Diabetes

Question 1

the diabetes association defines hyperglycemia as?

Answer 1

a consistent blood glucose between 100-126 mg/dl

Question 2

define “fasting” hyperglycemia

Answer 2

blood sugar > 126 mg/dL (> 7 mmol) after no eating/drinking for at least 8 hours

Question 3

define “postprandial” hyperglycemia?

Answer 3

aka “after meal hyperglycemia”

blood sugar > 180 mg/dL within 2 hrs of eating

Question 4

people without diabetes typically have blood sugar under what levels following a meal?

Answer 4

< 140 mg/dL

Question 5

diabetes symptoms can remain latent until what blood glucose?

Answer 5

250-300 mg/dl

15-20 mmol/L

Question 6

the dx of diabetes is contingent on what parameters being met?

Answer 6

• Fasting (8 hrs post meal) blood glucose - 126 mg/dl
• Random (postprandial) blood glucose - 200 mg/dl
• Glycosylated Hb (HbA1c) - 6.5
• 2 hour glucose tolerance test – not used often

Question 7

wat blood glucose levels can lead to organ damage?

Answer 7

chronic levels > 125 mg/dl

Question 8

describe the clinical presentation of diabetes insipidus

Answer 8

• excessive urination (polyuria) - like DM
  
  • but, it is due to insufficient ADH (vasopressin) secretion
    
    • so, no glucose dysregulation seen

Question 9

type I vs type II diabetes - cause / onset / tx

Answer 9

Type1

• insulin dependent DM (IDDM)
• juvenile onset
• tx: insulin supplementation

Type 2

• non - insulin dependent DM (NIDDM)
• adult onset
• tx: inability to maintain normal glucose levels even via hyperinsulemic state

Question 10

what are other causes of DM outside of Type I & Type II?

Answer 10

• gestational DM- hyperglycemia goes away post-delivery
• DM secondary to drugs - antiphsycotics/fertility drugs
• DM due to Klinefelters syndrome (XXY)

Question 11

pathogenesis of Type I DM

Answer 11

• insufficient insulin synthesis due to destruction of pancreatic B-cells
  
  • auto-Abs to beta cell proteins in the pancreas islets
    
    • auto-Abs possibly formed due to abnormal MHC gene: MHCs that see native proteins as foreign
      
      • possibly triggered by viral event
• glucagon predominates due to low-insulin state:
  
  • induces
    
    • blood glucose inc
      
      • • gluconeogenesis
      • • glycogenolysis
      • • glucose uptake
    • general breakdown
      
      • lipolysis –> FAs –> ketosis

Question 12

pathogenesis of type II diabetes

Answer 12

• no pancreatic destruction - insulin made in proper quantities
• dietary / enviornmental factors lead to peripheral insulin resistance that persists despite heightened insulin secretion by beta-cells (hyperinsulinema)
  
  • so state is “insulin predominant” (not glucagon) —> building state
    
    • no gluconeogenesis/glycogenolysis
    • no fat breakdown (no ketoacidosis)
    • synthesis of: glycogen & FAT: Fat > glcyogen = hyperlipidemia
  • but, this insulin doesn’t induce “uptake”
    
    • glucose (especially) & fat (?)

Question 13

excess glucose molecules in hyperglyemica can form what products?

what is their significance?

Answer 13

formed by “glycation” of glucose:

• HbA_1c: 1-amino-deoxyketose linked to Hb’s B-globin
  
  • indicative of blood glucose levels:
    
    • normal: 6% = 120 mgl/dl glucose
    • high: 6.5% = 126 mg/dl glucose
• AGE: end glycation products derived from 1-amino-deoxyketose
  
  • accumulae in ECM (vasculature)–> retinopathy, nephropathy

formed by “polyol pathway

• sobrital (polyols)​
  
  • ​can lead to –> cataracts, neuropathy

Question 14

what are the major chonic complications of DM and what are they caused by?

Answer 14

macrovascular complications

• atherosclerosis - hyperlipidemia (DM II?)

microvascular complications

• nephropathy - AGEs
• retinopathy - AGEs
• neuropathy - polyol accumulation (disrupts myoinositol metabolism)

Question 15

tx of Type I diabetes?

Answer 15

insulin

Question 16

tx of type II diabetes?

Answer 16

1. diet/exercise
2. oral hypoglycemia drugs: Metformin, Glyburide, TZD
3. insulin