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RUSVM Pharmacology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the targets of drugs action to treat a hypo endocrine disorder?

A

Replacing an endogenous substance

  • > hypoglycemia - dextrose
  • > hypocalcemia - calcium gluconate

Indirectly helps body to regain normal homeostasis
-> hypocalcemia -> VitD/Calcitrol

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2
Q

What is the usual underlying cause to cause excess of a substance in the body?

A

Lack of response to normal feedback

  • hyperplasia
  • benign neoplasia
  • malignant neoplasia
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3
Q

What are the drug targets to treat hyper endocrine disorders?

A

Destroy abnormal tissue/get ride of the source

Inhibit production of substance

Enhance elimination of substance

Inhibit function of substance

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4
Q

Generally, acute changes should be addressed (slowly/fast) and chronic changes should be reversed (slowly/fast)

A

Fast; slow

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5
Q

What is the function of thyroid?

A

Increase metabolic rate and O2 consumption

Positive inotropic and chronotropic (increase # and affinity of B adrenergic receptors)

Enhance catecholamine response

Catabolic effects on muscle and adipose tissue

Stimulate erythropoiesis

Increase body temp

Regulate cholesterol

Essential for growth and development

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6
Q

Most commonly you will see dogs with ______-thyroidism and cats with ________-thyroidism

A

Hypo; hyper

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7
Q

What is the goal of therapy to treat hypothyroidism in dogs?

A

Replace hormone the body is not producing

Liothyronine (T3) or Levothyroxine (T4)

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8
Q

What thyroid replacement drug requires less dosing and has a lower risk of causing thyrotoxicosis (excess T4)

A

levothyroxine (t4)

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9
Q

In large patients, dosing of levothyroxine is usually done in what measurements?

A

Mg/m^2

Body surface area reflects metabolism

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10
Q

How is hypothyroidism monitored?

A

By measuring T4

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11
Q

What is the only Veterinary approved produce to treatment of hypothyroidism?

A

Thyro-tabs

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12
Q

What is the goal of therapy to treat hyperthyroidism in cats?

A

Stop excessive hormone production

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13
Q

What are non-pharmacological ways of treating hyperthyroidism?

A

Diet -prevent production (iodine uptake)
Surgery
Radioactive iodine

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14
Q

What are the targets for pharmacological therapies for hyperthyroidism?

A

Prevent production/interfere with synthesis
Prevent release of preformed hormone
Prevent conversion of T4 to T3 in tissue

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15
Q

What drugs will inhibit thyroid hormone synthesis

A

Methimazole, carbimazole, propylthiouracil

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16
Q

What drug will inhibit thyroid hormone synthesis and inhibit conversation of T4 to T3?

A

Propylthiouracil

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17
Q

Iodines and iodinated contrast agents have what effect?

A

Inhibit thyroid hormone synthesis
Inhibit release of preformed hormone
Inhibit T4 to T3 conversion (contrast agents)

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18
Q

What do we use in practice to treat hyperthyroidism in cats. Why is it the best choice?

A

Methimazole

Consistently efficacious
Side effects are uncommon and most are manageable

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19
Q

What products contain the active methimazole

A

Tapazole

Felimazole

Transdermal methimazole (not a product -> compounded

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20
Q

What are the side effects of methimazole

A

Mild/common: GI signs (vomiting) and transient hematologist changes on CBC

Severe/uncommon: refractory GI signs, idiosyncratic rxn (facial excoriation, hepatopathy, bone marrow suppression)

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21
Q

Can severe and acute hypocalcemia be life-threatening

A

Yep

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22
Q

What are clinical signs of hypocalcemia?

A 
Hyperesthsia/pawing at face 
Tremors -> flaccid paralysis 
Seizures
Hyperthermia 
Bradycardia
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23
Q

What do you call hypocalcemia due to a sudden increased use of calcium, generally associated with birth and lactation

A

Eclampsia

milk fever

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24
Q

What route of administration should be used if our need emergency calcium replacement?

A

Parenteral

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25
Q

What are the parenteral calcium options?

A

Ca Gluconate

Ca Chloride

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26
Q

Can you give Ca Chloride SQ or IM?

A

Caustic

Irritating to tissue

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27
Q

What can occur if your give Ca too rapidly?

