DIABETES MELLITUS GNUR 401 2023 GROUP.ppt

SCHOOL OF NURSING & MIDWIFERY
COLLEGE OF HEALTH SCIENCES
UNIVERSITY OF GHANA, LEGON
DR. KWADWO AMEYAW KORSAH, (PhD, MPhil,
BA, FWACN, SRN)
Department of Adult Health
1

Session Overview
This session covers brief information about the
pancreas and its major functions. A major
disorder of the pancreas, diabetes mellitus is
also discussed.
2

Outline of Presentation
• Brief information about the pancreas
• Definition of diabetes
• Types of diabetes –type 1, causes, clinical
manifestations, Diabetic Ketoacidosis (DKA)
• Type 2 diabetes mellitus – causes
• Hyperglycaemic Hyper-Osmolar Non-Ketotic
State (HONK)
• Gestational Diabetes Mellitus
3

Outline of Presentation contd.
• Other types of diabetes
• Clinical Manifestations of diabetes mellitus
• Diagnosis of Diabetes Mellitus
• Medical Management of diabetes mellitus
• Nursing management of diabetes mellitus
• Complications
• Diabetes screening
• UK model of diabetes prevention
• Somogyi Effect and Dawn Phenomenon
• Insulin Therapy and Kinetics with examples.
4

Session Objectives
At the end of the session, the student should be able to:
• Indicate the role of the pancreas in the regulation of
blood sugar.
• Describe the three major types of diabetes.
• Identify patients with clinical manifestations of diabetes
mellitus.
• Describe treatment protocols available for the treatment
of patients living with diabetes mellitus
• Identify ways to empower individuals living with diabetes
mellitus.
5

Brief information about the pancreas
Functions of the Pancreas
• The pancreas is involved in blood sugar
control and metabolism within the body, and
also in the secretion of substances which help
digestion.
6

Brief information about the pancreas
contd.
• Basically, the roles are divided into (1)
endocrine role, associated with the secretion
of insulin and other hormones within
pancreatic islets and helping control blood
sugar levels and metabolism within the body,
and (2) an exocrine role, about the secretion
of enzymes involved in digestion of substances
such as trypson and chymotrypson to digest
protein, amylase for digestion of
carbohydrates, and lipase to break down fats 7

Brief information about the pancreas contd.
Primary hormones secreted by the pancreas
include:
• Glucagon (secreted by alpha cells): Glucagon
helps maintain normal blood glucose by working
in the opposite way of insulin. It stimulates the
cells to release glucose, and this raises the blood
glucose level (Young, 2006). In simple terms alpha
cells produce the hormone glucagon, which raises
blood glucose.
11

• Insulin (secreted by beta cells): This hormone
regulates blood glucose level by allowing
many of the body’s cells to absorb and use
glucose. It implies that beta cells produce the
hormone insulin, which lowers blood glucose
levels.
• In turn, this maintains blood glucose levels
(Hall, 2011).
12

• Somatostatin (secreted by delta cells): When
levels of other pancreatic hormones, such as
insulin and glucagon, get too high,
somatostatin is secreted to maintain a balance
of glucose and/or salt in the blood (Young,
2006).
• In other words, somatostatin inhibits the
secretion of pancreatic hormones, including
glucagon and insulin.
13

14
Diabetes Mellitus (DM)
Diabetes Mellitus (DM) is a long-lasting and
incapacitating illness associated with raised
blood sugar levels in affected individuals.
Hyperglycaemia results from disturbances
related to carbohydrate, protein and fat
metabolism due to malfunctioning of the
pancreas in terms of insulin secretion, insulin
action or the two together (Melmed et al.,
2011).

Diabetes Mellitus (DM) contd.
• It causes variations/changes in metabolism of
carbohydrates, proteins as well as fats. When
insulin is discharged by the pancreas, the body
is able to regulate how and when fats,
proteins and carbohydrates are metabolized.
15

16
The subsequent deficiency of insulin leads to
increased blood and urine glucose.
The body’s central source of energy are
carbohydrates. Carbohydrates are
transformed/changed into glucose and
provide the required nutrients for the body
when they are processed or digested.

17
• Insulin is discharged uninterruptedly by the
pancreas according to the body’s
requirements (Melmed et al., 2011).

18
Grouping of Diabetes Mellitus:
• Diabetes mellitus type 1 (T1D or type 1
diabetes) is a form of diabetes mellitus that
results from the autoimmune destruction of
the insulin-producing beta cells in the
pancreas (Longo et al., 2012).
• Formerly it was known as Insulin-Dependent
Diabetes Mellitus (IDDM) or Juvenile Diabetes
(JD).

Type 1 Diabetes contd.
• A number of explanatory theories have been
put forward, and the cause may be one or
more of the following: genetics or viruses or
autoimmune response (single-handedly or
blend of these factors).
• Another theory also postulates that the cause
of type 1 diabetes is unknown.
• Other causative factors include chemicals and
drugs (Longo et al., 2012).
19

• Globally, about 5-10% of people with diabetes
have type 1 DM. It was projected/estimated
that about 80,000 children develop the
disease each year (Chiang, Kirkman, Laffel and
Peters, 2014).
20

• Most people with this type are diagnosed
before the age 30 (Chiang, Kirkman, Laffel and
Peters, 2014). In the affected individuals
there is inadequate supply of insulin in this
type, so patients require exogenous/external
source of insulin.
21

23
Causes of type 1 diabetes mellitus
• Autoimmune destruction of the insulin-
producing beta cells:
• The disease process in diabetes type 1 is a
destruction of beta cells in the pancreas,
regardless of which risk factors or causative
entities have been present, in which the
immune system attacks the insulin-secreting
cells of the pancreas (Longo et al., 2012) .

• Type 1 diabetes results from the destruction
of the beta cells in the islets of Langerhans in
the pancreas. This destruction usually results
from immunological defect that produces
antibodies against the beta cells (Chiang,
Kirkman, Laffel and Peters, 2014) .
• These antibodies may be present for months
or years before clinical symptoms of diabetes
develop in the affected person.
24

25
• Genetic predisposition/causes of diabetes
mellitus type 1:
• Type 1 diabetes is a disease that implicates
many genes. Over 50 genes are linked to type
1 diabetes (Bluestone, Herold and Eisenbarth,
2010).
• For example, research with the Human Leukocyte
Antigen (HLA) System that is used in tissue typing has
demonstrated a relationship with some HLA antigens
and diabetes.

