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Diabetes Mellitus
Urinalysis
Glycosuria
Limitations of urinalysis : renal threshold (varies between
individual); urinary concentration (fluid intake and urine
concentration may effect); neuropathic bladder (reduce the
accuracy); hypoglycemia (this can not be detect)
Urinary ketones
Semi-quantitatif test for acetoacetat; Ketosis-prone diabetes
Glycated haemoglobin
HbA1c is formed by the post-translational, non-enzymatic glycation
Glycaemic targets
Frequency of measurement (every 3 or 6 months)
Limitations of HbA1c measurements : daily patern of blood
glucose levels? ; blood loss/haemolysis/reduced red cell (low
HbA1c)
Blood glucose
Before breakfast (fasting)
2 hour post prandial
ADA1,2
AACE3
IDF4
(Western
Pacific region)
<7
< 6.5
< 6.5
HbA1c (%)
mg/dl
mmol/l
Fasting/preprandial
plasma glucose
90130
5.07.2
< 110
< 6.0
< 110
< 6.1
Postprandial plasma
glucose
< 180
< 10.0
< 140
< 7.8
< 145
<8.0
1. ADA. Diabetes Care 2004; 27: S1535; 2. ADA Diabetes Care 2002; 25: S3549;
3. Feld S. Endocrine Pract 2002; 8 (Suppl 1): 4082; 4. Asian-Pacific Type 2 Diabetes Policy Group.
Type 2 diabetes: Practical targetsand treatment. 4th Edn; Hong Kong: Asian-Pacific Type 2 Diabetes Policy Group, 2005.
HbA1c
< 7%
Fasting BG
mg/dl
< 100
Post prandial BG
mg/dl
< 140
Blood pressure
mmHg
< 130/80
LDL-cholesterol
Complications of Diabetes
Mellitus
Chronic Complications of
Diabetes Mellitus
Microvascular
Acute Complications of
Diabetes Mellitus
Hyperglycemia crisis
Hypoglycemia
Macrovascular
Pathophysiology of
Microvascular
Complications
Diabetic Retinopathy
Diabetic Retinopathy
Blindness is primarily the result of progressive diabetic retinopathy and
clinically significant macular edema.
Diabetic retinopathy is classified into two stages: nonproliferative and
proliferative.
Nonproliferative diabetic retinopathy : marked by retinal vascular
microaneurysms, blot hemorrhages, and cotton wool spots
The appearance of neovascularization in response to retinal hypoxia is
the hallmark of proliferative diabetic retinopathy.
Diabetic Nephropathy
Hyperglycemia
Renal
vasodilatation
Protein glycation
Increased
intraglomerular
capillary pressure
Increased glomular
filtration rate
Hypertension
Increased
protein excretion
Microalbuminuria or
macroalbuminuria
Glomurular
damage
Nephropathy
Diabetic Nephropathy
Diabetic nephropathy is the leading cause of ESRD in the US.
Individuals with diabetic nephropathy almost always have diabetic
retinopathy.
Declining GFR
End stage renal failure
Diabetic Neuropathy
METABOLIC
myoinositol
VASCULAR
glucose
Altered membrane
potensial
Slow nerve
conduction
sorbitol
AGE
formation
nerve
oedema
Arterial
narrowing
vasoconstriction
NO
production
Impairing
axonal transport
Vessel
occlusion
H2O
Diabetic Neuropathy
Diabetic neuropathy occurs in approximately 50% of
individuals with long-standing type 1 and type 2 DM.
The development of neuropathy correlates with the duration
of diabetes and glycemic control; both myelinated and
unmyelinated nerve fibers are lost.
Several stage :
Intraneural biochemical abnormalities; sorbitol
accumulation, myoinositol depletion
Impairement of electrophysiological measurement;
decreased nerve conduction velocity; asymptomatic
Clinical neuropathy; detectable using clinical methods;
maybe symptomatic. Histological changes evident
End stage complications. Exp are ulceration and Charcot
neuroarthropathy; major derangements of neural
structure and function.
