The document summarizes the history and origins of the word diabetes, the discovery of the pancreas and insulin, and provides details on the types, causes, symptoms, investigations and management of diabetes. It traces the term diabetes back to ancient Greece and describes observations of the disease made by ancient Egyptians, Indians and Persians. It discusses key discoveries like the roles of the pancreas by Minkowski and von Mering in 1889 and the discovery of insulin by Banting, Best and Macleod in 1921-1922.

1. MSM INSTITUTE OF AYURVEDA
Department of swasthavritta
Diabetes
Submitted to- Dr. Veena Aggarwal. Submitted by - Neha
Dr. Pawan. Roll no. 20083031
Ms. Manita

2. ORIGIN OF THE WORD DIABETES
The term diabetes is the shortened version of the full name
diabetes mellitus.
Diabetes mellitus is derived from the Greek word diabetes
meaning siphon - to pass through and the Latin word mellitus
meaning honeyed or sweet. This is because in diabetes excess
sugar is found in blood as well as the urine.
It was known in the 17th century as the "pissing evil" .
https://www.news-medical.net/health/History-of-Diabetes.aspx

3. The term diabetes was probably coined by Apollonius of Memphis
around 250 BC.
Diabetes is first recorded in English, in the form diabete, in a medical
text written around 1425.
It was in 1675 that Thomas Willis added the word “mellitus” to the
word diabetes. This was because of the sweet taste of the urine. This
sweet taste had been noticed in urine by the ancient Greeks, Chinese,
Egyptians, Indians, and Persians as is evident from their literature.

4. In Ebers papyrus, dated back to 1500 BC, we may find passages
describing patients who suffer from excessive thirst, copious
urination and they are treated by plants' extracts. However,
according to the Egyptian endocrinologist historian of medicine and
translator of the Ebers papyrus Paul Ghalioungui (1908-1987), the
description of a probable diabetes, in Ebers, is regarded as
unsatisfactory and probably wrong.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4707300/

5. In Kahun papyrus (c. 2000 BC) there is just the title of a recipe for the
Treatment of a thirsty woman, but the text is missing. So, we may assume
that ancient Egyptians could not recognize behind the symptoms of
specific disease entity such as diabetes.
Around the 5th century BC, the famous Indian surgeon Sushruta, in his
work Samhita, identified diabetes, by using the term madhumeha (honey-
like urine) and pointed out not only the sweet taste of the urine but also
its sticky feeling to the touch and its ability to attract the ants. Sushruta
further mention that diabetes affects primarily the rich castes and is
reated to the excessive food consumption as the rice, cereals and sweets.

6. In ancient China, Chang Chung-Ching (ca. 160-ca. 219), referred to as
"the Chinese Hippocrates', described polyuria, polydypsia and loss of
weight as symptoms of a specific disease, while in 7th century AD Chen
Chuan recorded the sweet urine in diabetes mellitus and named the
disease Hsiao kho ping mentioning its characteristic symptoms:
intense thirst, copious drinking and large amounts of urine which is
tasted sweet. In an attempt to treat that disease his colleague Li Hsuan
proposed the abstinence from wine, salt and sex.

7. From the 8th century onwards, physicians observed the tendency of diabetic
patients to develop skin infections as furuncles, rodent ulcers and troubles of
the eyesight. In 11th century AD, the celebrated Arabo-islamic physician
Avicenna (980-1037) in his textbook El-Kanun (Canon of Medicine) described
diabetes and mentioned gangrene and sexual dysfunction as its complication.
Years later, the medieval scholar Moises Maimonides (1138-1204) described
in detail diabetes. including the symptoms of acidosis

8. Ancient Egyptians, Indians, Chinese and Arabs tried to describe the
clinical signs and symptoms of diabetes mellitus.
However, few are the main protagonists in the history of diabetes
mellitus who contributed significantly, not only to its diagnosis and
treatment but also to the development of our current notions on the
disease, paving the way for further study and establishing a new
medical sub specialty, diabetology

