Ayurvedic Description of Prameha, Madhumeha and Modern medical perspective of Diabetes mellitus.

1. Madhumeha
(Diabetes mellitus)
Dr. Narendra P. Giri
MD Resident
TUATH, Kirtipur
05/03/2020

2. Madhumeha
 The term ‘Madhumeha’ is used interchangeably with ‘Prameha’
but it is one among the 4 Vataj Prameha.
 Prameha is one of the eight Maharoga described in Ayurveda.
 All the types of Prameha if not treated properly on time or if
neglected turns out to be Madhumeha. (advanced stage of
Prameha)

3. Prameha
 Literally, Pra= Abundant, Meha=passing of large quantity of urine
 Although the main presenting symptom of the disease is excess and
sweet urine, it involves all the three doshas and 10 dushyas including
shukra and oja.
 Ikshumeha and Seetameha (types of Kafaj Prameha) have Mutra
Madhurya (Glycosuria) as a presenting feature which causes
Dhatukshya and vitiation of Vata resulting in Madhumeha in long run.
 Similarly, Kaphapitta Kshaya in a Kapha-Pitta Pramehi associated with
chronicity and Dhatukshaya leads to aggravation of Vata resulting in
Madhumehaa (Vataja Meha).

4. Etiology of Prameha
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 Enjoying sedentary habits and the pleasure of sleep excessively,
 too much use of yoghurt and its preparation,
 meat juice of domestic, aquatic and swampy animals,
 milk and its preparation,
 newly harvested cereals,
 new/ fresh wines, preparations of jaggery (canesugar preparations)
and
 all other Kapha-aggravating factors are the causes of the diabetes
syndrome

5. 10 dushyas in Prameha
 Dosha- Kafa, Pitta and Vata ( in the sequential order)
 Dushya- Medha, Rakta, Sukra, Ambu ( saririk Kleda), Vasa,
Lasika, Majja, Rasa, Oja and Mamsha

6. Classification of Prameha
 According to Dosha and Prognosis
a. Kafaj-10 types
 Sadhya due to Samakriyatwat and meda dhatu not being totally
dusthi
b. Pittaj-6 types
 Yapya due to Visham kriyatwat, moderate dusthi of medo dhatu,
samsrustha dosha in medosthan
c. Vataj-4 types
 Asadhya due to Gambhira dhatu ashraya, severe dusthi of dhatus
and Biparita kriyatwat

7. Classification of Prameha
Kafaj-10 types Pittaj- 6 types Vataj- 4 types
Udakmeha Ksharmeha Vasameha
Ikshumeha Kalameha Majjameha
Shandrameha Nilameha Hastimeha
Shandraprasadmeha Lohitameha Madhumeha
Suklameha Manjisthameha
Sukrameha Haridrameha
Sheetameha
Sikatameha
Shanairmeha
Alalameha

8. Classification of Prameha
According to Etiological causes- 2 types
1. Sahaja/ Jatapramehi (Hereditary)- due to bija dosha and
is incureable,
 usually the patient is krisha.
2. Apathyanimitttaja (Acquired)-
a. Avaranajanya and Dhatu apakarsanajanya-due to
avarana of Vata by kafa and pitta and due to vitiation
of vata by dhatukshya
b. Santarpanajanya and Apatarpanjanya
c. Anilatmaka and Kafasambhava

9. Samprapti of Prameha
1. Nidana sevan
2. Dosha Dusti
3. Dusta Dosha Enters Medha dhatu
4. Meda vilayana due to pitta
5. Kleda Vriddhi
6. Excess Kleda shifts to basti
7. Gradually involves other dhatus as well
8. Involvement of other dosha also
9. Prameha rogotpatto

10. Madhumeha
 One of the Vataj Prameha
 Literaly, Madhu=Honey, Meha=Urine
 The disease in which the urine is similar to honey in
colour, taste, smell and consistency.
 Even the body gets sweetness in madhumeha.
 Synonyms-Kshaudrameha, Ojomeha
 Chronic and incureable in nature

11. Madhumeha-Nidan
 All the Prameha on being neglected or not treated properly
turns to be Madhumeha.
 All the things that produce excessive kafa, medha and mutra
are the etiologies.
 All the Aahara Vihara having Snigdha, Sheeta, Guru, Pichhila,
Madhura, Slakshna properties that vitiate dushya causes
Madhumeha.
 These factors mainly cause excessive burden on metabolism at
cellular level resulting in intermediate metabolites which leads
to excess production of meda, kleda, lasika, mutra, sweda and
deposition of meda at various sites.

