Diabetes by dr arshid rafiq

Diabetes Mellitus
Dr Arshid Rafiq
(Diploma in diabetes. Fellowship in diabetes)
Under supervision of
Dr Rakesh Gupta MD (medicine).FIACM
Senior consultant physician
Indraprastha Apollo Hospitals

 Pancreas secretes 40-50 units
of insulin daily in two steps:
 Secreted at low levels during
fasting ( basal insulin secretion)
 Increased levels after eating
(prandial)
 An early burst of insulin occurs
within 10 minutes of eating
 Then proceeds with increasing
release as long as hyperglycemia
is present

Insulin
 Insulin allows glucose to move into
cells to make energy
 Inhibits glucagon activity

DIABETESMELLITUS
 is a chronic disorder of
carbohydrate, protein,
and fat metabolism
resulting from insulin
deficiency or abnormality
in the use of insulin

Types
1.Type I
 formerly known as Insulin –
Dependent Diabetes Mellitus (IDDM)
Autoimmune (Islet cell antibodies)
•Early introduction of cow’s milk and
cereals
•Intake of medicine during pregnancy
•Indoor smoking of family members
destruction of beta cells of the
pancreas  little or no insulin
production
requires daily insulin admin.
 may occur at any age, usually appears
below age 15

2. Type II
 formerly known as Non Insulin–Dependent
Diabetes Mellitus (NIDDM)
 probably caused by:
 disturbance in insulin reception in the cells
  number of insulin receptors
 loss of beta cell responsiveness to glucose
leading to slow or  insulin release by the
pancreas
 occurs over age 40 but can occur in children
 common in overweight or obese
 w/ some circulating insulin present, often do
not require insulin

Gestational diabetes
3.Gestational Diabetes ;
a).blood sugar levels are high during
pregnancy in women
b) .Women who give birth to children
over 9 lbs.
c). high risk of type 2 diabetes and
cardiovascular disease

Pre-Diabetes
 Impaired fasting glucose (IFG)
 FPG- 100-125mg/dL
 Impaired glucose tolerance (IGT)
 OGTT 140-199mg/dL
 HbA1c 5.7-6.4%

Risk Factors
 Obesity
 Race
 History of CVD
 HTN
 Physical inactivity
 Familial history
 Polycystic Ovary Syndrome
 Gestational Diabetes
? ? ? ? ? ? ?

“Of course too
much is bad for
you”

Fasting plasma glucose (FPG)
≥126 mg/dL (7.0 mmol/L)
OR
2-h plasma glucose ≥200 mg/dL
(11.1 mmol/L) during an OGTT
OR
A1C ≥6.5%
OR
Random plasma glucose
≥200 mg/dL (11.1 mmol/L)
Criteria for the Diagnosis of
Diabetes
American Diabetes Association Standards of Medical Care in Diabetes.
Classification and diagnosis of diabetes. Diabetes Care 2016; 39 (Suppl. 1): S13-S2216

Clinical Manifestations ( Signs and Symptoms)
- Polyuria - weakness
- Polydipsia - fatigue
- Polyphagia -  blood sugar / glucose level
- weight loss - (+) glucose in urine (glycosuria)
- nausea / vomiting
- changes in LOC (severe hyperglycemia)
(sleepiness, drowsiness  coma)
- recurrent infection, prolonged wound healing
- altered immune and inflammatory response, prone to
infection (glucose inhibits the phagocytic action of WBC 
resistance)
- genital pruritus – (hyperglycemia and glycosuria favor fungal
growth : candidal infection – resulting in pruritus, common
presenting symptom in women)
- Erectile dysfunction

Oral Glucose Tolerance Test
(OGTT)

Glycoselated Hemoglobin (HbA1c)
 HbA1c is a test that measures the
amount of glycated hemoglobin in
your blood. Glycated hemoglobin is a
substance in red blood cells that is
formed when blood sugar (glucose)
attaches to hemoglobin.

Urinalysis
 Glycosuria
 Ketone bodies

Diabetes Mellitus
Summary Treatable, but not curable.
 Preventable in obesity, adult client.
 Controllable- DIET and EXERCISE
 Diagnostic Tests
 Signs and symptoms of hypoglycemia
and hyperglycemia.
 Treatment of hypoglycemia and
hyperglycemia – diet and oral
hypoglycemics.
 Nursing implications – monitoring,
teaching and assessing for
complications.

