MANAGEMENT OF TYPE 2

DIABETES AND ITS

CHALLENGES
KAREN PHILLIPS
MBBS,DM (Internal Medicine) MSc (Diabetes and
Endocrinology)
 Case Vignette
 32 y.o obese male presented to his PCP with a 1/52 h/o polyuria,
polydipsia and fatigue. He has no h/o chronic medical illnesses
but admits that he does not have good diet or exercise plan…
 What other symptoms might you expect
 What other question would you ask?

 On examination he was a pleasant male with BMI of 34kg/m2.

Of note he had no signs of insulin resistance… and his systemic
examination was normal.
 Cont’d
 What findings might you expect on systemic examination?

 His GMR was noted at 24.1 mmol/l and his urinalysis revealed
ketones 4+

 Formal labs were significant for:

Glucose 34.1mmol/l HbA1C 13%
Na 129 CO2 13 Hb 17 Chol 6.5 HDL 0.8
BUN 19.0 CK 330 WBC 13 LDL 4.5
Creat 150 TNI neg Plt 150 Tg 1.8
 Cont’d
 What is your diagnosis?
 What other investigations would you request?

 You decide to admit him despite his protests..

 What is your management plan?

 One week later he has improved significantly and is ready for home.
 What medication are you going to discharge him on?
 What advice would you give him??
Type 2 diabetes is characterised by:
Chronic hyperglycaemia with disturbances of
carbohydrate, fat and protein metabolism
Defects in insulin secretion (-cell
dysfunction) and insulin action (insulin
resistance)

Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications.

Department of Noncommunicable Disease Surveillance, World Health Organization, Geneva 1999.
A serious, progressive disease
 Characterised by two fundamental defects:
 insulin resistance

 -cell dysfunction

 Accounts for 90% of diabetes cases worldwide

 Associatedwith serious microvascular and macrovascular
complications
 Represents a significant disease burden
 Represents a considerable economic burden

Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. World Health Organization, 1999. Diabetes
Mellitus. Fact Sheet No 138. World Health Organization, 2002.
 Growing problem
 Estimated 7% of US population is diabetic
 Twice that many have prediabetes
 21% of those over 60 have diabetes
 45% of new diagnoses are being made in children and adolescents
 Diabetes
 Type I—beta cells destroyed by autoimmune process
 Type 2—decreased insulin production and decreased sensitivity to
insulin
 Type 1 Diabetes Mellitus
 Genetic susceptibility
 Autoimmune
 Glycosuria
 Fat breakdown
 DKA
 Type 2 Diabetes Mellitus
 Resistance
 Decreased production
 Generally no fat breakdown
 HHNS
 Type 2 Diabetes Mellitus
 Exercise enhances action of insulin
 Weight loss is cornerstone of treatment
 Gestational Diabetes
 Glucose intolerance during pregnancy
 Placental hormones contributes to insulin resistance
 High risk: glycosuria, family history, marked obesity
 Native Americans, African Americans, Hispanics and Pacific
Islanders
 Gestational Diabetes
 Women of average risk tested between 24-28 weeks of gestation
 Goals for glucose levels during pregnancy are 105 or less before
meals; 130 or less after meals
 Will have greater risk of developing Type 2 DM later in life if
weight not controlled
 Clinical Manifestations
 Polyuria
 Polydipsia
 Polyphagia
 Fatigue, tingling or numbness in hands, slow healing wounds and
recurrent infections
 Criteria for the Diagnosis of
Type 2 Diabetes
Plasma Glucose Level (mmol/L)

Stage of Fasting Plasma 2-hr Plasma Glucose in a

Glycemic Control Glucose (mmol/L) 75-g. OGTT (mmol/L)

Normal < 6.1 < 7.8

IFG 6.1 – 6.9

IGT 7.8 - 11.0

Diabetes 7.0* 11.1

* Or casual plasma glucose 11.1 mmol/L (casual PG = regardless of time since last meal) + symptoms of diabetes
(polyuria, polydipsia, unexplained weight loss)

