2. Diabetes Mellitus - Dr. Ryan (3 hours) - 9-1-2017 - Friday

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Diagnosis of GDM - 2-step strategy

1) 50g OGTT (non-fasting) •1H ≥130mg/dL 2) Proceed to step 2 (on another day) 100g OGTT (fasting) FPG ≥95mg/dL • 1H ≥180mg/dL • 2H ≥155mg/dL • 3H ≥140mg/dL 1) You'll drink a solution with 50 grams of sugar. An hour later, you'll give a blood sample. A lab technician will use this sample to measure your blood sugar level. 2) The second step is generally only conducted *if the first step has a positive result* Step two is a is a three-hour version of the OGTT used in the one-step approach above. In the three-hour version of the test, a healthcare provider will ask you to consume a syrupy glucose solution that contains 100 grams of sugar. They'll draw your blood when you're fasting and at the one-, two-, and three-hour marks after you've drunk the glucose solution.

United Kingdom Prospective Diabetes Study UKPDS - Comment about BP Control

1) BP144/82 mmHg = significant reduction in Strokes Diabetes related deaths Heart failure Visual loss Microvascular complications 2) Continuous relationship as you decrease bp 3) No threshold identified - they didn't find a level BP below which there was no relationship

Treatment Goals for HTN for diabetics - JNC 8 Guidelines

1) Blood pressure <140/<90mmHg 2) Moderate evidence ACEI, ARB, CCB, thiazide in non-black population CCB or thiazide in black population

Diagnostic Criteria for DKA & HHS - slide

1) Differences don't matter between mild moderate and seerfe 2) DKA at glucose lvels as low as 250 3) Hhs develops at lot higher 4) DKA you will have acidosis - your bicarb o will be low in DKA versus HHS 5) Osmolallity in DKA is variable but in HHS it will be high because perosn is much more dehydarteed b/c longer process 6) Also gap acidsosis in DKA and mores severe mental status changes in HHS.

Normoglycemia values

1) FPG (fasting plasma glucose) <100 mg/dL(from 100-120 - prediabetes) 2) 2-h PG (Postprandial Glucose) <140 mg/dL

Diabetes - FPG value, 2-hPG, casual plasma glucose level, HbA1C value, test repeated or not?

1) FPG ≥126 mg/dL 2) 2-h PG ≥ 200 mg/dL when given OGTT (oral glucose tolerance test) of 75 g of glucose is given 3) Symptoms of DM plus casual plasma glucose ≥ 200 mg/dL, 4) HbA1C ≥ 6.5% Repeat test on subsequent day unless unequivocal symptoms (like diabetic ketoacidosis) unquivocal = leaving no doubt that the person is diabetic

GDM complications

1) Fetal macrosomia 2) Neonatal hypoglycemia => 1. The fetus's pancreas is kicking out the high levels of insulin that the fetus is being exposed to so after delivery the pancreas is still working and fetus becomes hypoglycemic. 3) Cesarean delivery (b/c large baby)

Examples of Miscellaneous DM

1) Genetic defects of ß-cell function MODY (not secreting enough insulin, usually pt< 25, mildly hyperglycemia) 2) Genetic defects in insulin action Ranges from mild to extreme insulin resistance 3) Diseases of the exocrine pancreas a) CF, (have problems with all the exocrine function - cant secrete insulin from pancreas) b) trauma & infection both of these 2 can also affect beta cell function 4) Drug or chemical induced 5) Endocrinopathies

Other Types of DM

1) Gestational diabetes 2) Miscellaneous

Natural History of Type 2

1) Glucose on y axis and years on x 2) Yellow: post meal is kept under control at first but eventually patient loses control 3) At the bottom graph: insulin resistance is increasing overtime and it is flattening and the red is insulin level - you're hyper-insulinemic at first to take care of the glucose levels that rise substantially after a meal 4) Note Decrease in incretin and beta cell function effect

DKA and HHS result from

1) Insulin deficiency—primary abnormality whether Absolute or relative and 2) Elevated counter-regulatory hormones such as Glucagon, catecholamines, cortisol, GH 3) Also Metabolic decompensation (making things worse)

Management of Moderate Hypoglycemia

1) May need assistance 2) Treat as with mild reaction 3) but May need repeated treatment, patient May be combative (because of the mood changes) with Longer recovery time

