Diabetes mellitus an overview

Objectives of the Lecture
 Be able to define diabetes mellitus
 Be able to classify diabetes mellitus
 Be able to list predisposing factors
 Be able to list clinical features of diabetes mellitus
 Be able to list drugs used in treatment of diabetes
mellitus
Diabetes Mellitus: An Overview 229/03/2014

Outline
 DM definition
 DM epidemiology
 Types of DM
 Clinical features
 Investigations
 Treatment
 Complications
29/03/2014 3Diabetes Mellitus: An Overview

What is Type 2 Diabetes Mellitus (T2DM)?
– Current ADA definition1
• T2DM is a metabolic disease characterized by
hyperglycemia, resulting from a combination of
resistance to insulin action and an inadequate insulin
secretory response
– T2DM involves 2 primary pathogenic processes:
• progressive decline in pancreatic islet function
(↓ insulin secretion and inadequately suppressed
glucagon secretion)2,3
• diminished tissue responses to insulin (insulin
resistance)2,4
ADA=American Diabetes Association
1American Diabetes Association. Diabetes Care. 2006; 29 (Suppl 1): S43–S48; 2Weyer C, et al. J Clin Invest. 1999; 104: 787–794;
3Müller WA, et al. N Engl J Med. 1970; 283: 109–115; 4Ahrén B, Pacini G. Diabetes Obes Metab. 2005; 7: 2–8.

Epidemiology
 More than 285 million (2010) people affected
worldwide
 By 2030, some 566 million people are projected to
have diabetes.
 3.2% (12.1million) from Africa in 2010
 By 2030, 3.7% (23.9 million) from Africa 2010

CLASSIFICATION AND
DIAGNOSIS

Classification of Diabetes
 Type 1 diabetes
 β-cell destruction
 Type 2 diabetes
 Progressive insulin secretory defect
 Other specific types of diabetes
 Genetic defects in β-cell function, insulin action
 Diseases of the exocrine pancreas
 Drug- or chemical-induced
 Gestational diabetes mellitus

TYPE 1 DM
 Due to B-cell destruction.
 Require insulin for survival.
 Presence of certain autoantibodies.
 Type 1A – presence of autoantibodies (anti-GAD, IA2, ICAA,
and anti-insulin antibodies).
 Type 1B – absence of autoantibodies (idiopathic)

Type 2 DM
 Most common form of DM
 Characterized by disorder in insulin action and insulin secretion or
both.
 Specific etiology unknown
 Insulin resistance
 Progressive B-cell failure.
 They are obese.

Predisposing Factors
 Obesity
 Hypertension
 Strong family history
 Sedentary lifestyle
 Lack of exercise
 Alcoholism
 Smoking
 Western diet
 Advancing age
 Diabetogenic drugs
 Low birth weight
 Artificial or cow milk
formulae in neonates
 Viruses
 Migration

Urbanisation/Westernisation

Gestational diabetes
 Carbohydrate intolerance associated with
hyperglycemia of variable severity with the onset
or first recognition during pregnancy.
 In early pregnancy, fasting and post prandial
glucose concentration are normally lower than in
non pregnant women

Risk of developing GDM
 Old women
 Previous history of glucose intolerance
 History of babies large for gestational age

Underlying causes of Type 2 Diabetes
Obesity
Insulin
resistance
-cell
defect
Impaired
glucose
tolerance
Early
diabetes
Late
diabetes
Hyperinsulinaemia
Decreased insulin
secretion
-cell failure
Saltiel AR. J Clin Invest 2000;106:163–164.
ACE/CDR/05/20746/1

Hyperinsulinaemia
Hyperglycaemia
Plasma
insulin
Blood
glucose
Insulin resistance Pancreatic
failure
Diagnosis of
type 2 diabetes
Insulin resistance
Edelman SV. Type 2 diabetes mellitus. Adv Int Med 1998; 43:449–500.
Underlying factors in type 2 diabetes are insulin
resistance and -cell dysfunction
ACE/CDR/05/20746/1

