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Pharmacology 1 choefsho > Endocrine pharmacology > Flashcards

Endocrine pharmacology Flashcards

1
Q

Which drugs would you use to replace an endogenous substance for hypoglycemia?

A

Dextrose

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2
Q

Which drugs would you use to replace an endogenous substance for hypoadrenocorticism “Addison’s”?

A

DOCP/Fludrocortisone and prednisone

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3
Q

Which drug with would you use to replace an endogenous substance for hypothyroidism?

A

Levothyroxine

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4
Q

Which drug would you use to replace an endogenous substance for hypocalcemia?

A

Calcium gluconate

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5
Q

Which drug would you use to replace something that allows the body to regain normal homeostasis for hypocalcemia from low PTH (indirect)?

A

Vitamin D/Calcitriol

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6
Q

What would you use to increase the elimination of calcium?

A

Saline diuresis

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7
Q

Which drug would you use to inhibit the production of substances from the thyroid?

A

Methimazole

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8
Q

Which drug would you use to inhibit the production of substances from the adrenals?

A

Trilostane

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9
Q

Which drug would you use to destroy the abnormal tissue in thyroids?

A

I131

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10
Q

Which drug would you use to destroy the abnormal tissue in the adrenals?

A

Lysodren

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11
Q

T or F. If there is an acute change, it needs to be reversed acutely and if there is an extremely gradual change, then it should be reversed over a period of time.

A

True

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12
Q

What are the consequences of correcting the endocrine imbalance too quickly?

A

Rebound effects, transient clinical signs, risk of toxicity

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13
Q

Matching! Which condition is more common in which species?

A. Dogs

B. Cats

  1. Hyperthyroidism
  2. Hypothyroidism
A

A. Dogs: 2. Hypothyroidism

B. Cats: 1. Hyperthyroidism

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14
Q

Which of the following is NOT true about thyroid function?

  1. Stimulates erythropoiesis
  2. Enhance response to catecholamines
  3. Increase metabolic rate in most tissues
  4. Increase oxygen consumption in most tissues
  5. Psotive cardiac inotropy and chronotropy
  6. Increase number/affinity of beta adrenergic receptors
  7. Regulate cholesterol synthesis and degradation
  8. Anabolic effects on muscle and adipose tissue
  9. Essential for normal growth and development
  10. Increase body temperature
  11. Increases gluconeogenesis and mobilization of glycogen
  12. Increase proportion of alpha-myosin heavy chains
A
  1. Anabolic effects on muscle and adipose tissue

Should be: CATABOLIC effects on muscle and adipose tissue

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15
Q

Which drug is used to treat hypothyroidism in dogs, and is the preferred drug because it requires less frequent dosing and has a lower risk of causing thyrotoxicosis (excessive T4 levels)?

  1. Liothyronine (T3)
  2. Levothyroxine (T4) (Soloxine)
A
  1. Levothyroxine (T4) (Soloxine)
  • Dosed mg/kg orally BID (sometimes SID, half-life is variable)
  • Injectable only used for rare situations like myxedema coma
  • Reduce risk of oversupplementation in large patients (>50lb) by dosing mg/m^2 instead of mg/kg
  • Replaces the hormone the body is not producing
  • For-life drug
  • Monitored by measuring T4 levels
    • Timing of sample important
    • Start measuring 4 weeks after starting therapy
  • Soloxine brand may give better control in some individuals over generic products
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16
Q

Which drugs could interfere with thyroid test results when monitoring levothyroxine (Soloxine)?

A

Phenobarbital, zonisamide, sulfonamides, glucocorticoids, phenylbutazone, quinidine

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17
Q

You just diagnosed hyperthyroidism in a cat, what treatment options can you give the client besides drugs?

A

y/d (iodine restrictive) diet, surgery (not common anymore), radioactive iodine (very selective, very good)

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18
Q

Which drug is used to treat hyperthyroidism in cats by stopping excessive hormone production?

A

Methimazole in North America and carbimazole in the UK and Australia

  • Tapazole human approved
  • Felimazole vet approved
  • Transdermal methimazole: good bioavailability, compounded
  • Carbimazole is converted in the body to methimazole

Uncommon drugs: Thioureylenes and propylthiouracil PTU, iodides (inhibit organification and release of thyroid hormones but are not as effective), and iodinated contrast agents (inhibit T4 > T3 conversion in periphery)

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19
Q

What are the side effects of using methimzole to treat hyperthyroidism in cats?

