UANE&S 400814

Pancreatic Dysfunction - Diabetes Mellitus

Prepared by Gabrielle Metelli & Kathleen Dixon - 2009

University of Western Sydney 2009 1

Diabetes Mellitus - Definition

¾ “Diabetes is a long-term (chronic) condition in which blood glucose levels

become too high because the body produces little or no insulin, or cannot
use insulin properly.” (Australian Institute of Health & Welfare, 2006).

¾ Disorder of carbohydrate, protein and fat metabolism due to an imbalance

between insulin availability and insulin need. (Porth, 2005).

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 Diabetes Mellitus - Facts
¾ The incidence and prevalence of diabetes are on the rise worldwide

¾ In Australia, about 3.5% of the population reported having diabetes

¾ Around 1 million Australians are estimated to have Diabetes.

¾ Expected to increase over the decade.

¾ Diabetes and its associated complications, which include cardiovascular,

nerve, kidney and eye diseases, compromise the quality of life of a large
number of Australians

¾ They are also a sharply increasing component of health care costs

¾ Diabetes is currently one of the top 10 causes of death in Australia.

(Australian Institute of Health & Welfare, 2006).

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Diabetes Mellitus - Classification

¾ Type 1 diabetes

¾ Type 2 diabetes

¾ Other specific types of diabetes

¾ Gestational diabetes mellitus

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 Type 1 Diabetes Mellitus
¾ previously known as Insulin Dependent Diabetes Mellitus (IDDM)

¾ absence of insulin production by the pancreas

¾ results in hyperglycaemia

¾ often diagnosed in childhood (juvenile)

¾ accounts for 10-15% of all diabetes

¾ requires insulin injections to control blood glucose levels (BGL)

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Type 1 Diabetes Mellitus

Aetiology
¾ Type 1 diabetes is thought to be
the result of
¾ a gene-environment interaction,
¾ with the strongest genetic risk
markers in the HLA region of
chromosome 6.
Pathophysiology
¾ Catabolic disorder leading to a
breakdown of fats & proteins &
an elevation in BGL’s
¾ Absolute absence of insulin leads
to lipolysis, & the conversion of
fatty acids to ketones
¾ Excess ketones leads to
ketoacidosis

¾ Glucagon levels remain elevated

because of lack of insulin.

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 Type 2 Diabetes Mellitus
¾ Type 2 DM previously known as NIDDM or mature onset diabetes.

¾ The most common type of DM

¾ 85- 90% of cases in the community.

¾ In 2004, 5% or 2,419 deaths were related to diabetes

(Public Health Division, 2006).

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T2DM -
Aetiology Pathophysiology
¾ Family history and obesity are the ¾ Type 2 diabetes is a chronic
most important risk factors. condition

¾ Pancreas continues to produce ¾ marked by reduced levels of

insulin insulin and/or
¾ Insulin secretion is inadequate
and/or ¾ the inability of the body to use
¾ Is poorly utilised by the tissues insulin properly (insulin
resistance).

¾ Results from
¾ Impaired beta cell function and
insulin secretion
¾ Peripheral insulin resistance
¾ Increased hepatic glucose
production
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 T2DM
Insulin Impaired Beta Cell Function
Resistance Pathophysiology Pathophysiology
¾ Begins before onset of symptoms ¾ Can arise from:
¾ Genetic decrease in beta cell
¾ Occurs in muscle, fat and liver cells mass
¾ Increased beta cell apoptosis
¾ Beta cell exhaustion
¾ Casues include:
¾ Chronic hyperglycaemia
¾ Genetics
¾ Chronic elevation of free fatty
¾ Ageing
acids
¾ Sedentary lifestyle
¾ Amyloid deposition in the beta
¾ Central obesity cell

¾ Beta cells increase insulin

production to compensate
eventually leading to beta cell
failure
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Diabetes Mellitus - Signs & Symptoms

¾ Polyuria & glycosuria

¾ Elevated blood glucose levels (hyperglycaemia) cause osmotic diuresis;

¾ The amount of glucose filtered by the glomeruli of the kidney exceeds that
which can be reabsorbed by the renal tubules;
¾ Leading to large losses of water along with glucose.

¾ Polydipsia

¾ Because of elevated blood glucose levels, water is osmotically drawn from

body cells
¾ Resulting in intracellular dehydration and stimulation of thirst in the
hypothalamus

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 Diabetes Mellitus - Signs & Symptoms
¾ Polyphagia
¾ Depletion of cellular stores of carbohydrates, fats, and protein results in cellular
starvation and a corresponding increase in hunger in T1DM only.

¾ Weight loss occurs because of fluid loss in osmotic diuresis

¾ In T1DM weight loss occurs because of body tissue wasting as fats & proteins
are used for energy.

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Diabetes Mellitus
Complications
¾ Chronic hyperglycaemia leads to:
¾ Microvascular disease
¾ Macrovascular disease.

¾ Occurs in both Type 1 & Type 2 DM

¾ Microvascular disease results in:

¾ Diabetic retinopathy
¾ Diabetic nephropathy
¾ Diabetic neuropathy
¾ Macrovascular disease results in:
¾ Cerebrovascular disease
¾ Cardiovascular disease
¾ Peripheral vascular disease

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 Diabetes Mellitus
Microvascular Complications
¾ Retinopathy
¾ Capillary structure undergoes alterations in blood flow, leading to;
¾ Retinal ischaemia
¾ Microaneurysm formation
¾ Neovascularisation
¾ Scarring
¾ Retinal detachment

¾Nephropathy
¾A disease of the kidneys characterised by the presence of albumin in the urine,
hypertension, oedema and progressive renal insufficiency.

