Endocrine Flashcards
what drug is commonly used to treat the effects of pheochromocytoma?
phenoxybenzamine
T/F: dogs commonly get hyperthyroidism
FALSE, rare. they more commonly get hypothyroidism
T/F: 89% of T4 and T3 are bound to plasma proteins
FALSE, 99%! remaining 1% is free
where is most of T4 made?
in follicular cells and stored as colloid in thyroid gland
T/F: T3 is made in follicular cells of the thyroid gland and is stored as colloid
FALSE, T4 is made here and converted to T3 in the cell where its needed
what is the goal of therapy for hypothyroidism in dogs?
REPLACE hormone the body isn’t producing
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
FALSE, levothyroxine (T4)
thyrotoxicosis
excessive T4 levels
how might you reduce the risk of oversupplementation in large patients (>50lb)?
instead of dosing mg/kg, dose mg/m2 (body surface area dosing)
is levothyroxine given IV, PO, or IM?
PO, IV only used in rare situations like myxedema coma
T/F: when treating patients via mg/kg instead of mg/m2 it is more common to underdose small dogs and overdose large dogs
TRUE, smaller dogs have higher metabolisms
what should you monitor when treating a patient long term for hypothyroidism?
measure T4 levels, 4 wks after starting therapy
T/F: phenobarbital can interfere w/ thyroid test results
TRUE, as well as zonisamide, sulfonamides, glucocorticoids, phenylbutazone, quinidine, etc.
what is the goal of therapy for hyperthyroidism in cats?
stop excessive hormone production
how does Hill’s y/d help treat hyperthyroidism in cats and what patient would you be concerned about using diet therapy with?
prevents production (iodine uptake), watch out for in outdoor cats!! w/ diet therapy they must be strict in sticking to the diet
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
FALSE, biologically iodides and iodinated contrast agents do more things in the body to go towards the treatment of hyperthyroidism
T/F: carbimazole is a prodrug that is metabolized to its active form methimazole
TRUE
what makes methimazole the drug of choice for hyperthyroidism in cats
- consistently efficacious
- side effects are uncommon and most are manageable
why would you choose to use methimazole over propylthiouracil (PTU) when treating hyperthyroidism in cats?
PTU, like methimazole, is thioureylene and is efficacious but it has a higher incidence of serious side effects
T/F: iodides/iodinated contrast agents have variable efficacy and are transient
TRUE, don’t work well in all cats and is clinically unreliable
what are three drugs that are considered methimazoles?
- tapazole (human approved, use extra label)
- felimazole
- transdermal methimazole (acquire from compounding)
T/F: methimazole is a drug product used for hyperthyroidism in cats
FALSE, methimazole is an active ingredient and therefore not considered a “product”, FDA does not register pure active ingredients
matilda the cat is given felimazole and is shows an idiosyncratic rxn. can you prescribe her tapazole instead?
NO, idiosyncratic reactions are not dose dependent, all about the drug and it’s metabolites. tapazole also has methimizole as it’s active ingredient
facial excoriation is an idiosyncratic rxn you might see when what drug is given to a cat with hyperthyroidism?
methimazole (tapazole, felimazole, transdermal methimazole)
what mild side effects might you see with a cat with hyperthyroidism given methimazole?
GI signs, transient hematologic changes in CBC
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?
switch him to transdermal methimazole
T/F: clinical signs for acute hypocalcemia include hyperesthesia/pawing at face, tremors, progressing to flaccid paralysis, seizures, hypethermia, and bradycardia
TRUE
what causes ‘milk fever’ in cows and eclampsia in dogs?
periparturient hypocalcemia, sudden increase in calcium usage (i.e. lactating, after whelping) in which patient can’t adapt readily enough
daisy the cow has milk fever, how do you treat her?
replace her calcium deficit until she catches up
what are two parenteral calcium options used for acute treatment of hypocalcemia?
Ca Gluconate or Ca Chloride
T/F: Ca Chloride is administered PO/SQ
FALSE, it’s caustic and parenteral, NEVER give SQ/IM
rapid administration of what can cause arrhythmias?
calcium, monitor ECG
what are two oral options used to treat chronic hypocalcemia (hypoPTH)?