9. DISCOVERY OF PANCREAS
Joseph von Mering and Oskar Minkowski in 1889 discovered the role of
pancreas in diabetes. They found that dogs whose pancreas was
removed developed all the signs and symptoms of diabetes and died
shortly afterwards.
In 1910, Sir Edward Albert Sharpey-Schafer found that diabetes resulted
from lack of insulin. He termed the chemical regulating blood sugar as
insulin from the Latin "insula", meaning island, in reference to the
insulin-producing islets of Langerhans in the pancreas.
https://www.news-medical.net/health/History-of-Diabetes.aspx

10. DISCOVERY OF INSULIN
In 1921 Sir Frederick Grant Banting and Charles Herbert Best repeated the
work of Von Mering and Minkowski and went ahead to demonstrate that
they could reverse induced diabetes in dogs by giving them an extract from
the pancreatic islets of Langerhans of healthy dogs. Banting, Best and their
chemist colleague Collip purified the hormone insulin from pancreases of
cows at the University of Toronto. This led to the availability of an effective
treatment for diabetes in 1922. For this, Banting and laboratory director
MacLeod received the Nobel Prize in Physiology or Medicine in 1923, both
shared their Prize money with others in the team who were not recognized,
in particular Best and Collip.
https://www.news-medical.net/health/History-of-Diabetes.aspx

11. HISTORY OF TREATMENT OF DIABETES
Sushruta, Arataeus, and Thomas Willis were the early pioneers of the
treatment of diabetes. Greek physicians prescribed exercise - preferably on
horseback to alleviate excess urination. Some other forms of therapy applied
to diabetes include wine, overfeeding to compensate for loss of fluid weight,
starvation diet, etc.
In 1776, Matthew Dobson confirmed that the sweet taste of urine of diabetics
was due to excess of a kind of sugar in the urine and blood of people with
diabetes
https://www.news-medical.net/health/History-of-Diabetes.aspx

12. In ancient times and medieval ages diabetes was usually a death sentence.
Aretaeus did attempt to treat it but could not give a good outcome.
Sushruta (6th century BCE) an Indian healer identified diabetes and
classified it as "Madhumeha". Here the word "madhu" means honey and
combined the term means sweet urine.
The ancient Indians tested for diabetes by looking at whether ants were
attracted to a person's urine. The Korean, Chinese, and Japanese words for
diabetes are based on the same ideographs which mean "sugar urine
disease".

13. In Persia Avicenna (980-1037) provided a detailed account on diabetes
mellitus in "The Canon of Medicine". He described abnormal appetite and
the decline of sexual functions along with sweet urine. He also identified
diabetic gangrene.
Avicenna was the first to describe diabetes insipidus very precisely. It was
much later in the 18th and 19th century that Johann Peter Frank (1745-
1821) differentiated between diabetes mellitus and diabetes insipidus

14. INTRODUCTION
Diabetes is a lifelong (chronic)
disease and is a group of
metabolic disorder characterized
by high levels of sugar in blood
(hyperglycemia) resulting from
defects in insulin secretion or
resistance to insulin or both.

15. EPIDEMIOLOGY
In 2014, 8.5% of adults aged 18 years and older had diabetes. In
2019, diabetes was the direct cause of 15 lakh deaths and 48% of
all deaths due to diabetes occurred before the age of 70 years.
Another 4,60,000 kidney disease deaths were caused by diabetes,
and raised blood glucose causes around 20% of cardiovascular
deaths.

17. Between 2000 and 2019, there was a 3% increase in age-standardized
mortality rates from diabetes. In lower-middle-income countries, the
mortality rate due to diabetes increased 13%.
By contrast, the probability of dying from any one of the four main
noncommunicable diseases (cardiovascular diseases, cancer, chronic
respiratory diseases or diabetes) between the ages of 30 and 70
decreased by 22% globally between 2000 and 2019.

