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Type 2 Diabetes
Mellitus

 http://crisbertcualteros.page.tl
Etiology
• Insulin resistance:
 – decrease peripheral utilization of glucose
 elevated PPG
 - Increase liver glucose output -> elevated
FBS
• Beta cell dysfunction
• Alpha cell dysfunction – lack suppression of
   glucagon secrection
Pathophysiology of Diabetes
           FBS         2Hr PP      Insulin      Insulin     Treatment
                                   Resistance   Secretion



Phase 1    Normal      Normal      increased    increased   none
                       OGTT



Phase 2    Normal or   increased   Markedly     increased   Diet, a-
           increased               increased                glucosidase,
                                                            metformin


Phase 3    increased   increased   increased    increased   OHA, insulin
diagnosis
• Any of: (ADA, 2008)
Symptoms of DM + RBS >200
FBS > 126
     (normal: <100)
     IFG: 100 – 125
75 gm OGTT
  a) 2hr Plasma glucose: > 200  DM
     normal: <140
  b) 2hr Plasma Glucose: 140 – 199  IGT
Goals of treatment
HBA1C: <7
Preprandial plasma glucose: 90 – 130
Peak post-prandial plasma glucose: < 180
Hospitalized patient:
  – Critically ill: kept as close to 110; gen. <140;
    insulin needed
  – Non-critical: FBS <126; RBS<180
Goals of treatment
BP: <130/80
LDL: <100
Triglycerides: <150
HDL: >140
DM Management
• All DM with HPN ACEI or ARB
• Annual influenza vaccine
• Atleast 1 lieftime pneumococcal vaccine
• >40yo: give statin to achieve LDL reduction
  of 30-40%
• <40yo: medical tx if diet modification is
  failed
• Aspirin tx
DM Management
Monotx: for FBS<140; 2PPBS<180
1st line:
1. metformin: dec liver glucose output
2. Sulfonylurea: inc insulin secretion
3. TZD: inc insulin sensitivity
Alternative tx:
1. Non-SU insulin secretagogue: inc insulin
   secretion
2. Glucosidase inhibitor: delays GI absortion
   of carbohydrates
Combination TX: if FBS>140; 2PPBS>180
1. If on SU: add metfomin or TZD
2. If on metformin: add SU or TZD
3. If on TZD: add SU or metformin

Insulin TX: if blood sugar is not controlled
http://crisbertcualteros.page.tl

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Type 2 Diabetes Mellitus Pathophysiology and Treatment

  • 1. Type 2 Diabetes Mellitus http://crisbertcualteros.page.tl
  • 2. Etiology • Insulin resistance: – decrease peripheral utilization of glucose  elevated PPG - Increase liver glucose output -> elevated FBS • Beta cell dysfunction • Alpha cell dysfunction – lack suppression of glucagon secrection
  • 3.
  • 4.
  • 5. Pathophysiology of Diabetes FBS 2Hr PP Insulin Insulin Treatment Resistance Secretion Phase 1 Normal Normal increased increased none OGTT Phase 2 Normal or increased Markedly increased Diet, a- increased increased glucosidase, metformin Phase 3 increased increased increased increased OHA, insulin
  • 6. diagnosis • Any of: (ADA, 2008) Symptoms of DM + RBS >200 FBS > 126 (normal: <100) IFG: 100 – 125 75 gm OGTT a) 2hr Plasma glucose: > 200  DM normal: <140 b) 2hr Plasma Glucose: 140 – 199  IGT
  • 7. Goals of treatment HBA1C: <7 Preprandial plasma glucose: 90 – 130 Peak post-prandial plasma glucose: < 180 Hospitalized patient: – Critically ill: kept as close to 110; gen. <140; insulin needed – Non-critical: FBS <126; RBS<180
  • 8. Goals of treatment BP: <130/80 LDL: <100 Triglycerides: <150 HDL: >140
  • 9. DM Management • All DM with HPN ACEI or ARB • Annual influenza vaccine • Atleast 1 lieftime pneumococcal vaccine • >40yo: give statin to achieve LDL reduction of 30-40% • <40yo: medical tx if diet modification is failed • Aspirin tx
  • 10. DM Management Monotx: for FBS<140; 2PPBS<180 1st line: 1. metformin: dec liver glucose output 2. Sulfonylurea: inc insulin secretion 3. TZD: inc insulin sensitivity
  • 11. Alternative tx: 1. Non-SU insulin secretagogue: inc insulin secretion 2. Glucosidase inhibitor: delays GI absortion of carbohydrates
  • 12. Combination TX: if FBS>140; 2PPBS>180 1. If on SU: add metfomin or TZD 2. If on metformin: add SU or TZD 3. If on TZD: add SU or metformin Insulin TX: if blood sugar is not controlled