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ACVIM General Exam > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Corticotrophs:

  1. Anterior/Posterior Pituitary
  2. What do they produce?
  3. How are they stimulated?
A
  1. Anterior
  2. Adrenocotrophic hormone (ACTH)
  3. Corticotrophin Releasing Hormone (CRH)
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2
Q

Thyrotrophs:

  1. Anterior/Posterior Pituitary
  2. What do they produce?
  3. How are they stimulated?
A
  1. Anterior
  2. Thyroid stimulating hormone (TSH)
  3. Thyrotropin releasing hormone (TRH)
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3
Q

Gonadotrophs:

  1. Anterior/Posterior Pituitary
  2. What do they produce?
  3. How are they stimulated?
A
  1. Anterior
  2. Leutinizing hormone (LH) and Follicle stimulating hormone (FSH)
  3. Gonadotropin releasing hormone (GnRH)
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4
Q

Somatotrophs:

  1. Anterior/Posterior Pituitary
  2. What do they produce?
  3. How are they stimulated?
  4. How are they inhibited?
A
  1. Anterior
  2. Growth Hormone (GH)
  3. Growth Hormone Releasing Hormone (GHRH)
  4. Growth Hormone Inhibitory Hormone (GHIH) and Somatostatin
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5
Q

Lactotrophs:

  1. Anterior/Posterior Pituitary
  2. What do they produce?
  3. How are they stimulated?
  4. How are they inhibited?
A
  1. Anterior
  2. Prolactin
  3. Thyrotropin releasing hormone (TRH)
  4. Prolactin Inhibitory Hormone (PIH)
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6
Q

Which hormones are stored in the posterior pituitary gland (neurohypophysis)?

A
  1. Vasopressin (ADH)

2. Oxytocin

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7
Q

Where is ADH produced?

A
  1. Supraoptic nuclei of the hypothalamus

* Stored in the posterior pituitary for release

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8
Q

Where is oxytocin produced?

A
  1. Paraventricular nuclei of the hypothalamus

* Stored in the posterior pituitary for release

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9
Q

What are the functions of Growth Hormone?

A
  1. Increase protein synthesis
  2. Increase mobilization of fatty acids from adipose tissue
  3. Decreased utilization of glucose throughout the body
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10
Q

What mediates the actions of growth hormone?

A
  1. Insulin like growth factors (IGFs, aka somatomedins)
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11
Q

Draw the hypothalmic/pituitary/target axis for growth hormone

A

See notes

Axis

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12
Q

When does growth hormone predominate?

A
  1. During the fasted state
    * Lipolysis and fatty acid oxidation (protein sparing effect) during fasting
    * Insulin antagonism
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13
Q

What are the functions of IGH-1?

A
  1. Production increased by Growth hormone when there is sufficient nutrient intake and a high insulin concentration in the portal vein
  2. Antilipolytic activity
  3. Insulin like activity
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14
Q

What are the effects of growth hormone on the following?

  1. Insulin (CHO)
  2. Fat
  3. Protein
  4. Chondrocytes
A
  1. Antagonism
  2. Lipolysis
  3. Protein synthesis
  4. Epiphyseal growth
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15
Q

What are the effects of IGF-1 on the following?

  1. Insulin (CHO)
  2. Fat
  3. Protein
  4. Chondrocytes
A
  1. Insulin like activity
  2. Antilipolytic activity
  3. Protein synthesis
  4. Epiphyseal growth
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16
Q

What stimulates Growth Hormone secretion?

A
  1. Decreased 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
  9. GHRH
  10. Ghrelin
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17
Q

What inhibits Growth Hormone secretion?

A
  1. Increased BG
  2. Increased FFH
  3. Aging
  4. Obesity
  5. GHIH (Somatostatin)
  6. Somatomedins (IGFs)
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18
Q

Which breeds are predisposed to pituitary dwarfism?

A
  1. German shepherd, Karelian Bear dog
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19
Q

What is the pathophysiology of pituitary dwarfism?

A
  1. Autosomal recessive LHX3 mutation
  2. Pituitary hypoplasia (pituitary cysts)
    * Will have combined GH, TSH, and prolactin deficiencies
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20
Q

Acromegaly predominates in (males/females)

A

Males (88%)

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21
Q

What is the pathophysiology for acromegaly?

A
  1. GH-producing acidophil pituitary adenoma
  2. GH + IGF-1 → proliferation of bone, cartilage, soft tissues, and increase in size of organs
  3. Increased IGF-1 levels unable to counteract insulin resistance by excessive GH concentrations
  4. β cell failure → diabetes
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22
Q

What clinical signs are attributed to acromegaly?

A
  1. Signs related to diabetes mellitus
    - PU/PD
    - Plantigrade
  2. Polyphagia
  3. Weight loss → stabilization → weight gain (different from diabetic cats)
  4. Insulin resistance
  5. Broadening of the head
  6. Prognathia infeior
  7. Widening of interdental spaces
  8. Organomegaly
  9. CNS signs (10-15%)
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23
Q

What is the diagnostic test of choice for diagnosis acromegaly?

A
  1. Measuring IGF-1
    * Reflects 24 hour GH secretion
    * Poorly controlled diabetes may decrease IGF-1
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24
Q

When could IGF-1 be normal in a cat with acromegaly? When should IGF-1 testing be done?

A
  1. If the cat is an uncontrolled diabetic

2. Recommend testing a minimum of 6-8 weeks after insulin therapy is initiated

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25
Q

How is acromegaly treated?

A
  1. Pituitary surgery → gold standard
  2. Medical therapy
    - Somatostatin analogs (pasireotide, octreotide)
    - Dopamine agonist (L-deprenyl)
    - All showed very little effect except pasireotide
  3. Radiation
    - 2/3 will show improvement in symptoms
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26
Q

How is the etiology of acromegaly different in dogs?

A
  1. It is almost always induced by endogenous or exogenous progestogens giving rise to GH hypersecretion from the mammary gland
    * Swedish and Norwegian Elkhounds, Border Collies, and Beagles are overrepresented
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27
Q

What is the precursor of ACTH?

A

POMC

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28
Q

What are the functions of cortisol?

A
  1. Increase blood glucose
  2. Decrease insulin sensitivity
  3. Decrease inflammation and immune system function
  4. Increase protein mobilization
  5. Increase mobilization of fat
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29
Q

What is the etiology of hyperadrenocorticism? Which is most common?