Management of DM
Classification and diagnosis of diabetes. Diabetes Care 2016; 39 (Suppl. 1): S13-S2225

The major components of the
treatment of diabetes are:
• Medical NutritionTherapy
(Diet and Exercise) [MNT]1
• Oral Antihyperglycemic Drug
[OAD]2
• Insulin & Other Injectables3
26

Medical Nutrition Therapy
(MNT)
● An individualized MNT program is
recommended for all people with type 1 and type 2
diabetes.
● For people with T1DM or those with T2DM who
are on a flexible insulin program, education on carb
counting or estimation.
American Diabetes Association Standards of Medical Care in Diabetes. Foundations of care
and the comprehensive medical evaluation. Diabetes Care 2017; 39 (Suppl. 1): S23-S3527

…….MNT
● For patients on a fixed insulin
program, having a consistent pattern of
carbohydrate intake with respect to time
and amount can result in improved
glycemic control and a reduced risk of
hypoglycemia.

 Adults with diabetes: at least 150 min/wk of
moderate-intensity aerobic activity or 30
minutes brisk walking over at least 3
days/week with no more than 2
consecutive days without exercise
Physical Activity

 Children with diabetes/prediabetes:
at least 60 min/day physical activity
Physical Activity

 All individuals, including those with diabetes,
should reduce sedentary time, particularly by
breaking up extended amounts of time (>90
min) spent sitting.
Physical Activity

 Advise all patients not to use cigarettes, other
tobacco products, or e-cigarettes.
 Include smoking cessation counseling and other
forms of treatment as a routine component of
diabetes care.
Smoking Cessation

A complete medical evaluation should be performed
at the initial visit to:
 Confirm & classify diagnosis
 Detect complications & potential comorbid
conditions
Comprehensive Medical
Evaluation

Components of the Comprehensive
Diabetes Evaluation
Laboratory Evaluation
 A1C, if results not available within past 3
months

….Components of the Comprehensive Diabetes Evaluation
If not performed/available within past year:
 Fasting lipid profile
 Liver function tests
 Spot urine albumin-to-creatinine ratio
 Serum creatinine and eGFR
 Thyroid-stimulating hormone in patients with
type 1 diabetes or dyslipidemia or women aged
>50 years

 Two primary techniques available for health
providers and patients to assess effectiveness of
management plan on glycemic control
1. Patient self-monitoring of blood glucose
(SMBG)
2. A1C
..Glycemic Control
Glycemic targets. Diabetes Care 2017; 39 (Suppl. 1): S39-S4637

 CGM or interstitial glucose may be a useful
adjunct to SMBG in selected patients.
Glycemic Control

 Patients on multiple-dose insulin (MDI) or insulin
pump therapy should do SMBG
 Prior to meals and snacks
 At bedtime
 Prior to exercise
 When they suspect low blood glucose
Glucose Monitoring

 When they suspect low blood glucose
 After treating low blood glucose until they are
normoglycemic
 Prior to critical tasks such as driving
 Possibly also post-prandially
Glucose Monitoring

 Perform the A1C test at least twice annually in
patients that meet treatment goals (and have stable
glycemic control).
 Perform the A1C test quarterly in patients whose
therapy has changed or who are not meeting
glycemic goals.
A1C Testing

 Perform the A1C test quarterly in patients whose
therapy has changed or who are not meeting glycemic
goals.
 Use of point-of-care (POC) testing for A1C provides
the opportunity for more timely treatment changes.
A1C Testing

 Lowering A1C to <7% has been shown to reduce
microvascular complications and, if implemented
soon after the diagnosis of diabetes, is associated
with long-term reduction in macrovascular
disease.
Glycemic Goals in Adults

 Consider more stringent goals (e.g. <6.5%)
for select patients if achievable without
significant hypos or other adverse effects.
Glycemic Goals in Adults

A1C <7.0%*
Preprandial capillary
plasma glucose
4.4–7.2 mmol/L*
(80–130 mg/dL)
Peak postprandial
capillary plasma
glucose†
<10.0 mmol/L*
(<180 mg/dL)
Glycemic Recommendations for
Nonpregnant Adults with Diabetes
* Goals should be individualized.
† Postprandial glucose measurements should be
made 1–2 hours after the beginning of the meal.