***A tissue type test (may also be called HLA
typing) is a blood test that identifies substances
called antigens on the surface of body cells and
tissues. Examining the antigens helps to find if
donor tissue is safe (compactible) for transplant
to another person. Based on the antigens, the
immune system can tell the difference between
normal body tissue and foreign tissue (for
example, tissue from another person's body).
26

• Some of these antigens are reliably found in
patients with insulin-dependent diabetes
mellitus (type 1 diabetics). Typical examples
are D,A,Q & B genes (Bluestone, Herold and
Eisenbarth, 2010).
27

28
• Similarly, selected researchers have also
observed a relationship between various HLA
antigens and persons with long term
complications of diabetes (Bluestone, Herold
and Eisenbarth, 2010).
• However, not all persons with these antigens
develop diabetes mellitus type 1.
• This limitation renders this theory futile or
pointless.

29
• The viral theory:
• One theory proposes that type 1 diabetes is a
virus-triggered autoimmune response in
which the immune system attacks virus-
infected cells along with the beta cells in the
pancreas (National Institute of Health, 2013).

• The virus (environmental factor) is believed to act to
trigger the autoimmune response. It is also believed
that the genetic make up of cells in an individual
probably determines whether the virus can attach
itself to the cell surface, enter the cell, and change its
metabolism.
• This certainty/belief has been traced to HLA
genotypes, though the connection between them
and the triggering of an autoimmune reaction
remains poorly understood (National Institute of
Health, 2013).
30

31
• The characteristically abrupt appearance of
insulin-dependent diabetes (type 1) could be
the result of an infection with a diabetogenic
virus in a person already genetically
predisposed. And that the infection might
cause an autoimmune reaction (antigen-
antibody reaction).

32
• In order for type 1 to develop, at least 90% of
the individual’s beta cells must stop producing
insulin. This could result from one very potent
viral attack or it could be the result of a series
of viral infections that eventually destroy the
beta cells (National Institute of Health, 2013).

33
• Antibodies against one of the suspected
viruses (Coxsackie B4) have been found in the
blood of patients newly diagnosed with
insulin-dependent diabetes and not in Non-
Insulin Dependent Diabetics.
• Similarly, rubella is also implicated, even
though the evidence is
inconclusive/questionable.

34
Evidence/Proof: Evidence that suggests a viral
cause for Insulin-Dependent Diabetes (type
1) include the following:
1. It usually occurs in young people whose
systems are more prone to viral infections.
2. It occurs suddenly, like viral infection
3. It usually occurs when viral infections are
prevalent.

35
4. Beta cells are inflamed early in the viral
infection.
5. A viral infection may develop before the
diabetes develops (from health history of the
patient).
6. It may develop in a child with no family
history of diabetes mellitus.
(National Institute of Health, 2013)

• As noted already the Coxsackie virus, family or
rubella is implicated, although the evidence is
inconclusive.
• This vulnerability/susceptibility is not shared
by everyone, because it is not every person
infected by the suspected virus who develops
type 1 diabetes.
36

• Chemicals and drugs
• Some chemicals and drugs destroy pancreatic
cells.
• For example, Pyrinuron (Vacor), a rodenticide
(for rodent control [pale yellow crystalline
solid, odourless]) made known in the United
States in 1976, particularly destroys pancreatic
beta cells, resulting in type 1 following its
ingestion by humans.
37

• If it is ingested by humans in high doses, it may
selectively destroy insulin-producing beta cells in
the pancreas and cause type 1 diabetes (Vogel,
1982).
• May also cause death resulting from
cardiovascular and respiratory failures and central
nervous system dysfunction. Human survivors
gradually develop an insulin-deficient, ketosis-
prone form of diabetes millitus (EPA, 1998).
38

• It was withdrawn from the U.S. market in 1979
but is still used in some countries.
• Similarly, Streptozotocin (Zanosar), an
antibiotic and antineoplastic agent employed
in chemotherapy for the treatment and
management of pancreatic cancer, destroys
beta cells, resulting in loss of insulin
production (EPA, 1998).
39

40
Family History of T1DM
• Although the exact mechanism of how other
people get the condition in families is not well
understood, blood relatives of known patients
with diabetes need to maintain life-long vigilance
for this condition. Obese persons and mothers
who have delivered large babies are also
susceptible. These high risk individuals should be
examined regularly for signs of diabetes.

• Reading Assignment: Some books also employ lay
perspectives to explain causes of chronic conditions
such as DM I & II by using (1) naturalistic, (2)
personalistic, and (3) emotionalistic disease causal
theories. So far we have focused our attention on
naturalistic model of disease causation, nevertheless
you should consider reading the other 2 models of
illness causality by Kottak (2014) in order to offer
appropriate care to people with varied cultural and
ethnic backgrounds who get diabetes.
41

42
Type 1 Diabetes Mellitus (DM) contd.
Clinical Manifestations:
When diagnosed individuals have four cardinal
clinical manifestations:
1. Weight loss and muscular wasting due to
breakdown of protein and lipids
(catabolism).

43
2. Frequent urination (polyuria) because glucose
attracts water and an osmotic diuresis occurs.
This polyuria results in the loss of water and
electrolytes, particularly Na, Cl, K and
Phosphate.

44
3. Excessive thirst (polydpsia). The loss of water
and sodium results in thirst and increases fluid
intake.
4. Eat excessively (polyphagia). Extreme hunger
and increased food intake are triggered as the
cells become starved of their fuel.

45
Clinical Manifestations of type 1 DM
contd.
In addition:
1. It usually begins in childhood but may also
occur at any age.
2. Measurable circulating insulin may still be
present early in the course of the disease,
but it soon disappears
3. As insulin production decreases,
hyperglycemia develops as a result of the
body’s inability to use glucose

46
Clinical Manifestations of type 1 DM
contd.
4. If the concentration of glucose in the blood is
sufficiently high, the kidney may not reabsorb all of
the filtered glucose; the glucose then may appear in
urine (Glucosuria).
Fluid loss through the kidneys result as the kidneys
work to excrete the increased load of glucose,
producing loss of water, Na, magnesium, calcium,
potassium chloride, and phosphate.
(Longo et al., 2012)

47
Summary (type 1 DM)
It may develop through:
1. Active autoimmunity
2. Genetic Predisposition
3. Viral factor/Environmental trigger
4. Chemical or drug factor
5. There is progressive beta dysfunction
6. Overt diabetes mellitus

48
Diabetic Ketoacidosis (DKA)
When there is deficiency of insulin, muscles
cannot utilize glucose. Free fatty acids are
then mobilized from the adipose tissue cells
and broken down by the liver into ketone
bodies for energy (Melmed et al., 2011). In
other words, there is a severe lack of insulin.
For this reason the blood glucose, although
very high, can not be utilized for energy
production. Fat is broken down instead,
producing toxic chemicals called ketones.

Diabetic Ketoacidosis (DKA) contd.
(Ketones are end-products of fat metabolism in
the body. That is, they are formed when fat is
burned for energy by the muscles. Chemically,
they are strong acids known as ketone bodies
which are very dangerous to organs of the body
(Melmed et al., 2011). For example, the brain.
49

50
Ketoacidosis is therefore characterized by
excessive ketone bodies in the blood. Patients
with ketoacidosis exhibit loss of Na, kcl, and
water from the body. The net metabolic result
of acute, uncontrolled diabetes mellitus is loss
of fat stores, cellular protein, electrolytes and
water. There is severe dehydration and
electrolyte imbalance (Longo et al., 2012).