12. Madhumeha- Purvarupa
 burning sensation in the palms and soles,
 body (skin) becoming unctuous and slimy,
 heaviness in body,
 urine is sweet, bad in smell and white in color,
 stupor,
 debility,
 profound thirst,
 dyspnea,
 more accumulation of dirt in the palate, throat, tongue and teeth,
 hairs of the head adhering to one another and more growth of the
hairs and nails.

13. Madhumeha-Rupa
 The general feature of the diabetes syndrome is the
passage of a profuse and/ or turbid urine, the urine
becomes like honey and the entire body becomes very
sweet.
 Sushrutacharya also says that Sahajameha Rogi are
usually Krisha (Thin built) while Apathyanimittaja Rogi are
usually Sthula (Obese).

14. Madhumeha-Samprapti

15. Samprapti of Madhumeha in the light of Kriyakala
Risk Factors Symptoms Modern
Explanation /
Investigation
Management Strategy
Sanchaya Consumption of
excessive heavy to
digest,oily,sweet,sour
and salt diet,
sedentary life style,
day sleep
Cold intolerability,
Recurrent
Respiratory
discomforts,
Laziness, sleepy,
feeling of heaviness
in body
High risk factors
like sedentary life
style, over
nutrition,
Abnormal fasting
lipid profile
Life style modifications,
following Ayurvedic
Dincharya, Ritucharya,
Sleshma viruddha
Upakrama esp. regular
Udvartana, vyayama,
langhana etc
Prakopa Above plus Drava
atisevana, Madhura and
Medura atisevana
Sweda Adhikya,
Sthoola laxyana,
Exertional
dyspnoeas, sphik-
stanodara
lambhanam
Prediabetic-
Abnormal GTT,
GCT in pregnancy
Primary Prevention, Life
style modifications,
Sthoulya Chikitsa,
consumption of tikta
rasa
Prasara Above + Stress, Ushna Karapada daha and
some other purva
rupa
Abnormal GTT,
FBS=100-125
Above + Nisha Aamalaki
prayoga for prevention

16. Risk Factors Symptoms Modern
explanation/Investiga
tions
Management
Strategy
Sthana
Samshraya
Above nidana+
Mutrala Aahara
Full fledged purva rupa,
Kafa Prameha Upadrava
Early Diabetic
FBS<125,PPBS<160
Kafa Prameha
chikitsa+
secondary
Prevention
Vyakti Above+ Rakta
Pradoshakara
Nidana
Prabhoota Avila
mutrata, loosing
weight, Pitta Prameha
Upadrava
Persistent Glycosuria
FBS< 180
Pitta Prameha
chikitsa,
Secondary
prevention
Bheda Above+
Apatarpana
nidana like severe
diet control,
excessive
medication
Above+ Vata Prameha
Upadrava
Uncontolled High
blood sugar, Chronic
diabetes with
complications
Tertiary
prevention,
Dhanwantari
Ghritam, Vasanta
kusmakara rasa,
Chandraprava vati
etc

17. Prameha-Chikitsa
Chikitsa sutra- as per Charak
 Sthula and Balawan Prameha rogi are subjected to Samsodhana
first then santarpan is done whereas Krisha and Durbala rogi are
subjected to Brimhan chikitsa.
 Samsodhana ayogya Pramehi should be treated by samsamana.
 Mantha (Sattu mixed in water), Kasaya, powder of yawa,
Avaleha and laghu food should be given to pacify doshas.

18. Sworas Kwath Churna Ghrita
Amalaki Vidangadi Triphaladi Dhanvantarghrita
Haridra Phalatrikadi Mustadi Trikantakadighrita
Nimba patra Mustadi Gokshuradi Sinhamritaghrita
Bilwapatra Manjisthadi Arkadi Dadimadighrita
Guduchi Pathadi Shalmalighrita
Avaleha Guggulu Paka Vati Modaka
kushavleha Gokshuradi
Guggul
Puga paka Chandraprabha
Vati
Kastur
Modaka
Bangavleha Ashwagandhadi
paka
Indra vati
Draksha Paka Pramehantak
Vati

19. Rasaushadhi Aasava Aristha
Vasantkusumakar Rasa Lodhrasava
Mehamudgar Rasa Dantyasava
BrihatVangeshwar Rasa Madhukasava
Prameha gajkesri Rasa Devdarvyadiarishta
Trivanga Bhasma Lodhrarishta
Vasant tilaka Rasa