Anaesthesia;nu
mbness
Loss of pain
perception
Altered
sensation:
Paraesthesiae
Dysaesthesiae
Pain
Burning
Signs
Sensory loss
Diminished/absent tendon
reflexs
Muscle wasting and
weakness
Autonomic dysfunction
Foot uleration
Treatment of Symmetric
Neuropathy
Glucose control
Pain control
Tricyclic antidepressants
Amitriptyline,desipramin, nortriptilin,
trazodone
Anticonvulsants
Carbamazepine, gabapentin
Topical creams
capsaicin
Foot care
Autonomic Neuropathy
DM-related autonomic neuropathy can involve multiple
systems, including the cardiovascular, gastrointestinal,
genitourinary, sudomotor, and metabolic systems.
Autonomic neuropathies affecting the cardiovascular system
cause a resting tachycardia and orthostatic hypotension.
Gastroparesis and bladder emptying abnormalities are often
caused by the autonomic neuropathy seen in DM (discussed
below).
Hyperhidrosis of the upper extremities and anhidrosis of the
lower extremities result from sympathetic nervous system
dysfunction.
Anhidrosis of the feet can promote dry skin with cracking,
which increases the risk of foot ulcers.
Autonomic neuropathy may reduce counterregulatory hormone
release, leading to an inability to sense hypoglycemia
appropriately ((hypoglycemia unawareness)
Pathophysiology of
Macrovascular
Complications
Macrovascular Complication
Macrovascular complications of diabetes mellitus
are condition characterized by atherosclerotic
occlusive disease of cerebral, myocard and
lower extremities.
Atherothrombosis is the most common cause of
macrovascular complications
Atherothrombosis is characterized by a sudden
(unpredictable) atherosclerotic plaque disruption
(rupture or erosion) leading to platelet activation
and thrombus formation
Atherothrombosis is the underlying condition that
results in events leading to myocardial infarction,
ischemic stroke, amputation and vascular death
Macrophages
bind to and enter
intima wall
Uptake of Lipids by
Macrophages
Macrophages
become foam
cells & fatty
streak formed
Smooth muscle
cells (SMCs)
migrate into the
intima
Result: Atherosclerotic
plaque2
Myocardial
infarction
Angina:
Stable
Unstable
Macrovascular Disease in
Diabetes Mellitus
Cardiovascular and cerebrovascular disease account
for up 70% of death in patients with type 2 DM
All patients with type 2 diabetes have greater
predipostition to macrovascular disease, often having a
constellation of risk factors, which have been term
insulin resistance.
It has been hypotethesized that insulin resistance and
hyperinsulinemia (environmental and genetic factors),
are central to development :
Glucose intolerance
Hypertension
Dyslipidemia
Coagulopathy
Neuropathy
Motor
dysfunction
Abnormal
Foot posture
Neuropathy
Neuropathy
Microvascular
disease
Reduced pain
Sensation and
proprioception
Increased foot
prssure
Dry, cracked
skin
Poor tissue
nutrition and
oxygenation
Cheiroarthropathy
Arteriovenous
shunting
Callus
Trauma
Mechanical,
thermal,
chemical
Ulcer
Ischemia
Macrovascular
disease
Hyperglycemia crisis
Diabetic ketoacidosis (DKA)
Hyperglycemic Hyperosmolar
State (HHS)
Hypoglycemia
Pathophysiolgy of Hyperglycemia
Crisis
Precipitating Factors
often 30-50%
primarily due to underlying vascular or infectious event
Definition of HHS
Extreme hyperglycemia
Increased serum osmolality
Severe dehydration without significant
ketosis or acidosis
Precipitating Factors
Laboratory Findings
DKA
HHS
Approach to Therapy
Correcting the hyperosmolar state and
dehydration is the initial aim of therapy.
Insulin therapy should be undertaken
only after the patient is stable
hemodynamically.
Glucose and H2O
Hypoglycemia
Clinical Manifestations of
Hypoglycemia
Whipples triadsymptoms consistent with hypoglycemia,a low
Patient
unconscious
Oral glucose
(10-20gr)
Recovered
Acute hypoglycemia
Check BG after
15-20 min
Not
recoverd
Patient
unconscious
10% glucose
IV infusion
Patient
conscious
Repeat oral
glucose
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