Anti-Diabetes Flashcards by Jerry Sojan

Insulin of choice in emergent sitautions

IV regular insulin

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Low risk of hypoglycemia insulins VRS High risk of hypoglycemia insulins. Name please

rapid acting (lispro, aspart, glulisine) and long acting (glargine, detremir) = low risk VRS higher risk: short acting (regular insulin) and intermediate (NPH)

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drugs that can interefere with diabetic meds and make them more prone to hyPOglycemia

beta blockers - stop effects of catecholamines
EtOH - prevents gluconeogenesis
Salicylates - increases insulin secretion and acts a wee bit like insulin @ periphery

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drugs that can interfere wtih diabetic meds and make pts more prone to hyPERglycemia

epinephrine, corticosteroids, atypical antipsychotics, HIV protease inhibitors = make tissue less responsive

phenyoin, clonidine, calcium channel blockers = decreased insulin secretion

diuretics = deplete K (alters ability of K to play roel in exocytosis of insulin in response to sugra SUR/KIR channel)

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first gen sulfonylureas please

tobutamide - short duration of action

chlorporpamide - longer duration of action

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a/se of chlorporpamide

hyperglycemia @ elderly = dont give
hyperemic flush @ OH = dont drink
SIADH = dont pee

DONT GIVE OLD, DONT DRINK LOTS, DONT PEE MUCH

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second gen sulfonylureas, now preferred bc better a/se profile = ?

glyburide - hyperglycemia @ 20-30%
glupizine - hyperglycemia @ least DOC***
glimepride - hyperglycemia @ 3-4%

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anti-diabetic drugs that cause WEIGHT GAIN

1) sulfonlyureas - tolbutamide, chlorpropamide, glyburide, glipizine, glimepride
2) meglinitides - repaglinide, nateglinide

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Please name the Meglitinides

Repaglinide

Nateglinide

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Describe kinetics and use of the meglitinides

shorter duration of action and more rapid onset than sulfonylureas –> thefeore used for post pradial (omit if you skip a meal)

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A/se of meglitinides

repaglinide and natiglinide: hypoglycemia and weight gain

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MOA of meglitinides and sulfonylureas

bind to SUR of ATP-K sensitive –> causes less K+ out of cell –> depolarizes –> opens vg Ca++ channels –> depolarizes –> exocytosis of insulin and increased transcription of insulin –> hurrah

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MOA of metformin key words please

no insulin increase (decreases insulin levels due to improved glycemic control)
stops gluconeogen @ liver
increases insulin effects @ muscle and liver

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Effects unique to metformin *small group too , high yeild probly

decreases TAG

does not cause weight gain

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First line for DMii

metformin (because doesnt cause weight gain and decreases TAG)

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When I say metformin, you think of this intracellular protein causeing all its effects

AMPK

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A/se of metformin

a) gi messy time
b) B12 deficeincy - bc of gi messy time
c) lactic acidosis - bc liver cant use lactic acid for gluconeogenesis since metformin blocks it via AMPK

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Dont use metformin for these 4 types of patients

liver dz
renal dz
OH-ics
hypoxic patients - resp dz

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TZDs name them please

pioglitazide

rosiglitazone

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MOA TZDs please

pioglitazide, rosiglitazone

a) decrease insulin resistance
b) agonists of PPARgamaa = alter gene expression and therefore take weeks to months to take effect

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What does pioglitazone do better than rosiglitazone?

all good things

decreased LDL particle concentration and size
increase HDL
decreased TAG

What blood tests MUST you order if pt is taking TZDs

liver function tests (also perform with alpha glucosidase inhibitors - acarbose)

SHARK STYLE: If you have a diabetic patient with liver problems, dont give these drugs if you can

metformin
TZDs
acarboseo - glucosidase inhibitor

SHARK STYLE: If you have a diabetic patient with a crapy lipid profile, these drugs will help

metform
TZDs (the glitta-zones)
insulin
coveleselam (decreases LDL but icnreases TAG)

