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Flashcards in Oral Glycemic 1 Deck (30)
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1
Q
What are the two primary techniques to assess glycemic control?
A
patient self-monitoring glucose levels

Hemoglobin A1C
2
Q
What is the difference between Type 1 and Type 2 DM?
A
1- autoimmune, beta cell destruction--> no insulin production
2- progressive insulin secretory defect
3
Q
Outside of DMT1 and DMT2, what are some other specific types of Diabetes?
A
Gestational diabetes
genetic defects in beta cell function/ insulin action
diseases of exocrine function
drug/chemical induced
4
Q
The lecture described two studies relating glycemic control to complications of DM, what was the result?
A
better glucose control decreases both microvascular and macrovascular complications
5
Q
How do you treat Type 1 DM? Type 2?
A
Type 1: insulin required
Type 2: 1st diet and exercise + initiate metformin
- if they are markedly symptomatic +/- elevated blood glucose/ A1c--> consider insulin
- if noninsulin monotherapy at max dose does not reach target A1c--> add second oral agent


6
Q
How does Type 2 DM develop?
A
alpha cells dysfunction-->secrete inappropriately high levels of glucagon + amyloid plaques + fewer beta cells --> secrete insufficient levels of insulin=> HYPERGLYCEMIA
beta cell mass decreases over time => disease progression
7
Q
what are incretin hormones?
A
-synthesized in L cells in the ileum and colon
-secreted in response to incoming nutrients
-stimulate insulin secretion
8
Q
how were incretin hormones first discovered?
A
insulin response to oral glucose was greater than the response to IV glucose
9
Q
what is the most important incretin hormone in humans?
A
glucagon-like peptide 1 (GLP1)
10
Q
What is the t1/2 of GLP1? Where are GLP1 receptors? How is it metabolized?
A
t1/2: 2-3 min
receptors in islet cells, CNS, plus more
metabolized by DPP-4
*secretion impaired by DMT2
11
Q
What does GLP1 do?
A
-enhances glucose-dependent insulin secretion
-slows gastric emptying
-suppresses glucagon secretion
-promotes satiety
-enhances beta cell proliferation (probably only in rodents)
-may improve insulin sensitivity
12
Q
What are the pathophys. mechanisms of DMT2?
A
decreased incretin effect
increased hepatic glucose prouction
decreased peripheral glucose uptake
increased pancreatic glucagon secretion
decreased pancreatic insulin secretion
13
Q
What is the target HbA1C for diabetics?
pre-prandial plasma glucose?
post-prandial plasma glucose?
A
<180
14
Q
What class is metformin in?
A
biguanides
15
Q
what is the mechanism of metformin (biguanides)?
A
activates AMP-kinase--> decreases hepatic glucose production and intestinal glucose absorption, increases insulin action
16
Q
how do sulfonylureas work? what are some of their names?
A
they close the K-ATP channels on beta cell plasma membranes--> increases insulin secretion
Glibenclamide/Glyburide
Glipizide
Gliclazide
Glimepiride
17
Q
What class are Repaglinide and Nateglinide in? How do they work?
A
class: meglitinides
mech: same as sulfonylureas
18
Q
Pioglitazone: class and MOA?
A
class: Thiazolidinediones
MOA: activates nuclear transcription factor PPAr-gamma--> increases peripheral insulin sensitivity
19
Q
Why is Pioglitazone infrequently used?
A
lots of side effects: weight gain, edema, HF, bone fractures, increased risk of bladder cancer
20
Q
what is the newer Thiazolidinedione that has less side effects than Pioglitazone?
A
Rosiglitazone
21
Q
what are the alpha-glucosidase inhibitors and what is their MOA?
A
acarbose and miglitol
MOA: inhibits intestinal alpha-glucosidase--> slows carb breakdown
**nonsystemic, must take with every meal, no as effective as metformin in reducing A1c
22
Q
GLP1 Receptor agonists: names and MOA
A
Exenatide, liraglutide
MOA: activates GLP1 receptors--> increased insulin secretion, decreased glucagon secretion, slows gastric emptying, increased satiety
23
Q
What is unique about the mode of delivery for the GLP1 receptor agonists?
A
they are only injectable, unlike most other non-insulin tx for DMT2
24
Q
What are the DPP4 inhibitors and how do they wrk?
A
Sitagliptin, Vildagliptin, saxagliptin, linagliptin
moa: inhibits DPP4 activity--> increase GLP1, GIP and insulin concentration, decrease glucagon
**expensive
25
Q
what class is Canagliflozin? moa?
A
sodium glucose cotransporter 2 inhibitor = SGLT2
moa: reduces glucose resorption in the kidney--> increases urinary glucose excretion
**no hypoglycemia
***may cause volume depletion, genital mycotic infections, UTIs, expensive
26
Q
What are the bile acid sequestrants and how do they work? when is it used?
A
Colesevelam
moa: binds bile acids/ cholesterol
this is primarily used for HTN but it shows a modest reduction in A1c so it could be a good drug for diabetics with HTN
27
Q
Bromocriptine is a ________ agonist. It works by______. What does it do to insulin? Side effects?
A
bromocriptine is a dopamine-2 agonist
it works by activating dopaminergic receptors--> alters hypothalamic regulation of metabolism and increases insulin sensitivity
* bonus: No hypoglycemia
Side effects: dizziness/ syncope, nausea, fatigue, rhinitis
28
Q
Name the non-insulin tx for DMT2 that cause weight gain
A
sulfonylureas
meglitinides
thiazolidinediones

29
Q
Name the non-insulin tx for DMT2 that cause weight loss
A
GLP1 receptor agonists
SGLT2
30
Q
What two classes of non-insulin tx for DMT2 are both cheap and work well when used together?
A
Biguanides (metformin) and sulfonylureas (glibenclamide, Glipizide, Gliclazide, Glimepiride)