19. ETIOLOGY
● Elevated blood sugar (glucose) levels due to absolute or relative
insufficiencies of insulin,
● Type 1-Beta cell destruction completely leading to absolute
insulin deficiency
● Type 2 –combination of insulin resistance and Beta cell
dysfunction

20. CLINICAL FEATURES
● Increased Thirst Frequent Urination
● Unexpected Weight Loss
● Increased Fatigue
● Blurred vision
● Numbness and tingling specially in hands and feet

22. HORMONE CONTRIBUTIONS
● 15-20% α cells synthesize and secrete GLUCAGON
● 70- 80% β cells synthesize and secrete INSULIN
● 1-8% δ cells synthesize and secrete STOMATOSTATIN and
GASTRIN
● 1-2% F- cells secrete PANCREATIC POLYPEPTIDE which decreases
the absorption of food from the GIT

23. TYPES OF DIABETES
● TYPE 1 diabetes mellitus (IDDM)
● TYPE 2 diabetes mellitus (NIDDM)
● GESTATIONAL diabetes mellitus
● OTHER TYPES NEONATAL diabetes mellitus .

24. TYPE 1 DIABETES MELLITUS
● insulin- dependent diabetes mellitus (IDDM)
● Also known as “juvenile diabetes”
● Common among 10-14 yrs age group
● 90% is autoimmune mediated
● 10% is idiopathic

25. TYPE 2 DIABETES MELLITUS
● Non insulin- dependent diabetes mellitus
(NIDDM)
● Also known as “adult-onset diabetes".
● The primary cause is excessive body weight
and not enough exercise.
● Begins as insulin resistance,as the need for
insulin rises, pancreas gradually loses its
ability to produce insulin.

26. GESTATIONAL DIABETES MELLITUS
● diagnosed during pregnancy
● Gestational diabetes is caused when the
insulin receptors do not function
properly
● Having no past diabetic history

27. COMPARISON OF TYPE 1 & 2 DIABETES
Features Type 1 Type 2
Onset Sudden Gradual
Age at onset Mostly in children Mostly in adults
Ketoacidosis Common Rare
Autoantibodies Usually present Absent

28. PATHOPHYSIOLOGY OF TYPE 1 DIABETES
● By loss of the insulin-producing beta cells of the islets of
Langerhans in the pancreas, leading to insulin deficiency.
● This type can be further classified as immune-mediated or
idiopathic.
● The majority of type 1 diabetes is of the immune- mediated
nature, in which a T-cell- mediated autoimmune attack leads to
the loss of beta cells and thus insulin.

30. Cont.
● Affected people are otherwise healthy and of a healthy weight
when onset occurs.
● Sensitivity and responsiveness to insulin are usually normal,
especially in the early stages.
● Type 1 diabetes can affect children or adults, but was
traditionally termed "juvenile diabetes" because a majority of
these diabetes cases were in children.

31. PATHOPHYSIOLOGY OF TYPE 2 DIABETES
● Type 2 DM is characterized by insulin resistance.
● The defective responsiveness of body tissues to insulin is believed
to involve the insulin receptor.
● Type 2 DM is due primarily to lifestyle factors and genetics.
● Early stage of type 2, the predominant abnormality is reduced
insulin sensitivity.

33. ● Obesity
● Lack of physical activity and poor diet
● Stress
● Dietary factors also influence the risk of developing type 2 DM
such as sugar-sweetened drinks
● Type of fats in diet saturated fats and trans fatty acids increasing
the risk of diabetes.
● Lifestyle factors

34. PATHOPHYSIOLOGY OF GESTATIONAL
DIABETES
● Involves a combination of relatively inadequate insulin secretion
and responsiveness.
● It occurs in about 2–10% of all pregnancies and may improve or
disappear after delivery.
● Pregnancy related factors like human placental lactogen
interferes with susceptible insulin receptors.

35. RISK FACTORS
● Non modifiable :-
Age - 45 or more
Race- African, American,Asian American
Family history - parents or siblings with diabetes

36. ● MODIFIABLE:
Pre diabetes Heart and blood disease
Hypertension
Low HDL cholesterol and high triglycerides.
Obesity
Polycystic ovary syndrome
Physical inactivity

37. COMPLICATIONS
● Diabetic retinopathy
● Diabetic nephropathy,
● Diabetic neuropathy,
● Diabetes related foot problems (such as diabetic foot ulcers)
● Macular edema

39. INVESTIGATIONS
● Fasting blood sugar level
● Oral glucose tolerance test (OGTT)
● HbA1C
● Lipid Profile – To diagnose dyslipidaemia
● RBS can be done only if the patient follows up for the diagnostic
tests after a meal

40. HbA1c Test
The hemoglobin A1c (glycated hemoglobin, glycosylated hemoglobin,
HbA1c, or A1c) test is used to evaluate a person's level of glucose
control. The test shows an average of the blood sugar level over the
past 90 days and represents a percentage. The test can also be used to
diagnose diabetes.

