Diabetes - Hockerman Flashcards by Kappa Epsilon Pi Chapter

Generic Name for Humalog

Insulin Lispro

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Generic Name for Novolog

Insulin Aspart

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Generic Name for Apidra

Insulin Glulisine

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Generic Name for Lantus

Insulin Glargine

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Generic Name for Levemir

Insulin Detemir

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Generic Name for Tresiba

Insulin Degludec

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List the VERY Rapid Onset/Short Action Insulins

Lispro, Aspart, Glulisine

humalog, novolog, apidra

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List the rapid onset/short action insulins

Regular (R)

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List the intermediate onset/action insulins

NPH (N)

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List the slow onset/long action insulins

glargine, detemir, degludec

lantus, levemir, Tresiba

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Describe “lente” insulins

insulin is complexed with Zinc to make an insoluble precipitate….

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Explain NPH Insulin

Insulin is complexed with Protamine to delay absorption!

It is NOT genetically modified

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Modification made to make Lispro Insulin?

lysine and proline switch positions on insulin B chain

P28 and K29

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Modification made to make Aspart Insulin?

Proline 28 switched to aspartate

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Modification made to make Glulisine Insulin?

Asn3 and Lys29 in B chain are switched to Lys and Glu

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Modification made to make Glargine Insulin?

Asn 21 of alpha chain is changed to Gly

- 2 Arg Residues added to end of beta-chain

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Modification made to make Detemir Insulin?

Thr 30 of b chain is deleted - Lys 29 is myristylated (aka fatty acid added so it can bind to serum albumin extensively)

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Modification made to make Degludec Insulin?

Thr 30 of b chain is replaced by Glu and fatty acid added (so it can bind to serum albumin)

(what is added “gamma-Glu/C16 fatty acid)

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Examples of Mixture Insulins

NPH and Regular (Humulin 70/30 and 50/50)

NPL and Lispro (Humalog 75/25 & 50/50)

Ryzodeg (70% degludec and 30% aspart)

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what is Afrezza?

inhaled insulin

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Qualities that allow Afrezza to be inhaled?

large surface area and it is a small particle

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4 routes of administration for insulin

SQ, Infusion Pump, IV, Inhalation

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Uses of Insulins in Diabetics:

1) ________ liver glucose output
2) _________ fat storage
3) _________ glucose uptake

decrease; increase; increase

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List Adverse Reactions to Insulin

Hypoglycemia
Lipodystrophy
Lipoatrophy
Insulin Resistance

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Signs/Sx of hypoglycemia

weakness, sweating, hunger, tachycardia, increased irritability, tremor, blurred vision, seizures, coma, increased sympathetic output

Hypoglycemia = blood glucose is < ______

60 mg/dL

what is lipodystrophy?

lump of fat at over used injection site of insulin

what is lipoatrophy?

concavities in SQ tissue

Agents that can interact with Insulin/ cause an INCREASE in blood glucose

- catecholamines - glucocorticoids - Oral contraceptives - thyroid hormone - calcitonin - somatropin - isoniazid - Phenothiazines - morphine

Agents that increase the risk of insulin hypoglycemia

``` ETHANOL beta adrenergic receptors ACE inhibitors Fluoxetine Somatostatin Anabolic Steroids MAO Inhibitors ```

What Antidiabetic drugs will decrease glucose production

- Biguanides | - Insulin

What Antidiabetic drugs will decrease glucose absorption

- alpha-glucosidase inhibitors | - amylin mimetics

What Antidiabetic drugs will increase glucose excretion

SGLT2 inhibitors

What Antidiabetic drugs will increase glucose utilization

- thiazolidinediones | - insulin

What Antidiabetic drugs will increase insulin secretion

- sulphonylureas - meglitinides - GLP-1 Activators - DPP-4 Inhibitors

type 1 or type 2 diabetes - which one uses antidiabetics

Type 2!