20.  Baladi Churnam Kshaya- Harita Samhita
 Gokantkadyavaleha– Bhava Prakasha
 Kharpara rasayanam– Rasa Ratna samucchyaya
 Manjisthadyam Ghrutam– Gada Nigraha
 Sinhamrut Ghrutam– Chakradutta
 Khadirradi Kashaya– Gada Nigraha
 Pashanbhed Kashaya– Sahasra Yoga
 Pashanbhed Pak– Yoga Ratnakara
 Asanadi Yoga- Bhava Prakash

21.  Indra vati – Rasendrasara sangraha
 Vedvidya vati –Bharata Bhaishajya Ratnakara Vol 4
 Bahumootrantaka ras– Sahasrayoga
 Maskmruganka ras–Rasarajasundaram
 Meha Kesari ras–Rasendrasara Sangraha
 Pramadananda ras–Bruhatyoga Tarangini
 Sarweshwar ras–Bhaishajya Ratnavali

22.  Somanath ras–Rasendra Chintamani
 Vangeshwara ras–Yoga Ratnakara
 Taala Maranam–Bharata Bhaishajya Ratnavali vol-2
 Umashambhu Ras–Rasa Ratnasamucchya

23. Yogasanas
 Utthita Trikonasana
 Parivritta Trikonasana
 Prasarita Padottanasana
 Jathara Parivartanasana
 Pavanamuktasana
 Viparitakarani
 Bhujangasana
 Dhanurasana
 Mandukasana
 Ardha Matsyendrasana
 Paschimottanasana
 Ardha Ustrasana

24.  PRANAYAMA
 Nadishodhana/Anuloma Viloma Pranayama
 Bhramari Pranayama
 KRIYAS:
 Agnisara Kriya
 Kapalabhati Kriya
 CYCLIC MEDITATION –AVARTANA DHYANA

25. Pathya Aahara
 Shook Dhanya: Jeerna Shali, Shashtika, Kodrava, Yava,
Godhuma, Uddalaka,Shyamaka
 Shimbi Dhanya: Chanaka, Adhaki, Kulattha, Mudga
 Shaka Varga: The leafy vegetables with a predominance of
tikta-kashaya rasa, Patola, Karvellaka, Shigru
 Phala Varga: Jambu, Dadima, Shringataka, Amalaki,
Kapittha, Tinduka, Kharjura, Kalinga, Navina Mocha.

26.  Mamsa Varga: Vishkira mamsa, Pratuda, Jangala mamsa
 Taila Varga: Danti, Ingudi, Sarshapa, Atasi
 Udaka Varga: Sarodaka, Kushodaka, Madhudaka
 Kritanna Varga: Apupa, Saktu,Yavodana,Vatya,Yusha
 Others: Madhu, Hingu, Saindhava, Maricha, Lasuna

27. Pathya Vihara
 To have walk as much as possible
 traveling on elephants, horses
 different plays and games
 different forms of marshal arts practice
 roaming in different places other than temples using
umbrella
 following “Sadvrutta”
 Dry Massage (Udvartan)
 Bath (Snana)
 Yoga

28. Apathya Aahara
 Shuka Dhanya (Cereals) - White Newly harvested Rice (within One
year) & its preparations, Aromatic Rice (Basmati) ,Maida & its
preparations, Bread, Noodles, Pasta, Maida biscuits, Murukku, Puri ,
Jalebi
 Shami Dhanya (Pulses) - Black Tila (Sesame), Masha (Udad/ black
gram & its preparations ), Rajamasha (Cow pea), Matara (Pea),
 Mamsa Varga (Nonveg) - Gramyaudakanuparasa (meat soup of the
domestic, aquatic and marshy animals) , Meat soup of pork, buffalo,
fish etc.
 Phala Varga (Fruits) - Banana, Custard apple, Jack fruit , Grapes,
Dates, Plum, Pineapple, Mango , Papaya, Watermelon, Guava,
Sapota

29.  Shaka Varga: Kanda (tubers)- Potato, sweet potato, beetroot,
cabbage and its preparations,
 Madya Varga ( Drink) - Navamadyapana (freshly brewed alcoholic
drinks), Sweet alcoholic drinks, Better to avoid all kinds of alcohol
 Pana (Water)- Varsha Ritu Jala, Soft drinks, Soda, Cold drinks,
Sweet fruit juices
 Gorasa Varga (Dairy products) - Dugdha (Milk), Dadhi (Curd),
Butter, Cheese , Ghrita (ghee) , Milk preparations eg. Paneer, Kheer,
Icecreams
 Ikshuvikara (Jaggery and its preparations) - Jaggery , Sugar
 Navanna (new/fresh grains, cereals) - Cereals and grains that are
less than one year old

