Cology, Oral Hypogly

Front 1

igt and type 2 dm has a slower/fast rise in insulin

Back 1

f

slower rise

Front 2

igt and type 2 dm has a longer/shorter peak than norm w/ insulin

Back 2

longer

Front 3

who has the lowest plasma glucose:

norm/igt/type 2 dm

Back 3

norm

Front 4

insulin peaks for ngt/dm

Back 4

ngt

Front 5

who has higher glucagon: ngt or dm

Back 5

dm

Front 6

drugs that stimulate the pancreas to make more insulin

Back 6

sulfonylureas

meglitinides

oral hypoglycemics

Front 7

drugs that sensitize the body to insulin and/or control hepatic glucose production

Back 7

thiazolidinediones

biguanides

oral antihyperglycemics

Front 8

drugs that slow the absorption of starches

Back 8

alpha-glucosidase inhibitors

Front 9

suppress glucagon

decrease gastric emptying

food intake

Back 9

incretins (glucagon like peptides)

DPP4 inhibitors

Front 10

1st gen oral hypoglycemics/sulfonylureas

Back 10

acetohexamide

chlorpropamide

tolazamide

tolbutamide

Front 11

oral hypoglycemics/sulfonylureas
2nd gen

Back 11

glimepiride

glipizide

glyburide

Front 12

sulfonylureas

block -- dependent --- channel on beta cells in pancrease

Back 12

atp

K

Front 13

sulfonylureas

depolarization induced:

Back 13

increase insulin release

Front 14

sulfonylureas

decrease --- --- glucose production

Back 14

basal hepatic

Front 15

sulfonylureas

decrease glu---- and gly---

Back 15

decrease gluconeogenesis

glycogenolysis

Front 16

sulfonylureas

increase insulin --- ----

increase --- #

Back 16

insulin receptor sensitivity

receptor #

Front 17

sulfonylureas

decrease --- levels

Back 17

glucagon (secondary to increase insulin and somatostatin release)

Front 18

sulfonylureas

almost all metabolized in the ---

Back 18

liver

some active metabolites

Front 19

sulfonylureas

excreted in the --

Back 19

urine

Front 20

sulfonylureas

higly --- bound

Back 20

protein

Front 21

sulfonylureas

caution w/ - insufficiency

Back 21

hepatic

renal

Front 22

sulfonylureas

cross/does not cross the placenta

Back 22

cross

so may deplete insulin from fetal pancreas

Front 23

sulfonylureas: chlorpropamide

avoid in -----

long/short acting

Back 23

elderly

long (48 hrs)

Front 24

sulfonylureas: chlorpropamide

highest/lowest se

Back 24

highest

Front 25

sulfonylureas: chlorpropamide

--- like rxn w/ etoh

Back 25

disulfram

Front 26

-- and -- most likely to produce hypoglycemia

Back 26

chlorpropamide

glyburide

Front 27

sulfonylureas: glimepiride

may enchance sensitivity of -- --- to insulin

Back 27

peripheral tissue

Front 28

sulfonylureas: glimepiride

use in combo w/ --, may decrease dose of -- required

Back 28

insulin

insulin

Front 29

sulfonylureas: glimepiride

more rapid/slow glucose control

Back 29

rapid

Front 30

sulfonylureas: glimepiride

may enchance --glycemia

Back 30

hypo

Front 31

sulfonylureas: glimepiride

dosing

Back 31

once per day

Front 32

sulfonylureas: glyburide

dosing

Back 32

once daily

Front 33

sulfonylureas: glyburide

most frequent ---

Back 33

hypoglycemia

Front 34

sulfonylureas: glyburide

may suppress -- inhibition of insulin release

Back 34

glucose

Front 35

sulfonylureas: glipizide

when should it be taken

Back 35

30 min before meals

Front 36

sulfonylureas: glipizide

short/long t1/2

Back 36

short t1/2

Front 37

sulfonylureas: glipizide

more/less hypoglycemia

Back 37

less hypoglycemia

Front 38

what can block the s/s of hypoglycemia

Back 38

beta blockers

Front 39

sulfonylureas

--glycemia

weight gain/loss

-- --- ---

Back 39

hypoglycemia

weight gain

constipation/n/v

Front 40

sulfonylureas ae of skin:

Back 40

rash

pruritis

increased sensitivity to sunlight

Front 41

sulfonylureas ae

---penia

--penia

--- anemia

Back 41

leucopenia

throbocytopenia

aplatic anemia

rare

Front 42

what may develop over time w/ sulfonylureas

Back 42

resistance

so might need insulin in 10-15 yrs

Front 43

ci w/ sulfonylureas

Back 43

diabetic ketoacidosis w/ or w/out coma

type 1 dm

pregnancy

breastfeeding

Front 44

sulfonylureas

di:

-- binding

-- drugs decrease effectiveness

--- like rxns

Back 44

protein

hyperglycemic

disulfiram

Front 45

s/s of hypoglycemia:

