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Lecture 10

NURSING 2LA2 Lecture Notes - Lecture 10: Glucokinase, Northern Hemisphere, Fibrinolysis

Course Code
Ruth Hannon

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Module 2: Alterations in Hormonal Regulation – Diabetes
Diabetes Mellitus Part 1
This module will cover Type 1 and Type 2 Diabetes, as well as briefly addressing
gestational diabetes. Learning about the disease of diabetes requires you to have a basic
understanding of the anatomy and physiology of the pancreas, liver, and the regular
hormonal influences on these organs. I will cover the basics of the anatomy and
physiology as it relates to diabetes mellitus. This includes glucose, fat, and protein
metabolism, pancreas, hormones of the endocrine pancreas, glucose regulating hormones,
the action of insulin on cells.
I have included some recommended readings from the School of Nursing’s
science textbooks. There is a lot of content in this module. Some of should be a review
from previous science courses and some of it will be new or add on to previous learning.
The overall aim of this module is to provide the basic science content related to diabetes
so that you are then able to apply it into clinical practice. Remember, you will have
further opportunity to discuss and apply this content in tutorial sessions and clinical
setting. Please note that there is a reference list at the PowerPoint presentation and
specific references for each slide are found in the notes section of each slide. Also, the
term diabetes will be used interchangeably with diabetes mellitus in this presentation.
Diabetes actually means the excessive excretion of urine. Diabetes mellitus refers
to the disorder of carbohydrate, fat and protein metabolism with absolute or relative
insulin deficiency. Diabetes insipidus will not be covered in this module.
Learning Outcomes
At the end of this module, you should be able to:
-Describe current Canadian trends in the prevalence diabetes mellitus
-Describe the etiology of diabetes comparing type 1 & 2 DM and gestational
-Describe glucose, fat and protein metabolism
-Identify glucose-regulating hormones and describe their function
-Describe the pathophysiology of type 1 and type 2 diabetes mellitus
-Link the pathogenesis of DM to the clinical manifestations and evaluation of the
-Provide scientific rationale for interventions
-Provide scientific rationale for patient teaching
Complication of diabetes mellitus will be very briefly discussed. The second module on
diabetes mellitus will cover in detail, the acute and chronic complications of the disease.

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Prevalence of Diabetes
According to the National Diabetes Surveillance System in Canada:
-In 2006/07 prevalence of diagnosed diabetes increased by 4% from the previous
year and 21% from 2002/03 to 2006/07
-Type 2 DM accounts for app. 90% of diabetes cases
Type 1 DM accounts for another 10% with gestational diabetes
mellitus and others making up the remaining
-2 million (1 in 16) Canadians are diagnosed with diabetes (2006/07)
-> 9 million Canadians live with diabetes or prediabetes
As future nurses, I hope that this statistic and the previous one
leads you to recognize the opportunity and need for health
education to address prediabetes
-Prevalence 6.2% (5.9% females, 6.2% males)
Aged one year and older
-Prevalence of diabetes lower in children than adults
The prevalence among children and adolescents is 0.3% while that
of the adult is 6.4%.
Among adults, the prevalence increases with age from about 2% of
adults in their 30s, peaking at 23% or 1 in 5 adults aged 75-79
years old
-Personal costs of premature death and complications
Include reduced quality of life, an increased rate of heart disease,
stroke, kidney disease, blindness, amputation, and erectile
A staggering 80% of people with diabetes will die as a result of
heart disease or stroke
Canadian adults with diabetes are twice as likely to die
Type 1 diabetic’s life expectancy may be shortened by as much as
15 yrs
Type 2 diabetic’s life expectancy may be shortened by 5-10 yrs
-Financial burden
There is tremendous personal societal financial burden to diabetes
A diabetic incurs medical cost that are 2-3 times higher than
someone without diabetes
oPersonal annual medical cost $1000 - $15 000
oDiabetes estimated to cost $16.9 billion/year by 2020
Etiology Type 1 DM
Type 1 Diabetes Mellitus is characterized into two types:
Autoimmune Type 1A
-accounts for 90-95% of T1D cases
Idiopathic Type 1B

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Autoimmune Type 1A
-In type 1A there is a autoimmune mediated specific loss of beta cells in the
pancreatic islets Langerhans
As a whole, T1D includes cases of diabetes that are primarily the
result of beta cells destruction which leads to absolute insulin
deficiency and is prone to ketoacidosis. This is believed to be the
result of genetic-environment interaction.
-Genetic-environment interaction
There is research underway looking at the genetic susceptibility to
The strongest association and most studied is the inheriting Major
histocompatibility complex (MHC) on chromosome 6
In particular, HLA-DR 3 and HLA-DR 4 is associated with an
increased risk of Type 1A diabetes, that is 20-40 times higher than
that of the general population
It should be noted that some specific human leukocyte antigens are
thought to decrease the risk of developing T1D, including HLA-
DR 2
There is also an insulin gene which regulates beta cell replication
and function on chromosome 11, which is worth mentioning
There are polymorphisms of multiple genes that have been
identified as influencing the risk of Type 1A diabetes that will not
be identified in this module
In most cases, there is likely a polygenic inheritance of T1D,
meaning that susceptible individuals have more than one genetic
Between 10-13% of individuals with newly diagnosed T1D have a
first degree relative with T1D
Identifying genes that predispose individuals to diabetes has many
advantages but also carries many ethical and legal issues
A discussion of the pros and cons of the genetic testing is beyond
the scope of this module, but definitely worth thinking about as it
becomes more and more prevalent and relevant to most clinical
practice areas
oMHC genes on chromosome 6 encode for human leukocyte antigens
oChromosome 11- insulin gene regulating beta cell replication & function
-Autoantibodies specific to beta cell destruction include: insulin autoantibodies,
islet cell autoantibodies, antibodies directed at other islet autoantigens (glutamic
acid decarboxylase-GAD & tyrosine phosphatase IA-2)
-Environmental factors: drugs & chemicals; nutritional intake; viruses
As mentioned before, environmental factors interact with genes
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