``` ADA Diagnosis Criteria: A1C Fasting Plasma Glucose 2-hours plasma glucose Random Plasma Glucose ```

> 6.5%; > 126 mg/dL; > 200 mg/dL; > 200 mg/dL

Type 1 diabetes - when beta cell mass is decreasing - is there positive or negative results for ICA and IAA

positive! (antibodies against ICA and IAA can cause

Pathophysiology of Diabetes: Hyperglycemia seen when... - _______ glucose uptake in cells where glucose uptake is insulin dependent - _________ glycogen synthesis - ________ conversion of amino acids to glucose

decreased; decreased; increased

Will see Hyperlipidemia in Diabetes because...... | increased _________ and increased ________

fatty acid mobilization from fat cells; fatty acid oxidation (ketoacidosis)

Complications of Diabetes - Neuropathy: | increased blood glucose levels lead to increased utilization of the __________ (_________)

polyol pathway; Aldose Reductase;

Complications of Diabetes - Neuropathy: | Increased _________ in neural cells

cystosolic

Complications of Diabetes - Nephropathy: | what issues are present?

renal vascular changes and changes in the glomerular basement membrane

Complications of Diabetes - Ocular: | what can happen?

cataracts, retinal microaneurysms, hemorrhage

Ideal Ranges for Blood Glucose: | Fasting

70 - 90 mg/dL

Ideal Ranges for Blood Glucose: | Pre-Parandial

70 - 105 mg/dL

Ideal Ranges for Blood Glucose: | Post-Prandial

< 120 - 160 mg/dL

Acceptable Ranges for Blood Glucose: | Fasting

70 - 110 mg/dL

Acceptable Ranges for Blood Glucose: | Pre-Parandial

70 - 130 mg/dL

Acceptable Ranges for Blood Glucose: | Post meal

< 180 mg/dL

Insulin's Effect on the Liver

Inhibits: Gluconeogenesis; Ketogenesis; Glycogenolysis Stimulates: Glycogen Synthesis; Triglyceride Synthesis

Insulin's Effect on the Skeletal Muscle

stimulates: glucose transport and amino acid transport

Insulin's Effect on the Adipose Tissue

stimulates triglyceride storage and glucose transport

Insulin Receptor has 2 subunits

alpha and beta

role of the alpha subunit in the insulin receptor

it is a regulatory unit of the receptor - will represses activity of beta subunit - repression gets relieved by insulin

Insulin _______ is a clear solution at a pH of 4.0 - but when administered it will precipitate

glargine

Hypoglycemia S/Sx: | _______ sympathetic output

increased

How to treat hypoglycemia

glucagon/glucose

For the use of sulfonylureas - what MUST be functioning

beta cells

Sulfonylureas will help diabetics how? (affect glucose or insulin more directly?)

will increase release of insulin

Effects of Sulfonylureas on Beta Cell Insulin Release: 1) binds to _________ 2) _______ K+ channel 3) _________ cell polarization 4) Activates ________ channels 5) Increases ______ and activity of _____ 6) Increased exocytosis of ______ containing granules

sulfonylurea receptor; inhibits; decreases; voltage sensitive Ca2+; Ca2+; microfilaments; insulin

Does the drug increases or decrease blood glucose? | Catecholamines

increase

Does the drug increases or decrease blood glucose? | Glucocorticoids

increase

Does the drug increases or decrease blood glucose? | Oral Contraceptives

increase

Does the drug increases or decrease blood glucose? | thyroid hormone

increase

Does the drug increases or decrease blood glucose? | Calcitonin

increase

Does the drug increases or decrease blood glucose? | Somatropin

increase

Does the drug increases or decrease blood glucose? | Isoniazid

increase

Does the drug increases or decrease blood glucose? | Phenothiazines

increase

Does the drug increases or decrease blood glucose? | Morphine

increase

Does the drug increases or decrease blood glucose? | Ethanol

decrease

Does the drug increases or decrease blood glucose? | Beta-adrenergic blockers

decrease

Does the drug increases or decrease blood glucose? | ACE Inhibitors

decrease

Does the drug increases or decrease blood glucose? | Fluoxetine

decrease

Does the drug increases or decrease blood glucose? | Somatostatin

decrease

Does the drug increases or decrease blood glucose? | Anabolic steroids

decrease

Does the drug increases or decrease blood glucose? | MAO Inhibitors

decrease

What Classes of Antidiabetic Drugs Increase Insulin Secretion

- Sulphonylureas - Meglitinides - GLP-1 activators - DPP-4 Inhibitors

What Classes of Antidiabetic Drugs decrease glucose absorption

- alpha-glucosidase inhibitors | - amylin mimetics

What Classes of Antidiabetic Drugs increase glucose excretion

SGLT2 inhibitors

What Classes of Antidiabetic Drugs decrease glucose production

- biguanides | - insulin

What Classes of Antidiabetic Drugs will increase glucose utilization

- thiazolidineodiones | - Insulin

Explain the Idea behind insulin being release from pancreatic beta cells

Glucose gets taken in by GLUT2; Glucose encounters glucokinase --> G6P --> metabolism --> less ATP and more ADP More ADP will close the K+ channel; causes depolarization; Ca2+ comes into cell; Ca2+ and microfilaments cause insulin granules to go to surface of cell and release insulin

