Clinical Aspects of Diabetes Mellitus: Diagnosis, Types, Management

Clinical Aspects
of
Diabetes Mellitus
Alaa Wafa . MD
Associate Professor of Internal Medicine
PGDIP DM Cardiff University UK
Diabetes & Endocrine Unit.
Mansoura University

CASE 6: SWEET PEE
Ian, a 14-year-old male child
drinking anything available & more frequently to micturate.
drowsy and confused.
breathing quickly& deeply, and breath smells of nail varnish
remover.
blood pressure is 80 / 40mmHg and pulse rate 140 /minute.
immediate management - fluid, NaCl, insulin by infusion
IV Insulin then twice daily SC insulin therapy .

Glucose Homeostasis Research Timeline
• 1552 BC: Ebers Papyrus in ancient Egypt.First known written
description of diabetes. (excessive urination)
• 1st Century AD: Arateus — “Melting down of flesh and limbs Into urine.”
• 1776: Matthew Dobson conducts experiments showing sugar in blood and urine
of diabetics.
• Mid 1800s: Claude Bernard studies the function of the pancreas and liver, and
their roles in homeostasis.
• 1869: Paul Langerhans identifies cells of unknown function in the pancreas.
These cells later are named “Islets of Langerhans.”
• 1889: Pancreatectomized dog develops fatal diabetes.
• 1921: Insulin “discovered” — effectively treated pancreatectomized dog.
• 1922: First human treated with insulin.
• 1923: Banting and Macleod win Nobel Prize for work with insulin.
• 1983: Biosynthetic insulin produced.
• 2001: Human genome sequence completed.
1552BC 1st Century AD 1776 1869 188918th Century 1921-23 1983 2001

- Hatshepsut’s mummy is that of an obese, diabetic
50 year old woman with bad teeth.
- She died from metastatic cancer.
Diabetes

Worldwide
prevalence of 8.3%
IDF Diabetes Atlas Update 2013

 Diabetes mellitus (DM) is a group of diseases
characterized by high levels of blood glucose
resulting from defects in insulin production, insulin
action, or both.
 The term diabetes mellitus describes a metabolic
disorder of multiple aetiology characterized by
chronic hyperglycaemia with disturbances of
carbohydrate, fat and protein metabolism resulting
from defects in insulin secretion, insulin action, or
both.

 Diabetes mellitus may present with
characteristic symptoms such as thirst,
polyuria, blurring of vision, and weight loss.
 In its most severe forms, ketoacidosis or a
non–ketotic hyperosmolar state may develop
and lead to stupor, coma and, in absence of
effective treatment, death.

 Polyuria / Nocturia
 Excessive thirst and appetite
 Weight Loss
 Lethargy
 Blurred Vision
 Skin infections
 Vaginal infections

 Type 1 Diabetes Mellitus
 Type 2 Diabetes Mellitus
 Gestational Diabetes
 Other types:
LADA
MODY
Secondary Diabetes Mellitus

 Was previously called insulin-dependent diabetes mellitus
(IDDM) or juvenile-onset diabetes.
 Type 1 diabetes develops when the body’s immune system
destroys pancreatic beta cells, the only cells in the body
that make the hormone insulin that regulates blood
glucose.
 This form of diabetes usually strikes children and young
adults, although disease onset can occur at any age.
 Type 1 diabetes may account for 5% to 10% of all
diagnosed cases of diabetes.

Risk factors for type 1 diabetes may include
 Autoimmune
 Genetic
 Environmental factors

 Was previously called non-insulin-dependent
diabetes mellitus (NIDDM) or adult-onset
diabetes.
 Type 2 diabetes may account for about 90% to
95% of all diagnosed cases of diabetes.
 It usually begins as insulin resistance, a
disorder in which the cells do not use insulin
properly. As the need for insulin rises, the
pancreas gradually loses its ability to produce
insulin.

