Adult Medical-Surgical Adult Medical-Surgical Nursing Nursing

Endocrine Module: Endocrine Module:

Diabetes Mellitus Diabetes Mellitus

(Lecture 1): Introduction(Lecture 1): Introduction

The Role of InsulinThe Role of Insulin

Anabolic role: regulates the Anabolic role: regulates the uptakeuptake and storage of glucose by the cells: and storage of glucose by the cells: insulin binds to cell surface receptors insulin binds to cell surface receptors allowing uptake of glucose (storage allowing uptake of glucose (storage as glycogen)as glycogen)

Controls the level of glucose in the Controls the level of glucose in the blood (together with glucagon) blood (together with glucagon)

Diabetes Mellitus: DefinitionDiabetes Mellitus: Definition

Diabetes is a metabolic problem of Diabetes is a metabolic problem of hyperglycaemia resulting from defects in hyperglycaemia resulting from defects in either or both of the following:either or both of the following:

Insulin production: pancreatic Insulin production: pancreatic ββ cells may cells may stop secreting insulin (type 1)stop secreting insulin (type 1)

Insulin action: the body cells may stop Insulin action: the body cells may stop responding to insulin (insulin resistance) responding to insulin (insulin resistance) (type 2)(type 2)

Diabetes Mellitus: ClassificationDiabetes Mellitus: Classification

Type 1: (5-10% of cases)Type 1: (5-10% of cases)

Type 2: (90-95% of cases)Type 2: (90-95% of cases)

Gestational DM (in pregnancy, similar Gestational DM (in pregnancy, similar to type 2 but resolves at end of to type 2 but resolves at end of pregnancy: may lead to type 2 at pregnancy: may lead to type 2 at later date)later date)

Complications of Diabetes MellitusComplications of Diabetes Mellitus

Hyperglycaemia leads to both acute Hyperglycaemia leads to both acute and longterm complicationsand longterm complications

Acute Complications of Diabetes Acute Complications of Diabetes MellitusMellitus

Diabetic ketoacidosis (type 1 DM)Diabetic ketoacidosis (type 1 DM)

Hyperglycaemic hyperosmolar non-Hyperglycaemic hyperosmolar non-ketotic syndrome (type 2 DM)ketotic syndrome (type 2 DM)

Hypoglycaemia and comaHypoglycaemia and coma

Longterm Complications of Longterm Complications of Diabetes MellitusDiabetes Mellitus

Macrovascular → coronary artery Macrovascular → coronary artery disease, cerebro-vascular disease, disease, cerebro-vascular disease, peripheral vascular diseaseperipheral vascular disease

Chronic microvascular → Chronic microvascular → nephropathy, retinopathynephropathy, retinopathy

NeuropathyNeuropathy

Diabetes Mellitus: USA FactsheetDiabetes Mellitus: USA Factsheet

Leading cause of blindness in working-Leading cause of blindness in working-age adults, non-trauma amputation age adults, non-trauma amputation and end-stage renal diseaseand end-stage renal disease

Leading cause of hospitalisationLeading cause of hospitalisation Third leading cause of death from Third leading cause of death from

disease: mainly coronary artery disease: mainly coronary artery disease and cerebro-vascular diseasedisease and cerebro-vascular disease

Source: Centre for Disease Control, 2008; American Source: Centre for Disease Control, 2008; American Diabetic Association, 2008 in Brunner & Suddarth, Diabetic Association, 2008 in Brunner & Suddarth, 1212thth edition, 2010 edition, 2010

Diabetes Mellitus: Type 1Diabetes Mellitus: Type 1

AbsenceAbsence of insulin secretion due to auto- of insulin secretion due to auto-immune destruction of the immune destruction of the ββ cells of the cells of the Islets of LangerhansIslets of Langerhans

Usually onset at a younger age(<30 years)Usually onset at a younger age(<30 years) Acute onset requiring urgent treatmentAcute onset requiring urgent treatment Genetic predisposition: HLA tissue-typing Genetic predisposition: HLA tissue-typing

DR3/DR4 has ↑ risk up to 20 times, but DR3/DR4 has ↑ risk up to 20 times, but stressors may trigger or enhance disorderstressors may trigger or enhance disorder

InsulinInsulin required as treatment required as treatment

Type 1 Diabetes Mellitus: Type 1 Diabetes Mellitus: PathophysiologyPathophysiology

Auto-immune destruction of Auto-immune destruction of ββ cells: ↓ cells: ↓ insulin and unchecked hyperglycaemiainsulin and unchecked hyperglycaemia

If > renal threshold (9.9 m mol/l) kidneys If > renal threshold (9.9 m mol/l) kidneys may not reabsorb glucose → glycosuriamay not reabsorb glucose → glycosuria