which glucose transporter (GLUT#) has the HIGHEST Km

GLUT2

where is the highest Km GLUT# found?

beta cells (in pancreas)/liver

why does the pancreas and liver have a GLUT with such a high Km?

- high Km = more glucose needed to stimulate response - don't want beta cells to pump out insulin for just little amounts of glucose...

which glucose transporter (GLUT#) is insulin induced

GLUT4

where is GLUT4 found?

skeletal muscle/adipocytes (GLUT4- insulin induced)

which glucose transporter (GLUT#) has the lowest Km, where is it found, and why

GLUT3; its in neurons; very low because you wants neurons/brain to be able to take in glucose even at low levels because you constantly need glucose for functioning

What types of cells are found in islet of langerhans

alpha, beta, delta

what cell in the islet of langerhan releases glucagon

alpha

what cell in the islet of langerhan releases somatostatin

Delta

what cell in the islet of langerhan releases insulin

beta

what cell in the islet of langerhan releases amylin

beta

beta cells in the islet of langerhan release what?

insulin AND amylin

alpha cells in the islet of langerhan release what?

glucagon

delta cells in the islet of langerhan release what?

somatostatin

what does Amylin do in the body?

- slows gastric emptying - decreases food intake - inhibits glucagon secretion

Insulin processing: | insulin is made in beta cells and is made as a ________ peptide that is deposited where?

single; secretory granules

In the secretory granule, insulin is cleaved into what two things

1) alpha/beta chain | 2) C connecting peptide (C peptide)

List the sulfonylureas

1st gen (Tolbutamide, Chlorpropamide, Tolazamide) 2nd gen (glipizide, glimeperide, glyburide)

Sulfonylureas work intermittently or constitutively?

constitutively (can wear out the cells!!)

list the 2nd gen sulfonylureas

glipizide, glimeperide, glyburide

Main difference between 1st and 2nd gen of sulfonylureas?

potency

What drug class acts similarly to sulfonylureas but acts for a very short amount of time

Meglitinides (or the "glinides")

Describe the qualities of the "glinide" antidiabetic drug class (Metiglinides)

- MOA: like sulfonylureas - V SHORT DURATION OF ACTION (1 hr = half life) - TAKE TABLET BEFORE EACH MEAL

how should/how often should glinides be taken

before each meal (bc short acting)

Examples of Glinides

Repaglinide, Nateglinide

which glinide is selective for K(ATP) channels in the pancreas, and not the hear?

Nateglinide

which glinide has a shorter half life?

Nateglinide (nate - works only at pancrease but v short half life)

ADE's for Sulfonylureas

- lasting and prolonged hypoglycemia (b/c long af half life) - G.I. problems - Wt gain/ - INCREASED # of SECONDARY FAILURES

Drug Interactions for Sulfonylureas: Which drugs may enhance the action of sulonylureas/increase risk of hypoglycemia due to the DISPLACEMENT of sulfonylureas from protein binding sites

- salicylates - phenylbutazone - sulfonamides - clofibrate (Atromid S)

"types" of drug interactions for sulfonylureas

- may cause hypoglycemia (by displacing sulfonylureas from protein binding sites OR a drug has their own hypoglycemic effect and add as an additive) - drugs cause hyperglycemia

what drugs can interact with sulfonylureas by having their own hypoglycemic effect

alcohol | high dose salicylates

what are some drug interactions that can oppose the action of sulfonylureas

- oral contraceptives - corticosteroids - epinephrine - thyroid - thiazide diuretics

why does oral glucose give a higher insulin release than IV glucose?

incretin effect

Idea behind "incretin effect"

peptide hormones (GIP and GLP-1) are released from the intestine after a meal - and go to islet of langerhans to stimulate beta cells

what peptide hormones are released from the small intestine that will be used to stimulate beta cells