Blood glucose
Insulin and Glucagon Regulate Normal Glucose
Homeostasis
Glucose output Glucose uptake
Glucagon (α cell)
Insulin
(β cell)
Pancreas
Liver
Muscle
Adipose
tissue
Fasting state Fed state

Porte D Jr, Kahn SE. Clin Invest Med. 1995;18:247–254.
Adapted with permission from Kahn CR, Saltiel AR. In: Kahn CR et al,
eds. Joslin’s Diabetes Mellitus. 14th ed. Lippincott Williams & Wilkins; 2005:145–168. 4

Islet dysfunction
Adapted from Buse JB et al. In Williams Textbook of Endocrinology. 10th ed. Philadelphia, Saunders, 2003:1427–1483; Buchanan TA Clin
Ther 2003;25(suppl B):B32–B46; Powers AC. In: Harrison’s Principles of Internal Medicine. 16th ed. New York: McGraw-Hill, 2005:2152–2180;
Rhodes CJ Science 2005;307:380–384.
The Pathophysiology of Type 2 Diabetes Includes
Multiple Defects
Pancreas
Insulin deficiency
Liver
Muscle & Fat
Excess
glucagon Diminished
insulin
Beta cell
produces
less insulin
Alpha cell
produces
excess
glucagon
Insulin resistance
(decreased glucose uptake)
Excess Glucose Output
HYPERGLYCEMIA

Time
Pancreatic Islet Cells in Type 2 Diabetes
B cells
α cells
B cells
α cells

The Core Defects in type 2 diabetes:
Insulin resistance in
peripheral tissues
Excess Hepatic
Glucose Production
due to
1) increased glucagon
2) insulin insufficiency
3) insulin resistance
Insulin deficiency due
to insufficient
pancreatic insulin
release

Reprinted from Primary Care, 26, Ramlo-Halsted BA, Edelman SV, The natural history of type 2
diabetes. Implications for clinical practice, 771–789, © 1999, with permission from Elsevier.
Development and Progression of
Type 2 Diabetes and Related Complications*
*Conceptual representation.
Insulin level
Insulin resistance
Hepatic glucose
production
Postprandial
glucose
Fasting plasma
glucose
Beta-cell function
Progression of Type 2 Diabetes Mellitus
Impaired Glucose Tolerance
Diabetes Diagnosis
Frank Diabetes
4–7 years
Development of Macrovascular Complications
Development of Microvascular Complications

Risk Factors for Developing Type 2 Diabetes
Type 2
Diabetes
Certain
racial and
ethnic
groups Low HDL
cholester
ol or high
triglycerid
es
Gestation
al
Diabetes
Overweight
Lack of
regular
exercise
regularly
Family
history of
diabetes
Age  45
years
Reprinted from Primary Care, 26, Ramlo-Halsted BA, Edelman SV, The natural history of type 2
diabetes. Implications for clinical practice, 771–789, © 1999, with permission from Elsevier.

Type 2 diabetes
Type 2 diabetes is associated:
 Older age,
Obesity,
Family history of diabetes,
History of gestational diabetes,
 Impaired glucose metabolism
 Physical inactivity .
 Type 2 diabetes is increasingly being diagnosed
in children and adolescents.

24
Features of Type1DM and Type 2 DM
Feature T1DM T2DM
1) Age of onset Usually < 30 Usually > 30
2) Rate of onset Rapid Slow
3) Body weight Thin Obese
4) Ketosis Common Rare
5) Prevalence < 0.5% > 2%
6) HLA association Present Absent
7) Concordance – identical
twins
< 50% > 95%
8) Islet cell mass Greatly reduced Slightly reduced
9) Association with
endocrinopathies
Occasional Rare

 A form of glucose intolerance that is diagnosed
in some women during pregnancy.
 It is common among obese women and women
with a family history of diabetes.
 During pregnancy, gestational diabetes requires
treatment to normalize maternal blood glucose
levels to avoid complications in the infant.

 Other specific types of diabetes result from
specific genetic conditions (such as maturity-
onset diabetes of youth), surgery, drugs,
malnutrition, infections, and other illnesses.
 Such types of diabetes may account for 1% to
5% of all diagnosed cases of diabetes.

 MODY – Maturity Onset Diabetes of the
Young
 MODY is a monogenic form of diabetes with
an autosomal dominant mode of inheritance:
◦ Mutations in any one of several transcription
factors or in the enzyme glucokinase lead to
insufficient insulin release from pancreatic ß-cells,
causing MODY.
◦ Different subtypes of MODY are identified based
on the mutated gene.

 Latent Autoimmune Diabetes in Adults (LADA) is
a form of autoimmune (type 1 diabetes) which is
diagnosed in individuals who are older than the
usual age of onset of type 1 diabetes.
 Alternate terms that have been used for "LADA"
include Late-onset Autoimmune Diabetes of
Adulthood, "Slow Onset Type 1" diabetes, and
sometimes also "Type 1.5
 Often, patients with LADA are mistakenly thought
to have type 2 diabetes, based on their age at the
time of diagnosis.