51
Often the diagnosis of DM is first made when the
patient is brought to the hospital in coma state
due to Ketoacidosis. Diabetic ketoacidosis is the
commonest cause of death among patients with
diabetes in Ghana. It is common in newly
diagnosed diabetics, example children, young
adults and other Type 1 diabetes patients.
What factors may contribute to DKA among these
patients?

Causes:
1. Previously undiagnosed diabetes
2. Interruption of insulin therapy (usually for
financial reasons or for alternative
treatment)
3. Stress of intercurrent illness (e.g. infection,
myocardial infarction, stroke etc.)
4. Other factors including “Healer Shopping”

Clinical Manifestations:
• Passing excess urine
• Dehydration with dry skin, reduced skin
turgor or sunken eyes
• Drinking excess amounts of water
• Relatives may report changes in sensorium
• etc.

Investigations:
• Blood glucose is usually greater than
18mmol/L.
• Urine glucose is usually more than 3+
• Urine ketones (usually higher than 2+).
• Blood urea and electrolytes (usually low,
however if in renal failure urea and
potassium are high)
• Other test may be ordered.

Management of Diabetic Ketoacidosis
(DKA)
• Bed rest/Admission of patient
• Administration of IVF with fast acting insulin (soluble
regular insulin) Normal Saline/Dextrose
Saline/5%Dextrose Water?? etc.
• Liberal oral fluids (water if patient can drink)
• Intake and Output Monitoring
• Monitoring of blood glucose levels (sliding scale)
• Monitoring of urine ketones
• General observation of the patient
• Etc.
55

56
Complications
Over a period of years, blood glucose levels that
are consistently above normal appear to cause
complications that affect the large vessels in
the brain, heart, kidneys and extremities and
small vessels in the eyes, kidneys and nerves
(Beare and Myers, 2003).

Read on:
Pancreas transplantation: In some persons,
pancreas transplant may restore proper glucose
regulation. Nevertheless, the surgery involved
may be more costly and risky than continued
insulin replacement therapy (Lakey et al., 2003).
57

Read on:
Islet cell transplantation: Islet cell
transplantation may be a choice for some
people with type 1 diabetes that are not well
controlled with insulin. Difficulties include
finding donors that are a compactible, getting
the new islets to survive, and the side effects
from the medications used to prevent rejection
(Lakey et al., 2003).
58

59
2. Type 2 Diabetes (Non-Insulin-Dependent
Diabetes Mellitus). Diabetes mellitus type 2 is
a long term metabolic disorder that is
characterized by high blood sugar, insulin
resistance, and relative lack of insulin (Beare
and Myers, 2003).

• The development of type 2 diabetes is caused
by a combination of lifestyle and genetic
factors (Beare and Myers, 2003).
• Some of these factors are under personal
control, such as diet and obesity, other factors
are not, such as increasing age and genetics.
60

• In type 2 DM, genetics and obesity play a
more significant role. The exact role that
heredity and obesity play is not yet completely
understood, though they contribute. There is
apparently no relationship between viruses
and the etiology of NIDDM.
61

Lifestyle causes of diabetes mellitus type 2:
A number of lifestyle factors are known to be
important to the development of type 2
diabetes, including:
• obesity and being overweight
• lack of physical activity
• poor diet
• Urbanization (Beare and Myers, 2003).
62

• Dietary factors influence the risk of developing
type 2 diabetes.
• Consumption of sugar-sweetened drinks in
excess is associated with an increased risk.
• The type of fats in the diet are also important,
with saturated fats increasing the risk.
63

• Eating lots of white rice appear to also play a
role in increasing risk.
• A lack of exercise is believed to cause 7% of
cases.
64

Genetic causes of diabetes mellitus type 2:
• Most cases of diabetes involve many genes, with
each being a small contributor to an increased
probability of becoming a type 2 diabetic.
• For example, if one identical twin has diabetes, the
chance of the other developing diabetes within his
lifetime is greater than 90%, while the rate for non-
identical siblings is 25–50% (Merck’s Medical
Manual, 2002).
65

Medical conditions and drugs that can predispose
persons to T2DM.
• There are a number of medications and other
health problems that can predispose to diabetes.
Some of the medications include: glucocorticoids,
cortisol, prednisolone, etc. Those who have
previously had gestational diabetes are at a
higher risk of developing type 2 diabetes (Merck’s
Medical Manual, 2002.
66

• Other health problems that are associated
include: Cushing's syndrome etc (Beare and
Myers, 2003).
67

68
Basically, type 2 DM results from a decrease in
the amount of insulin produced or an
insensitivity of the cell to insulin. About 90-
95% of people with diabetes have type 2.
Individuals have onset after age 40 years.
Classic symptoms are not present when first
diagnosed (Beare and Myers, 2003).

69
In some Non-Insulin Dependent Diabetes
persons, insulin secretion is increased,
resulting in higher circulating insulin levels.
Although excessive insulin is present, it is not
utilized because of an inadequate number of
insulin receptors present in cells.

71
This mechanism has been observed in obese
non-insulin dependent patients. With weight
loss the number of insulin receptors on the
cells increase, thereby allowing glucose to
enter the cell. This may result in return of a
normal glucose utilization (Merck’s Medical
Manual, 2002).

72
Diabetes Mellitus type 2 contd.
Although the symptomatology of type 2
diabetes is less obvious than that of type 1,
this classification of diabetes is accompanied
by vascular and neuropathic complications.

73
DM type 2 contd.
Typically, they are not absolutely dependent on
exogenous insulin for survival, although
insulin therapy is often employed to lower
their blood glucose levels. **Note that being
treated with insulin supplements does not
change the classification of Type 2 to Type 1
(NIDDM to IDDM)** (Standard Treatment
Guideline for Ghana, 2010).

DM type 2 contd.
• Insulin therapy may be required temporarily in
Type 2 patients during severe stress e.g.
severe infections, acute myocardial infarction,
surgical operations, trauma, hyperosmolar
state.
74

75
DM type 2 contd.
In practice:
1. These patients may not require insulin and
are usually managed adequately with
exercises and diet alone.
2. The majority (about 80%) of patients with
NIDDM are overweight when the condition
is first diagnosed unless due to one or two
reasons the diagnosis is delayed.

76
DM type 2 contd.
3. Symptoms may be so minor that the disease
is undetected for many years (Develops
slowly/Insidious).
4. Diagnosis may be suspected as a result of a
routine urinalysis or during presentation of
another condition like HPT/screening.

