1

DIABETES MELLITUS
 2

Diagnosing and screening

of diabetes
SYMPTOMATIC INDIVIDUALS 3

Any individual who has symptoms suggestive of T2DM

 Fatigue

 Lethargy

 Polyuria, nocturia, polydipsia, polyphagia

 Weight loss
 Pruritus vulvae
 Balanitis
4
5
S C R E E N IN G 6
TESTS
Screening test
Capillary plasma glucose
- RANDOM BLOOD SUGAR >7.8, FASTING > 5.6, need
confirmatory test

Diagnostics
► Oral glucose tolerance test (OGTT)
► Fasting blood glucose
► HBA1C
7
8
9
Cardiovascular Risk Estimation
ASSESSMENT UPON DIAGNOSIS 11
12
13
Physical examination of newly diagnosed 14
patient with T2DM
 BASELINE 15
INVESTIGATIO
N
► Fasting plasma glucose (FPG)
► HbA1c
► Renal profile
► Lipid profile
► Liver function test
► Urinalysis for albumin, microalbuminuria if
albuminuria is absent
► ECG
 16

Management of Diabetes Mellitus

General Management 17

Medical nutrition therapy- mainstay of

prevention and treatment

Increase physical activities

-Duration of exercise of 150
mins/week

Tobacco cessation
 18
MEDICATIONS
 OHA
 Biguanides
 Sulphonylurea
 s Meglitinides
 Alpha glucosidase inhibitor
 Thiazolidinediones
 Dipeptidyl peptidase 4 inhibitor
 Sodium glucose
cotransporter 2 inhibitor
 Biguanides (metformin) 19

► Lowers blood glucose especially FBG by

decreasing hepatic glucose production.
► Not accompany by hypoglycemia
► Reduces HBA1c up to 1 . 5 %
► ADR: nausea, anorexia, diarrhea
► Lactic acidosis is rare, usually in renal
impairment patient
 Sulphonyureas 20

► Reduces blood glucose by increasing

secretion with insulin HB A1 c
0.46-1.62% averag e reduction of
► Major A D R is hypog lycem ia. Hig her risk in
elderly, renal impairment and liver cirrhosis
► S econd g enerations ( g liclazide, g liplizide
glimiperide
, preferred over S u s as they cause less
hypoglycemia and weight gain)
DRUGS AND DOSES
21
Drug Mechanism Things to take note
of action
Biguanides Reduces insulin GI sides effects,
resistance lactic acidosis,
(Metformin helps weight
) loss
TZD (Pioglitazone) (PPAR- agonist) Precipitates heart
Reduces insulin failure, oedema
resistance

Sulfonylureas Increases insulin Hypoglycemia,

(Glibenclamide, secretion weight gain,
Gliclazide) GI side effects
Meglitinides Increases insulin Hypoglycemia,
(Repaglinide) secretion weight gain, GI
sides effects
Drug Mechanism Things to take note
of action
Alpha- Glucosidase Inhibits alpha- GI side
inhibitor glucosidase hence effects,
(Acarbose) reducing glucose flatulance
absorption

Dipeptidyl Increases insulin Weight neutral,

peptidase-4 secretion + minimal risk
inhibitors delays gastric of
(Sitagliptin) emptying hypoglycemia

SGLT2 inhibitor Increases glucose Diuresis,

(Dapalgiflozin) excretion by glucosuria,
kidneys dehydratio
n 2
1
 TYPES OF
INSULIN

PRANDIAL INSULIN
administered pre-meal because of its
short or rapid
onset of action in controlling
postprandial glucose excursion.
BASAL INSULIN
administered once or twice daily. The
intermediate or long
acting pharmacokinetic profile
covers the basal insulin requirements
in between meals and through the
night.
25
How to Initiate Insulin? 26
► An ideal insulin regimen should mimic the physiological insulin response
to meals and endogenous hepatic glucose production.
► Option for initiation include:
1. basal insulin
- can be initiated at 10U a day or 0.1-0.2 U/kg/day,
- set FPG target and choose evidence-based titration algorithm e.g.
- increase by 2 U every 3 days to reach target FPG without
hypoglycaemia; OR
- Adjust 2 U every week based on 3 days’ glucose
readings.

2. Premixed insulin once or twice daily.

► Advice patient to perform self-monitoring of blood glucose (SMBG) and
empowered to self-adjust their insulin doses
► After titration of basal insulin, if the HbA1C is not at target but 27
FASTING PLASMA GLUCOSE is at target, intensification of
insulin therapy, by adding prandial insulin or converting to
premixed insulin is needed.
28
Target for Controls for Risk Modification 29
30
 31

MANAGEMENT OF
CHRONIC
COMPLICATIONS
DIABETIC 32
► SCREENING
R ETIN O PATHY ▪ visual acuity assessment – Snellen chart
▪ fundus camera photography
► EYE EXAMINATION
▪ Referral to ophthalmologist at the time of diagnosis of
T2DM
33
M ANAG EMENT

DELAY
ONSET

 Glucose
Intensive glucose-lowering has been shown to prevent and/or delay onset
 Blood pressure
Lowering blood pressure (BP) decreases retinopathy progression, although lowering BP
intensively (systolic BP <120 mmHg) does not impart additional benefit.
 Fenofibrate use
Retinopathy progression may be slowed by addition of fenofibrate particularly in those with
non-proliferative diabetic retinopathy (NPDR).
PROGRESSION
 Photocoagulation therapy
Laser photocoagulation remains the standard practice for treating diabetic retinopathy. Laser therapy is
indicated for severe NPDR and proliferative diabetic retinopathy.

