Welcome to Scribd, the world's digital library. Read, publish, and share books and documents. See more
Standard view
Full view
of .
Look up keyword
Like this
0 of .
Results for:
No results containing your search query
P. 1
Diabetic Peripheral Neuropathy: The Biopsychosocial Approach

Diabetic Peripheral Neuropathy: The Biopsychosocial Approach

Ratings: (0)|Views: 47|Likes:
An essay for the 2011 Undergraduate Awards (Lecturer Nomination) Competition by Manuela Cristea. It is nominated by Lecturer Catherine Redmond of University College Dublin in the category of Nursing & Midwifery
An essay for the 2011 Undergraduate Awards (Lecturer Nomination) Competition by Manuela Cristea. It is nominated by Lecturer Catherine Redmond of University College Dublin in the category of Nursing & Midwifery

More info:

Published by: Undergraduate Awards on Sep 01, 2012
Copyright:Attribution Non-commercial


Read on Scribd mobile: iPhone, iPad and Android.
See more
See less


AssignmentDiabetic Peripheral Neuropathy: The Biopsychosocial Approach
Diabetic peripheral neuropathy (DPN) as a long term complication of diabetes mellitus is achronic condition accounting for high morbidity as a result of nerve damage to the limbsand poor quality of life due to its overwhelming impact
on all aspects of people’s
lives.However, a dichotomous approach to care (biological/psychological) is no longer feasible,rather a complementary perspective is suggested. While there are several physiological andpsychological theories attempting to address this pathology, this essay will argue the needfor a unified approach to health care, which integrates biological processes with the humanexperience of illness, hence contends the need for a biopsychosocial model of care (Engle,1977).Diabetic peripheral neuropathy (DPN) is a microvascular complication of both type 1(66%) and 2 diabetes (59%), manifesting with increased blood sugar levels and decreasedblood flow (Sadosky et al, 2008) which consequently affect the sensory and motor nervesof the lower and upper limbs in a distal symmetrical stocking and glove fashion. It presentswith positive symptoms like loss of sensation (risk of ulcers and amputations) andproprioception (risk of falls and fractures), negative symptoms (highly debilitating pain andparesthesia), or no symptoms at all (Davies et al, 2006). Such clinical manifestations reflecteither neuronal demyelination or axonal atrophy and degeneration of the type of nerve fiberinvolved in the neuropathy: with the large ones affected first (fast conducting, longmyelinated fibers) and accounting for loss of sensation and vibration, deficient thermalperception, impaired proprioception and ataxia; while the damage to the smallunmyelinated fiber (conducive to maladaptive hyper-excitability) is responsible for painand numbness (Fazan et al, 2010).
The primary risk factors for developing DPN is hyperglycemia, while the duration of diabetes, the age and height (the longer the neuronal fiber the higher the risk), smoking,hypertension, high cholesterol levels and alcohol intake also enhance the risk (Onge, 2008).Its pathogenesis is not yet clear, but there is some evidence that oxidative stress, advancedglycated end products (AGE), activation of protein C kinase and the polyol pathway, alllinked to hyperglycemia are directly involved (Vanotti et al, 2007).Although the neuronal cells can function independent of the insulin action, the diabetesinduced hyperglycemia is damaging to the nerves as the glycosylated proteins are exposedto the action of free radicals. The excess of glucose will enter and activate the
where it will be converted in sorbitol (via aldose reductose and NADPH) andconsequently fructose (via the oxidation with NAD+ by the sorbitol dehydrogenase). Suchpathway is conducive to neuropathy as high levels of sorbitol have an osmotic effect on theneuronal cell impairing the functioning of the Na+/K+ ATPase pump on the plasmamembrane, and decreasing the levels of nitric oxide thus generating vasoconstriction andincreased vascular permeability (Kles and Vinik, 2006).Hyperglycemia also causes the formation of 
Advanced Glycated End Products
(AGEs)via glucose autooxidation and the glycation of essential proteins. Besides causing aninflammatory reaction (antibodies), AGEs alter the cell surface interactions by binding totheir receptors RAGE and consequently causing cellular malfunctions, thickening of thevessels, evident in the etiology of DPN ( Kles and Vinik, 2006). They also contribute tothe production of 
oxidative stress
. Hyperglycemia increases glycolysis and lypolysis, andas a result, this intensified cellular chemical activity- whereby sugars and other proteins

You're Reading a Free Preview

/*********** DO NOT ALTER ANYTHING BELOW THIS LINE ! ************/ var s_code=s.t();if(s_code)document.write(s_code)//-->