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Pharm Exam II > Endocrine > Flashcards

Endocrine Flashcards

1
Q

what drug is commonly used to treat the effects of pheochromocytoma?

A

phenoxybenzamine

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2
Q

T/F: dogs commonly get hyperthyroidism

A

FALSE, rare. they more commonly get hypothyroidism

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3
Q

T/F: 89% of T4 and T3 are bound to plasma proteins

A

FALSE, 99%! remaining 1% is free

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4
Q

where is most of T4 made?

A

in follicular cells and stored as colloid in thyroid gland

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5
Q

T/F: T3 is made in follicular cells of the thyroid gland and is stored as colloid

A

FALSE, T4 is made here and converted to T3 in the cell where its needed

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6
Q

what is the goal of therapy for hypothyroidism in dogs?

A

REPLACE hormone the body isn’t producing

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7
Q

T/F: liothyronine is the drug of choice for hypothyroidsm in dogs because of its T3 form, less frequent dosing, and lower risk of causing thyrotoxicosis

A

FALSE, levothyroxine (T4)

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8
Q

thyrotoxicosis

A

excessive T4 levels

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9
Q

how might you reduce the risk of oversupplementation in large patients (>50lb)?

A

instead of dosing mg/kg, dose mg/m2 (body surface area dosing)

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10
Q

is levothyroxine given IV, PO, or IM?

A

PO, IV only used in rare situations like myxedema coma

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11
Q

T/F: when treating patients via mg/kg instead of mg/m2 it is more common to underdose small dogs and overdose large dogs

A

TRUE, smaller dogs have higher metabolisms

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12
Q

what should you monitor when treating a patient long term for hypothyroidism?

A

measure T4 levels, 4 wks after starting therapy

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13
Q

T/F: phenobarbital can interfere w/ thyroid test results

A

TRUE, as well as zonisamide, sulfonamides, glucocorticoids, phenylbutazone, quinidine, etc.

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14
Q

what is the goal of therapy for hyperthyroidism in cats?

A

stop excessive hormone production

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15
Q

how does Hill’s y/d help treat hyperthyroidism in cats and what patient would you be concerned about using diet therapy with?

A

prevents production (iodine uptake), watch out for in outdoor cats!! w/ diet therapy they must be strict in sticking to the diet

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16
Q

T/F: based on biological mechanisms thioureylenes would be a much better choice in treatment of hyperthyroidism in cats than iodides and iodinated contrast agents

A

FALSE, biologically iodides and iodinated contrast agents do more things in the body to go towards the treatment of hyperthyroidism

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17
Q

T/F: carbimazole is a prodrug that is metabolized to its active form methimazole

A

TRUE

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18
Q

what makes methimazole the drug of choice for hyperthyroidism in cats

A
  • consistently efficacious

- side effects are uncommon and most are manageable

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19
Q

why would you choose to use methimazole over propylthiouracil (PTU) when treating hyperthyroidism in cats?

A

PTU, like methimazole, is thioureylene and is efficacious but it has a higher incidence of serious side effects

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20
Q

T/F: iodides/iodinated contrast agents have variable efficacy and are transient

A

TRUE, don’t work well in all cats and is clinically unreliable

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21
Q

what are three drugs that are considered methimazoles?

A
  • tapazole (human approved, use extra label)
  • felimazole
  • transdermal methimazole (acquire from compounding)
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22
Q

T/F: methimazole is a drug product used for hyperthyroidism in cats

A

FALSE, methimazole is an active ingredient and therefore not considered a “product”, FDA does not register pure active ingredients

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23
Q

matilda the cat is given felimazole and is shows an idiosyncratic rxn. can you prescribe her tapazole instead?

A

NO, idiosyncratic reactions are not dose dependent, all about the drug and it’s metabolites. tapazole also has methimizole as it’s active ingredient

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24
Q

facial excoriation is an idiosyncratic rxn you might see when what drug is given to a cat with hyperthyroidism?

A

methimazole (tapazole, felimazole, transdermal methimazole)

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25
Q

what mild side effects might you see with a cat with hyperthyroidism given methimazole?

A

GI signs, transient hematologic changes in CBC

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26
Q

oden the cat has been on felimazole for hyperthyroidism and is continuing to show mild GI signs (vomiting). what can you prescribe him to alleviate these symptoms?

A

switch him to transdermal methimazole

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27
Q

T/F: clinical signs for acute hypocalcemia include hyperesthesia/pawing at face, tremors, progressing to flaccid paralysis, seizures, hypethermia, and bradycardia

A

TRUE

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28
Q

what causes ‘milk fever’ in cows and eclampsia in dogs?

A

periparturient hypocalcemia, sudden increase in calcium usage (i.e. lactating, after whelping) in which patient can’t adapt readily enough

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29
Q

daisy the cow has milk fever, how do you treat her?

A

replace her calcium deficit until she catches up

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30
Q

what are two parenteral calcium options used for acute treatment of hypocalcemia?