• 5. Frequently the disease is discovered when
the patient seeks health care treatment of
complications such as deteriorating vision,
pain in legs or impotence or reduction in
feeling for sex.
• 6. Often blood glucose tests are normal, with
hyperglycemia being seen only in postprandial
(following a meal).
(Standard Treatment Guideline for Ghana, 2010)
77

78
DM type 2 contd.
7. Onset is insidious/sneaky and may take years
to develop.
Other warning symptoms of type 2 DM are:
Fatigue, itching of the skin (of the vulva in
females), skin wounds that heal poorly,
cramps in the muscle, blurring of vision etc.

• Individuals with type 2 diabetes mellitus may
present with hyperosmolar hyperglycemic
state (a condition of very high blood sugar
level associated with/without decreased level
of consciousness and low blood pressure).
• The blood pressure may however be high in
an already a hypertensive patient.
(Longo et al., 2012).
79

DM type 2 contd.
Hyperglycaemic Hyper-Osmolar Non-Ketotic State
(HONK)/Hyperosmolar Hyperglycaemic State.
Coma (HONK) is a dangerous condition brought
on by very high blood glucose levels in type 2
diabetes (e.g. above 33 mmol/L).
• The condition of very high blood glucose without
signs of ketosis may also be called Hyperosmolar
Hyperglycaemic State.
80

DM type 2 contd.
Coma is a short term complication requiring
immediate treatment by a healthcare
professional (Standard Treatment Guideline
for Ghana, 2010).
81

DM type 2 contd.
Clinical manifestations of HONK
• Before loss of consciousness and coma takes
place, patients may show signs of very high blood
sugar levels with associated manifestations which
may include:
• Extreme thirst
• Frequent need to urinate
• Disorientation
• Nausea
82

DM type 2 contd.
Causes of HONK
• May be due to undiagnosed type 2 diabetes
that has been developing over a number of
years.
• On the other hand, HONK may be brought
about by not taking diabetic medication or
• Due to very high blood glucose levels resulting
from long period of illness.
83

DM type 2 contd.
Treatment for HONK
• Treatment for hyperglycaemic hyperosmolar non-
ketotic coma will include fluids being given to the
patient and insulin administered intravenously
(Standard Treatment Guideline for Ghana, 2010;
Beare and Mters, 2003).Similar to the management
of DKA
Differentiate between Hyper-Osmolar Non-Ketotic
State and Diabetic Ketoacidosis.
84

DM type 2 contd.
• Hyperglycaemic hyperosmolar non-ketotic
state results from very high blood glucose
levels in a patient with normal ketone levels.
• If very high blood glucose levels are combined
with high ketone levels, the state is likely to be
ketoacidosis.
85

Gestational Diabetes Mellitus
3. Gestational Diabetes Mellitus (GDM) also called
Pregnancy Induced Diabetes. GDM applies only to
women in whom glucose intolerance develops or
discovered during pregnancy. After pregnancy
diagnostic classification may be changed to IDDM or
NIDDM. Women who had the disease before the
pregnancy are not included in this classification.
Women with GDM have an increased future risk for
progression to NIDDM or rarely IDDM (Beare and Myers,
2003).
88

Gestational Diabetes Mellitus contd.
What are the possible causes of GDM?
• Women without previously diagnosed
diabetes exhibit high blood glucose (blood
sugar) levels during pregnancy (especially
during their third trimester). Gestational
diabetes is caused by improper insulin
responses.
89

Pregnancy and Diabetes Development
Pregnancy is diabetogenic due to increased
production of insulin antagonists such as
human placental lactogen, placental insulinase,
cortisol, oestrogens and progesterone.
Insulin requirements increases during pregnancy
due to increased production of insulin
antagonists while it decreases postpartum
90

Risk factors of GDM
• Classic risk factors for developing gestational
diabetes are:
• A previous diagnosis of gestational
diabetes/Pregnancy Induced Diabetes or pre-
diabetes
• A family history showing a first-degree relative
with type 2 diabetes.
92

• Maternal age – a woman's risk factor
increases as she gets older (especially for
women over 35 years of age).
• Ethnicity (those with higher risk factors
include African-Americans, Afro-Caribbeans,
and people originating from South Asia region
• Being overweight, obese or severely obese
increases the risk T2DM.
93

• Management of GDM (Lifestyle)
• Assessment and Counseling before pregnancy
and multidisciplinary management are
important for good pregnancy outcomes.
• Since insulin resistance is highest in mornings,
breakfast carbohydrates need to be restricted more.
Intake of more fiber in foods with whole grains, or
fruit and vegetables can also reduce the risk of
gestational diabetes.
94

• Regular moderately intense physical exercise
is advised, although there is no consensus on
the specific structure of exercise programs for
GDM.
• However, this should be done with
caution/care.
(Chiang, Kirkman, Laffel and Peters, 2014).
95

Other types of Diabetes
Other types of Diabetes include:
1. Impaired Glucose Tolerance (IGT) is the term
used to describe fasting glucose levels
between 120 and 200 mg/dl. The term IGT
replaces borderline diabetes.
(Beare and Myers, 2003)
96

Other types of Diabetes contd.
2. Secondary DM as a result of other disorders.
Causes include pancreatic disorders like
pancreatitis and pancreatectomy etc. Therapy is
similar to that of treating diabetes using
modalities of meal planning, exercises and
medication and also looking at the underlying
cause. Read on other types such as drug
induced DM etc.
97

General Clinical Manifestations
As already noted in type 1 DM:
When diagnosed individuals have four cardinal
clinical manifestations:
1. Weight loss and muscular wasting due to
breakdown of protein and lipids
(catabolism).
98

Clinical manifestations contd.
2. Frequent urination (polyuria) because glucose
attracts water and an osmotic diuresis occurs.
This polyuria results in the loss of water and
electrolytes, particularly Na, Cl, K and
Phosphate.
99

Clinical manifestations contd.
3. Excessive thirst (polydpsia). The loss of water
and sodium results in thirst and increases fluid
intake.
4. Eat excessively (polyphagia). Extreme hunger
and increased food intake are triggered as the
cells become starved of their fuel.
100

If the concentration of glucose in the blood is
sufficiently high, the kidney may not reabsorb all of
the filtered glucose; the glucose then may appear in
urine (Glucosuria).
Fluid loss through the kidneys results as the kidneys
work to excrete the increased load of glucose,
producing loss of water, Na, magnesium, calcium,
potassium chloride, and phosphate.
(Longo et al., 2012)
101

102
Diagnosis of Diabetes
1. Based on classic clinical manifestations which are:
Polyuria, polydipsia, polyphagia, rapid weight loss.
2. Elevated Fasting Blood Glucose on more than one
occasion (above 5.5mmol/L). The presence of
abnormally high blood glucose levels is the
criterion on which the diagnosis of diabetes should
be based. Blood glucose levels elevated above
(5.5mmol/L or more, more than one occasion
suggest a diagnosis of diabetes.

