DIABETES MELLITUS

SUSAN NYABATE
OUTLINE
• Define diabetes mellitus • Investigations
• Aetiology and • Diagnostic criteria for
classification of DM DM
• Epidemiology of DM: • Management of DM
Prevalence, incidence
and mortality • Comorbidities in
• Pathophysiology
diabetes
of DM
• Prevention and control
• Risk factors
• Clinical manifestations
OBJECTIVES
1. To define Diabetes Mellitus
2. To classify Diabetes Mellitus
3. To understand the modifiable and non-modifiable
risk factors of DM
4. To learn how to diagnose DM
5. To understand the management of Type 1 DM, Type
2 DM, and Gestational diabetes.
6. To understand how to manage comorbidities in DM.
7. To understand how to prevent DM and its
complications
DEFINITION
• Diabetesmellitus is a chronic metabolic
disorder characterised by sustained
elevated serum glucose resulting from
defects in insulin secretion, action or
both.
• It
is a complex illness that requires
continuous medical care with
multifactorial risk reduction strategies
beyond glycaemic control.
AETIOLOGY AND
CLASSIFICATION
• Classification is based on the aetiology of
disease.
• Include:
1. Type 1 diabetes
2. Type 2 diabetes
3. Gestational diabetes
4. Other types of diabetes
Type 1 Diabetes
• Resultsfrom autoimmune destruction of the
pancreatic beta cells leading to absolute insulin
deficiency
• Usuallypresents in childhood, adolescence and young
adulthood although it might present as early as 6 months.
• Type1 diabetes that presents at a later age is known as
Latent Autoimmune Diabetes in Adults.
• It is insulin dependent diabetes mellitus.
Type 2 Diabetes
• Progressiveloss of beta cell insulin secretion
frequently on the background of insulin
resistance.
• More common among adults (30-40 years) but
increasingly been diagnosed in younger
people who are obese or overweight.
• Is
the most common (about 90%) form of
diabetes and it is insulin independant.
Gestational Diabetes Mellitus
• Thisis diabetes diagnosed in second and third
trimester in a pregnant woman who was
previously not known to have diabetes.
• It
is often asymptomatic and has to be
screened for.
• It
is associated with poor pregnancy outcomes
especially if untreated but usually resolves
after delivery.
Maturity Onset Diabetes of the Young
• MODY is a rare form of DM that is inherited in
an autosomal dominant manner. It is caused by
a mutation in one of 11 genes involved in
insulin production.
• Itis different from Type 1 and Type 2 DM and
is believed to account for 5% of all diabetes
mellitus cases.
• It is also referred to as monogenic diabetes.
 Other Types of Diabetes

• Lesscommon and include:

1. Genetic disorders such as Down’s syndrome
2. Infections e.g. Coxsackie virus, CMV
3. Diseases of the exocrine pancreas
(pancreatitis, cancer of the pancreas)
4. Endocrinopathies (hyperthyroidism,
Cushing’s syndrome, Acromegaly)
5. Drug induced (corticosteroids,
antipsychotics, Protease inhibitors, thiazide
diuretics)
 Differences between Type 1 and Type 2
DM
CHARACTERISTIC TYPE 1 DM TYPE 2
S
Onset Sudden, acute and sub-acute Slow, insidious and progressive
Age Usually <30-35 years Older patients >35 years
Typical symptoms Moderate to severe symptoms Often symptomatic because of slow
present onset of disease
Weight Lean, with rapid weight loss Normal to overweight at diagnosis
before diagnosis
Insulin secretion Insulin deficient, needs insulin Initially inadequate insulin secretion
treatment at diagnosis with progressive deficiency over time
Chronic Uncommon Common because of late diagnosis
complications at
diagnosis
Insulin resistance Absent Present
CHARACTERISTI TYPE 1 DM TYPE 2 DM
CS

C peptide levels Very low or absent Normal or reduced

Differences…
Immune markers Autoimmune disease: anti-GAD, Absence of autoimmune markers
ICA, IA-2

Heredity Less common More common

Metabolic Absent Present (cluster of CVD risk factor)