30. Apathya Vihara
 Atimatra sevana (excessive eating)
 Aasyasukham (enjoying comfortable sitting or luxury)
 Swapnasukham (enjoying the pleasure of excessive
sleeping )
 Avyayam (lack of exercise and physical activity )
 Diwaswapa (sleeping in the daytime/afternoon)
 Aalasya (lazyness)

31. Diabetes Mellitus
 In the first century B.C., a Greek physician, Aretus the Cappadocian,
coined the name diabainein, meaning "a siphon," referring to the
excessive urination associated with the disease diabetes.
 In the western medicine, the word diabetes was first recorded in
1425.
 The Greek word mellitus, “like honey,” was added in 1675, to reflect
the sweet smell and taste of the patient’s urine.
 However, the metaphor “Urine similar to honey” was extant
centuries before that and is exactly reflected in the Ayurvedic term
“Madhumeha” which literally means “honey-like urine”.

32.  Diabetes mellitus is a metabolic disorder of multiple etiology,
characterized by chronic hyperglycemia with disturbances of
carbohydrate, fat and protein metabolism resulting from
defects in insulin secretion, insulin action, or both.
 The long-term specific effects of diabetes include retinopathy,
nephropathy and neuropathy, among other complications.
 People with diabetes are also at increased risk of other diseases
including heart, peripheral arterial and cerebrovascular disease,
obesity, cataracts, erectile dysfunction, and nonalcoholic fatty
liver disease.
 They are also at increased risk of some infectious diseases, such
as tuberculosis.

33. Epidemiology
 Diabetes is found in every population in the world and in all regions, including
rural parts of low- and middle-income countries.
 The number of people with diabetes is steadily rising, with WHO estimating
there were 422 million adults with diabetes worldwide in 2014. The age-
adjusted prevalence in adults rose from 4.7% in 1980 to 8.5% in 2014, with the
greatest rise in low- and middle-income countries compared to high-income
countries.
 In addition, the International Diabetes Federation (IDF) estimates that 1.1
million children and adolescents aged 14–19 years have T1DM.
 Without interventions to halt the increase in diabetes, there will be at least 629
million people living with diabetes by 2045.
 High blood glucose causes almost 4 million deaths each year and the IDF
estimates that the annual global health care spending on diabetes among adults
was US$ 850 billion in 2017.

34. Diagnostic criteria
 Four diagnostic tests for diabetes are currently recommended,
including measurement of fasting plasma glucose; 2-hour (2-h) post-
load plasma glucose after a 75 g oral glucose tolerance test (OGTT);
HbA1c; and a random blood glucose in the presence of signs and
symptoms of diabetes.
 People with fasting plasma glucose values of ≥ 7.0 mmol/L (126
mg/dl), 2-h post-load plasma glucose ≥ 11.1 mmol/L (200 mg/dl),
HbA1c ≥ 6.5% (48 mmol/mol); or a random blood glucose ≥ 11.1
mmol/L (200 mg/ dl) in the presence of signs and symptoms are
considered to have diabetes.
 If elevated values are detected in asymptomatic people, repeat
testing, preferably with the same test, is recommended as soon as
practicable on a subsequent day to confirm the diagnosis.

35. Classification of Diabetes
Diabetes can be classified into the following general categories:
1. Type1 diabetes (due to autoimmune β-cell destruction, usually leading to
absolute insulin deficiency)
2. Type 2 diabetes (due to a progressive loss of β-cell insulin secretion
frequently on the background of insulin resistance)
3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or
third trimester of pregnancy that was not clearly overt diabetes prior to
gestation)
4. Specific types of diabetes due to other causes, e.g., monogenic diabetes
syndromes (such as neonatal diabetes and maturity-onset diabetes of the
young [MODY]), diseases of the exocrine pancreas (such as cystic fibrosis
and pancreatitis), and drug- or chemical induced diabetes (such as with
glucocorticoid use, in the treatment of HIV/AIDS, or after organ
transplantation).

36. Aetio-pathogenesis of DM
 The aetiology and pathogenesis of diabetes can be described
simplistically as problems with insulin sensitivity and insulin
secretion, but the underlying specific defects are complex and
not well understood.
 While some specific defects have been identified (e.g. genetic
abnormalities resulting in insulin secretory problems), defining
the mechanisms underlying common forms of diabetes remains
challenging as they are increasingly recognized to involve a
complex interplay of genetic, epigenetic, proteomic and
metabolomic processes.

