Week 2 Day 1

Front 1

Diabetes mellitus is a disease of.....

Back 1

Metabolism affecting lipid, carbohydrate and protein metabolism

Front 2

List the lab values for diagnosing diabetes

Back 2

HbA1c >6.5% (it is a 3 month average of blood sugar)
Fasting plasma glucose >126 mg/dL (above this value is where you can begin to get retinopathy)
2 hour plasma Glucose >200 mg/dL
Random Glucose >200 mg/dL

Front 3

What are the lab values for diagnosis of pre-diabetes?

Back 3

Fasting plasma glucose 100-125 mg/dL
2 hour plasma glucose 140-199 mg/dL (after 75 grams of oral glucose)
A1c 5.7-6.4%

Pre-diabetes can be lowered to about 5%/year with improved lifestyle

Front 4

What are the short term complications of DM

Back 4

Poor wound healing
Fatigue
Impaired immune defenses
Electrolyte abnormalities
Prolonged hospital stay
Increased inpatient morbidity
Can become hypoglycemic d/t aggressive treatment

Front 5

What are the long term microvascular complications of DM?

Back 5

Retinopathy-->blindness
Nephropathy-->kidney failure
Neuropathy-->amputations

Front 6

What are the long term macrovascular complications of DM?

Back 6

Coronary Artery Disease-->heart attacks
Peripheral Vascular Disease-->Strokes

Front 7

List the pathways for the development of DM complications

Back 7

Accumulation of advanced glycosylation end products
Accumulation of sorbitol
Disruption of hexosamine pathway
Activation of poly (ADP-ribose) polymerase pahtway
Increased oxidative stress (free radicals)

Front 8

Autoimmune B-cell destruction with lack of insulin

Back 8

Type I DM

Front 9

Insulin resistance with relative insulin deficiency

Back 9

Type II
or Gestational (has some B-cell dysfunction; need to send nutrients to the fetus-in rare cases can induce Type I diabetes)

Front 10

What are other causes of DM other than Type I, II, or Gestational

Back 10

Genetic defects in B-cell function
Exocrine pancreas diseases
Cushings disease
drug induced

Front 11

What are the defects in Type II diabetes mellitus

Back 11

Insulin resistance--> kidneys and liver make too much glucose and cant take-up glucose by insulin responsive tissues
Inadequate insulin secretion

Front 12

Insulin (medication)

Back 12

Most powerful; binds to insulin receptor to increase glucose uptake by insulin responsive tissues

Front 13

Sulfonylurea-GLIMEPIRIDE

Back 13

Binds to receptor that regulates K+ channel to stimulate insulin release

Inexpensive can cause hypoglycemia

Front 14

Meglitinide-Repaglinide and mateglinide

Back 14

Increase insulin secretion by binding to K+ channel
Short T1/2

Used in Chronic Renal disease
Can cause hypoglycemia

Front 15

Biguanide (METFORMIN)

Back 15

Decrease systemic glucose output (from kidneys and liver)

DONT use in chronic renal disease, pulmonary disease, liver disease, or heart disease

Front 16

Alpha-glucosidase inhibitor-Acarbose

Back 16

Delays digestion of complex carbs

Increased GAS production

Front 17

Thiazolidinediones-Glitazones, rosiglitazone, pioglitazone

Back 17

Binds to PPAR receptors and appears to sensitize insulin responsive tissues to insulin

Fluid overload that can cause heart failure
Acute coronary syndrome
Bladder cancer

Front 18

Incretin analogues-Exenatide and Liraglutide

Back 18

Bind to incretin receptors to increase prandial insulin secretion and delay gastric emptying

Nausea
Pancreatitis
Expensive;newer drug

Front 19

DPP-4 inhibitor-Stiagliptin

Back 19

Inhibits the breakdown of incretins

Pancreatitis/pancreatic cancer

Front 20

Sodium glucose co-transporter 2 inhibitor

Back 20

Inhibits glucose reabsorption of filtered glucose in the kidney

Limited data
Increased UTIs

Front 21

What is the first line agent for diabetes?

Back 21

Metformin

Front 22

List the requirements of metabolic syndrome (need 3)

Back 22

Waist circumference (>40in in men and 35 in women)
Hypertriglyceridemia (>150 mg/dl)
Low HDL (<40 mg/dL in men, <50mg/dL in women)
Hypertension (>130/85 mmHg; or on antihypertensives)
Impaired Fasting glucose (>100 mg/dL; or taking medication)

Front 23

Outline the basic pathophysiology of metabolic syndrome

Back 23

Adipose mass-->release FFA to liver-->increase Glucose and triglycerides and secrete VLDL

FFA also reduce insulin sensitivity in muscle by inhibiting uptake

The increased glucose--->increased insulin secretion-->increased Na+ and SNS activation-->hypertension

Adipocytes produce IL-6 and TNF-a-->insulin resistance and liplysis of adipose tissue (Il-6 increases hepatic glucose production)

Increased fibrinogen (hepatic) and plasminogen activating inhibitor (adipocyte)-->prothrombic state

Front 24

Upper body obesity (visceral fat)

Back 24

more strongly correlated to insulin resistance than lower-body fat (d/t higher accumulation of lipid in muscles and liver)

Front 25

Pronlonged stimulation of beta cells leads to...