Testing for Diabetes in
Asymptomatic Patients
 Consider testing overweight/obese adults (BMI ≥25 kg/m2)
with one or more additional risk factors
 In those without risk factors, begin testing at age 45 years
 If tests are normal
 Repeat testing at least at 3-year intervals
 Use A1C, FPG, or 2-h 75-g OGTT
 In those with increased risk for future diabetes
 Identify and, if appropriate, treat other CVD risk factors

Diagnostic Criteria
Fasting Glucose
mg/dL
2-h OGTT
mg/dL
Random Glucose
mg/dL
A1c
Normal <100 <140 <200 <5.7%
Prediabetes 100-125
(IFG)
140-199
(IGT)
5.7-6.4%
Diabetes ≥ 126 ≥ 200 ≥ 200 ≥ 6.5%
Note: In the absence of unequivocal hyperglycemia, result(s) should be
confirmed by repeat testing.

DIAGNOSTIC CRITERIA FOR GDM
ADA ADA WHO
75g oral
glucose
(Mg/dL)
100g oral
glucose
(Mg/dL)
75g oral
glucose
(Mg/dL)
Fasting 95 95 >/= 126
1 hour 180 180
2 hour 155 155
3 hour NA 140 >/= 140

Clinical features
 Classical symptoms:
 Polyuria
 Polydipsia
 Polyphagia
 Complications :
 Acute
 Chronic

Acute complications
 Diabetic ketoacidosis (DKA)
 Hyperglyceamic hyperosmolar state(HHS)

Eyes
(retinopathy, glaucoma,
cataracts)
Brain and Cerebral
Circulation
(stroke, TIA)
Heart and Coronary
Circulation
(angina, MI, CHF)Kidneys
(nephropathy, ESRD)
Peripheral Nervous
System
(peripheral neuropathy) Peripheral Vascular Tree
(peripheral vascular disease,
gangrene, amputation)
Tissue Damage in Many Organ Systems Leads to
Serious Long-term Complications in T2DM
CHF=congestive heart failure; ESRD=end-stage renal disease; MI=myocardial infarction; TIA=transient ischemic attack; T2DM=type 2 diabetes mellitus
Adapted from International Diabetes Federation. Complications. Available at: www.eatlas.idf.org/complications Accessed February 17, 2009.

Chronic Complications
 Affects many organ systems.
 Vascular :
 Microvascular
 Macrovascular
 Non vascular:
 Gastroparesis
 Sexual dysfunction
 Skin changes

Mechanism of Complications
 There are 3 major theories (not mutually
exclusive);
 Formation of Advanced Glycosylation End Products (AGEs)
via the nonenzymatic glycosylation of cellular protein.
 Increase glucose metabolism via the sorbitol pathway by
enzyme aldose reductase.
 Increase formation of diacyglycerol leading to activation of
certain isoforms of protein kinase C (PKC).

Complications
 Ophthalmologic
 Renal
 Neuropathy
 Cardiovascular
 Lower extremities
 Infections
 Dermatologic

Laboratory Diagnosis,
Monitoring and Evaluation
of Diabetes Mellitus

Outline
 Purpose of laboratory testing
 Confirmation of diagnosis of DM
 Assessment of severity and level of DM control
 Identification of co-morbidities and complications
 Effect of treatment
 Self urine and blood glucose monitoring
 Laboratory monitoring

Confirmation of diagnosis
 FPG and 2hrPP
 Urinalysis
 HBA1c
 Serum lipids
 Serum electrolytes
 Imaging studies

Aims of treatment
 Reduce the symptoms of hyperglycaemia
 Limit adverse effects of treatment
 Maintain quality of life and psychological well-
being
 Prevent or delay vascular complications of
diabetes

Basis of Treatment
 Reducing insulin resistance
 Replacing or augmenting insulin secretion
 Reducing gluconeogenesis
 Treating effects of lipolysis and reducing lipolysis