41. ● For an HbA1c test to classify as
normal, or in the non-diabetic
range, the value must be below
5.7 %.
● Anyone with an HbA1c value of
5.7 % to 6.4 % is considered to be
prediabetic,
● while diabetes can be diagnosed
with a HbA1c of 6.5% or higher.

42. HOW THE TEST
WORKS
The sugar in your blood is called
glucose. When glucose builds up
in your blood, it binds to the
hemoglobin in your red blood
cells.
The A1c test measures how much
glucose is bound.

43. ORAL GLUCOSE TOLERANCE TEST
For this test, you fast overnight, and the fasting blood sugar level is
measured. Then you drink a sugary liquid, and blood sugar levels are
tested periodically for the next two hours. A blood sugar level:-
● <140 mg/dL (7.8 mmol/L) is normal.
● > 200 mg/dL (11.1 mmol/L) after two hours indicates diabetes.
● A reading between 140 and 199 mg/dL (7.8 mmol/L and 11.0
mmol/L) indicates prediabetes.

44. FASTING BLOOD SUGAR TEST
A blood sample will be taken after an overnight fast.
A fasting blood sugar level
● <100 mg/dL (5.6 mmol/L) is normal.
● A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9
mmol/L) is considered prediabetes. If it's 126 mg/dL (7 mmol/L) or
higher on two separate tests, you have diabetes.

45. WHO DIABETES DIAGNOSTIC CRITERIA
Condition 2 Hour
glucose
Fasting
glucose
HbA1c
Unit mmol/l (mg/dl) mmol/l (mg/dl) DCCT%
Normal <7.8(<140) <6.1(<110) <6.0
Diabetes
mellitus
≥11.1 (≥200) ≥7.0(126) ≥6.5

46. Condition
fasting
2 HRS
Glucose
Glucose HbA1C
Unit Mg/dl Mg/dl %
Normal <140 <110 <6
Impaired
glucose
tolerance
>140 <126 6-6.4
DM >200 >126 >6.5

47. MANAGEMENT
● Medical nutrition ( Diet & excercise)
● Oral hypoglycemic therapy
● Insulin therapy

48. DIET MANAGEMENT
● Follow individualized meal plan and snacks as scheduled diet
based on pts. wt., age, occupation and activity.
● Balanced diabetic diet - 50% CHO, 30% fats, 20% CHON(Co2, H20,
02, Nitrogen), vitamins and minerals.
● Meal should include more fiber and starch and fewer simple or
refined sugars.

49. EXERCISE
● Avoid trauma to extremities
● Avoid during poor metabolic control
● Physical activity promotes weight reduction and improves insulin
sensitivity, thus lowering blood glucose levels.
● Patients have BS>200 mg/ dl and who have urine ketones should
not begins excercise until urine test are negative.

50. INSULIN THERAPY
Short-term use:
● Acute illness,surgery,stress,emergencies
● Pregnancy
● Breast-feeding
● Insulin may be used as initial therapy in type 2 diabetes
● Severe metabolic decompensation(diabetic ketoacidosis,
hyperosmolar nonketotic coma , lactic acidosis)

51. Long term use :-
● If targets have not been reached after optimal dose of
therapy,then consider change multi - dose insulin therapy.
COMPLICATIONS OF INSULIN THERAPY
● Hypoglycemia
● Systemic allergic reactions
● Insulin resistance

52. ACTION OF INSULIN
It helps in the transportation of glucose across the cell membrane.
Insulin activate GLUT-4 (Transporter of glucose) as a result of that
glucose transportation occur across the cell
● It helps in the formation of glycogen; insulin stimulate Glycogen
synthase enzyme Glucose Glycogen. Insulin inhibit the
phosphorylase enzyme which convert the glycogen into glucose.
● Phosphorylase Insulin Glucose Glycogen Glucose

53. METHODS OF INSULIN
THERAPY
● Insulin syringe
● Insulin pens
● Jet injectors
● Insulin pumps

54. INSULIN DOSES
Insulin doses are given in two main ways:
● Basal insulin- provides a steady amount of insulin delivered all
day and night. This helps maintain blood glucose levels by
controlling how much glucose the liver releases (mainly at night
when the time between meals is longer).