37. Type 1 DM
 Data on global trends in T1DM prevalence and incidence are not
available, but data from many high income countries indicate an
annual increase of between 3% and 4% in the incidence of T1 DM in
childhood.
 Males and females are equally affected.
 Despite T1DM occurring frequently in childhood, onset can occur in
adults and 84% of people living with T1DM are adults.
 T1DM decreases life expectancy by around 13 years in high-income
countries.
 People with T1DM are also prone to other autoimmune disorders such
as Hashimoto thyroiditis, Graves disease, Addison disease, celiac
disease, vitiligo, autoimmune hepatitis, myasthenia gravis, and
pernicious anemia.

38. Type 1 DM- Etiology
1. Immune-Mediated Diabetes:
 This form, previously called “insulin dependent diabetes” or “juvenile-
onset diabetes”, accounts for 5–10% of diabetes and is due to cellular-
mediated autoimmune destruction of the pancreatic β-cells.
 Autoimmune markers include islet cell autoantibodies and
autoantibodies to GAD (GAD65), insulin, the tyrosine phosphatases IA-2
and IA-2b, and ZnT8.
 Type1 diabetes is defined by the presence of one or more of these
autoimmune markers.
 The disease has strong HLA associations, with linkage to the DQA and
DQB genes. These HLA-DR/DQ alleles can be either predisposing or
protective.

39. 2. Idiopathic Type 1 Diabetes:
 Some forms of type 1 diabetes have no known etiologies.
 These patients have permanent insulinopenia and are
prone to DKA, but have no evidence of β-cell
autoimmunity.
 Although only a minority of patients with type 1 diabetes
fall into this category, of those who do, most are of
African or Asian ancestry.
 This form of diabetes is strongly inherited and is not HLA
associated.

40. Type 1 DM- Treatment
 Most people with type 1 diabetes should be treated with multiple
daily injections of prandial and basal insulin, or continuous
subcutaneous insulin infusion.
 Generally, insulin requirements can be estimated based on
weight, with typical doses ranging from 0.4 to 1.0 units/kg/day.
Higher amounts are required during puberty, pregnancy, and
medical illness.
 Most individuals with type 1 diabetes should use rapid-acting
insulin analogs to reduce hypoglycemia risk.
 Consider educating individuals with type 1 diabetes on matching
prandial insulin doses to carbohydrate intake, premeal blood
glucose levels, and anticipated physical activity.

41. Noninsulin Treatments for Type 1 Diabetes:
 Pramlintide is based on the naturally occurring β-cell peptide
amylin and is approved for use in adults with type1 diabetes.
Results from randomized controlled studies show variable
reductions of HbA1C (0–0.3%) and body weight (1–2 kg) with
addition of pramlintide to insulin.
Surgical treatment for Type 1 Diabetes:
 Pancreas and islet transplantation normalizes glucose levels
but requires lifelong immunosuppression to prevent graft
rejection and recurrence of autoimmune islet destruction

42. Type 2 Diabetes
 Type 2 diabetes, previously referred to as “noninsulin-dependent
diabetes” or “adult-onset diabetes,” accounts for 90– 95% of all
diabetes.
 This form encompasses individuals who have relative (rather than
absolute) insulin deficiency and have peripheral insulin resistance.
 At least initially, and often throughout their lifetime, these individuals
may not need insulin treatment to survive.
 There are various causes of type 2 diabetes. Although the specific
etiologies are not known, autoimmune destruction of β-cells does not
occur and patients do not have any of the other known causes of
diabetes.
 Most but not all patients with type 2 diabetes are overweight or obese.
Excess weight itself causes some degree of insulin resistance.

43.  Many factors increase the risk of developing T2DM including
age, obesity, unhealthy lifestyles and prior gestational
diabetes (GDM).
 There are particular populations that have a higher occurrence
of type 2 diabetes, for example Native Americans, Pacific
Islanders, and populations in the Middle East and South Asia.
 It is also often associated with strong familial, likely genetic
or epigenetic predisposition.