Secondary causes of Diabetes mellitus include:
 Acromegaly,
 Cushing syndrome,
 Thyrotoxicosis,
 Pheochromocytoma
 Chronic pancreatitis,
 Cancer

 Drug induced hyperglycemia:
◦ Atypical Antipsychotics - Alter receptor binding
characteristics, leading to increased insulin resistance.
◦ Beta-blockers - Inhibit insulin secretion.
◦ Corticosteroids - Cause peripheral insulin resistance and
gluconeogensis.
◦ Fluoroquinolones - Inhibits insulin secretion by blocking ATP
sensitive potassium channels.
◦ Thiazide Diuretics - Inhibit insulin secretion due to
hypokalemia. They also cause increased insulin resistance due
to increased free fatty acid mobilization.

34
Diagnosis of Pre-diabetes and Diabetes
Test Fasting Plasma Glucose
(FPG)
Oral Glucose Tolerance Test
(OGTT
Random/Casual
Plasma Glucose
(with symptoms)
How
performed
Bd glucose is measured
after at least an 8 hr fast
75 gm glucose load (drink) is
ingested after at least an 8hr
fast
Blood glucose is measured at
2 hrs
Blood glucose is
measured at any
time regardless
of eating
Normal < 100mg/dl (5.6 mmol/L) < 140 mg/dl (7.8 mmol/L)
Pre-
diabetes
IFG
100-125 mg/dl
(5.6-6.9 mmol/L)
Pre-
diabetes
IGT
140-199 mmol/dl
(7.8-11 mmol/L)
Diabetes
Mellitus
≥ 126 mg/dl (7 mmol/L) ≥ 200mg/dl (11.1 mmol/L) ≥ 200mg/dl
(11.1 mmol/L)
(with symptoms)

Prediabetes: Impaired glucose tolerance and
impaired fasting glucose
• Prediabetes is a term used to distinguish
people who are at increased risk of
developing diabetes.
• IFG :100 to 125 mg/dl
• IGT :140 to 199 mg/dL

Management of
Diabetes Mellitus

ANTI-HYPERGLYCEMIC THERAPY
• Therapeutic options: Lifestyle
- Weight optimization
- Healthy diet
- Increased activity level
ADA-EASD Position Statement Update:
Management of Hyperglycemia in T2DM, 2015
Diabetes Care 2012;35:1364–1379; Diabetologia 2012;55:1577–1596

DPP-4 inhibitors3
(stimulates glucose dependant
insulin secretion from
b-cells and lowers glucagon
secretion from -cells)
Sulphonylureas
and rapid-acting
secretagogues1
(stimulates insulin
secretion)
Thiazolidinediones1
(reduces insulin resistance
in target tissues)
Metformin1
(reduces hepatic
glucose production and increases
peripheral glucose uptake)
-glucosidase inhibitors1
(delays digestion and
absorption of intestinal
carbohydrate)
Mainclasses ofglucose-lowering medications
SiteandMOA*
1. Krentz AJ, Bailey CJ. Drugs. 2005;65:385-411. 2. Cheng A, Fantus G. Can Med Assoc J. 2005;172:213-26.
3. Barnett A. Int J Clin Pract. 2006;60:1454-70. 4. Chao EC. Discov Med. 2011 Mar;11(58):255-63.
Intestinal lipase
inhibitors2
(blocks free fatty acid
absorption from
the intestine)
MOA*; Mode Of Action

peripheral
glucose
uptake
hepatic
glucose
production
pancreatic
insulin
secretion
pancreatic
glucagon
secretion
gut
carbohydrate
delivery &
absorption
incretin
effect
HYPERGLYCEMIA
?
Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011
Multiple, Complex Pathophysiological
Abnormalities in T2DM
_
_
+
renal
glucose
excretion

peripheral
glucose
uptake
hepatic
glucose
production
pancreatic
insulin
secretion
pancreatic
glucagon
secretion
gut
carbohydrate
delivery &
absorption
incretin
effect
HYPERGLYCEMIA
?
Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011
Multiple, Complex Pathophysiological
Abnormalities in T2DM
_
_
+
renal
glucose
excretion
DA
agonists
T Z D sMetformin
S U sGlinides
DPP-4
inhibitors
GLP-1R
agonists
A G I s
Amylin
mimetics
Insulin
Bile acid
sequestrants

