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Endocrinology > Pancreatic Hormones, Anti-diabetic agents and Hyperglycemic Drugs > Flashcards

Pancreatic Hormones, Anti-diabetic agents and Hyperglycemic Drugs Flashcards

1
Q

Pancreatic ‘juice’ comes from ______ cells –> is delivered to the

A

acinar cells –> duodenum via the ductal system

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2
Q

Beta cells secrete

A

insulin

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3
Q

Alpha cells secrete

A

glucagon

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4
Q

Omega cells secrete

A

somatostatin

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5
Q

High blood glucose levels stimulates

A

higher secretion rate

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6
Q

Low blood glucose levels stimulates

A

glucose transport into cells
inhibits glycogenolysis (breakdown of glycogen -> glucose)
inhibits gluconeogenesis

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7
Q

Type 1 DM is usually diagnosed in

A

early childhood to early adulthood

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8
Q

Type 1 DM is the

A

absolute deficiency of insulin (autoimmune disorder where your body destroys beta cells)

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9
Q

Treatment of Type 1 DM

A

insulin

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10
Q

Concerns for type 1 DM

A

DKA
infection
end-organ damage from untreated hyperglycemia

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11
Q

Type 2 DM risk factors

A

genetic factors
obesity
aging plays a role

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12
Q

Type 2 DM is

A

peripheral insulin resistance (decrease uptake of glucose in tissue)
insulin secretion does not maintain glucose homeostasis

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13
Q

Complications of DM

A

retinopathy
nephropathy
neuropathy
CV complications
gastroparesis, autonomic insufficiency

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14
Q

Insulin options

A

long acting
intermediate acting
rapid acting
short acting

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15
Q

Insulin is degraded in

A

the GI tract - so administered subcutaneously most commonly
IV administration for emergencies and DKA

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16
Q

Goals of giving insulin

A

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

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17
Q

Long acting insulin (basal insulin) includes

A

insulin glargine (Lantus)
insulin detemir (Levemir)

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18
Q

Insulin Glargine =
peak =
onset =
effective duration =
dosing =

A

long acting
no peak - flat prolonged effect
onset - 1-1.5 hours w/ max effect after 4 hours
effective duration - up to 24 hours
dosing - daily

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19
Q

Insulin Detemir =
onset =
peak =
effective duration =
dosing =

A

long acting
peak is 6-8 hours
effective duration up to 24 hours
dosing - twice daily

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20
Q

Intermediate acting insulin includes

A

NPH - neutral protamine Hagedorn

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21
Q

NPH - Neutral protamine Hagedorn =
administration =
onset =
peak =
duration of action =

A

intermediate acting insulin
subQ only (therefor not used for DKA)
onset 4-12 hours
peak 5.5 hours
duration of action 18-24 hours

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22
Q

Short acting insulin includes

A

regular (humulin, novolin)

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23
Q

Regular - Humulin, Novolin =
onset =
peak =
effective duration =
administration =

A

short acting insulin
onset - 30 min -5 hours
peak - 2-3 hours
effective duration - 8-12 hours
subQ and IV options

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24
Q

Rapid acting insulin includes:

A

insulin lispro (Humalog)
insulin aspart (Novolog)
insulin glulisine (Apidra)