Pro-GIP and PRO-glucagon (will become GLP-1)

Modes of Action for GLP-1: | _______ insulin secretion

stimulate

Modes of Action for GLP-1: | _________ glucagon secretion

suppress

Modes of Action for GLP-1: | ________ gastric emptying

slows

Modes of Action for GLP-1: | _________ food intake

reduces

Modes of Action for GLP-1: | _________ beta cell mass and _______ beta cell function

increases; maintains

Modes of Action for GLP-1: | ________ insulin sensitivity

improves

Modes of Action for GLP-1: | __________ glucose disposal

enhances

GLP-1 Receptor Signaling: | GLP-1 is a small peptide ______ (agonist, partial, antagonist) for _______ (what kind of receptor)

agonist; GPCR

GLP-1 Receptor Signaling: Gs, Gq, and G(beta/gamma) pathways - will all (indirectly or directly) cause ________ (_____) which will cause increase in gene transcription and beta-cell proliferation

cause glucose-stimulated ERK1/2 phosphorylation (GSEP);

GLP-1 Receptor Signaling: | what pathways lead to GSIS (Glucose stimulated insulin secretion)

Gs and Gq

Recap on Signaling Pathways: | GPCR ---> Gs ---> ______ --> ______

AC; cAMP

Recap on Signaling Pathways: | GPCR ---> Gq ---> ______ --> ______

PLC; Ca2+

Recap on Signaling Pathways: | GPCR ---> G(beta/gamma) ---> ______ --> ______

PI3K; phosphorylation...

GLP-1 is secreted from ______ cells in the ______

"L"; intestine

GLP-1 levels may be ______ in T2DM

decreased!

How to combat low levels of GLP-1 in T2DM

- provide a long-lasting GLP-1 analog | - prevent degradation of endogenous GLP-1

Benefits of GLP-1 treatment for T2DM: - _______ hyperglycemia with ____ risk of hypoglycemia - _____ loss - Increase _________

reduce; low; weight; beta cell mass

List the GLP-1 Analogs

- Exenatide (Exendin 4; Byetta) - Victoza (Liraglutide) - Tanzeum (Albiglutide) - Dulaglutide (Trulicity) - Lixisenatide (Adlyxin) "tide-s"

What drugs are are inhibitors of DPP-4

-Gliptins! (januvia, tradjenta, onglyza, Nesina) (sitagliptin, linagliptin, saxagliptin, alogliptin)

DPP-4 inhibitors = GLP-1 _______

modulators

which DPP-4 inhibitor(s) are NOT extensively metabolized

januvia, nesina, tradjenta

which DPP-4 inhibitor(s) are extensively metabolized

onglyza (CYP3A4/5 substrate)

which DPP-4 inhibitor(s) are excreted in the urine (kidney)

Januvia, Nesina, Onglyza

which DPP-4 inhibitor(s) are excreted in the feces (liver)

Tradjenta

ADE's of GLP-1 Modulators

N/V; Constipation; HA; SEVERE SKIN REACTIONS

DPP-4 is also present on _______ cells

immune

DPP-4 is on present cells: leads to reduced ________ --> _______ Potential increased risk of _______

WBCs; infections; cancers

Amylin Analog name?

Symlin (Pramlintide)

Amylin Analog - useful in type 1 or type 2 or both?

both!

MOA of alpha-glucosidase inhibitors

decrease absorption of carbohydrates from the intestine by inhibiting gut alpha glucosidases

what enzymes does alpha-glucosidase inhibitors inhibit?

- sucrase - maltase - glucoamylase

What are some examples of alpha-glucosidase inhibitors

Acarbose and Miglitol

ADE's for alpha-glucosidase inhibitors (and reasoning behind it)

diarrhea, nausea, flatulence (enzymes are not digesting it, so bacteria in gut DO digest it and leads to gas etc...)

Acarbose has risk of _____ damage when doses exceed _______

liver; 100 mg TID

what do SGLT2 inhibitor drug names end in...