A

Ca Gluconate or Ca Chloride

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31
Q

T/F: Ca Chloride is administered PO/SQ

A

FALSE, it’s caustic and parenteral, NEVER give SQ/IM

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32
Q

rapid administration of what can cause arrhythmias?

A

calcium, monitor ECG

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33
Q

what are two oral options used to treat chronic hypocalcemia (hypoPTH)?

A

Ca Carbonate (small animal), Ca Propionate (large animal, food additive)

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34
Q

what is the control booth for calcium metabolism?

A

parthyroid glands! no PTH means the GIT can’t absorb Ca

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35
Q

T/F: hypoparathyroidism results in the inability of the body to convert Vitamin D to it’s active form (calcitriol)

A

TRUE

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36
Q

what three areas of the body are involved in calcium metabolism in the body?

A
  • bone (storage)
  • kidneys (excretion)
  • gut (absorption)
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37
Q

what is the most potent activated form of vitamin D?

A

calcitriol, rapid

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38
Q

what is the biggest potential side effect of calcitriol?

A

hypercalcemia (monitor serum calcium levels!)

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39
Q

T/F: calcitriol is the best vet approved drug of choice for treatment of hypocalcemia from hypoPTH

A

FALSE, no vet approved form, only human-approved products

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40
Q

T/F: calcitriol capsules are in mcg which means they have a narrow therapeutic index (TI)

A

TRUE

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41
Q

what must you replace in the lifelong management of hypocalcemia from hypoPTH?

A

replace vitamin D

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42
Q

what might you try first when a patient is exhibiting signs of acute/transient hypoglycemia?

A

frequent, small meals with complex carbohydrates

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43
Q

T/F: ongoing IV dextrose solutions should be NO LESS than 5% concentration

A

FALSE, they should be NO MORE than 5% concentration

44
Q

quick!! puss the cat was acting lethargic so you gave him a small meal and now he’s seizing!! what do you give him?

A

intravenous bolus of dextrose, use in emergency situations (usually 1ml/kg of 50% dextrose diluted 1:4)

45
Q

what toxin causes a massive insulin release in dogs?

A

xylitol, keep that sugar free gum hidden!

46
Q

what must you address and alter when it comes to treating chronic hypoglycemia?

A
  • address the cause

- alter glucose production/use by body (diet, corticosteroids)

47
Q

what corticosteroids do you use in the treatment of chronic hypoglycemia?

A

prednisone/prednisolone

48
Q

what usually causes hyperglycemia?

A
  • something that doesn’t require therapy (STRESS)

- diabetes mellitus (DM)

49
Q

what is the primary goal of diabetes mellitus therapy?

A

address the insulin deficiency

50
Q

diabetes mellitus =

A

insulin deficiency

51
Q

T/F: amino acid sequence of insulin is highly preserved across species

A

TRUE, dog=pig

52
Q

insulin is produced by what cells of the islets of langerhans in what organ?

A

beta-cells, endocrine pancreas

53
Q

when BG rises what channels close causing depolarization and insulin release?

A

energy-dependent K+ channels

54
Q

where in the body is glucose used as an energy source?

A

liver, muscle, adipose, heart

55
Q

T/F: in peripheral tissues insulin binds to insulin receptors allowing glucose to enter the cell and be utilized

A

TRUE

56
Q

T/F: human approved insulin formulas are 40 IU/mL and veterinary approved insulin formulas are 100 IU/mL

A

FALSE, opposite

57
Q

what are three major factors you must consider when using exogenous insulin?

A
  • concentration (big impact on dose)
  • duration of action (short, intermediate, long)
  • potency (what impact will the drug have)
58
Q

in what order of duration (shortest to longest) are NPH, regular insulin, and protamine zinc/PZI?

A

regular insulin>NPH>protamine zine/PZI

59
Q

which insulins are given SQ only?

A

intermediate (NPH, Lente, Vetsulin) and long-acting (protamine zinc/PZI, glargine, detemir)

60
Q

T/F: regular insulin is the only insulin that can be administered IV

A

TRUE! IV, IM or SC

61
Q

what type of insulin is most commonly used for hospitalized patients?

A

regular insulin, can be given IV CRI or intermittent IM/SC

62
Q

T/F: an insulin with fast onset and shorter duration gives you as a vet more control

A

TRUE, more predictable

63
Q

what two insulin types are added to delay absorption and extend clinical effect?

A

protamine (NPH) and zinc (lente)

64
Q

what type of insulin is the “go to”, especially for canines?

A

vetsulin (porcine lente insulin)

65
Q

T/F: vetsulin may cause a longer duration in felines

A

FALSE, SHORTER

66
Q

T/F: a more potent insulin will be harder to dose because of smaller doses (i.e. small dogs)

A

TRUE, (i.e. 0.5 IU increments are very hard to draw up in a syringe accurately)

67
Q

which insulin type is generally the “go to” for cats?

A

glargine

68
Q

what causes glargine to have very gradual absorption (‘flat’ curve)?

A

it forms microprecipitates in the body, slowly doles out insulin

69
Q

what two long-acting insulin types are human approved?

A

glargine and detemir

70
Q

which insulin type is known to be the most potent?

