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Role of Panchakarma in the Management of Madhumeha
1. ROLE OF PANCHAKARMA IN
THE MANAGEMENT OF
MADHUMEHA
Dr. PRASHANTH. A. S.
M.D.(Ayu), Ph.D. P.G.M.H., M.H.A.
PROFESOR
AYURVEDA MAHAVIDYALAYA, HUBLI
MO. 9448135575
Email:drprashanthayurved@gmail.com
ROLE OF PANCHAKARMA IN
THE MANAGEMENT OF
MADHUMEHA
Dr. PRASHANTH. A. S.
M.D.(Ayu), Ph.D. P.G.M.H., M.H.A.
PROFESOR
AYURVEDA MAHAVIDYALAYA, HUBLI
MO. 9448135575
Email:drprashanthayurved@gmail.com
5. What is diabetes?
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.
The effects of diabetes mellitus include long–term
damage, dysfunction and failure of various organs.
6. Diabetes
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.
Often symptoms are not severe, or may be absent, and
consequently hyperglycaemia sufficient to cause
pathological and functional changes may be present for a
long time before the diagnosis is made.
7. Diabetes Long-term Effects
The long–term effects of diabetes mellitus include
progressive development of the specific complications of
retinopathy with potential blindness, nephropathy that may
lead to renal failure, and/or neuropathy with risk of foot
ulcers, amputation, Charcot joints, and features of
autonomic dysfunction, including sexual dysfunction.
People with diabetes are at increased risk of
cardiovascular, peripheral vascular and cerebrovascular
disease.
8. Burden of Diabetes
The development of diabetes is projected to reach pandemic proportions
over the next10-20 years.
International Diabetes Federation (IDF) data indicate that by the year
2025, the number of people affected will reach 333 million –90% of these
people will have Type 2 diabetes.
In most Western societies, the overall prevalence has reached 4-6%, and
is as high as 10-12% among 60-70-year-old people.
The annual health costs caused by diabetes and its complications
account for around 6-12% of all health-care expenditure.
10. Type 1 diabetes
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,
and environmental factors.
11. Type 2 diabetes
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.
Type 2 diabetes is associated with older age, obesity, family history
of diabetes, history of gestational diabetes, impaired glucose
metabolism, physical inactivity, and race/ethnicity.
African Americans, Hispanic/Latino Americans, American Indians,
and some Asian Americans and Native Hawaiians or Other Pacific
Islanders are at particularly high risk for type 2 diabetes.
Type 2 diabetes is increasingly being diagnosed in children and
adolescents.
37. Signs of background diabetic retinopathy
Microaneurysms usually
temporal to fovea
Intraretinal dot and
blot haemorrhages
Hard exudates
frequently
arranged in clumps or
rings
Retinal oedema seen as
thickening on biomicroscopy
38. Diffuse diabetic maculopathy
• Diffuse retinal thickening • Generalized leakage on FA
• Guarded prognosis
• Grid photocoagulation• Frequent cystoid macular oedema
• Variable impairment of visual acuity
39. Ischaemic diabetic maculopathy
• Macula appears relatively normal • Capillary non-perfusion on FA
• Poor visual acuity • Treatment not appropriate
41. D.N.- Pathogenesis
Familial - Genetic
Only 35-40% patients with IDDM develop DN.
There is an increased risk of DN in a patient with
family member having DN.
42. D.N.- Pathogenesis
Glycemic Control-in both expt & human
DN does not occur in euglycemic patients.
Confirmed role of hyperglycemia in pathogenesis of DN.
Renal transplant with early DN showed structural recovery in euglycemic
receipient. (Abouna)
44. D.N.- Pathogenesis
Extracellular matrix accumulation
- Imbalance between synthesis & degradation of
ECM components
- Linkage between glucose concentration & ECM
accumulation
- Transforming growth factor-Beta associated with
increased production of ECM molecules
45. D.N.- Pathogenesis
Extracellular matrix accumulation
- TGF-B can down regulate synthesis of ECM
degrading enzymes & upregulate inhibitors of
these enzymes
- Angiotensin II can stimulate ECM synthesis
through TGF-B activity
- Hyperglycemia activates protein kinase C,
stimulating ECM production through cyclic AMP
Pathway
54. Classification of diabetic peripheral
neuropathies
Somatic:
Polyneuropathies (bilateral
sensory)
Paresthesias, including
numbness and tingling
Impaired pain, temperature,
light touch, two-point
discrimination, and vibratory
sensation
Decreased ankle and knee-jerk
reflexes
Mononeuropathies
Involvement of a mixed nerve
trunk that includes loss of
sensation, pain, and motor
weakness.