Confirmatory glucose test must be done in all cases on another day

CDA 2003 CPG, Can J Diabetes 27(Suppl 2):S7 2003

 ß Cell Failure and the
Progression of Diabetes
There is a progressive decline in insulin secretion when stratified by
2-hour plasma glucose (2hPG) in individuals spanning a range of glucose
tolerance

Insulin secretion / insulin resistance

(ΔI/ΔG /IR 0-120 min [mL/min * kg

NGT IGT T2D Obese
45 Non-obese

30
index

FFA])

15
[n=388 with NGT*,
IGT* or type 2
diabetes]

* NGT = Normal glucose tolerance;

2hPG (mmol/L)
* IGT = Impaired glucose tolerance

Gastaldelli et al. Diabetologia 2004;47(1):31-9.

Hyperglycemia Can Cause Serious Long-
Term Problems
Good News for Type 1
Diabetes
Good News for Type 2
Diabetes
Outpatient Glucose Targets for Nonpregnant Adults

Parameter Treatment Goal

Individualize on the basis of age, comorbidities,

duration of disease, and hypoglycemia risk:
A1C, % • In general, ≤6.5 for most*
• Closer to normal for healthy
• Less stringent for “less healthy”

FPG, mg/dL <6.1mmol/l

2-Hour PPG, mg/dL <7.7mmol/l

*Provided target can be safely achieved.

FPG = fasting plasma glucose; PPG = postprandial glucose.

20
Monitoring Your Diabetes: Target Blood
Glucose Levels
Without With Diabetes With Diabetes
Diabetes (normal) (target)

Before meals 3.8 -  6.1 4.0 - 7.0mmol/l

6.3mmol/l mmol/l

Before bedtime 3.8 -  6.6mmol/l 5.5 –

6.6mmol/l 8.3mmol/l

Hemoglobin A1c  6%  7%  7%
 Self-Care

 Patients should be educated to practice self-care. This allows the patient to

assume responsibility and control of his / her own diabetes management. Self-
care should include:

◦ Blood glucose monitoring

◦ Body weight monitoring
◦ Foot-care
◦ Personal hygiene
◦ Healthy lifestyle/diet or physical activity
◦ Identify targets for control
◦ Stopping smoking
 Therapeutic Lifestyle Changes
Parameter Treatment Goal

Weight loss
(for overweight and Reduce by 5% to 10%
obese patients)
150 min/week of moderate-intensity exercise (eg, brisk walking) plus
Physical activity
flexibility and strength training

• Eat regular meals and snacks; avoid fasting to lose weight

• Consume plant-based diet (high in fiber, low calories/glycemic index,
and high in phytochemicals/antioxidants)
Diet • Understand Nutrition Facts Label information
• Incorporate beliefs and culture into discussions
• Use mild cooking techniques instead of high-heat cooking
• Keep physician-patient discussions informal

23
Healthful Eating Recommendations
Carbohydrate Specify healthful carbohydrates (fresh fruits and vegetables, legumes, whole grains); target 7-10
servings per day
Preferentially consume lower-glycemic index foods (glycemic index score <55 out of 100:
multigrain bread, pumpernickel bread, whole oats, legumes, apple, lentils, chickpeas, mango,
yams, brown rice)
Fat Specify healthful fats (low mercury/contaminant-containing nuts, avocado, certain plant oils,
fish)
Limit saturated fats (butter, fatty red meats, tropical plant oils, fast foods) and trans fat; choose
fat-free or low-fat dairy products
Protein Consume protein in foods with low saturated fats (fish, egg whites, beans); there is no need to
avoid animal protein
Avoid or limit processed meats
Micronutrients Routine supplementation is not necessary; a healthful eating meal plan can generally provide
sufficient micronutrients
Chromium; vanadium; magnesium; vitamins A, C, and E; and CoQ10 are not recommended
for glycemic control
Vitamin supplements should be recommended to patients at risk of insufficiency or deficiency