Back 25

Beta cell failure with a decrease in insulin

possibly due to lipotoxicity

Front 26

adiponectin and leptin increase or decrease with insulin resistance?

Back 26

decrease

Front 27

TNFa increase or decrease with insulin resistance?

Back 27

Increase

Front 28

Inflammation hypothesis for insulin resistance

Back 28

enlarged fat cells attract macrophages and excrete inflammatory signals that work in the muscle cell, via the kinase JNK, to block an insulin receptor substrate (IRS-1)

Front 29

Lipid overload hypothesis for insulin resistance

Back 29

enlarged fat cells leak fatty acids, causing diacylglycerols (DAGS) to accumulate in muscle cells.
These inhibit insulin signaling through protein kinase Cs (nPKCs) and then block the insulin receptor substrate IRS-1.

Front 30

At what age is metabolic syndrome usually diagnosed?

Back 30

Middle age (40-60)

Prevalence increases with age

Front 31

Other complications associated with the metabolic syndrome

Back 31

Fatty liver disease
Polycystic ovary syndrome
Obstructive Sleep Apnea
Gout (hyperuricemia)
Increased risk of cancer

Front 32

Lipid profile in matabolic syndrome

Back 32

The typical lipid profile in the metabolic syndrome is a low HDL, elevated triglycerides and mild or moderate increase in the LDL cholesterol. The LDL particles are smaller and more atherogenic.

Front 33

Insulin suppresses hepatic glucose production by what types of mechanisms

Back 33

Direct: decrease glycogenolysis and gluconeogenesis
Indirect: Decrease free fatty acid flux to liver and decrease glucagon secretion

Front 34

What is the nonpharnmacologic therapy for metabolic syndrome

Back 34

Weight loss
Limit fats in diet
Physical activity
Smoking cessation
Consider bariatric surgery in management of obesity

Front 35

Orlistat

Back 35

Treatment of obesity/metabolic syndrome
reversible inhibitor of gastric and pancreatic lipases
Can inhibit the absorption of dietary fats by 30%

Front 36

HTN in metabolic syndrome tx

Back 36

Consider ACE inhibitor or ARB

Front 37

LDL cholesterol in metabolic syndrome tx

Back 37

Statins are first line agents
Ezetimibe is second line therapy

Front 38

>200 triglyerides in metabolic syndrome treatment

Back 38

Fibric acid derivatives
Niacin

Front 39

Low HDL metabolic syndrome tx

Back 39

Exercise and weight loss
Fibrates or Niacin

Front 40

Treat prediabetes

Back 40

Diet, exercise and weight loss
Nutrition counseling
Metformin-->patients with class II or III obesity who are young; those with a history of gestational diabetes of GDM

Front 41

CV risk factors in metabolic syndrome tx

Back 41

Aspirin

Front 42

Pathophys of Type I diabetes in children

Back 42

Environmental trigger-->B-cell antigen released-->CD4 recognizes as foreign-->CD4 Th1 response-->CD8 cytotoxic T cell and cytokines attack pancreatic B-cells

Need a genetic predisposition

Front 43

What are the electrolyte changes in untreated Type I diabetes

Back 43

Hyponatremia-->osmotic dilution of plasma (diluted in free water; water released d/t hyperglycemia)
Hypokalemia
Low CO2-->ketoacidosis (acid levels go up)
Phosphate: Decreased phosphate intake and phosphaturia

Front 44

When is the peak age of diagnosis in Type one DM

Back 44

10-14 yo

Front 45

Does oral or IV glucose create a bigger spike in insulin?

Back 45

Oral glucose
But IV glucose creates a quicker rise in insulin (presynthesized insulin)

Front 46

Diabetic ketoacidosis occurs in the presence of...

Back 46

Absolute insulin deficiency-->poor calorie consumpton, prolonged poor glycemic control and concomitant illness

Compensatory hyperpnea (Kussmaul respiration)

Front 47

What are the short acting insulin preps?

Back 47

Aspart, Glulisine, Lispro

Front 48

What are the long acting insulin preps?

Back 48

NpH, Detemir, Glargine (longest; 24 hours)

Front 49

Sx of insulin overdose

Back 49

Shakiness, headaches, dizziness, sweatiness, tachycardia, hunger, or fatigue (tx with fast acting carbs)
Moderate hypoglycemia-->confusion, poor coordination, slurred speech (tx frosting, sugar gel in buccal mucosa)

Severe hypoglycemia-->stupor, seizure, and coma (tx emergency care with glucagon injections)

Front 50

T1DM causes weight gain or loss?

Back 50

loss

Front 51

What is the most common treatment for Type 1 DM?

Back 51

Multiple daily injections

Front 52

Impact of fiber, protein, and fat diets in type I DM

Back 52

take longer to digest-->causing a more gradual rise and fall in blood sugars

Want to have a protein/fat snack before bed to prevent hypoglycemia