Back 45

tremor

elevated hr

sweating

adrenergic activation

Front 46

meglitinides

Back 46

repaglinide

nateglinide

Front 47

meglitinides

block --dependent --- channel in -- cells

Back 47

atp

K

beta

Front 48

meglitinides

increase --- secretion

Back 48

insulin

Front 49

meglitinides

insulin release relative to --- level

Back 49

glucose

(meglitinides more porportional to norm glucose release)

Front 50

meglitinides

highly -- bound

-- metabolism

Back 50

protein

hepatic

Front 51

meglitinides

when should they be taken

Back 51

before meals

repaglinide: 30 min

nateglinide: 1-10 min

Front 52

meglitinides

peak effectiveness -- hr

duration ----- hours

Back 52

1

3-4

Front 53

meglitinides

may be combined w/ -- but not other oral agents

Back 53

metformin

(not w/ others esp sulfonylureas)

Front 54

meglitinides

what do you do if you miss a meal

Back 54

skip dose

Front 55

ae of meglitinides:

--- --- infections

--- glycemia

weight gain/loss

--ache

--

-- pain

use w/ caution in -- problems

Back 55

upper resp infections

hypoglycemia

weight gain

ha

nausea

joint pain

use w/ caution in liver problems

Front 56

meglitinides


which cause more hypoglycemia

Back 56

repaglinide > nateglinide

Front 57

metformin

decrease -- glucose production

increase --- glucose uptake and utlization

increase -- sensitivity

Back 57

hepatic

peripheral

tissue insulin

Front 58

metformin

decease --- --- form gi tract

Back 58

glucose absorption

Front 59

metformin

limited ---

Back 59

hypoglycemia

cuz not affecting insulin secretion directly

Front 60

metformin

t/f

metabolized in the liver

Back 60

f

not

yet, ci in hepatic disease due to lactic acid

Front 61

metformin

protein bound?

Back 61

no

Front 62

t/f

metformin excreted unchanged by kidneys via renal tubular excretion

Back 62

t

not used in renal impairment

Front 63

metformin

t/f

not useful in obese patients w/ insulin resistance and hyperlipidemia

Back 63

f

useful

Front 64

t/f

metformin causes weight gain

Back 64

f

no weight gain!

Front 65

ae of metformin:

GI

Back 65

unpleasant or metallic taste

anorexia

constipation

diarrhea

heartburn

Front 66

metformin ae:

-- acidosis:

increased incidence in -- impairment,

--- and after sx

Back 66

lactic

renal

aging

Front 67

t/f

metformin can cause a rash

Back 67

t

Front 68

metformin

can cause -- anemia

Back 68

megaloblastic

decreased vit b12 absorption

Front 69

ci w/ metformn


-- failure

--disease

---- --- acidosis or ---ia

-- disease

Back 69

heart

renal

metabolic

hypoxia

hepatic

Front 70

metformin

------ drugs compete for --- excretion

Back 70

cationic

tubular

Front 71

metformin

should be stopped:

Back 71

before sx

withhold drug for 48 hrs after sx due to increase in lactic acid

Front 72

thiazolidinediones

Back 72

pioglitazone

rosiglitazone

troglitazone

Front 73

thiazolidinediones

selective and potent --- form --- ---- --

Back 73

agonist

peroxisome proliferator activated receptor gamma (PPAR-y)

Front 74

thiazolidinediones

PPAR regulates transcription of --- responsive genes

Back 74

insulin

Front 75

thiazolidinediones

PPAR

genes involved in -- and -- metabolism

Back 75

lipid

gluocose

(does not affect insulin. .. just affects glucose utilizatin)

Front 76

thiazolidinediones

increase --- glucose uptake and utilization

decrease --- glucose production

Back 76

peripheral (increase tissue insulin sensititivity)

hepatic

Front 77

thiazolidinediones

highly --- bound

Back 77

protein

Front 78

thiazolidinediones

-- metabolism

Back 78

liver

Front 79

thiazolidinediones

max effect may require 6-12 ----

Back 79

weeks

Front 80

ae of thiazolidinediones

--- --- infection

Back 80

resp tract

Front 81

thiazolidinediones ae

expanded --- --, ---

--ache

---

-- pain

weight gain/loss

Back 81

resp tract infection

bl volume, edema

ha

fatigue

muscle pain

Front 82

thiazolidinediones ae

increaed ----

monitor ---- ---- q 2 mo for the 1st year

Back 82

increased HDL, LDL, variable on TG

liver enzymes

Front 83

when do you stop taking thiazolidinediones

Back 83

ALT > 3x norm

Front 84

which thiazolidinediones has increased incidence of mi and deaths

Back 84

rosiglitazone

Front 85

when can you give rosiglitazone

Back 85

if there are no cv risk factors

Front 86

alpha-glucosidase inhibitors

Back 86

acarbose

miglitol

Front 87

alpha-glucosidase inhibitors

are competitive/noncompetitive inibitors of a-amylase and ------ enzymes in -- brush broder