 An A1C goal of <7.5% is recommended across all
pediatric age-groups.
Type 1 Diabetes: Glycemic
Control
Children and adolescents. Diabetes Care 2017; 39 (Suppl. 1): S86-S9346

Blood glucose goal range
A1C Rationale
Before meals
Bedtime/
overnight
5.0–7.2 mmol/L
(90–130 mg/dL)
5.0–8.3 mmol/L
(90–150 mg/dL)
<7.5%
A lower goal (<7.0%)
is reasonable if it can
be achieved without
excessive hypos
T1 DM: Glycemic Control
1. Goals should be individualized; lower goals may be reasonable.
2. Modify BG goals in youth w/ frequent hypos or hypoglycemia unawareness.
3. Measure postprandial BG if discrepancy between preprandial BG and A1C & to
assess glycemia in basal–bolus regimens.American Diabetes Association Standards of Medical Care in Diabetes.
Children and adolescents. Diabetes Care 2017; 39 (Suppl. 1): S86-S93
47

Approaches
to Glycemic Treatment
48

 Most people with T1DM should be treated with
multiple dose insulin (MDI) injections (3–4 injections
/day of basal & prandial insulin) or continuous
subcutaneous insulin infusion (CSII).
 Individuals who have been successfully using CSII
should have continued access after they turn 65 years
old.
Pharmacological Therapy for
T1DM
American Diabetes Association Standards of Medical Care in Diabetes. Approaches to
glycemic treatment. Diabetes Care 2017; 39 (Suppl. 1): S52-S5949

Pharmacological Therapy for T1DM
 Consider educating individuals with T1DM on
matching prandial insulin dose to carbohydrate
intake, premeal blood glucose, and anticipated
activity.
 Most individuals with T1DM should use insulin
analogs to reduce hypoglycemia risk.

Pramlintide
 FDA approved for T1DM
 Amylin analog
 Delays gastric emptying, blunts pancreatic
glucose secretion, enhances satiety
 Induces weight loss, lowers insulin dose
 Requires reduction in prandial insulin to reduce
risk of severe hypos

 Can normalize glucose but require lifelong
immunosuppression.
 Reserve for T1D patients:
 Undergoing renal transplant
 Following renal transplant
 With recurrent ketoacidosis or severe hypos
Pancreas and Islet Cell Transplantation

 Can normalize glucose but require lifelong
 Islet cell transplant investigational
 Consider for patients requiring pancreatectomy
who meet eligibility criteria.
Pancreas and Islet Cell Transplantation

Pharmacological
Therapy for T2DM

Noninsulin Agents Available
for T2DClass Primary Mechanism of Action Agent(s) Available as
-Glucosidase
inhibitors
 Delay carbohydrate absorption from
intestine
Acarbose
Miglitol
Precose or generic
Glyset
Amylin analogue
 Decrease glucagon secretion
 Slow gastric emptying
 Increase satiety
Pramlintide Symlin
Biguanide
 Decrease HGP
 Increase glucose uptake in muscle
Metformin Glucophage or generic
Bile acid sequestrant
 Decrease HGP?
 Increase incretin levels?
Colesevelam WelChol
DPP-4 inhibitors
 Increase glucose-dependent insulin
secretion
Alogliptin
Linagliptin
Saxagliptin
Sitagliptin
Nesina
Tradjenta
Onglyza
Januvia
Dopamine-2 agonist  Activates dopaminergic receptors Bromocriptine Cycloset
Glinides  Increase insulin secretion
Nateglinide
Repaglinide
Starlix or generic
Prandin
56
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.
. How are glycemic targets achieved forT2D?
Continued on next slide

Noninsulin Agents Available
for T2DClass Primary Mechanism of Action Agent(s) Available as
GLP-1 receptor
agonists
 Increase glucose-dependent insulin
secretion
 Slow gastric emptying
 Increase satiety
Albiglutide
Dulaglutide
Exenatide
Exenatide XR
Liraglutide
Tanzeum
Trulicity
Byetta
Bydureon
Victoza
SGLT2 inhibitors  Increase urinary excretion of glucose
Canagliflozin
Dapagliflozin
Empagliflozin
Invokana
Farxiga
Jardiance
Sulfonylureas  Increase insulin secretion
Glimepiride
Glipizide
Glyburide
Amaryl or generic
Glucotrol or generic
Diaeta, Glynase,
Micronase, or generic
Thiazolidinediones
 Increase glucose uptake in muscle
and fat
 Decrease HGP
Pioglitazone
Rosiglitazone
Actos
Avandia
57
Q4. How are glycemic targets achieved forT2D?
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

