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of Diabetes
Are they Preventable???
13th October, 2009
BY
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Presentation
outline
(Prevention)
PRESENTATION
OUTLINE
(Prevention)
Can we
prevent those
dreadful
complication ?
Why?
How?
MACROVASCULAR COMPLICATIONS
THE WEAPON
PATHOPHYSIOLOGY of Atherosclerosis
Atherosclerosis is the leading cause of death & disability in
the world
Key processes in atherosclerosis are the intimal thickening
& lipid accumulation that produce the characteristic
atheromatous plaques
Atherosclerosis is a slow & progressive disease that often
begins as early as infancy
MACROVASCULAR COMPLICATIONS
CARDIAC COMPLICATIONS
10
Vice like
Constricting pain
Heart Attack
+
Acute heart failure
+
Shock
)Very High death rate (
Acute drop in BP
Heart Attack
Acute
heart
failureSOB
followed
by chest
pain. 11
Chest Pain
12
1. Unstable Angina
2. Non STEMI
3. STEMI
Ballooning
Stenting
Before
After
Coronary bypass
Before
After
14
MACROVASCULAR COMPLICATIONS
CEREBROVASCULAR COMPLICATIONS
15
16
HEMORRHAGIC
ISCHEMIC
17
18
19
20
MACROVASCULAR COMPLICATIONS
21
Asymptomatic
20% to 50%
Intermittent claudication
10% to 35%
5-Year Outcomes
Cardiovascular
Disease
Limb Morbidity
Stable
Worsening
1-Year Outcomes
Alive, no amputation, 50%
Amputation, 25%
Nonfatal
20%
Fatal
15% to 30%
Death, 25%
*Chronic ischemic rest pain, ulcers, or gangrene attributable to atherosclerotic occlusive disease.
PAD = peripheral arterial disease.
22
5
23
PATHOPHYSIOLOGY OF PAD
Atherosclerotic disease process
becomes symptomatic when
occlusive lesions cause limb
ischemia
In patients with IC, limb blood
flow may be normal during rest
but markedly inadequate during
exercise
In time, ischemia can cause
neurologic and metabolic
changes in skeletal muscle that
lead to functional impairment of In this angiogram, the right
common iliac artery exhibits
the affected limb
INTERMITTENT CLAUDICATION
A subset of patients with symptomatic PAD
Leg pain
Produced by exercise
Relieved by rest
Caused by arterial occlusive disease
Dependent on location and extent of occlusion
Leading to deconditioning of muscle
Resulting avoidance of activity leads to
deconditioning of muscle
25
Retinopathy
Proved Evidences
MICROVASCULAR COMPLICATIONS
R ETINOPATHY
Micro aneurysms
Dot Hemorrhages
Intraretinal MicroVascular
Abnormalities
Venous Beading
Retinal Ischemia
NVEs
Occluded Vessel
NVD
NVE
NVD
NVD
Subhyaloid Hemorrhages
NVE
Exudative maculopathy
Subhyaloid Hemorrhages
Exudative maculopathy
Exudative Maculopathy
Gliosis of Vessels
Ischemic Retinopathy
Photo Coagulation
Diabetic
Macular
Edema
Proliferative
Diabetic
Retinopathy
Nonproliferative
Diabetic
Retinopathy
Preclinical
None, or blurred
vision
Non, or reduced
vision or floaters
None
Symptoms
Swelling of
retina due to
leaky capillaries
Increased
capillary leakage
Fluid
accumulation in
retinal layers
Retinal
vasodilatation
Beading
IRMAs
Neovascularization or optic
disc, retina, &/ or
iris
Retinal vasodilatation
Microaneurysms
Nerve fiber layer
infarcts
Intraretinal
hemorrhages
IRMAs
Venous bleeding
Normal
appearing
retina
Clinical
signs
indicating
need for
referral
32
No abnormalities
No apparent retinopathy
Microaneurysm only
Recommended first
examination *
Yearly
Yearly
At time of diagnosis of
diabetes
Type 2 diabetes
Physician discretion
pending results of first
