - causes selective necrosis of the zona fasciculata and reticularis (it’s thought the zona glomerulosa is resistant)

126
Q

Why is mitotane not preferred for ADH treatment over trilostane?

A

MST not statistically different between drugs, and more side effects with mitotane

127
Q

What is the prognosis for untreated HAC based on a 2017 study?

A

MST 506 if untreated vs. MST not reached with treated group

New consensus is to treat b/c it does increase lifespan

128
Q

T/F: HAC is rare in cats and most are adrenal dependent.

A

False - it is rare, but most are pituitary dependent (80% PDH, 20% ADH)

129
Q

What percentage of feline adrenal tumors are adenomas vs. carcinomas?

A

50% adenomas, 50% carcinomas

130
Q

What are clinical signs of HAC in cats?

A

80% of cats are diabetic at time of diagnosis
PU/PD - not present until development of DM
**SKIN FRAGILITY
Weight loss (not weight gain)

131
Q

How do chemistry findings in cats with HAC differ from dogs?

A
  • High ALP activity is NOT a consistent finding (10-20%) - cats don’t have the corticosteroid induced isoenzyme like dogs
  • Hyperglycemia, glucosuria in 90% of cats
  • Hypercholesterolemia in 50% of cats
  • Elevated ALT in 33% of cats
132
Q

T/F: The ACTH stim test is just as sensitive in cats as dogs.

A

FALSE - has poor sensitivity in cats (30-50%), best used to look for Addisons

133
Q

What is the test of choice to diagnose HAC In cats and how does it vary from dogs?

A

LDDST - use the HDDST dog dose of dexamethasone (0.1mg/kg)

134
Q

Are mitotane or ketoconazole recommended for treatment of HAC in cats?

A

NO b/c of side effects

135
Q

What is the prognosis for HAC in cats?

A

<50% survive beyond one year b/c o the skin stuff and DM

136
Q

Why does the body need cortisol (aka what does it mediate in the body)?

A
  • Hepatic gluconeogenesis and glycogenesis
  • Protein and fat metabolism
  • Maintain vascular reactivity to catecholamines
  • Maintain endothelial integrity
  • Maintain GI mucosa (via influence of digestion and intestinal absorption, and increasing brush border enzymes)
137
Q

What are consequences of hypocortisolemia?

A
  • Hypoglycemia
  • Muscular weakness, increased susceptibility to stress
  • Hypotension
  • Increased vascular permeability leading to hypoalbuminemia and hypovolemia
  • Vomiting/diarrhea, weight loss
  • Hypoalbuminemia, hypoglobulinemia, hypocholesterolemia
138
Q

What regulates aldosterone secretion (4 pathways)?

A
  1. Renin-angiotensin axis
  2. Increased plasma potassium concentration
  3. Increased plasma sodium concentration (minor)
  4. Increased plasma ACTH concentration (minor)
139
Q

What is the most prominent promoter of aldosterone release?

A

Angiotensin II

Also K+

140
Q

If you remove the pituitary, will you have a mineralocorticoid deficiency?

A

NO - b/c ACTH is a minor player in mineralocorticoid secretion

141
Q

What cells within the collecting duct does aldosterone act on?

A

Principle cells - activates NaKATPase pump to increase potassium into cell and moving it into urine, pulls sodium into cell and puts that out into plasma —> conserve body salt

Intercalated cells - results in H+ ions being excreted into urine

142
Q

What electrolyte changes are seen with hypoaldosteronism?

A

Hyponatremia - b/c not able to absorb it from urine
Hypochloremia - b/c chloride follows sodium
Hyperkalemia - b/c there’s no exchange for sodium at principal cells

143
Q

What is the mechanism through which hypotension develops with hypoaldosteronism?

A

Hyponatremia leads to concurrent loss of water —> decreased ECF —> hypovolemia —> hypotension

144
Q

Most hypoadrenocorticism is PRIMARY or SECONDARY

A

PRIMARY (95%) - affecting adrenal glands, not pituitary

145
Q

How much of the adrenal glands must be lost before hypoadrenocorticism develops?

A

> = 90%

146
Q

What is atypical Addison’s?

A

Deficiency of glucocorticoids but not mineralocorticoids

(Typical Addison’s lacks both)

147
Q

What is secondary hypoadrenocorticism?