¾Most common cause of renal failure requiring dialysis or transplantation.

¾It occurs because of thickening of the basement membrane of the glomeruli.

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Diabetes Mellitus

Microvascular Complications Macrovascular Complications

¾Macrovascular Disease:
¾ Neuropathy
¾affects coronary, peripheral and
¾ affects sensorimotor and
cerebrovascular circulation
autonomic nerves and contributes
to many problems such as:
¾increased risk for:
¾ foot ulcers
¾ Constipation
¾Ischaemic heart disease
¾ postural hypotension
¾ impotence ¾Myocardial infarction

¾Peripheral Vascular Disease

¾Amputation

¾Cerebrovascular accident

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 Type 1 Diabetes Mellitus
Hyperosmolar Hyperglycaemic
Diabetic Ketoacidosis (DKA) Non-Ketotic Syndrome
(HHNKS):
¾ Hyperglycaemia (BSL > 15 ¾ severe hyperglycaemia >34
mmol/L
mmol/L)
¾ absence of ketonaemia &
¾ Bicarbonate (< 15 mEq/L) ketoacidosis (due to some insulin
availability)

¾ pH (< 7.3) ¾ profound dehydration - serum

hyperosmolality

¾ Polydipsia

¾ Polyuria

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Diabetes Mellitus
Blood Tests Criteria for Diagnosis
¾ fasting blood glucose test ¾ Symptoms + casual plasma
¾ fast 8 - 12 hrs glucose of >11.1 mmol/L
¾ glucose level measured

¾ FPG > 7 mmol/L

¾ random blood glucose
¾ taken without regard to food or time
¾ OGTT post 2 hours > 11.1
mmol/L
¾ oral glucose tolerance test
¾ given concentrated glucose solution
¾ plasma tested at 1 - 2 hourly intervals
¾ BGL should be normal after 3hrs

¾ glycated haemoglobin
¾ Test A1C

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 Diabetes Mellitus - Drug Therapy

Insulin Oral hypoglycaemic agents:

¾ all insulin's come in same ¾ Biguanides – metformin
strength (100 international ¾ Decrease glucose production in the
units per ml) liver
¾ Increase glucose utilisation in
peripheral tissues
¾ most patients are on human
insulin ¾ Decrease absorption of glucose
¾ Does not affect B-cells
¾ Does not increase insulin secretion
¾ Types:
¾ Preferred for overweight patients
¾ ultra-short acting; as it is less likely to increase
¾ short-acting; weight.
¾ intermediate-acting;
¾ long-acting

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Diabetes Mellitus - Drug Therapy

Oral hypoglycaemic agents:

¾ Sulfonylureas – glibenclamide, glipizide, gliclazide

¾ Promote insulin release.
¾ Increase cellular sensitivity to insulin
¾ Decrease glycogenolysis and gluconeogensis
¾ Reduce BGL
¾ Take with meals to reduce hypoglycaemia

¾Alpha-glucosidase inhibitor – acarbose

¾Delays digestion and absorption of carbohydrates
¾Lowers post-prandial BGLs
¾Lowers post-prandial endogenous insulin requirements

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 Diabetes Mellitus - Drug Therapy

Oral hypoglycaemic agents:

¾ Repaglinide
¾ Stimulates insulin production
¾ Improves insulin secretion
¾ Binds at a different site to sulfonylureas

¾ Glitazones – rosiglitazone, pioglitazone

¾ Enhance sensitivity of peripheral tissues and liver to insulin
¾ Reduce insulin resistance

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References
¾ AIH&W. (14th November 2006).Diabetes link to the world diabetes day,
14 November 2006 fact sheet. Retrieved on 4th July, 2007, from
www.aihw.gov.au/diabetes/index.cfm
¾ Black, J. M., & Hawks, J. (2005). Medical-surgical nursing: Clinical
management for positive outcomes (7th ed.). Philadelphia:W.B.
Saunders.
¾ Brown, D., & Edwards, H. (Eds.). (2008). Lewis’s medical-surgical
nursing assessment and management of clinical problems. (2nd
ed.). Sydney: Elsevier.
¾ Bryant, B., Knights, K., & Salerno, E. (2007). Pharmacology for health
professionals (2nd ed.). Sydney: Mosby/Elsevier (Australia).
¾ Chang, E., Daly, J., & Elliot, D. (2006). Pathophysiology applied to
nursing practice. Sydney: Elsevier (Australia).
¾ Guthrie, R. A., & Guthrie, D. W. (2004). Pathophysiology of diabetes
mellitus. Critical Care Nursing Quarterly ,27(2), 113-125.

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 References
¾ Lehne, R. A. (2007). Pharmacology for nursing care (6th ed.).
Philadelphia:Saunders
¾ Lemone, P., & Burke, K. (2008). Medical surgical Nursing : Critical
thinking in client care (4th. ed.). Upper Saddle River, New Jersey:
Prentice - Hall.
¾ Marieb, E. N. (2007). Human anatomy and physiology (7th ed.). California:
Benjamin/Cummings.
¾ Porth, C. M. (2005). Pathophysiology: Concepts of altered health states
(7th ed.). Philadelphia: Lippincott.
¾ Public Health Division, The health of the people of New South Wales –
Report of the chief health officer. Sydney NSW Department of Health.
Retrieved on 4th July, 2007, from
www.health.nsw.gov.auchoindex.htm

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