syndrome

Treatment Insulin therapy Initially lifestyle changes +/- oral

glucose lowering agents +/- Insulin

Acute complications DKA HHS but may cause DKA

Treatment associated Treatment associated hypoglycaemia
hypoglycaemia

Chronic More prone to microvascular High risk for macrovascular

complications of complications complications but may also develop
Diabetes microvascular complications.
 EPIDEMIOLOGY
• According to the World Health organisation, the global
prevalence of diabetes among adults over 18 years was 8.5%
in 2014.
• In2016, an estimated 1.6M deaths globally resulted directly
from diabetes.
EPIDEMIOLOGY
• Prevalenceof diabetes in Kenya is estimated to be 3.1-
4.6% with mortality being at about 1% of total deaths.
(WHO,2016). An estimated 1 in every 17 Kenyans have
diabetes and 12,800 Kenyans died from diabetes and
high blood sugar in 2014.
• It
is estimated that about two thirds of people with
diabetes worldwide are undiagnosed.
 PATHOPHYSIOLOGY
• The
pancreas secretes digestive enzymes and
hormones insulin and glucagon into the
bloodstream that control the amount of glucose in the
body.
• Release
of insulin lowers blood glucose levels by
allowing glucose to enter the cells where it is
metabolised.
• Glucagonis released to stimulate the release of
glucose from the liver following a drop in blood
glucose levels
 Endogenous insulin
• Insulinis a small protein of MW 5808 that is made up of 2
chains (a and b) of 51 amino acids joined by disulphide bonds
• Pro-insulinis processed within the Golgi apparatus of the beta
cells and packaged into granules where it is hydrolysed into
insulin and a C-peptide (has no hypoglycaemic effect)
segment.
• Insulin
and C-peptide are secreted in equimolar amounts in
response to insulin secretagogues.
• Granules inside the beta cells store the insulin in the form of
crystals containing 2 zinc atoms and six molecules of insulin
Endogenous insulin
 Determinants of insulin secretion
Stimulate release Inhibit release
Glucose Chronically elevated glucose
Other sugars like mannitol
Amino acids esp the gluconeogenic
ones

Hormones like GLP-1, GIP and Hormones like insulin and leptin
glucagon

High concentration of fatty acids Low concentration of fatty acids

Beta adrenergic stimulation Alpha adrenergic stimulation
Insulin secretagogues and quinine Inhibitory drugs like vinblastine,
colchicine, phenytoin
Insulin secretion
Endocrine effects of insulin
 Pathophysiology of Type 1 DM

• Lossof insulin secretion results from the autoimmune

destruction of insulin producing beta cells is triggered
by environmental factors such as viruses and toxins in
genetically susceptible individuals
• Sincethe capacity of normal beta cells to secrete insulin
far exceeds the normal amounts needed to control
metabolism, the clinical onset of diseases is preceded by
an extensive asymptomatic period during which beta cells
are destroyed.
Pathophysiology of Type 1 DM
• Beta
cell destruction usually occurs over a period of
weeks, months or years
• Deficiencyof insulin results in:
1.Increased hepatic glycogenolysis and impaired non-
hepatic glucose utilisation
2.Kidneys capacity to reabsorb glucose is surpassed leading
to glucosuria which results in polyuria, polydipsia and
polyphagia
3.Uncontrolled lipolysis leads to elevated levels of free fatty
acids that when oxidised leads to generation of ketones
4.Increased proteolysis with weight loss
Pathophysiology of Type 2 DM
• Type 2 DM is characterised by impaired
insulin secretion and insulin resistance,
however, the exact pathophysiology is not
known.
• Basalinsulin levels are typically normal
or elevated at diagnosis.
Pathophysiology of Type 2 DM
• There is islet cell dysfunction in which the
reciprocal relationship between alpha and
beta cells is lost leading to reduced insulin
production in response to glucose.
• This results in postprandial hyperglycaemia
• With time, beta cells lose their ability to
respond to elevated glucose concentrations
leading to increasing loss of glucose
control.
Pathophysiology of Type 2 DM
• Mostindividuals with type 2 DM exhibit
decreased tissue response to insulin.
• Excessweight or hyperglycaemia may contribute
to hyperinsulinemia which in time may lead to a
downregulation of the number of insulin
receptors on target tissues and organs.
• Decreased peripheral glucose uptake and
utilisation in muscle is the primary site of insulin
resistance and results in post prandial
hyperglycaemia
Pathophysiology of Type 2 DM
• Resistancemay be secondary to decreased
number of receptors, decreased affinity of
receptors or defects in insulin signalling
and action that follows receptor binding.
• Patientswith Type 2 DM also exhibit
increased hepatic glucose production
reflected by elevated blood glucose levels
Pathophysiology of Type 2 DM
• Ultimately,a vicious cycle caused by
untreated fasting and postprandial
hyperglycaemia resulting from by
decreased glucose uptake and increased
hepatic glucose production,
hyperinsulinemia and increased insulin
resistance inflicts ongoing damage to
tissues and organs
 RISK FACTORS FOR TYPE 2
DIABETES MELLITUS
MODIFIABLE RISK FACTORS NON-MODIFIABLE RISK
FACTORS
Overweight and obese Age > 40 years
Physical inactivity First degree relative with diabetes
Unhealthy diet Polycystic ovarian syndrome
Impaired glucose tolerance Previous gestational diabetes or
large baby >4kg
Dyslipidaemia African and Asian ancestry
Alcohol abuse and tobacco use
Hypertension
 CLINICAL MANIFESTATIONS
MOST COMMON LESS COMMON

