4 Endocrine Glucose

Front 1

Rxs for DM type I

Back 1

Insulins
Pramlintide acetate (symlin)

Front 2

Rapid onset insulins

onset and DOA

Back 2

Insulin-lispro
Insulin-aspart
Insulin-glulisine
10-30 min------3-5 hr

Regular insulin
30-60 min-------5-12 hr

A little LISPro ASPART GLU the INSULIN

Front 3

intermediate onset insulins
onset dOA

Back 3

Insulin Lispro Protamine
Isophane insulin
1-2h------10-20 h
Insulin zinc
2-4 h------12-20 h

The lispro's PROtAMIne ISOPHINE ZING!

Front 4

Long acting insulin

Back 4

Extended insulin zinc,
2-4 h 16-24 h
Insulin detemir
1 h-----20 h
Insulin glargine
1-2 h 24 h
The EXTENDED ZING is DETEMIR and G-LARGin

USually one takes a long acting guy and then a short acting PRN tailored to the needs

Front 5

Pramlintide acetate
indications
MOA
SEs

Back 5

AMYLIN analog----cosecreted with insulin---dec G.EMPTYING,^satiety, decr post meal glucose and glucagon prod in liver
for use in DM type I (taken at a meal) UNCONTROLLED*****on insulin
SE-HYPOGLYCEMIA*****

Front 6

Insulin SEs

Back 6

• Hypoglycemia
 Beta blockers mask symptoms
 Warning symptoms are blocked (e.g., tachycardia)

• Develop Ab’s to insulin
 Does NOT interfere with therapy

• Hypokalemia
 Insulin ↑ cellular uptake of K+

• Injection at same site repeatedly
 Lipodystrophic injection site reaction
NOTE Strenuous exercise ↓ amount of insulin needed(glucagon,cortisol, GH secreted)

Front 7

Insulin Moa

Back 7

RECEPTOR pr. TK---->MAPK (mitogenic)
&------->+p-IRS--IPS/akt--->protein/glycogen/fat synth, mobilize GLUT4 t-porter (via CBL protooncogene) to PM in adipose and muscle to sequester glucose and some AAs

Front 8

classes of drugs used to treat DM type II

Back 8

sulfonylureas
Biguanides
thiazolidinediones
DPP-4 (-)
meglitinides
a-glucosidase (-)
incretin analogs
glucagon/glucose

Front 9

Sulfonylureas 1st generation

Back 9

Tolbutamide
Chlorpropamide
acetaheximide
tolazamide


(CHLO-PROPA acetOhexi TOLAZAM TOLBUTA)

Front 10

Sulfonylureas 2nd generation

Back 10

Glyburide
Glipizide
Glicazide
Glimepiride

Front 11

Sulfonylureas 1st generation
SEs

Back 11

• tolbutamide is More cardiotoxicity than other sulfonylureas (but has a short T1/2 and is good for pts prone to hypoglycemia)
ALL 1st GEN-
• Extensive protein binding
 LOTS of interactions
 Displacement = hypoglycemia
• Flushing & hypotension when taken with alcohol
 Disulfran reaction
(inhibit alcohol dehydrogenase and increase acetaldehyde)

Front 12

Sulfonylureas 2nd generation
SEs

Back 12

• Fewer drug interactions (less protein binding)

• Often minimal side effects
 Persistent hypoglycemia
 Muscle weakness
 Dizziness
 Confusion

• Weight gain (exacerbates diabetes)

• Note: side effects don’t usually cross over
 However, if patient doesn’t respond to 1 sulfonylurea …probably fail to respond to others as well
this is for both generations
some say they increase Heart attacks

Front 13

Sulfonylureas
mOA

Back 13

blocks ATP K+ channel in B-cells
= depolarize-----increase insulin secretion

Front 14

glucovance

Back 14

metformin +Glyburide

Front 15

Biguanides
named

Back 15

metformin

Front 16

metformin
MOA
advantages

Back 16

increased post receptor action
increased GLUT-4, dec gluconeo, dec insulin resistance

GOOD-no hypoglyc or ^insulin secretion, good lipid profile, dec DIs than sulfonyls

Front 17

metformin
SEs
CIs

Back 17

• Fewer drug interactions than sulfonylureas
•  Lactic acidosis*****
 Phenformin removed from market for this
• GI distress
• Metallic taste
• Contraindications
 Lactic acidosis
 Renal, hepatic, cardiac disease
 Excess alcohol ingestion
 Acute infection / severe stress
 Severe caloric restriction / exhausting exercise
 Pulmonary insufficiency
 Pregnancy or breastfeeding

Front 18

Thiazolidinediones
named

Back 18

the GLITAZONES

Rosiglitazone
Pioglitazone

Thi-azol-i-dined before ROSI & PIO S' GLITA-ZONE PPARtY the agony the INSOLENT Sensitive muscle....