24
 CHALLENGES
 Time to exercise
 Safety Concerns
 Expense
 Time to prepare healthy meals
Noninsulin Agents Available for T2D
Class Primary Mechanism of Action Agent(s) Available as
-Glucosidase  Delay carbohydrate absorption from Acarbose Precose or generic
inhibitors intestine Miglitol Glyset
 Decrease glucagon secretion
Amylin analogue  Slow gastric emptying Pramlintide Symlin
 Increase satiety
 Decrease HGP
Biguanide Metformin Glucophage or generic
 Increase glucose uptake in muscle
 Decrease HGP?
Bile acid sequestrant Colesevelam WelChol
 Increase incretin levels?

 Increase glucose-dependent insulin Alogliptin Nesina

Linagliptin Tradjenta
DPP-4 inhibitors secretion
Saxagliptin Onglyza
 Decrease glucagon secretion Sitagliptin Januvia
Dopamine-2 agonist  Activates dopaminergic receptors Bromocriptine Cycloset
Nateglinide Starlix or generic
Glinides  Increase insulin secretion
Repaglinide Prandin

DPP-4 = dipeptidyl peptidase; HGP = hepatic glucose production.

Garber AJ, et al. Endocr Pract. 2013;19(suppl 2):1-48. Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379.
Continued on next slide 26
 Noninsulin Agents Available for T2D
Class Primary Mechanism of Action Agent(s) Available as
 Increase glucose-dependent insulin Albiglutide Tanzeum
secretion Dulaglutide Trulicity
GLP-1 receptor
 Decrease glucagon secretion Exenatide Byetta
agonists
 Slow gastric emptying Exenatide XR Bydureon
 Increase satiety Liraglutide Victoza

Canagliflozin Invokana
SGLT2 inhibitors  Increase urinary excretion of glucose Dapagliflozin Farxiga
Empagliflozin Jardiance

Glimepiride Amaryl or generic

Gliclazide Diamicron MR or
Sulfonylureas  Increase insulin secretion Glyburide generic
Diaeta, Glynase,
Micronase, or generic
 Increase glucose uptake in muscle and
Pioglitazone Actos
Thiazolidinediones fat
Rosiglitazone Avandia
 Decrease HGP

GLP-1 = glucagon-like peptide; HGP = hepatic glucose production; SGLT2 = sodium glucose cotransporter 2.
Garber AJ, et al. Endocr Pract. 2013;19(suppl 2):1-48. Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379.
Continued from previous slide 27
 Acute Complications of Diabetes
Hypoglycemia
DKA
HHNS
 DKA is a serious acute complications of Diabetes Mellitus. It carries
significant risk of death and/or morbidity especially with delayed
treatment.
 The prognosis of DKA is worse in the extremes of age, with a
mortality rates of 5-10%.
 With the new advances of therapy, DKA mortality decreases to > 2%.
Before discovery and use of Insulin (1922) the mortality was 100%.
Pathophysiology
 Secondary to insulin deficiency, and the action of counter-regulatory
hormones, blood glucose increases leading to hyperglycemia and
glucosuria. Glucosuria causes an osmotic diuresis, leading to water
& Na loss.
 In the absence of insulin activity the body fails to utilize
glucose as fuel and uses fats instead. This leads to ketosis.
Pathophysiology/2
The excess of ketone bodies will cause metabolic acidosis, the later is
also aggravated by Lactic acidosis caused by dehydration & poor
tissue perfusion.
Vomiting due to an ileus, plus increased insensible water losses due
to tachypnea will worsen the state of dehydration.
Electrolyte abnormalities are 2ry to their loss in urine & trans-
membrane alterations following acidosis & osmotic diuresis.
Pathophysiology/3
Because of acidosis, K ions enter the circulation
leading to hyperkalemia, this is aggravated by
dehydration and renal failure.
 So, depending on the duration of DKA, serum K
at diagnosis may be high, normal or low, but the
intracellular K stores are always depleted.
 Phosphate depletion will also take place due to
metabolic acidosis.
 Na loss occurs secondary to the hyperosmotic
state & the osmotic diuresis.
Pathophysiology/4
 The dehydration can lead to decreased kidney perfusion and acute
renal failure.
 Accumulation of ketone bodies contributes to the abdominal pain
and vomiting.
 The increasing acidosis leads to acidotic breathing and acetone
smell in the breath and eventually causes impaired consciousness
and coma.
Precipitating Factors
New onset of type 1 DM: 25%
Infections (the most common cause): 40%
Drugs: e.g. Steroids, Thiazides, Dobutamine &
Turbutaline.
Omission of Insulin: 20%. This is due to:
 Non-availability (poor countries)
 fear of hypoglycemia
 rebellion of authority
 fear of weight gain
 stress of chronic disease
DIAGNOSIS
 You should suspect DKA if a diabetic patient presents with:
 Dehydration.
 Acidotic (Kussmaul’s) breathing, with a fruity smell (acetone).
 Abdominal pain &\or distension.
 Vomiting.
 An altered mental status ranging from disorientation to coma.
DIAGNOSIS/2
To diagnose DKA, the following criteria must be
fulfilled :
1. Hyperglycemia: of > 300 mg/dl & glucosuria
2. Ketonemia and ketonuria
3. Metabolic acidosis: pH < 7.25, serum bicarbonate < 15 mmol/l.
Anion gap >10.
Anion gap= [Na]+[K] – [Cl]+[HCO3].
This is usually accompanied with severe
dehydration and electrolyte imbalance.
Management
The management steps of DKA includes:
Assessment of causes & sequele of DKA by taking a
short history & performing a scan examination.