A

Reduced secretion of ACTH from the pituitary gland. Leads to glucocorticoid deficiency ONLY

148
Q

If you took a biopsy of the adrenal glands in a dog with Addison’s, what would you expect to see?

A

Severe lymphoplasmacytic inflammation and adrenocortical atrophy involving all layers of the adrenal cortex

This is suspected to be immune-mediated adrenal it is in majority of cases.

149
Q

When you abruptly withdraw exogenous corticosteroids, do you cause primary or secondary hypoadrenocorticism?

A

SECONDARY

150
Q

What is the typical signalment of a patient with Addison’s?

A
  • Canine
  • Breeds are typically Standard poodles, Portuguese water dogs, Nova Scotia Duck Tolling Retrievers, Bearded Collies, Great Danes
  • Typically female (~70%) but this is not true for predisposed breeds
  • Median age of onset 4y (younger in DTR (3y) and Great Danes
151
Q

What breeds typically get Addison’s and what is the pattern of inheritance?

A

Standard poodle, Portuguese water dog, Nova Scotia Duck Tolling retriever - autosomal recessive

Bearded Collie - pattern of inheritance is unknown

152
Q

What clinical signs of addison’s are attributed to glucocorticoid deficiency only?

A

Anorexia, vomiting, diarrhea, weight loss, lethargy/depression, weakness/shaking/shivering, rarely seizures

153
Q

What clinical signs are attributed to mineralocorticoid deficiency?

A

PU/PD, hypovolemia shock, collapse, dehydration

154
Q

What CBC findings might you see in an Addisonian patient?

A

Non-regenerative anemia (27% of cases)

LACK OF STRESS LEUKOGRAM
- Lymphocytosis (10%)
- Eosinophilia (20%)
- Neutrophilia (32%)

155
Q

What abnormalities might you see on the chemistry panel of an Addisonian patient?

A

***HYPERKALEMIA (more common than Hyponatremia)
Hyponatremia
Hypercalcemia (30%)
Azotemia (88%)
Hyperphosphatemia (68%)
Hypoglycemia (17%)
Hypoalbuminemia (39%)
Hypocholesterolemia (7%)
Increased liver enzymes (40%)

156
Q

What parasites can cause pseudo-Addison’s?

A

Whipworms

157
Q

What changes might you expect on the urinalysis of an Addisonian dog?

A

Isosthenuria to minimally concentrated urine

This is due to hyponatremia which causes medullary washout (1.008-1.020)

158
Q

How is Addison’s diagnosed?

A

Baseline cortisol: if >2ug/dL it rules out Addison’s

If <= 2ug/dL you need further testing with ACTH stim

159
Q

How is Addison’s treated in the acute setting?

A
  • Fluids
  • Glucocorticoid supplementation (dexamethasone)
  • Deoxycorticosterone pivalate (DOCP)
160
Q

Why is it okay to use dexamethasone in and acute Addisonian crisis?

A

It does not cross react with the cortisol assay acutely (<24h), but can after several doses

161
Q

How is Addions’s treated chronically/long term?

A
  • Glucocorticoid supplementation (prednisone 0.05-0.2mg/kg/d) - double during times of stress
  • Deoxycorticosterone pivalate (DOCP; 2.2mg/kg q28d)

Alternative is fludrocortisone (0.02mg/kg/d) which has both cortisol and mineralocorticoids, but has to be given daily and usually you need more glucocorticoids vs. mineralocorticoids so dose adjustment is challenging

162
Q

How do you treat atypical Addions’s?

A

Mineralocorticoids only but most convert and need glucocorticoids too

163
Q

What is prognosis for Addison’s?

A

Excellent!!

DOCP can be expensive in large dogs and might lead to euthanasia

Pred side effects may also lead to euthanasia

EDUCATE

164
Q

T/F: Addison’s in cats is common

A

FALSE - very rare

165
Q

What is the typical signalment of a cat with Addison’s?

A

1.5-14y
All DLH or DSH
Male = female

166
Q

Is it common or uncommon to see bloodwork changes in cats with Addison’s?

A

UNCOMMON

167
Q

Hyperaldosteronism is more common in CATS/DOGS

A

Cats

168
Q

In feline hyperaldosteronism, is renin elevated or decreased?

