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SAM I again > Settles Endocrine > Flashcards

Settles Endocrine Flashcards

1
Q

What is the MOST active form of the thyroid hormone in a cell?

A

FREE T3! It is free because it is not attached to a protein. Do NOT confuse this with rT3. rT3 is the result of deiodination of T4 to inactive

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2
Q

What test is used to dx hypoadrenocorticsm?

A

ATCH stim

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3
Q

Is diabetes mellitus ever reversible?

A

Yes

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4
Q

What are common clinical signs of hypercalcemia?

A

seizures! weird ECGs

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5
Q

What is your T4 level if you have primary hypothyroidism?

A

LOW

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6
Q

What are some additional causes of low T4?

A

iatrogenic (if P had I131 tx), euthyroid sick syndrome, drug therapy

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7
Q

What is the typical hypothyroid signalment

A

middle age, medium to large breed

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8
Q

What are your typical hypothyroid CSs?

A

Generalize weight gain, slow/”old”, lethargic, alopecia (truncal), hyperpigmentation, rat tail, seborrhea

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9
Q

What is a specific accompanying condition with hypothyroid patients?

A

hypothyroid myxedema. Occurs around peripheral nerves. It is the deposition of mucopolysaccharides in the dermis

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10
Q

If you have hypothyroid as a Ddx, what steps are you going to take next?

A
  1. CBC, chem, U/A.
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11
Q

What will you see on your CBC if your patient is hypothyroid?

A

mild anemia, HYPERCHOLESTEROLEMIA!!!

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12
Q

If you submit a T4, what would rule out hypothyroidism?

A

Normal T4 level

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13
Q

What do low levels of T4 indicate?

A

hypothyroidsim or ESS

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14
Q

If you have low T4 and HIGH TSH, what is this supportive of?

A

Hypothyroid dz!

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15
Q

What do you treat hypothyroidism with?

A

Levothyroxine

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16
Q

Monitoring therapy: what will you see in 1-2 weeks

A

attitude improvement

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17
Q

Monitoring therapy: what will you see in 4-6 weeks

A

improvement in derm signs

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18
Q

Monitoring therapy: what will you see in 2-4 months?

A

hair regrowth!

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19
Q

When I say hyperthyroidism, you say?

A

CATS

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20
Q

What is the etiology of hyperthyroidism?

A

excessive production of T4 and T3

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21
Q

What is the most common cause of hyperthyroidism?

A

functional adenoma (70% of cats have this bilaterally)

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22
Q

What does the thyroid hormone do to glucose?

A

Increases it!!!! it increases gluconeogenic enzymes

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23
Q

What happens to muscles with excess thyroid hormone?

A

thinner muscles due to myosin heavy chain destruction

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24
Q

What does your typical hyperthyroid patient look like?

A

skinny (weight loss), unkempt, scraggly coat, PU/PD, GI signs (THEY ARE EATING BUT THEY ARE STILL LOSING WEIGHT!)

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25
Q

What are you going to find on PE on a hyperthyroid patient?

A

goiter, “thyroid slip”, tachycardia, murmur/gallop

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26
Q

What indicates a thyroid storm?

A

HR >220, hypertensive, blown retinas

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27
Q

What are you going to see on your lab work of a hyperthyroid patient?

A

CBC: stress leukogram (increased WBC, increased neutrophils, decreased lymphocytes)
Chem: INCREASED ALT!!!
U/A: +/- dilute

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28
Q

What are your four treatments available for hyperthyroid patients?

A
  1. medical
  2. dietary
  3. surgical
  4. radioactive
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29
Q

What is your number one drug for hyperthyroid patients

A

methimazole

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30
Q

How does methimazole work?

A

inhibits thyroid hormone synthesis by blocking incorporation of iodine

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31
Q

What kind of diet should you place a hyperthyroid patient on?

A

low iodine

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32
Q

What is the surgical tx for hyperthyroidism?

A

thyroidectomy

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33
Q

What type of radiation tx are you going to do on your hyperthyroid patient?

A

I131

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34
Q

What is hyperadrenocorticism?

A

excessive production of glucocorticoids by the adrenal glands

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35
Q

How many forms of hyperadrenocorticism are there?

A

3! pituitary dependent, adrenocortical neoplasia, iatrogenic

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36
Q

what percentage of cases does pituitary dependent cushing’s account for?

