Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm II > Diabetes Meds > Flashcards

Diabetes Meds Flashcards

1
Q

2016 ADA criteria for dx of diabetes?

A

any of the following:
confirmed fasting blood glucose greater than or equal to 126
HgbA1c of 6.5% or greater
non-fasting blood glucose of 200 or greater in pt presenting w/sxs or exam findings consistent w/diabetes
(+) oral glucose tolerance test resulting in blood glucose of 200 or greater at 2-3 hrs after a bolus of glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

DM type 1 is dt what? usu presents at what age? ssxs? what happens to the pancreas? what abs are present?

A

DM type 1 usu dt relative or absolute insulin deficiency
usu less than 20 yo when sxs onset
dt autoimmunity against pancreatic beta cells and insulin
overall leads to islet cell fibrosis and atrophy
anti-islet cell abs as well as glutamic acid decarboxylase abs are present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how to differentiate btw type 1 and type 2 DM?

A

type 1 DM will have insulin abs and a low amount of C-peptide
type 2 DM will not have insulin abs and will have normal or high C-peptide
insulin abs can also be used to differentiate type 1.5 from type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is C peptide? when do you see it?

A

peptide that is made when pro-insulin is split into insulin and C peptide
splitting occurs before pro-insulin is released from endocytic vesicles w/in the pancreas
pts w/newly diagnosed diabetes may have C-peptide levels measured as means of distinguishing btw type 1 and 2 DM: will be low in type 1 and normal or high in type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

cause of DM type 2? often associated with what? abs present?

A

type 2 is dt insulin resistance and over time a relative insulin deficiency in addition to excess hepatic glucose production
most often associated with obesity and generally age of onset is 30 years or older
NO antibodies present
90-100% concordance for development for type 2 DM in identical twins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is type 1.5 DM? how to determine dx? initially respond well to what tx, then what is necessary?

A

latent-onset adult diabetes (LADA)
are insulin resistant similar to type 2 DM but at levels less than type 2
often (+) for islet cell antibodies
may respond well to lifestyle changes or to oral DM meds but beta cells continue to be destroyed and type 1.5 quickly progress to needing insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when should type 1. 5 DM be considered?

A

in a previously diagnosed type 2 DM pt who demonstrates a rapid failure of glucose control despite oral DM meds which had previously worked well to prevent hyperglycemia
when anti-islet antibodies are present
low levels of C-peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

meds for type 2 DM?

A 
biguanides
sulfonylureas
meglitinides
alpha-glucosidase inhibitors
thiazolidinediones (glitazone)
dipeptidyl peptidase-4 inhibitors
insulin can be given in conjunction with any of the above drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pts on oral diabetic meds are generally switched to what prior to any in-patient surgery?

A

insulin (sliding scale)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MOA of metformin? MOA of sulfonylureas and meglitinides? MOA of alpha-glucosidase inhibitors? MOA of thiazolidinediones (glitazones)? MOA of DPP-4 inhibitors?

A

metformin: inhibits glucose production by the liver and decreases insulin resistance
sulfonylureas + meglitinides increase secretion of insulin
alpha-glucosidase inhibitors delay absorption of glucose by intestine
thiazolidinediones (glitazones) decrease insulin resistance
DPP-4 inhibitors promote release of insulin from pancreas after eating a meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when might a diabetic pt using oral meds need to switch to insulin?

A

with severe acute infxns b/c of potential for worsening glucose control; before any in-patient surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

standard of care for type 2 DM who become PG or develop gestational DM?

A

insulin rather than oral meds b/c the oral meds affect baby’s pancreas as well and can lead to macrosomia
also insulin provides greater glucose control
may need to increase insulin dosing during last TM b/c increased HPL decreases insulin receptor sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

metformin was derived from what? MOA? effect on blood glucose? PG category?