A

Mild common reactions: vomiting, transient hematologic changes

Severe idiosyncratic reactions: facial excoriation, hepatopathy, severe bone marrow suppression

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20
Q

In which type of hypocalcemia will you see hyperesthesia/pawing at face, tremors progressing to flaccid paralysis, seizures, hyperthermia, bradycardia?

  1. Acute
  2. PTH/Vitamin D deficiency
A
  1. Acute hypocalcemia
    * Periparturient hypocalcemia: “Milk fever”, eclampsia (body needs more calcium all of a sudden, but cannot produce it fast enough; associated with birth/lactation)
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21
Q

How would you treat acute hypocalcemia?

A
  • Replace the calcium deficit until the patient can ‘catch up’
  • Oral vs. IV calcium (depends on emergency)
  • Ca chloride is caustic so NEVER give SQ/IM
  • Ca gluconate should be diluted if giving SQ (IV better)
  • Caution: rapid IV administration can cause arrhythmias (monitor ECG!) and Ca is incompatible with some fluids and drugs
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22
Q

Why does PTH/Vitamin D deficiency cause hypocalcemia?

A
  • Inability of the body to convert vitamin D to calcitriol (active form)
  • No PTH > GIT can’t absorb Ca (so treat with calcitriol)
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23
Q

How would you treat hypocalcemia due to PTH deficiency?

A

Oral Ca carbonate in small animals and Ca proprionate as a food additive; there are many! GI tract must be able to absorb calcium

  • May need to treat as for acute hypocalcemia in the short term (parenteral calcium vs. oral calcium)
  • Lifelong management of the underlying problem necessary
    • Replace Vitamin D
    • Calcitriol (most potent, significantly increases the absorption of Ca from GIT and reduce loss through kidney; dosing in nanograms so tricky), DHT (dihydrotachysterol), ergocalciferol
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24
Q

How would you treat acute/transient hypoglycemia?

A
  • Diet (frequent, small meals with complex carbs)
  • Dextrose 50% solution (emergencies)
    • Mucosal absorption decent (Karo syrup on gums)
    • IV dextrose can be given as a bolus, diluted 1:4
    • Ongoing IV dextrose must not be > 2.5-5% = phlebitis
    • Do not give dextrose SQ (tissue irritation)
  • Glucagon IV in nanograms (not common)
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25
Q

FYI

If you had a patient on IV fluids with 600mL left in their bad and you wished to make it a 2.5% dextrose solution, how much 50% Dextrose (stock solution) would you add to the bag?

A

30mL

  • (% desired / % stock) x volume in bag
  • (2.5% / 50%) x 600mL = 30mL
26
Q

What are the causes of hyperglycemia?

A

Stress, sepsis, diabetes mellitus

  • Think about DM as ‘insulin deficiency’ and that the hyperglycemia is just a side-effect of not being able to put the glucose into tissue
27
Q

Which oral hypoglycemic agent is used for type II diabetes in cats by stimulating the secretion of insulin?

A

Glipizide (only clinically relevant drug used in vet med )

  • Sulfonylurea drug
  • Stimulates insulin secretion ty the pancreatic beta-cells (via blocking K+ channels to trigger an AP)
  • They also increase tissue sensitivity to insulin
  • Not perfectly ‘safe’
  • May accelerate beta-cell loss
28
Q

Where is insulin naturally produced?

A

Beta-cells of the islets of Langerhans in the endocrine pancreas (stored in vesicles)

  • When blood glucose levels rise, energy-dependent K+ channels close causing membrane depolarization and insulin release
  • Amino acid sequence highly preserved across species (human and pig are 1AA different, dog and pig are the same), so we can use cross-species
29
Q

In peripheral tissues, where does insulin bind?

A

Tyrosine kinase receptors; it makes available glucose transporters than can allow glucose to enter the cell (liver, muscle, adipose, heart)

  • Low blood glucose suppresses insulin release, when insulin levels fall the glucose transporters move back inside the cell
30
Q

How is insulin as a drug administered?

A

All are injectable (IV, SQ, IM)

31
Q

What is the human approved formula concentration and what is the veterinary formula concentration of insulin?

A
  • Humans: 100 IU/mL
  • Veterinary: 40 IU/mL
  • Use the appropriate syringe for the insulin type!
32
Q

How is the duration of insulin categorized?