A

80-85%.

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37
Q

What determines a pituitary dependent cushing’s patient

A

functional ACTH secreting pituitary tumor! It will cause bilateral adrenocortical HYPERplasia

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38
Q

Why would you classify a chushing’s patient, as iatrogenic cushing’s?

A

excessive exogenous steroids; bilateral adrenal atrophy

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39
Q

What classifies an adrenal dependent cushing’s patient?

A

adrenocoritcal tumors! usually atrophy of the contralateral gland

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40
Q

What is your typical signalment of a cushing’s patient?

A

poodles, boxers, dachshunds, schnauzers, boston terriers, GSDs; Middle aged-old; RARE in cats!

41
Q

What is your typical hx and CSs in a cushing’s patient?

A

PU/PD; polyphagia; pendulous abdomen; panting; thin skin; muscle/ligament weakness and atrophy; calcinosis cutis!!!; hyperpigmentation; CNS signs

42
Q

How are you going to dx cushings?

A

Hx and CSs usually!

43
Q

But because this is Settles, how are you REALLY going to dx cushings?

A

With ultrasound, duhhhh

44
Q

What are you going to see on a CBC of a cushings patient?

A

polycythemia, stress leukogram

45
Q

What are you going to see on a chem of a cushings patient?

A

HYPERCHOLESTEROLEMIA!

INCREASED ALP!

46
Q

what other dx test are you going to perform on a cushings patient other than a CBC and chem?

A

UA! specifically a urine culture and UPC

47
Q

What is important about a UPC in a cushings patient?

A

a negative UPC will make cushings unlikely. a positive test WILL make cushings likely but it is NOT diagnostic!

48
Q

Is LDDST a diagnostic test?

A

yes! 95% dx with PDH, 100% dx with AT. Cushingoid dogs do NOT supress

49
Q

What is the test of choice for addisons dz (hypoadrenocorticisim?)

A

ATCH stim

50
Q

Are you going to use HDDST to diagnose cushings?

A

Nope!! but if you note suppression, chances are it’s a PDH

51
Q

When are you going to use ACTH stim?

A

with a mild CS/lab abnorm.
patients with concurrent non-adrenal dz
patients with suspected IATROGENIC cushing’s dz
patients on phenobarb

52
Q

When are you going to use LDDST?

A

patients with severe CSs and no evidence of non-adrenal dz

patients with suspected AT

53
Q

What are your tx options for hyperadrenocorticism?

A

Mitotane, selegiline, Trilostane, ketoconazole, surgical, radiation

54
Q

What does mitotane do?

A

it is an adrenal cytoTOXIC agent used to treat PDH

  • causes severe, progressive necrosis of the zona fasciculata and zona reticularis
  • PERMANENT adrenal atrophy
55
Q

What does selegiline do?

A

MAO-B inhibitor that may be useful for cognitive dysfunction syndrome in dogs/cats/or PDH patients

  • cheap tx
  • use on Ps that are negative on labwork but have mild CSs of cushings
56
Q

What does trilostane do?

A

competitive inhibitor of 3-beta hydroxysteroid dehydrogenase

  • reduces the synthesis of cortisol, aldosterone, and adrenal adrogens
  • inhibition is REVERSIBLE
  • can cause hyperkalemia
57
Q

What does ketoconazole do?

A

palliative tx in dogs with large, malignant, or invasive AT.

- reversible inhibitor of steroidogenesis

58
Q

Prognosis of cushing’s patients?

A

PDH - good
malignant AT - POOR
good prognosis if ZERO evidence of local invasion/benign AT

59
Q

What are the two hormones made in the posterior pituitary?

A

ADH/vasopressin and oxytocin

60
Q

What is the function of ADH/vasopressin?

A

promotes the reabsorption of water int he CT of the kidneys

61
Q

How does aldosterone work?

A

promotes Na, Cl reabsorption, K excretion

62
Q

What are the major regulators of aldosterone secretion?

A

Plasma K+ levels and RAS

63
Q

Where is ADH made?

A

in the hypothalamus. The nerve cells transport ADH to the pituitary gland where it is released into the blood stream

64
Q

What does ADH do?

A

decreases urine production, decreases sweating, increased BP

65
Q

If patient is dehydrated?

A

ADH is released! It wants to conserve water!

66
Q

If patient is overhydrated?

A

ADH is inhibited! It wants to get rid of excess water!

