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Pharm3: Mod1: Endocrine > Mod 1 lecture 3: pancreatic hormones, anti-diabetic agents and hyperglycemic drugs > Flashcards

Mod 1 lecture 3: pancreatic hormones, anti-diabetic agents and hyperglycemic drugs Flashcards

1
Q

what is the pancreatic duct

A

begins in tail of pancreas
runs through parenchyma of pancreas, merges with bile duct
conducts exocrine activity: pancreatic ‘juice’ from acinar cells is delivered to duodenum via a ductal system

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2
Q

what is the bile duct

A

with pancreatic duct empties into duodenum via the hepatopancreatic ampulla with control via the hepatopancreatic sphincter

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3
Q

What are Pancreatic Islets (of Langerhans)

A

Beta cells secrete insulin
alpha cells secrete glucagon
__ cells secrete somatostain

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4
Q

where is insulin released from

A

pancreatic beta cells at a basal rate

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5
Q

what stimulates higher secretion of insulin

A

high blood glucose
increased amino acids concentration
increased fatty acid concentration
certain hormones (GIP, GLP-1)
vagal activity

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6
Q

what are the actions of insulin

A

lower BG levels: facilitate glucose transport into cells, inhibits glycogenolysis, inhibits gluconeogenesis
regulates fat metabolism
regulates protein metabolism
increased K+ uptake into cells

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7
Q

What is the typical presentation of type 1DM

A

usually diagnosed in early childhood to early adulthood
absolute deficiency of insulin
caused by autoimmune destruction of the beta cells of the pancreas

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8
Q

what is the treatment for type 1 diabetes

A

insulin

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9
Q

what are the concerns with type 1DM

A

DKA
infection
end-organ damage from untreated hyperglycemia

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10
Q

What is the presentation of type 2DM

A

more common than type 1
genetic factors, obesity, and aging play a role
inability of beta cells to produce appropriate quantities of insulin; insulin resistance; other defects

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11
Q

What is normal glucose tolerance for FBG, 2 hours p glucose load, HgbA1c

A

FBG: <100
2 hours: <140
HgbA1c: 5.7

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12
Q

what is the impaired glucose tolerance for FBG, 2 hours p glucose load, HgbA1c

A

FBG: 100-125
2 hours: 140-199
HgbA1c: 5.7-6.4

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13
Q

what is DM for FBG, 2 hours p glucose load, HgbA1c

A

FBG: >126
2 hours: >200
HgbA1c: >6.5

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14
Q

What are complications of DM

A

retinopathy
nephropathy
neuropathy
CV complications
Gastroparesis, autonomic insufficiency

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15
Q

What are the different lengths on insulin treatments

A

long acting
intermediate acting
rapid acting
short acting

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16
Q

What is the PK of insulin

A

degraded in the GI tract
administered subcutaneously, m/c
IV administration for emergencies and DKA

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17
Q

What are the goals of insulin

A

to replicated normal physiologic insulin secretion
to replace basal insulin (overnight, fasting and between meal)
to provide bolus at meal time

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18
Q

What are the long acting insulins

A

Insulin Glargine (lantus)
Insulin determir (Levemir)

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19
Q

What is the PK of Insulin glargine (lantus)

A

no peak
flat, prolonged effect
onset: 1-1.5 hours with max effect after 4 hours
effective duration: up to 24 hours
dosing: daily

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20
Q

What is the PK of insulin determir (levemir)

A

onset: 1-2 hours
peak: 6-8 hours
effective duration: up to 24 hours
dosing: twice daily

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21
Q

What is the intermediate acting insulin

A

NPH (neutral protamine Hagedorn)

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22
Q

what is the PK of NPH

A

subcutaneous only (not used for DKA)
onset: 4-12 hours
peak: 5.5 hours
duration of action: 18-24 hours

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23
Q

What is the short acting insulin

A

Regulat (Humulin, Novolin)

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24
Q

what is the PK for Humulin, Novolin

A

onset: 30min- 5 hours
Peak: 2-3 hours
effective duration: 8-12 hours
SubQ or IV options

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25
Q

What are the rapid acting insulins

A

Insulin Lispro (Humalog)
Insulin Aspart (Novolog)
Insulin Glulisine (Apidra)

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26
Q

What is the timing of Insulin Lispro (Humaglog)

A

onset: 10-15 minutes
peak > 30-90 minutes
effective duration: 3-4 hours

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27
Q

what is the timing of insulin aspart (novolog)

A

onset: 15-20 min
peak > 1-2 hours
effective duration: 3-5 hours

28
Q

what is the timing of Insulin Gluisine (apidra)

A

onset: 20-30 minutes
peak: 55 minutes
effective duration: 1-2.5 hours

29
Q

What are AE of Insulin

A

weight gain
somogyi effect
Dawn phenomenon
hypoglycemia

30
Q

what is somogyi effect

A

if blood sugar levels drops too low in early morning hours, hormones are released.
these help reverse the low blood sugar levels but may lead to blood sugar levels that are higher than normal in the morning

31
Q

What is the Dawn phenomenon

A

normal rise in blood sugar as a person’s body prepares to wake up
in the early hours

This may cause higher blood sugar i the morning (before eating)