Weight loss Excessive hunger

Polyuria/bedwetting in young Blurred vison

children
Excessive thirst (polydipsia) Mood changes

Fatigue Skin infections

Polyphagia Oral or vaginal thrush

Abdominal pain
 DIAGNOSIS OF DIABETES
MELLITUS
TEST IMMEDIATE DIABETES
HYPERGLYCAEMIA

Fasting blood glucose 6.1 – 7.0 mmol/L ≥ 7.0mmol/l

OR 2 hour OGTT 7.8 – 11.0 mmol/L ≥ 11.1 mmol/L

OR Random blood glucose ≥ 11.1 mmol/L

in a symptomatic patient

OR HbA1C ≥ 6.5%
 PREDIABETES
• Prediabetesis a term used to distinguish people
who are at increased risk of developing diabetes.
• Thesepatients either have impaired fasting
glucose (IFG) or impaired glucose tolerance
(IGT)
• The WHO and ADA define it as:

IFG FBG of 5.6mmol/l-6.9mmol/l

IGT 2 hour OGTT of 7.8-11.0 mmol/l
HbA1C 5.7-6.4%
PREDIABETES
• Progression to diabetes is not inevitable and can
be mitigated by weight loss, physical activity and
dietary control.
• Metformin may be administered to these patients.
• Frequent screening, as recommended should be
done.
SCREENING FOR TYPE 2 DM
• Screeningand early diagnosis of diabetes is
important considering the insidious nature of
symptoms, misdiagnosis and poor health
seeking behaviour.
• It
should be repeated annually if found to be
normal.
• Screening should be considered for:
 All individuals with any risk factors
 Across all populations using the relevant cut
offs
POPULATION GROUP/RISK PARAMETERS
Overweight or obese BMI greater than 25
First degree relative with diabetes
Women previously diagnosed with GDM or
delivered baby weighing >4kg

History of CVD
Hypertension Blood pressure greater than 140/90
mmHg on therapy for hypertension

Blood lipids
Women with PCOS
Physical inactivity <150mins of moderate activity per
week

Other clinical conditions associated with

insulin resistance

Unhealthy diets
INVESTIGATIONS
• Complete medical and family history
• Physical examination
1.Height and weight measurement for BMI assessment
(done at every visit)
2.Blood pressure measurement (every visit)
3.Injection site assessment (every visit)
4.Oral cavity assessment for dental carries and gum
disease (initial visit and annually thereafter)
5.Eye assessment for visual acuity and fundoscopy
(initial visit and annually there after)
 Investigations

• Laboratory tests
1.Glucose (every visit)
2.HbA1c (done at initial visit then six monthly if on target,
or every three months if problematic)
3.TSH (at initial visit then annually there after)
4.Lipid profile (done annually)
5.UECs (initially then annually)
6.HIV (at initial visit and annually there after)
7.Urinalysis (at initial visit then annually thereafter or as
needed)
MANAGEMENT OF
TYPE I DIABETES
PHARMACOLOGICAL
MANAGEMENT
 INSULIN THERAPY
• Insulin is the mainstay in the treatment of Type I DM
• The most common regimens are
1.Basal bolus regimen (aka Multiple daily injections)
using short/rapid acting insulin given with main meal
and intermediate or long acting insulin given OD or
BD
Is the preferred method
2. Twice daily insulin
Using premixed insulin or short acting and
intermediate acting insulin
Calculation of Total Daily Insulin
Requirements
• Although the total daily insulin is calculated as
0.5-0.75 U/kg/day, there are two formula that
can be utilised
• Based on BMI
• BMI > 25 then the patient is considered obese
and thus use the formula 0.6 Units/kg/day
• BMI ≤ 25 then the patient is considered
normal and thus use the formula 0.5
Units/kg /day
• TDI = 0.55 * patient’s weight (kg)
 Basal bolus regimen
COMBINATION ADMINISTRATION

Short acting and Short acting insulin analogue (60%) (round off to the nearest Long acting insulin
long acting insulin whole number) analogue (40%)
analogues

Before breakfast Before lunch Before dinner Before dinner

20% 20% 20% 40%

OR

Short acting and Short acting insulin analogue (70%) (round off to the nearest Intermediate acting
intermediate acting whole number) insulin analogue
insulin analogues (30%)

Before breakfast Before lunch Before Dinner Before dinner

70%/3 70%/3 70%/3 30%

 Twice daily injections

• Thisinvolves the giving of premixed insulin or short acting and

intermediate acting insulin in to divided doses that is, 2/3 in the
morning before breakfast and 1/3 in the evening before
dinner.
• Insulinrequirements may decrease during the honeymoon period
before rising again
• TDI generally increases as a child grows
• Duringperiods of regular changes in food consumption, TDI
should not be increased but should be redistributed according
to amount and timing of carbohydrate intake.
Twice daily injections
 Question
• A 55year old man with T2DM was initiated with SC
soluble insulin 24U TDS. His BMI was 30. Four
months later, he was switched from soluble to Mixtard
• A)calculate the weight in kgs and height in m the man
• B)Determine the appropriate dose and dosing schedule
for Mixtard, where his BMI had reduced to 24.9
• C)Mixtard is available in 10ml vial with a strength of
100U/ml. Determine the number of days that one
mixtard vial would last
Answers
• A) 120kg and 2m
• B)34Umorning 30mins before breakfast
and 17U evening 30mins before dinner
• C) 20 days
 Proper insulin injection technique using
syringe