Quick diagnosis of DKA at the ER.

Baseline investigations.

Treatment, Monitoring & avoiding complications.

Transition to outpatient management.

Assessment
 History:
Symptoms of hyperglycemia, precipitating factors ,
diet and insulin dose.
 Examination:
 Look for signs of dehydration, acidosis, and
electrolytes imbalance, including shock,
hypotension, acidotic breathing, CNS status…etc.
 Look for signs of hidden infections (Fever
strongly suggests infection) and If possible, obtain
accurate weight before starting treatment.
Quick Diagnosis
 Known diabetic children confirm D hyperglycemia, K ketonuria
& A acidosis.
 Newly diagnosed diabetic children be careful not to miss because
it may mimic serious infections like meningitis.
 Both Hyperglycemia (using glucometer) glycosuria, & ketonuria
(with strips) must be done in the ER and treatment started, without
waiting for Lab results which may be delayed.
Baseline Investigations
The initial Lab evaluation includes:
 Plasma & urine levels of glucose & ketones.
 ABG, U&E (including Na, K, Ca, Mg, Cl, PO4, HCO3), & arterial
pH (with calculated anion gap).
 Venous pH is as accurate as arterial (an error of 0.025 less than
arterial pH)
 Complete Blood Count with differential.
 Further tests e.g., cultures, X-rays…etc , are done when needed.
Pitfalls in DKA
 High WCC: may be seen in the absence of infections.
 BUN: may be elevated with prerenal azotemia secondary to
dehydration.
 Creatinine: some assays may cross-react with ketone bodies, so it
may not reflect true renal function.
 Serum Amylase: is often raised, & when there is abdominal pain, a
diagnosis of pancreatitis may mistakenly be made.
Treatment
Principles of Treatment:
 Careful replacement of fluid deficits.
 Correction of acidosis & hyperglycemia via
Insulin administration.
 Correction of electrolytes imbalance.
 Treatment of underlying cause.
 Monitoring for complications of treatment.
Manage DKA in the PICU. If not available it can
be managed in the special care room of the
pediatric inpatient ward.
Treatment
Principles of Treatment:
 Careful replacement of fluid deficits.
 Correction of acidosis & hyperglycemia via
Insulin administration.
 Correction of electrolytes imbalance.
 Treatment of underlying cause.
 Monitoring for complications of treatment.
Manage DKA in the PICU. If not available it can
be managed in the special care room of the
pediatric inpatient ward.
Fluids replacement
 Determine hydration status:
A. Hypovolemic shock:
administer 0.9% saline, Ringer’s lactate or a plasma
expander as a bolus dose of 20-30 ml/kg. This can
be repeated if the state of shock persists. Once the
patient is out of shock, you go to the 2nd step of
management.
Fluids replacement/2
B- Dehydration without shock:
1. Administer 0.9% Saline 10 ml/kg/hour for an
initial hour, to restore blood volume and renal
perfusion.
2. The remaining deficit should be added to the
maintenance, & the total being replaced over 36-
48 hours. To avoid rapid shifts in serum
osmolality 0.9% Saline can be used for the initial
4-6 hours, followed by 0.45% saline.
Fluids replacement/3
 When serum glucose reaches 250mg/dl change fluid to
5% dextrose with 0.45 saline, at a rate that allow complete
restoration in 48 hours, & to maintain glucose at 150-
250mg/dl.
 Pediatric saline 0.18% Na Cl should not be used even in
young children.
Insulin Therapy
start infusing regular insulin at a rate of
0.1U/kg/hour using a syringe pump. Optimally,
serum glucose should decrease in a rate no faster
than 100mg/dl/hour.
If serum glucose falls < 200 prior to correction
of acidosis, change IV fluid from D5 to D10, but
don’t decrease the rate of insulin infusion.
The use of initial bolus of insulin (IV/IM) is
controversial.
Insulin Therapy/2
Continue the Insulin infusion until acidosis is
cleared:
 pH > 7.3.