A

Decreased - excess circulating aldosterone leads to renin suppression

169
Q

What are the consequences of too much aldosterone?

A
  • Hypernatremia
  • Hypokalemia
  • Hypertension
  • Weakness
170
Q

Is feline hyperaldosteronism typically unilateral or bilateral?

A

Unilateral

Usually unilateral adrenocortical adenoma (39%) or carcinoma (48%)

171
Q

What is the typical age at which feline hyperaldosteronism is diagnosed?

A

Middle aged to older, mean age 12-13y

172
Q

What are clinical manifestations of hypokalemia in feline hyperaldosteronism?

A

Hypokalemic polymyopathy - persistent and progressive weakness; ventroflexion of neck b/c they lack a nuchal ligament

173
Q

At what degree of hypokalemia do you typically see hypokalemic polymyopathy

A

<3mg/dL

174
Q

What clinical signs are typically associated with hypertension in feline hyperaldosteronism?

A
  • Acute blindness and/or sudden change in eye color (can be due to intraocular hemorrhage or retinal detachment)
  • Cardiac changes (murmur, cardiomegaly, ventricular hypertrophy)
175
Q

What changes might you see on a chemistry panel with hyperaldosteronism?

A
  • Hypokalemia (although absence does not rule it out)
  • Serum sodium typically normal
  • Elevated CK (especially with hypokalemic myopathy)
  • +/- mild azotemia
176
Q

When should you consider evaluation for feline hyperaldosteronism?

A

Any cat with
- An adrenal nodule and unexplained hypokalemia or hypertension
- Hypertension or hypokalemia refractor to therapy

177
Q

How is feline hyperaldosteronism diagnosed?

A
  1. Aldosterone:Renin ratio - will distinguish primary from secondary
    • Primary: high ratio
    • Secondary: low ratio

Problem is renin is not widely commercially available and is effected by meds like ACEis and beta-blockers, as well as dietary salt; additionally, aging and neutering cats may decrease plasma renin concentration in healthy ranges

  1. Urine Aldosterone: Creatinine Ratio
  2. Plasma Aldosterone concentration - markedly elevated in most cats with hyperaldosteronism; may be within upper end of RI in mild cases, so consider in light of serum potassium concentration (low potassium concentration is a potent suppressor of aldosterone secretion)
178
Q

How is feline hyperaldosteronism treated?

A

Surgery for solitary adrenal masses —> typically curative

If unresectable, or if there is evidence of metastasis or bilateral hyperfunction:
- Address the hypokalemia w/mineralocorticoid receptor blockers (spironolactone) and potassium supplementation
- Address hypertension with calcium channel blockers (amlodipine) +/- ACEis

179
Q

Per the ACVIM consensus statement on hypertension, are ACEis first line therapy for cats?

A

NO - they are in dogs, but cats don’t respond as robustly so typically they’re used for Proteinuria

180
Q

The enzyme that is responsible for conversion of norepinephrine to epinephrine is under the influence of what despite being located in the adrenal medulla?

A

Cortisol

181
Q

Typically NOREPINEPHRINE/EPINEPHRINE is more predominant in the adrenal medulla?

A

Epinephrine (70% vs. norepinephrine 30%)

182
Q

Where are alpha 1 receptors located and what effect do they have?

A

Vascular smooth muscle —> vasoconstriction

183
Q

Where are beta1 receptors found and what is their effect?

A

Myocardium —> increased HR and contractility

184
Q

Where are beta2 receptors found and what is their effect?

A

Vascular smooth muscle —> vasodilation in skeletal muscle, arterioles, coronary arteries, and veins

Bronchioles smooth muscle —> relaxation/bronchial dilation

Intestinal smooth muscle —> decreases intestinal motility

185
Q

In the urinary bladder, what type of receptors (alpha or beta) are responsible for increased sphincter tone and which are responsible for relaxing the detrusor

A

Alpha - increased sphincter tone

Beta - relax detrusor

186
Q

In adipose tissue, what receptor type is responsible for increasing lipolysis?

A

Beta

187
Q

What cells and where in the adrenal gland do pheochromocytomas arise?

A

Arise from catecholamine-producing chromaffin cells in the adrenal medulla

188
Q

Are pheochromocytomas typically unilateral or bilateral?

A

Unilateral

189
Q

What is the typical signalment of a pheochromocytoma patient?