Diagnosis of Diabetes contd.
• Normal value ranges may differ slightly
among different laboratories due to different
test devices. The normal blood glucose level
(tested while fasting) should be between 3.9
and 5.5 mmol/L (70 to 100 mg/dL). The mean
normal blood glucose level in humans is
about 5.5 mmol/L (100 mg/dL).
103

104
3. If fasting glucose levels are normal or nearly
normal, the diagnosis must be based on
Glucose Tolerance Test (Gold Standard
Method). Glucose Tolerance Test: Oral Glucose
Tolerance Test
(Standard Treatment Guideline for Ghana,
2010).

Eg. Two hour glucose tolerance test after
ingesting the standardized 75 Gm glucose
solution, the blood sugar level is then checked
again.
1. Blood glucose is checked before the test.
2. Glucose is administered and blood sugar level
rechecked exactly after two hours.
105

4. Glycosylated Hemoglobin or
Glycated Hemoglobin - HbA1c or A1c test is
used as a guide to know what is the average
blood glucose level during the past 2 or 3
months/usually 3 months. Glucose tends to
stick to red blood cells and more the glucose
in the blood, the more the number of red cells
that have glucose on its surface.
106

Normally 4 to 6 red cells in 100 have glucose
attached to its surface; hence the range of
HbA1c in a normal person is 4 to 6%. Better
control of glucose means lesser the
complications of diabetes to the heart, blood
vessels, kidneys, brain, nerves, eyes and feet
etc. (Chiang, Kirkman, Laffel and Peters, 2014).
107

• HbA1c has the advantages that fasting is not
required and results are more stable but the
disadvantage is that the test is more costly
and takes some time before the result is
available.
• HbA1c may be useful to diagnose individuals
in whom the clinical manifestations are not
clear and straight forward to support decision
making for diagnosis.
108

110
5. Urine Tests: Urine tests should not be used
because both false-negative and false-positive
results occur. Renal glucosuria occurs when
the renal threshold for glucose is decreased
(LeMone and Burke, 1996).

111
In this instance, glucose appears in the urine
despite normal blood glucose values. In the
elderly, renal threshold levels are higher than
normal, so no glucose is found in the urine
despite elevated blood glucose values/levels.

SOME BASIC INVESTIGATIONS UPON
DIAGNOSIS
The following investigations are important for
each patient upon diagnosis to serve as a
reference point.
• ECG/Chest X-Ray/Scan of the Heart
• Renal Function Test (Kidney Function Test)
• Liver Function Tests (LFTs)
• Eye Tests including Scan of the Eye
• Others

Management of DM
Therapeutic objectives:
The objectives of long-term diabetes
treatment are to:
1. Relieve symptoms and maintain fasting (4 –
6mmol/L) and 2-hourly post meal (4 –
8mmol/L) blood glucose levels within the
normal limits.

Management of DM contd.
2. Prevent acute diabetes complications such as
hypoglycaemia, ketoacidosis state, HONK etc.
3. Prevent the chronic complications of diabetes,
namely; blindness, limb amputation, kidney
disease, nerve damage, hypertensive heart
disease etc.
2010).

Other therapeutic objectives are:
• To achieve a Glycated haemoglobin 6.5 % or
less
• To ensure weight reduction in overweight and
obese individuals
• To maintain blood pressure less than 130/80
mmHg in patients with diabetes and
• To maintain cholesterol level at less than 2.5
mmol/L (Beare and Myers, 2003).
115

These objectives may be achieved by strict
blood glucose control and regular screening
for diabetes complications. Regular follow-up
of all individuals with diabetes is therefore
important to assess their metabolic control.

Practically, these objectives may be achieved
based on the following components of
management:
1. Diet
2. Exercise
3. Medication
4. Monitoring
5. Education
6. Other factors
117

118
Achievement and maintenance of metabolic control
requires the judicious use of:
1. Medication
A. Insulin and
Oral medications:
B. Biguanides e.g. Metformin Hydrochloride 500mg-1g
12 hourly with, or soon after meals. Metformin
decreases insulin resistance and increases insulin
sensitization.
(Standard Treatment Guideline for Ghana, 2010).

C. Sulphonylureas: All sulphonylureas are of equal
potency and efficacy. The recommended total
daily doses for the commonly available ones are –
1. Tolbutamide, oral, 250mg-1g, 8-12 hourly.
2. Gliclazide, oral, 40-160mg 12 hourly
3. Glibenclamide, 2.5-10mg as a single dose in the
morning (if required, not more than 5mg could
additionally be given in the evening, maximum
total dose 15mg per day.

• Sulphonylureas are best taken with meals.
Tolbutamide and Gliclazide are short-acting
and are preferred in the elderly and those
with mild kidney disease.
• In general sulphonylureas should be avoided
in all patients with liver disease and used
with care in kidney disease.

D. Thiazolidinediones are additional oral
medications which may be used either alone
or in combination with metformin or a
sulphonylurea in type 2 diabetics.

• Examples of Available Thiazolidinediones
are:
• Pioglitazone, oral, 15-45 mg, as single daily
dose
• Or
• Rosiglitazone, oral, 4-8 mg, as single daily dose
2010).
122

• E. Combined Oral Therapy: Individuals with
Type 2 diabetes not responding to maximum
tolerable doses of a sulphonylurea, metformin
or a thiazolidinedione alone, could be given
combined oral therapy with two or three oral
anti-diabetic medications. However, two
different products from the same group (e.g.
Two sulphonylureas) should never be used
together.
123

For Oral Hypoglycaemic Medications:
Note
• Patients, who usually have Type 2 diabetes,
exercise and diet alone should be tried first.
When diet and exercise fail to achieve
satisfactory control within 3 months, non-
obese patients are preferably, but not
compulsorily or exclusively, be treated with a
sulphonylurea, and obese patients with
metformin.
124

• Avoid metformin and long-acting oral anti-
diabetic drugs, such as Glibenclamide in the
individuals with poor kidney and liver
functions.
• Oral anti-diabetic drugs should be avoided in
Type 1 patients and should not be used
during pregnancy and breast-feeding.

• Insulin is always indicated in a patient who
has been in ketoacidosis, and in most young
patients who usually have type 1 diabetes.
• Insulin is also indicated in older or Type 2
patients when oral anti-diabetic drugs cease
to be effective and in all pregnant and breast-
feeding women.

• The starting dose of any long-term treatment
for diabetes must initially be low, with
increments in the dose over several days or
weeks according to results of blood glucose
testing.
• Hypoglycaemia is a potential side-effect with
most of the anti-diabetic drugs, so patient
should be observed closely. (Read on
Hypoglycaemia).