Ca Carbonate (small animal), Ca Propionate (large animal, food additive)
what is the control booth for calcium metabolism?
parthyroid glands! no PTH means the GIT can’t absorb Ca
T/F: hypoparathyroidism results in the inability of the body to convert Vitamin D to it’s active form (calcitriol)
TRUE
what three areas of the body are involved in calcium metabolism in the body?
- bone (storage)
- kidneys (excretion)
- gut (absorption)
what is the most potent activated form of vitamin D?
calcitriol, rapid
what is the biggest potential side effect of calcitriol?
hypercalcemia (monitor serum calcium levels!)
T/F: calcitriol is the best vet approved drug of choice for treatment of hypocalcemia from hypoPTH
FALSE, no vet approved form, only human-approved products
T/F: calcitriol capsules are in mcg which means they have a narrow therapeutic index (TI)
TRUE
what must you replace in the lifelong management of hypocalcemia from hypoPTH?
replace vitamin D
what might you try first when a patient is exhibiting signs of acute/transient hypoglycemia?
frequent, small meals with complex carbohydrates
T/F: ongoing IV dextrose solutions should be NO LESS than 5% concentration
FALSE, they should be NO MORE than 5% concentration
quick!! puss the cat was acting lethargic so you gave him a small meal and now he’s seizing!! what do you give him?
intravenous bolus of dextrose, use in emergency situations (usually 1ml/kg of 50% dextrose diluted 1:4)
what toxin causes a massive insulin release in dogs?
xylitol, keep that sugar free gum hidden!
what must you address and alter when it comes to treating chronic hypoglycemia?
- address the cause
- alter glucose production/use by body (diet, corticosteroids)
what corticosteroids do you use in the treatment of chronic hypoglycemia?
prednisone/prednisolone
what usually causes hyperglycemia?
- something that doesn’t require therapy (STRESS)
- diabetes mellitus (DM)
what is the primary goal of diabetes mellitus therapy?
address the insulin deficiency
diabetes mellitus =
insulin deficiency
T/F: amino acid sequence of insulin is highly preserved across species
TRUE, dog=pig
insulin is produced by what cells of the islets of langerhans in what organ?
beta-cells, endocrine pancreas
when BG rises what channels close causing depolarization and insulin release?
energy-dependent K+ channels
where in the body is glucose used as an energy source?
liver, muscle, adipose, heart
T/F: in peripheral tissues insulin binds to insulin receptors allowing glucose to enter the cell and be utilized
TRUE
T/F: human approved insulin formulas are 40 IU/mL and veterinary approved insulin formulas are 100 IU/mL
FALSE, opposite
what are three major factors you must consider when using exogenous insulin?
- concentration (big impact on dose)
- duration of action (short, intermediate, long)
- potency (what impact will the drug have)
in what order of duration (shortest to longest) are NPH, regular insulin, and protamine zinc/PZI?
regular insulin>NPH>protamine zine/PZI
which insulins are given SQ only?
intermediate (NPH, Lente, Vetsulin) and long-acting (protamine zinc/PZI, glargine, detemir)
T/F: regular insulin is the only insulin that can be administered IV
TRUE! IV, IM or SC
what type of insulin is most commonly used for hospitalized patients?
regular insulin, can be given IV CRI or intermittent IM/SC
T/F: an insulin with fast onset and shorter duration gives you as a vet more control
TRUE, more predictable
what two insulin types are added to delay absorption and extend clinical effect?
protamine (NPH) and zinc (lente)
what type of insulin is the “go to”, especially for canines?
vetsulin (porcine lente insulin)
T/F: vetsulin may cause a longer duration in felines
FALSE, SHORTER
T/F: a more potent insulin will be harder to dose because of smaller doses (i.e. small dogs)
TRUE, (i.e. 0.5 IU increments are very hard to draw up in a syringe accurately)
which insulin type is generally the “go to” for cats?