1. Wash your hands using proper hand washing technique

2. Check the insulin for lumps, crystals and discoloration. If okay,
roll between your hands until uniformly cloudy. Do not shake.
3. Wipe the top of vial with an alcohol swab
4. Pull the plunger down to let required number of units of air into
the syringe
5. Push the air into the insulin bottle and leave the needle in the
bottle
6. Turn the insulin bottle and syringe upside down and pull the
plunger down to let the required number of units of insulin in
 Proper insulin injection technique

7.Look for air bubbles in the syringe. If present, push the insulin
back into the vial and repeat step 6
8. Clean the injection site with an alcohol swab
9. Pinch up the area of the skin.
10. Holding the syringe like a pencil, push the needle at 90 degrees
into the skin. Push the plunger
11. Release the pinch, then pull the syringe needle out of the skin.
12. Dispose of the syringe into sharps container.
Sites of injection: thigh, abdomen, gluteus, upper and outer arm
Monitoring insulin therapy in Type 1
DM
 Interpretation of BGL
• Pre-meal BGL is always high: preceding dose of intermediate or
long acting insulin is insufficient
• Pre-meal BGL is always low: previous dose of intermediate or long
acting insulin is too high
• Pre meal BGL is sometimes very high and at times very low: either
insulin, food or exercise are not consistent and should be reviewed
• BGL 2 hours after meals is too high: the meal dose of regular
insulin was too low
• BGL 2 hours post meal is too low: the previous meal dose of regular
insulin was too high
• Note that the level of blood glucose in the early morning can rise
(dawn phenomenon)
 Adjusting insulin dose
• Before
adjusting the insulin dose consider the
following:
 Rule out other causes of deviations such as infections,
noncompliance and alcohol consumption
 Do not adjust or omit the insulin dose that follows a deviant
glucose level
 If insulin requirements are increased when a patient has an
infection, remember to lower the dose after recovery
 Adjusting insulin dose
• Before adjusting insulin dose consider:
 While a patient is hospitalised, they usually do not consume
their normal diet. This should be considered before making
adjustments

 If patients have unusual readings while in hospital, check

their usual injection site. If a different sit is used while in
hospital, absorption may differ slightly. If the same site is
used every time, lipodystrophy may cause erratic insulin
absorption.
 Adjusting insulin dose
• Always fix the lows first and the highs later
• Adjust one insulin at a time if they are on different types
• Nightmares, restless sleep, headache on waking, a wet
pillow or sheets may be signs of sleeping through an
episode of hypoglycaemia
Adjusting the insulin dose
• If
the patient is on • Ifthe patient is on
short and rapid intermediate acting,
acting insulin: long acting and
• Adjust by no more premixed insulin
than 2 units (or 10% • Adjustby no more
of the dose daily) than 2 units or 10%
(whichever is
greater) every 3-4
days
Somogyi effect
• Thisis rebound hyperglycaemia in response to
low blood glucose
• Insulinusers may experience high blood glucose
in the morning as a result of an overabundance of
insulin at night leading to prolonged nocturnal
hypoglycaemia
• The body responds by releasing glucagon,
epinephrine and cortisol elevating blood glucose
that may be seen the following morning.
Dawn phenomenon
• Thisis morning rise in blood sugar in
response to waning insulin and a
growth hormone surge.
Honeymoon period in diabetes
• The honeymoon period is a time after diagnosis
where symptoms subside often after change in diet or
introduction of medication
• This is especially common in people with LADA
• Inmany newly diagnosed diabetes, not all beta cells are
destroyed. After initiation of insulin, aerobic metabolism
resumes and glucose is transported into cells and
metabolised for energy.
• After the body starts utilising glucose, the remaining
islets cells may begin to recover the ability to produce
insulin, resulting in a honeymoon period.
NON-PHARMACOLOGICAL
MANAGEMENT
• Patient and family education
 Ensures that the patient and their family is
equipped with enough information to
adequately manage the disease and correctly
identify and prevent complications
• Nutritional management
 Nutritional counselling should emphasise the
need for a healthy diet with food in proportions
appropriate to age and stage of disease
MANAGEMENT OF
TYPE 2 DM
Goals of management
1. Management of hyperglycaemia (maintenance
of euglycemia)
2. Prevention and treatment of complications of
diabetes mellitus
NON-
PHARMACOLOGICAL
MANAGEMENT
Patient education
• Thisis important in ensuring good glycaemic
control and prevention of diabetic complications
• It
is a continuous, individualised process that
should be offered to all patients at time of
diagnosis and consolidated at regular intervals
thereafter.
Patient education
• It
may touch on:
1.Overview of diabetes
2.Self- glucose monitoring
3.Need for physical activity
4.Preventing and delaying diabetic
complications
5.Managing stress
6.Dietary control
Dietary management
• Thisis based on the principle of healthy eating
in the context of socioeconomic, cultural and
psychological influences of food choices.
Dietary management
• Principles
of dietary management:
1.Follow a healthy, balanced eating plan
2.Monitoring carbohydrate intake is key in achieving
optimum glycaemic control. Carbohydrates
should make up 45-60% of the total energy
intake.
3.For individuals with normal renal function, no
modification of usual protein intake is needed.
Proteins should make up 15-20% of the total
energy intake.
 Dietary management
4. Fat intake should be restricted to <35% of the
total energy intake with abundance of
unsaturated fats and limitation of saturated fats to
<7%
5. Limit all kinds of salt intake
6. Supplement vitamins and minerals in special
groups such as elderly, lactating and pregnant
women and vegans
7. Moderate alcohol consumption.
Tools used in meal planning
1.Plate model
2.Hand portion guide
3.Glycaemic index and glycaemic load
4.Food groups and food serving
5.Carbohydrate counting
Physical Activity
• Regularphysical activity improves metabolic
control, increases insulin sensitivity, improves
cardiovascular health and helps weight loss and
its maintenance.
• Typesof physical activity:
1.Aerobic or endurance exercise e.g. walking
2.Anaerobic or resistance exercise e.g. lifting
weights
 Physical activity and exercise
 Aerobic form is usually preferred.
 A detailed physical evaluation of cardiovascular and
renal systems, eye, neurological and foot status should be
performed before starting an exercise program.
Physical activity and exercise
 The prescribed physical activity programs should be
appropriate for the age, socioeconomic status, state of
physical fitness, lifestyle and level of glycaemic
control.
 Physical activity should regular (3 days/week, last
at least 20-30 minutes per session and be at least of
moderate intensity.)
PHARMACOLOGICAL
MANAGEMENT
Oral Glucose Lowering Agents
(OGLAs)
• Indications
 Individuals with type 2 DM whose glycaemic targets
are not met by combination of dietary modifications
and physical/exercise
 Indicated at first presentation of diabetes i.e. FBS>
11mmol/L or RBS >15mmol/L
• The first line is Metformin unless contraindicated
Factors to consider when choosing an
OGLA
• Patient’s characteristics
• Lifestyle
• Degree of glycaemic control
• Cardiovascular and renal risks
• Access to drugs
• Economic status
• Agreement between the doctor and the
person living with diabetes
OGLA
• Useof the stepped up care approach is
recommended as monotherapy is seldom sufficient
• Combination therapy should be considered as initial
choice if HbA1C is greater than 8%
• Threedrug combination therapy can be used when 2
drug regimens fail to achieve target values. However,
this may create compliance problems.
• Fixed dose combinations increase but may inhibit the
flexibility of dosing prescription.
CLASS DRUG DOSE MAJOR SIDE
EFFECTS