Some newer medications:
Tab Galvus Met: This is a combination of
Metformin and Vildagliptin
Metformin belongs to Biguanide and
Vildagliptin belongs to class of medicines
known as islet enhancers. E.g 50 mg
Vildagliptin and 500 mg of Metformin.
Forxiga (Dapaglifloxin) is also used as daily dosage to
manage type 2 DM- belongs to sodium-glucose
cotransporter 2 inhibitor

2. Non-pharmacological treatment (Standard
Treatment Guideline for Ghana, 2010). All
patients with diabetes require diet therapy.
Diet (Meal Plan)-Breakfast, Lunch,
(**Afternoon Snack**), Supper, Bed time.
All patients with diabetes require diet
therapy. All patients and close relations who
cook or control their meals must be referred
to a dietician or diet nurse for individualized
meal plans.

• In practice, patients must avoid ‘free’ or
refined sugars, such as soft drinks, or adding
sugar to their beverages. ‘Diet’ soft drinks,
which contain a sweetener and not glucose,
may however be used but care must always
be taken as we may have false nutritional
information these days.
• Diet must be selected.

They should not eat plenty at one point in
time. We should encourage enough fibre
intake. Some healthcare professionals advice
patients to eat only one diet etc. This practice
is improper and must be discouraged.

• Carbohydrates (60%), protein (15%) and fat
(25%) mostly of plant-origin and low in animal
fat. (Moderate consumption of……)
• Increase in the amount of fibre e.g.
vegetables, fruits and cereals.
132

GLYCAEMIC INDEX (GI) AND GLYCAEMIC LOAD (GL): (read on
these, get examples)
• A food with a high GI raises blood sugar more
than a food with a medium to low GI. But the
glycemic index does not take into account the
amount of carbohydrate in a food. So
glycemic load is a better indicator of how a
carbohydrate food will affect blood sugar.
(read on these, get examples)
133

134
3. Exercise (Activity):
• Is good for both type 1&2 DM.
• Diet and exercise may be used to control
blood glucose levels in individuals with type
2 DM but when the response to these
measures is inadequate, oral agents are
tried.

• Regular, simple exercise (e.g. walking 1 hour
daily) is helpful in ensuring good glucose
control. All advice on exercise must give
consideration to the patient’s age and the
presence of complications and co-morbid
conditions.
• Regular, simple exercise e.g. 30 minutes brisk
walking at least 3 days a week in ambulant
patients.

136
Activity contd.
Exercise is an important part of the medical
management and deserves careful and
thorough explanation before implementation.
Activity is a wonderful insulin sensitizer,
enhancing glucose uptake into skeletal
muscle. The exact mechanism is unknown but
it occurs in both type 1 and type 2 DM.

137
Activity contd.
Benefits of Exercises
1. Improve insulin sensitivity
2. Lowers blood glucose
3. Assists with weight loss
4. Preserve with cardiovascular fitness
5. Improves sense of wellbeing and leads to.
6. High Quality of Life (HQoL)
(LeMone and Burke, 1996)

138
Activity contd.
For effective activity/exercise in the
management of Diabetes Mellitus consider:
• Frequency (F)
• Intensity (I)
• Time (T)
Risk of exercise is hypoglycemia which is a
diabetes emergency. (Read on this please)

139
Monitoring
4. Monitoring: For example monitoring blood
glucose levels using sliding scale:

140
Sliding Scale contd.
Blood Glucose less than 6mmol/L= Urine Glucose Negative=
Blue colour = No insulin ( in adults)= No insulin (in
children)
6.1-9.0mmol/L=1+= Green = 4units= 0.06 units/kg
9.1-12mmo/L=2+= Yellow = 6units=0.09units/kg
12.1-15mmol/L= 3+= Brown = 8units=0.12units/kg
15.1-18mmol/L=4+= Brick Red =10Units=0.15/kg
In this instance monitor blood or (**urine**) glucose 4
hourly and give the corresponding amount of insulin as
ordered by the doctor. Insulin therapy and kinetics is
fully discussed at the end with examples.

141
Monitoring contd.
i. Self monitoring (Use of symptoms as a guide
for self monitoring.
ii. Use of diary to record date, time and
monitoring results by the use of glucometers
and test strips.

142
Monitoring contd.
iii. Other diary notations may include
medications, food intake, activity levels, and
illness so that the person can begin to see the
relationship between blood glucose or urine
ketones and treatment regimen.
As patients gain flexibility and self
determination, they may manipulate insulin,
diet, and exercise independently on the basis
of monitoring results.

143
Monitoring contd.
iv. Tell patient the importance of performing a
home blood glucose test to correlate a
subjective symptom.

144
5. Education – meal plan to control weight,
glucose, and lipids composition of diet,
reading nutritional labels, monitoring and use
of results, performing test accurately,
interpreting test results, behavioral change
strategies, risk factor reduction (Beare and
Myers, 2003).

145
Exercises and activity- benefits and risk,
preparing for exercises, medication- goal of
treatment, injection techniques, complications
of treatment: hypoglycemia etc.
So by its nature, diabetes can be significantly
influenced by each of these management
components.

Questions
• Achievement and maintenance of metabolic
control in DM requires the judicious use of
Medication, Diet, Monitoring, Exercise and
Education. Discuss
• Effective use of standardized protocol for the
management of DM is a predictor of a better
Glycated Haemoglobin level (HbA1c or A1c).
Discuss
146

• Part of the Answer Q. 2 For people without
diabetes, the normal range for the
haemoglobin A1c test is between 4% and 6%.
Because studies have repeatedly shown that
out-of-control of diabetes results in
complications from the disease, the goal for
people with diabetes is an hemoglobin
A1c less than 7%. The higher the hemoglobin
A1c, the higher the risks of developing
complications related to diabetes.
147

148
Nursing Management of DM
1. Myths about the disease must be dispelled
through education: This determines direction
of education that must be given.
2. Health History- Psychosocial/emotional status
(perception of the meaning of the diagnosis,
how it affects the patient’s life and future
plans, day to day activities, coping
mechanisms that are employed by the person:
How do they affect glycemic control?

149
Nursing Management of DM contd.
3. Physical Examination
4. Patient Education- Insulin self administration,
family involvement and social support,
diabetes as a family challenge, stress and
psychological adjustment, adaptation to living
with a chronic disease, foot, skin, and dental
care: daily self care measures: the need for
regular evaluation of feet and teeth

150
Nursing Management of DM contd.
Use of health care systems and community
resources: planned follow ups, emergency
care: patient tag, planning for travel, patient’s
responsibility: name and telephone numbers
of her/his nurse, avoid group eating etc.
5. Promoting Adequate Nutrition
6. Managing Medications
7. Decreasing fear

151
Complications of DM
Complications of diabetes are associated with
the development of microvascular and
macrovascular diseases.
Microvascular disease is a disease of small blood
vessels, capillaries and precapillaries
arterioles.
Macrovascular disease is a large vessel disease.

