1Insulin is synthesized in the
beta cells of islets of langerhans
2How is insulin made?
cleavage of proinsulin to produce the c-peptide and insulin
3How many peptide chains is insulin made of?
two
4What does insulin do?
carb, protein and lipid metabolism
regulates electrolytes
5Which test shows the gycated hemoglobin which reflects the average blood glucose levels of the prior 8-12 weeks?
hemoglobin A1C
6What is the most sensitive test?
oral glucose tolerance test
7How many hours does the patient have to fast for the fasting plasma glucose test?
more than 8 hours
8What are the rapid acting insulins?
lispro
aspart
glulisine
9What is the onset of rapid acting insulin? WHat is the peak onset and duration?
5-15 minutes
1 hour
3-4 hours
10What is the onset of short acting insulin? What is the peak and duration?
30 minutes
2-3 hours
4-6 hours
11What is the only insulin available for IV use?
short acting insulin
12What is the intermediate acting insulin?
NPH
13What is the onset, peak and duration for intermediate acting insulin?
1-2 hour
6-10 hours to peak
duration is 10-16 hours
14What are the long acting insulins?
glargine
detemir
degludec
15What is the onset, peak and duration of mixed insulin ?
1-4 hours
flat (not defined)
duration is 24 hours
16What is the mixed insulin made of?
NPH and rapid acting insulin (LAG)
17What should be administered in addition to dexamethasone?
detemir
glargine
18What is the average carb to insulin ratio
1 unit of insulin for 15 carbs
191 unit of insulin lower the blood glucose level by
30-40 mg/dL
20What are some AE assocated with insulin?
hypoglycemia
weight gain
lipodystrophy at the injection site
pain and erythema at injection site
hypokalemia
edema
21What DDIs decrease insulin demand?
analgesics
antibiotics
antimalarial drugs
MOAIs
fibrates
haloperidol
22Which drugs increase insulin demand?
thiazide and loop diuretics
heparin
glucocorticoids
opiods
immunosupressive durgs
TCAs
antipsychtic drugs
lithium
protease inhibitors
thryoid hormones
estrogen
dobutamine (beta adrenergic agnoists)
epinephrine
derivatives of nicotinic acid
23What drugs can either increase or decrease insulin demand?
ethanol
beta blockers
24Coverage that keeps glucose stable throughout the entire day including between meals and fasting?
basal
25Additional covrage for the acute increases in glucose?
bolus
26What is the MOA of biguanides?
decreases hepatic gluconeogensis
decreases intestinal absorption of glucose
improves insulin sensitivity by increaseing peripheral glucose uptake and utilization
27t/f biguinides stimulate the release of insulin?
false
28What is the glycemic efficacy of biguanides?
lowers HbA1c by 1.2-2% over 3 months
29T/F metformin rarely causes hypoglycemia?
true
30What are the SE associated with metformin?
weight loss
GI
decreases b12
metallic taste in mouth
31What are the CI to biguanides?
renal failure
IV iodinated contrast medium
heart failure
alcoholism
severe liver failure
chronic pancreatitis
stravation ketosis
ketoacidosis
sepsis
32What are the second generate sulfonylureas?
glipizide
glyburide
glimepiride
33What is the MOA of sulfonylureas and meglitinides?
block ATP-sensitive potassium channels of the pancreatic beta cells which causes depolarization of the cell membrance which leads to calcium influx then insulin secretion
decreases hepatic gluconeogensis
increases peripheral insulin sensitivity
34What is the glycemic efficacy of sulfonylureas?
lowers HbA1c by 1.2% over 3 months
35What are the SE of sulfonylureas?
hypoglycemia
coma
weight gain
n/v
anemia
36What are the CI to sulfonylureas?
type I DM
pregnancy
lactation
sulfa allergy
beta blockers
hepatic or renal insufficiency
severe CV comorbidity
obesity
37Patients on sulfonylureas will have an increased hypoglycemia risk with what?
alcohol
antifungals
anticoagulants
TCAs
38Which drug is associated with the highest risk of hypoglycemia?
sulfonylureas
39t/f the risk of hypoglycemia increases when sulfonylureas are with in combination therapy?
true
40How much do meglitinide derivatives reduce A1c levels?