Initial Evaluation - Post diagnosis of diabetes

1) Medical history 2) Dietary history 3) Physical activity 4) Physical exam 5) Lab exam 6) Referrals 7) Immunizations

GDM Treatment

1) Medical nutritional therapy (MNT) -> 3 meals, 3 snacks 2) Moderate physical activity 3) Insulin therapy 4) Oral therapy - but most physicians don't like it 5) Breastfeeding - see http://www.diabetesincontrol.com/breastfeeding-and-diabetes/ 6) Screen for DM 4-12 weeks post-partum

Recommendations to treat hyperlipidemia with statins in diabetics

1) No evidence to treat lipids if below 40 years old and no risk factors. ] 2) If there is risk factors or history of CVD then statin is recommended that's all she said.

Properties typical of type 2 diabetics: (T or F?) a) Obesity b) Hyperinsulinemia c) Absolute insulin deficiency d) Impaired glucose tolerance

1) Obesity 2) Hyperinsulinemia 3) Relative insulin deficiency - insulin levels insufficient relative to the high glucose levels in the blood 4) Impaired glucose tolerance - FYI - "means that blood glucose is raised beyond normal levels, but not high enough to warrant a diabetes diagnosis" - so they probably have that before a diabetes diagnosis?

Gestational Diabetes Risks to mother

1) Obesity 2) Insulin resistance (pregnancy increases the risk b/c progestrone and other factors) 3) Diabetes

Risk Factors for Type 2 DM

1) Overweight (note not obese) (BMI ≥ 25 kg/m2) BMI ≥ 23 kg/m2 in Asian Americans (diff in bone structure) 2) Physically inactive 3) Family history of DM (1st degree relative) 4) History of GDM in women 5) HTN Or on antihypertensive therapy 6) HDL <35mg/dL ± triglyceride >250mg/dL 7) Meeting criteria for "increased risk" - see later flash card

More risk factors for Type 2 DM

1) Poly-cystic ovarian syndrome "The raised level of insulin in the bloodstream is thought to be the main underlying reason why PCOS develops" => - mark of insulin resistance 2) Signs of insulin resistance - (folds in the back of the neck) 3) History of CVD 4) High risk race/ethnicity African American Latino Native American Asian American Pacific Islander

HypERglycemia Signs/Symptoms

1) Polyuria - b/c a lot of glucose and they want to pee it out 2) Polydipsia 3) Polyphagia 4) Blurred vision 5) Fatigue (b/c insulin reistance - body not using glucose 6) Infections, slow healing - "People with diabetes are more susceptible to developing infections, as high blood sugar levels can weaken the patient's immune system defenses. In addition, some diabetes-related health issues, such as nerve damage and reduced blood flow to the extremities, increase the body's vulnerability to infection."

Idiopathic Type 1 diabetes

1) Rare 2) Not autoimmune (strange!) 3) Marked by variable insulin deficiency between episodes 4) Strongly inherited

Management of Severe Hypoglycemia

1) Requires assistance 2) Pt unable to swallow 3) Hence use Buccal CHO 4) Or Parenteral glucagon 5) but glycogen stores may be exhaused so Next level - IV dextrose

Screen for Gestational diabetes:

1) Screen for DM2 if High risk (BMI ≥ 25kg/m2; - PLUS 1 or more risk factors for DM2) 2) If Average risk - screen for gestational diabetes 24-48 weeks gestation

Which of the following properties about Immune-mediated Type 1 diabetes is not true 1) Prescence of seriological markers 2) Rate of beta-cell destruction varies between children and adults 3) Rate of beta-cell destruction in children is slow 4) Rate of beta-cell destruction in children is slow

1) Seriological markers 2) Rate of beta-cell destruction variable Children (usually rapid) - that's why they get type 1 diabetes at a young age. Adults (slower onset)

DKA—Oxymoronic State - why?

1) The fact that the body enters a catabolic state b/c it's breaking down body tissue to produce *more glucose* b/c body thinks hypoglycemia 2) Decreased PO intake (despite no glucose is being used by body tissues) - especially in DKA b/c there are abdominal symptoms too

Classifications of Diabetes Mellitus

1) Type 1 (DM1) a) LADA 2) Type 2 (DM2) 3) Gestational (GDM) 4) Miscellaneous

Prevention/Delay of DM; also frequency of monitoring

1) Weight loss 5-10% = Referral to support group 2) Increase physical activity 3) Consider metformin for those at high risk Provides glucose control, no evidence of β cell protection but will help them lose weight 4) Yearly monitoring

Properties of DKA

1) hyperglycemia 2) ketonemia (not in HHS) 3) metabolic acidosis (not in HHS)

Discuss how Nutrition, Exercise, Alcohol & drugs can cause hypoglycemia?