A

Canine
Mean age 12y
No breed or sex predilection

190
Q

When you have metastasis with a pheochromocytoma, do you typically see more norepinephrine or epinephrine?

A

Norepinephrine because there’s no cortisol in the blood to convert it to epinephrine

191
Q

What are epinephrine and norepinephrine metabolized to and by what enzyme?

A

Epinephrine —> metanephrine
Norepinephrine —> Normetanephrine

COMT enzyme (catechol-O-methyltransferase)

192
Q

Why do we measure normetanephrine and metanephrine rather than epi/norepinephrine?

A

Epi/norepinephrine are short lived

193
Q

What are clinical signs associated with pheochromocytomas?

A

A LOT - they’re typically episodic and random, and can be many things. Severity is typically associated with tumor size

194
Q

How are pheochromocytomas diagnosed?

A
  • Hypertension (BP >300mmHg only identified in dogs with pheos)
  • Urine metanephrines - specifically normetanephrines are more helpful than metanephrine
195
Q

What is the treatment of choice for pheochromocytomas?

A

Adrenalectomy

196
Q

What is the MOA of phenoxybenzamine?

A

Oral, non-competitive, non-selective alpha-adrenoreceptor blocker

197
Q

What are negative prognostic factors for pheochromocytoma

A

Tumors >5cm
Evidence of metastasis or thrombosis

198
Q

TRH released from the hypothalamus acts on ___ in the anterior pituitary to stimulate release of __, which travels to the thyroid gland and stimulates secretion of __ and __.

A

TRH released from the hypothalamus acts on THYROTROPHS in the anterior pituitary to stimulate release of TSH, which travels to the thyroid gland and stimulates secretion of T3 and T4.

199
Q

The thyroid gland is composed of __ that are filled with __.

A

Composed of follicles

Filled with colloid

200
Q

What is colloid in thyroid follicles?

A

A glycoprotein that is the base of what thyroid hormones are made of; also traps iodide

201
Q

How many molecules of iodine are attached to T3 and T4?

A

T3 has 3
T4 has 4

202
Q

How are T3 and T4 moved from colloid to blood stream?

A

T3 and T4 are bound to thyroglobulin in the colloid of thyroid follicles. When TSH binds the TSH receptor, a conformation change happens in the cuboidal cells lining the follicles and they take Thg-T3 and Thg-T4 into the cell, where they combine with lysozymes which cleave the thyroglobulin. T3 and T4 are released into blood stream, thyroglobulin is recycled.

203
Q

What enzyme plays and important role in development of thyroid hormones within the colloid (basically getting iodine to connect to thyroglobulin-tyrosine complexes to form T3 and T4)?

A

Thyroid peroxidase (TPO)

204
Q

What are the three roles of thyroid peroxidase?

A
  1. Oxidates iodide to iodine
  2. Organification - Attaching iodine to tyrosine residues of thyroglobulin to form monoiodotyrosine (MIT) and diiodotyroxine (DIT)
  3. Coupling - combining MIT and DIT to form T3, or two DITs to form T4
205
Q

What is the active form of thyroid hormone?

A

T2 - triiodothyronine

206
Q

Which form of thyroid hormone increases with stress in people?

A

Reverse T3 - helps differentiate euthyroid sick syndrome in people, but not available in dogs

207
Q

Thyroid hormone is secreted in primarily what form?

A

T4

208
Q

What protein primarily transports thyroid hormone in the blood?

A

Thyroxine-binding globulin

209
Q

Thyroid hormone has a HIGH/LOW affinity for plasma-binding proteins?

A

HIGH - released slowly to tissue cells (T3 faster than T4)

210
Q

What enzyme converts T4 to T3 at the level of the tissues?

A

Deiodinases

211
Q

What are genomic functions of thyroid hormones?

A
  1. Activate nuclear receptors
  2. Thyroid hormone receptor forms heterodimer with retinoid X receptor (RXR) at specific thyroid hormone response elements —> these are important for development of CNS, growth, cardiovascular effects
212
Q

What are non-genomic functions of thyroid hormone?

A
  1. Regulation of ion channels - has been show to increase activity of NaKATPases
  2. Oxidative phosphorylation
213
Q

What are the effects of thyroid hormone on growth and development?