Healthy eating, weight control, increased physical activity & diabetes education
Metformin
high
low risk
neutral/loss
GI / lactic acidosis
low
If HbA1c target not achieved after ~3 months of monotherapy, proceed to 2-drug combination (order not meant to denote
any specific preference - choice dependent on a variety of patient- & disease-specific factors):
Metformin
+
Metformin
+
Metformin
+
Metformin
+
Metformin
+
high
low risk
gain
edema, HF, fxs
low
Thiazolidine-
dione
intermediate
low risk
neutral
rare
high
DPP-4
inhibitor
highest
high risk
gain
hypoglycemia
variable
Insulin (basal)
Metformin
+
Metformin
+
Metformin
+
Metformin
+
Metformin
+
Basal Insulin +
Sulfonylurea
+
TZD
DPP-4-i
GLP-1-RA
Insulin§
or
or
or
or
Thiazolidine-
dione
+
SU
DPP-4-i
GLP-1-RA
Insulin§
TZD
DPP-4-ior
or
or GLP-1-RA
high
low risk
loss
GI
high
GLP-1 receptor
agonist
Sulfonylurea
high
moderate risk
gain
hypoglycemia
low
SGLT2
inhibitor
intermediate
low risk
loss
GU, dehydration
high
SU
TZD
Insulin§
GLP-1 receptor
agonist
+
SGLT-2
Inhibitor
+
SU
TZD
Insulin§
Metformin
+
Metformin
+
or
or
or
or
SGLT2-i
or
or
or
SGLT2-i
Mono-
therapy
Efficacy*
Hypo risk
Weight
Side effects
Costs
Dual
therapy†
Efficacy*
Hypo risk
Weight
Side effects
Costs
Triple
therapy
or
or
DPP-4
Inhibitor
+
SU
TZD
Insulin§
SGLT2-i
or
or
or
SGLT2-i
or
DPP-4-i
If HbA1c target not achieved after ~3 months of dual therapy, proceed to 3-drug combination (order not meant to denote
If HbA1c target not achieved after ~3 months of triple therapy and patient (1) on oral combination, move to injectables, (2) on GLP-1 RA, add
basal insulin, or (3) on optimally titrated basal insulin, add GLP-1-RA or mealtime insulin. In refractory patients consider adding TZD or SGL T2-i:
Metformin
+
Combination
injectable
therapy‡
GLP-1-RAMealtime Insulin
Insulin (basal)
+
Figure 2. Anti-hyperglycemic therapy
in T2DM: General recommendations Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442

Metformin
high
low risk
neutral/loss
low
Metformin
+
Metformin
+
Metformin
+
Metformin
+
Metformin
+
high
low risk
gain
edema, HF, fxs
low
Thiazolidine-
dione
intermediate
low risk
neutral
rare
high
DPP-4
inhibitor
highest
high risk
gain
hypoglycemia
variable
Insulin (basal)
Metformin
+
Metformin
+
Metformin
+
Metformin
+
Metformin
+
Basal Insulin +
Sulfonylurea
+
TZD
DPP-4-i
GLP-1-RA
Insulin§
or
or
or
or
Thiazolidine-
dione
+
SU
DPP-4-i
GLP-1-RA
Insulin§
TZD
DPP-4-ior
or
or GLP-1-RA
high
low risk
loss
GI
high
GLP-1 receptor
agonist
Sulfonylurea
high
moderate risk
gain
hypoglycemia
low
SGLT2
inhibitor
intermediate
low risk
loss
GU, dehydration
high
SU
TZD
Insulin§
GLP-1 receptor
agonist
+
SGLT-2
Inhibitor
+
SU
TZD
Insulin§
Metformin
+
Metformin
+
or
or
or
or
SGLT2-i
or
or
or
SGLT2-i
Mono-
therapy
Efficacy*
Hypo risk
Weight
Side effects
Costs
Dual
therapy†
Efficacy*
Hypo risk
Weight
Side effects
Costs
Triple
therapy
or
or
DPP-4
Inhibitor
+
SU
TZD
Insulin§
SGLT2-i
or
or
or
SGLT2-i
or
DPP-4-i
Metformin
+
Combination
injectable
therapy‡
Insulin (basal)
+
Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442