decrease -- absorption

Back 87

competitive

a-glucosidae

intestinal

glucose

Front 88

alpha-glucosidase inhibitors

t/f

ok to give as monotx

Back 88

f

not much effect on type 2 so use in combo

Front 89

alpha-glucosidase inhibitors

acarbose absorbed/not absorbed

Back 89

not absorbed

metabolized by intestinal flora

Front 90

alpha-glucosidase inhibitors

miglitol has -- absorption

excreted by the -----

Back 90

saturable

kidney

Front 91

alpha-glucosidase inhibitors

when should u take

Back 91

w/ first bite of each meal

Front 92

alpha-glucosidase inhibitors

monitor ---- w/ miglitol

Back 92

liver fx

Front 93

alpha-glucosidase inhibitors

usu used in comb w/

Back 93

oral agents or insulin

Front 94

ae of alpha-glucosidase inhibitors

-- pain

--


----

Back 94

abd pain

diarreha

flatulence. . . undigested carbs in colon

Front 95

alpha-glucosidase inhibitors ci

--- --- disease

gi --- or ---

chronic --- disease

Back 95

inflammatory bowel disease

gi obstruction or ulceration

chronci intestinal disease

Front 96

incretin:

--- like ----

Back 96

glucagon like peptide

t1/2: 2 minutes

Front 97

incretin glucose dependent/independent insulintropic polypeptide

Back 97

dependent

Front 98

incretin

when is glucose increased

Back 98

after meal

Front 99

increase increase --- secretion form l cell of intestine

Back 99

GLP

Front 100

incretin increase gluccose dependent ----- release from ---

Back 100

insulin

pancreas

Front 101

incretin

increase/decrease gastric emptying and food intake

Back 101

decrease

Front 102

glp 1 stimulate release, biosynthesis, and gene transcription of -----

Back 102

insulin

Front 103

glp 1 metabolized by --- ---

Back 103

dipeptidlyl peptidase

(DDP-IV)

Front 104

glp 1 secreted upon:

Back 104

ingestion of food

Front 105

type 2 dm have dimished level of insulin as well as decreased postprandial ---- induced insulin secretion

Back 105

glp 1

Front 106

type 2 dm have increased -- after meals

Back 106

glucagon

Front 107

glp-1 suppress -- levels after meals,

increase -- during fasting

increase --- production

Back 107

glucagon

glucagon

glucose

Front 108

incretins also decrease gastric emptyiing which will:

Back 108

slow peak glucose absorption

Front 109

incretins will increase -----

Back 109

satiety

Front 110

incretins: exenatide

indications

Back 110

type 2 dm taking metformin and sulfonylureas or comb and not controlled

Front 111

incretins: exenatide

will cause weight loss/gain

Back 111

lossa

Front 112

dose of exenatide:

Back 112

5-10 mcg 2 x day

0-60 min before a meal

Front 113

route of exenatide

Back 113

sq

prefilled pen-injectors

Front 114

ae if exenatide

--- -----

--glycemia w/ sulfonylurease

----- absorption of other meds

inappropriated use for:

Back 114

n/v

hypoglycemia

delay absorption of other oral meds

inappropriate use for weight loss

Front 115

incretins: liraglutide

human glp-1 analog linked to -- --- binds -- to be released slowly

Back 115

fatty acid

albumin

Front 116

t 1/2 of liraglutide

Back 116

12 hrs

Front 117

ae of liraglutide

Back 117

thyroid ca

pancreatitis

n/v

hypoglycemia

ha

dizziness

Front 118

dipeptidyl peptidase 4 inhibitors

Back 118

vildagliptin

sitagliptin

saxagliptin

Front 119

dipeptidyl peptidase involed the breakdown of --- and ----

as well as several peptides;

including peptides:

Back 119

glp 1

gip

peptide y

neuropeptide y

growth hormone

Front 120

dipeptidyl peptidase also involed in -- activation

Back 120

T cell

Front 121

ae of dipeptidyl peptidase 4 inhibitors

Back 121

diarrhea

ha

angioedema

anaphylaxis

skin rash (stevens johnson)

Front 122

sglt inhibitors:

Back 122

dapagliflozin

canagliflozin

Front 123

sglt responseible for

na glucos transporters inte -- ----- responsible for glucose reaborption

also glucose uptake in the -----

Back 123

proximal tubule of the kidney

GI

Front 124

t/f

sglt inhibitors will decrease serum glucose and increase weight loss

Back 124

t

Front 125

ae of sglt inhibitors

Back 125

uti

ha

diarrhea

hypoglycemia

Front 126

glp-1 or dpp-4 inhibition

more reduction of glucagon

Back 126

glp 1

Front 127

glp-1 or dpp-4 inhibition

more gastric emptying

Back 127

glp 1

Front 128

glp-1 or dpp-4 inhibition

satiety, n/v, appetite suppressed, wieght loss, antibody formation

Back 128

glp 1

Front 129

admistiration of glp

Back 129

injectable

Front 130

adminstrationof dpp-4 inhibition

Back 130

oral

Front 131

glp 1 can cause

Back 131

pancreatitis

Front 132

dpp-4 inhibitors can cuase

Back 132

stevens johnson