A
  1. Thyroid hormone acts synergistically with GH and IGF-1
  2. Promotes Chandra genesis
214
Q

What are the effects of thyroid hormone on metabolism?

A
  1. Increased lipid metabolism —> fat mobilization
    - Increases concentrations of FFAs in plasma
    - Enhances oxidation of fatty acids
    - Increases cholesterol synthesis BUT increases cholesterol reabsorption because it increases cholesterol conversion to bile acids, which lowers plasma cholesterol
  2. Carbohydrate metabolism
    - Enhances insulin-dependent entry of glucose into cells
    - Increases gluconeogenesis and glycogenolysis
  3. Protein metabolism
    - Anabolic and catabolic —> when increased, catabolic predominates
215
Q

What are the effects of thyroid hormone on vitamin consumption?

A

Thyroid hormone increases quantities of enzymes. Vitamins are essential parts of enzymes and coenzymes, so you get relative vitamin deficiency

216
Q

What are the effects of thyroid hormone on the cardiovascular system?

A
  1. Vascular
    - Promotes vasodilation —> decreases SVR —> enhances blood flow
    - Direct stimulation of erythropoietin synthesis —> erythrocytosis —> increases circulating blood volume which causes an increase in preload
    - Decreased SVR will lead to RAAS activation, causing renal sodium retention by aldosterone, resulting in increased circulating blood volume —> increased preload
  2. Heart
    - Positive chronotropic effect: increases HR
    - Positive iontropic effect: increases cardiac contractility
    - Increased HR and contractility leads to increased cardiac output (b/c remember CO = HR x SV, and thyroid hormone is increasing both)
217
Q

What are the effects of thyroid hormone on the GIT?

A
  1. Increases appetite and food intake
  2. Increases rate of digestive secretions
  3. Increases motility of GIT such that we can see
    - Hyperthyroidism —> diarrhea
    - Hypothyroidism —> constipation (more in people than dogs)
218
Q

What are the effects of thyroid hormone on the CNS?

A

Thyroid hormone is important for brain and neuronal development, specifically differentiation of oligodendrocytes making myelin

Excitatory effects on CNS
- Too much = anxiety, nervousness
- Too little = sluggish/dull

219
Q

What are the three forms of hypothyroidism and some Ddx for each?

A
  1. Primary = thyroid dysfunction
  2. Secondary = TSH deficiency; issue is in the pituitary (ddx pituitary malformation, pituitary destruction from a mass/surgery/RT, Thyrotroph suppression from concurrent illness)
  3. Tertiary = problem in hypothalamus; RARE; (Ddx hypothalamic mass)
220
Q

What form of hypothyroidism is most common in dogs?

A

Primary - 95% of cases

221
Q

What is the most common etiology primary hypothyroidism in dogs?

A

Lymphocytic thryroiditis - thyroid gland is invaded by lymphocytes, plasma cells, macrophages. Thought to be immune-mediated (thyroglobulin and TPO = main antigens)

222
Q

What percentage of thyroid tumors cause neoplasticism destruction leading to hypothyroidism?

A

10%

223
Q

How much of the thyroid gland needs to be destroyed before clinical signs will appear?

A

80%

224
Q

Are thyroid tumors in dogs typically functional or nonfunctional?

A

Nonfunctional

225
Q

What is the typical age of a hypothyroid dog?

A

Middle aged to older

226
Q

What dog breeds are predisposed to hypothyroidism?

A

Golden retrievers
Doberman pinschers

227
Q

What clinical manifestations of hypothyroidism do we see?

A
  1. Metabolic - lethargy/inactivity, weight gain, mental dullness, cold intolerance
  2. Dermatological - endocrine alopecia, hyperpigmentation, pyoderma, myxedema
  3. Neuromuscular - Polyneuropathy/myopathy, vestibular signs (central or vestibular), facial/trigeminal nerve paralysis, seizures, disorientation, myxedema coma, laryngeal paralysis
  4. Cardiovascular - bradycardia, cardiac arrhythmias
  5. GI - esophageal hypomotility (megaE maybe but usually doesn’t get better when hypoT is treated so unclear the cause and effect); consolation (more common in people)
  6. Repro - infertility, prolonged parturition
228
Q

What is myxedema coma?