A

Short, intermediate, and long-acting

33
Q

T or F. The potency of various formulations of insulin is usually all different.

A

False, they are usually very similar; except detemir which is 4x more potent (dogs)

34
Q

Which of the following is a short-acting insulin most commonly used for hospitalized patients who are not eating and is the only one that can be administered IV?

  1. Protomine Zinc/ PZI (Prozinc)
  2. Glargine
  3. Detemir
  4. NPH (Isophane)
  5. Vetsulin/Caninsulin
  6. Regular insulin (Humulin-R, Novalin-R)
A
  1. Regular insulin (Humulin-R, Novalin-R)
    * IV (CRI, not boluses), IM or SQ
35
Q

Which drug is an intermediate-acting insulin that is a good starting insuline type for canines? (pick 2)

  1. Protomine Zinc/ PZI (Prozinc)
  2. Glargine
  3. Detemir
  4. NPH (Isophane)
  5. Vetsulin/Caninsulin (vet formula)
  6. Regular insulin (Humulin-R, Novalin-R)
A
  1. NPH and 5. Vetsulin/Caninsulin
  • ONLY SC
  • Protamine (NPH) or zinc (Lente) are added to delay absorption and extend clnical effect (good because we don’t want glucose levels to fluctuate that much)
  • May not provide adequate control (duration) in felines
  • Insulin pens available for Vetsulin/Caninsulin (ease of use and precision dosing, $$$)
36
Q

Which long-acting insulin has a much higher potency in dogs (4x) so it requires special dosing and may be difficult to dose for small dogs?

  1. Protomine Zinc/ PZI (Prozinc)
  2. Glargine
  3. Detemir
  4. NPH (Isophane)
  5. Vetsulin/Caninsulin
  6. Regular insulin (Humulin-R, Novalin-R)
A
  1. Detemir (Levemir)
  • SQ only
  • Human drug
37
Q

Which long-acting insulin forms a microprecipitate in physiologic pH which results in very gradual absorption (‘flat curve)?

  1. Protomine Zinc/ PZI (Prozinc)
  2. Glargine
  3. Detemir
  4. NPH (Isophane)
  5. Vetsulin/Caninsulin
  6. Regular insulin (Humulin-R, Novalin-R)
A
  1. Glargine
  • SQ only
  • Human drug
38
Q

Which long-acting insulin is a veterinary approved product and may have a shorter duration than the rest of the long-acting insulins?

  1. Protomine Zinc/ PZI (Prozinc)
  2. Glargine
  3. Detemir
  4. NPH (Isophane)
  5. Vetsulin/Caninsulin
  6. Regular insulin (Humulin-R, Novalin-R)
A
  1. Protomine Zinc/PZI (Prozinc)
  • SQ only
  • Good starting drug for cats
39
Q

Review your adrenal gland microanatomy!

A
40
Q

Where in the adrenal gland are glucocorticoids produced?

A

Zona fasciculata of the cortex

  • Cortisol is the endogenous hormone
  • Regulated by the hypothalamus/pituitary through release of CRH (corticotropic releasing hormone) and ACTH (adrenocorticotrophic hormone)
41
Q

What are glucocorticoids used for?

A

Anti-inflammatory effects

  • May have small amounts of mineralocorticoid activity
  • Prednisone, prednisolone, dexamethasone, triamcinolone, methylpredisolone
42
Q

Where do non-genomic effects of glucocorticoids occur?

A

Glucocorticoid receptors in the membrane: rapid effects

43
Q

Where do genomic effects of glucocorticoids occur?

A

Nuclear type GCRs in the cytoplasm: after binding move into the nucleus to increase or decrease gene expression (takes hours to days)

44
Q

What are the physiologic effects of glucocorticoids?

A
  • Increase calcium excretion
  • Reduce fever (be careful that they don’t have an infection!)
  • Suppress immune response (dose/duration dependent)
  • Lymphotoxic
45
Q

What are the adverse effects of using glucocorticoids?

A
  • Alters water metabolism (PU/PD) by altering ADH and Na+ retention
  • Generally catabolic (opposite of insulin so avoid in diabetics; lose muscle mass, gain fat)
  • Important in parturition but inhibit fertility
  • Cause a ‘stress’ leukogram
  • Impair healing
  • Chronic use can cause calcinosis cutis, osteoporosis, thin skin and alopecia (bilaterally symmetrical)
  • Increase GI acid and decrease mucus (risk with NSAIDS!)
  • Increase fat absorption/deposition, increase liver enzymes (ALP)
46
Q

When would you use glucocorticoids for diagnostic testing?