A
  1. Pituitary dependent → 85%
  2. Adrenal dependent → 15%
  3. Iatrogenic!
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30
Q

Hyperadrenocorticism:
Small breed dogs are more likely to have (pituitary/adrenal) dependent hyperadrenocorticism and large breed dogs are more likely to have (pituitary/adrenal)

A
  1. Pituitary

2. Adrenal

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31
Q

What are the clinical signs associated with Cushing’s disease?

A
  1. PU/PD → cortisol inhibits ADH’s action on V2 receptors in the collecting duct
  2. Polyphagia
  3. Muscle wasting
  4. Alopecia, thin skin, hyperpigmentation
  5. Decrease immune function
  6. Calcinosis cutis → Ca and P deposition increased due to secondary hyperparathyroidism
  7. Potbelly
  8. Panting
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32
Q

What % of Cushing’s dogs have a high PTH? Why?

A
  1. 90%

2. Secondary hyperparathyroidism

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33
Q

What are the characteristics of a stress leukogram?

A

SMILED

  1. Neutrophils (segs), monocytes → increased
  2. Lymphocytes, eosinophils → decreased
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34
Q

What changes can be found on a CBC in a Cushing’s patient?

A
  1. Stress leukogram
  2. Mild polycythemia
  3. Thrombocytosis (75-80%)
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35
Q

What changes can be found on a chemistry in a Cushing’s patient?

A
  1. ALP»>ALT
  2. Hypercholesterolemia (90%)
  3. Hypertriglyceridemia
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36
Q

What % of Cushing’s dogs have proteinuria?

A

> 50%

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37
Q

What % of Cushing’s dogs have UTI? What % show clinical signs?

A
  1. 50%

2. <5%

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38
Q

What is the effect of Cushing’s disease on thyroid function?

A
  1. Secondary hypothyroidism

- Cortisol alters thyroid hormone binding to plasma proteins

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39
Q

What are complications associated with Cushing’s?

A
  1. Urinary calculi
  2. Hypertension (31-86%)
  3. Gallbladder mucocele (23%)
  4. Pulmonary thromboembolism
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40
Q

The urine cortisol to creatinine ratio is very good at ruling (in/out) Cushing’s disease

A
  1. Out

2. High sens, low spec

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41
Q

What are you looking for in an ACTH stimulation test?

A

An exaggerated response to ACTH one hour post administration

  • Normal <18
  • Grey Zone: 18-22
  • Exaggerated: >22
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42
Q

Low Dose Dexamethasone Suppression Test:
The 8-hour level is >1.4
This patient (is/is not) Cushinoid

A

Is!

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43
Q

What are the criteria for pituitary dependent hyperadrenocorticism on a low dose dexamethasone suppression test?

A
  1. Suppress below 1.4 at the 4 hour mark and then are above 1.4 at the 8 hour
  2. Are at 50% of baseline at either the 4 hour or the 8 hour
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44
Q

ACTH Stim vs Low Dose Dex

- More sensitive

A

Low Dose Dex

*Less specific → can get a false positive from stressed dogs in the hospital

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45
Q

ACTH Stim vs Low Dose Dex

- More specific

A

ACTH Stim

  • Can trust a positive test
  • Less sens → if neg, need to do a low dose dex
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46
Q

ACTH Stim vs Low Dose Dex

- Can separate PDH from ADH

A

Low dose dex

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47
Q

What is the purpose of the HIGH dose dex suppression test? What is it NOT able to do?

A
  1. Differentiating test

2. Will NOT tell you if a dog has Cushing’s disease

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48
Q

What are the treatments for Cushing’s disease?

A
  1. Adrenalectomy → esp. if tumor >2 cm
  2. Hypophysectomy
  3. Medical Management
    - Trilostane
    - Mitotane
    - Ketoconazole
  4. Radiation not effective
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49
Q

What is the MOA of triolostane?

A

Competitive inhibitor of 3β-hydroxysteroid dehydrogenase

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50
Q

What are the adverse effects of trilostane?

A
  1. Vomiting
  2. Lethargy
  3. Electrolyte shifts (iatrogenic Addison’s, less common)
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51
Q

What are the monitoring recommendations for dogs on trilostane?

A
  1. ACTH stim 10-14 days post dose change (4-6 hours post pill)
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52
Q

What is the MOA of mitotane?

A
  1. Selective necrosis of the zona fasciculata and reticularis
    * Non-reversible
    * Zona glomerulosa is resistant
  2. Also inhibits steroid biosynthesis
    - 11β-hydroxylase
    - Cholesterol desmolase
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53
Q

What are the adverse effects for mitotane?

A
  1. Anorexia
  2. Lethargy
  3. Weakness
  4. Diarrhea
  5. Hepatotoxicity
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54
Q

What is a unique clinical presentation for cats with Cushing’s disease?

A
  1. Skin fragility

2. High ALP is not a consistent finding

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55
Q

Why does the body need cortisol?

A
  1. Hepatic gluconeogenesis and glycogenesis
  2. Protein and fat catabolism
  3. Maintain vascular reactivity to catecholamines
  4. Maintain endothelial integrity
  5. Maintain GI mucosa
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56
Q

What are regulators of Aldosterone secretion?

A
  1. RAAS
    - Increased Angiotensin II
  2. Increased plasma K concentration
    Minor players
    - Increased plasma Na
    - Increased plasma ACTH
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57
Q

Hypophysectomy (will/will not) result in a mineralocorticoid deficiency

A
  1. Will not

- ACTH is only a minor player in aldosterone regulation

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58
Q

What are the consequences of hypocortisolemia?

A
  1. Hypoglycemia
  2. Muscular weakness
  3. Hypotension
  4. Increased vascular permeability
  5. Vomiting, diarrhea, weight loss
  6. Hypoalbuminemia
  7. Hypoglobulinemia
  8. Hypocholesterolemia
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59
Q

What % of dogs have primary hypoadrenocorticism? Secondary?

A
  1. 95%

2. 5%

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60
Q

What is the difference between primary and secondary hypoadrenocorticism?

A
  1. Primary has glucocorticoid and mineralocorticoid deficiency whereas secondary only has glucocorticoid deficiency
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61
Q

What % of dogs are reported to have atypical Addison’s?

A
  1. 30%

* Normal electrolytes at diagnosis

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62
Q

What % of the adrenal glands must be destroyed to have primary Addison’s?