GOALS OF MANAGEMENT

Glycemic Recommendations
*Individualize goals based on these values.
†Postprandial glucose measurements should be made 1–2 h after the
beginning of the meal, generally peak levels in patients with diabetes
Target Treatment
Goal
AACE/ACE 2011 ADA 2012
A1c ≤6.5% <7%
Fasting Glucose FPG <110 mg/dl Preprandial PG 70-
130mg/dl
Postprandial
Glucose
2-hr postprandial
<140mg/dl
Peak <180mg/dl

Blood Pressure and Lipid Goals
Blood pressure <130/80 mmHg†
Lipids
LDL cholesterol <100 mg/dL (<2.6
mmol/L)‡
†Based on patient characteristics and response to therapy, higher or lower
systolic blood pressure targets may be appropriate.
‡In individuals with overt CVD, a lower LDL cholesterol goal of <70 mg/dL
(1.8 mmol/L), using a high dose of statin, is an option.

Approach to Patient with DM
History
Physical examination
Laboratory assessment.

Management contd
 Requires a multidisciplinary team:
 Primary care provider
 Endocrinologist/Diabetologist
 Certified diabetic educator
 Nutritionist

Management contd
 When complication arises, the team will
include;
Neurologist
Nephrologists
Cardiologist
Vascular surgeon
Ophthalmologist
podiatrist

Treatment
Non pharmacologic
Pharmacologic
Surgical.

Non pharmacologic treatment
 Education of patients:
 Individualized or
group based
 Done by various
health professionals
 Repetitive,
interactive
 Address causes,
course, treatment
 Define target for DM
control
29/03/2014 Diabetes Mellitus: An Overview 39

 Lifestyle Modification:
Quit smoking
Quit drinking
alcohol
Regular exercise
Healthy diet
Weight reduction
29/03/2014 Diabetes Mellitus: An Overview 40
Non Pharmacologic Treatment

Dietary Management of DM
 Individualized, simple instructions
 Aim to achieve ideal body weight and encourage
healthy eating habits and lifestyle modification
 Calculate activity level and caloric requirements to
achieve above
 Diet should be able to reduce hyperglycaemia,
glucotoxicity and lipotoxicity

The Ideal or Paleolithic Diet
 50 -65% carbohydrate, complex carbohydrates
derived mainly from whole grains and legumes, low
glycaemic index
 0.6g/kg body weight proteins (15-20%) derived from
game animals or fish, insects
 15 -25% fat derived from vegetable and nut oils.
 High fiber 25 – 30g daily

EXERCISE IN DIABETES
 Dynamic or isotonic
 Graduated & individualised
 Regular with adequate warm up
 Appropriate footcare
 Precautions in OHA or insulin dose
 Contraindicated in some conditions

Exercise Therapy
 Benefits
 Increase insulin sensitivity
 Improved long term glycaemic control – lower HbA1c
 Improved circulating lipid profile
 Improved BP control
 May promote redistribution of body fat ( reduce CVD
risk)
 Health benefits – 3 days wkly

 Individualized regimen
 State of control
 Stretching & warm-up
 Aerobic level sustainable for 30mins
 Cool down
 Full evaluation before prescribing exercise
 Complications/risks
 Precautions for patient

Pharmacotherapy
 Oral glucose lowering agents.
 Injectables:
Insulin
Insulin analogues
Incretin mimetic agents.
 Newer agents.