Sulfonyureas Glibenclamide 2.5mg od or bd (max Hypoglycaemia,

15mg/d) with meals weight gain, skin
rashes
Glimepiride 1mg od (max 4mg/d) Hypoglycaemia,
with meals weight gain, skin
rashes
Biguanides Metformin 500mg OD (max 2g/d) GI disturbances, lactic
with meals acidosis, B12
deficiency
Thiazolidinediones Pioglitazone 15mg OD (max Hepatotoxicity,
45mg/d) dilutional anaemia,
osteoporosis, weight
gain
Meglitinides Repaglinide 1mg bd, tds or qid Hepatotoxicity,
(max 16mg/d) before dilutional anaemia,
meals weight gain

Alpha glucosidase Acarbose 25mg tds (max 300mg) Dyspepsia, diarrhoea,

inhibitors with meals flatulence
CLASS DRUG DOSAGE MAJOR SIDE
EFFECT

DPP 4 Inhibitors Vidagliptin 50mg OD or BD (max Urticaria, angioedema,

100mg/d) acute pancreatitis

Sitagliptin 100mg OD

SGLT2 inhibitors Dapagliflozin 5mg OD (max Polyurea, UTI, DKA,

10mg/d) candidiasis,
hypotension

Canagliflozin 100mg OD (max

300mg/d)
Insulin Therapy in Type 2 Diabetes
• Indications for Insulin
1.Poor glycaemic control
2.HbA1C still ≥ 8% despite previous attempts to
improve lifestyle modification and maximum oral
therapy.
3.Patient is symptomatic (weight loss, polyuria,
polydipsia, recurrent infections)
4.Steroid-induced diabetes
5.Patient unable to tolerate or has contradiction to
OGLAs
 Insulin therapy in type 2 DM
6. Gestationaldiabetes or diabetes in pregnancy not
controlled on OGLAs
7. Painful neuropathy
8. Foot ulceration and infection
9. Presentation in hyperglycaemic emergency
10.Peri-operative period especially major or emergency
11. Organ failure or other medical conditions requiring
tight glycaemic control e.g. acute MI
 Dosing of insulin in type 2 DM
• The regimen and dose of insulin therapy varies from patient to patient
• Initiate basal insulin with metformin +/- other OGLA at 10U/day or
0.1-0.2U/kg/day then adjust once or twice weekly to reach glycaemic
control
• If HbA1C is not controlled, consider combination injectable therapy
 Add 1 rapid-acting insulin injection before largest meal
4 units, 0.1U/kg or 10% basal dose adjusted by increasing the dose by 1-
2U once or twice weekly until targets are met OR
 Add GLP-1 RA OR
 Change to premixed insulin twice daily (before breakfast and supper)
DIABETES IN
PREGNANCY
 Classification