A
  1. Bilateral >90% destruction

* Immune mediated adrenalitis is suspected in the majority

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63
Q

Addison’s is more common in (males/females)

A

Females

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64
Q

Addison’s disease most commonly has what type of inheritance?

A
  1. Autosomal recessive

* Poodles are common breed

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65
Q

What is the median age of onset for Addison’s?

A

4 years

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66
Q

What changes can be seen on a CBC for dogs with Addison’s?

A
  1. Non-regenerative anemia (27%)

2. Lack of a stress leukogram

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67
Q

What changes can be seen on a chemistry for dogs with Addison’s?

A
  1. Hyperkalemia (96%)
  2. Hyponatremia (81%)
    * 30% have normal electrolytes
  3. Hypercalcemia (31%)
  4. Azotemia (88%) and Hyperphosphatemia (68%)
  5. Hypoglycemia (17%)
  6. Hypoalbuminemia (39%)
  7. Reduced cardiac output
  8. Reduced renal perfusion
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68
Q

What parasite can cause Addison like changes?

A

Whipworms

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69
Q

What does a baseline cortisol >2 indicate? <= 2?

A
  1. Ruled out Addison’s

2. Needs further testing

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70
Q

What result on an ACTH stimulation test would indicate Addison’s disease?

A

Flat-line

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71
Q

Dexamethasone (does/does not) cross react with the cortisol assay

A

Does not

*One benefit for giving it in an acute setting for a suspect addison’s

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72
Q

What is used for treatment of Addison’s?

A

Acute
1. Fluid therapy
2. Glucocorticoid supplementation (dexamethasone)
3. DOCP
Chronic
1. Glucocorticoid supplementation → double during times of stress
2. DOCP

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73
Q

What is the most common adrenal disease in cats?

A
  1. Hyperaldosteronism

* Many have concurrent CKD, is likely underdiagnosed

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74
Q

What are the clinical signs of hyperaldosteronism?

A
  1. Weakness (may be episodic)
  2. Lethargy
  3. PU/PD
  4. Neck ventroflexion
  5. Blindness
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75
Q

When should primary hyperaldosteronism be strongly considered in cats?

A
  1. Adrenal nodule and unexplained hypokalemia or hypertension
  2. Hypertension or hypokalemia refractory to therapy
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76
Q

What is the gold standard test for feline hyperaldosteronism?

A

Aldosterone:Renin Ratio

*Is not very easy to do

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77
Q

What is the most clinically useful diagnostic for hyperaldosteronism?

A
  1. Plasma aldosterone concentration
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78
Q

How is hyperaldosteronism treated?

A 
Surgery
- Treatment of choice
Medical Mangement
1. Hypokalemia
- Mineralocorticoid receptor blockers → spironolactone
- K supplementation
2. Hypertension
- Calcium channel blockers → amlodipine
- +/- ACEi
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79
Q

How many transmembrane segments do G protein linked receptors have? Enzyme linked hormone receptors?

A
  1. 7 transmembrane segments

2. 1 transmembrane segment

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80
Q

How does the adenylyl cyclase-cAMP second messenger system function?

A
  1. Converts ATP → cAMP → activates cAMP dependent protein kinase → phosphorylation of specific proteins in the cell
  2. cAMP also activates protein kinase A → downstream causes increased or decreased activity of RNA polymerases and transcription of target genes
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81
Q

How does the phospholipase C second messenger system function?

A
  1. Attached to the inside projections of receptors and catalyzes the breakdown of the phospholipids in the cell membrane → PIP2 → IP3 + DAG
  2. Activates protein kinase C → phosphorylates other proteins
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82
Q

Adenylyl Cyclase vs Phospholipase C

- Angiotensin II (epithelial cell of proximal tubule, thick ascending LoH, distal tubule, and collecting duct)

A

Adenylyl Cyclase

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83
Q

Adenylyl Cyclase vs Phospholipase C

- Catecholamines (β receptor)

A

Adenylyl cyclase

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84
Q

Adenylyl Cyclase vs Phospholipase C

- Vasopressin (V2 receptors)

A

Adenylyl Cyclase

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85
Q

Adenylyl Cyclase vs Phospholipase C

- Calcitonin/PT

A

Adenylyl Cyclase

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86
Q

Adenylyl Cyclase vs Phospholipase C

- ACTH

A

Adenylyl Cyclase

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87
Q

Adenylyl Cyclase vs Phospholipase C

- FSH

A

Adenylyl Cyclase

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88
Q

Adenylyl Cyclase vs Phospholipase C

- TSH (on Thyroid)

A

Adenylyl Cyclase

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89
Q

Adenylyl Cyclase vs Phospholipase C

- LH

A

Adenylyl Cyclase

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90
Q

Adenylyl Cyclase vs Phospholipase C

- CRH

A

Adenylyl Cyclase

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91
Q

Adenylyl Cyclase vs Phospholipase C

- Glucagon

A

Adenylyl Cyclase

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92
Q

Adenylyl Cyclase vs Phospholipase C

- Secretin

A

Adenylyl Cyclase

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93
Q

Adenylyl Cyclase vs Phospholipase C

- Somatostatin

A

Adenylyl Cyclase

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94
Q

Adenylyl Cyclase vs Phospholipase C

- Angiotensin II (vascular smooth muscle)

A

Phospholipase C

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95
Q

Adenylyl Cyclase vs Phospholipase C

- Catecholamines (α receptors)

A

Phospholipase C

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96
Q

Adenylyl Cyclase vs Phospholipase C

- Vasopressin (V1 receptor on vessels, vascular smooth muscle)

A

Phospholipase C

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97
Q

Adenylyl Cyclase vs Phospholipase C

- Oxytocin

A

Phospholipase C

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98
Q

Adenylyl Cyclase vs Phospholipase C

- GnRH

A

Phospholipase C

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99
Q

Adenylyl Cyclase vs Phospholipase C

- GHRH

A

Phospholipase C

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100
Q

Adenylyl Cyclase vs Phospholipase C

- TRH

A

Phospholipase C

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101
Q

Adrenocortical hormones are synthesized from what?

A

Cholesterol

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102
Q

What is the primary source of cholesterol?

A

LDL

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103
Q

How is LDL converted to cholesterol?