Injectables
Insulin
Insulin analogues
Exenatide
Liraglutide

Indications for Use of Insulin
 All type 1DM patients
 High risk type 2 DM patients
 All pregnant diabetics not controlled with diet
 All acutely or chronically ill persons with DM
 All patients preparing for or just having surgery
 All diabetics who have trauma, leg ulcers,
gangrene, moderately severe nephropathy,
myocardial infarction.
 Any person who desires strict control

INSULIN DOSAGE
 0.6-1.0 units/kg body weight (ideal body weight)
 Divide this dose into tds if soluble insulin OR into bd if
70/30 insulin (humulin) used
 Additional 0.3 units/kg body weight added if infection,
sepsis or DKA present
 Insulin to be given 30 minutes premeals if 30:70 or
soluble insulin and 30-45 min premeal if Isophane or
Lente (Humulin N) insulin
 Do not add insulin to N/Saline infusion
 Do not give Humulin 30:70 or Isophane (Humulin
N)insulin I.V
 Adjust insulin dose with blood sugar

Targets for Control
 Absence of symptoms, well being
 Ideal body weight, BMI 20-23, maximum waist 88cm
in females and 94 in males
 Blood pressure 130/80mmHg
 FBS 70 -90mg/dL
 2hpp 70 – 140mg/dL
 HbA1c 6 – 7%
 Total cholesterol <5mmol(200mg)
 No proteinuria

Non-Insulin Hypoglycemic Agents
Oral
Biguanides
Sulfonylureas
Meglitinides
Thiazolidinediones
Alpha Glucosidase
inhibitors
Incretin Enhancers
(DPP-IV inhibitors)
Resin binder
Parenteral
 Amylin analogs
 Incretin mimetics
Diabetes Mellitus: An
Overview29/03/201451

Pharmacology - Biguanides
Class Biguanides
Compound Metformin
Mechanism Activates AMP-kinase
Action(s) • Hepatic glucose production
• Intestinal glucose absorption
• Insulin action
Glucose
Lowering Effect
• Fasting
• Post Prandial
Advantages • No weight gain
• No hypoglycemia
• Reduction in cardiovascular events and mortality (UKPDS
f/u)
Disadvantages • Gastrointestinal side effects (diarrhea, abdominal
cramping)
• Lactic acidosis (rare)
• Vitamin B12 deficiency
• Contraindications: reduced kidney function
Cost Low
Diabetes Mellitus: An Overview29/03/201452

Pharmacology - SulfonylureasClass Sulfonylureas (2nd generation)
Compound • Glibenclamide/Glyburide
• Glipizide
• Gliclazide
• Glimepiride (3rd generation)
Mechanism Closes KATP channels on β-cell plasma membranes
Action(s) Insulin secretion
Advantages • Generally well tolerated
• Reduction in cardiovascular events and mortality (UKPDS f/u)
Disadvantages • Relatively glucose-independent stimulation of insulin
secretion: Hypoglycemia, including episodes necessitating
hospital admission and causing death
• Weight gain
• Primary and secondary failure
Cost Low

Pharmacology – Meglitinides
Class Meglitinides
Compound • Repaglinide (Prandin®)
• Nateglinide (Starlix®)
Mechanism Closes KATP channels on β-cell plasma membranes
Action(s) Insulin secretion
Advantages Accentuated effects around meal ingestion
Disadvantages • Hypoglycemia, weight gain
• Dosing frequency
Cost Medium

Pharmacology – Thiazolidinediones
(TZD)
Class Thiazolidinediones (Glitazones)
Compound Pioglitazone (Actos®)
Mechanism Activates the nuclear transcription factor PPAR-
Action(s) Peripheral insulin sensitivity
Advantages • No hypoglycemia
• HDL cholesterol
• Triglycerides
Disadvantages • Weight gain
• Edema
• Heart failure (CI with stage III and IV)
• Bone fractures
Cost High

Pharmacology – Thiazolidinediones
(TZD)
Class Thiazolidinediones (Glitazones)
Compound Rosiglitazone (Avandia®)
Mechanism Activates the nuclear transcription factor PPAR-
Action(s) Peripheral insulin sensitivity
Advantages No hypoglycemia
Disadvantages • LDL cholesterol
• Weight gain
• Edema
• Heart failure (CI with stages III and IV)
• Bone fractures
• Increased cardiovascular events (mixed evidence)
• FDA warnings on cardiovascular safety
Cost High