44. Type-2 Diabetes-Treatment
 Metformin is the preferred initial pharmacologic agent for the
treatment of type 2 diabetes.
 Once initiated, metformin should be continued as long as it is tolerated
and not contraindicated; other agents, including insulin, should be
added to metformin. Long-term use of metformin may be associated
with biochemical vitamin B12 deficiency, and periodic measurement of
vitamin B12 levels should be considered in metformin-treated patients,
especially in those with anemia or peripheral neuropathy.
 The early introduction of insulin should be considered if there is
evidence of ongoing catabolism (weight loss), if symptoms of
hyperglycemia are present, or when HBA1C levels (10% [86 mmol/mol])
or blood glucose levels (≥300 mg/dL [16.7 mmol/L]) are very high.

45.  Consider initiating dual therapy in patients with newly diagnosed type 2
diabetes who have HbA1C ≥1.5% (12.5 mmol/mol) above their glycemic
target.
 A patient-centered approach should be used to guide the choice of
pharmacologic agents. Considerations include comorbidities
(atherosclerotic cardiovascular disease, heart failure, chronic kidney
disease), hypoglycemia risk, impact on weight, cost, risk for side effects,
and patient preferences.
 Among patients with type 2 diabetes who have established atherosclerotic
cardiovascular disease, sodium–glucose cotransporter 2 inhibitors, or
glucagon-like peptide 1 receptor agonists with demonstrated cardiovascular
disease benefit are recommended as part of the antihyperglycemic
regimen.
 Among patients with atherosclerotic cardiovascular disease at high risk of
heart failure or in whom heart failure coexists, sodium–glucose
cotransporter 2 inhibitors are preferred.

46.  For patients with type 2 diabetes and chronic kidney disease,
consider use of a sodium– glucose co-transporter 2 inhibitor or
glucagon-like peptide 1 receptor agonist shown to reduce risk of
chronic kidney disease progression, cardiovascular events, or both.
 In most patients who need the greater glucose-lowering effect of an
injectable medication, glucagon-like peptide-1 receptor agonists
are preferred to insulin.
 Intensification of treatment for patients with type 2 diabetes not
meeting treatment goals should not be delayed.
 The medication regimen should be reevaluated at regular intervals
(every 3–6 months) and adjusted as needed to incorporate new
patient factors.

48. Oral Hypoglycemic Agents
Class Drug Dose Route Remarks
Biguanides Metformin 500
mg/850/1000
mg
Oral First line, no
Hypoglycemia, High
Efficacy
Sulfonylureas Glimepiride 4 mg Oral Can cause
hypoglycaemia,High
efficacy
Glipizide 10 mg
Glyburide 6 mg
Thiazolidinedi
ones
Pioglitazone 45 mg Oral No hypoglycaemia,
High efficacy
Rosiglitazone 4 mg

49. α-
Glycosidage
Inhibitor
Acarbose 100 mg Oral No Hypoglycaemia
Miglitol 100 mg
Meglitinides
(Glinides)
Nateglinide 120 mg Oral May cause
Hypoglycaemia,
High efficacyRepaglinide 2 mg
DPP-4
Inhibitors
(Dipeptidyl
peptidase-4
inhibitor)
Alogliptin 25 mg Oral No Hypoglycaemia,
Intermediate
efficacy, costlySaxagliptin 5 mg
Linagliptin 5 mg
Sitagliptin 100mg

50. SGLT2
Inhibitors
Ertugliflozin 15 mg Oral No
hypoglycaemia,Inter
mediate efficacy,
Costly
Dapagliflozin 10 mg
Canagliflozin 300 mg
Empagliflozin 25 mg
GLP-1
receptor
agonists
Exenatide (extended
release)
2 mg powder for
suspension or pen
SC No Hypoglycaemia,
High efficacy,
Costly
Exenatide 10 mg pen
Dulaglutide 1.5/0.5 mL pen
Semaglutide 1 mg pen
Liraglutide 18 mg/3 mL pen
SGLT2 Inhibitors=Sodium glucose cotransporter 2 inhibitor,
GLP-1 RA-Glucagon Like peptide 1 Receptor Agonists

51. Insulin Therapy
 Many patients with type 2 diabetes eventually require and
benefit from insulin therapy.
 But risk of Hypoglycaemia should be brone in mind.
Basal Insulin:
 Basal insulin alone is the most convenient initial insulin regimen
and can be added to metformin and other oral agents.
 Starting doses can be estimated based on body weight (e.g., 10
units a day or 0.1–0.2 units/kg/day) and the degree of
hyperglycemia, with individualized titration over days to weeks
as needed.

52. Prandial Insulin:
 Individuals with type 2 diabetes may require doses of
insulin before meals in addition to basal insulin.
 The recommended starting dose of mealtime insulin is
either 4 units or 10% of the basal dose at each meal.
 Titration is done based on home glucose monitoring or
HbA1C. With significant additions to the prandial insulin
dose, particularly with the evening meal, consideration
should be given to decreasing the basal insulin dose.