-gliflozin

what are the drugs that are SGLT2 inhibitors

- jardiance - invokana - Farxiga

how do SGLT2 inhibitors work?

they work in the kidney - they decrease the reabsorption threshold for glucose in the kidney ---- leads to more glucose being excreted into the urine (will decrease blood glucose levels!!)

are SGLT2 inhibitors for Type 1 , type 2 or both?

just type 2! should be used with diet/exercise

ADE's for SGLT2 inhibitors

- increased risk of UTIs/genital infections (more sugar down there ---- bacteria can grow better) - increased urine flow/volume - increased risk of hypoglycemia with sulphonylurea and insulin

what is the contraindication for SGLT2 inhibitors

pts with renal impairment!

which SGLT2 inhibitor should NOT be used in pts with BLADDER CANCER

Farxiga

Possible causes of insulin resistance

- polymorphisms in signaling pathways (rare) - Obesity (accum. of fat in abdominal cavity) - Inactivity

Effect of Insulin Resistance in Skeletal Muscle

- decreased glucose uptake

Effect of Insulin Resistance in Adipose Tissue

- impaired glucose uptake - impaired inhibition of lipolysis - mobilization of FAs to other tissues occurs

Effect of Insulin Resistance in the liver

impaired inhibition of glucose output (via gluconeogenesis and glycogenolysis)

Obese people - have ________ levels of free fatty acids

increased

_______ FFAs lead to Insulin Resistance (IR)

acutely raising

Insulin Resistance: | Polymorphism occurs how?

Ser gets phosphorylated (Tyr normally does!) this leads to inhibiting signaling

what things lead to polymorphisms of Insulin resistance/pathway signaling

promoted FA uptake, lipid-by products, inflammatory mediators (cytokines) aka Excess nutrients(like FFA), adpionectin, cytokines

Obesity Induced Inflammation and Insulin resistance: | _________ adipocytes are made by M1 infiltration

hypertrophied;

Obesity Induced Inflammation and Insulin resistance: | Hypertrophied adipocytes release what factors that will cause insulin resistance

- TNFa - IL-6 - MCP-1

Obesity Induced Inflammation and Insulin resistance: | _______ from the hypertrophied adipocyte will decrease adiponectin

MCP-1

Obesity Induced Inflammation and Insulin resistance: | ______ from hypertrophied adipocyte will go to monocyte

MCP-1

Obesity Induced Inflammation and Insulin resistance: | M# ---> M# due hyperphagia and due to lack of exercise

2 --> 1 | M1 is the hypertrophied adipocyte

Obesity Induced Inflammation and Insulin resistance: | what does MCP-1 stand for

monocyte chemoattractant protein - 1

Advantages of biguanide over sulfonylureas

- less chance of hypoglycemia | - rarely cause wt gain

Metformin has a lower risk of _______ compared to older biguanides

lactic acidosis

which drug is a part of the biguanide class?

metfomrin

MOA of Metformin: | is an activator of ________

AMPK (AMP-activated kinase)

MOA of Metformin: | increases efficiency/sensitivity of insulin where?

liver, fat, and muscle cells

Metformin's Action in the Liver: | Metformin binds to _______

OCT1

Metformin's Action in the Liver: | Metformin inhibits __________ at the mitochondria

oxidation at complex 1

Metformin's Action in the Liver: | Inhibited oxidation of mitochondria leads to ________ levels of AMP

increased (bc not making ATP = more AMP)

Metformin's Action in the Liver: | Inhibited oxidation of mitochondria leads to increased levels of ________

AMP

Metformin's Action in the Liver: | High AMP levels will inhibit what process _________

gluconeogenesis (bc it inhibits Fructose bisphosphase (FBP)) | remember ATP is needed for gluconeogenesis

Metformin's Action in the Liver: | High AMP levels will increase/activate _______

AMPK

Metformin's Action in the Liver: | High AMP levels will increase/activate AMPK which leads to _________

DECREASED lipid and cholesterol synthesis

where are the two main places that metformin affects

LIVER and SKELETAL MUSLCE

what does OCT stand for? (OCT 1 is the metformin receptor)

oragnic cation transporter

who is contraindicated for metformin

pts that have increased risk of lactic acidosis (ex: people w/ poor oxygenation - CHF pts...lung disease pts..)

Which drug leads to decreased abosorption of Vit. B12

metformin

Metformin leads to decreased absorption of _______

Vit. B12

Can metformin and sulfonylureas be used together?

yes!