TZDs and the FDA
 Rosiglitazone
 Restricted by FDA – can only be used by patients currently
benefiting from therapy or do not get adequate DM
treatment from other agents and not willing to use
pioglitazone
 1-800-AVANDIA
 Pioglitazone
 FDA alert – ongoing analysis of risk of bladder cancer
(with prolonged use >12 months)

Pharmacology – Alpha-Glucosidase
Inhibitors
Class α-Glucosidase inhibitors
Compound • Acarbose
• Miglitol
Mechanism Inhibits intestinal α-glucosidase
Action(s) Intestinal carbohydrate digestion and absorption
slowed
Advantages • Nonsystemic medication
• Postprandial glucose
Disadvantages • Gastrointestinal side effects (gas, flatulence,
diarrhea)
• Dosing frequency
Cost Medium

Pharmacology – Incretin Enhancers
Class DPP-4 inhibitors (incretin enhancers)
Compound • Sitagliptin (Januvia®)
• Vildagliptin (Galvus®)
• Saxagliptin (Onglza®)
• Linagliptin (Tradjenta®)
Mechanism Inhibits DPP-4 activity, prolongs survival of endogenously released
incretin hormones
Action(s) • Active GLP-1 concentration
• Insulin secretion
• Glucagon secretion
• Weight “neutrality”
Disadvantages • Occasional reports of urticaria/angioedema
• Cases of pancreatitis observed
• Long-term safety unknown (cancer ?)
Cost High

SGLT-2 Inhibitors
 Sodium glucose cotransport 2 inhibitors
 These are drugs which inhibit the reabsorption of
glucose in the distal tubules of the kidney
 Idea for using these drugs emanated from people with
the rare familial glycosuria patients
 Dapagliforzin, Canagliforzin are the first 2 in this group
 Cause weight loss and reduce weight by glycosuria
 Dapagliforzin failed FDA approval early last year
 Canagliflorzin (Invokana) was approved by FDA in
March 2013
 Side effects are nasal stuffiness and mild increase in UTI
29/03/2014
Overview60

Pharmacology – Incretin Mimetics
Class GLP-1 receptor agonists (incretin mimetics)
Compound • Exenatide (Byetta®)
• Liraglutide (Victoza®)
Mechanism Activates GLP-1 receptors (β-cells/endocrine pancreas;
brain/autonomous nervous system
Action(s) • Insulin secretion (glucose-dependent)
• Glucagon secretion (glucose-dependent)
• Slows gastric emptying
• Satiety
Advantages • Weight reduction
• Potential for improved β-cell mass/function
Disadvantages • Gastrointestinal side effects (nausea, vomiting, diarrhea)
• Cases of acute pancreatitis observed
• C-cell hyperplasia/medullary thyroid tumors in animals (liraglutide)
• Injectable
• Long-term safety unknown
Cost High

Pharmacology – Amylin Analog
Class Antihyperglycemic Synthetic Analog
Compound • Pramlintide (Symilin®)
Mechanism • Amylinomimetic
Action(s) • Glucagon secretion (glucose-dependent)
• Slows gastric emptying
• Satiety
Advantages • Potential weight loss
Disadvantages • Meal time injections
• Nausea
• Hypoglycemia in combination with insulin
Cost High
Diabetes Mellitus: An Overview
Lexi-Drugs Online [Internet]. Hudson (OH) : Lexi-Comp, Inc. 1978-2012[cited 2012
August 1].
29/03/201463

Pharmacology – Bile Acid
Sequestrants
Class Bile acid sequestrants
Compound Colesevelam (Welchol®)
Mechanism Binds bile acids/cholesterol
Action(s) Bile acids stimulate receptor on liver to produce
glucose
Results • Lowers fasting and post prandial glucose
• LDL cholesterol
Disadvantages • Constipation
• Triglycerides
• May interfere with absorption of other medications
Cost High

