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Pharmacology I > unit 1- endocrine medications > Flashcards

unit 1- endocrine medications Flashcards

1
Q

hypoglycemic drugs

A
  • lower blood sugar
  • insulin
  • PO hypoglycemic
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2
Q

insulin dynamics

A
  • increase glucose uptake/storage
  • triglyceride synth
  • protein synth
  • encourages movement of K+ into cells
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3
Q

insulin kinetics

A
  • absorption: SubQ, IM, IV, pump (PO destroyed by stomach acid)
  • distribution: wide (skeletal muscle/adipose tissue)
  • metab: hepatic (some renal/muscle)
  • excretion: renal
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4
Q

rapid acting insulins

A
  • insulin lispro (Humalong)
  • insulin aspart (Novolog)
  • insulin glulisine (Apidra)
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5
Q

rapid acting insulin onset/peak/duration

A
  • less than 15 min
  • 0.5-1 hr
  • 3-4 hf
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6
Q

short acting insulins

A

•Regular insulin (Novolin R; Humulin R)

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7
Q

short acting insulin onset/peak/duration

A
  • 0.5-1 hr
  • 2-3 hr
  • 5-7 hr
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8
Q

intermediate acting insulins

A
  • NPH insulin (Humulin N)

* insulin determir (Levemir)

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9
Q

intermediate acting insulin peak/onset/duration

A
  • 1-2 hr
  • 4-12 hr
  • 18-24 hr
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10
Q

long acting insulin

A

•insulin glargine (Lantus)

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11
Q

long acting insulin onset/peak/duration

A
  • 1 hr
  • none
  • 24 hr
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12
Q

selecting insulin syringe/needle

A
  • use syringe corresponding to concentration of insulin being admin (U-100 insulin w/ U-100 syringe)
  • 25-26 g needle (½-¾ inches)
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13
Q

insulin storage

A
  • unopened vials in fridge
  • open vials 1 month room temp
  • premixed vial for 3 months in fridge
  • premixed syringe 1-2 wk in fridge
  • syringe in vert position w/ needle pointing up
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14
Q

mixing insulin

A
  • draw short acting first, then long to prevent injecting longer acting into the short vial
  • rotate vial in hand to disperse particles
  • don’t admin cloudy regular
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15
Q

3 types of mixed insulin

A
  1. premixed NPH (int) and regular (short)
  2. premixed lispro protamine (int) and insulin lispro (short)
  3. premixed aspart protamine (int) and insulin aspart (rapid)
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16
Q

hypoglycemia

A
  • blood sugar too low
  • ↑HR, palpitations, sweating, nervousness, HA, confusion, drowsiness, fatigue
  • tx w/ carbs PO; glucagon admin; IV D10/D50W
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17
Q

hypoglycemia causes

A
  • decreased intake of food
  • increased alcohol intake
  • increased exercise
  • parturition (L & D)
  • vomiting/diarrhea
  • stress
  • insulin therapy EXCEEDING needs
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18
Q

hypoglycemia tx

A
  • make sure conscious first (safe swallow)
  • carbs PO (simple sugar)
  • glucagon admin
  • IV D10 or D50W
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19
Q

hyperglycemia

A
  • blood sugar too high

* may be due to insulin therapy being INSUFFICIENT

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20
Q

drugs posing hypoglycemic effects r/t insulin interaction

A
  • sulfonylureas
  • meglitinides
  • beta blockers
  • etoh
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21
Q

drugs posing hyperglycemic effects r/t insulin interaction

A
  • thiazide diuretics

* glucocorticoids

22
Q

lipoatrophy

A

•loss of subQ tissue producing depression in skin
•immunlogic rxn
*why rotating injection sites is important

23
Q

lipohypertrophy

A

•accumulation of subQ tissue

24
Q

Digoxin and insulin interaction

A
  • Dig slows HR
  • combined insulin potentiates dig’s effects and causes extreme bradycardia
  • dysrhythmias also occur b/c it lowers K+ levels
25
Q

beta blockers and insulin (or OHA) interaction

A
  • beta-adrenergic agents slow HR, CO, etc

* mask SNS response making hypo hard to ID

26
Q

oral hypoglycemic agents (OHA)