A

Accursed due to accumulation of mucopolysaccharides and hyaluronic acid in the dermis that binds water. Leads to profound weakness, hypothermia, bradycardia, non-pitting edema, hypo ventilation, and stupor leading to coma.

THIS IS RARE

229
Q

What changes might you see on the CBC of a dog with hypothyroidism?

A
  1. Normocytic, normochromic, non-regenerative anemia (30% of cases)
  2. Target cells - due to cholesterol loading
230
Q

What changes might you see on the chemistry panel of a dog with hypothyroidism?

A
  1. Lipemia!!
  2. Fasting Hypercholesterolemia in 75% of cases
  3. Fasting hypertriglyceridemia
  4. Mild increases in ALT, AST, and ALP activities
231
Q

What is the gold standard diagnostic test for canine hypothyroidism?

A

TSH stimulation test - not done frequently b/c of expense of recombinant TSH

232
Q

If a TSH stimulation test cannot be performed, what values are recommended to assess for hypothyroidism in a dog?

A

T4
fT4
TSH

233
Q

Total T4 is lower in what breeds?

A

Sighthouds

234
Q

A __ total T4 with a __ fT4 provides diagnosis of hypothyroidism when clinical signs and lab work are consistent.

A

Low normal total T4
Low fT4

235
Q

Circulating cTSH is usually __ in primary hypothyroidism.

A

increased

**do not measure this alone, must be used in conjunction with T4 and fT4

236
Q

What medications can affect thyroid testing?

A

Sulfonamides (↓ TT4, ↓ fT4, ↑ TSH)
- Block iodination of thyroglobulin
- Effect on thyroid function depends on dose & duration
- Only one that actually results in clinical signs of hypothyroidism!

Phenobarbital (↓ TT4, ↓ fT4, may ↑ TSH)
- NO clinical disease!

Glucocorticoids (↓ TT4, ↓ fT4, ↓ TSH)
- Influence peripheral metabolism of thyroid hormones
- Inhibit TSH release

Clomipramine (↓ TT4, ↓ fT4, does not affect TSH) - tricyclic antidepressant

237
Q

What is levothyroxine?

A

Synthetic L-T4 sodium

238
Q

Why do we treat hypothyroidism with T4 and not T3 if T3 is the active form?

A

So the body can determine how much T3 it needs

239
Q

How long after starting treatment would you reassess thyroid levels in a hypothyroid dog?

A

6-8 weeks

240
Q

What is the most common cause of primary hyperthyroidism in cats?

A

Adenomatous hyperplasia
- Usually bilateral (70%)

241
Q

What are the environmental risk factors for hyperthyroidism?

A
  1. Excess or deficient iodine in diets
  2. Canned cat food with pop top lids
  3. Soy isoflavones - genistein and daidzein inhibit TPO; diets with soy cause increased T4 and fT3
  4. Selenium
  5. Goitrogens - bisphenol (epoxy resins, polycarbonate plastics), polybrominated diphenyl ether flame retardants (PBDEs)
242
Q

What is the typical age of a cat with hyperthyroidism?

A

13 years

243
Q

What cat breeds are associated with a decreased risk of hyperthyroidism?

A

Tonkinese
British shorthairs
Burmese
Siamese
Himalayan
Abyssinian

244
Q

What are the clinical manifestations of feline hyperthyroidism?

A
  1. Metabolic - polyphagia, weight loss, hyperactivity, heat intolerance/cool seeking
  2. Dermatologic - unkempt hair coat, alopecia, matted fur
  3. Neuromuscular - tremors, weakness
  4. Cardiovascular - tachycardia, heart murmur, gallop rhythm, hypertension
  5. GI - vomiting (direct action of T4 on CTZ; also b/c they are overeating and have increased GI motility); diarrhea (due to increased GI motility)
  6. Renal - PU/PD
245
Q

What CBC changes might you see in a cat with hyperthyroidism?

A
  1. Erythrocytosis - T4 stimulates BM precursors and EPO production
  2. Increased MCV (in 22% of cases) - due to decreased RBC maturation time
  3. Heinz bodies - cause more oxidative damage
  4. Lymphopenia
  5. Leukocytosis
246
Q

What chemistry changes might you see in a cat with hyperthyroidism?