1. Nutrition and drugs - some foods and drugs can increase insulin absorption => hypoglycemia 2. alcohol can cause delayed hypoglycemia - like hypoglycemia in the morning after drinking at night

Insulin's effect on K+ and phosphate ions

"In addition to insulin's effect on entry of glucose into cells, it also stimulates the uptake of amino acids, again contributing to its overall anabolic effect. When insulin levels are low, as in the fasting state, the balance is pushed toward intracellular protein degradation. Insulin also increases the permiability of many cells to potassium, magnesium and phosphate ions. The effect on potassium is clinically important. Insulin activates sodium-potassium ATPases in many cells, causing a flux of potassium into cells. Under certain circumstances, injection of insulin can kill patients because of its ability to acutely suppress plasma potassium concentrations. "

For Clarification - FYI - Antihypertensiive therapy and onset of diabetes

"Numerous studies have consistently demonstrated that certain classes of antihypertensive medications have differential effects on carbohydrate and lipid metabolism in humans. In general, higher doses of thiazide diuretics (i.e., ≥25 mg/day hydrochlorothiazide) and β-blockers, at any antihypertensive dose, worsen glycemic control, with β-blockers worsening insulin sensitivity"

Why is there a beta cell failure in type 2 diabetes? Is it because we're producing too much insulin leading to failure of the cells because they're overworked

"Type 2 diabetes mellitus is a complex disease characterized by beta-cell failure in the setting of insulin resistance. In early stages of the disease, pancreatic beta-cells adapt to insulin resistance by increasing mass and function. As nutrient excess persists, hyperglycemia and elevated free fatty acids negatively impact beta-cell function. This happens by numerous mechanisms, including the generation of reactive oxygen species, alterations in metabolic pathways, increases in intracellular calcium and the activation of endoplasmic reticulum stress. These processes adversely affect beta-cells by impairing insulin secretion, decreasing insulin gene expression and ultimately causing apoptosis. In this review, we will first discuss the regulation of beta-cell mass during normal conditions."

BMI Value that poses a risk for type 2 DM

(BMI ≥ 25 kg/m2) BMI ≥ 23 kg/m2 in Asian Americans (diff in bone structure)

Mild symptoms of hypoglycemia

(autonomic sx) Tremors Palpitations Sweating Hunger

Moderate Hypoglycemia

(neuroglycopenic in addition to the autonomic sx from before) Headache Mood change Irritability Decreased attentiveness Drowsiness Confusion Impaired judgment Weakness

Describe how Insulin errors can cause hypoglycemia

(too much insuulin, mixing insulins or taking wrong type at wrong time)

Normal anion gap ≈

12meq/L Ketones (anionic) in DKA lead to anion gap acidosis

Gestational diabetes usually happens when during the pregnancy

2nd or 3rd trimester (about 7% of pregnancies)

Which of the following goals is appropriate in a 34 YO male with type 2 diabetes and no comorbodities 1) HBa1c < or equal to 6% 2) BP < 120/80 mmHg 3) LDL <70 mg/dL 4) Fasting BG <130 mg/dL 5) All of the above 6) None of the above

4

Diagnosis of GDM - 1-step strattegy

75g OGTT (fasting) - *don't need to know numbers but know that we use OGTT* FPG ≥92mg/dL • 1H ≥180mg/dL • 2H ≥153mg/dL A two-hour 75-gram oral glucose tolerance test (OGTT) is used to test for diabetes. A healthcare provider will take a fasting lab draw to test your fasting glucose level first. They'll then ask you to drink 8 ounces of a syrupy glucose solution that contains 75 grams of sugar. You'll then wait in the office for two hours. At the one-hour and two-hour mark they'll measure the glucose level in the blood sample again.