Amyotrophy
Associated with muscle
weakness, wasting, and severe
pain of muscles in the pelvic
girdle and thigh.
Autonomic:
Impaired vasomotor function
Postural hypotension
Impaired gastrointestinal function
Gastric atony
Diarrhea, often postprandial
and nocturnal
Impaired genitourinary function
Paralytic bladder
Incomplete voiding
Impotence
Retrograde ejaculation
Cranial nerve involvement
Extraocular nerve paralysis
Impaired pupillary responses
Impaired special senses
56. Presentations
3 types of neuropathy:
1. Progress steadily with increasing duration of
diabetes and associated with other diabetic
complications-common
2. Acute onset with resolution over period of
months-rare
3. Pressure palsies
61. Autonomic Neuropathy
Closely associated with sensorimotor
neuropathy
Signs are common if looked for (40%
subjects have abnormal CVS tests) but
symptoms are rare (<1%)
Affects the response to hypos but not
awareness
If symptoms: mortality=30-50% over 10
years
66. Macro-vascular Complications
Ischemic heart disease
Cerebrovascular disease
Peripheral vascular disease
Diabetic patients have a 2 to 6 times higher risk for
development of these complications than the
general population
67. Macro-vascular
Complications
The major cardiovascular risk factors in the
non-diabetic population (smoking,
hypertension and hyperlipidemia) also
operate in diabetes, but the risks are
enhanced in the presence of diabetes.
Overall life expectancy in diabetic patients is
7 to 10 years shorter than non-diabetic
people.
68. Macro-vascular
Disease
Once clinical macro-vascular disease
develops in diabetic patients they have a
poorer prognosis for survival than
normoglycemic patients with macrovascular
disease
The protective effect females have for the
development of vascular disease are lost in
diabetic females
69. Cardiovascular disease
Cardiovascular disease (also called heart disease) is a
class of diseases that involve the heart, the blood
vessels (arteries, capillaries, and veins) or both.
Cardiovascular disease refers to any disease that affects
the cardiovascular system, principally cardiac disease,
vascular diseases of the brain and kidney, and peripheral
arterial disease. The causes of cardiovascular disease are
diverse but atherosclerosis and/or hypertension are the most
common. Additionally, with aging come a number
of physiological and morphological changes that alter
cardiovascular function and lead to subsequently increased
risk of cardiovascular disease, even in healthy asymptomatic
individuals.
70. Coronary artery
disease (CAD)
Coronary artery disease (CAD) also known
as atherosclerotic heart disease,coronary heart
disease,[
or ischemic heart disease (IHD),the
most common type of heart disease and cause
of heart attacks.The disease is caused
by plaque building up along the inner walls of the
arteries of the heart, which narrows the arteries
and reduces blood flow to the heart.
71. Micrograph of a coronary artery with
the most common form of coronary
artery disease(atherosclerosis) and
marked luminal narrowing.
72. Peripheral vascular
disease
Peripheral vascular disease (PVD), commonly referred to
as peripheral artery disease (PAD) or peripheral artery
occlusive disease (PAOD) or peripheral obliterative
arteriopathy, refers to the obstruction of
large arteries not within the coronary, aortic arch vasculature,
or brain. PVD can result
from atherosclerosis, inflammatory processes leading
to stenosis, an embolism, or thrombus formation. It causes
either acute or chronic ischemia (lack of blood supply). Often
PVD is a term used to refer to atherosclerotic blockages found
in the lower extremity.
73. The illustration
shows how P.A.D.
can affect arteries in
the legs. Figure A
shows a normal
artery with normal
blood flow. The inset
image shows a
cross-section of the
normal artery. Figure
B shows an artery
with plaque buildup
that's partially
blocking blood flow.
The inset image
shows a cross-
section of the
narrowed artery.