A
  1. Increased liver enzymes (90% have increase in >= 1 LEZ)
    - ALT can be mild to moderate (up to 4x)
    - ALP - bone isoenzyme
    - Hyperbilirubinemia
  2. Azotemia
    - Increased BUN
    - Increased creatinine due to muscle catabolism and/or concurrent CKD
    - Hyperphosphatemia - due to bone metabolism and/or concurrent CKD
  3. Hyperglycemia (d/t stress or b/c thyroid hormone stimulates release of glucose in the bloodstream)
  4. Hypokalemia - not as common as with hyperaldosteronism or CKD
247
Q

What abnormalities might you see on the UA of a cat with hyperthyroidism?

A
  1. Variable USG - most will have USG >1.035, 4% of cases have USG <1.015; SHOULD NOT BE <1.008 b/c the PU/PD is secondary to medullary washout
  2. Proteinuria - resolves with treatment of hyperthyroidism
  3. Bacteriuria infrequently, usually not clinical for it
  4. Ketonuria due to high metabolic state
248
Q

How is feline hyperthyroidism diagnosed?

A

Baseline total T4

249
Q

T/F: If you have a cat with clinical signs of hyperthyroidism but get a normal tT4 on your first screening, you have ruled out hyperthyroidism.

A

NO - if they have clinical signs you should recheck a T4 in 1 month if signs are mild to moderate. If signs are severe, check an fT4, thyroid scintigraphy, or T3 suppression test

250
Q

T/F: A tT4 in the upper half of the RI with a high fT4 is diagnostic for hyperthyroidism in a cat with appropriate clinical signs.

A

True

251
Q

What is the MOA of methimazole?

A

Inhibition of thyroid peroxidase

252
Q

What are side effects of methimazole?

A
  1. GI - usually related to tablet and not transdermal form
  2. Facial excoriation - can happen with either oral or transdermal form
  3. Blood dyscrasias (bone marrow suppression) - Thrombocytopenia, neutropenia
  4. Hepatotoxicity
  5. Acquired myasthenia gravis - rare
253
Q

What is the MOA of I131 treatment?

A

I131 emits gamma rays and beta particles. The beta particles (1-2mm) cause follicular cell death

254
Q

What is the mechanism of the Y/D diet?

A

Deficient in iodine, and thyroid needs iodine to make thyroid hormone

255
Q

What produces parathyroid hormone?

A

Chief cells of the parathyroid gland

256
Q

Where does parathyroid hormone act? 3 sites

A

Renal tubules
Bone
Duodenum

257
Q

Parathyroid hormone __ calcium and __ phosphorus.

A

Increases calcium
Decreases phosphorus

258
Q

What is the main source of vitamin D in dogs?

A

Diet

This is why dogs with chronic enteropathy can have hypovitaminiosis D

259
Q

What two organs are important for activation of vitamin D?

A

Kidneys
Liver

260
Q

Where does vitamin D act? 2 sites

A

GI tract
Bone

261
Q

Vitamin D __ calcium and __ phosphorus.

A

Increases calcium
Increases phosphorus

262
Q

Where is calcitonin produced?

A

C cells of the thyroid

263
Q

Where does calcitonin act?

A

Bone

264
Q

Calcitonin __ calcium and __ phosphorus.

A

Decreases calcium
No action on phosphorus

265
Q

What two main types of neoplasia have hypercalcemia mediated by PTHrp?

A

Lymphoma
AGASACA

266
Q

What are ddx for hypercalcemia?

A

HOGS IN YARD (DRAGON SHIT)
Hyperparathyroidism
Osteolytic
Granulomatous (fungal)
Spurious (hyperlipemia)
Idiopathic (#1 in cats)
Neoplasia (MM, LSA, AGASACA)
Young
Addison’s
Renal
D - vitamin D toxicity

267
Q

What are ddx for hypocalcemia?

A

Hypoparathyroidism
Vit D deficiency (PLE, EPI)
Pancreatitis
Eclampsia
Hypoalbuminemia (total)
Phosphate enema toxicity

268
Q

Are parathyroid nodules usual singular or multiple, and are they benign or malignant?

A

Singular in 80-90% of cases
Typically adenomas (87% of cases)

269
Q

What breed is the poster child for primary hyperparathyroidism?

A

Keeshonds

270
Q

What chemistry panel abnormalities might you see with primary hyperparathyroidism?

