This document discusses the role of Panchakarma in managing Madhumeha (diabetes mellitus). It begins by defining diabetes as a metabolic disorder characterized by high blood glucose levels due to defects in insulin production or action. It then describes the types and complications of diabetes, including retinopathy, nephropathy, and neuropathy. The document emphasizes that Panchakarma helps manage diabetes by eliminating toxins from the body and controlling high blood sugar levels.

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

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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.

9. Types of Diabetes
Type 1 Diabetes Mellitus
Type 2 Diabetes Mellitus
Gestational Diabetes
Other types:
LADA (
MODY (maturity-onset diabetes of youth)
Secondary Diabetes Mellitus

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.

13. Gestational diabetes

29. Vascular complications of diabetes
Microangiopathic
.Retinopathy
.Nephropathy
.Neuropathy
Macroangiopathic
.Coronary artery disease
.Cerebro-vascular disease
.Peripheral vasc. disease

32. DIABETIC RETINOPATHY
1. Adverse risk factors
2. Pathogenesis
5. Clinically significant macular oedema
6. Preproliferative diabetic retinopathy
3. Background diabetic retinopathy
4. Diabetic maculopathies
Focal
Diffuse
Ischaemic
7. Proliferative diabetic retinopathy

33. Adverse Risk Factors
1. Long duration of diabetes
• Obesity
• Hyperlipidaemia
2. Poor metabolic control
3. Pregnancy
4. Hypertension
5. Renal disease
6. Other
• Smoking
• Anaemia

34. Healthy Retina Diabetic
Retinopathy

35. Pathogenesis of diabetic retinopathy

36. Consequences of chronic leakage

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

40. Diabetic Nephropathy
DM +
Persistent albuminuria,
Worsening proteinuria,
Hypertension &
progressive renal failure

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)

43. D.N.- Pathogenesis
Glomerular Hyperfiltration
Glomerular Hypertension
Glomerular Hypertrophy
GBM thickening
Mesangial Expansion

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

46. Diffuse and Nodular Glomerulosclerosis
in Diabetic Nephropathy

47. Advanced Diabetic
Glomerulosclerosis

48. Diabetic Nephropathy

49. Functional changes*
Natural History of IDDM
Proteinuria
End-stage
renal disease
Clinical type 1 diabetes
Structural changes†
Proteinuria
Rising serum
creatinine levels
Rising blood pressure
Onset of
diabetes
2 5 10 20
Years
* Kidney size ↑, GFR ↑.
†
GBM thickening ↑, mesangial expansion ↑
Microalbuminuri
a
30
CV events

50. Functional changes*
Natural History of NIDDM
Proteinuria
End-stage
renal disease
Clinical type 2 diabetes
Structural changes†
Rising blood pressure
Rising serum
creatinine levels
Cardiovascular death
Microalbuminuria
Onset of
diabetes
2 5 10 20 3
0
Years
* Kidney size ↑, GFR ↑.
†
GBM thickening ↑, mesangial expansion ↑

51. Effect of Angiotensin Blockade
Afferent arteriole
Efferent arteriole
↓Glomerular pressure
↓(↓ GFR)
Glomerulus
Bowman’s Capsule
Angiotensin II
Proteinuria
A II blockade:

52. DIABETIC
NEUROPATH
Y

53. Pathology
Axonal loss, focal demyelination &
regeneration
↓ conduction velocity and ↑
sensory thresholds

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

55. Pathophysiology-biochemical and vascular
factors

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

57. Presentations
Diffuse symmetrical sensorimotor
polyneuropathy
Predominantly sensory
Predominantly feet
↓ pain and temperature sensation
Parasthesiae and numbness
Neurogenic pain/allodynia
Neuropathic oedema
Wasting occurs only if severe

58. Diffuse symmetrical sensorimotor
polyneuropathy
Problems:
Pain and oedema
Diabetic foot ulceration
Present in 80% of foot ulcers
Principle cause in 39% of ulcers
Partly responsible in 36% of ulcers

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

62. www.plymouthdiabetes.org.uk/

63. www.plymouthdiabetes.org.uk/

64. Mononeuropathies
Acute ? Secondary to ischaemia
Pain and weakness (severe)
Resolve over months
Amyotrophy (Older ♂>♀)
3rd
nerve
6th
nerve
Truncal radiculopathies

65. Macro Vascular
Complications

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.

74. DIABETIC
VASCULOPATH
Y

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.

77. Diabetic carbuncle

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.

83. Diabetic
Dermopathy

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.

94. Management
1.Diet
2.Use of oral Hypoglycemic drugs.
3.Exercise

95. CHIKITSA SUTRA

96. EKMOOLIKA PRAMEHAGHANA
DRAVYA
COMMON

97. SPECIFIC ACCODING TO TYPE-

98. MINERAL PRAMEHAGHANA
DRAVYA

99. DIFFERENT HERBAL AND HERBO-
MINERAL FORMULATIONS