• Classified as either diabetes in pregnancy or gestational diabetes

mellitus
DIABETES IN PREGNANCY GESTATIONAL DM

DEFINITION Pregnancy in a patient known to Hyperglycaemia diagnosed for the 1 st

previously have DM time in pregnancy (2nd or 3rd trimester)

HYPERGLYCAEMIA Hyperglycaemia diagnosed for the 1st
time during pregnancy that meets the
WHO criterion for DM in non-pregnant
state
OCCURRENCE May occur at any time during pregnancy
including the first trimester
Hyperglycaemia levels do not meet
WHO criterion for DM
May occur at any time during
pregnancy but usually after 24 weeks
Diagnostic criteria
 Management of Diabetes in pregnancy
• Give appropriate preconception and pregnancy planning
and care that ensures that glycaemic control is optimised
at least 3 months before conception
• Insulinin the medication of choice for pregnant
patients with diabetes. If sugars are well controlled,
manage the patient on metformin and glibenclamide
• Glycaemiccontrol during labour and delivery is of
utmost importance to avoid adverse neonatal outcomes
• Bloodglucose should be monitored hourly during labour
and delivery ensuring it is maintained at 4-7mmol/L
Management of diabetes in pregnancy
• Give IV glucose, potassium and insulin injections (10%
dextrose 500ml +10 mmol KCl + 10-14 units soluble
insulin depending on BGL to run 5 hours) at the onset of
labour.
• Afterdelivery and removal of the placenta reduce the
insulin in GKI infusion by half to prevent hypoglycaemia.
• Once the mother is able to feed, give pre-pregnancy doses
of insulin or OGLA
• Measure BGL in the neonate at birth and encourage
breastfeeding
 Management of GDM

• Women at high risk of GDM include:

 BMI >30
 Age >35 years
 Previous history of GDM
 Persistent glycosuria
 Previous large baby (>4kg)
 Poor obstetric history (miscarriages, still births, congenital
anomalies)
 Family history of diabetes
 Pregnancy with polyhydramnios
 PCOS
 Multiple gestation
 Management of GDM
• Advise patient on importance of healthy diet and glucose
optimisation (FBS<5 mmol/L)
• If blood glucose is not optimised within 2 weeks put the patient on
Metformin or Insulin
• Delivery at 38 weeks is advised if sugars are well controlled
• Stop OGLA and Insulin after delivery and monitor blood glucose.
• If RBS >7.8mmol/L or FBS >6.1mmol/L postdelivery, manage as
pre-existing diabetes.
• If BGL are normal post delivery, repeat OGTT at 6 weeks the
annually thereafter
 Complications of DIP and GDM
Maternal Foetal/Neonatal
In Pregnancy Miscarriages Macrosomia > 4kg
UTI Congenital malformations

Pre-eclampsia/eclampsia Sudden foetal death

Polyhydramnios
Pre-term labour
Intra and postpartum Complications of having a large baby

Long term CV disease Obesity

GDM in subsequent pregnancies Diabetes

Overt DM Metabolic syndrome

Hypertension
COMORBIDITIES IN
DIABETES
Comorbidities
• Theseare diseases that coexist with the primary
disease
• Comorbidities that exist with diabetes include
but are not limited to:
1.Hypertension
2.Dyslipidaemia
3.Mental health
4.HIV
5.Tuberculosis
6.Cancer
 HYPERTENSION
• BP inpeople with Type 2 DM should be determined at
every visit
• BP ≥ 140/90 mmHg should be classified as hypertensive.
• BP targetsof therapy are 130/80 mmHg or lower for
patients with microalbuminuria
• Non-pharmacologic measures such as healthy diet, exercise
and weight loss, reduction of alcohol and tobacco cessation.
• Pharmacological
therapy is indicated when BP ≥ 140/90
mmHg persists despite lifestyle modification.
• Multiple agents may be required.
 Management of hypertension algorithm
BP≥140/90mmHg in adults >18 years

Start lifestyle changes (lose weight, reduce dietary salt and alcohol and stop smoking

Stage 1: 140-159/90-99 (without Hypertension with

other CV risk factors or Stage 2: ≥ 160/100 comorbidities/complica
abnormal findings tions

Monitored lifestyle management

up to 3 months

Start antihypertensive therapy

Goal BP achieved (<140/90)

Continue follow up
 Potential problems with certain
antihypertensives
1. Diuretics in large doses inhibit insulin release
2. Beta blockers may blunt or mask symptoms of
hypoglycaemia and exacerbate peripheral vascular
disease
3. Dyslipidaemia may be worsened by beta blockers and
diuretics
4. Impotence and postural hypotension may be precipitated
by alpha blockers and centrally acting agents
5. ACEIs may induce hyperkalaemia, renal failure or
persistent cough
CLASS DOSAGE REGIMEN COMMENTS