A

derived from French lilac plant
MOA: decreases hepatic glucose production to a lesser extent, enhances insulin sensitivity in skeletal muscle
causes hypoglycemia (but not to a detrimental level)
PG category B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

similar effects of metformin and sulfonylureas? dissimilar effects of metformin and sulfonylurea on weight?

A

reduce pts fasting serum glucose, non-fasting serum glucose and A1c levels
metformin can cause a pt to experience modest reduction of wt whereas sulfonylureas can cause weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SEs of metformin? can decrease major SE by doing what? what do you need to supplement with while using metformin?

A

SEs: abd cramping and nausea; metallic taste; lactic acidosis (rare but can be fatal)
to decrease the cramping and nausea can use the slow or extended release forms of the drug
need to supplement w/B12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

population who is at most risk for the most severe SE of metformin use? how to decrease the occurrence of this SE?

A

lactic acidosis risk increases in those who are renally impaired
can decrease risk for developing lactic acidosis by decreasing or lowering EtOH consumption while taking metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

guidelines for using metformin in pts w/renal impairment?

A

should not be started or if started stopped in pts w/serum creatinine greater than 1.5 mg/dL in males and greater than 1.4 in females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

metformin use + what two things can increase the risk for renal insufficiency?

A

increase use of iodinated contrast material can also increase the risk for renal insufficiency
high EtOH use can increase the risk of lactic acidosis dt renal insufficency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MOA of sulfonylureas?

A

stimulate intact beta cells of the pancreas to release more insulin
this occurs as a result of the interaction of a sulfonylurea with the ATP sensitive potassium channels in beta cell membranes
by blocking potassium channels, the time a beta cell spends in the calcium release stage of cell signaling is increased which initiates more insulin release from the affected beta cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

2, 1st generation sulfonylureas still in use today?

A

chlorpropamide/diabinese

tolbutamide/orinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

3, 2nd generation sulfonylureas still in use today?

A

glipizide/glutotrol
glyburide/micronase/diabeta
glimepiride/amaryl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

most common adverse effects w/sulfonylureas?

A

cardiovascular events leading to mortality hypoglycemia, esp in those with renal or hepatic impairment
might also have wt gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

PG category of sulfonylureas?

A 
category C (for 2nd generation sulfonylureas dt insufficient human drug studies)
have been shown to cause fetal hypoexmia as a result of medication induced hyper-insulinemia which can extract oxygen from fetal blood by the fetus beyond the ability of the placenta to supply it leading to fetal hypoxemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

C/I to sulfonylurea use?

A

renal or KD impairment as this increases the risk of hypoglycemia
pregnancy dt high risk for fetal hypoxemia as well as congenital malformations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

dt sulfonylureas MOA, how long can they be utilized as an effective tx?

A

b/c sulfonylureas act by increasing total beta cell fxn and the pancreas is failing in DM, this means that sulfonylureas can only be utilized for 5-10 years

26
Q

btw gyburide, glimepiride and glipizide which has the greatest hypoglycemic effect?

A

gyburide appears to have the greatest incidence of hypoglycemia events

27
Q

are sulfonylureas effective in type 1 diabetes or post-pancreatectomy?

A

NO b/c there is an absolute deficiency of insulin production

28
Q

what was the initial monotherapy for DM for a long time? what has it been replaced with and why?

A

initial therapy used to be a sulfonylurea but now its metformin b/c of the wt loss associated with it’s use
and in about 10-20% of pts initial use of sulfonylurea alone is ineffective in controlling blood glucose levels

29
Q

what is triple therapy? how often is it used?

A

med regiment when one oral DM medication is not effective at lowering blood glucose levels
can add metformin or a thiazolidinedione to a sulfonylurea
ultimately insulin may be required
triple therapy of a sulfonylurea, biguanide and a TZD is generally discouraged but some still prefer this over insulin

30
Q

MOA of meglitinides? two drugs currently? also referred to as what? how to take?