 Bicarbonate > 15 mmol/l

 Normal anion gap 10-12.

Correction of Acidosis
 Insulin therapy stops lipolysis and
promotes the metabolism of ketone bodies.
This together with correction of dehydration
normalize the blood PH.
 Bicarbonate therapy should not be used unless
severe acidosis (pH<7.0) results in hemodynamic
instability. If it must be given, it must infused
slowly over several hours.
 As acidosis is corrected, urine KB appear to rise.
Urine KB are not of prognostic value in DKA.
Insulin Therapy/3
If no adequate settings (i.e. no infusion or
syringe pumps & no ICU care which is the
usual situation in many developing
countries) Give regular Insulin 0.1
U/kg/hour IM till acidosis disappears and
blood glucose drops to <250 mg/dl, then us
SC insulin in a dose of 0.25 U/kg every 4
hours.
When patient is out of DKA return to the
previous insulin dose.
Correction of Electrolyte Imbalance
 Regardless of K conc. at presentation, total body K is low. So, as soon
as the urine output is restored, potassium supplementation must be
added to IV fluid at a conc. of 20-40 mmol/l, where 50% of it given as
KCl, & the rest as potassium phosphate, this will provide phosphate
for replacement, & avoids excess phosphate (may precipitate
hypocalcaemia) & excess Cl (may precipitate cerebral edema or adds
to acidosis).
Potassium
 If K conc. < 2.5, administer 1mmol/kg of
KCl in IV saline over 1 hour. Withhold
Insulin until K conc. becomes> 2.5 and
monitor K conc. hourly.
 If serum potassium is 6 or more, do not give potassium till you
check renal function and patients passes adequate urine.
Monitoring
A flow chart must be used to monitor fluid
balance & Lab measures.
 serum glucose must be measured hourly.
 electrolytes also 2-3 hourly.
 Ca, Mg, & phosphate must be measured initially
& at least once during therapy.
 Neurological & mental state must examined
frequently, & any complaints of headache or
deterioration of mental status should prompt rapid
evaluation for possible cerebral edema.
Complications
 Cerebral Edema
 Intracranial thrombosis or infarction.
 Acute tubular necrosis.
 peripheral edema.
Cerebral Edema
 Clinically apparent Cerebral edema occurs in 1-2% of children with
DKA. It is a serious complication with a mortality of > 70%. Only
15% recover without permanent damage.
 Typically it takes place 6-10 hours after initiation of treatment, often
following a period of clinical improvement.
Causes of Cerebral Edema
The mechanism of CE is not fully understood, but
many factors have been implicated:
 rapid and/or sharp decline in serum osmolality
with treatment.
 high initial corrected serum Na concentration.
 high initial serum glucose concentration.
 longer duration of symptoms prior to initiation of
treatment.
 younger age.
 failure of serum Na to raise as serum glucose falls
during treatment.
Presentations of C. Edema
Cerebral Edema Presentations include:
deterioration of level of consciousness.
 lethargy & decrease in arousal.
 headache & pupillary changes.
 seizures & incontinence.
 bradycardia. & respiratory arrest when brain stem
herniation takes place.