Outline
 Acute complications of DM
 - Hypoglycaemic emergencies
 - Hyperglycaemic emergencies
 Chronic complications of DM
 - Vascular
 - Neuropathic
 - Mixed

DIABETIC KETOACIDOSIS
 Definition
 Epidemiology
 Aetiopathogenesis/Pathophysiology
 Clinical features
 Investigations
 Treatment
 Prognosis

Definition
 An acute metabolic complication of DM
 Hyperglycaemia (>300mg/dL)
 Acidosis , blood pH <7.3
 Increased total blood ketones, > 5 mmol/L
 In clinical practice it is suspected when there is
ketonuria++ in the face of hyperglycaemia

Epidemiology of DKA
 Few published Nigerian data
 Europeans and Americans quote 10 – 30 cases
per 100, 000 population.
 Commoner in females
 Commoner in non-whites
 Mortality higher in the elderly

Aetiopathogenesis/Pathophysiology
 Insulin deficiency and glucagon excess leads to
excess acetyl-CoA
 Acetyl CoA is converted to acetoacetate
 Some acetoacetate is converted to other
ketones
 These ketones require to be buffered and thus
bicarbonate is used up as pH drops
 The respiratory centre is stimulated and
Kussmaul’s breathing occurs

Aetiopathogenesis/Pathophysiology
 Urine becomes acidic, osmotic diuresis occurs
 H and Na and K are lost in the urine together
with ketones
 FFAs are increased due to lipolysis from
stimulation of lipoprotein lipase
 A major role for initiating all the events is
elevation of counter-regulatory hormones

Clinical Features
 Risk factors of
infection, trauma,
omission of
medication
 Malaise
 Weight loss
 Polyuria, polydipsia,
 Nausea, vomiting,
abdominal distension
 Confusion, lethargy
 Hypotension,
arhythmias
 Severe dehydration
 Acetone breath
 Glycosuria and
ketonuria

Clinical Features contd
 Deep coma and or seizures may occur
 Acute abdomen may be present and confused
with surgical abdomen
 Fluid loss is in range of 6 – 8 litres in adults

Role of Insulin

Investigations
 Urinalysis
 Ketostix
 Electrolytes and urea
 Haemogram incl WBC
 Blood pH and ketones
 ECG,
 Urine and blood culture
 Blood sugars

Treatment
 Admit to emergency or ICU, NPO, resuscitate
 Intravenous saline 6 – 8 litres in 24 hours in adults
 Saline given 1 litre fast, then 1 litre in an hour, then
1 litre in 2hrs, then 1 litre 4 hourly
 Soluble insulin 10 units IM or IV stat, then give 6
units hourly till RBS <250mg/dL
 Sugars should drop at 50-70mg/dL per hour
 If not dropping double the dose of insulin

Treatment (contd)
 When RBS <250mg/dL change the IV fluids to
5% dextrose to run 1 pint 4 hourly and add KCl
20 – 40mmol per pint with soluble insulin 4-6
units per pint
 When patient fully conscious and rehydrated
then change insulin to s/c t.d.s pre-meals at
dose of 0.2 – 0.3 units/kg body weight and allow
patient eat

Treatment 4
 Antibiotics may be indicated if sepsis present but
it should be remembered that leucocytosis is a
regular feature of DKA
 NG tube may be required if there is gastric
dilatation
 Dysequillibrium syndrome is a complication of
excessive rapid lowering of blood sugar

Prognosis
 This is good if treatment commenced early and
adequate monitoring of sugars, electrolytes and
fluid balance is done.