A
  1. ACTH stimulates uptake of LDL by the adrenal gland (as well as enzymes needed to liberate cholesterol from LDL)
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104
Q

What is the rate limiting step in steroid synthesis? What is this step stimulated by?

A
  1. Cholesterol desmolase: Conversion of cholesterol to pregnenalone
    * Occurs in the mitochondria
  2. Stimulated by ACTH and Angiotensin II
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105
Q

How do glucocorticoids stimulate gluconeogenesis in the liver?

A
  1. Stimulates enzymes to convert amino acids into glucose
  2. Mobilizes amino acids from the peripheral tissues
  3. Insulin antagonist
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106
Q

What are the primary substrates for gluconeogenesis?

A
  1. Amino acids
  2. Glycerol
  3. Lactate
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107
Q

How do glucocorticoids stimulate protein metabolism?

A
  1. Stimulates protein catabolism in peripheral tissues to mobilize amino acids to the liver for gluconeogenesis
  2. While peripheral protein stores are decreased, plasma proteins and liver proteins are increased
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108
Q

How do glucocorticoids stimulate fat metabolism?

A
  1. Stimulates breakdown of triglycerides in adipose tissue
  2. Stimulates hormone sensitive lipase
  3. Stimulates lipoprotein lipase
109
Q

What are the two main regulators of Aldosterone secretion?

A
  1. Increased plasma K concentration

2. Increased Angiotensin II concentration

110
Q

What are the effects of Aldosterone on the principal cells of the collecting tubules?

A
  1. Increase Na-K ATPase

2. Increase Na channels

111
Q

What are the effects of Aldosterone on the intercalated cells of the collecting tubules?

A
  1. Increased H secretion

* Causes metabolic alkalosis

112
Q

What suppresses Aldosterone release?

A
  1. ANP
  2. Dopamine
  3. Heparin
113
Q

Primary hyperaldosteronism is most likely to be caused by what?

A
  1. Unilateral adenoma/carcinoma of the zona glomerulosa
114
Q

What laboratory findings can be found with hyperaldosteronism?

A
  1. Hypokalemia (primary abnormality)
  2. Elevated aldosterone
  3. Metabolic alkalosis
  4. Urinary fraction excretion of potassium is elevated
  5. Hypertension
115
Q

What is unique about secondary hypoadrenocorticism?

A

There is only a glucocorticoid deficiency

116
Q

What is atypical Cushing’s?

A

Overproduction of cortisol precursors or sex hormones

117
Q

What can be elevated in dogs with atypical Cushing’s?

A
  1. 17-hydroxyprogesterone
  2. Progesterone
  3. Estradiol
  4. Testosterone
  5. Androstenedione
118
Q

What % of dogs with Cushing’s will have hypothyroidism? Why?

A
  1. 50%

2. Negative feedback of cortisol on pituitary secretion of TSH and also due to alterations in peripheral T4 metabolism

119
Q

What is Nelson’s syndrome?

A

When cortisol lowering therapy has the potential to stimulate pituitary adenoma growth

120
Q

What is the MOA of ketoconazole in the context of Cushing’s therapy?

A
  1. Inhibits steroid biosynthesis via inhibition of p450 dependent enzymes
    - 11β hydroxylase
    - Cholesterol desmolase
121
Q

What are the adverse effects of using ketoconazole for treating Cushing’s disease?

A
  1. GI
  2. Hepatotoxicity
  3. Thrombocytopenia (rare)
  4. Reversible lightening of the hair coat
122
Q

When is ketoconazole used to treat Cushing’s disease?

A

Usually in mitotane resistant adrenocortical tumors

123
Q

What is the MOA of using etomidine in treating Cushing’s disease?

A
  1. Inhibition of:
    - 11β hydroxylase
    - Cholesterol desmolase
124
Q

What is Levodeprenyl used for?

A

FDA approved for treatment of PDH in dogs

125
Q

What is the MOA of levodeprenyl for treatment of hyperadrenocorticism?

A
  1. Reversible inhibition of MAO-B → increased central dopamine levels since it is not broken down
  2. Dopamine then acts to inhibit ACTH secretion by the pars intermedia
    * FDA approved for treatment of PDH and cognitive dysfunction in dogs
126
Q

How is ACTH used to monitor levodeprenyl therapy?

A

DONT USE ACTH STIM - this drug is neither adrenolytic nor an inhibitor of steroidigenesis

127
Q

What are the effects of RT in treating Cushing’s disease for:

  1. Neurological signs
  2. Endocrine control
A
  1. 50% will have complete resolution of neuro signs

2. Only 25% will have endocrine control

128
Q

When can melatonin be used for the treatment of Cushing’s disease?

A
  1. Dogs with atypical Cushing’s if they have NO OTHER signs of HAC
129
Q

Cats with HAC are (more/less) likely to have macro adenomas than dogs?

130
Q

What % of dogs with HAC have microadenomas?

131
Q

Why is the ACTH stim test important in the context of iatrogenic Cushing’s?

A
  1. It is used to rule out iatrogenic cushing’s
  2. There should be no stim in iatrogenic cases
    * the Hypothalamic/Pituitary axis is shut down from excessive exogenous cortisol
132
Q

Why is an elevated ALP not found in cats with Cushing’s disease?

A

They do not have a steroid inducible form of ALP

133
Q

Why do excessive glucocorticoids in HAC cause hypertension?

A
  1. Cortisol increases sensitivity to endogenous vasoconstrictors (increases the number and function of α1 and β receptors)
  2. Inhibits NO production
  3. Improves myocardial function
  4. Lessens the downregulation of adrenergic receptors secondary to catecholamine therapy in shock
  5. Also has anti-ADH activity → retains sodium but also becomes PU/PD
    - Decrease ADH release from pituitary
    - Decrease renal sensitivity to ADH
134
Q

What is the disease?

  1. Feline
  2. Sudden onset blindness
  3. Present with muscle weakness and cervical ventroflexion
  4. Hypertension noted
  5. Hypokalemic on chemistry
A

Primary Hyperaldosteronism

135
Q

Why does azotemia occur in patients with primary hyperaldosteronism?

A

Due to negative feedback to the RAAS system → Loss of angiotensin drops total renal blood flow

136
Q

What is the stimulus for ADH release?

A
  1. Increased osmolality (osmoreceptors in the supraoptic nucleus)
  2. Decreased blood volume (decreased stretch by atrial stretch receptor)
137
Q

What is the function of Thyroid Stimulating Hormone (TSH)

A
  1. Stimulates T3 and T4 secretion
138
Q

What are the components of colloid?