glargine
what causes glargine to have very gradual absorption (‘flat’ curve)?
it forms microprecipitates in the body, slowly doles out insulin
what two long-acting insulin types are human approved?
glargine and detemir
which insulin type is known to be the most potent?
detemir, 4x in dogs!!
which insulin type is difficult to dose in small dogs and why?
detemir because of its potency
which insulin type is now offered as a dosing pen?
vetsulin, provides ease and precision of dosing but $$
what do oral ‘antidiabetic’ drugs cause?
hypoglycemia
what is the main oral hypoglycemic agent used in veterinary medicine?
glipizide
what type of diabetes do you use oral hypoglycemic agents for?
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
in which animal do you NOT use hypoglycemic agents?
dogs
why should you monitor patients that are given oral hypoglycemic agents?
can cause SIGNIFICANT hypoglycemia
if oral hypoglycemic agents are capable of causing significant hypoglycemia and accelerate beta-cell loss, why would a vet prescribe them for a patient?
owners!! some owners are deathly afraid of needles
T/F: glipizide is safer because it’s oral
FALSE, can still have significant adverse effects
where are mineralcorticoids produced?
in the zona glomerulosa in the adrenal cortex
where are glucocorticoids produced?
in the zona fasciculata in the adrenal cortex
mineralcorticoids =
aldosterone (endogenous hormone)
glucocorticoids =
cortisol (endogenous hormone)
T/F: glucocorticoids should NOT be given concurrently w/ NSAIDs
TRUE, can cause ulcers
T/F: prednisone, prednisolone, dexamethasone, triamcinolone and methylprednisolone are examples of mineralcorticoids
FALSE, glucocorticoids
what are the two mechanisms of action of glucocorticoids?
- 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
why are glucocorticoids used (in general)?
anti-inflammatory effects
when is it contraindicated to use topical glucocorticoids?
corneal ulcers, infection (active), or diabetes
T/F: glucocorticoids antagonize insulin
TRUE! avoid in diabetes
what are the clinical uses for glucocorticoids?
-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)
T/F: glucocorticoids are protein bound
- specific transporter transcortin (high affinity, low capacity)
- albumin secondary (low affinity, high capacity)
why should you administer prednisolone topically rather than prednisone?
if it’s topical it’s localized so the drug wont’ have the chance to be hydrolyzed, need to give in active form
why is it preferred to give cats prednisolone rather than prednisone?
because cats aren’t great at hydrolyzing prednisone to prednisolone (active form)
what are two main considerations in using glucocorticoids?
- potency (significant differences between products)
- duration (base steroid has certain duration, formulation will lengthen)
how much more potent is dexamethasone than prednisone?
7.5 x! (relative potency = 30)
T/F: prednisone/prednisolone has a longer duration than dexamethasone
FALSE, prednisone/prednisolone< triamcinolone< dexamethasone
what two excipients can be added to injectable steroids?
- salt esters (succinate, phosphate)
- insoluble esters (pivalate)
what do salt/soluble esters do when added to a glucocorticoid?
- make steroid soluble
- makes suitable for IV admin
- faster onset (DURATION UNCHANGED)
what do insoluble esters such as pivalate do when added to a glucocorticoid?
- cause delayed onset, long duration (‘depot’)
- NOT FOR IV USE
- i.e. depo-medrol (stays in muscle as depot and is slowly released)
name three important mineralcorticoids
- aldosterone (endogenous)
- DOCP
- fludrocortisone
T/F: aldosterone excretes Na and retains K
FALSE, opposite
T/F: Addison’s disease is a disease that causes a deficiency in aldosterone
TRUE
which is longer acting, fludrocortisone or DOCP?
DOCP, contains pivalate
which corticosteroid shows a small amount/the most glucocorticoid activity of the mineralcorticoids?
fludrocortisone, also has more Na retention compared to DOCP
what would you measure when monitoring mineralcorticoids?
K+/Na+
T/F: fludrocortisone is given parentally (IM, SC) and DOCP is given orally
FALSE, opposite, remember DOCP has pivalate added so NO IV USE