Eggregious eleven - Alpha cell defect

= producing glucagon too much which is not good especially if person is already diabetic - shouldn't be doing that

Prevention/Delay of DM - Increase of physical activity

= ≥150 minutes/week moderate activity (moderate - can talk but can't carry on a conversation) or vigorous activity but moderate is good enough

Management of mild symptoms of Hypoglycemia

=> Self-treatment 1) 15 grams (1 serving) of CHO a) 4-6oz sweet drink (fruit juice, soda) => can of coke has 12 oz b) 5-6 lifesavers (4 lifesavers ~ 14 grams so makes sense) c) Glass of milk d) Fruit

Answer

A

Which of the following characteristcs are associated with type 1 diabetes A. Immune mediated B. Insulin resistance C. Obesity D. High prevalence

A. Immune mediated

Initial Evaluation - Post diagnosis of Diabetes - Lab work

A1C Renal function Urinalysis Lipid panel

DM risk (prediabetes) - A1C

A1C 5.7—6.4%

Equation for calculating anion gap

AG = Na+ - (Cl- + HCO3 )

Hypoglycemia—Glucagon - Adult dosing

ASAP 1 mg; may repeat in 20 minutes Also Give CH O or IV dextrose if no improvement, call 911 (after two administrations)

DKA happens more frequencly in children/adults

Adults > children; however #1 COD in children with DM1

Screening for DM2 - General population

Age ≥ 45 at 3 year intervals (as you age, risk factors increase so start screening at 45)

Therapy that poses a risk for Type 2 DM

Anti-hypertensive therapy

Gestational diabetes frequency

Approximately 7% of pregnancies

Answer -

B

Which of the following characteristcs are associated with type 2 diabetes A. Immune mediated B. Insulin resistance C. Obesity D. High prevalence

B, C and D

Treatment Goals for HTN for diabetics - 2016 ADA Guidelines

Blood pressure <140/<90mmHg <130/<80mmHg in younger patients ?

Discuss blurred vision in type 2 diabetes

Blurred vision: 2 types in diabetes - on the short-term - glucose infuses into the eyes and there is an enzyme that reducies it to sorbitol which is an osmotically active molecule

Eggregious eleven - brain

Brain: decrease in morning dopamine (FYI- "For certain people, poor production of the hormone dopamine in their brain might promote overeating, pushing them toward diabetes and obesity.); increased appetite b/c insulin Resistance => you're not using that glucose,

Answer

C 6.5 is the diagnsotic, below 7 is what we want them to be but below 6.5 is great b/c it means they're not diabetic

Answer

C That's the first you should do - if it's still low - thaen haver have a snack

Eggregious eleven - colon/biome

Colon/biome: huge area of research - if fix, then you've fixed much of the glucose problem

Answer

D

DKA or HHS Fruity ketone breath

DKA

DKA or HHS N/V & CRAMPS

DKA

DKA or HHS Three P's

DKA

DKA or HHS Weight loss

DKA

Develops due to emotional stress - DKA/HHS

DKA

Develops quickly - DKA/HHS

DKA

DKA or HHS Kussmaul's respirations

DKA (b/c of the metabolic acidosis i think) - No Kussmaul's in HHS

DKA or HHS Dehydration s/sx

DKA (she diddn't emphasize but makes sense because of polyuria) and HHS (more severe in that)

DKA or HHS Δ mental status

DKA and HHS but in DKA change is not as severe as in HHS

Prevalence of DM

Diabetes ~30.3 million ~9.4% (about 10%) population ~ 24% undiagnosed Pre diabetes ~86 million

Initial Evaluation - Post diagnosis of Diabetes - Referrals

Dilated eye exam Podiatry Dietician DSME ="programs provides knowledge and skills for people who want to manage their type 2 diabetes" Dental = "All persons with diabetes should have a comprehensive dental examination including prevention, early detection and treatment of periodontal disease" - see: http://diabetescoalitionofcalifornia.org/wp-content/uploads/2013/11/2011DentalExaminationAlgoSub.pdf

Eggregious eleven - immune system/inflammation

Dysregualtion of immunity and increased inflammation

Answer

E

Answer -

E (A doesn't make sense b/c macrosomia is a term that refers to newborns with excessive birth weight)

Answer

E - we don't screen for type 1

We screen for Type 1 diabetes b/c there are serological markers that we can look for (T or F)

F. There are Seriological markers (but can't do anything about it - so no reason to screen)

Describe how Erratic insulin absorption - can cause hypoglycemia

For instance activity that can increase insulin absorption can lead to hypoglycemia

What is Diabetes Mellitus?