A

MOA: stimulate beta cells to release insulin; bind to ATP-sensitive potassium channels on beta cells and thereby increase insulin release
meglitinide drugs: nateglinide and repaglinide
these are both chemically unrelated to the sulfonylureas and are referred to as non-sulfonyurea secretagogues
generally given 3-4 times a day before meals (tid-qid ac)

31
Q

of the two meglitinides, which is proven to be equally effective as sulfonylureas?

A

repaglinide appears to be equally effective as sulfonylureas in improving blood glucose control and lowering A1c levels

32
Q

SEs of meglitinides? monotherapy or can it be used in combination?

A

SEs: hypoglycemia, wt gain
can be combined with metformin or w/a TZD (glitazone class) but DO NOT combine with a sulfonylurea dt increased risk of hypoglycemia

33
Q

onset of meglitinides? how to take?

A

rapidly absorbed from GI causing insulin to peak w/in 30-60 minutes and is rapidly cleared
take 3-4 times a day before each meal and if a meal is missed drug should not be taken

34
Q

MOA of thiazolidinediones/glitazones? two examples?

A

MOA: improve insulin sensitivity in skeletal muscle cells, fat cells adn liver cells and also help decrease hepatic glucose production
rosiglitazone/avandia and pioglitazone/ACTOS are examples

35
Q

how to give avandia and ACTOS? how long to achieve maximum effect? drugs they can be combined with?

A

give once a day
the glitazones can take 6-14 wks to achieve their maximum effects
avandia and ACTOS are approved for monotherapy or in combo w/metformin or a sulfonylurea
only ACTOS is approved for concurrent use with insulin

36
Q

SE of glitazones?

A

avandia and ACTOS both increase the risk for congestive heart failure and possibly MI
also possible reduction in bone density and subsequent risk for increased fractures
wt gain of 5-10 lbs has also been reported

37
Q

when initiating glitazone tx, what test needs to be performed and what needs to be monitored?

A

before initiating tx need to measure LFTs

with continued use need to recheck LFTs at month 1 and again at month 3 to check for a rise in AST

38
Q

two alpha-glucosidase inhibitors that can be used to tx DM? MOA?

A

examples are acarbose and miglitol
MOA: inhibit alpha-glucosidase enzymes that line the brush border of the SI which interferes w/the hydrolysis of carbs and delays the absorption of glucose and other monosaccharides

39
Q

how to take alpha-glucosidase inhibitors? risk of hypoglycemia?

A

in order to lower postprandial glucose levels they must be taken with each meal
alone, neither alpha-glucosidase inhibitor will cause hypoglycemia, but when given with a sulfonylurea or insulin the risk for hypoglycemia increases

40
Q

SEs of alpha-glucosidase inhibitors? why do you get this SE?

A

SEs: abd pain, diarrhea, flatulence
these SEs happen because alpha-glucosidase inhibitors cause carbs to not be absorbed so stay in lumen of the gut and then get these SEs dt osmotic effects of sugars and bacterial fermentation of sugars

41
Q

two severe SEs of acarbose? PG category of acarbose and miglitol?

A

in high doses, has been associated with moderate transaminase elevations and in rare events has caused fatal hepatic failure
both are PG category B (can be used in PG)

42
Q

how to tx hypoglycemia dt alpha-glucosidase inhibitors? C/I to using acarbose or miglitol?

A

need to give pt glucose rather than sucrose b/c alpha-glucosidase inhibitors interfere w/the breakdown of sucrose
C/Is: chronic intestinal dzs, IBD, colonic ulceration or any degree of intestinal obstruction

43
Q

MOA of dipeptidyl peptidase-4 inhibitors?

A

DPP-4 enzyme normally breaks down incretins GLP-1, GIP that are released following a meal
so inhibition of DPP-4 in the periphery diminishes degree of inactivation of GLP-1 which augments insulin secretion and diminishes inflammation of the islet cells and inhibits glucagon secretion
all of this in turn increases glucose utilization and diminishes hepatic glucose production which through reduction in postprandial and fasting glucose reduces HgbA1c

44
Q

MOA of sitagliptin/januvia? used to tx what? use alone or in combo?

