Ptx 1 Dm

Front 1

In diagnosis of DM, random BG value?

Back 1

200mg/dL

Front 2

Diabetes: Fasting plasma glucose: (FPG)

Back 2

≥ 126 mg/dL; confirmed with 2nd test

Front 3

Diabetes: 2-hour blood glucose

Back 3

200 mg/dL; confirmed with 2nd test

Front 4

Diabetes: A1C

Back 4

6.5% (Normal 4-5.6%); conformed with 2nd test

Front 5

Pre-Diabetes: Fasting plasma glucose: (FPG)

Back 5

100-125 mg/dL (impaired fasting glucose – IFG)

Front 6

Pre-Diabetes: 2-hour blood glucose

Back 6

140-199 mg/dL (impaired glucose tolerance – IGT)

Front 7

Pre-Diabetes: A1C

Back 7

5.7- 6.4% (Normal 4-5.6%)

Front 8

Formulas for expressing A1c as average glucose

Back 8

eAG = 28.7 X A1c- 46.7

Front 9

Goals of DM therapy: Preprandial glucose

Back 9

70 - 130 mg/dL

Front 10

Goals of DM therapy: Postprandial glucose

Back 10

<180 mg/dL

Front 11

Goals of DM therapy: A1c

Back 11

<7%

Front 12

Goals of DM therapy: Blood pressure

Back 12

< 130/80

Front 13

Drugs of choice in DM for lowering BP

Back 13

CE inhibitor or ARB

Front 14

Goals of DM therapy: Lipid Levels: LDL

Back 14

<100 mg/dL

Front 15

Goals of DM therapy: Lipid Levels: HDL, male

Back 15

>40 mg/dL

Front 16

Goals of DM therapy: Lipid Levels: HDL, female

Back 16

>50 mg/dL

Front 17

Goals of DM therapy: Lipid Levels: Triglycerides

Back 17

<150 mg/dL

Front 18

Drugs of choice in DM for lowering lipids

Back 18

Statins

Front 19

What are the types of insulin for mealtime covereage

Back 19

Rapid and short acting insulin

Front 20

What are the types of insulin for basal control

Back 20

Intermediate and long acting insulin

Front 21

Algorithm for Type 2 DM: step 2 (well-validated)

Back 21

Lifestyle, metformin and basal insulin OR sulfonylurea

Front 22

Accute complication of DM: too much glucose

Back 22

Diabetic ketoacidosis (DKA), Hyperglycemic hyperosmolar nonketotic syndrome (HHNS)

Front 23

Accute complication of DM: too little glucose

Back 23

Hypoglycemia, Blood glucose &lt; 60

Front 24

What are the 4 Microvascular chrionic complications of DM

Back 24

Peripheral neuropathy, Autonomic neuropathy, Retinopathy, Nephropathy

Front 25

What are the 2 Macrovascular chronic complication of DM

Back 25

Myocardial infarction and stroke

Front 26

What is the effect of Peripheral neuropathy

Back 26

Numbness, tingling, pain; can lead to foot damage

Front 27

What is the effect of Autonomic neuropathy

Back 27

Impotence, Diabetic gastroparesis, Neurogenic bladder, Hypoglycemic unawareness

Front 28

What is the effect of Retinopathy

Back 28

Leading cause of blindness

Front 29

What is the effect of Nephropathy

Back 29

Leading cause of kidney failure; Characterized by proteinuria

Front 30

What are the treatments for Retinopathy

Back 30

Photocoagulation, modify other risk factors, get regular eye exams

Front 31

What are the treatments for Nephropathy

Back 31

ACE inhibitors, ARBs, restrict protein intake

Front 32

What is the treatment for the Macrovascular chronic complications

Back 32

ASA therapy, 75-162 mg daily

Front 33

know the insulin therapy for DM

Back 33

Front 34

when should short acting insulin be given?

Back 34

30 minutes before a meal

Front 35

what is amylin?

Back 35

Amylin is a hormone that is co-secreted w/ insulin from the cells of the pancreas

Front 36

what is amylin release in DM 1 & 2?

Back 36

w/ type II, we still have working of cells so we still have release of amylin but we don’t get that spike that we get in a normal person.
In type I, there is no release of amylin

Front 37

how can amylin work in treatment of DM? what is the SE?

Back 37

So amylin would be a good treatment for type I DM or type II DM that requires insulin.
What amylin does when it is released w/ insulin is it reduces our emptying gastric time so we don’t empty the stomach as quickly. So glucagon is not released, it makes us feel full. The side effect of a slower emptying is nausea & it can also cause hypoglycemia. So it’s recommended that those who start on should decrease the rapid acting insulin or mealtime insulin by 50%

Front 38

What is synthetic analog of amylin?

Back 38

symlin

Front 39

A patient with Type 1 DM is found to have a high blood glucose during an office visit. Which of the following insulin preparations could be administered in the office to bring the blood glucose down in a timely manner?

A.Insulin detemir (Levemir)
B.Insulin glargine (Lantus)
C.Insulin lispro (Humalog)
D.NPH insulin (Humulin or Novolin R)

Back 39

C is the correct answer

Front 40

What is the effect of sulfonylureas on A1C?

Back 40

reduces it by 1-2%

Front 41

What are the 3 sulfonylureas covered in lecture?

Back 41

Glimepiride, glipizide, glyburide,

Front 42

This drug is given for newly diagnosed type 2 DM?

Back 42

metformin

Front 43

This drug could be considered for pre-diabetes?

Back 43

Metformin

Front 44

what SCr levels should not be given metformin?

Back 44

SCr > 1.5 males; > 1.4 females

Front 45

How are glinides different from sulfonyureas?

Back 45

They have faster onset & shorter duration of action. They are dosed before a meal so if u skip a meal, u skip the dose whereas w/ sulfonylureas since they are long acting, if u skip a meal, a person will be hypoglycemic at the end of the day

Front 46

MOA of glucosidase inhibitors?

Back 46

Inhibit breakdown of complex CHO & decrease postprandial glucose

Front 47

This drug should not be given to those w/ heart failure?

Back 47

Thiazolidnediones

Front 48

What are the thizoldinediones?

Back 48

Pioglitazone & rosiglitazone

Front 49

Adverse effects of thiazolidnediones?

Back 49

Fluid retention, edema, bone fractures & cardiac risk

Front 50

How do incretin hormones work?

Back 50

Increase postprandial insulin & decrease postprandial glucagon. They also delay gastric emptying & enhance satiety

Front 51

Incretin mimetics are aka what?

Back 51

GLP-1 agonists

Front 52

What are the 2 GLP-1 agonists?

Back 52

GLP-1 agonists

Exenatide &
liraglutide

Front 53

What are the adverse effects of GLP-1 agonists?

Back 53

Nausea & vomiting, pancreatitis, & Ab can develop against them

Front 54

What are the DPP-4 inhibitors?

Back 54

Sitaglipitin & saxagliptin

Front 55

MOA of DPP-4 inhibitors?

Back 55

They inhibit dipeptidyl peptidase 4 enzyme w/c is responsible for breaking down incretins

Front 56

What are the adverse effects of DPP-4 inhibitors?

Back 56

Nasopharyngitis, headache

Front 57

Too much glucose can lead to what 2 things?

Back 57

DKA & hyperglycemic hyperosmolar nonketotic syndrome (HHNS)

Front 58

What complications occur w/ too little glucose?

Back 58

Hypoglycemia w/ glucose <60