Group of disorders that result in hyperglycemia - for example: Defect in insulin secretion, Or problem in insulin action. Or combination of both

HDL value that poses a risk for type 2 DM

HDL <35mg/dL ± triglyceride >250mg/dL

Develops slowly - DKA/HHS

HHS

Develops usually due to Undiagnosed DM - DKA/HHS

HHS

total body water deficit = much more profound in DKA/HHS than DKA/HHS

HHS (7-12 L) DKA (5-7 L fluid loss)

No ketones in DKA/HHS

HHS because no lipolysis and hence no ketogensis

Answer

He is not obese - he is overweight - obesity is BMI over 30 He has hypertension He doesn't have family history with type 1 diabetes NOT type 2 diabetes. He is overweight Polynesian islan So answer is F.

Initial Evaluation - Post diagnosis of Diabetes - physical exam

Ht/wt Vitals Foot exam Thyroid => "Your doctor will check this gland by feeling it while you swallow. Thyroid problems sometimes develop in people who have diabetes."

HHS stands for

Hyperglycemic hyperosmotic syndrome

Eggregious eleven - kidney:

Hyperglycmeia - kidney: if too much, normal kidney will pee out, people with dibates can retiain it for such a high level though

Why is there Hyponatremia in both DKA and HHS

Hyponatremia = sodium level is low because glucose is osmoticall active so draws water from inside the cell to outside - she said "correct sodium for glucose in both cases"

Diabetes Control & Complications Trial (DCCT)

Hypothesis: complications of DM1 are directly related to elevated plasma glucose - After treatment 60% RR (relative reduction) Diabetic retinopathy Nephropathy Neuropathy Delay in onset & progression of complications

United Kingdom Prospective Diabetes Study UKPDS

Hypothesis: complications of DM2 are related to elevated plasma glucose 4 monotherapies (like insulin or metformin) vs. diet Microvascular complications decreased 25% Linear relationship between glycemic control & complications 35% reduction in complications per1% reduction HbA1c No significant decrease in macrovascular events AMI & sudden death decreased 16% (not statistically signficiant)

Marked by variable insulin deficiency between episodes

Idiopathic Type 1 diabetes

This type of diabetes is strongly inherited

Idiopathic Type 1 diabetes

Screening for DM2 - Children

If A) Overweight 1) BMI > 85th percentile for age & sex or 2) weight for height > 85th percentile 3) Weight > 120% ideal for height Plus any 2 of the following: 1) FH of DM2 in 1st or 2nd degree relative (like uncles or grandparents) 2) High risk race/ethnicity 3) Signs of insulin resistance or associated conditions (HTN or hyperlipidemia) 4) Maternal history of DM or GDM

Explain insulin effect on Ketogensis

In the liver insulin increases fatty acid synthesis and esterification. At the same time malonyl-CoA formation is increased, which inhibits the acylcarnitine transferase system and thus *decreases the transport of fatty acids into mitochondria and hence fatty acid oxidation and ketogenesis*

Hormone that helps control glucose level in concert with insulin

Incretin hormone:

What's the primary abnomrality in diabetes?

Insulin deficiency whether absolute (type 1) or relative (type 2)

LADA

LADA = latent autoimmune diabetes in Adults = they don't look like typical type 1 (for example - not children)

HHS Less/More prevalent than DKA LowHigh mortality Older/Younger patients

Less prevalent than DKA High mortality • 5-25% Older patients due to Often undiagnosed DM

Eggregious eleven - liver

Liver : increasing glucose levels even though person is hyperglycemic

Screening for DM2 - More frequent/earlier screening

More frequent/earlier screening for those with risk factors BMI ≥ 25 kg/m2 plus additional risk factor(s) BMI ≥ 23kg/m2 if Asian descent

Eggregious eleven - muscle tissue

Muscle: insulin resiistnace

Answer

Not a loss Not because slow process Maybe Hypertension - yes - Nope Very possible - yes

Child & Adolescent Obesity 2011-2012

Notice that obesity is increasing with age for both genders

Gestational diabets risks to offspring

Obesity Glucose intolerance Diabetes

Pathophysiology—Obesity & DM2

Obesity ➜ (leads to) chronic inflammation of Adipose tissue, Liver, Pancreas, hypothalamus etc => Sets up systemic insulin resistance & eventual β-cell dysfunction

Having 1st degree, 2nd degree, both pose a risk factor for type 2 DM

Only 1st degree (a person's parent, sibling, or child)

