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of diabetes mellitus
Complications of Diabetes Mellitus
Chronic Complications of Acute Complications
Diabetes Mellitus of Diabetes Mellitus
Microvascular Hyperglycemia crisis
Retinopathy Diabetic ketoacidosis
(nonproliferative/proliferative) Hyperglycemia
Nephropathy hyperosmolar State
Neuropathy Lactic acidosis
Sensory and motor (mono- Hypoglycemia
and polyneuropathy)
Autonomic
Macrovascular
Coronary artery disease
Peripheral vascular disease
Cerebrovascular disease
Genetic and
environmental risk
factors impact
inflammation,
autoimmunity, and
metabolic stress are
leading to
hyperglycemia
Vasoactive
Loss of tight
factors
junction
Retinal
ischemia
Growth Macular
factors oedema
New vessels
-Low resistance
- No pericyte/autoregulation
Advanced diabetic eye disease
Retinal ischemia
Neovascularitation
Pericyte Preretinal
loss haemorrhage
Blindness
Diabetic retinopathy
Microalbuminuria or Glomurular
macroalbuminuria damage
Nephropathy
Diabetic nephropathy
Diabetic nephropathy is the leading cause of ESRD in the US.
Individuals with diabetic nephropathy almost always have
diabetic retinopathy.
The stages of diabetic nephropathy are :
Hyperfiltration
Microalbuminuria
Overtproteinuria
Declining GFR
End stage renal failure
Microalbuminuria is defined as 30 to 300 mg/d in a 24-h collection
or 30 to 300 g/mg creatinine in a spot collection (preferred
method).
The appearance of microalbuminuria (incipient nephropathy) in
type 1 DM is an important predictor of progression to overt
proteinuria (300 mg/d) or overt nephropathy.
Hypertension more commonly accompanies microalbuminuria
or overt nephropathy in type 2 DM
Diabetic nephropathy - treatment
The optimal therapy for diabetic nephropathy is prevention.
Interventions effective in slowing progression from
microalbuminuria to overt nephropathy include:
near normalization of glycemia,
strict blood pressure control, and
administration of ACE inhibitors or ARBs, and
treatment of dyslipidemia.
Blood pressure should be maintained at 130/80 mmHg in
diabetic individuals without proteinuria.
A slightly lower blood pressure (125/75) should be considered
for individuals with microalbuminuria or overt nephropathy
A consensus panel of the ADA suggests modest restriction of
protein intake in diabetic individuals with microalbuminuria (0.8
g/kg per day) or overt nephropathy (<0.8 g/kg per day)
Diabetic neuropathy
Mechanism of nerve damage in diabetes
METABOLIC VASCULAR
myoinositol
glucose
Altered membrane
potensial
Arterial
Slow nerve sorbitol narrowing
conduction AGE
formation
nerve vasoconstriction
oedema 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.
Clinical features symmetrical
sensorimotor neuropathy
Symptoms Signs
Loss of sensation ; Sensory loss
Anaesthesia;’numbness’
Diminished/absent tendon
Loss of pain perception
reflexs
Altered sensation:
Muscle wasting and
Paraesthesiae
Dysaesthesiae weakness
Pain Autonomic dysfunction
Burning Foot uleration
Hyperalgesia/allodynia
Neuralgia – lancinating pain
Cramps ; restless leg
Burning, feeling like the feet are on fire Freezing, like the feet are on ice,
although they feel warm to touch
Macrophages
bind to and enter
intima wall
Macrophages
become foam Chemo-attractants such as PDGF
Uptake of Lipids by cells & fatty released from activated macrophages
Macrophages streak formed
Myocardial
infarction Angina:
• Stable
• Unstable
Reduced pain
Sensation and
proprioception
Abnormal
Foot posture
Arteriovenous
shunting
Callus
Ulcer
Mechanical,
Trauma thermal, Macrovascular
chemical Ischemia
disease
Acute Complication of Diabetes
Mellitus
Hyperglycemia crisis
Diabeticketoacidosis (DKA)
Hyperglycemic Hyperosmolar State (HHS)
Hypoglycemia
Diabetic ketoacidosis
(DKA)
Hyperglycemic Hyperosmolar State
(HHS)
Pathophysiolgy of hyperglycemia crisis
Diabetic ketoacidosis (DKA)
DKA was formerly considered a hallmark of type 1
DM
The symptoms and physical signs of DKA
Symptoms : Nausea/vomiting, Thirst/polyuria, Abdominal
pain, Shortness of breath
Physical findings : Tachycardia, Dry mucous
membranes/reduced skin turgor, Dehydration / hypotension,
Tachypnea / Kussmaul, respirations/respiratory distress,
Abdominal tenderness (may resemble acute pancreatitis or
surgical abdomen), Lethargy /obtundation / cerebral edema
/ possibly coma
Precipitating factors
Inadequate insulin administration
Infection (pneumonia/UTI/
Gastroenteritis/sepsis
Infarction (cerebral, coronary, mesenteric,
peripheral)
Drugs (cocaine)
Pregnancy
HHS: Differences from DKA
Patients usually older- typically 60 or more
Major pathophysiologic differences
longer uncompensated osmotic diuresis
greater volume depletion
Acidemia (pH > 7.3) and ketosis are mild
Higher mortality -
often 30-50%
primarily due to underlying vascular or infectious event
Occurs in Type 2 diabetics, often mild or unrecognized
Definition of HHS
Extreme hyperglycemia
Increased serum osmolality
Severe dehydration without significant ketosis or
acidosis
ECF ICF
H2O
H2O