32
Q

What are symptoms of hypoglycemia

A

HA
Tachycardia
vertigo
anxiety
confusion
diaphoresis

33
Q

What is the pharmacotherapy of GLP-2 Agonists/incretin mimetics

A

release of incretin is reduced in DMT2
GLP-1receptor agonist actions

34
Q

what are the GLP-1 Receptor agonist actions

A

promotes insulin secretion
enhances satiety
decreases postproandial glucagon secretion
promotes beta cell proliferation

35
Q

release of incretin is reduced in DMT2 with agnoist/incretin mimetis

A

gut releases incretin hormones in response to a meal
incretin hormones are responsible for 60-70% of postprandial insulin secretion

36
Q

What are the GLP-1 agonists/incretin mimetic medications

A

Exendatide: Byetta
Liraglutide: Victoxa
Dulaglutide: Truliciy

all injectables = no oral form

37
Q

What are the oral agents available for DM that stimulate insulin secretion

A

sulfonylureas
megalitinides

38
Q

what are oral agents available for DM that increase insulin sensitivity

A

Biguanides (metformin)
thiazolidinediones (“glitazones”)

39
Q

what are other oral agents available for DM

A

alpha-glucosidase inhibitors
dipeptidyl peptidase-4 inhibitors
sodium-glucose co transporter 2 inhibitors

all for T2DM

40
Q

what are the Sulfonyleureas

A

first generation (not in use)
second generation:
Glyburide (micronase)
Glipizide (glucotrol)
Glimepiride (amaryl)

41
Q

what is the MOA for sulfonyleureas

A

stimulates release of insulin from pancreatic beta cell
reduces production of hepatic glucose
increases sensitivity of insulin in the periphery

42
Q

What are the AE of sulfonylureas

A

weight gain, hyperinsulinemia, hypoglycemia

43
Q

what are the contraindications of sulfonylureas

A

sulfa allergy and pregnancy
use caution with: hepatic insufficiency, renal insufficiency, geriatric patients

44
Q

What are Meglitinides “Glinides”

A

repaglinide (prandin)
Nateglinide (starlix)

of historical interest, but used very infrequently at present

45
Q

what is the MOA for glinides

A

release insulin from beta cells of the pancreas
-chief difference from sulfonlureas: rapid onset and short duration

46
Q

What are the AE of glinides

A

hypoglycemia
use caution with renal and hepatic insufficiency (prandin)

47
Q

What is Metformin (glucophage) and the MOA

A

biguanides
MOA: decrease hepatic gluconeogenesis, increase insulin sensitivity (enhances peripheral utilization)

48
Q

what are the AE of Metformin

A

abdominal discomfort

49
Q

what are the contraindications for metformin

A

hepatic and renal impairment
DKA
AMI
CHF
IV contrast
Alcoholism

Use with caution in elderly

50
Q

What are the thiazolidinediones (“glitazones” or “TZDs”)

A

Rosiglitazone (avandia)
Pioglitazone (actos)

51
Q

what is the MOA for glitazones

A

increase insulin sensitivity
enhances peripheral uptake of glucose
reduces hepatic glucose production

enhanced insulin sensitivity in peripheral tissues and liver by activation of ppar-gamma receptors

52
Q

what are contraindications for glitazones

A

Heart Failure

53
Q

what are the AE of glitazones

A

weight gain
osteopenia
HA
anemia

use with caution in patients with hepatic impairment

54
Q

What are the alpha-glucosidase inhibitors

A

acarbose (precose)
Miglitol (glyset)

55
Q

what is the MOA for alpha glucosidase inhibitors

A

inhibitor of alpha-glucosidease in intestinal brush border
delay digestion of carbohydrates -> lower postprandial glucose levels

56
Q

what are the AE of alpha-glucosidase inhibitors

A

GI intolerance

57
Q

what are the contraindications of alpha-glucosidase inhibitors

A

IBD
colon Ca or other conditions which predispose to obstruction of perforation

58
Q

What are the dipeptidyl peptidase - 4 inhibitors (DPP-4 inhitors - “Gliptins”)

A

sitagliptin (Januvia)
Saxagliptin (onglyza)

59
Q

what is the MOA for DDP-4 inhibitor/Gliptins

A

inhibits the enzyme DDP-4 (DPP-4 inactivates GLP-1) -> increase release of insulin and decrease release of glucagon

60
Q

what is GIP

A

glucose-dependent insulinotropic polypeptide

61
Q

What is GLP-1

A

glucagon-like peptide

62
Q

What are the sodium-glucose cotransporter 2 (SGLT2) inhibitors

A

canagliflozin (invokana)
Dapagliflozin (Farxiga)
empagliflozin (Jardiance)

63
Q

what is the MOA for SGLT2

A

reabsorbs filtered glucose in tubular lumen of the kidney; therefore, by inhibiting the cotrnsporter, there will be decreased reabsoprtion of glucose

64
Q

what are the AE of SGLT2

A

can cause vaginal candidiasis, UT

65
Q

What are the main side effects of:
glinides sulfonylureas:
Biguanides alpha glucosidase inhibitors:
sulfonylureas, glinides, thiazolidinediones:
Biguanides:
thazolidinediones:

A

glinides sulfonylureas: hypoglycemia
Biguanides alpha glucosidase inhibitors: GI disturbances
sulfonylureas, glinides, thiazolidinediones: Weight gain
Biguanides: Nausea
thazolidinediones: Cardiovascular risk

Pharm3: Mod1: Endocrine (5 decks)

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