A
  • Low-dose dexamethasone suppression test (LDDS)
  • High-dose dexamethasone suppression test (HDDS)
47
Q

When would you use glucocorticoids as physiologic replacement therapy?

A

Hypoadrenocorticism (Addison’s disease)

48
Q

When would you use glucocorticoids as anti-inflammatories?

A

Allergies: skin allergies, asthma, etc.

49
Q

When would you use glucocorticoids as an immunosuppressive?

A

Immune-mediated diseases (IMHA, immune polyarthritis, etc)

50
Q

T or F. Glucocorticoids are generally well absorbed orally or parenterally and are protein bound drugs.

A

True

  • Protein bound
    • Specific transporter transcortin (high affinity, low capacity)
    • Albumin secondary (low affinity, high capacity)
51
Q

Which glucocorticoids are hydrolyzed to release the steroid base?

A
  • Prednisone > prednisolone (in cats and in liver disease, would prefer to use prednisolone so it doesn’t have to metabolize in the liver)
  • Cortisone > cortisol
  • Methylprednisone > methylprednisolone
52
Q

T or F. Glucocorticoids are excreted in bile.

A

False, urine.

53
Q

T or F. When you look at the doses for glucocorticoids, most assume you are using prednisone.

A

True! There are significant differences between products

(potency)

54
Q

T or F. The base steroid has a certain duration and the formulation then can further lengthen the duration of physiologic activity.

A

True

  • For repeated dosing, we’re going to use pred
  • Cumulation can occur with daily use of dexamethasone
55
Q

For injectable steroids, which exipients may be added?

A
  • Salt esters (succinate, phosphate)
    • Makes the steroid soluble for IV administration
    • Emergency situations
    • Na succinate, Na phosphate
    • Onset faster but duration unchaged
  • Insoluble esters (pivalate, acetate, acetonide, etc.)
    • The less soluble the ester, the longer it will take to absorb (delayed onset, long duration)- “depot” (acts as a slow release)
    • Opaque suspensions: NOT FOR IV USE!
    • IM, SQ, joint
56
Q

How much can insoluble esters prolong duration?

A

Weeks to months (compared to 12-36 hours)

  • Try to avoid using this because it only really works clinically the first few weeks and can see side effects as it builds up in the body
57
Q

What are the side effects of using glucocorticoids short term (3-5 days)?

A
  • Usually not serious unless concurrent factors
  • Labwork changes (stress leukogram, decreased thyroid values)
  • PU/PD/PP
  • Fetal abnormalities/abortion
  • More severe side effects can occur
58
Q

What are the side effects of using glucocorticoids long term (>1 week)?

A
  • Increased susceptibility to infection
  • Skin changes (hyperpigmentation, thinning, alopecia)
  • Collagen disease (cruciate injury), delayed wound healing
  • Hypertension, thromboembolic disease
  • Panting
  • Addisonian signs (with withdrawal- ‘iatrogenic Addison’s)
    • Dose must be tapered if on steroids more than a few days!
  • Less common: myopathy, calcinosis cutis, osteoporosis
59
Q

Where in the adrenal glands are mineralocorticoids produced?

A

Zona glomerulosa

  • Aldosterone is the endogenous hormone
  • Regulate Na+ retention/K+ excretion by the kidney
60
Q

What are mineralocorticoids used for?

A

Used for their Na+ retention effects (retaining water)

  • May have small amount of glucocorticoid activity (fludrocortisone)
61
Q

Which mineralocorticoid is given orally BID?

  1. Fludrocortisone
  2. DOCP (desoxycorticosterone pivalate, Percorten-V)
A
  1. Fludrocortisone
    * Monitor by measuring K+/Na+
    * Do not confuse this for fluticasone!
62
Q

Which mineralocorticoid is given parenterally (IM, SQ) every 25 days or longer?

  1. Fludrocortisone
  2. DOCP (desoxycorticosterone pivalate, Percorten-V)
A
  1. DOCP (desoxycorticosterone pivalate, Percorten-V)
    * Monitor by measuring K+/Na+

Pharmacology 1 choefsho (13 decks)

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