Metformin
high
low risk
neutral/loss
low
Metformin
+
Metformin
+
Metformin
+
Metformin
+
Metformin
+
high
low risk
gain
edema, HF, fxs
low
Thiazolidine-
dione
intermediate
low risk
neutral
rare
high
DPP-4
inhibitor
highest
high risk
gain
hypoglycemia
variable
Insulin (basal)
Metformin
+
Metformin
+
Metformin
+
Metformin
+
Metformin
+
Basal Insulin +
Sulfonylurea
+
TZD
DPP-4-i
GLP-1-RA
Insulin§
or
or
or
or
Thiazolidine-
dione
+
SU
DPP-4-i
GLP-1-RA
Insulin§
TZD
DPP-4-ior
or
or GLP-1-RA
high
low risk
loss
GI
high
GLP-1 receptor
agonist
Sulfonylurea
high
moderate risk
gain
hypoglycemia
low
SGLT2
inhibitor
intermediate
low risk
loss
GU, dehydration
high
SU
TZD
Insulin§
GLP-1 receptor
agonist
+
SGLT-2
Inhibitor
+
SU
TZD
Insulin§
Metformin
+
Metformin
+
or
or
or
or
SGLT2-i
or
or
or
SGLT2-i
Mono-
therapy
Efficacy*
Hypo risk
Weight
Side effects
Costs
Dual
therapy†
Efficacy*
Hypo risk
Weight
Side effects
Costs
Triple
therapy
or
or
DPP-4
Inhibitor
+
SU
TZD
Insulin§
SGLT2-i
or
or
or
SGLT2-i
or
DPP-4-i
Metformin
+
Combination
injectable
therapy‡
Insulin (basal)
+
Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442
HbA1c
≥9%
Metformin
intolerance or
contraindication
Uncontrolled
hyperglycemia
(catabolic features,
BG ≥300-350 mg/dl,
HbA1c ≥10-12%)

Diabetes Mellitus - Complications

Complications of diabetes mellitus
Acute (Metabolic)
Chronic
(Angiopathy)
Macro Vascular
Complications
Micro Vascular
Complications
 Diabetic Ketoacidosis
(DKA)
 Hyperosmolar non-
ketomic Coma (HONK)
 Hypoglycemia
1. Young MJ, Boulton AJ, MacLeod AF, Williams DR, Sonksen PH. Diabetologia 1993;36(2):150-4.
2. Caro, J. J., A. J. Ward, et al. (2002). Diabetes Care 25(3): 476-81.

 Infections
 Trauma
 MI
 Stroke
 Surgery
 Emotional stress
 Inadequate intake or poor compliance

 Fruity breath
 Kussmaul’s
 Hypotension
 N&VAbdominal pain
 Anorexia
 Dehydration
 Weight loss
 Polyuria
 Somnolence
 Tachycardia
 Thirst
 Visual disturbances
 Warm, dry skin
 Weakness

 Hyperglycemia
 Dehydration
 Electrolyte imbalances
 Metabolic acidosis

 Most commonly occurs in older adults with
Type II diabetes
 Always look for precipitating factors

 Drugs (beta Blocker or diuretics)
 Procedures
 Chronic illness (stroke , P.E, silent MI)
 Acute illness (severe infections)

55
 Overdose of insulin
 Omitting a meal
 Overexertion
 Nausea and vomiting
 Alcohol intake

 Hypoglycemia = development of symptoms or a
plasma glucose <70 mg/dl.
Symptoms of hypoglycemia
Autonomic Neuroglycopenic
Trembling
Palpitations
Sweating
Anxiety
Hunger
Nausea
Tingling
Angina
Arrhythmi
a
Difficulty concentrating
Vision changes
Difficulty speaking
Headache
Dizziness
Confusion
Weakness
Drowsiness
Tiredness
T1AS
Severity of hypoglycemia
Mild: Autonomic symptoms are present. The individual is able to self-treat.
Moderate: Autonomic and neuroglycopenic symptoms are present. The
individual is able to self-treat.
Severe: Individual requires assistance of another person. Unconsciousness
may occur. Plasma glucose is typically <50 mg/dl.