A
  1. Total hypercalcemia
  2. Low normal to hypophosphatemia
  3. Most NOT azotemic (PTH renal protective) - about 4% have azotemia
  4. Increased ALP activity (40%) - bone isoenzyme (ALT typically normal)
271
Q

What UA abnormalities might you see in a dog with hyperparathyroidism?

A
  1. Mean USG 1.012
  2. Hematuria
  3. Pyuria
  4. Bacteria
  5. Calcium oxalate and calcium phosphate stones possible
272
Q

T/F: Primary hypoparathyroidism is common.

A

False - rare

273
Q

What are the five cell types of the endocrine pancreas and what do they secrete?

A

Alpha cells - produce glucagon

Beta cells - produce insulin

Gamma cells (aka PP cells or F cells) - produce pancreatic polypeptide

Delta cells - produce somatostatin

Epsilon cells - produce grehlin

274
Q

What is the chemical structure of insulin?

A

Protein composed of A & B chains connected by two disulfide bridges

275
Q

Canine insulin is most similar to what other species?

A

Porcine

276
Q

Feline insulin is most similar to what other species?

A

Bovine

277
Q

What are the net affects of insulin?

A

Lower blood concentrations of glucose, FAs & amino acids

Promote intracellular conversion to their storage forms of glycogen, triglycerides & protein

278
Q

Presence of insulin required to move glucose into cells EXCEPT in what organs/cell types?

A

brain, liver, WBC, RBC

279
Q

What stimulates insulin secretion?

A

Hyperglycemia
Increased free fatty acids in blood
Increased amino acids in blood
GI hormones (gastrin, CCK, secretin, GIP)

280
Q

What is the rate limiting step for steroid hormone synthesis?

A

Cholesterol desmolase

281
Q

How does insulin decrease gluconeogenesis?

A

Promoting protein synthesis in peripheral tissues

Decreasing activities of hepatic enzymes involved in conversion of amino acids to glucose

282
Q

Hyperglycemia stimulates __ of insulin from __

A

Synthesis and release of insulin from pancreatic islet cells

283
Q

Oral intake of glucose provides release of what GI hormones that also stimulate insulin?

A

Gastric
CCK
Gastric inhibitory polypeptide (GIP)

284
Q

Glucagon stimulates beta cells in the pancreas to secrete what 4 compounds?

A

Insulin
Somatostatin
Epinephrine
Norepinephrine

285
Q

In what three locations is glucagon produced?

A

Alpha cells of pancreas
Stomach (gut glucagon)
Small intestine (glicentin)

286
Q

Where does glucagon exhibit it’s main effects and what does it do there?

A

Liver: increases cAMP which leads to decreased glycogen synthesis, increased glycogenolysis, and increased gluconeogenesis to increase blood glucose concentrations

Also promotes lipolysis and increases in FAs which negatively feed back on glucagon production

287
Q

What factors stimulate glucagon secretion?

A

Hypoglycemia = MAIN FACTOR
Intestinal hormones (except secretin)
Increased blood amino acids

288
Q

What factors inhibit glucagon secretion?

A

Increased somatostatin levels
Hyperglycemia

289
Q

Glucagon levels will be ____ in syndromes of insulin insufficiency

A

Paradoxically elevated

290
Q

Where is somatostatin synthesized and stored?

A

Pancreatic delta cells

291
Q

What stimulates somatostatin release?

A

Hyperglycemia
Increased amino acids
Increased fatty acids
GI hormones released from upper GIT

292
Q

Where does somatostatin act?

A

LOCALLY (paracrine fashion) - acts on islets of langerhans to decrease insulin and glucagon secretion

293
Q

What are the primary actions of somatostatin?

A

Inhibits digestive processes by decreasing nutritive absorption and digestion

Decreases motility and secretory activity of the GIT and gallbladder

Inhibits secretion of all endocrine cell types of the islets of langerhans (effects are greater on alpha cells compared to beta cells) —> inhibits glucagon secretion

294
Q

Of the pancreatic hormones, only __ stimulates somatostatin production.

A

Glucagon

295
Q

What factors decrease insulin secretion?

A

Hypoglycemia
Fasting
Increased somatostatin
Alpha-adrenergic activity/leptin
Glucagon, growth hormone, and cortisol

ACVIM Generals (16 decks)

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