0.4%-0.9%
41What are the meglitinide derivatives?
repaglinide
nateglinide
42What are the CI for meglitinide derivatives?
severe liver failure
renal failure
43Which meglitinide is okay to give with milder CKD?
repaglinide
44What are the alpha glucosidase inhibitors?
acarbose
miglitol
45What are the SE associated with alpha glucosidase inhibitors?
flatulence
hypoglycemia
hepatotoxicity
bloating
diarrhea
46What are the CI for alpha-glucosidase inhibitors?
severe renal failure
IBD
conditions associated with malabsorption
47Which alpha-glucosidase inhibitor causes less hepatotoxicity?
miglitol
48What is the MOA for acarbose/miglitol?
inhibit alpha-glucosidase which causes a delayed and decrease intestinal glucose absorption and decrease carb breakdown
49How much do alpha glucosidase inhibitors reduce HbA1c?
0.5-1.0%
50What are the thiazolidinediones?
rosiglitazone
pioglitazone
51What is the MOA?
insulin sensitizers
52T/F thiazolidinediones need the presences of insulin to work
true
53Which diabetic medication has been show to slow the progression of diabetes?
thiazolinediones
54What are the common side effects of TZDs?
weight gain
edema
fluid retention
left sided HF
skeletal fractures
hepatotoxicity
55What is the glycemic efficacy of TZDs?
1% in 3 months
56Which TZD has no efect on triglycerides?
rosiglitazone
57What are the CI for TZD?
heart failure (stage III or IV)
liver failure
58What is the box warning associated with TZDs?
CHF
59What is a risk associated with rosiglitazone?
increased LDL cholesterol
60What are the CI associated with pioglitazone?
h/o bladder cancer or active bladder cancer
macrohematuria of unknown orgin
61What are the GLP-1 agonists?
gulaglutide
liraglutide
semaglutide
62GLP-1 agonists are known for
risk reduction for major CV events
63What is the mOA of GLP-1 agonists?
mimic the endogenous incretin GLP-1 causing stimulation of glucose dependent insulin release, reduce glucagon and slow gastric emptying
64Purpose of slowing gastric emptying in GLP-1 receptor agonists?
increase feeling of satiety
decreases weight
65What is the glycemic efficacy of GLP-1 agonists?
lowers HbA1c by 0.5-1.5% over 3 months
66What are the SE of GLP-1 agonists?
n/v/d
h/a
67What are the CI for GLP-1 agonists?
symptomatic GI motility disorders
chronic pancreatitis
family hx of pancreatic tumors
hx of family hx of MTC or MEN type 2
68What are the dipeptidyl peptidase IV (DDP-4) inhibitors?
sitagliptin
saxagliptin
69What is the MOA of DDP-4 inhibitors?
indirectly increase the endogenous incretin effect by inhibiting the DPP-4 that breaksdown GLP-1 which causes increase insulin secretion and delays gastric emptying
70What are the SE associated with DPP-4 inhibitors?
GI symptoms
arthralgia
h/a
dizziness
increased feeling of satiety
nasopharyngitis and URT infection
UTI
pancreatitis
71What are the CI associated with DPP-4 inhibitors?
hypersensitivity
liver failure
renal failure
72What are the SGLT-2 inhibitors?
end in glifozin
73What is the MOA of SGLT-2 inhibitors?
reversible inhibition of the sodium-dependent glucose cotransporter in the proximal tubule of the kidney which reduces glucose reabsorption in the kidney
74SGLT-2 inhibitors cause
glycosuria
polyuria
75What are the indications for SGLT-2 inhibitors?
young patients with treatment compliant type 2 DM without significant renal failure
76What are the clinical characterisitics of SGLT-2 inhibitors?
lowers HbA1c by 0.6% over 3 months
promotes weight loss
decrease BP
decreased risk CV mortality
77What are the SE of SGLT-2 inhibitors?
UTI
genital infections
dehydration
DKA
increase risk of lower limb amputation
carcinogenic effect
78What are the CI of SGLT-2?
CKD
recurrent UTIs