55. ● Bolus insulin( premeal ) insulin :
Provides a dose of insulin at meals to help move absorbed sugar
from the blood into muscle and fat. Bolus doses can also help
correct blood sugar when it gets too high. Bolus doses are also
called nutritional or meal-time doses. Sometimes, a bolus dose
must also be taken with large snacks.

56. DOSES
● T1DM patients should receive multidose injections (3 - 4 a day) of
basal and premeal insulin or insulin pump therapy
● Most individuals with T1DM should use rapid-acting insulin
analogs to reduce hypoglycemia risk

57. THERAPY DOSES
● Insulin dosing in T1DM will vary based on patient's age, weight,
and residual pancreatic insulin activity
● T1DM patients will typically require a total daily insulin dose of
0.4 - 1.0 units/kg/day
● A typical starting dose in metabolically-stable patients is 0.5
units/kg/day

58. ORAL ANTI- DIABETIC AGENTS
There are currently four classes of oral anti-diabetic agents:-
i. Biguanides
ii. Insulin Secretagogues - Sulphonylureas
iii.Insulin Secretagogues - Non-sulphonylureas
iv.a-glucosidase inhibitors SETES
v. Thiazolidinediones (TZDs)

60. METFORMIN
● This is the only drug of this class presently available in market It does
not cause hypoglycaemia
● MOA : They increase glucose uptake and utilisation in skeletal
muscle (thereby reducing insulin resistance) and reduce hepatic
glucose production (gluconeogenesis).
● Pharmacokinetic : Metformin has a half-life of about 3 hours and is
excreted unchanged in the urine.

61. SIDE EFFECTS OF METFORMIN
● Dose-related gastrointestinal disturbances
● lactic acidosis is a rare but potentially fatal toxic effect
● Long-term use may interfere with absorption of vitamin B12
● Contra indicatioions :-
Renal failure Hepatic disease Heart failure or shock.

62. INSULIN SECRETAGOGUES SULFONYLUREAS :
Inhibit KATP Channel of ß-cells
First-generation agents :- Tolbutamide ,Acetohexamide ,Tolazamide
Chlorpropamide
Second-generation :- Glipizide ,Glyburide ,Glimepiride

63. NON-SULFONYLUREA SECRETAGOGUES
MEGLITINIDES
● Inhibit KATP Channel of ß-cells
● Very fast onset of action, rapidly metabolized by liver enzymes, with a
peak effect within 1 hour, the duration of action is 5–8 hr. • Short
duration of action and a low risk of hypoglycaemia.
● Medications in this Class: Repaglinide, Nateglinide.

64. THIAZOLIDINEDIONES
● ↓ Insulin resistance by making muscle and adipose cells more
sensitive to insulin.
● They also suppress hepatic glucose production.
Side effects: weight gain, oedema, Hypoglycemia (if taken with insulin)
Contraindication: patients with abnormal LFT or CHF
Medications in this class: Pioglitazone, Rosiglitazone,

65. Drugs Dose Dosage/day Duration of
action
Metformin 500-2000 mg 2-3 times daily 6-12 h
Glipizide 2.5-20 mg 1-2 times daily 12-24 h
Gliclazide 40-320mg Once daily -
Nateglinide 60-180 mg 3times daily < 4 h

66. TREATMENT OF
DIABETES TYPE 1
● Maintain blood sugar levels.
● Insulin therapy
● Diet
● Exercise

67. TREATMENT OF DIABETES TYPE2
MONOTHERAPY
● If glycaemic control is not achieved (HbA1c > 6.5%) with lifestyle
modification within 1-3 months, ORAL ANTI-DIABETIC AGENT
should be initiated.
● In the presence of marked hyperglycaemia in newly diagnosed
symptomatic type 2 diabetes (HbAlc> 8%, FPG> 11.1 mmol/L), oral
anti- diabetic agents can be considered at the outset together
with lifestyle modification.