A
  1. Thyroglobulin - glycoprotein

2. Concentrated iodide

139
Q

How is Iodine brought into thyroid cells?

A

Na-I Symporter

140
Q

What is thyroglobulin made from? How is it put into the follicle?

A
  1. Made in the thyroid cell from carbohydrates and amino acids
  2. Packaged into apical vesicles for movement into the follicle
141
Q

What happens when TSH binds to its receptor?

A
  1. The thyroid cell undergoes a conformational change
  2. Allows Thg-T3 and Thg-T4 to be brought into the thyroid cell
  3. Lysozymes separate the thyroglobulin from T3 and T4
  4. T3 and T4 are then able to enter the bloodstream
142
Q

What enzyme plays an important role in the development of thyroid hormones within the colloid?

A

Thyroid peroxidase

143
Q

What are the roles of thyroid peroxidase?

A
  1. Oxidation → Oxidizes iodide to iodine
  2. Organification → Incorporates iodine into tyrosine residues of thyroglobulin
    - Forms monoidotyrosine (MIT) and diiodotyoxine (DIT)
  3. Coupling → Combines MIT and DIT into triidothyroxine (T3) OR combines DIT and DIT into thyroxine (T4)
144
Q

What are the products of thyroid hormone synthesis? Which are active?

A
  1. T3 → active
  2. T4
  3. Reverse T3 → Inactive
    - the iodines are in the wrong places
145
Q

How much of the iodinated tyrosine in thyroglobulin never becomes T4/T3? What happens to it?

A
  1. 3/4

2. Remains as MIT and DIT and is NOT secreted into the blood → the iodine is cleaved from them by diodinase and recycled

146
Q

Which is secreted more from the thyroid - T4 or T3?

A
  1. T4 - 93%

2. T3 - 7%

147
Q

How is T4 transported in the blood?

A

Bound to thyroxine binding globulin

148
Q

Thyroid hormones have a (high/low) affinity for plasma binding proteins

A

High

  • Released slowly to tissue cells
  • Results in them having a slow onset of action
149
Q

What happens to T4 at the level of the tissues?

A
  1. Converted to T3 by deiodinases
150
Q

What are the functions of the thyroid hormones? (Broad/Big Picture)

A
  • Genomic and Non-Genomic Functions*
    1. Activate nuclear receptors
    2. Thyroid hormone receptor forms heterodimer with retinoid x receptor (RXR) at specific thyroid response elements → allows regulation of specific DNA elements/transcription
    3. Nongenomic → regulates ion channels and oxidative phosphorylation
151
Q

What are the effects of thyroid hormone in the context of growth and development?

A
  1. Act synergistically with GH and IGF-1

2. Promotes chondrogenesis

152
Q

What are the effects of thyroid hormone in the context of metabolism?

A
  1. Mobilize Fat
    - Increase FFA in plasma
    - Enhance oxidation of fatty acids
    - Increase cholesterol synthesis but increase cholesterol reabsorption
    - Increase cholesterol conversion to bile acids → lowers plasma cholesterol overall
  2. Carbohydrate
    - Enhances insulin dependent glucose entry into cells
    - Increases gluconeogenesis and glycogenolysis
  3. Protein
    - Anabolic and catabolic → when increased catabolic predominates
153
Q

What are the effects of thyroid hormone in the context of vitamin consumption?

A
  1. Causes a relative vitamin deficiency
    - One paper showed that hyperthyroid cats were deficient in B12 before being treated
    - Due to thyroid hormone increasing quantities of enzymes and vitamins are an essential part of enzymes and co-enzymes
154
Q

What are the effects of thyroid hormone in the context of the vasculature?

A
  1. Promotes vasodilation (due to increased tissue metabolism) → decreased systemic vascular resistance → enhanced blood flow
  2. Direct stimulation of erythropoietin synthesis → increases circulating blood volume → increase in preload
  3. Decreased SVR → RAAS activation → renal sodium retention → increase circulating blood volume → increase preload
155
Q

What are the effects of thyroid hormone in the context of the heart?

A
  1. Positive chronotropic effect
  2. Positive inotropic effect → increase stroke volume
  3. Increased cardiac output → due to increased HR and contractility
156
Q

What are the effects of thyroid hormone in the context of the GI?

A
  1. Increase appetite and food intake
  2. Increase rate of digestive secretion
  3. Increase motility of GI
157
Q

What are the effects of thyroid hormone in the context of CNS?

A
  1. Important for brain and neuronal development
    * Differentiation of oligodendrocytes
  2. Excitatory effects on CNS
    * Too much → anxiety/nervousness
    * Too little → sluggish
158
Q

What are the effects of thyroid hormone in the context of reproduction?

A
  1. Fertility
  2. Pregnancy
  3. Ovulation
159
Q

What are the possible etiologies for hypothyroidism?

A
  1. Primary → Thyroid dysfunction
  2. Secondary → TSH deficiency, pituitary malformation, pituitary destruction (mass, SRT), thyrotroph suppression (concurrent illness)
  3. Tertiary → TRH deficiency (rare)
160
Q

What is the most common underlying etiology of hypothyroidism in dogs?

A
  1. Primary - 95% of cases
161
Q

What is the thought to be the underlying cause of primary hypothyroidism in dogs?

A
  1. Immune mediated → 80% of the gland destroyed before clinical signs
  2. Neoplastic destruction → 10% of thyroid tumors
  3. Idiopathic atrophy → follicles replied by adipose tissue, some think this may be secondary to immune destruction
  4. Iodine deficiency
162
Q

What changes can be seen on CBC with hypothyroidism?

A
  1. Normocytic, normochromic, nonregenerative anemai (30%)
  2. Target cells → due to cholesterol loading
  3. Thrombocytosis
163
Q

What changes can be seen on chemistry with hypothyroidism?

A
  1. Fasting hypercholesterolemia (75%)
  2. Fasting hypertriglyceridemia
    * May result in atherosclerosis
164
Q

What is the gold standard test for diagnosing hypothyroidism?

A
  1. TSH stimulation test

* Not typically done clinically

165
Q

What are the recommended diagnostics to diagnose hypothyroidism?

A
  1. T4
  2. fT4
  3. TSH
166
Q

Which form of T4 is biologically active? What does it do?