HYPEROSMOLAR
HYPERGLYCAEMIC STATE (HHS)
 Definition
 Epidemiology
 Aetiopathogenesis/Pathophysiology
 Clinical Features
 Investigations
 Treatment
 Prognosis

Definition of HHS
 Similar to DKA but:
 Blood sugars in range of 600 – 2000mg/dL
 No ketonuria or trace ketones
 No anion gap or mild anion gap <10
 Often have azotaemia, increased Na, K
 Normal blood pH

Epidemiology
 HHS is not as common as DKA
 Commoner in elderly patients who are often
institutionalised or with cognitive impairment
 Males slightly more commonly affected
 Seen in type 2 DM
 Rare in type 1 DM

Aetiopathogenesis
 Patient is fairly insulin sensitive
 There is still some circulating insulin sufficient to
suppress ketosis but insufficient to suppress
gluconeogenesis
 Renal impairment couple with dehydration from
reduced fluid intake over a period
 Often patient on diuretic
 Hyperosmolarity ensues with thrombogenicity

Clinical features
 Polyuria, polydipsia and then oliguria
 Confusion or coma
 Severe dehydration
 No Kussmaul’s respiration
 DVT or PE is common

Clinical Features
 Severe dehydration, fluid deficit 8 – 10 litres
 Altered sensorium, seizures, etc
 Thromboembolic events eg DVT, PE, CVA, , MI,
etc
 Vomiting and gastroparesis
 Gastric erosions and haematemesis common

Investigations
 E/U/C
 Urinalysis
 Blood sugars
 Sepsis workup
 Plasma osmolarity, plasma pH
 ECG, CXR, D-dimer tests

Treatment
 Very similar to DKA treatment
 Admit, NPO
 Rehydrate with 6 – 10 litres of fluid preferably
half normal saline
 Hourly soluble insulin 4-6 units after a stat
10units IV
 Use heparin or enoxaparin to anticoagulate
 Watch out for fluid overload if CKD present

Prognosis
 Poorer than DKA, mortality being 50 – 90% in
most centres
 Mortality may follow cerebral oedema, embolic
events or uraemia

Hypoglycaemia
 Defined as low blood sugar
 Blood sugars below 2.2mmol/L taken as
hypoglycaemia in general population
 In DM patients the threshold for hypoglycaemia
is lower so coma may occur in blood sugars 50 –
80mg/dL and in those with rapid decline in blood
sugars

Definition
 Thus Whipple’s triad often used to identify and
confirm hypoglycaemia in DM patient
 Triad is made up of
 - hypoglycaemic symptoms
 - biochemically proven low blood sugar
 - relief of symptoms after administration of sugar
or carbohydrate containing drink/meal

Aetiopathogenesis of Hypoglycaemia
 Excess insulin whether from injections or
secretagogue
 Inadequate calorie intake
 Inadequate counter-regulatory response
 Continued insulin secretion or insulin action

Risk factors for Hypoglycaemia
 Skipping or postponing meals
 Overdose of hypoglycaemic agents
 Poor monitoring of blood sugars
 Age – extremes of age, the very young and the
elderly
 Alcohol and other substances that potentiate
hypoglycaemic drugs

Clinical features
 Adrenergic symptoms: eg palpitations, tremors,
sweating
 Neuroglycopenic symptoms: dizziness,
headache, coma, seizures, confusion, etc
 Glucagon related symptoms : nausea, vomiting,
borboygmi

Investigations
 Blood sugars
 Insulin assays
 C-peptide
 Liver, renal function tests

Treatment
 Resuscitate with glucose containing soft drink, sugar
or glucose at home if conscious
 Admit to hospital if unconscious or if first aid with
sugar at home not working
 Resuscitate and give IV 10% glucose or diluted 50%
glucose via wide bore access
 Give IM glucagon 1mg if available
 Continue to monitor blood sugars, omit insulin or
OHAs patient was taking

Treatment contd
 When conscious and alert encourage to eat
 If delay in regaining consciousness KIV stroke,
MI, uraemia or other co-morbidities
 Thus CT scan, ECG, E/U/C may be required
 Prevent recurrence by drug dose adjustment
and patient education

Conclusion
 Early detection and recognition of metabolic
complications is vital for full recovery
 Self glucose monitoring will prevent these
conditions

QUESTIONS
Overview29/03/201499

Diabetes mellitus an overview

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