75. Hypertension in Type 1
and 2 Diabetes
Type 1
Develop after
several years of
DM
Ultimately affects
~30% of patients
Type 2
Mostly present at
diagnosis
Affects at least 60%
of patients
76. Diabetic Carbuncle
A carbuncle is an abscess larger than a boil, usually with
one or more openings draining pus onto the skin. It is
usually caused by bacterial infection, most
commonly Staphylococcus aureus, or Streptococcus namo
kines, which can turn lethal. However, the presence of
carbuncles is actually a sign that the immune system is
working. The infection is contagious and may spread to
other areas of the body, or other people; those living in the
same residence may develop carbuncles at the same time.
78. Cutaneous
Manifestations
Nearly all patients with diabetes eventually develop
cutaneous manifestations of the disease.
Can be first sign that a patient has diabetes.
Cutaneous signs of diabetes can be valuable to
physician for diagnosis, management, and
treatment.
79. Necrobiosis Lipoidica
Diabeticorum
Degenerative disease of collagen in the
dermis and subcutaneous fat
with an atrophic epidermis.
Precedes onset of diabetes
in 15-20% of patients
Lesions progress to ulcers
if predisposed to trauma
Location:
85% anterior aspect-pretibial region of
lower extremeties, 15% hands,
forearms, face, scalp
80. Necrobiosis Lipoidica Diabeticorum
Etiology unknown: seem to occur and persist independent of
hyperglycemic control
Theory one: immunologic role-release of cytokines from
inflammatory cells may lead to destruction of the collagen
matrix.
Theory two: Microvascular effects of diabetic retinopathy
and neuropathy lead to a degradation of collagen.
Women > Men
81. Necrobiosis Lipoidica
Diabeticorum
Treatment: Lesions can spontaneously resolve, however most
do not. No standard therapy.
-used to arrest progression
Support stockings/rest
NSAIDs
Intrelesional, systemic,
topical corticosteriods
Aspirin and dipyridamole
Tumor necrosis factor
Laser surgery
Excision/grafting
82. Diabetic Dermopathy
Also known as shin spots, most common cutaneous finding in
diabetics (approximately 50% of diabetics).
Round to oval atrophic hyperpigmented lesions on the
pretibial areas of the lower extremities. Early lesions usually
raised, then flatten. Brownish hyperpigmentation due to
hemosiderin deposits.
Occur bilateral with asymmetrical distribution.
84. Diabetic Bullae
Blisters occur spontaneously in diabetic patients,
atraumatic/asymptomatic lesions on feet and legs.
Patients tend to have adequate circulation in the
affected extremities and peripheral neuropathy.
Three types of Diabetic Bullae:
-Most common: Sterile fluid
containing that heal without
scarring.
-Hemorrhagic, heals with
scarring.
-Multiple nonscarring on
sun exposed/tan skin.
85. Diabetic Bullae
Usually resolve without treatment within 2-5 weeks.
Therapy should be aimed at preventing ulceration and
secondary infection.
86. Diabetic Bullae
When they occur in the feet can resemble friction blisters,
however usually an absence of trauma.
87. Eruptive Xanthomas
Occur in hyperlipidemic/hyperglycemic states: uncontrolled
diabetic patients.
Most common in young men with Type 1 diabetes
Resistance to insulin makes it difficult for the body to clear the
fat from the blood.
88. Eruptive Xanthomas
Usually asymptomatic firm, waxy, yellow papules in
the skin.
Enlargements can have erythematous halo, can itch.
Occurs most often on the back of hands/feet,
arms/legs, buttocks, face-eyes.
89. Eruptive Xanthomas
Increase risk of developing pancreatitis.
Eruptions can resolve in a few weeks with
hyperlipidemic/hyperglycemic control, lipid lowering
medications.
90. Acanthosis Nigricans
Hyperpigmentation and thickening of epidermis
Precedes diabetes, considered a marker for the disease,
most common in overweight diabetic patients.
Usually occurs in skin folds, often described as velvety
Neck, back, axillae, groin region, over joints in the
hands/feet.
91. Kyrle’s Disease
Also known as perforating dermatosis.
Rare condition, except in setting of diabetes with
chronic renal failure.
Large papules with central keratin plugs,
widespread pattern seen in patients undergoing
dialysis.
Itching/scratching present
92. Kyrle’s Disease
Primary location: extensor surfaces of the lower
extremity, but can occur on face and trunk.