Effects of Agents Available
for T2D
58
AGI = -glucosidase inhibitors; BCR-QR = bromocriptine quick release; Coles = colesevelam; DPP4I = dipeptidyl peptidase 4 inhibitors;
FPG = fasting plasma glucose; GLP1RA = glucagon-like peptide 1 receptor agonists; Met = metformin; Mod = moderate; PPG =
postprandial glucose; SGLT2I = sodium-glucose cotransporter 2 inhibitors; SU = sulfonylureas; TZD = thiazolidinediones.
*Mild: albiglutide and exenatide; moderate: dulaglutide, exenatide extended release, and liraglutide.
Met GLP1RA SGLT2I DPP4I TZD AGI Coles BCR-QR
SU/
Glinide
Insulin Pram
FPG
lowering
Mod
Mild to
mod*
Mod Mild Mod Neutral Mild Neutral
SU: mod
Glinide:
mild
Mod to
marked
(basal
insulin or
premixed)
Mild
PPG
lowering
Mild
Mod to
marked
Mild Mod Mild Mod Mild Mild Mod
Mod to
marked
(short/
rapid-
acting
insulin or
premixed)
Mod to
marked
Continued on next slide

for T2D
59
AGI = -glucosidase inhibitors; BCR-QR = bromocriptine quick release; Coles = colesevelam; DPP4I = dipeptidyl peptidase 4 inhibitors;
GLP1RA = glucagon-like peptide 1 receptor agonists; Met = metformin; Mod = moderate; NAFLD, nonalcoholic fatty liver disease;
SGLT2I = sodium-glucose cotransporter 2 inhibitors; SU = sulfonylureas; TZD = thiazolidinediones.
*Especially with short/ rapid-acting or premixed.
SU/
Glinide
Insulin Pram
NAFLD
benefit
Mild Mild Neutral Neutral Mod Neutral Neutral Neutral Neutral Neutral Neutral
Hypo-
glycemia
Neutral Neutral Neutral Neutral Neutral Neutral Neutral Neutral
SU: mod
to severe
Glinide:
mild to
mod
Mod to
severe*
Neutral
Weight Slight loss Loss Loss Neutral Gain Neutral Neutral Neutral Gain Gain Loss

for T2D
60
. How are glycemic targets achieved forT2D?
SU/
Glinide
Insulin Pram
Renal
impair-
ment/ GU
Contra-
indicated
in stage
3B, 4, 5
CKD
Exenatide
contra-
indicated
CrCl <30
mg/mL
GU
infection
risk
Dose
adjust-
ment
(except
lina-
gliptin)
May
worsen
fluid
retention
Neutral Neutral Neutral
Increased
hypo-
glycemia
risk
Increased
risks of
hypo-
glycemia
and fluid
retention
Neutral
GI adverse
effects
Mod Mod* Neutral Neutral* Neutral Mod Mild Mod Neutral Neutral Mod
CHF Neutral Neutral Neutral Neutral† Mod Neutral Neutral Neutral Neutral Neutral Neutral
CVD
Possible
benefit
Neutral Neutral Neutral Neutral Neutral Neutral Safe ? Neutral Neutral
Bone Neutral Neutral Bone loss Neutral
Mod bone
loss
Neutral Neutral Neutral Neutral Neutral Neutral
AGI = -glucosidase inhibitors; BCR-QR = bromocriptine quick release; Coles = colesevelam; CHF = congestive heart failure; CVD =
cardiovascular disease; DPP4I = dipeptidyl peptidase 4 inhibitors; GI = gastrointestinal; GLP1RA = glucagon-like peptide 1 receptor
agonists; GU = genitourinary; Met = metformin; Mod = moderate; SGLT2I = sodium-glucose cotransporter 2 inhibitors; SU =
sulfonylureas; TZD = thiazolidinediones.
*Caution in labeling about pancreatitis.
†Caution: possibly increased CHF hospitalization risk seen in CV safety trial.

 The progressive nature of T2DM should be
regularly & objectively explained to T2DM
patients.
 For T2DM patients not achieving glycemic goals,
promptly initiate insulin therapy.
 Avoid using insulin as a threat, describing it as a
failure or punishment.
 Give patients a self-titration algorithm.
Insulin Therapy in T2DM

64
Insulin initiation in Type 2 DM:
When
1. HbA1c ≥ 10% [start combination insulins] (ADA 2017) but if
HbA1c ≥ 9%, Basal alone may be initiated
2. Symptomatic hyperglycemia
3. PPG > 19.4 mmol/L, FPG> 16.6 moml/L
4. If the glycemic target is not achieved by using three non-insulin
agents (metformine/pioglitazone, secretagogue,
ɑGi/DPP4i/SGLT2i) by at least 3 months
5. In some specific situations