A
  1. fT4

2. Enters cells, exerts negative feedback inhibition on pituitary TSH, the form that is deiodinated in the cell

167
Q

What is the total T4?

A

The sum of bound and free T4

168
Q

What is the total T3?

A

The sum of bound and free T3

*Not particularly helpful

169
Q

Why are T4 autoantibodies important?

A
  1. They will falsely increase the total T4 concentration

* Will also increase free T4 if you dont use non-equilibrium dialysis

170
Q

How will the following factors affect thyroid testing?

  1. Age
  2. Size
  3. Breed
  4. Athletic Training
A
  1. Progressive decline in T4 with age (20-40% lower in older dogs)
  2. T4 greater in small vs medium to large breed, T3 greater in medium vs small and large breed
  3. Sighthounds have lower T4
  4. After sprint racing, tT4 but not fT4 decreased
171
Q

Which drugs may affect your thyroid testing?

A
  1. Glucocorticoids
  2. Phenobarbital
  3. Antibiotics (Sulfonamide)
  4. NSAIDs
  5. Tricyclic antidepressants
172
Q

What is the treatment of hypothyroidism?

A
  1. Levothyroxine (Synthetic L-T4 sodium)
173
Q

Why do we use synthetic T4 instead of T3 for treating hypothyroidism?

A

It still leaves control with the cells for how much they need

174
Q

When do you expect to see responses to hypothyroid therapy in the following areas:

  1. Mental alertness
  2. Clinical pathology
  3. Obesity
  4. Myocardial function
  5. Hair Growth
A

Minimum of 6-8 weeks before reassessing testing

  1. Within first week
  2. 2-4 weeks
  3. 2 months
  4. 2-12 months
  5. 3-5 months
175
Q

What kind of testing should be performed for follow-up hypothyroidism after starting therapy?

A
  1. T4 and cTSH 4-6 hours post pill

* T4: Should be in the upper half of the reference range to slightly high

176
Q

What is the prognosis for hypothyroidism?

A
  1. Normal life expectancy if properly treated
177
Q

What is the difference between thyroid dependent dwarfism vs growth hormone dependent dwarfism?

A
  1. Thyroid dependent will have disproportionate dwarfism whereas growth hormone is proportionate
178
Q

What is the etiology of hyperthyroidism?

A
  1. Primary hyperthyroidism
    * 98% due to benign changes
    * 2% due to malignant thyroid carcinoma
    * 3-5% can have ectopic tissue
179
Q

Which cat breeds have a DECREASED risk of hyperthyroidism?

A
  1. Tonkinese
  2. British shorthairs
  3. Burmese
  4. Siamese
  5. Himalayan
  6. Abyssinian
180
Q

What are the clinical manifestations of feline hyperthyroidism?

A
  1. Polyphagia
  2. Weight loss
  3. Hyperactivity
  4. Heat intolerance
  5. Unkempt hair coat
  6. Alopecia, matted fur
  7. Tremors, weakness
  8. Tachycardia
  9. Heart murmur, gallop rhythm
  10. Hypertension
  11. Vomiting
  12. Diarrhea
181
Q

What changes can be seen on CBC with hyperthyroidism?

A
  1. Erythrocytosis
  2. Increased MCV
  3. Heinz bodies
  4. Lymphopenia
  5. Leukocytosis
182
Q

What changes can be seen on chemistry with hyperthyroidism?

A
  1. Increased liver enzymes (90%)
  2. Azotemia
  3. Hyperglycemia (5%)
  4. Hypokalemia
183
Q

What is the diagnostic test of choice for hyperthyroidism?

A
  1. Total T4

* If elevated, the sens 91% and spec 100% for hyperthyroidism

184
Q

Hyperthyroidism (should/should not) be excluded based on 1 normal total T4 in a cat with appropriate clinical signs

A

Should not

  • If signs moderate → repeat in 1 month
  • If signs severe → fT4, thyroid scintigraphy, T3 suppression test
185
Q

How is feline hyperthyroidism treated?

A
  1. Methimazole
186
Q

What is the MOA of methimazole?

A
  1. Inhibits thyroid peroxidase
187
Q

What are the side effects of methimazole?

A
  1. GI: Vomiting, diarrhea, anorexia (15%)
  2. Facial excoriations (2-3%)
  3. Blood dyscrasias (3-9%)
  4. Thrombocytopenia
  5. Neutropenia
  6. Heptatotoxicity
    7 Acquired myasthenia gravis - RARE
188
Q

What is the MOA of radioactive iodine for treatment of feline hyperthyroidism?

A
  1. I131 emits gamma rays and beta particles

2. Beta particles cause follicular cell death

189
Q

What are the success rates of I131 treatment?

A
  1. 93% euthyroid after one treatment
  2. 2-5% require second treatment
  3. 1-2% hypothyroid
190
Q

What cells produce parathyroid hormone?

A

The chief cells of the parathyroid gland

191
Q

Where does parathyroid hormone function? What does it do?

A
  1. Renal tubules, bone, duodenum

2. Increase Ca, Decrease P

192
Q

Where do dogs get vitamin D?

193
Q

Where is vitamin D activated?

A

Liver and kidneys

194
Q

Where does vitamin D act? What does it do?

A
  1. Gastrointestinal tract, Bone

2. Increase Ca, Increase P

195
Q

What cells produce calcitonin?

A
  1. C cells of the thyroid
196
Q

Where does calcitonin act? What does it do?

A
  1. Bone

2. Decrease Ca

197
Q

What are causes for HYPERcalcemia?

A
  1. Hyperparathyroidism
  2. Osteolytic
  3. Granulomatous (Fungal)
  4. Spurious (Hyperlipidemia)
  5. Idiopathic (#1 in cats)
  6. Neoplasia
  7. Young
  8. Addison’s
  9. Renal
  10. Vitamin D Toxicity
    * HOGS IN YARD*
198
Q

What are causes for HYPOcalcemia?

A
  1. Hypoparathyroidism
  2. Vitamin D Deficiency
  3. Pancreatitis
  4. Eclampsia
  5. Hypoalbuminemia (total Ca)
  6. Phosphate enema toxicity
199
Q

What is the pathogenesis of primary hyperparathyroidism?

A
  1. 80-90% single nodule
  2. Adenoma (87%)
  3. Primary hyperplasia (8%) → typically involves all of the glands
  4. Carcinoma (5%)
200
Q

What is the most common breed of dog with primary hyperparathyroidism?