Seen with DM, CHF, hepatic abnormalities-alcoholic
cirrhosis, renal disease
Elimination of collagen and elastin throughout
epidermis.
93. Kyrle’s Disease
Can be difficult to treat: have to manage underlying systemic
disorder
Antihistamines, antipruritics, topical corticosteriods,
Retinoic acid, UV light therapy, laser therapy
Rapid improvement and resolution of lesions is seen once
underlying disease is treated.
Diabetic nephropathy can be divided into 4 phases: microalbuminuria (urinary albumin excretion 30-300 mg/24 h), macroalbuminuria or proteinuria (&gt;300 mg/24 h), the nephrotic syndrome, and chronic renal failure (Grundy et al, 1999). Microalbuminuria is the first clinical sign of diabetic damage to the kidney and is a harbinger of progressive kidney damage. Microalbuminuria also reflects a higher risk for cardiovascular disease. Once microalbuminuria is present, it progresses over 5-10 years to macroalbuminuria in 22%-50% of patients (Mogensen, 1984; Cooper et al, 1988; Haneda et al, 1992; Ravid et al, 1992; John et al, 1994; Lebovitz et al, 1994). Macroalbuminuria denotes significant diabetic nephropathy and will be followed by a decline in glomerular filtration rate (GFR). Once a patient with type 2 diabetes develops macroalbuminuria, further decline in renal function appears to be inevitable; GFR declines at a rate of 4-12 mL/min/year (Pugh et al, 1993; Gall et al, 1993; Hasslacher et al, 1993). Some patients develop the nephrotic syndrome, which usually heralds progressive renal insufficiency and end-stage renal disease.
In diabetic nephropathy studies, where the time of onset of type 2 diabetes is known, these patients follow a time course similar to that seen in patients with type 1 diabetes. However, the date of onset of type 2 diabetes is often unknown and usually precedes the clinical diagnosis by several years (Grundy et al, 1999). By the time patients are diagnosed with type 2 diabetes, many have already developed hypertension, signs of nephropathy (including microalbuminuria or even macroalbuminuria) and cardiovascular disease (Mogensen et al, 1992; The Hypertension in Diabetes Study Group, 1993a; American Diabetes Association, 1998). Whereas patients with type 1 diabetes are usually normotensive until overt renal disease develops, hypertension commonly occurs in patients with type 2 diabetes before the onset of overt diabetic nephropathy, and about 40% of newly diagnosed patients with type 2 diabetes are already hypertensive (The Hypertension in Diabetes Study Group, 1993a). Both the onset of microalbuminuria and the progression of renal disease after the onset of macroalbuminuria are accelerated by hypertension (Epstein and Sowers, 1992).
The majority of patients with type 2 diabetes who have macroalbuminuria also have hypertension (Grundy et al, 1999). In these patients, control of hypertension slows the decline in GFR. The main goal of any treatment for patients with type 2 diabetic nephropathy should be to prevent the natural progression from microalbuminuria to macroalbuminuria to end-stage renal disease. Effective antihypertensive treatment is the best inhibitor of diabetic nephropathy (Ravid et al, 1993). Since reducing albuminuria delays progression of diabetic nephropathy, this parameter can be used as a benchmark for measuring the efficacy of therapeutic interventions (Rossing et al, 1994).
Note that the high risk of cardiovascular mortality in patients with type 2 diabetes, even early in their disease, may not allow for the development of nephropathy (Ismail et al, 1999).
Diabetic nephropathy can be divided into 4 phases: microalbuminuria (urinary albumin excretion 30-300 mg/24 h), macroalbuminuria or proteinuria (&gt;300 mg/24 h), the nephrotic syndrome, and chronic renal failure (Grundy et al, 1999). Microalbuminuria is the first clinical sign of diabetic damage to the kidney and is a harbinger of progressive kidney damage. Microalbuminuria also reflects a higher risk for cardiovascular disease. Once microalbuminuria is present, it progresses over 5-10 years to macroalbuminuria in 22%-50% of patients (Mogensen, 1984; Cooper et al, 1988; Haneda et al, 1992; Ravid et al, 1992; John et al, 1994; Lebovitz et al, 1994). Macroalbuminuria denotes significant diabetic nephropathy and will be followed by a decline in glomerular filtration rate (GFR). Once a patient with type 2 diabetes develops macroalbuminuria, further decline in renal function appears to be inevitable; GFR declines at a rate of 4-12 mL/min/year (Pugh et al, 1993; Gall et al, 1993; Hasslacher et al, 1993). Some patients develop the nephrotic syndrome, which usually heralds progressive renal insufficiency and end-stage renal disease.