Short term use of insulin therapy in patients
with T2DM may also be considered in the
following conditions:
• Acute illness, surgery, stress and emergencies
• Pregnancy and lactation
• As initial therapy in T2DM with severe
hyperglycemia
• Severe metabolic decompensation (eg. DKA,
HHS)

Types of insulin;
Type of Insulin Onset Peak Duration
Role in Blood Sugar
Management
Rapid-Acting
Lispro 15-30 min. 30-90 min 3-5 hours Covers insulin needs for
meals eaten at the same
time as the injection.Aspart 10-20 min.
40-50
min.
3-5 hours
Glulisine 20-30 min.
30-90
min.
1-2½ hours
Short-Acting
Regular (R)
30 min- 60
min
2-5 hours 5-8 hours
Covers insulin needs for
meals eaten within 30-60
minutes
Intermediate-Acting
NPH (N) 1-2 hours
4-12
hours
18-24 hours
Covers insulin needs for
about half the day or
overnight.

Types of insulin
Name of
Insulin
Onset Duration
Role in Blood
Sugar
Management
Long-Acting
Long-acting
insulin covers
insulin needs
for about one
full day.
Degludec 30-90 min
No peak:
insulin is
delivered at a
steady level.
Longer than 24
hours
Glargine 30-90 min Up to 24 hours
Detemir 1-120 min 20-24 hours

Types of insulin
Type of Insulin Onset Peak Duration
Role in Blood Sugar
Management
Pre-Mixed*
30/70 30 min. 2-4 hours 14-24 hours These products are
generally taken two
or three times a day
before mealtime.
50/50 30 min. 2-5 hours 18-24 hours
25/75 15 min.
30 min.-2½
hours
16-20 hours
Inhaler
Exubera Banned
Afrezza With in min 12 to 15 min 2-3 hours
Post prandial
effects.
*Premixed insulins are a combination of specific proportions of intermediate-
acting and short-acting insulin in one bottle or insulin pen (the numbers the brand
name indicate the percentage of each type of insulin).

Common Insulin Regimens
Split Mix Regimens
 Two injections (intermediate + soluble) per day
* before breakfast & before bedtime
 Proportion/dosage of insulin titrated based on
BG profile
 Drawback
Mixing insulins is tedious and problematic
Inaccuracy of dose
Not preferred –more problems for patients
69

Basal insulin
Usually given at night
 Proportion/dosage of insulin titrated based on FBG
 Drawback
Expensive
Fasting blood glucose is primary targeted
May be with sensitizer and or secretagogue
70

Basal Plus
 Basal insulin at night
 Any rapid acting insulin premeal.
 May be useful during early years of T2DM and in
uncomplicated well motivated patients.
 May be needed to shifted to Basal bolus
regimen
 titrated based on BG profile
 Drawback
 Mixing insulins is tedious and problematic
 Inaccuracy of dose 71

CommonInsulin Regimens (4)
Basal Bolus
 Basal insulin at night and one rapid acting insulin
immediately before each major meal (3 times).
 Basal insulin is titrated following FBG
 Rapid acting insulin is titrated by post meal BGs
 Drawback
 Expensive
 4 times needle prick a day.
Most preferred –most flexible
72

Management of
Diabetes
in Pregnancy
73

 Provide preconception counseling that
addresses the importance of tight glycemic
control, ideally <6.5%, to reduce the risk of
congenital anomalies.
Pregestational Diabetes
American Diabetes Association. Management of diabetes in pregnancy.
Standards of Medical Care in Diabetes-2016. Diabetes Care 2017;39(Suppl. 1):S94–S9874

75
• Family planning should be discussed
and effective contraception should be
prescribed and used until a woman is
prepared and ready to become
pregnant.