 Anti-vascular endothelial growth factor (anti-VEGF)

Vascular endothelial growth factor (VEGF) plays an important role in diabetic retinopathy, particularly in
the development of diabetic macular oedema. Anti-VEGF therapy is superior to laser photocoagulation,
improves vision and is the treatment of choice in centre-involving diabetic macular oedema. Potential
adverse effects of anti-VEGFs include transient increases in intraocular pressure and injection-related
infectious endophthalmitis
 DIABETIC KIDNEY DISEASE 36

► D K D is a major cause of chronic kidney disease.

► Diagnosis is made clinically – based on presence of
albuminuria and/or reduced eGFR in the absence of other
causes of kidney disease
Estimation of GFR

Measure serum creatinine at least annually regardless of degree of albumin excretion.

An eGFR <60 ml/min / 1.73m2 is considered abnormal and should be repeated after 3 months
to diagnose DKD. However, eGFR thresholds may vary in older adults and should be
interpreted with caution in elderly individuals >70 years.
When eGFR <60ml/min /1.73m2 screening for complications such as volume overload,
electrolyte abnormality, metabolic acidosis, anemia and renal bone disease should be
considered.
Prognosis of DKD
based on GFR
and albuminuria
M ANAG EMENT
Prevention progression of DKD

► BP control (<130/80 mmHg)

► Glycaemic control
 Renin Angiotensin System blockade (ACE inhibitor/ARB)
 SGLT2 inhibition
► Protein and salt intake
► Weight reduction
 DIABETIC 40
NEUROPATH
Y

Diffuse neuropathies
• distal symmetric
polyneuropathy (DSPN)and
diabetic autonomic neuropathy
(DAN) particularly CV
autonomic neuropathy
Focal neuropathies
• mononeuritis and
radiculopathies.
41
MANAGEMENT
 Intensive lifestyle intervention
► Intensive glycemic control
► No pharmacologic therapy has been shown to be effective in treating DSPN
► Opioids
► Tricyclic antidepressants
 Cardiovascular disease

► Coronary heart disease

► Cerebrovascular disease (Stroke)

Lifestyle modification
Smoking cessation
Glycaemic control
BP control
Antiplatelet therapy
Revascularisation
Peripheral arterial disease (PAD)

 Risk factors for PAD in T2DM include:

 Older age
 Longer duration of T2DM
 Higher HbA1c
 Elevated SBP
 Low HDL-C levels
 Previous CVD
 Smoking
 Non-invasive
bedside tests for
evaluation of
PAD
 MANAG EMENT

 Smoking cessation and lifestyle modification.

 Statins for secondary prevention of CV events; aim for LDL-C <1.4mmol/L or LDL-
C reduction of at least 50% from baseline.
 Adequate blood pressure and glycaemic control.
 Anti-thrombotic therapy
 Single anti-platelet therapy (SAPT) is recommended only in symptomatic PAD or
after revascularization.
 Combination therapy of low-dose rivaroxaban (2.5 mg bd) and aspirin (100 mg od)
can be considered in patients with chronic symptomatic PAD and T2DM who do not
have a high risk of bleeding.
 Diabetic foot

► Peripheral neuropathy which is asymptomatic in up to 50% of patients,

predisposes to ulcerations and vasculopathy further retards the healing
process.

 PREVENTION
-proper care of feet including nail and skin care
- daily visual inspection of feet with a mirror, in those with Loss of protective sensation (LOPS),
- check for presence of foreign or penetrating objects before putting on footwear,
-advise not to walk barefoot outdoors or indoors, selection of appropriate footwear according
to foot risk, including certain prescribed footwear for high risk patients
-seek early treatment in presence of active diabetic foot problems (e.g. ulceration,
infection, gangrene or limb ischaemia).
MANAGEMENT

 Patients with active diabetic foot problems (ulceration, infection,

gangrene,critical limb ischaemia, acute Charcot neuroarthropathy) should
be referred urgently and seen within 2 4 hours in secondary/tertiary care,
and preferably managed by a multidisciplinary foot care team.
 Trauma induced ulcers with no other risk factors will require the standard wound
care and close follow-up until full recovery.
 Antibiotics should be used as an adjunct to surgical debridement for diabetic
foot ulcers with local or systemic infection but should not be used to
prevent infection.
 Appropriate analgesia should be given for adequate pain relief in those with
painful neuropathy .
 Mental health issues
Symptoms to look for:
 appetite changes,
 loss of interest in daily activities,
 Feeling of despair,
 inappropriate sense of guilt,
 sleep disturbance,
 weight loss,
 suicidal thoughts.

 MANAGEMENT
 Referral to a mental health specialist
 Behavioral treatment interventions which include cognitive behavioural therapy and exercise
 Sexual dysfunction

 Erectile d y s fu n c ti o n
MANAGEMENT
-Optimization of glycaemic control, management of other co-morbidities and
lifestyle modifications should be encouraged.(Level III)
-Psychosexual counselling is recommended in functional ED.
-Referral to a urologist
-Phosphodiesterase-5 (PDE-5) inhibitors e.g. sildenafil, tadalafil and vardenafil
should be offered as first-line therapy
Female sexual dysfunction

MANAGEMENT
Emphasis should be made to treat psychosocial disorders and relationship
disharmony.
Optimisation of glycaemic control should be encouraged.
Avoid drugs that may affect sexual function such as beta blockers, alpha blockers,
calcium channel blockers, diuretics,oral contraceptive pills.
 52

THANK YOU!