201
Q

What are the clinical signs of primary hyperparathyroidism?

A
  1. Majority dont have clinical signs
    * 20-50% of owners do not appreciate any clinical signs
  2. Lower urinary tract signs most common (50%)
  3. PU/PD
  4. Weakness
  5. Exercise intolerance/Lethargy
  6. GI
202
Q

What is the treatment of choice for primary hyperparathyroidism?

A
  1. Parathyroidectomy
203
Q

What bloodwork changes can you see with primary hypoparathyroidism?

A
  1. Hypocalcemia

2. Hyperphosphatemia

204
Q

Transdermal methimazole has a significantly (higher/lower) incidence of GI effects

205
Q

What are the dermatologic clinical signs seen with hypothyroidism?

A
  1. Bilaterally symmetric non-pruritic alopecia that spares the head and extremities (25-88% - MOST COMMON)
  2. Rat Tail (12%)
  3. Myxedema
  4. Pyoderma
    * Hairs remain in inactive growth (telegenic), fall out
206
Q

What is myxedema coma in context of hypothyroidism?

A
  1. Accumulation of acid and neutral mucopolysaccharides and hyaluronic acid in the dermis → bind water and lead to thickening/edema of the skin and forehead/face
  2. Can become obtunded, hypothermic, hypovolemic, hypotensive, bradycardic
  3. Treat with slow warming, restore blood volume, increase blood pressure, supplement with injectable levothyroxine
207
Q

What are the neurologic signs seen with hypothyroidism?

A
  1. Polyneuropathy (weakness) - MOST COMMON
  2. Facial nerve paralysis
  3. Peripheral vestibular disease
  4. Hyporeflexia
  5. Denervation on EMG
208
Q

Why does myalgia occur in hypothyroidism?

A
  1. Muscle cramping secondary to poor oxidative capacity and impaired glycogenolysis
209
Q

What are the cardiovascular clinical signs seen with hypothyroidism?

A
  1. Decreased cardiac output/impaired myocardial contractility
  2. Increased systemic vascular resistance
  3. Decreased blood volume
  4. Artherosclerosis → ischemia/infarction causing arrhythmias
210
Q

What are the reproductive consequences seen in hypothyroidism?

A
  1. Males → decreased fertility
  2. Females → infertility
  3. Intact bitches → hyperprolactemia
  4. Prolonged anestrus, decreased libido, abortion
211
Q

What are sulfonamides important in the context of hypothyroidism? Why?

A
  1. The only drug that can cause CLINICAL hypothyroidism along with testing changes
  2. Blocks iodination of thyroglobulin
212
Q

What would be the result for the following values in a patient being administered sulfonamides or phenobarbital?

  1. T4
  2. fT4
  3. TSH
A
  1. Decreased
  2. Decreased
  3. Increased
213
Q

What is euthyroid sick syndrome?

A
  1. Low total T3 or Total T4

2. Free T4 and TSH will be normal

214
Q

What is the underlying mechanism in euthyroid sick syndrome?

A
  1. Changes in hormone binding to serum carrier proteins, peripheral hormone distribution, and metabolism
  2. Inhibition of TSH secretion
  3. Inhibition of thyroid hormone synthesis
215
Q

What is the most accurate single hormone measurement for diagnosis of hypothyroidism?

A
  1. Free T4 by equilibrium dialysis
216
Q

What test for hypothyroidism will not be influenced by non-thyroidal factors?

A
  1. NONE → even free T4 can be affected by some drugs and non-thyroid diseaes
217
Q

Why is TSH recommended to be used along with T4?

A

It has a poor sensitivity by itself but increases to 100% when used in conjunction

218
Q

What causes the HCM-like syndrome observed in hyperthyroidism?

A
  1. Induced production of myosin isoform that increases the speed of myosin/actin interaction → increases contractility
  2. Increased activity of SR Ca-ATPase and CA pumps → increase contractility and speed of diastole
  3. Increased activity of ion channels
  4. Increased number of β adrenergic receptors
219
Q

What is the most common arrhythmia seen in hyperthyroidism?

A

Sinus tachycardia

220
Q

What happens to diastolic and systolic pressures in hyperthyroidism?

A
  1. Systolic pressure → increased

2. Diastolic pressure → decreased

221
Q

How might renal disease be masked in hyperthyroidism cats?

A
  1. Hyperthyroidism → reduced muscle mass → falsely decreased creatinine that may mask renal disease
222
Q

What is the preferable test for diagnosing hyperthyroidism in cats?

A
  1. T4
    * T4 and T3 are both very SPECIFIC for hyperthyroidism but T4 is preferred because T3 can be normal in some scenarios despite an increased T4
223
Q

How should free T4 be used in the diagnosis of feline hyperthyroidism?

A
  1. Very sensitive but not as specific as T4

* Always use concurrently with T4, NEVER ALONE

224
Q

Why might β blockers be used in the treatment of hyperthyroidism?

A

They block the conversion of T4 to T3

225
Q

What is the TRH response test?

A 
In healthy cats:
- TRH → Increases TSH → Increase T4
- Should have increase in T4 >60%
In hyperthyroid cats
- This pathway is less functional due to chronic TSH suppression from excess T4 secretion
- Increase in T4 after TRH <50%
226
Q

What is the best test for confirming euthyroidism and ruling out hyperthyroidism in cats?

A

T3 suppression test

227
Q

How does calcitonin decrease Ca

A
  1. Decrease osteolytic effect on bone resorption

2. Decreases osteoclast activity

228
Q

What is secreted from pancreatic a cells?

229
Q

What is secreted from pancreatic β cells?

230
Q

What is secreted from pancreatic d cells?

A

Somatostatin

231
Q

Which glucose transporters are insulin dependent? Independent?

A
  1. GLUT4

2. GLUT1, GLUT2, GLUT3, GLUT5

232
Q

Where are GLUT-2 receptors found?

A
  1. Liver
  2. Pancreas β cell
  3. Intestine
233
Q

What is the function of the GLUT5 transporter?

A

Facilitated diffusion of fructose in the intestine

234
Q

What are SGLT transporters?

A

Na-dependent glucose transporters

235
Q

What is the mechanism for insulin release?