Front 19

Rosiglitazone
Moa

Back 19

Thiazolidinedione
PPARγ agonists
(Peroxisome proliferation activated receptor gamma)
Mediates DNA-directed, RNA-mediated protein synthesis

Front 20

Pioglitazone
actions

Back 20

 Increases Transcription of “insulin sensitive” genes
 Stimulates glucose transport
• Stimulates Glut 4 receptors
 Inhibits Glucose production
 Stimulates Regulation of FA metabolism
Increases sensitivity of target cells to insulin******
Improve lipid profile

Front 21

Thiazolidinediones
specific to each and as a group
SEs
CIs

Back 21

Rosiglitazone-may increase MI

Pioglitazone-Induces CYP 3A4 Decreases availability of other drugs
e.g. oral contraceptives

BOTH-• Fluid retenti---Edema---careful in CHF
CIs hepatic dis, HF, PREG (?)(as with all NEW dmII drugs have not been proven USE INSULIN)
in Polycystic ovary disease Women may resume ovulation (Use contraception)
NEW WARNING may increase fractures in funky spots in old women

Front 22

DPP-4 inhibitors

Back 22

sitaglipin phosphate (increased incretin scene)

DiPP-4 INCRETable stuff ShIT-A-GLIP-TIN (phosphate) was everywhere…… With the truly INCRETable…………EXE-NATI (de) who was everywhere……

( the incretins..^insulin,satiety dec-Gluca,GE)

Front 23

sitaglipin phosphate
Moa

Back 23

dpp-4 inhibitor (dipeptidyl peptidase ?)
enzyme that degrades incretins like GLUCAGON LIKE peptide-1 (GLP-1)(inhibits glucagon) that are secreted pre and post a meal
this increase in incretins basically increases INSULIN and decreases GLUCAGOn.....and other insulin type stuff

Front 24

meglitinides
named

Back 24

the glinides (similar to sulfonylureas)2nd line drugs
nateglinide
repaglinide

Front 25

repaglinide
MoA
and everything

Back 25

nateglinide also
like sulfonyls
increase insulin secretion
preg not established

Oral
Short acting
Taken before each meal
Metabolized by CYP 3A4

Front 26

alpha-glucosidase inhibitors
named

Back 26

miglotol
acarbose

Front 27

miglotol
MoA

Back 27

miglotol
acarbose
oligosacharides---Inhibit enzyme on brush border of enterocytes in small intestine (inhibits α-glucosidase)
Delay carbohydrate digestion & absorption (NOT prevented)
Plasma insulin response is blunted

Front 28

alpha-glucosidase inhibitors
named
SEs of each and both

Back 28

miglitol NO Hepatotoxicity
•  Not well tolerated
 GI (Flatulence***, diarrhea, etc.)
ACARbose  Hepatic toxicity
•  Not well tolerated
 GI (Flatulence, diarrhea, etc.)

Front 29

alpha-glucosidase inhibitors
indications

Back 29

miglotol
acarbose
for severe!! hyperglycemia
(not moderate)

Front 30

GLP-1 analog
named

Back 30

EXEnatide
incretin

Front 31

EXEnatide
MOA
indications

Back 31

GLP-1 analog (from a lizard)
^insulin & satiety
DEcrease-glucagon and G. emptying
(use as anti obese ?)
approved if uncontrolled on others
this is the only injectable DM II drug
TAKEN PRE MEAL

Front 32

Tx algorythm for TYPE II DM

Back 32

start with diet blah
then metformin (he's the man)
then others add prn
insulin is third and final (except in pregnancy)

Front 33

gestational Diab Tx

Back 33

diet number one
insulin if needed must keep tight control
in polycystic ovary disease may keep on metformin not thiazolidin.....

Front 34

Tx HYPOglycemia

Back 34

glucose (ER IV dextrose)
glucagon

Front 35

GLUCAGON
Moa
indication

Back 35

Increases Blood glucose
 Increases Glycogenolysis & gluconeogenesis
• Positive Inotrope/chronotrope on heart
• Relaxes GI smooth mm.
indications-
• Hypoglycemia
• Beta blocker toxicity
• Verapamil toxicity
• Radiologic exam of GI tract
• Overdose of sulfonylurea or insulin

IM good if combative

Front 36

QUinilones and DM

Back 36

cause up and down blood glucose

Front 37

Hypoglycemia in a diabetic can
result from:

Back 37

insulin overdose
-excessive exercise
-delayed or decreased food intake