A

Arrhythmia -Monitor ECG

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28
Q

What are the oral Ca options

A

Ca Carbonate (small animal)

Ca Propionate (large animal)

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29
Q

Hypoparathyroidism results in inability of the body to covert vitamin D to ___________

A

Calcitriol

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30
Q

What is the biggest potential side effect of calcitriol?

A

Hypercalcemia

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31
Q

How do you treat acute/transient hypoglycemia

A

Diet
Dextrose 50% solution
Glucagon

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32
Q

How would you treat hypoglycemia with diet?

A

Frequent small meals with complex carbohydrates

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33
Q

How do you administer glucagon?

A

IV (dosed in nanograms)

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34
Q

How is dextrose administered?

A 
Mucosal absorption 
IV bolus (emergency)
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35
Q

An IV dextrose should not be more than ______ concentration.

A

5%

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36
Q

You need to make a 5% dextrose solution using a 1000mL fluid bag. How much 50% dextrose stock do you need to add?

A

V1 x C1 = V2 x C2
1000ml x 5% = ? X 50%

?= 1000mL x 5% / 50%

100mL

37
Q

You have a patient on IV LRS with 600ml left in their bag and you want to make it 2.5% dextrose solution. How much 50% dextrose should you add?

A

600ml x 2.5% = ? X 50%

?= (600ml x 2.5%) / 50%

30ml

38
Q

What is usually the cause of hyperglycemia?

A

Stress, exercise, or steroids (does not require therapy)

Diabetes mellitus (DM)

39
Q

What is the primary goal of therapy in treating diabetes mellitus?

A

To address the insulin deficiency

-> secondarily brings down glucose

40
Q

Insulin is produced by ?

A

B cells of the islets of Langerhans

41
Q

Insulin binds to ___________ receptors to up regulate GLU4 allowing glucose to enter the cell

A

Tyrosine kinase

42
Q

In the absence of insulin, tyrosine kinase receptors are not activated, and _________ receptors remain in the cell

A

GLUT4
(Insulin dependent expression)

Insulin is not taken up into the cell–> hyperglycemia

43
Q

All exogenous insulin formulations are administered how?

A

injectable (IV, SQ or IM)

44
Q

What differs between human and vet formulations of insulin

A

Concentration

Human 100IU/mL
Vet 40IU/mL

45
Q

What is the duration of action of insulin

A

Depending of formation can be short, intermediate, or long-acting

46
Q

What is the difference between potency and concentration of a drug?

A

Potency is the amount required to produce an effect of given intensity

Concentration is the amount of drug per amount of volume

47
Q

What is the most important short acting insulin type?

A

Regular insulin

48
Q

How do you administer regular insulin?

A

IV, IM, or SC (only one that can be IV)

49
Q

How does the onset and duration of IV regular insulin compare to IM/SC regular insulin?

A

IV- immediate onset and duration 1-4hrs
IM/SC- 10-30mins and duration 3-10hrs

Usually only used in hospitalized patients (CRI)

50
Q

What are the intermediate acting insulin types?

A

NPH, Lente, Vetsulin/Caninsulin

51
Q

How are the intermediate acting insulin administered?

52
Q

protamine in ________ or zinc in _________ are added to delay absorption and extended clinical effect

A

NPH; Lente

53
Q

_____________ is a porcine lente insulin and is a veterinary formulation, therefore the concentration is _________

A

Vestsulin/Caninsulin

40IU/mL

54
Q

What is the onset and duration of intermediate acting insulin

A

Onset 30min-2hrs

Duration 4-24hrs

55
Q

What are the long acting insulins?

A

Protamine zinc/ PZI
Glargine
Determined

56
Q

_________ forms miroprecipetates in physiological pH which results in gradual absorption

A

Glargine (long acting insulin)

57
Q

____________ has a much higher protect in dogs (4x) and requires special dosing

A

Detemir

Dosing may be difficult to dose for small dogs
The only insulin with a different potency

58
Q

What is the duration and action of the long-acting insulin types?

A

Onset 1-4hrs

Duration 6-28hrs

59
Q

What is the effect of glipizide? And when is it used?

A

Oral hypoglycemic agent -> CAUSE hypoglycemia, they don’t treat it

Only useful in type II diabetes (only in cats)

60
Q

What is the MOA of glipizide?