Diabetes Ramifications

Organ damage Eyes Kidneys Nerves (both peripheral and autonomic) Heart Blood vessels

DKA is marked by overproduction of

Overproduction of β-hydroxybutyric acid & acetoacetic acid (Ketones)

Initial Evaluation - Post diagnosis of Diabetes - Immunizations

Pneumovax Influenza

Glucagon MoA

Promotes hepatic glycogenolysis & gluconeogenesis

Screen for DM2 - Children - what age

Recommended screening at Age 10 or onset of puberty if earlier (Q3 years)

Treatment Goals for DM

Symptom free, complication free Glycemic control=> A1C <7.0%* (don't worry about numbers)

Intensive insulin therapy can lead to hypoglycemia (T or F)

T

Whether patient enters DKA or HHS state, either way, insulin deficiency is the primary abnormality (T or F)

T.

Brain doesn't depend on insulin for glucose uptake (T or F)

T. (Thank God)

Glucagon - Adverse Effects

Tachycardia (she didn't discuss but interesting) Nausea, vomiting

FYI - Fasting Plasma Glucose Test - how does it work?

The fasting plasma glucose test is performed after a person has fasted for at least 8 hours. A sample of blood is taken from a vein in the arm. If the blood glucose level is greater than or equal to 126 mg/dl, *the person is retested* and, if the results are consistent, diagnosed with diabetes

Egregious Eleven in Diabetes

These are all the body systems affected and being affected by diabetes

Insulin deficiency leads to Tissues "thriving" or "starving" Protein catabolism/anabolism Lipolysis/lipogensis Decreased/Increased Glucose Decreased/Increased Ketones

Tissues "starving" Protein catabolism Lipolysis Increased Glucose and Ketones

Absolute deficiency of insulin secretion

Type 1

Caused by Genetic predisposition & lifestyle

Type 2

Characterized by Insulin resistance (not deficiency)

Type 2

Is there ketoacidosis in type 1/type 2

Type 2 Circulating insulin typically inhibits lipolysis No lipolysis ∴ no ketogenesis = No ketoacidosis However: Catacholamines May suppress β-cell function Progression to DKA Type 1 Lipolysis + Ketogenesis = Ketoacidosis

Presentation for type 2 diabetes

Variable 1) They can just be Hyperglycemia or 2) Complications (if they've never been screeneed before) 3) Can also be asymptomatic and they just happen to be diagnosed during screening.

Answer

Yes loss of bladder control because of polyuria Yes infection Lethargy - yes Hypertension - not in type 1 Normal bmi - yes Weight loss - - not gonna be on an exam.

We don't screen for type 1 diabetes. Why? Does T1D have low prevalence?

bec prevalnece is low and there is nothing that we can do about it anyway

Ketones are

breakdown of fats, levels increase when insulin levels are low; used an energy source

Egregious eleven - Stomach/small intestine:

decrease in incretin

Screen for DM 4-12 weeks post-partum if

diagnosed with GDM (bec/ GDM is risk for type 2)

Eggregious eleven - Adipose tissue -

increased lipolysisi to produce more glucose (I think i might have misheard her here, it is probably increased lipolysis to generate fatty acids which contribute to insulin resistance)

Severe hypoglycemia sympoms

neuroglycopenic sx 1) Unresponsive 2) Unconscious 3) Convulsions (compared to only tremors and palpitations in mild/moderate hypoglycemia)

Egregious Eleven in Diabetes - Pancreatic issue =

not making enough insulin

Incretin effect =

released in the gut; plays a role in glucose processing by promoting insulin secretion (FYI- an example is GLP-1 - which we discussed as an en emerging treatment with Dr. Mills), function decreased in Diabetes (one of the egregious eleven)

Describe the "normal" way insulin is secreted

there is insulin that is pre-made waiting to be released As soon as you put food in your mouth, this pre-made is released to help take care of the post-meal glucose and then some insulin will be relelased after that to take care of the rest - this is impaired in diabetics.

DM risk (prediabetes) - Impaired glucose tolerance (IGT)

• 2-h PG (Post-prandial Glucose) 140-199 mg/dL (compare with normoglycemia values)

DM risk (prediabetes) - Impaired fasting glucose (IFG)

•FPG 100-125 mg/dL - note post prandial level is useless here doesn't tell you antyhing about IFG (compare with normoglycemia values)