67
Q

What is aldosterone?

A

a hormone that affects Na reabsorption. It gets released if blood is diluted and low in volume. It causes more sodium to be reabsorbed

68
Q

is ACTH needed for aldosterone release?

A

NO!

69
Q

What are your main indicators for an addisonian patient?

A

dogs, young-middle aged, females >males, ADR, anorexia, lethargy, dehydration, weakness, polyuria

70
Q

What is the definition of “typical” hypoadrenocorticism?

A

deficient in mineralocorticoids and glucocorticoids due to primary lesions

71
Q

What is something you will not see on the CBC of an addisonian patient

A

you will NOT see a stress leukogram!!!!

72
Q

What are some clinpath abnormalities you’ll see in an addisonian patient?

A

hyponatremia, hyperkalemia, USG will be isosthenuric, mild hypoglycemia

73
Q

What is going to be your typical maintenance therapy for your addisonian patients?

A

percorten injections. DOCP injections do NOT possess any glucocorticoid activity; florinef - has some glucocorticoid activity

74
Q

What is the definition of Type I DM

A

failure of pancreatic beta cells, immune cells destroy beta cells in the pancreas

75
Q

What is the definition of Type II DM

A

insulin resistance and beta cell burnout with time

  • pancreas produces less insulin
  • more glucose is in the blood
  • insulin moves less glucose into the bells
76
Q

Which diabetes is most common in cats?

A

Type II DM

77
Q

Which diabetes is most common in dogs

A

Type I DM

78
Q

What are CSs of diabetes in dogs?

A

PU/PD/polyphagia

weightgain leading to weight loss

79
Q

what are some diabetic neuropathies?

A

pantigrade posture; sensorimotor neuropathy in BOTH pelvic and thoracic limbs

80
Q

Why do you get nerve structural abnormalities with diabetes?

A

increases in fructose and sorbitol

81
Q

What are CSs of a healthy diabetic?

A

PU/PD, +/- weightloss, polyphagia, dry/flaky skin, plantigrade stance

82
Q

What are the 3 types of insulin?

A

short, intermediate, and long

83
Q

What is short insulin?

A

Ex: regular (glargine, R-insulin)
15 min onset
5-6h duration

84
Q

What is intermediate insulin?

A

Ex: NPH, lente (vetsulin)
15 min onset
6-12h duration

85
Q

What is long insulin?

A

Ex: PZI, ultralente
1-2h onset
8-24h duration

86
Q

What kind of dietary therapy are you going to place a diabetic pet on?

A

high protein, low carb

87
Q

What is weird about fructosamine levels in cats?

A

Fructosamine levels will be falsely lowered in cats with hypoproteinemia and hyperthyroidism

88
Q

What is total calcium made up of?

A

iCa - 50%
chelated Ca - 10%
protein bound - 40%

89
Q

What are some sources of active vitamin D?

A

Fortified food!
fish
dairy

90
Q

What does calcitonin do?

A

Tones down the Ca! It increases Ca deposition in bones, decreases Ca uptake in intestines, and decreases Ca reabsorption from urine

91
Q

What does the PTH do?

A

increases Ca release from the bones, increases Ca uptake in intestines, and increases Ca reabsorption from urine

92
Q

What are the CSs of hypercalcemia?

A

PU/PD, weakness lethargy, inappetence, V+/d+

93
Q

The important Ddx of hypercalcemia

A

DRAGONSHIT
D= hypervitaminosis D
A= addisons
H= hyperparathyroidism

94
Q

Calcium and phosphorus have what kind of relationship?

A

INVERSE! Also if the product of [Ca][P] = >70, you will have mineralization of soft tissues!!!

95
Q

Hypocalcemia will result in what?

A

minor drop in Ca = increase in PTH

major drop in Ca = increase in PTH and Vitamin D3

96
Q

Etiologies of hypocalcemia

A
  1. primary hypoparathyroidism

2. eclampsia

97
Q

How do you dx hypocalcemia?

A

serum iCa, PTH levels, ECG

98
Q

Calcitriol is:

A
  • manmade
  • 1,25-dihydroxycholecalciferol
  • Vitamin D3
99
Q

Calciferol is:

A

ergocalciferol –> 25 hydroxyvitamin D –> 1,25 dihydroxyvitamin D (ACTIVE FORM!)

SAM I again (4 decks)

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