152
Complications of DM contd.
Generally, microvascular diseases predominate
in patients diagnosed early in life i.e. IDDM
where as macrovascular diseases are
common in those later diagnosed i.e.
NIDDM.

153
Microvascular Disease
The most common chronic complications of DM
include:
1. Retinopathy (Eye)
2. Nephropathy (Kidneys)
3. Neuropathy (Nerves)
The main degenerative changes in diabetes occur
because of a thickening of the capillary basement
membrane. Read on these.

155
Macrovascular Diseases
1. Coronary Heart Disease (CHD)- Usually these
individuals who suffer from CHD tend to be
overweight and often have hypertension and
hyperlipidemia. These risk factors are
particularly evident in persons with type 2 DM

156
2. Hypertension
3. Hyperlipidemia

157
4. Diabetic foot-persons with DM are prone to
foot problems for a number of reasons. E.g.
Microvascular and Macrovascular diseases
may result in ischemia and delayed healing.
Problems associated with neuropathy,
including absence of sensation resulting in
lack of pain awareness contribute to the
development of foot lesions. Necrosis and
ulcerations may develop later.

158
Manifestation of autonomic neuropathy can
result in excessive dryness and cracking of the
skin, which also contribute to infection.
Microvascular and macrovascular alterations
produce tissue ischemia and may lead to
sepsis.

159
The triad of Neuropathy, Ischemia and Sepsis
results in gangrene and possible amputation
(Merck’ Medical Manual, 2002; Beare and
Myers, 2003).
Other Complications
1. Skin disorders, frequent infections, reduced
blood circulation in vessels of the skin.

161
1. Oral complications: commonly associated with
Type 1 DM is periodontitis manifested by eventual
tooth loss. The reduced vascular perfusion may
reduced oxygen consumption. This provides
optimal consideration for anaerobic microorganism
growth. Thus dental education, care and follow up
are critical to the overall health of the diabetic
patient.

162
Infections due to alterations in host defenses,
vascular insufficiency that limits infection
fighting factors.
Read on Prevention of DM
Prevention of type 1 DM is under active
research. It focuses on arresting the
autoimmune process.
Primary Prevention of type 2 DM:

163
Read on Prevention of DM contd
It involves identification and modification of risk
factors. It should be directed toward lifestyle
changes which include
1. Exercises
2. Weight control
3. Knowledge of risk factors. Be made aware of
familial tendencies and risk for siblings of
the individuals with either type of diabetes
etc.
4. Choice of diet and preparation

164
Read on Prevention of DM contd.
Secondary Prevention of types 1 and 2:
Treatment at the hospital or clinic based on:
3Rs
• Reporting early
• Right diagnosis and
• Right treatment

165
Read on Prevention of DM contd.
Tertiary Prevention of DM: The aim is to prevent
complications based on early detection of sign
and symptoms of complications. The major
emphasis of tertiary preventive education will
be on the ability of the nurse to counsel the
patient about the early detection of and
interventions for complications (Patient
Empowerment)

Diabetes Screening
• Fasting blood glucose screening should begin
at age 30-45 and be repeated at least every
three years (Melmed et al, 2011).
• Earlier and more frequent screening should be
conducted in at-risk individuals. The risk
factors for which screening is important are
listed below:
166

Diabetes Screening contd.
• Family history(parent or sibling)
• Overweight or obese
• History of gestational diabetes or infant born
with birth weight greater than 4 kg
• High cholesterol level
167

Diabetes Screening contd.
• High risk ethnic group
• Hypertension
• High fasting blood glucose value at a particular
point in time
• Etc.
(Melmed et al., 2011)
168

UK MODEL FOR PREVENTION OF DM AND
CHRONIC CONDITIONS
• UK introduced sugar tax on soft drinks
• The tax was introduced to improve children's
health due to increasing obesity and other
problems among children (BBC News Report,
2015).
169

CHRONIC CONDITIONS CONTD.
• Drinks with more than 8 grams of sugar per
100 millilitres was taxed at a higher rate than
drinks with less than 5 grams of sugar per 100
millilitres.
170

CHRONIC CONDITIONS CONTD.
• Companies were to pay the tax but the
government expected some manufacturers to
pass on the costs to customers making soft-
drinks more expensive, and consumed less.
• The UK government spends the revenue on
fitness programs and extend school hours for
children so they can take part in more sports.
•
171

UK MODEL FOR PREVENTION OF DM AND CHRONIC
CONDITIONS CONTD.
• Scandinavian countries, Hungary, Mexico and
France, Chile and Dominica also have similar
sugar tax.
• Denmark also introduced a soft drink tax and
fat tax and then repealed/cancelled them
because it was not successful.
172

173
Somogyi Effect and Dawn Phenomenon
Somogyi Effect: Somogyi effect results from
excessive insulin administration which results
in blood glucose fluctuations.

174
contd.
The hypoglycemia provokes secretion of insulin
antagonists (glucagon) or hypoglycemia in
persons with diabetes stimulates the
production of counter regulatory hormones
(glucocorticoids, growth hormone,
epinephrine) (Beare and Myers, 2003).

175
contd.
Usually, this situation coupled with intake of
carbohydrate to combat symptoms of low
blood sugar results in hyperglycemia. Many
hypoglycemic episodes occur during sleep,
and an early morning hyperglycemia results.

176
contd.
The person then chases elevated morning blood
glucose levels with increased insulin doses,
which can lead to increased hypoglycemia
episodes.

177
contd.
The signs and symptoms of Somogyi effect can
be any of those associated with hypoglycemia
but consist mainly of:
Night time sweats
Night mares
Restless sleep
Early Morning Headache (EMH)

178
contd.
Dawn Phenomenon: An elevation in blood
glucose between 5am and 9am with no
recorded episodes of nocturnal hypoglycemia
is referred to as the dawn phenomenon

179
contd.
Persons with type 1 DM may find that they
require more insulin in the morning to cover
their breakfast. Likewise, persons with type 2
DM may find that their fasting blood glucose is
always higher when they wake up in the
morning as opposed to their late blood
glucose.

180
contd.
Both situations can be the result of the dawn
phenomenon. As dawn approaches, the level
of certain hormones in the blood naturally
increase. These hormones probably, growth
hormone and cortisol, cause blood sugar
levels to rise (Beare and Myers, 2003, Longo et
al., 2012).

181
Difference Between Somogyi Effect and
Dawn Phenomenon
1. In the Somogyi effect hypoglycemia will be
identified and then followed by hyperglycemia.
2. In dawn phenomenon there is no overnight
hypoglycemia, rather there is consistent rise in
blood glucose levels overnight.
Decreasing the dose of insulin precipitating the
hypoglycemia treats the Somogyi effect.