Effect on lipid panel with metformin

- decreased serum LDL | - decreased TGs

How do thiazolidinediones decrease insulin resistance/improve target cell response

activates PPARy (PPAR gamma) aka a transcription factor

what does PPARy stand for

peroxisome proliferator activated receptor GAMMA

main target cells for thiazolidinediones

Adipocytes

how do thiazolidinediones affect Adipocytes

- enhance adipocyte differentiation - enhance FFA uptake into SQ Fat - reduce serum FFA

_____ FFA = less insulin resistance

less

Skeletal Muscles & Exercise: | ______ accumulates during exercise and will activated ______

AMP; AMPK | more AMP b/c using ATP during exercise...duh

Skeletal Muscles & Exercise: | _____ phosphorylates TBC1D(1/4) which will promote ______ activity of _______

AMP; GTPase; Rab

Skeletal Muscles & Exercise: | Once Rab dissociates from ______ - it can translocate to the membrane

GLT4 (GLT4 will go to membrane)

How will metformin work in the skeletal muscle to increase insulin sensitivity?

metformin will increase AMPK AMPK will phosphorylate TBC1D(1/4) - which increases GTPase activity of Rab - Rab comes off of GLUT4 - which allows GLUT4 to go to the membrane and bring in glucose!

what drugs are thiazolidinediones?

the "glitazone"s - Pioglitzaone - Rosiglitazone (Remember pioglitzaone - looks like pig - pigs are fat - thiazolidinediones work on fat cells)

which thiazolidinediones is assoc. w/ increased risk of bladder cancer

Pioglitazone

Thiazolidinediones - can they cause hypoglycemia?

No!

what is the contraindication for thiazolidinediones?

CHF (b/c of fluid retention)

what are Adipokines

hormones that come adipose tissue

what type of adipokine can cause insulin dependent glucose upake

adiponectin

Structure and Function of PPAR-gamma: | PPAR has to bind to _____ - to make a _____ to regulate gene transcription

RXR; dimer

Structure and Function of PPAR-gamma: | List components of the structure of PPAR-y

Ligand independent activation domain; Ligand- dependent activation domain; DNA binding domain Ligand binding/Dimerization domain

List the factors that are regulated by activation of PPARy

- resistin - adiponection - TNF-a - leptin - angiotensinogen (AGE) - plasminogen activator inhibitor (PAI-1)

what does leptin do in the body?

suppresses appetite; tells brain that the body is "fed"

PPARy is in control of releasing certain factors- all the factors are specifically released from

WAT - white adipose tissue

Is it low or elevated in Obesity/T2DM? | Leptin

???

Is it low or elevated in Obesity/T2DM? | Angiotensinogen

increased! --- leads to HTN in obesity

Is it low or elevated in Obesity/T2DM? | PAI-1 (plasminogen activator inhibitor)

increased! --- leads to increased risk of clots in obesity

Is it low or elevated in Obesity/T2DM? | Resistin

elevated

what does resistin do?

stimulates glucose export by liver & stimulates insulin resistance

what does adiponectin do?

decreases blood glucose and insulin resistance

what does TNF-a do?

stimulates lipolysis in WAT (white adipose tissue) & stimulates insulin resistance in skeletal muscle

when a TZD drug is given - what happens to levels of resistin

mRNA levels for resistin are DECREASED

when a TZD drug is given - what happens to levels of adiponectin

mRNA levels for adiponectin are INCREASED

when a TZD drug is given - what happens to levels of TNFa

mRNA levels for TNFa are DECREASED

Metformin or TZD? | molecular target is AMPK

metformin

Metformin or TZD? | molecular target is PPARy

TZD

Metformin or TZD? | pharmacologic action is to suppress HGP (hepatic glucose production)

metformin

Metformin or TZD? | pharmacologic action is enhanced insulin sensitivity

TZD

Metformin or TZD? | which one decreases A1c quite significantly

metformin!

Metformin or TZD? | which one reduces FFA quite significantly

TZD (bc they work on fat cells)

Metformin or TZD? | which one stimulates adiponectin quite significantly?

TZD

Metformin or TZD? | which on can cause wt gain

TZD

Metformin or TZD? | which one can cause peripheral edema

TZD

Metformin or TZD? | which one has increased risk of fracture and why/how

TZD; (TZD's decrease differentiation of mesenchymal stem cells into osteoblasts!