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25
Insulin Lispro (Humalog) = onset = peak = effective duration =
rapid acting insulin onset - 10-15 min peak - 30-90 min effective duration - 3-4 hours
26
Insulin Aspart (Novolog)= onset = peak = effective duration =
rapid acting insulin onset = 15-20 min peak > 1-2 hours effective duration - 3-5 hours
27
Insulin Glulisine (Apidra) = onset = peak = effective duration =
rapid acting insulin onset - 20-30 min peak - 55 min effective duration - 1-2.5 hours
28
long acting insulin is mostly used for
replacing normal bodies insulin, what their metabolic need is
29
rapid, short or intermediate acting insulin is used for
controlling sugars that we obtain when eating
30
Typical dosing =
0.1 - 1.2 units/ kg/ day Type 2 may require higher dosing due to resistance
31
Adverse reactions to insulin
wt gain somogyi effect dawn phenomenon hypoglycemia
32
What is the somogyi effect?
If the blood sugar level drops too low in the early morning hours, hormones such as growth hormone, cortisol and catecholamines are released - these help reverse the low blood sugar level but may led to blood sugar levels that are higher than normal in the morning
33
What is the Dawn Phenomenon?
a normal rise in blood sugar as a person's body prepares to wake up in the early morning hours, hormones () cause the liver to release large amounts of sugar into the bloodstream - for most people the body produces insulin to control the rise in blood sugar - if the body doesn't produce enough insulin blood sugar levels can rise, causing high blood sugar in the morning before eating
34
GLP-1 Agonists/ incretin Mimetics include
Exentidine Liraglutide Dulaglutide All injectables - no oral form
35
GLP-1 Agonists/ Incretin Mimetics MOA
promotes insulin secretion enhances satiety decreases postprandial glucagon secretion promotes beta cell proliferation
36
Oral Agents that primarily stimulate insulin secretion include
Sulfonylureas Meglitinides
37
Oral agents that increase insulin sensitivity include
Biguanides (metformin) Thiazolidinediones ("glitasones")
38
Other oral agents
alpha-glucosidase inhibitors dipeptidyl peptidase-4 inhibitors sodium-glucose co-transporter 2 inhibitors
39
Sulfonylureas MOA
stimulates release of insulin from the pancreatic beta cells reduces production of hepatic glucose increases sensitivity of insulin in the periphery
40
Adverse reactions of Sulfonylureas
wt gain hyperinsulinemia hypoglycemia
41
contraindications of Sulfonylureas
sulfa allergy pregnancy
42
Sulfonylureas: Use caution in
hepatic insufficiency renal insufficiency geriatric patients
43
Sulfonylureas include
first generation: tolbutamide, Chlorpropamide second generation: glyburide, glipizide, glimepiride
44
Meglitinides "Glinides" include
repaglinide nateglinide
45
Meglitinides "Glinides" MOA
release insulin from the beta cells of the pancreas rapid onset and short duration - chief difference from sulfonylureas
46
Adverse reactions of Meglitinides "Glinides"
hypoglycemia use caution with renal and hepatic insufficiency (Repaglinide)
47
Biguanides: Metformin MOA
Decreases hepatic gluconeogenesis Increases insulin sensitivity (enhances peripheral utilization)
48
Metformin adverse reactions
abdominal discomfort
49
Metformin contraindications
hepatic and renal impairment DKA AMI CHF IV contrast Alcoholism used with caution in the elderly
50
Thiazolidinediones (glitazones or TZDs)
Rosiglitazone Pioglitazone
51
Thiazolidinediones (glitazones or TZDs) MOA
Increases insulin sensitivity - by activation of ppar-gamma receptors (regulates transcription of a number of insulin responsive genes) enhances peripheral uptake of glucose reduces hepatic glucose production
52
Thiazolidinediones (glitazones or TZDs) contraindications
heart failure
53
Thiazolidinediones (glitazones or TZDs) adverse reactions
wt gain osteopenia HA Anemia use with caution in patients with hepatic impairment
54
Alpha-Glucosidase Inhibitors include
acarbose miglitol
55
Oral medications are only used for ______ DM
type 2
56
Alpha-Glucosidase Inhibitors MOA
inhibitor of alpha-glucosidase in intestinal brush border delay digestion of carbohydrates -> lower postprandial glucose levels
57
Alpha-Glucosidase Inhibitors adverse reactions
GI intolerance
58
Alpha-Glucosidase Inhibitors contraindications
IBD colon CA or other conditions which predispose to obstruction or perforation
59
Dipeptidyl peptidase-4 inhibitors include
Sitagliptin (Januvia) Saxagliptin (Onglyza)
60
Dipeptidyl peptidase-4 inhibitors MOA
inhibits the enzyme DPP-4 --> DPP-4 inactivates GLP-1 --> increase release of insulin and decrease release of glucagon
61
Sodium- glucose co-transporter 2 inhibitors include
Canagliflozin Dapagliflozin Empagliflozin (Jardiance)
62
Sodium- glucose co-transporter 2 inhibitors MOA
the SGLT2 reabsorbs filtered glucose in the tubular lumen of the kidney; therefore, by inhibiting this cotransporter, there will be decreased reabsorption of glucose increased urinary excretion of glucose -> decreased serum glucose
63
Sodium- glucose co-transporter 2 inhibitors adverse reactions
can cause vaginal candidiasis UTI

Endocrinology (5 decks)

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