A 
•sulfonylureas
•biguanides
•alpha-glucosidase inhibitors
•thiazolidinediones
•gliptin
•meglitinide
•SGLT2 inhibitors
*NIDD (type 2) can use
27
Q

common characteristics of OHAs

A
  • extensive protein binding -> interact w/ other drugs

* A/E of hypoglycemia

28
Q

1st generation sulfonylureas (2)

A
  • tolbutamide (Orinase)

* chlorpropamide

29
Q

2nd generation sulfonylureas (3)

A 
•glipizide (Glucotrol, Glucotrol XL)
•glyburide (DiaBeta)
•glimepiride (Amaryl)
*"gl"
*more potent and less interactions than 1st gen.
30
Q

sulfonylureas dynamics

A
  • stimulate insulin release from pancreas

* increase tissue responsiveness

31
Q

sulfonylureas kinetics

A
  • absorption: PO (food can delay)
  • distribution: wide (protein binding)
  • metab: hepatic
  • excretion: kidney
32
Q

biguanides (1)

A

•metformin (Glucophage)

33
Q

biguanide dynamics

A

•decrease glucose production in liver
•increase glucose uptake and use
•decrease GI absorption of glucose
*A/E of GI issues

34
Q

biguanide kinetics

A
  • absorption: PO slow from small bowel

* excretion: unchanged via kidney

35
Q

alpha-glucosidase inhibitor (1)

A

•Acarbose (Precose)

  • need to take w/ iron
  • A/E of GI issues
36
Q

thiazolidinediones (2)

A
  • Pioglitazone (Actos)

* Rosiglitazone (Avandia)

37
Q

thiazolidinediones dynamics

A

•reverse insulin resistance by increasing glucose utilization and diminishing glucose production

38
Q

thiazolidinediones kinetics

A
  • good PO absorption
  • 99% protein bound
  • excreted in feces/urine
39
Q

thiazolidinediones A/E

A 
•dizziness
•fluid retention
•flatulence
•diarrhea
•potential for hepatic toxicity
•increased LDL
*increases metab of CCBs and steroids
40
Q

Gliptin

A
  • Sitagliptin (Januvia)
  • stimulates release of insulin
  • suppresses postprandial release of glucagon
41
Q

meglitinide

A
  • Repaglinide, Nateglinide
  • given 0-30 min before meal
  • well tolerated
  • increases release of insulin
  • short t½
42
Q

SGLT2 inhibitors (2)

A
  • Dapagliflozin (Farxiga)
  • Canagliflozin (Invokana)
  • block reabsorption of glucose in kidney
  • AE of UTI and yeast infection
43
Q

PO glucagon

A
  • attempt to raise glucose levels when treating hypoglycemia
  • stimulates alpha cells in pancreas to make glucagon, which then goes to the liver to initiate glycogenolysis
  • AE: N/V; hyposensitivity
  • effects w/in 20 min
44
Q

thyroid hormone

A
  • Levothyroxine (synthroid)

* synthetic form of thyroid hormone (T4)

45
Q

Levothyroxine dynamics

A
  • increases metabolic rate, protein synth, cardiac output, renal perfusion, O2 use, body temp, blood volume, and growth processes
  • contraindicated for MI pt
46
Q

Levothyroxine kinetics

A
  • T4 converted to T3
  • 99% protein bound
  • 7 day t½
  • takes 1 month to get to therapeutic range
  • PO qd
47
Q

anti-thyroid medications (4)

A
  • methimazole (Tapazole)
  • propylthiouracil (PTU)
  • iodine solution (Lugol’s sol.)
  • radioacive iodine
48
Q

methimazole (Tapazole) & propylthiouracil (PTU) pharmacodynamics

A
  • block synth of thyroid hormone
  • prevent oxidation of iodine
  • block conversion of T4 to T3
49
Q

non-radioactive iodine (Lugol’s sol) pharmacodynamics

A

•creates high levels of iodide, which reduce iodine uptake by thyroid
•inhibit thyroid hormone production
•block release of thyroid hormones into bloodstream
*used for reduction of gland; thyrotoxicosis

50
Q

radioactive iodide pharmacodynamics

A

•destroys some of the thyroid hormone producing cells
•at high doses destroys thyroid cells
•used for hyperthyroidism and cancer
*full effects in 2-3 months

51
Q

glucocorticosteroids (3)

A

•cortisol (Hydrocortisone)
•prednisone
•dexamethasone
*anti-inflam./immunosuppressive

Pharmacology I (9 decks)

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