 In adults, mild to moderate hypoglycaemia should be treated by the
oral ingestion of 15g. of carbohydrate, preferably as glucose or
sucrose tablets or solution. These are preferable to orange juice
and glucose gels.
 Patients should be encouraged to wait 15 minutes, retest BG and
retreat with another 15g. of carbohydrate if the BG level remains
<70 mg/dl.
 If > 70 mg/dl a snack is allowed
Examples of 15g. of carbohydrate for treating
mild to moderate hypoglycemia
 15 g of glucose in the form of glucose tablets
 15 ml (3 teaspoons) or 3 packets of table sugar dissolved in water
 175 ml (3/4 cup) of juice or regular soft drink
 6 Life Savers™ (1 = 2.5 g carbohydrate)
 15 ml. (1 tablespoon) of honey

Chronic complications
of
Diabetes Mellitus

chronic complications
Microvascular
disease
Eyes
Kidneys
Nerves
Macrovascular disease
Ischaemic heart disease
Strokes
Peripheral vascular
disease
Feet
HypertensionHyperglycaemia
Dyslipidaemia
Coagulopathy
Smoking
1. Young MJ, Boulton AJ, MacLeod AF, Williams DR, Sonksen PH.
Diabetologia 1993;36(2):150-4.
2. Caro, J. J., A. J. Ward, et al. (2002). Diabetes Care 25(3): 476-81.

1 Fong DS, et al. Diabetes Care. 2003; 26 [Suppl. 1]:S99–S102.
2 Molitch ME, et al. Diabetes Care. 2003; 26 [Suppl.1]:S94–S98.
3 Kannel WB, et al. Am Heart J. 1990; 120:672–676.
4 Gray RP & Yudkin JS. In Textbook of Diabetes. 1997.
5 Mayfield JA, et al. Diabetes Care. 2003;26 [Suppl. 1]:S78–S79.
Diabetic
retinopathy
Leading cause
of blindness in working-age adults1
Diabetic
nephropathy
Leading cause of
end-stage renal disease2
Cardiovascular
disease
Stroke
2- to 4-fold increase in
cardiovascular
mortality and stroke3
Diabetic
neuropathy
Leading cause of non-
traumatic lower extremity
amputations5
8/10 diabetic patients
die from CV events4
DiabetesisaSeriousChronicDisease
~50%ofpatientspresentedwithcomplication

Neuropathy
– Peripheral
– Autonomic
Kidney Nerves
Retinopathy
- Cataract
- Glaucoma
Nephropathy
– Microalbuminuria
– Gross albuminuria
Blindness Kidney failure Amputation
Disability and/or death
Eye
Microvascular disease

 Fluorescein
angiogram. This
shows abnormalities
in the capillaries of
the retina in the
diabetic.

Diabetic Retinopathy
Cotton wool spots

Proliferative Retinitis:
Neovascularization
Haemorrhagia
Fibroplasia
Retinal detachment
Laser cauterization

 Micro aneurisms
 Scattered exudates
 Hemorrhages(flame
shaped, Dot and Blot)
 Cotton wool spots (<5)
 Venous dilatations
Background retinopathy

 New vessels (on disc,
elsewhere)
 Fibrous proliferation (on
disc, elsewhere)
 Hemorrhages
(preretinal, vitreous)
Panretinal photo-coagulation

 Diabetes has become the most common
cause of end stage renal failure in the US and
Europe
 About 20 – 30% of patients with diabetes
develop evidence of nephropathy

Stage Description GFR
1 Kidney damage/normal GFR >90ml/min
2 Mild renal insufficiency 89-60
3 Moderate renal insufficiency 59-30
4 Severe renal insufficiency 29-15
5 Kidney Failure/ERF/ESRD <15
DKD: Diabetic kidney disease
DKD Classification

 Sensorimotor neuropathy (acute/chronic)
 Autonomic neuropathy
 Mononeuropathy
Spontaneous
Entrapment
External pressure palsies
 Proximal motor neuropathy

 128 Hz tuning fork for
testing of vibration
perception

Cranial nerve palsies
(most common are n.
IV,VI,VII)

 Ulceration (painless)
 Neuropathic edema
 Charcot arthropathy

 Male sex
 Increasing age
 Peripheral vascular disease
 Neuropathy
 Infection
 Low socioeconomic status
 Limited joint mobility
 Poor education of patient

Cellulitis of the foot (diabetic)

Patient should
◦ check feet daily
◦ Wash feet daily
◦ Keep toenails short
◦ Protect feet
◦ Always wear shoes
◦ Look inside shoes
before putting them
on
◦ Always wear socks
◦ Break in new shoes
gradually

Take Control Of Your Patient Life,
Otherwise…………
Diabetes Will Control It . !!!

Thank
you
dralaawafa@hotmail.com

Clinical Aspects of Diabetes Mellitus: Diagnosis, Types, Management

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Clinical Aspects of Diabetes Mellitus: Diagnosis, Types, Management