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Diabetic Foot
Introduction ,[object Object],[object Object],[object Object],[object Object]
Pathogenesis of Chronic Complication of diabetes mellitus
Hyperglyceamia Nonenzymatic glycosylation  of collagen and other proteins in interstitial tissue and blood vessel wall Formation of irreversible advanced glycosylation end products  ( AGES ) ‏ Cause  cross link   between polypeptides  Trap  plasma and interstitial proteins including  LDL Promote the  deposition of cholesterol   in the blood vessel intima  Accelerated the process of  atherogenesis Formation of  atherosclerotic plaque Atherosclerosis
Glucose Sorbitol Fructose NADPH + H + NADP + NAD + NADH + H + Aldose reductase Polyol dehydrogenase Disturbance in polyol pathway GSH (reduced) GSSG (oxidized) Glutathione reductase
Hyperglycaemia  stimulate polyol pathway   accumulation sorbitol + fructose in Schwann cells Increase IC osmolality  influx of water    osmotic cell injury  damage schwann cell (demyelination )  axon degeneration irreversibly  disrupt neural function  Diabetic neuropathy
Diabetic foot result from: ,[object Object],[object Object],[object Object],[object Object]
a) Predisposing peripheral vascular disease Atherosclerosis  (medium-sized vessels below the knee) Compromised blood supply Coagulative necrosis Dry gangrene Infection Wet gangrene Ischemia Ulcer
Predisposing peripheral vascular disease Artheroma plaque narrowing the arterial lumen Ischaemic toes due to artherosclerosis
b) Neuropathy Neuropathy Motor Sensory Autonomic ↓  nociception ↓  Proprioception, Unawareness of foot position Reduced  sweating Dry skin Fissures and cracks Muscle wasting Foot weakness Postural deviation Deformities, stress and shear pressures Trauma Stress on bones & joints Plantar pressure Callus formation Infection Ulcer
Neuropathy  ,[object Object],[object Object],[object Object],[object Object]
Claw toe Severe atrophy of the intrinsic foot muscles (lumbrical & interossei) ‏ d/t motor neuropathy resulted in imbalance of foot muscles & cocked-up toes.
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Neuropathy
[object Object],[object Object],Neuropathy
c) Infection ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
d) Osteoporosis ,[object Object],[object Object]
 
Clinical presentation of diabetic foot
Diffentiation of  Ischaemic  and Neuropathy Ulcer Painless Sites of pressures (metatarsal heads, heels) Painful At the distal and over bony prominences Ulceration Warm palpable pulses Cold Pulseless Palpation High arch + clawing of toes No trophic changes Surrounded by callus Dependent rubor Trophic changes Gangrenous digits Inspection Usually painless Or painful neuropathy Claudication Rest pain Symptoms Neuropathy Ischaemia
Ischemic foot ulcer
Neuropathic foot ulcer Callus formation on its surrounding ulcer lesion.
Charcot Joint ,[object Object],[object Object],[object Object],[object Object],[object Object]
Charcot Joint Rocker bottom charcot foot
Gangrene  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
 

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Diabetic foot + gangrene

  • 2.
  • 3. Pathogenesis of Chronic Complication of diabetes mellitus
  • 4. Hyperglyceamia Nonenzymatic glycosylation of collagen and other proteins in interstitial tissue and blood vessel wall Formation of irreversible advanced glycosylation end products ( AGES ) ‏ Cause cross link between polypeptides Trap plasma and interstitial proteins including LDL Promote the deposition of cholesterol in the blood vessel intima Accelerated the process of atherogenesis Formation of atherosclerotic plaque Atherosclerosis
  • 5. Glucose Sorbitol Fructose NADPH + H + NADP + NAD + NADH + H + Aldose reductase Polyol dehydrogenase Disturbance in polyol pathway GSH (reduced) GSSG (oxidized) Glutathione reductase
  • 6. Hyperglycaemia  stimulate polyol pathway   accumulation sorbitol + fructose in Schwann cells Increase IC osmolality  influx of water  osmotic cell injury  damage schwann cell (demyelination )  axon degeneration irreversibly  disrupt neural function  Diabetic neuropathy
  • 7.
  • 8. a) Predisposing peripheral vascular disease Atherosclerosis (medium-sized vessels below the knee) Compromised blood supply Coagulative necrosis Dry gangrene Infection Wet gangrene Ischemia Ulcer
  • 9. Predisposing peripheral vascular disease Artheroma plaque narrowing the arterial lumen Ischaemic toes due to artherosclerosis
  • 10. b) Neuropathy Neuropathy Motor Sensory Autonomic ↓ nociception ↓ Proprioception, Unawareness of foot position Reduced sweating Dry skin Fissures and cracks Muscle wasting Foot weakness Postural deviation Deformities, stress and shear pressures Trauma Stress on bones & joints Plantar pressure Callus formation Infection Ulcer
  • 11.
  • 12. Claw toe Severe atrophy of the intrinsic foot muscles (lumbrical & interossei) ‏ d/t motor neuropathy resulted in imbalance of foot muscles & cocked-up toes.
  • 13.
  • 14.
  • 15.
  • 16.
  • 17.  
  • 18. Clinical presentation of diabetic foot
  • 19. Diffentiation of Ischaemic and Neuropathy Ulcer Painless Sites of pressures (metatarsal heads, heels) Painful At the distal and over bony prominences Ulceration Warm palpable pulses Cold Pulseless Palpation High arch + clawing of toes No trophic changes Surrounded by callus Dependent rubor Trophic changes Gangrenous digits Inspection Usually painless Or painful neuropathy Claudication Rest pain Symptoms Neuropathy Ischaemia
  • 21. Neuropathic foot ulcer Callus formation on its surrounding ulcer lesion.
  • 22.
  • 23. Charcot Joint Rocker bottom charcot foot
  • 24.
  • 25.  
  • 26.  

Editor's Notes

  1. Esp in tissues that do not require insulin for glucose transport, eg nerve, lens, kidneys, blood vessels.