trimester exam
Priority to conception
& during first trimester
Patient group
Eye exam should be performed through dialed pupils by qualified eye specialist
MICROVASCULAR COMPLICATIONS
DIABETIC NEPHROPATHY
DEATH
37
38
38
When
Normal Range
Blood
pressure
< 130/80 mm Hg
Urinary
albumin
Type 2: Annually
beginning at
diagnosis
Type 1: Annually, 5
years post-diagnosis
40
41
MICROVASCULAR COMPLICATIONS
DIABETIC NEUROPATHY
42
43
Description
No neuropathy
2a
2b
44
Characteristics
Stages 0/1:
No clinical neuropathy
No symptoms or signs
Stage 2a:
Clinical neuropathy
Stage 2b:
Clinical neuropathy
Stage 3:
Disability/ late stage
Objectives
Referral
Stages 0/1:
No clinical
neuropathy
As required
Stage 2a:
Clinical
neuropathy
Diabetologist,
neurologist
Stage 2b:
Clinical
neuropathy
Stage 3:
Disability/ late
stage
Diabetologist,
neurologist,
chiropodist,
podiatrist, diabetes
specialist nurse,
diabetic foot clinic
if available
47
Sign/ Symptom
Treatment
Bladder dysfunction
Retrograde ejaculation
Antihistamine
Erectile dysfunction
Slidenafil, tadalafil
Dyspareunia
48
SYMPTOMS / SIGNS
Exercise intolerance
Postural hypotension
Silent Ischemia
TREATMENT
Discontinue aggravating drugs
Change posture (make postural changes slowly,
elevate bed)
Increase plasma volume
50
MICROVASCULAR COMPLICATIONS
DIABETIC FOOT
51
52
53
54
Deformities
Motor Neuropathy
Autonomic Neuropathy
Pedography
55
56
Parasthesia inspite of
lack of Sensation
Sensory Neuropathy
58
Portals of infection
59
2.
3.
4.
5.
programs,
or pharmacotherapy (including nicotine replacement
& bupropion.
6.
62
Recommendation
Approximate SBP
Reduction Range
Weight reduction
5-20 mmHg/10 kg
weight lost
8-14 mmHg
Restrict sodium
intake
2-8 mmHg
Physical activity
4-9 mmHg
2-4 mmHg
Adopt DASH
eating plan
Moderate
alcohol
consumption
64
65
VLDL
Carries triglycerides to peripheral cells
High levels may be associated with increased CHD risk
LDL
Carries cholesterol to cells
High levels linked to increased CHD risk
Primary target of cholesterol-reducing therapy
HDL
Removes cholesterol from cells
High HDL considered protective against CHD
HDL >60 mg/dL decreases CHD risk
Lipoprotein(a)
A complex of LDL and apolipoprotein(a)
Prevents LDL from being taken up by the Liver
Elevated Lp(a) is an independent risk factor for premature CHD
Triglycerides
A neutral fat stored in adipose cells
Positively correlated with risk for CHD
66
67
2. Statins
a. Great at lowering LDL levels
b. Not much affect on Lipoprotein(a), HDL,
or small dense LDL, and minor effects
on
Triglycerides
68
71
*BMI is calculated as the weight in kilograms divided by the body surface area in meters 2.
Overweight state is defined by BMI=25-30 kg/m2. Obesity is defined by a BMI >30 kg/m2.
71
ANTICOAGULATION RECOMMENDATIONS
ASPIRIN RECOMMENDATIONS
Start and continue indefinitely aspirin 75 to
162 mg/d in all patients unless
contraindicated
For patients undergoing CABG, aspirin (100 to
325 mg/d) should be started within 48 hours
after surgery to reduce saphenous vein graft
closure
Post-PCI-stented patients should receive 325
mg per day of aspirin for 1 month for bare
metal stent, 3 months for sirolimus-eluting
stent and 6 months for paclitaxel-eluting stent
74
CLOPIDOGREL RECOMMENDATIONS
76
78
B-BLOCKER RECOMMENDATIONS
INFLUENZA VACCINATION
For a Healthier
Beware
Community
the terrorists of
the Arteries
Diabetes
Hypertension
Cholesterol
Smoking