A
  1. Pancreatic β cell bind glucose on GLUT2 transporters
  2. Glucose enters the cells and is converted to Glucose-6-Phosphate
  3. G6P is converted to ATP which inhibits K channels
  4. Closed K channels depolarize the cell → open voltage gated Ca channels
  5. Influx of Ca stimulates release of insulin
236
Q

What factors stimulate insulin release?

A
  1. GLUCOSE
  2. Glucagon
  3. Amino acids → Lysine and arginine
  4. Growth hormone, Cortisol, Progesterone, Estrogen, Gastrin, Secretin, CCK, GIP, GLP-1
  5. Fatty acids
  6. Parasympathetic stimulation
  7. β adrenergic stimulation
237
Q

What factors inhibit insulin secretion?

A
  1. Epinephrine, Norepinephrine
  2. DECREASED GLUCOSE
  3. Fasting
  4. Somatostatin
  5. Leptin
238
Q

How do sulfonylurea drugs increase insulin secretion?

A

They bind to the ATP dependent K channels and close them

239
Q

How does insulin decrease blood glucose?

A

Promote glucose uptake by GLUT4

240
Q

When does muscle utilize glucose?

A
  1. During heavy exercise
  2. After a meal
  3. If there is a lot of glucose
    * Usually just uses fatty acids for energy
241
Q

What are the functions of insulin?

A
  1. Inactivates phosphorylase → typically converts glycogen to glucose
  2. Activates glucokinase (liver)/hexokinase (other tissues) → promotes adding P to glucose to make G6P (traps it in the cell)
  3. Activates glycogen synthase → promotes glycogen formation
  4. Inhibits glucose phosphatase
  5. Activates lipoprotein lipase on endothelial cells
  6. Inactivates hormone sensitive lipase in cells
  7. Promotes TG and protein storage
  8. decreases gastric emptying
  9. Increases satiety
  10. Decreases glucagon release
242
Q

What is the effect of insulin on the liver?

A
  1. Insulin promotes storage
  2. Activates glucokinase
  3. Inhibits liver phosphorylase
  4. Activates glycogen synthase
  5. Inhibits hepatic gluconeogenesis
    * The liver is the most important site of glucose storage
243
Q

What is the effect of insulin on fat metabolism?

A
  1. Glucose → FA → TG → VLDL → adipose tissue

2. insulin activates lipoprotein lipase → breaks down TG to fatty acids at adipose tissue to allow absorption

244
Q

What is the effect of insulin on protein metabolism?

A
  1. Increases protein synthesis in the liver by increasing uptake of amino acids
  2. Inhibits hepatic gluconeogenesis → spares amino acids
  3. Stimulates RNA translation
  4. Acts synergistically with GH to promote growth
245
Q

What are the functions of glucagon?

A

Acts to increase blood glucose

  1. Stimulates hepatic gluocneogenesis
  2. Activates cAMP in hepatocytes → promotes phosphorylase to break down glycogen to glucose
  3. Activates hormone sensitive lipase
  4. Enhances strength of the heart
  5. Utilizes amino acids for gluconeogenesis
  6. Increases blood flow
  7. Enhances bile acid secretion
  8. Inhibits fat storage, activates adipose cell lipase
  9. Inhibits gastric acid secretion
246
Q

What factors stimulate glucagon secretion?

A
  1. Low blood glucose
  2. Elevated amino acids
  3. Elevated cortisol
  4. Elevated insulin
247
Q

What is the function of somatostatin?

A

Inhibitory actions on:

  1. Insulin and glucagon
  2. Gastric secretion (esp on G cell)
  3. S cells
  4. I cells
  5. Motility
  6. GH release, TSH
248
Q

What are the most common disease that cause insulin resistance in the dog?

A
  1. Steroids
  2. Obesity
  3. Hyperadrenocorticism
  4. Diestrus
  5. Chronic pancreatitis
  6. Renal insufficiency
  7. UTI
  8. Hyperlipidemia
  9. Development of insulin antibodies in dogs treated with BEEF insulin
249
Q

What are the most common disease that cause insulin resistance in the cats?

A
  1. Obesity
  2. Chronic pancreatitis
  3. Renal insufficiency
  4. Hyperthyroidism
  5. Oral infection
  6. Acromegaly
  7. Hyperadrenocorticism
250
Q

What causes DKA to occur?

A

Insulin deficiency causes an increase in lipolysis → excessive ketone body production and acidosis

251
Q

What is the hallmark of DKA?

A
  1. Increased GLUCAGON:INSULIN ratio
252
Q

Duration of insulin action (short/intermediate/long)

- Regular

253
Q

Duration of insulin action (short/intermediate/long)

- NPH (Humulin or Novalin)

A

Intermediate

254
Q

Duration of insulin action (short/intermediate/long)

- Lente (Vetsulin)

A

Intermediate

255
Q

Duration of insulin action (short/intermediate/long)

- PZI

A

Long

*Not recommended since 90% beef

256
Q

Duration of insulin action (short/intermediate/long)

- Glargine

A

Long

*Insulin analog

257
Q

Duration of insulin action (short/intermediate/long)

- Ultralente

A

Long

*Longest acting but least potent

258
Q

What does fructosamine represent?

A
  1. Represents average BG over past 1-3 weeks
259
Q

What can cause a false decrease in fructosamine in dogs?

A
  1. Hypoproteinemia
  2. Hyperlipidemia
  3. Azotemia
260
Q

What can cause a false decrease in fructosamine in cats?

A
  1. Hypoproteinemia

2. Hyperthyroidism

261
Q

What should you be concerned about if you find a normal to low fructosamine in a diabetic patient?

A
  1. Be concerned with periods of hypoglycemia and insulin overdose
262
Q

What insulin should you start with in a diabetic dog?

A
  1. Lente or NPH
263
Q

What insulin should you start with in a diabetic cat?

A
  1. Glargine (or PZI)
264
Q

What should the nadir be in a diabetic dog?

265
Q

Diabetic ocular complications are (more/less) common in dogs compared to cats

266
Q

What % of cultured urine in diabetic cats has a UTI in the absence of pyuria?

267
Q

What are the mechanisms for non-insulin-dependent diabetes mellitus?

A
  1. Insulin receptor defect

2. Increased hepatic gluconeogenesis

268
Q

Diabetes will lead to (increased/decreased) triglyceride levels in serum?

A

Increased

*Insulin deficiency impairs LPL activity

269
Q

T3 has a (shorter/longer) half life than T4

ACVIM General Exam (15 decks)

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