68. PREVENTION
● Take fibrous diet
● Exercise and yoga
● Avoid junk food
● Avoid tobacco
● Maintain normal body weight

69. प्रमेह
● प्रभूताविलमूत्रता
प्रभूत मात्रा में विक
ृ त मूत्र का त्याग होना प्रमेह शब्द का अर्थ है।
● यह मेदिह स्रोतस की व्यावि हैं।
● इसमें १० दुष्य शावमल है - रस,रक्त, माांस, मेद, मज्जा, शुक्र, अांबु, िसा,
लसीका, ओज ।

70. निदाि
आस्यासुखं स्वप्नसुखं दधीनि ग्राम्यौदकािूपरसााः पयांनस ।
िवान्नपािं गुडवैक
ृ तं च प्रमेहहेतुाः कफक
ृ च्च सववम् ॥ ( च.नच ६/४)
● सुखपूिथक गद्देदार आसनोां पर बैठें रहना
● स्वप्नसुख-सुखपूिथक गद्देदार वबस्तरे पर सोना
● दही
● ग्राम्य

71. पूववरूप
स्वेदोऽङ्गगन्ध: निनिलाङ्गता च िय्यासिस्वप्नमुखे रनतश्च।
हन्नेत्रनिह्वाश्रवणोपदेहो घिाङ्गता क
े ििखानतवृद्धि॥ ( च.नच ६/१३)
● स्वेद और शरीर से गन्ध का आना, अङ्ोां में वशवर्लता, सुखपूिथक शयन-
आसन पर बैठने इच्छा होना, हृदयप्रदेश, नेत्र, जीभ और कान में मैलोां का
भरा रहना, शरीर का मोटा होना, क
े श और नख का अविक बढ जाना।

72. ● नूतन अन्न
● नूतन जल (िर्ाथ का जल)
● गुड़ का विकार (जैसे खााँड़, चीनी, वमश्री, वमठाई आवद)
● जलीय और आनूर् पशु-पवियोां क
े माांसोां को अविक रूप से सेिन करना, दू ि
का अविक सेिन
● कफ को उत्पन्न करने िाली वजतनी िस्तुयें हैं, जैसे-भात, खीर आवद ये सभी
िस्तुयें प्रमेह को उत्पन्न करने िाली होती हैं ।

73. प्रमेह क
े भेद
वत्रदोर् क
े कोप क
े कारण २० प्रकार क
े प्रमेह होते है : -
● िातज प्रमेह - ४
● वपत्तज प्रमेह - ६
● कब्ज़ प्रमेह -१०

74. वाति प्रमेह
1. िसामेह ( Chyluria/lipiduria)
2. मज्जामेह ( Pyuria)
3. हस्तस्तमेह ( Polyuria with Incontinence)
4. मिुमेह ( Diabetes Glycosuria)

75. नपत्ति प्रमेह
1. िारमेह (Alkaline Urine)
2. कलमेह (Haematuria)
3. नीलमेह ( Indicouria)
4. रक्तमेह ( Frank Haematuria)
5. मांवजष्ठामेह ( Haemoglobinouria)
6. हाररद्रमेह ( Biliuira)

76. कफि प्रमेह
1. उदकमेह (Diabetes Insipidus)
2.इिुबावलकामेह (Glysuria)
3. सान्द्रमेह (Phosphaturia)
4. सान्द्र प्रसाद मेह
(Phosphaturia)
5. शुक्लमेह ( Chyluira)
6. शुक्रमेह (Spermaturia)
7. शीतमेह ( Renal Glysuria)
8. वसकतामेह ( Crystalluria)
9. शनैमेह (Frequency)
10. आलालमेह (Albuminuria)