In diabetic nephropathy studies, where the time of onset of type 2 diabetes is known, these patients follow a time course similar to that seen in patients with type 1 diabetes. However, the date of onset of type 2 diabetes is often unknown and usually precedes the clinical diagnosis by several years (Grundy et al, 1999). By the time patients are diagnosed with type 2 diabetes, many have already developed hypertension, signs of nephropathy (including microalbuminuria or even macroalbuminuria) and cardiovascular disease (Mogensen et al, 1992; The Hypertension in Diabetes Study Group, 1993a; American Diabetes Association, 1998). Whereas patients with type 1 diabetes are usually normotensive until overt renal disease develops, hypertension commonly occurs in patients with type 2 diabetes before the onset of overt diabetic nephropathy, and about 40% of newly diagnosed patients with type 2 diabetes are already hypertensive (The Hypertension in Diabetes Study Group, 1993a). Both the onset of microalbuminuria and the progression of renal disease after the onset of macroalbuminuria are accelerated by hypertension (Epstein and Sowers, 1992).
The majority of patients with type 2 diabetes who have macroalbuminuria also have hypertension (Grundy et al, 1999). In these patients, control of hypertension slows the decline in GFR. The main goal of any treatment for patients with type 2 diabetic nephropathy should be to prevent the natural progression from microalbuminuria to macroalbuminuria to end-stage renal disease. Effective antihypertensive treatment is the best inhibitor of diabetic nephropathy (Ravid et al, 1993). Since reducing albuminuria delays progression of diabetic nephropathy, this parameter can be used as a benchmark for measuring the efficacy of therapeutic interventions (Rossing et al, 1994).
Note that the high risk of cardiovascular mortality in patients with type 2 diabetes, even early in their disease, may not allow for the development of nephropathy (Ismail et al, 1999).
Slide 21
Renal autoregulation
-If occurs in regions other than the legs, less association with diabetes.
-Anterior aspect of lower leg-shin typical location
-Posterior aspect of legs-B/L nature of the disease.
-Important-physcial exam….can advise pt. to see PCP for screening of DM
-Resolution/prognosis not related to glycemic control
-Treatment aimed at stopping progression and preventing ulceration/infection. Unless ulcerated do not have to treat.
-Many treatments because exact etiology is unclear, more than listed here.
-topical/intralesional steriods lessen the inflammation of early active lesions.
-Antiplatelet aggregation therapy, causes vasodilation, inhibits platelet aggregation.
-Recurrence common after excision/grafting due to underlying vascular damage.
-Can occur in anyone after an injury or trauma to the area. Can occur forearm, thighs, side of foot, scalp, trunk. &gt; 4 or more lesions indicative of diabetes. Can take up to 2 years to resolve.
-Lysis of erythrocytes leaves hemosiderin deposits causing brownish hyperpigmentation.
-No treatment necessary.
-Etiology-diabetes causes changes to small blood vessels that supply the skin. Leakage of blood products from vessels to skin
-Asympromatic, no treatment necessary.
-Small percentage of patients with diabetes develop spontaneous blistering on feet/legs.
-Heal without treatment, however can rupture-develop an ulcer and become infected secondarily.
-Picture: Intact blister
-Left: spontaneous blister with crusted region
-Right: ulcer and cellulitis that developed as a complication of a ruptured blister.
Again occur spontaneously etiology unkown: possible photosensitivity, increased in pressure resulting from edema of cardiac failure possible enough to result in blisters, decreased threshold to trauma.
One paper said develop more frequently in patients with uncontrolled diabetes and severe peripheral neuropathy.
-Close up of eruptive xanthoma
-Spontaneously resolve when serum lipids return to normal.
-Diet modifications, exercise-weight loss, medication
-Work up includes sugar levels, LFT, renal function-UA, creatinine
-Cause unknown, host inflammatory response, alteration of dermal connective tissue, inherited
-No known triggers