Treatment of C. Edema
 Reduce IV fluids
 Raise foot of Bed
 IV Mannitol
 Elective Ventilation
 Dialysis if associated with fluid overload or renal failure.
 Use of IV dexamethasone is not recommended.
 Hyperglycemic Hyperosmolar Nonketotic
Syndrome
 Predominated by hyperosmolarity and hyperglycemia
 Minimal ketosis
 Osmotic diuresis
 Glycosuria and increased osmolarity
 Occurs over time
 Blood sugar is usually over 600
 HHNS
 Occurs more often in older people
 Type 2 diabetes mellitus
 No ketosis
 Do not usually have the concomitant n/v
 Hyperglycemia, dehydration and hyperosmolarity may be more
severe than in DKA
 Medical Management
 Similar treatment as seen in DKA
 Watch fluid resuscitation if history of heart failure
 ECG
 Lytes monitoring
 Fluids with potassium replacement
 Nursing Management of HHNS
 Monitor neurologically
 Monitor ECG
 Monitor vital signs
 Labs
 Hourly blood glucose monitoring
 Insulin IV
 Cautious correction of hyperglycemia to avoid cerebral edema
 Consequences of Hypoglycemia
 Cognitive, psychological changes (eg, confusion, irritability)
 Accidents
 Falls
 Recurrent hypoglycemia and hypoglycemia unawareness
 Refractory diabetes
 Dementia (elderly)
 CV events
 Cardiac autonomic neuropathy
 Cardiac ischemia
 Angina
 Fatal arrhythmia

64
 Symptoms of Hypoglycemia
Blood Glucose
Classification Level Typical Signs and Symptoms
(mg/dL)

• Neurogenic: palpitations, tremor, hunger, sweating,

Mild hypoglycemia ~50-70
anxiety, paresthesia

• Neuroglycopenic: behavioral changes, emotional

Moderate hypoglycemia ~50-70
lability, difficulty thinking, confusion

• Severe confusion, unconsciousness, seizure, coma,

Severe hypoglycemia <50* death
• Requires help from another individual

*Severe hypoglycemia symptoms should be treated regardless of blood glucose level.

65
 Treatment of Hypoglycemia
Hypoglycemia symptoms
(BG <70 mg/dL)

Patient severely confused or

Patient conscious and alert
unconscious (requires help)

• Glucagon injection, delivered by

• Consume glucose-containing foods (fruit another person
juice, soft drink, crackers, milk, glucose
• Patient should be taken to
tablets); avoid foods also containing fat
hospital for evaluation and
• Repeat glucose intake if SMBG result treatment after any severe
remains low after 15 minutes
episode
• Consume meal or snack after SMBG has
returned to normal to avoid recurrence

BG = blood glucose; SMBG = self-monitoring of blood glucose.

66
 Hypoglycaemia
 Ask about symptomatic /asymptomatic hypoglycaemia at each
encounter
 Glucose 15 – 20 g preferred treatment for conscious individual
followed by meal/snack
 Glucagon for all individuals at increased risk of severe
hypoglycaemia
 Hypoglycaemia unawareness or episodes of severe
hypoglycaemia should trigger reevaluation of treatment
regimen
 Ongoing assessment of cognitive function
General Guidelines for Use of Oral Anti-Diabetic Agent in Diabetes

 In elderly non-obese patients, short acting insulin secretagogues can be

started but long acting Sulphonylureas are to be avoided. Renal
function should be monitored.