A

detemir, 4x in dogs!!

71
Q

which insulin type is difficult to dose in small dogs and why?

A

detemir because of its potency

72
Q

which insulin type is now offered as a dosing pen?

A

vetsulin, provides ease and precision of dosing but $$

73
Q

what do oral ‘antidiabetic’ drugs cause?

A

hypoglycemia

74
Q

what is the main oral hypoglycemic agent used in veterinary medicine?

A

glipizide

75
Q

what type of diabetes do you use oral hypoglycemic agents for?

A

TYPE II in cats, pancreas’ beta cells are still capable of secreting insulin but don’t secrete much. these drugs trigger insulin release (by blocking K+ channels) from the remaining cells

76
Q

in which animal do you NOT use hypoglycemic agents?

A

dogs

77
Q

why should you monitor patients that are given oral hypoglycemic agents?

A

can cause SIGNIFICANT hypoglycemia

78
Q

if oral hypoglycemic agents are capable of causing significant hypoglycemia and accelerate beta-cell loss, why would a vet prescribe them for a patient?

A

owners!! some owners are deathly afraid of needles

79
Q

T/F: glipizide is safer because it’s oral

A

FALSE, can still have significant adverse effects

80
Q

where are mineralcorticoids produced?

A

in the zona glomerulosa in the adrenal cortex

81
Q

where are glucocorticoids produced?

A

in the zona fasciculata in the adrenal cortex

82
Q

mineralcorticoids =

A

aldosterone (endogenous hormone)

83
Q

glucocorticoids =

A

cortisol (endogenous hormone)

84
Q

T/F: glucocorticoids should NOT be given concurrently w/ NSAIDs

A

TRUE, can cause ulcers

85
Q

T/F: prednisone, prednisolone, dexamethasone, triamcinolone and methylprednisolone are examples of mineralcorticoids

A

FALSE, glucocorticoids

86
Q

what are the two mechanisms of action of glucocorticoids?

A
  • non-genomic effects (receptors in membrane, rapid effects)

- genomic effects (nuclear type GCRs in cytoplasm, bind and move to nucleus, increase or decrease gene expression

87
Q

why are glucocorticoids used (in general)?

A

anti-inflammatory effects

88
Q

when is it contraindicated to use topical glucocorticoids?

A

corneal ulcers, infection (active), or diabetes

89
Q

T/F: glucocorticoids antagonize insulin

A

TRUE! avoid in diabetes

90
Q

what are the clinical uses for glucocorticoids?

A

-diagnostic testing
-physiologic replacement therapy (low doses, i.e. hypoadrenocorticism or Addison’s disease)
-anti-inflammatory
-immunosuppressive (high doses)
(depending on dose you’ll hit on these different uses)

91
Q

T/F: glucocorticoids are protein bound

A
  • specific transporter transcortin (high affinity, low capacity)
  • albumin secondary (low affinity, high capacity)
92
Q

why should you administer prednisolone topically rather than prednisone?

A

if it’s topical it’s localized so the drug wont’ have the chance to be hydrolyzed, need to give in active form

93
Q

why is it preferred to give cats prednisolone rather than prednisone?

A

because cats aren’t great at hydrolyzing prednisone to prednisolone (active form)

94
Q

what are two main considerations in using glucocorticoids?

A
  • potency (significant differences between products)

- duration (base steroid has certain duration, formulation will lengthen)

95
Q

how much more potent is dexamethasone than prednisone?

A

7.5 x! (relative potency = 30)

96
Q

T/F: prednisone/prednisolone has a longer duration than dexamethasone

A

FALSE, prednisone/prednisolone< triamcinolone< dexamethasone

97
Q

what two excipients can be added to injectable steroids?

A
  • salt esters (succinate, phosphate)

- insoluble esters (pivalate)

98
Q

what do salt/soluble esters do when added to a glucocorticoid?

A
  • make steroid soluble
  • makes suitable for IV admin
  • faster onset (DURATION UNCHANGED)
99
Q

what do insoluble esters such as pivalate do when added to a glucocorticoid?

A
  • cause delayed onset, long duration (‘depot’)
  • NOT FOR IV USE
  • i.e. depo-medrol (stays in muscle as depot and is slowly released)
100
Q

name three important mineralcorticoids

A
  • aldosterone (endogenous)
  • DOCP
  • fludrocortisone
101
Q

T/F: aldosterone excretes Na and retains K

A

FALSE, opposite

102
Q

T/F: Addison’s disease is a disease that causes a deficiency in aldosterone

A

TRUE

103
Q

which is longer acting, fludrocortisone or DOCP?

A

DOCP, contains pivalate

104
Q

which corticosteroid shows a small amount/the most glucocorticoid activity of the mineralcorticoids?

A

fludrocortisone, also has more Na retention compared to DOCP

105
Q

what would you measure when monitoring mineralcorticoids?

A

K+/Na+

106
Q

T/F: fludrocortisone is given parentally (IM, SC) and DOCP is given orally

A

FALSE, opposite, remember DOCP has pivalate added so NO IV USE

Pharm Exam II (6 decks)

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