 Women preexisting type 1 or type 2 diabetes
who are pregnant or planning to become
pregnant should be counseled on the risk of
development and/or progression of diabetic
retinopathy. Eye exams should occur before
pregnancy or in the first trimester & then be
monitored every trimester and for 1 year
postpartum as indicated by degree of
retinopathy.
Pregestational Diabetes

 Lifestyle change is an essential part GDM
mgmt. and may suffice for many women.
Add medications if needed to achieve
glycemic targets.
Gestational Diabetes Mellitus
(GDM)

 Preferred medications in GDM are insulin and
metformin; glyburide may be used but may have
higher rate of neonatal hypoglycemia &
macrosomia than insulin or metformin. Other
agents have not been adequately studied. Most
oral agents cross the placenta and all lack long-
term safety data. A
Gestational Diabetes Mellitus
(GDM)

The following targets for women with
pregestational type 1 or type 2 diabetes:
 Fasting ≤90 mg/dL (5.0 mmol/L)
 One-hour postprandial ≤130–140mg/dL (7.2–7.8
mmol/L)
 Two-hour postprandial ≤120 mg/dL (6.7 mmol/L)
Glycemic Targets in Pregnancy
(Preexisting Type 1 or Type 2)

Treatment of GDM
 MNT [Dietary Therapy, Exercise]
 Self BG monitoring
 Administration of Insulin if target blood
glucose level are not met by diet alone
 Fetal surveillance
 Intrapartum care
 Post partum care

Insulin therapy
Recommendations for starting Insulin (ADA
guideline)
FPG> 5.8mmol/l or
1 hr PG> 8.6 mmol/l
2hr PG > 7.2 mmol/l
Target blood glucose:
Pre prandial <5.3mmol/l
1 hr post prandial <7.8 mmol/l
2 hr post prandial <6.7 mmol/l

Insulin therapy cont.
Calculating dose:
Total insulin- 20-30 U/day
½ Basal or 2/3rd intermediate acting
½ Bolus or 1/3rd regular Insulin
Calculated daily dose of insulin:
1st trimester-0.8 unit ×kg BW
2nd trimester- 1 unit ×kg BW
3rd trimester- 1.3 unit×kg BW

The dose and type of insulin used is calculated
according to the blood glucose level
If the FBG is high then, a long acting (or
intermediate- acting insulin), is given before
bedtime.
If postprandial blood glucose levels are high,
then regular rapid-acting insulin are added before
meals.
Insulin Therapy cont.

Regular Insulin is withheld during labor; a
sliding scale of soluble insulin should be started
(or infusion pump as may be fit)
 Maternal hyperglycemia should be avoided
during labor to prevent fetal hyperinsulinemia
and subsequent neonatal hypoglycemia
Maternal blood glucose should be maintained
between 4- 5 mmol/L.
Peripartum Management:

Key Take-Home Messages
 MNT is the corner stone of diabetes
management.
 MNT is also essential to reach optimal
glycemic control with fewer hypoglycemic
episodes
85

Key Take-Home Messages
 OADs may attain or maintain good glycemic
control for a variable periods
 Insulin may need to be started in any time
mean while.
86

Diabetes Mellitus -
Complications

Complications of diabetes mellitus
Acute (Metabolic) Chronic (Angiopathy)
MacroVascular
Complications
MicroVascular
Complications

Risk factors and
complications
Microvascular
disease
Eyes
Kidneys
Nerves
Macrovascular disease
Ischaemic heart disease
Strokes
Peripheral vascular
disease
Feet
HypertensionHyperglycaemia
Dyslipidaemia
Coagulopathy
Smoking

Acute Complications
 Diabetic Ketoacidosis (DKA)
 Hyperosmolar non-ketomic
Coma (HONK)
 Hypoglycemia

Metabolic injury to large vessels
Heart Brain Extremities
Coronary artery
disease
– Coronary
syndrome
– MI
– CHF
Cerebrovascular
disease
Peripheral vascular
disease
– Ulceration
– Gangrene
– Amputation
Biology of Macrovascular
Injury

Hyperglycemia
Neuropathy
– Peripheral
– Autonomic
Kidney Nerves
Retinopathy
- Cataract
- Glaucoma
Nephropathy
– Microalbuminuria
– Gross albuminuria
Blindness Kidney failure Amputation
Death and/or disability
Eye
Biology of Microvascular
Injury

Microvascular Complications of
Diabetes-1
Retinopathy: Damage to blood vessels in and around
the retina. It could occur with varying degrees of severity.
Normal ------------- Small hemorrhages --------- Large hemorrhage

Nephropathy:
 Glomeruli are damaged in the kidneys.
 Results in loss of protein
 DIAGNOSTICVALUE-Normal
microalbumin level is 30mg/24 hours.
 May lead to kidney failure
Diabetes-2

Diabetes-3
Neuropathy
 Nerve fibres degenerate
 Blood vessels supplying the nerves are ‘grossly diseased’

96
Diabetes is Managed,
But it Does Not Go Away.
GOAL:
To maintain target
blood glucose

Diabetes by dr arshid rafiq

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