A

prevents activation of GLP-1 and GIP inactivation which potentiates duration of action of insulin following meals
used to tx type 2 DM
can combine with metformin or a TZD but not with insulin
combo w/metformin, a sulfonylurea or glitazone have shown consistent reductions in A1c concentrations

45
Q

severe SE of both januvia and janumet?

A

increased risk of developing acute pancreatitis, chronic pancreatitis which increases the risk for developing pancreatic cancer

46
Q

efficacy of new type 2 DM drugs compared to the old drugs?

A

newer drugs appear to be no better than the sulfonylureas and metformin which have been around for decades and some actually appear less effective and safe
generally newer drugs are also more expensive

47
Q

reasonable first choice for type 2 DM? what if adequate glucose control is not achieved? what if even that combo doesn’t get control?

A

metformin is a reasonable first choice
if cannot get adequate glucose control then can add a sulfonylurea to metformin
if metformin + a sulfonylurea doesn’t produce adequate glucose control then can add insulin as well, w/or w/o a sulfonylurea

48
Q

when used alone, oral DM meds lower HgbA1c by what %age?

A

0.5-1.5%

49
Q

which drug class increases risk of CHF, even though they are technically effective for glycemic control?

A

thiazolidinediones

50
Q

if you cannot achieve desired HgA1c with metformin alone, what can you add

A

a sulfonylurea

51
Q

what is the expected progression of oral medications in pts w/type 2 DM?

A

about 75% of pts w/type 2 DM will require multi-drug therapy or insulin w/in 10 years

52
Q

recommendation of when to initiate insulin?

A

initiation of insulin therapy should not be postponed when oral therapy fails to control plasma glucose

53
Q

which drug has been associated with increasing the risk of developing CHF or worsening heart failure and is actually more expensive than older agents?

A

glitazone such as ACTOS

54
Q

which drug has been associated with increasing the risk of pancreatitis and is more expensive than the older agents?

A

DPP-4 inhibiting drug such as januvia or janumet

55
Q

two new injectable meds approved by the FDA for treating both type 1 and type 2 DM?

A

pramlintide (synthetic form of amylin - hormone produced along w/insulin by the beta cells) and exenatide

56
Q

when can pramlintide/symlin be used?

A

in type 1 and type 2 DM pts whom cannot reach their HgbA1c level on insulin alone

57
Q

what is amylin?

A

hormone that plays a role in slowing gastric emptying and promotes satiety thereby preventing post-prandial spikes in blood glucose levels

58
Q

what does the use of symlin allow diabetic pts to do?

A

allows pts to use less insulin while still lowering average blood sugar levels and also substantially reduces the rise in blood sugar that often occurs immediately in diabetics immediately after meals

59
Q

can you combine pramlintide/symlin in the same injector?

A

NO

cannot be combined b/c of differences in chemistry and must be injected separately

60
Q

what is special about symlin?

A

notable for being the only drug to gain FDA approval for lowering blood sugar in type 1 diabetics since insulin was initially developed in the early 1920s

61
Q

what is exenatide/byetta? MOA?

A 
first in a new class of drugs referred to as incretin mimetics that have been developed for type 2 diabetes 
acts to lower blood glucose levels primarily by increasing insulin secretion 
ONLY has this effect w/elevated blood glucose levels so does NOT increase the risk of hypoglycemia although hypoglycemia can occur when taken in conjunction w/another hypoglycemic such as a sulfonylurea
62
Q

primary SE of exenatide/byetta? how to give? approved for use in who?

A

SE: nausea, tends to improve over time
injected w/meals and most will experience modest wt loss as well as improved glycemic control
approved use in type 2 DM who have not achieved their HgbA1c levels using metformin, a sulfonylurea or a combo med of metformin-sulfonylurea

Pharm II (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions