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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

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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
What are the rapid acting insulins
Insulin Lispro (Humalog) Insulin Aspart (Novolog) Insulin Glulisine (Apidra)
26
What is the timing of Insulin Lispro (Humaglog)
onset: 10-15 minutes peak > 30-90 minutes effective duration: 3-4 hours
27
what is the timing of insulin aspart (novolog)
onset: 15-20 min peak > 1-2 hours effective duration: 3-5 hours
28
what is the timing of Insulin Gluisine (apidra)
onset: 20-30 minutes peak: 55 minutes effective duration: 1-2.5 hours
29
What are AE of Insulin
weight gain somogyi effect Dawn phenomenon hypoglycemia
30
what is somogyi effect
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
What is the Dawn phenomenon
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
What are symptoms of hypoglycemia
HA Tachycardia vertigo anxiety confusion diaphoresis
33
What is the pharmacotherapy of GLP-2 Agonists/incretin mimetics
release of incretin is reduced in DMT2 GLP-1receptor agonist actions
34
what are the GLP-1 Receptor agonist actions
promotes insulin secretion enhances satiety decreases postproandial glucagon secretion promotes beta cell proliferation
35
release of incretin is reduced in DMT2 with agnoist/incretin mimetis
gut releases incretin hormones in response to a meal incretin hormones are responsible for 60-70% of postprandial insulin secretion
36
What are the GLP-1 agonists/incretin mimetic medications
Exendatide: Byetta Liraglutide: Victoxa Dulaglutide: Truliciy all injectables = no oral form
37
What are the oral agents available for DM that stimulate insulin secretion
sulfonylureas megalitinides
38
what are oral agents available for DM that increase insulin sensitivity
Biguanides (metformin) thiazolidinediones ("glitazones")
39
what are other oral agents available for DM
alpha-glucosidase inhibitors dipeptidyl peptidase-4 inhibitors sodium-glucose co transporter 2 inhibitors all for T2DM
40
what are the Sulfonyleureas
first generation (not in use) second generation: Glyburide (micronase) Glipizide (glucotrol) Glimepiride (amaryl)
41
what is the MOA for sulfonyleureas
stimulates release of insulin from pancreatic beta cell reduces production of hepatic glucose increases sensitivity of insulin in the periphery
42
What are the AE of sulfonylureas
weight gain, hyperinsulinemia, hypoglycemia
43
what are the contraindications of sulfonylureas
sulfa allergy and pregnancy use caution with: hepatic insufficiency, renal insufficiency, geriatric patients
44
What are Meglitinides "Glinides"
repaglinide (prandin) Nateglinide (starlix) of historical interest, but used very infrequently at present
45
what is the MOA for glinides
release insulin from beta cells of the pancreas -chief difference from sulfonlureas: rapid onset and short duration
46
What are the AE of glinides
hypoglycemia use caution with renal and hepatic insufficiency (prandin)
47
What is Metformin (glucophage) and the MOA
biguanides MOA: decrease hepatic gluconeogenesis, increase insulin sensitivity (enhances peripheral utilization)
48
what are the AE of Metformin
abdominal discomfort
49
what are the contraindications for metformin
hepatic and renal impairment DKA AMI CHF IV contrast Alcoholism Use with caution in elderly
50
What are the thiazolidinediones ("glitazones" or "TZDs")
Rosiglitazone (avandia) Pioglitazone (actos)
51
what is the MOA for glitazones
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
what are contraindications for glitazones
Heart Failure
53
what are the AE of glitazones
weight gain osteopenia HA anemia use with caution in patients with hepatic impairment
54
What are the alpha-glucosidase inhibitors
acarbose (precose) Miglitol (glyset)
55
what is the MOA for alpha glucosidase inhibitors
inhibitor of alpha-glucosidease in intestinal brush border delay digestion of carbohydrates -> lower postprandial glucose levels
56
what are the AE of alpha-glucosidase inhibitors
GI intolerance
57
what are the contraindications of alpha-glucosidase inhibitors
IBD colon Ca or other conditions which predispose to obstruction of perforation
58
What are the dipeptidyl peptidase - 4 inhibitors (DPP-4 inhitors - "Gliptins")
sitagliptin (Januvia) Saxagliptin (onglyza)
59
what is the MOA for DDP-4 inhibitor/Gliptins
inhibits the enzyme DDP-4 (DPP-4 inactivates GLP-1) -> increase release of insulin and decrease release of glucagon
60
what is GIP
glucose-dependent insulinotropic polypeptide
61
What is GLP-1
glucagon-like peptide
62
What are the sodium-glucose cotransporter 2 (SGLT2) inhibitors
canagliflozin (invokana) Dapagliflozin (Farxiga) empagliflozin (Jardiance)
63
what is the MOA for SGLT2
reabsorbs filtered glucose in tubular lumen of the kidney; therefore, by inhibiting the cotrnsporter, there will be decreased reabsoprtion of glucose
64
what are the AE of SGLT2
can cause vaginal candidiasis, UT
65
What are the main side effects of: glinides sulfonylureas: Biguanides alpha glucosidase inhibitors: sulfonylureas, glinides, thiazolidinediones: Biguanides: thazolidinediones:
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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