53. Other forms of Insulins:
 Premixed Insulin:- Premixed insulin products contain both a basal
and prandial component, allowing coverage of both basal and
prandial needs with a single injection.
 Concentrated Insulin Products:- Several concentrated insulin
preparations are currently available. U-500 regular insulin is, by
definition, five times more concentrated than U-100 regular
insulin.
 Inhaled Insulin:- Inhaled insulin is available for prandial use with a
limited dosing range; studies in people with type 1 diabetes
suggest rapid pharmacokinetics.

54. Need of Awareness in Diabetics for:
1. Hypoglycaemia-
 In those taking Insulin or Sulfonylureas or rarely with metformin the
blood glucose may fall below 3.5 mmol/l (63 mg/dl) in both types
of DM.
 So, tight regulation of glucose level in sensitive and elderly
diabetics is not recommended.
 Symptoms:
 Autonomic- Sweating, Trembling, Pounding Heart, Hunger, Anxiety
 Neuroglycopenic- Confusion, Drowsiness, Speech difficulty, Inability to
concerntrate, Incoordination
 Non specific-Nausea, Tiredness, Headache

55. 2. Diabetic Ketoacidosis:
 T1DM are more prone to DKA and specially children with T1DM may
present with DKA as a first presentation of the disease.
 It involves
 Hyperglycaemia of more than 200mg/dl,
 Hyperketonaemia
 Metabolic acidosis
3. Hyperglycaemic Hyperosmolar state:
 T2DM are more prone to HHS.
 It is characterized by hyperglycaemia >600mg/dl without significant
hyperketonaemia or acidosis.
 Severe dehydration and pre-renal uraemia are common.

56. Complications of DM
Microvascular/Neuropathic:
 Retinopathy, Cataract- Impaired vision
 Nephropathy- Kidney failure
 Periphreal Neuropathy- Sensory loss, motor weakness
 Autonomic Neuropathy- Postural Hypotension, GI Problems
(Gastroparesis, altered bowel habbit)
 Foot disease-Ulceration, arthropathy
Macrovascular:
 Coronary circulation- Myocardial ischaemia/Infraction
 Cerebral Circulation- TIA, Stroke
 Periphreal Circulation- Claudication, Ischaemia

57. Lifestyle modifications in DM
A simple and effective approach to glycemia and weight
management emphasizing portion control and healthy food choices
may be considered for those with type 2 diabetes who are not
taking insulin, who have limited health literacy or numeracy, or who
are older and prone to hypoglycemia.
1. Energy Balance:
 Weight loss (>5%) achievable by the combination of reduction of
calorie intake and lifestyle modification benefits overweight or
obese adults with type 2 diabetes and also those with
prediabetes. Intervention programs to facilitate weight loss are
recommended.

58. 2. Eating patterns and macronutrient distribution:
 There is no single ideal dietary distribution of calories among carbohydrates,
fats, and proteins for people with diabetes; therefore, meal plans should be
individualized while keeping total calorie and metabolic goals in mind.
 A variety of eating patterns are acceptable for the management of type 2
diabetes and prediabetes.
3. Carbohydrates:
 Carbohydrate intake should emphasize nutrient-dense carbohydrate sources
that are high in fiber, including vegetables, fruits, legumes, whole grains, as
well as dairy products.
 For people with type 1 diabetes and those with type 2 diabetes who are
prescribed a flexible insulin therapy program, education on how to use
carbohydrate counting and in some cases how to consider fat and protein
content to determine meal time insulin dosing is recommended to improve
glycemic control.

59. Carbohydrate contd:
 For individuals whose daily insulin dosing is fixed, a consistent pattern of
carbohydrate intake with respect to time and amount may be recommended
to improve glycemic control and reduce the risk of hypoglycemia.
 People with diabetes and those at risk are advised to avoid sugar-sweetened
beverages (including fruit juices) in order to control glycemia and weight and
reduce their risk for cardiovascular disease and fatty liver and should
minimize the consumption of foods with added sugar that have the capacity
to displace healthier, more nutrient-dense food choices
4. Protein:-
 In individuals with type 2 diabetes, ingested protein appears to increase
insulin response without increasing plasma glucose concentrations. Therefore,
carbohydrate sources high in protein should be avoided when trying to treat
or prevent hypoglycemia.