 Oral anti-diabetic agents are usually not the first line therapy in
diabetes diagnosed during stress, such as infections. Insulin therapy is
recommended for both the above

 Targets for control are applicable for all age groups. However, in
patients with co-morbidities, targets are individualized

 When indicated, start with a minimal dose of oral anti-diabetic agent,

while reemphasizing diet and physical activity. An appropriate duration
of time (2-16 weeks depending on agents used) between increments
should be given to allow achievement of steady state blood glucose
control
 C. Insulin Therapy

Short-term use:
 Acute illness, surgery, stress and emergencies
 Pregnancy
 Breast-feeding
 Insulin may be used as initial therapy in type 2 diabetes
 in marked hyperglycaemia
 Severe metabolic decompensation (diabetic ketoacidosis, hyperosmolar nonketotic coma, lactic
acidosis, severe hypertriglyceridaemia)

Long-term use:
 If targets have not been reached after optimal dose of combination therapy or BIDS, consider
change to multi-dose insulin therapy. When initiating this,insulin secretagogues should be
stopped and insulin sensitisers e.g. Metformin or TZDs, can be continued.
Overview of Insulin and Action
Different types of Insulin
 Barriers to Insulin Administration
(Patient Barriers)
 Myth based fear of insulin
 Fear of hypoglycaemia
 Concern about weight gain
 Fear of needles
 Self blame
 Social stigma
 Time consuming
 Cognitive impairment/ Low literacy
 Visual/dexterity impairment
 Provider Barriers
 Perceived patient resistance
 Patient’s adherence behaviour
 Concerns about hypoglycaemia, weight gain
 Provider time constraints
 Lack of resources/organisational structure to facilitate guideline
adherence
 Blood Pressure Targets
Parameter Treatment Goal
Individualize on the basis of age, comorbidities, and
Blood pressure
duration of disease, with general target of:
Systolic, mm Hg ~130
Diastolic, mm Hg ~80

 A more intensive goal (such as <120/80 mm Hg) should be considered for some
patients, provided the target can be safely reached without adverse effects from
medication.
 More relaxed goals may be considered for patients with complicated comorbidities or
those experience adverse medication effects.

77
 Comprehensive Management of CV Risk

 Manage CV risk factors

 Weight loss
 Smoking cessation
 Optimal glucose, blood pressure, and lipid control
 Use low-dose aspirin for secondary prevention of CV events in
patients with existing CVD
 May consider low-dose aspirin for primary prevention of CV events in
patients with 10-year CV risk >10%
 Measure coronary artery calcification or use coronary imaging to
determine whether glucose, lipid, or blood pressure control efforts
should be intensified
CV = cardiovascular; CVD = cardiovascular disease.
78
 Statin Use
 Majority of patients with T2D have a  Use a statin regardless of LDL-C level in
high cardiovascular risk patients with diabetes who meet the
 People with T1D are at elevated following criteria:
cardiovascular risk  >40 years of age
 ≥1 major ASCVD risk factor
 LDL-C target: <70 mg/dL—for the
 Hypertension
majority of patients with diabetes who
 Family history of CVD
are determined to have a high risk  Low HDL-C
 Smoking

ASCVD = atherosclerotic cardiovascular disease; CVD = cardiovascular disease; HDL-C = high density lipoprotein cholesterol;
LDL-C = low-density lipoprotein cholesterol.
79
 SUMMARY
 Type 2 Diabetes is a serious disease with significant clinical and
economic consequences
 Despite its challenges, Therapeutic Lifestyle Changes are
important as the first consideration in management
 Treatment must be individualised based on current guidelines and
patient preference to ensure compliance
 Diabetes selfcare is central to management
Thank You