ACEIs Enalapril 5mg OD optimized to 20mg bd First line therapy as it

Drug doses
(max 40mg/d) delays progression of
diabetic nephropathy

ARBs Losartan 50mg Od (max 100mg OD) Given if ACEI s/e are not
tolerated

CCBs Nifedipine 20mg bd (max 30mg bd) CCBs given as added

Amlodipine 5mg od (max 10mg od) combination therapy

Diuretics Furosemide 40mg morning Given in the event of

oedema

Beta Atenolol 50mg OD (max 100mg/d) Choose cardio selective

blockers betablockers
MENTAL HEALTH DISORDERS
• Psychosocial and emotional challenges exist in people
living with diabetes including:
 Depression
 Disordered eating behaviour
 Anxiety disorders
• Psychotropicagents may increase the incidence of
diabetes and may affect glycaemic control
 Clozapine
 Olanzapine
 Duloxetine
Management of mental disorders
• Screenindividuals at diagnosis and follow up
visits and refer for psychotherapy
• Counselling
is key for acceptance, medication
compliance and mitigation of mental disorder
• Considerthe effects of glycaemic control when
patients are on psychotropics
• Encourage support group involvement
 DYSLIPIDEMIA
• Riskof cardiovascular diseases in diabetics with
dyslipidaemia is very high.
• A lipid
profile should be done at initial contact and then
annually thereafter if normal or every 3-6 months if
abnormal or on treatment.
• Lifestylemanagement in regards to diet(decrease in
saturated fat intake), weight loss, exercise, reduction of
alcohol intake and tobacco cessation should be instituted.
• Statintherapy is initiated for people with type 2 DM > 40
years regardless of lipid level.
 Atorvastatin 20mg OD
 Dyslipidaemia
• Fibrates may be used in addition for persistent
hypertriglyceridemia
 Fenofibrate 200mg OD

• Lipid targets in patients with DM

LIPID TARGET (mg/dL)

Total cholesterol <93.6

LDL cholesterol <46.8

HDL cholesterol >19.8

TGs <30.6
CANCER
• Screen obese individuals with DM for frequently
for certain cancers: breast, bladder, pancreas,
endometrium
• Theassociated risk of cancers in diabetes is
probably due to shared risk factors of old age,
obesity, physical inactivity and smoking
HIV
• HIV and its treatment increase the development of diabetes
• Classification of HIV In patients with diabetes:
 Patients with pre-existing DM who contract HIV
 Those diagnosed with HIV and DM at the same time
 Those who develop hyperglycaemia post HAART initiation
• Drugs in HIV that may induce diabetes: Protease
inhibitors
• AllHIV positive patients should be screened for diabetes
for initiating HAART or when changing ARVs
• Diabeticpatients should be screened for HIV at initial
contact and annually thereafter
Management
• Treat opportunistic infections appropriately
• Lifestyle management
• Psychosocial support
• Reinforce compliance at every visit
• All
patients with Type 1 DM should be
managed with insulin therapy
 Management
• All patients with type 2 DM
 Metformin
 Drug of choice
 Avoided in patients with HIV associated enteropathy due
to GI side effects
 Contraindicated in HIV associated nephropathy, liver
disease
 Adjust dose if patient is on DTG
 Sulfonylureas
 Insulin
 Other drugs such as SGLT-2 inhibitors, Meglitinides or
DPP-4 inhibitors
TUBERCULOSIS
• Diabetes is associated with higher risks
of TB and adverse TB outcomes like
treatment failure and death since it
carries a higher risk of developing TB and
of latent TB infection, faster progression
of TB infection to disease and altered
clinical presentation of TB
• Alldiabetic patients should be screened
for TB: Fever, Night sweats, Cough,
Unexplained weight loss
Management of TB in DM
• All TB/DM patients should receive pyridoxine for the
duration of TB treatment
• Rifampicin may cause new onset dysglycaemia or
worsen glycaemic control of existing diabetes. It also
decreases the concentration of rosiglitazone and
pioglitazone. Insulin requirements may also increase.
• Monitor renal and liver function in patients with drug
resistant TB
CHRONIC KIDNEY DISEASE
• Diabetes mellitus in Chronic Kidney
Disease should may be managed with
Insulin, Glipizide and Thiazolidinediones.
Metformin is absolutely contraindicated if
CrCl is <30ml/min.
• Tightglycaemic control and management
of proteinuria is important in delaying
progression of CKD.
MONITORING OF
DIABETES MELLITUS
CARE
Methods for monitoring glycaemic
control
• Thestandard test is HbA1C. It should be
done every 3 months until BGL are well
controlled and subsequently every six months
• Self
monitoring of Blood Glucose should be
encouraged as it helps to titrate drug doses
• Clinical parameters should be monitored at
the initial visit, follow-ups and annually
 HbA1C test
• Also known as glycated haemoglobin or glycohaemoglobin test
• It is a measure of how much glucose, on average, has attached to
haemoglobin in the RBC.