182
Dawn Phenomenon contd.
Treatment of the dawn phenomenon consists of
increasing the dose of the insulin, which is
affecting nocturnal glucose levels.

183
Dawn Phenomenon contd.
A primary nursing role is to document reports of
hypoglycemia, glucose intake, and laboratory
results and to assess for the presence of night
sweats, night mares, and early morning
headaches.
The nurse should also correlate these
complaints and laboratory results with
mealtimes. Such data help identify the
phenomenon.

184
Insulin Therapy Regime
This is based on the needs of the patient.
Intensive multiple daily insulin injections has
become the gold standard. Convectional
therapies, which uses once and twice daily
insulin injection programmes, has been shown
to be less effective in the management and
control of diabetes. Note that Once or Twice
daily insulin therapy is still used with good
effect in Ghana (Standard Treatment
Guideline for Ghana, 2010).

Insulin Therapy Regime contd.
• Insulin therapy should usually begin with teaching
the patient the correct technique for subcutaneous
injections, as self-injections are to be strongly
encouraged.
• Patients should be made aware of the different
appearance of different kinds of insulin
(soluble/regular which is fast-acting = gin clear;
Neutral Protamine Hagedorn (NPH) or Lente which
are intermediate-acting = cloudy; pre-mixed insulin
preparations containing both soluble and NPH
insulin = cloudy) (Beare and Myers, 2003).

• Cloudy Insulin (intermediate-acting or pre-
mixed) can only be given subcutaneously and
SHOULD NOT be injected IM or IV. Only
soluble/regular insulin may be given by the
IM or IV route during emergency treatment.

• Most Insulins currently available in Ghana are
preferably injected 15-30 minutes before a meal.
Two injections daily (before breakfast and dinner) of
an intermediate-acting or pre-mixed insulin give
better blood glucose control than once daily
injections.
• Older patients and those with kidney disease may
sometimes be managed adequately on a single daily
injection (Beare and Myers, 2003).

• Two-thirds of the total daily insulin
requirement is given before breakfast, and
the remainder before the evening meal.
• Insulin requirements vary from patient to
patient irrespective of age and body weight.

189
Types of Insulin (Kinetics)
1. Quick-Acting Insulin e.g. Regular (onset
30min, duration 6-8 hrs) Lispro (onset
12min, duration 3hrs), Aspart (onset 12min,
duration 3hrs)
2. Intermediate Insulin e.g. Lente (onset 2½hrs,
duration 22hrs), Neutral Protamine
Hagedorn (NPH) onset 1½hrs, duration 22hrs

190
Types of Insulin (Kinetics) contd.
3. Long-Acting Insulin eg. Ultralente (onset 4hrs,
duration 28hrs), Glargine (onset 1-2 hours,
duration 24+hrs)
4. Combination Insulin (combined preparations) e.g.
Humulin (regular+neutral protamine
hagedorn(NPH), Novolin (regular+NPH, Humalog
Mix (NPH+Lispro): (onset 12-30 mins, duration 22
hours

191
Intensive Insulin Therapy Regime
Examples: Three injections per day: The three
injections per day method uses rapid and
intermediate-acting insulin for the pre-
breakfast dose, regular as a pre-supper dose,
and a small dose of intermediate-acting at
bedtime.

192
Intensive Insulin Therapy Regime contd.
Multidose Insulin: This therapy involves three or
four injections of short acting insulin before
meals coupled with long-acting preparations.
This regimen may also consist of three pre-
prandial doses of rapid-acting insulin coupled
with a dose of bed time lente.
(Longo et al., 2012; Beare and Myers, 2003).

193
Another option involves injecting long-acting insulin
once a day or divided into 2 equal doses given before
breakfast and supper.
Injection Sites: Read on sites for insulin injection for
practical demonstration at the skills laboratory at a
later date.
Right and Left buttocks
Right and Left abdomen
Right and Left thigh
Right and Left arm

194
Try to rotate these sites to avoid problems with
abscesses
Routes of Administration: Read on these.
Subcutaneous
IV is preferred during Ketoacidosis
Intra peritoneal for implantable insulin devices
IM may also be given

195
Hypoglycemia and Hyperglycemia
Read on signs and symptoms of hypoglycemia
and its management.

Sample Question
• Effective use of standardized protocol for the
management of DM is a predictor of a better
Glycated Haemoglobin level (HbA1c or A1c).
Discuss
• Plan
Medication
Diet
Monitoring
Exercise
Education
Then link with the concept of A1c results (normal values in individuals with DM)
196

Sample Question
• What is the link between coping strategies
utilized by patients newly diagnosed with type
2 diabetes mellitus and their levels of HbA1c.
• Plan
Positive coping methods
Negative coping methods
Link these with anticipated A1c results for the two extremes.
197

Sample Question
Achievement and maintenance of metabolic
control in DM requires the judicious use of
Medication, Diet, Monitoring, Exercise and
Education. Discuss
198

References
Beare, P. G. & Myers, J. L. (2003). Adult
Health Nursing, Medical-Surgical Nursing,
Health and Illness Perspectives.
7th Edition, Mosby 2003.
Chiang, J. L., Kirkman, M. S., Laffel, L. M. and
Peters, A. L. (2014). Type 1 diabetes through the
life span: a position statement paper of
American Diabetes Association (ADA) . Diabetes
Care, 2014, 141140.
199

References
• Lakey, JR; Burridge, PW; Shapiro, AM (September
2003). "Technical aspects of islet preparation and
transplantation.". Transplant international : official
journal of the European Society for Organ
Transplantation. 16 (9): 613–32. doi:10.1111/j.1432-
2277.2003.tb00361.x. PMID 12928769
• LeMone, P. & Burke, M. K. (1996). Medical Surgical Nursing:
Critical Thinking in Client Care. Addison Wesley – California,
USA.
200

References
Longo, D; Fauci, A; Kasper, D; Hauser, S; Jameson,
J; Loscalzo, J (2012). Harrison's
Principles of Internal Medicine (18th ed.).
NewYork: McGraw-Hill. pp. 2995–3000.
ISBN 978-0071748896.
Hall, J. (2011). Guyton and Hall textbook of
medical physiology (12th ed.).
Philadelphia, Pa.: Saunders/Elsevier. p. 781.
ISBN 978-1-4160-4574-8.
201

References
Melmed, S; Polonsky, KS; Larsen, PR;
Kronenberg, HM (2011). Williams Textbook
of Endocrinology (12th ed.). Saunders.
ISBN 978-1437703245
Merck’s Medical Manual 2002
Kottak, C. P. (2014). Windows on Humanity, New
York: McGraw-Hill
202

Reference
• Young, B., ed. (2006). Wheater's
functional histology : a text and colour
atlas (5th ed.). Churchill
Livingstone/Elsevier.
pp. 299–301. ISBN 978-0-443-06850- 8.
203

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