Osmotic diuresis: polyuria, dehydrationOsmotic diuresis: polyuria, dehydration NoNo insulininsulin to control catabolic action of to control catabolic action of

glucagon (glycogen, fat, protein) glucagon (glycogen, fat, protein) Breakdown of fat → ketone bodies Breakdown of fat → ketone bodies

(Diabetic ketoacidosis)may→ coma/ death(Diabetic ketoacidosis)may→ coma/ death

Type 1 DM: Clinical Manifestations Type 1 DM: Clinical Manifestations (Acute Onset)(Acute Onset)

Polyuria (↑ urine output)Polyuria (↑ urine output) Polydipsia (thirst)Polydipsia (thirst) Polyphagia (↑ appetite)Polyphagia (↑ appetite) Weight lossWeight loss Fatigue, weaknessFatigue, weakness Dehydration, dry skinDehydration, dry skin Recurrent infections, poor wound healingRecurrent infections, poor wound healing Maybe ↓ vision, numb, cool extremitiesMaybe ↓ vision, numb, cool extremities

Diabetes Mellitus: Type 2Diabetes Mellitus: Type 2

Reduced cell sensitivity to insulin (“insulin Reduced cell sensitivity to insulin (“insulin resistance”) therefore reduced uptake of resistance”) therefore reduced uptake of glucose: reduced glucose: reduced actionaction of insulin of insulin

Age of onset usually >30 yearsAge of onset usually >30 years Insidious, gradual onset (75% detected Insidious, gradual onset (75% detected

incidentally and may have complications)incidentally and may have complications) Family history commonFamily history common Associated with obesity: Diet to ↓ weight, Associated with obesity: Diet to ↓ weight,

and exercise are first line of treatment and exercise are first line of treatment

Type 2 Diabetes Mellitus: Type 2 Diabetes Mellitus: PathophysiologyPathophysiology

Insulin resistance reduces uptake of Insulin resistance reduces uptake of glucose by cells glucose by cells

In an attempt to control (reduce) blood In an attempt to control (reduce) blood glucose level, glucose level, ββ cells ↑ insulin production cells ↑ insulin production

Eventually inadequate insulin, relative to Eventually inadequate insulin, relative to elevated glucose levels → hyperglycaemia elevated glucose levels → hyperglycaemia (type 2 DM) (exhaustion of (type 2 DM) (exhaustion of ββ cells) cells)

As some insulin present, uncontrolled fat As some insulin present, uncontrolled fat breakdown and ketoacidosis is preventedbreakdown and ketoacidosis is prevented

Type 2 DM: Clinical Manifestations Type 2 DM: Clinical Manifestations (Gradual Onset)(Gradual Onset)

PolyuriaPolyuria PolydipsiaPolydipsia Maybe associated with obesity (central)Maybe associated with obesity (central) Fatigue, weaknessFatigue, weakness Dehydration, dry skinDehydration, dry skin Recurrent infections, poor wound healingRecurrent infections, poor wound healing Maybe ↓ vision, numb, cool extremitiesMaybe ↓ vision, numb, cool extremities *May be unaware until complications arise*May be unaware until complications arise

Diabetes Mellitus: DiagnosisDiabetes Mellitus: Diagnosis

Patient history and clinical picturePatient history and clinical picture Random blood glucoseRandom blood glucose Fasting blood glucoseFasting blood glucose Oral glucose tolerance test (GTT)Oral glucose tolerance test (GTT) Glycosylated Haemoglobin (Hb AGlycosylated Haemoglobin (Hb A1C1C)) Screen for complications: BP, ECG, arterial Screen for complications: BP, ECG, arterial

pulses, lipid profile, kidney function test, pulses, lipid profile, kidney function test, urine protein (24 hour), eye examination, urine protein (24 hour), eye examination, neurological assessmentneurological assessment

Positive Diagnosis of Positive Diagnosis of Diabetes MellitusDiabetes Mellitus

Random (RBS): >11.1 m mol/l (200mg/dl)Random (RBS): >11.1 m mol/l (200mg/dl) Fasting (FBS): >7 m mol/l (126mg/dl) Fasting (FBS): >7 m mol/l (126mg/dl)

(With symptoms or more than once)(With symptoms or more than once) GTT (fasting, 50-75g glucose orally): if 2 GTT (fasting, 50-75g glucose orally): if 2

hours postprandial, 11.1 m mol/l or abovehours postprandial, 11.1 m mol/l or above Glycosylated Haemoglobin (Hb AGlycosylated Haemoglobin (Hb A1C1C): >6%): >6% (When blood glucose elevated, molecules (When blood glucose elevated, molecules

attach to haemoglobin for lifespan of attach to haemoglobin for lifespan of RBCs: average 2-3 month glucose level)RBCs: average 2-3 month glucose level)

Diabetes Mellitus: Treatment PlanDiabetes Mellitus: Treatment Plan

Control blood glucose levelsControl blood glucose levels

Prevent acute or longterm Prevent acute or longterm complications which occur with lack complications which occur with lack of controlof control