SHARK STYLE: if someone drinks alcohol + DM

chronic - no metformin (contraindicated) | once in a while or chronic - no first gen sulfonylureas (tolbutamide, chlorporpramide)

MOA: exenatide

glucagon like polypeptide 1 - an incretin analoug = stimulates insulin secretion

the many effects of exenatide please.

enhances glucose dependent insulin secretion therefore suppresses postprandial glucagon release slows gastric emptying therefore keeps more food suppresse appetite drive = decreases appeitie may increase beta cell proliferation

a/se of exenatide

nausea, vomit, diarrhoe, ACUTE PANCREATITIS contraindicated in gastroparesis patients (but diabetes can cause gastropareisis :S) - bc causes gastric emptying slowing

how come exenatide doesnt get degraded

resistant to dipeptidyl peptidase IV

Sitagliptin MOA

DDP IV inhibitor --> increases levels of GLP-1 and insulin

a/se of sitagliptin

``` pancreatitis (just like exenatide - also GLP-1) hypersensitivity reactions (urticaria, angioedema, anaphylaxis, Steven Johnson etc) ```

Pramlintide MOA

analogue of amyline (cosecreted from beta cells) - decreased glucagon secretion - inhibits food intake - slows gastric emptying

Colesevelam

bile acid sequestrant used to lower LDL via MOA unknown

SHARK STYLE: what drug to not give people with III or IV CHF?

TZDs - glitter-zones

SHARK STYLE: which antidiabetic drugs do NOT cause weight gain

metformin alpha-glucosidase inhibitiors sitagliptine

SHARK STYLE: which antidiabetic drug causes weight loss?

exenatide**

SHARK STYLE: list dugs you shouldnt give if someone has issues with the following organ systems: a) heart/cvs b) pancreas c) Renal d) liver e) hyperesensivitiies f) gastroparesis

a) heart/chf - no TZDs b) pancrease - no exenatide or sitagliptine c) renal - no metformin d) liver - no metformin, monitor TZDs and acarbose (alpha glucosidase inhibitors) e) steven johnson - sitagliptine f) exenatide - slows gastric emptying

Effective treatment for people with HbA1c < 9%

metformin alone as monotherapy may be effective

If monotheraphy doesnt work over three motnhs

metformin PLUS oral agent, exenatide or insulin

SHARK STYLE: Which anti-diabetics do not cause weight gain

``` metformin alpha glucosidases exenatide - decreases sitaglitpine plamlitidine ```

If dual theraphy doesnt work then what would be the most ''robust'' option be

insuline

~*~* What level of HbA1c would favour the transition to insulin?

> 8,5%

What is the most effective of diabetes medications to lower glycemia?

Insulin - has no ceiling

~~~When is insulin warranted as INITIAL THERAPY

DM II use insuline as initial therapy when: @ significant hyperglycemic symptoms @ ketonuria @ HbA1c >10% (>8.5 for tri therapy addition) @ random glucose > 300 mg/dl

~ If a diabetic has X treat with ? series HYPERTENSION

ACEi and ARB

~If a diabetic has X treat with ? series albuminuria

If a diabetic has X treat with ? series

~If a diabetic has X treat with ? series distal symmetric polyneuropathy

``` ADGOPVV Amytriptyline Duloxetine Gabapentin Opioids Pregablin Valproate Venlafexin ```

~If a diabetic has X treat with ? series gastropareisis

CONTRAINDICATED - exenatide metoclopramide erythrmycin ME

~If a diabetic has X treat with ? series Erectile dysfunction

PDE5 inhibitor

~ DOC at pregos

regular insulin - short acting | IV (Emerg use of choice as well)

Glucagon uses times four please

1) severe hypoglycemia @ DM pts who o/d insulin 2) radiology of bowel b/c relaxes intestion 3) beta b poisoning - O/D antidote 4) glucagon C peptide test - to assess beta cell function

~ things i think will be super high yield and are bolded in notes ** things i think are high yield hurrah SHARK - get these before you move on to next card.

15 qs on last years exam.