Patient type Target

Young low risk <6.5%
Newly diagnosed with no CVD
Majority of patients <7% (T2DM) or 7.5% (T1DM)

Elderly high risk <8%

Hypoglycaemic unawareness
Poor short term prognosis
 Self monitoring blood glucose in Type 2
DM
• May take any of the following forms (to generate glucose profiles
that can identify daily glycaemic patterns and inform dosing):
 5-7 measurements per day over 1 to 3 days
 Staggered testing: pre and postprandial testing for alternating
meals over the course of a week
 Meal based SMBG (before and after selected meals that helps
individuals living with diabetes to understand the effects of their
treatment

Patient type Target FBS Target PPG

Young, low risk, newly 4.0-7.0 mmol/l 4.4-7.8 mmol/l
diagnosed, no CVD
Majority of patients 4.0 – 7.0 mmol/l 5.0-10.0 mmol/l
Elderly, high risk 4.0-9.8 mmol/l <11.0 mmol/l
 Clinical parameters
Parameter Targets
Male Female
BMI Between 18.5 and 24.9. A 10% weight loss
reduction in obese person is recommended
Waist circumference <90cm <84cm
Blood pressure <140/90 mmHg
BP in microalbuminuria <125/75 mmHg
Fasting lipid profile
Total cholesterol <4.8 mmol/l <4.8 mmol/l
LDL <2.6mmol/L <2.6mmol/l
HDL >1.0mmol/l >1.3mmol/l
TG <1.7 mmol/L <1.7mmol/l
PREVENTION AND
CONTROL OF
DIABETES MELLITUS
PRIMARY PREVENTION
• This are actions taken prior to the onset of diabetes
that reduce the possibility that diabetes will occur.
• It
can be achieved by health promotion which
includes health education, environmental
modification, nutritional intervention, lifestyle and
behavioural changes.
• This is achieved through population strategy and high
risk individual strategy.
SECONDARY PREVENTION
• Involvesactions that halt the progress
of diabetes at its early stage and prevent
complications
• Several studies have show that good
glycaemic control (HbA1C<7%), low
stable blood pressure (<140/80mmHg)
and lipid control prevent progression of
complications of DM.
TERTIARY DIABETES
• Actions taken when diabetes has progressed beyond
its early stages involving all measures available to
reduce or limit impairment and disabilities and
promote the patient’s adjustment to irreversible
conditions
• Involves
 Strict glycaemic control
 Diabetes education
 Effective treatment
 Screening and monitoring of complications
 Blood glucose, blood pressure and lipid control.
CASE STUDY
Case
PY is a 45 year old woman who is obese
(BMI=28kg/sq.m). She was referred to the DM clinic
by her gynecologist who has treated her for recurrent
vulvovaginal candidiasis and noted glucosuria.
On two separate occasions she was found to have a
FBS of 8.3mmol/L and 9.3mmol/L. Her HbA1C test
gave results of 7.9%. She denies symptoms of
polyphagia and polyuria although she admits to have
been more thirsty than usual of late. She complains of
lethargy and takes afternoon naps when she can.
Case
• Othermedical problems include hypertension that is
well controlled on lisinopril 20mg/d. She has 4
children, the last of whom was born at 5kg and she
was told during her last pregnancy that she is
“borderline diabetic”.
• Sheis a secretary and spends her weekends reading at
home. PY has been smoking at least 1 pack of
cigarettes per day for 20 years and drinks an
occasional glass of wine. Her family history is
significant for sister and grandmother who both have
diabetes and are obese. Her mother is alive and well
but her father died at 41 of a heart attack.
Case study
• On investigation, her FBS is 8.1mmol/L, Triglycerides
is 400mg/dL and a HbA1C of 7.7%. All other
parameters (FBC,UECs and LFTs) are normal. She is
diagnosed with Diabetes Mellitus.
• Questions:
1.What features of PY’s history (including risk factors)
and physical exam are consistent with this diagnosis?
2.What is the criteria used to diagnose DM?
3.What are the treatment goals in this case?
4.How do we manage PY??
5.How do we monitor therapy in PY?
Answers
• Features of history and physical exam
 Age >35 years
 High BMI with central obesity
 Physical inactivity and sedentary lifestyle
 Family history of diabetes
 Delivering a large baby (probably had gestational
diabetes)
 Symptoms of hyperglycaemia including
glucosuria, recurrent vulvovaginal candidiasis,
lethargy, thirst, hypertriglyceridemia
 High FBS on separate occasions and elevated
HbA1C
REFERENCES
• KenyaNational Clinical Guidelines for
the Treatment and Management of
Diabetes Mellitus. Second edition, 2018.
• Koda-Kimble and Young’s Applied
Therapeutics. 10th Edition
• American
Diabetes Association, Standards
of Medical care in Diabetes, 2017.