dodge 2

Question 1

Type 1 DM vs Type 2 DM

Answer 1

Type 1 VS Type 2

Absolute insulin deficiency vs Insulin resistance

younger, autoimmune vs older people

less genetic effect vs more genetic effect

Islet cell Ab, low C peptide vs High C peptide (initially)

Insulin tx early vs Insluin tx later (typically)

No oral medication vs Oral medications early (typically)

Question 2

PREDIABETES LAB VALUES

Answer 2

• Fasting plasma glucose = 100-125 mg/dL
• Glucose tolerance test = 140-199 mg/dL at two hours of glucose tolerance test
• Hemoglobin A1c = 5.7-6.4%

Question 3

Diabetes mellitus Lab values

Answer 3

• Fasting plasma glucose > 126 mg/dL
• Glucose tolerance test >200mg/dL at two hours of glucose tolerance test
• Random blood glucose > 200mg/dL with symtpoms of DM
• Hemoglobin A1c >6.5%

Question 4

Treatment recommendations based on A1c values

****

Answer 4

** 10-12% with KETOSIS and/or WEIGHT LOSS –> NEED TO BE ON INSULIN**

Question 5

describe the role lifestyle modifications have on treatment of DM

Answer 5

• ADA recommends 150 mins/week of moderate-intensity cardio workouts
  
  • 3x/wk, no more than 2 days off in between
• ADA also recommends resistance training at least two per week
• WEIGHT LOSS IS MOST IMPORTANT FACTOR in reducing A1c

Question 6

treatment goals of DM

Answer 6

• Hemoglobin A1c = < 7.0%
• Preprandial glucose (fasting) = 70-130 mg/dL
• Peak postprandial glucose = <180mg/dL

Question 7

Metoformin tx

Answer 7

• initial oral mono-therapy for Type 2 DM
• MoA
  
  • increased peripheral insulin sensitivity
  • decreased glucose production by liver
• Start at 500mg once or twice dailys, double every week if tolerated by pt until goal of 1000mg twice daily
• DO NOT USE with CHF, chronic hypoxia, pregnancy

Question 8

Sulfonylureas

Answer 8

• MoA: stimulate insulin secretion by pancreas beta cells
  
  • DECREASED MICROVASCULAR COMPLICATIONS (neuropathy, retinopathy etc)
• decreased efficacy with time, therefore will need increasing doses
• dont give to pregnant people

Question 9

Thiazolidinediones

Answer 9

• sensitive muscle, fat, hepatocytes to insulin (PPAR gamma)
• increased risk for bladder cancer with >1 year of use
• Increased risk of fluid retention and CHF; contraindicated in NYHA class II or IV

Question 10

Glitinides

Answer 10

• similar to sulfonylureas, stimulate beta cells; short half life = mealtime dosing
• increased weight gain and very expensive

Question 11

INSULIN THERAPY Type 1 vs Type 2 DM

Answer 11

• Type 1 DM
  
  • insulin REQUIRED
  • start at .5 units/kg/day
    
    • basal long acting insulin + prandial short acting insulin
    • OR.. Continuous infusion short acting insulin via pump
• Type 2 DM
  
  • Insulin MAY be required
  • start at .1-.2 units/kg/day
  • Initial goal to get morning fasting glucose to < 130mg/dL
    
    • check A1c
    • if stil not within goal, add prandial short acting insulin

Question 12

short acting insulin

Answer 12

Lispro, aspart, glulisine = short acting

glargine = long acting

Question 13

Mechanism of complications

Answer 13

• increased itnracellular glucose leads to formation of advanced glycoslyation end products (AGEs)
  
  • bind cell surface receptors, non enzymatic glycosylation
  • accelerate sthersclerosis, promote glomerular dysfunction, reduce NO syntheis, endothelial dysfunction
• Macrovascular: coronary, peripheral artery, and cerebreovascualr disease
• Microvascular: retinopathy, neuropathy, nephropathy

Question 14

CARDIOVASCULAR COMPLICATIONS

Answer 14

• increased cardiovascular disease (CHF, MI, PAD, CHD)
• DM = Coronary heart disease equivalent
• GOAL BLOOD PRESSURE = 130/80
• CONTROL OF RISK via:
  
  • Statin therapy (in certain populations with risk of MI, CVA)
  • smoking cessation
  • increased exercise
  • weight loss, diet

Question 15

Ophthalmologic complications

Answer 15

• DM is #1 cause of blindness in people age 20-74
  
  • more pronouced in african american and hispanic patients
  • DILATED COMPREHENSIVE EYE EXAM BY OPHTHALMOLOGIST (at time of diagnosiis of type 2 and within 5 years of onset of type 1 DM - followed by annual eye exams)
• PROLIFERATIVE RETINOPATHY
  
  • neovascularization due to hypoxemia –> new vessels rupture easier = hemorrhage
    
    • hemorrhage leads to aqueous fibrosis and eventual retinal detachment
• NON-PROLIFERATIVE RETINOPATHY
  
  • vascular micro aneurysms, blot hemorrhages, cotton-wool spots
  • retinal ischemia via change in retinal blood flow

Question 16

Nephrology complications

Answer 16

• number 1 cause of ESRD
• multiple mech: altered renal circualtion, glomerular chagnes
• measure urine albumin:CR ratio annually
  
  • starting at Dx of type 2 or within 5 years of type 1
  • IF >30mg/g
    
    • USE ACEi or ARB to reduce progression of proteinuria and decrease risk of END STAGE RENAL DISEASE

Question 17

NEUROPATHY COMPLICATIONS

Answer 17

• Distal symmetric polyneuropathy is most common (stocking-Glove distribution)
• Numbness, tingling, sharpness, burning
  
  • eventually los the painful sensation
• loss of proprioception, ankle reflexes and sensation

AUTONOMIC NEUROPATHY (noradrenergic, cholinergic)

• effects CV (orthostatic hypotension), GI (gastroparesis), Anhidrosis (dry skin)

YEARLY FOOT EXAMS

• at time of Dx of type 2 or at 5 years after onset of type 1 (skin inspection, pedal pusles, sensation testing)

Question 18

GI/GU Complications

Answer 18

• Gastroparesis with long-standing DM; delay gastric emptying
  
  • early satiety, anorexia, vomting
  • can use dopamine antagonist to promote gastric empyting (Metoclopramide)
• Genitourinary dysfunction
  
  • erectile dysfunction, female sexual dysfunction
  • Cystopathy (unable to sense full bladder)
  • increased UTI in postmenopausal women