77. कफि व नपत्त प्रमेह संप्राद्धि
मेदश्च मांसं च िरीरिं च क्लेदं कफो बद्धिगतं प्रदू ष्य ।
करोनत मेहाि् समुदीणवमुष्णैिािेव नपत्तं पररदृष्य चानप ॥ (च.नच ६/५)
● कफकारक िस्तुओां क
े सेिन करने से बढा हुआ कफ, मेद, माांस और बस्तस्त
में रहने िाले शारीररक क्लेद को दू वर्तकर प्रमेह को उत्पन्न करता है।
● उष्ण द्रव्योां क
े सेिन से बढा हुआ वपत्त मेद, माांस और शारीररक क्लेद उन्हें
उत्पन्न करता है ।

78. वाति प्रमेह सम्प्राद्धि
क्षीणेषु दोषेध्यवक
ृ ष्य बिी धातूि प्रमेहािनिलाः करोनत।
दोषो नह बद्धिं समुपेत्य मूत्रं संदृष्य मेहाञ्जियेद्यिास्वम् ।। (च.नच ६/६)
कफ और वपत्त दोर् जब िात की अपेिा िीण (न्यून) रहते है, तो बढा हुआ बात
िातुओां (िसा, मज्जा, ओज और लवसका) को मूत्राशय में खीांचकर ले आता है,
तब िातज प्रमेह को उत्पन्न करता है।

79. िीतनप्रयत्वं गलतालुिोषो माधुयवमास्ये करपाददाहाः
भनवष्यतो मेहगदस्य रूप मूत्रेऽनभधावद्धि नपपीनलकाश्च ॥ (च.नच ६/१४)
● शीतल द्रव्योां से अविक प्रेम करना,
● गला और तालु का सूखना,
● मुख का मीठा होना,
● हार्-पैर में जलन का होना,
● मूत्र चीवटयोां का लगना

80. साध्यासाध्यता
साध्यााः कफोत्था दि, नपत्तिााः षट् याप्या, ि साध्याः पविाच्चतुष्काः ।
समनियत्वानिषमनियत्वान्महात्ययत्वाच्च यिािमं ते ॥ (च.नच ६/७)
समवक्रय होने से कफजन्य दस प्रमेह साध्य होते हैं। विर्मवक्रय होने से वपत्तजन्य
६ प्रमेह बाध्य होते हैं। महात्यय होने से िातजन्य ४ प्रमेह असाध्य होते हैं।

81. नचनकत्सा सूत्र
स्िूलाः प्रमेही बलवानिहैकाः क
ृ ििचैकाः पररदुबवलच
संबृंहणं तत्र क
ृ िस्य कायव संिोधि दोषबलानधकस्य ॥ च.
नच६/१५)
● क
ृ श क
े वलए बृांहण वचवकत्सा करनी चावहए और
● वजस व्यस्तक्त में दोर्ोां की अविकता और बल की अविकता हो, उसमें सांशोिन
प्रयोग करना चावहए।

82. प्रमेह पीनडका
१० प्रकार की वपविकाये या फोड़े
उत्पन्न हो जाते है उनको प्रमेह
वपविकाये कहते है।
१ शराविका
२ कच्छवपका
३ जावलनी
४ अलजी
५ अलजी
६ मसूररका
७ सर्वपथका
८ पुवत्रणी
९ विदाररका
१० विद्रवि।

83. ● यह प्राय: सस्तन्धयोां, ममथस्र्लोां तर्ा अविक माांस युक्त स्र्ानोां में उत्पन्न होतीां
है।
● प्रमेह की उवचत वचवकत्सा न करने पर उक्त वपवड़का उत्पन्न होने लगती है।
प्रमेह नपनिका क
े उपद्रव :-
तृर्ा, श्वास, माांसपेवशयोां में सांकोच, मोह, वहक्का, मद, ज्वर, विसपथ, तर्ा
नावभ एिां ह्रदय आवद ममथस्र्लोां की गवत में रुकािट ।

84. आयुवेनदक योग
● वत्रकण्टकाद्य स्नेह
● फलवत्रकावदक्वार् (अनुपान- मिु)
● लोध्रासि
● उदक पान
● यि का प्रयोग
● व्यायाम
● वनदान पररिजथन

85. योगा