Professional Documents
Culture Documents
of 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
Biochemical
index
HbA1c (%)
ADA1,2
AACE
3
<7
< 6.5
IDF4
(Western
Pacific
region)
< 6.5
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.
treatment. 4th Edn; Hong Kong: Asian-Pacific Type 2 Diabetes Policy Group, 2005.
HbA1c
< 7%
Fasting BG
LDL-cholesterol
HDL-cholesterol
Men > 40 mg/dl (1.1 mmol/l)
Women > 50 mg/dl (1.3 mmol/l)
Triglycerides
Complications of Diabetes
Mellitus
Pathophysiology of
Microvascular
Complications
Diabetic Retinopathy
Diabetic Nephropathy
Hyperglycemia
Renal
vasodilatation
Increased glomular
filtration rate
Protein glycation
Increased
intraglomerular
capillary pressure
Hypertension
Increased
protein excretion
Microalbuminuria or
macroalbuminuria
Glomurular
damage
Nephropathy
Diabetic Nephropathy
Diabetic Neuropathy
METABOLIC
myoinositol
VASCULAR
glucose
Altered membrane
potensial
Slow nerve
conduction
sorbitol
nerve
oedema
AGE
formation
Arterial
narrowing
vasoconstriction
NO
production
Impairing
axonal transport
Vessel
occlusion
H2O
Symptoms
Loss of sensation ;
Anaesthesia;numbness
Loss of pain perception
Altered sensation:
Paraesthesiae
Dysaesthesiae
Pain
Burning
Hyperalgesia/allodynia
Neuralgia lancinating
pain
Cramps ; restless leg
Signs
Sensory loss
Diminished/absent
tendon reflexs
Muscle wasting and
weakness
Autonomic
dysfunction
Foot uleration
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
Pathology of Atherogenesis
Initiation:
Accumulation of lipids at
vascular junctions
experiencing high shear
forces
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
Ischemic stroke
Myocardial
infarction
Angina:
Stable
Unstable
Neuropathy
Motor
dysfunction
Abnormal
Foot posture
Microvascular
disease
Neuropathy Neuropathy
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
often 30-50%
Extreme hyperglycemia
Increased serum osmolality
Severe dehydration without significant ketosis or
acidosis
DKA
HHS
Hypoglycemia
Acute hypoglycemia
Patient
conscious
Patient
unconscio
us
Oral glucose
(10-20gr)
Recovere
d
Acute hypoglycemia
Check BG after
15-20 min
Not
recoverd
Patient
unconscio
us
10% glucose
IV infusion
Patient
conscious
Repeat oral
glucose
Thank you