A

Simulate insulin secretion by pancreatic B cells (blocking K+ channels)

Also increase tissue sensitive to insulin

61
Q

What are the adverse effects of glipizide?

A

Can accelerate beta cell loss

Only effective in 20-30% cats

62
Q

Glucocorticoids are produced by the ______________

A

Zone fasciculata

63
Q

What is the endogenous hormone produced by the zona fasiculata?

A

Cortisol (glucocorticoids )

64
Q

How is cortisol release regulated in the body?

A

Hypothalamus/pituitary -> released of CRH (corticotropin releaseing hormone) and ACTH (adrenocorticotropic homone)

65
Q

What is the MOA of glucocorticoids ?

A

Receptors in the membrane (cell cascade) or in the cytoplasm (gene expression)

66
Q

What are the glucocorticoids drugs and what are their main use?

A

Prednisone, prednisolone, dexamethasone, triamcinolone, methylprednisolone

Anti-inflammatory effects

67
Q

What are the effects of glucocorticoids ?

A

Suppress immune response
Increase Ca excretion (treat chronic hypercalcemia)
Reduce fever
Lymphotoxic

68
Q

Can you used glucocorticoids in a diabetic patient?

A

Nope

Glucocorticoids antagonize insulin

69
Q

What are the adverse effects of glucocorticoids ?

A

Alter water metabolism (PU/PD)
Catabolic
Antagonize insulin

Stress
Impair healing

Chronic use can cause calcinosis cutis, osteoporosis, thin skin, and alopecia

Increase GI acid and decrease mucus (dont use with NSAID!)

Increase fat absorption/deposition

70
Q

Topical glucocorticoids are used to treat what opthalamic conditions

A

Non-infectious keratitis, uveitis

71
Q

When is opthalamic topical glucocorticoids contraindicated?

A

Corneal ulcer, infection, or diabetes

72
Q

What re the topical glucocorticoids ?

A

Dexamethasone, and prednisolone

73
Q

What are the clinical uses of glucocorticoids ?

A

Diagnostic testing
Physiological replacement therapy
Anti-inflammatory
Immunosuppressive

-these effects are dose dependent, low to high

74
Q

What are some examples of glucocorticoid drugs that must be hyrdolyzed to their active form?

A

Prednisone -> prednisolone
Cortisone -> cortisol
Methylprednisone ->methylprednisolone

75
Q

How are glucocorticoids transported in the body

A

Protein bound

Transcoriton
Albumin (secondary)

76
Q

What are the glucocorticoids relative to their potency (low to high)

A

Cortisol (1)
Prednisolone (4)
Triamcinolone (5)
Dexamethasone (30)

77
Q

What excipients may be added to injectable glucocorticoids?

A 
Salt esters (Na succinate/ Na phosphate) 
Insoluble esters (pivalate, acetate, acetonide)
78
Q

What effect with a soluble ester have on glucocorticoids ?

A

Make steroid soluble
IV administration
Onset after but duration unchanged

79
Q

What effect with insoluble esters have on glucocorticoids ?

A

Less soluble
Not for IV use
Delay onset and longer duration

80
Q

What are the short term side effects of glucocorticoids ?

A

Lab changes

PU/PD/PP

Fetal abnormalities/abortion

81
Q

What are the long term side effects of glucocorticoids ?

A 
Increase susceptibility to infection 
Skin changes 
Collagen disease 
Hypertension, thromboembolic disease 
Panting 
Additions signs

Less common: myopathy, calcinosis cutis, osteoporosis

82
Q

What are the two mineralcorticoids you should know

A

Fludrocortisone

DOCP

83
Q

Mineralcorticoids are produced by the ___________

A

Zona glomerulosa

84
Q

What in the endogenous mineralcorticoids

A

Aldosterone

85
Q

What is the purpose of aldosterone

A

Regulate Na and K excretion in the kidney

86
Q

What is the effect of Fludrocortisone and DOCP?

A

Na retention -> mineralcorticoid effects

87
Q

How is Fludrocortisone administered

88
Q

How is DOCP administered?

A

Parenteral (IM or SC)

89
Q

T/F: fludrocortisone has a small amount of glucocorticoids activity

RUSVM Pharmacology (18 decks)

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