60. 5. Dietary Fat:-
 Data on the ideal total dietary fat content for people with diabetes are
inconclusive, so an eating plan emphasizing elements of a Mediterranean-style
diet rich in monounsaturated and polyunsaturated fats may be considered to
improve glucose metabolism and lower cardiovascular disease risk and can be an
effective alternative to a diet low in total fat but relatively high in
carbohydrates.
 Eating foods rich in long-chainn-3 fatty acids, such as fatty fish and nuts and
seeds, is recommended to prevent or treat cardiovascular disease; however,
evidence does not support a beneficial role for the routine use of n-3 dietary
supplements.
6. Micronutrients and Herbal suppliments:-
 There is no clear evidence that dietary supplementation with vitamins, minerals
(such as chromium and vitamin D), herbs, or spices (such as cinnamon or aloe
vera) can improve outcomes in people with diabetes who do not have underlying
deficiencies and they are not generally recommended for glycemic control.

61. 7. Alcohol:-
 Adults with diabetes who drink alcohol should do so in
moderation (no more than one drink per day for adult women
and no more than two drinks per day for adult men).
 Alcohol consumption may place people with diabetes at
increased risk for hypoglycemia, especially if taking insulin or
insulin secretagogues. Education and awareness regarding the
recognition and management of delayed hypoglycemia are
warranted.
8.Sodium:-
 As for the general population, people with diabetes should limit
sodium consumption to <2,300 mg/day.

62. 9. Nonnutritive sweeteners:-
 The use of nonnutritive sweeteners may have the potential to reduce
overall calorie and carbohydrate intake if substituted for caloric (sugar)
sweeteners and without compensation by intake of additional calories
from other food sources.
 For those who consume sugar-sweetened beverages regularly, a low-
calorie or nonnutritive-sweetened beverage may serve as a short-term
replacement strategy, but overall, people are encouraged to decrease
both sweetened and non-nutritive sweetened beverages and use other
alternatives, with an emphasis on water intake.

63. Physical Activities
 Children and adolescents with type 1 or type 2 diabetes or
prediabetes should engage in 60 min/day or more of moderate- or
vigorous-intensity aerobic activity, with vigorous muscle-
strengthening and bone-strengthening activities at least 3
days/week.
 Most adults with type 1 and type 2 diabetes should engage in 150
min or more of moderate to vigorous intensity aerobic activity per
week, spread over atleast 3 days/week, with no more than 2
consecutive days without activity.
 Shorter durations (minimum 75 min/week) of vigorous intensity or
interval training may be sufficient for younger and more physically
fit individuals.

64.  Adults with type 1 and type 2 diabetes should engage in 2–3 sessions/week of
resistance exercise on non consecutive days.
 All adults, and particularly those with type 2 diabetes, should decrease the
amount of time spent in daily sedentary behavior.
 Prolonged sitting should be interrupted every 30 min for blood glucose benefits,
particularly in adults with type 2 diabetes.
 Flexibility training and balance training are recommended 2–3 times/week for
older adults with diabetes.
 Yoga and tai chi may be included based on individual preferences to increase
flexibility, muscular strength, and balance.
 Hypoglycemia is less common in patients with diabetes who are not treated
with insulin or insulin secretagogues, and no routine preventive measures for
hypoglycemia are usually advised in these cases. Intense activities may actually
raise blood glucose levels instead of lowering them, especially if pre-exercise
glucose levels are elevated.

65. Smoking Cessation:
 Advise all patients not to use cigarettes and other tobacco products or e-
cigarettes.
Sleep:
 Adequate rest is also very important for maintaining energy levels and
well-being, and all patients should be advised to sleep approximately 7 h
per night.
 Evidence supports an association of 6 to 9 h of sleep per night with a
reduction in cardio-metabolic risk factors, whereas sleep deprivation
aggravates insulin resistance, hypertension, hyperglycaemia, and
dyslipidaemia.

66. Psychological Issues:
 Providers should consider assessment for symptoms of diabetes
distress, depression, anxiety, disordered eating, and cognitive
capacities using patient appropriate standardized and validated tools
at the initial visit, at periodic intervals, and when there is a change
in disease, treatment, or life circumstance.
 Consider screening older adults (aged >65 years) with diabetes for
cognitive impairment and depression.
 Routinely monitor people with diabetes for diabetes distress,
particularly when treatment targets are not met and/or at the onset
of diabetes complications.(The prevalence of DD is reported to be
18–45% with an incidence of 38–48% over 18 months )

67. Any Querries???