unit 1- endocrine medications Flashcards
(51 cards)
1
Q
hypoglycemic drugs
A
- lower blood sugar
- insulin
- PO hypoglycemic
2
Q
insulin dynamics
A
- increase glucose uptake/storage
- triglyceride synth
- protein synth
- encourages movement of K+ into cells
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
4
Q
rapid acting insulins
A
- insulin lispro (Humalong)
- insulin aspart (Novolog)
- insulin glulisine (Apidra)
5
Q
rapid acting insulin onset/peak/duration
A
- less than 15 min
- 0.5-1 hr
- 3-4 hf
6
Q
short acting insulins
A
•Regular insulin (Novolin R; Humulin R)
7
Q
short acting insulin onset/peak/duration
A
- 0.5-1 hr
- 2-3 hr
- 5-7 hr
8
Q
intermediate acting insulins
A
- NPH insulin (Humulin N)
* insulin determir (Levemir)
9
Q
intermediate acting insulin peak/onset/duration
A
- 1-2 hr
- 4-12 hr
- 18-24 hr
10
Q
long acting insulin
A
•insulin glargine (Lantus)
11
Q
long acting insulin onset/peak/duration
A
- 1 hr
- none
- 24 hr
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)
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
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
15
Q
3 types of mixed insulin
A
- premixed NPH (int) and regular (short)
- premixed lispro protamine (int) and insulin lispro (short)
- premixed aspart protamine (int) and insulin aspart (rapid)
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
17
Q
hypoglycemia causes
A
- decreased intake of food
- increased alcohol intake
- increased exercise
- parturition (L & D)
- vomiting/diarrhea
- stress
- insulin therapy EXCEEDING needs
18
Q
hypoglycemia tx
A
- make sure conscious first (safe swallow)
- carbs PO (simple sugar)
- glucagon admin
- IV D10 or D50W
19
Q
hyperglycemia
A
- blood sugar too high
* may be due to insulin therapy being INSUFFICIENT
20
Q
drugs posing hypoglycemic effects r/t insulin interaction
A
- sulfonylureas
- meglitinides
- beta blockers
- etoh
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
beta blockers and insulin (or OHA) interaction
* beta-adrenergic agents slow HR, CO, etc
| * mask SNS response making hypo hard to ID
26
oral hypoglycemic agents (OHA)
```
•sulfonylureas
•biguanides
•alpha-glucosidase inhibitors
•thiazolidinediones
•gliptin
•meglitinide
•SGLT2 inhibitors
*NIDD (type 2) can use
```
27
common characteristics of OHAs
* extensive protein binding -> interact w/ other drugs
| * A/E of hypoglycemia
28
1st generation sulfonylureas (2)
* tolbutamide (Orinase)
| * chlorpropamide
29
2nd generation sulfonylureas (3)
```
•glipizide (Glucotrol, Glucotrol XL)
•glyburide (DiaBeta)
•glimepiride (Amaryl)
*"gl"
*more potent and less interactions than 1st gen.
```
30
sulfonylureas dynamics
* stimulate insulin release from pancreas
| * increase tissue responsiveness
31
sulfonylureas kinetics
* absorption: PO (food can delay)
* distribution: wide (protein binding)
* metab: hepatic
* excretion: kidney
32
biguanides (1)
•metformin (Glucophage)
33
biguanide dynamics
•decrease glucose production in liver
•increase glucose uptake and use
•decrease GI absorption of glucose
*A/E of GI issues
34
biguanide kinetics
* absorption: PO slow from small bowel
| * excretion: unchanged via kidney
35
alpha-glucosidase inhibitor (1)
•Acarbose (Precose)
* need to take w/ iron
* A/E of GI issues
36
thiazolidinediones (2)
* Pioglitazone (Actos)
| * Rosiglitazone (Avandia)
37
thiazolidinediones dynamics
•reverse insulin resistance by increasing glucose utilization and diminishing glucose production
38
thiazolidinediones kinetics
* good PO absorption
* 99% protein bound
* excreted in feces/urine
39
thiazolidinediones A/E
```
•dizziness
•fluid retention
•flatulence
•diarrhea
•potential for hepatic toxicity
•increased LDL
*increases metab of CCBs and steroids
```
40
Gliptin
* Sitagliptin (Januvia)
* stimulates release of insulin
* suppresses postprandial release of glucagon
41
meglitinide
* Repaglinide, Nateglinide
* given 0-30 min before meal
* well tolerated
* increases release of insulin
* short t½
42
SGLT2 inhibitors (2)
* Dapagliflozin (Farxiga)
* Canagliflozin (Invokana)
* block reabsorption of glucose in kidney
* AE of UTI and yeast infection
43
PO glucagon
* 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
thyroid hormone
* Levothyroxine (synthroid)
| * synthetic form of thyroid hormone (T4)
45
Levothyroxine dynamics
* increases metabolic rate, protein synth, cardiac output, renal perfusion, O2 use, body temp, blood volume, and growth processes
* contraindicated for MI pt
46
Levothyroxine kinetics
* T4 converted to T3
* 99% protein bound
* 7 day t½
* takes 1 month to get to therapeutic range
* PO qd
47
anti-thyroid medications (4)
* methimazole (Tapazole)
* propylthiouracil (PTU)
* iodine solution (Lugol's sol.)
* radioacive iodine
48
methimazole (Tapazole) & propylthiouracil (PTU) pharmacodynamics
* block synth of thyroid hormone
* prevent oxidation of iodine
* block conversion of T4 to T3
49
non-radioactive iodine (Lugol's sol) pharmacodynamics
•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
radioactive iodide pharmacodynamics
•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
glucocorticosteroids (3)
•cortisol (Hydrocortisone)
•prednisone
•dexamethasone
*anti-inflam./immunosuppressive
