Endocrine - Pharm - Dm

Front 1

3 major types of insulin?

how are they categorized?

What rapid insulins are inhaled, and work faster than regular insulin?

Back 1

rapid acting, intermediate, long-acting

time of onset, duration of effect

Lispro, Aspart, Glulisine

Front 2

Insulin secretagogues are useful for which DM type?

oldest/longest medication class:

Insulin sensitizer, biquanide:

Effective in which DM type?

PPAR-G receptor activators:

Back 2

Type 2

oral sulfonylureas

Metformin

both T1, T2

rosi, pioglitazone (Gamma = glucose)

Front 3

Amylin analog:

incretin mimetic:

DP-4 inhibitor:

Back 3

pramlintide

exenatide

sitagliptin

Front 4

Explain physiology of insulin release:

Differentiating factors between DKA, NKDC:

Electrolyte imbalance, causing arrhythmias, needing insulin:

Back 4

B-cells in pancreas detect increased BS --> block ATP-dependent K+ channel --> depolarization, Ca++ influx --> insulin release

DKA - lower BS, fruity breath, Kussmaul respirations, acidosis

hyperkalemia

Front 5

onset/duration of rapid-acting insulins:

onset/duration of long-acting insulins:

Which type do you give right before meals?

Rapid-acting can mix with what other type of insulin?

Back 5

< 1hr, 4-8 h.

1-2 hrs, up to 24 h.

rapid acting

NPH - intermediate

Front 6

Which type of insulin cannot be mixed?

Which insulins are given SQ, not IV?

Non-clear insulins should not be given by ____.

How is Lispro structure different from human insulin?

Back 6

long-acting

glulisine, long-acting insulins

IV

Lys/Pro are switched in the chain

Front 7

How is Aspart different?

Glulisine differences?

Why is Lispro quicker acting than regular insulin?

Patient education with Lispro should include what?

Back 7

Aspartic acid for proline

Glutamic acid for proline

structure allows it to escape the SQ tissue

tell them to freakin' eat right after.

Front 8

Main difference between detemir and glargine?

When do you give rapid insulin?

How often is intermediate/long acting administered?

Monitoring levels for FPG, PPG, Hgb A1C, Urine glucose/ketones:

Back 8

detemir soluble at physiological pH - less variable absorption; glargine forms microprecipitates, soluble at acidic pH

immediately before meals

intermediate - BID, QD
long acting - usually QD

FPG - 90-130, PPG - <180, Hgb <7%, negative glucose/ketones

Front 9

Which DM type still needs insulin w/ a missed meal?

Two classic medications that raise glucose:

Dawn phenomenon, treatment:

Back 9

Type 1

glucocorticosteroids, BB's

early am hyperglycemia due to loss of activity - give more insulin, change to longer-acting

Front 10

Insulin secretagogues are used in which type of DM?

2 classes?

How often are OS and meglitinides given?

Which generation of OS are usually given and why?

Back 10

Type 2

oral sulfonylureas (1st gen -amides, 2nd gen -ides), meglitinides (-linides)

OS - QD (like long-acting insulins)
meglitinides - 15-30 min before meal

2nd gen - less active metabolites, less SE's

Front 11

Indications for secretagogues:

What should you monitor in OS/meglitinides:

chlorpropamide has what unique SE's?

MOA/indications of Metformin:

Back 11

type 2 uncontrolled by diet/exercise alone

OS - SCr/BUN, meg's - LFT's

disulfiram-like flushing, hyponatremia (SIADH)

insulin sensitizer - doesn't increase secretion - uncontrolled T2DM

Front 12

SE's of Metformin:

Contraindications:

A-glucosidase inhibitors, MOA, dosing, SE's:

Back 12

Metallic taste, GI, lactic acidosis, anemia

increased risk of lactic acidosis - COPD, liver disease

Acarbose, Miglitol - bind membrane A-glucoside hydrolase, amylase; blocks absorption of carbs; give TID

SE's - GI (farting, bloating, diarrhea); treat with DEXTROSE only

Front 13

PPAR-G activators:

MOA?

Unique non-glucose effects:

AE's:

Back 13

TZD's, glitazones - Rosi (Avandia), Pio (Actos)

bind PPAR-G receptor - regulate gene expression/proteins - better insulin sensitivity

Rosi - increases TC, LDL, TG
Pio - no effect on TC, LDL, decreased TG's

liver, weight gain, anemia, MI

Front 14

Amylin analogs, MOA:

Indications, administration:

AE's:

Back 14

Pramlintide - neuroendocrine peptide produced w/ insulin, slows GI emptying, suppresses glucagon, improves satiety

uncontrolled T1/T2 DM already on insulin; give SQ TID and reduce insulin by 1/2

N/V, rash, dizziness, HA

Front 15

Incretin mimetic, hormones it mimics, and effect on glucose/GI:

unique aspects of MOA:

Dosing, SE's:

Back 15

exenatide - GIP, GLP-1 - increased insulin secretion, decreased glucagon, gluconeogenesis, slowed gastric emptying, satiety

only increases insulin in high BS; doesn't affect normal response

given SQ BID, reduce dose of other drugs - SE's of N/V, GI, HA

Front 16

DPP-IV inhibitor, MOA:

Dosing, SE's:

What is the ultimate goal of Hgb A1C levels in tx of DM?

Back 16

sitagliptin (Januvia) - blocks DPP-IV, inhibits metabolism of GLP, GIP

give PO QD - SE's - GI, no wt loss

Hgb < 7