HRTD Medical Institute
PDT-Diabetology Courses

Post-Diploma Training in Diabetology

Table of Contents

Post-Diploma Training in Diabetology Courses

Post-Diploma Training in Diabetology. Mobile No. 01987-073965, 01797-522136. These Courses are 6 Months PDT-Diabetology, 1-Year PDT-Diabetology, and 2-Year PDT-Diabetology. 6 Month PDT Diabetology course Fee is Tk 35000/-, 1 Year PDT Diabetology Course Fee is Tk 65000/-, and 2 Years PDT Diabetology Course Fee Tk 125000/-. Each Semester of 6 Months contains 4 subjects and an exam mark of 400.

Post-Diploma Training in Diabetology

6 Months Post-Diploma Training in Diabetology (PDT-Diabetology 6 Months) Course Details

6 Months Post-Diploma Training in Diabetology that is PDT-Diabetology 6 Months Course Fee 35000/-. The payment system is an Admission Fee of Tk 10000/-, Monthly Fee of Tk 4000/- and Exam Fee of Tk 1000. 6 Months PDT-Diabetology Course contains 4 subjects. You can choose any 4 of these subjects Anatomy & Physiology of the Pancreas, Antidiabetic Drugs, Diabetology-1, Biochemistry of Diabetes, and Endocrine Glands & Their Functions.

PDT-Diabetology 6 Months Course Fee

1 Year Post-Diploma Training in Diabetology (PDT-Diabetology 1 Year) Course Details

1 Year Post-Diploma Training in Diabetology that is PDT-Diabetology 1 Year Course Fee Tk 65000/-. The payment system is an Admission Fee of Tk 15000/-, Monthly Fee of Tk 4000/- and Exam Fee of Tk 2000. 1 Year PDT-Diabetology Course contains 8 subjects. You can choose any 8 of these subjects Anatomy & Physiology of the Pancreas, Endocrine Glands & Their Hormones, Antidiabetic Drugs, Diabetology-1, Diabetology-2, Biochemistry of Diabetes, Endocrine Glands & Their Functions-1, Endocrine Glands & Their Functions-2.

PDT-Diabetology 1-Year Course Fee

Qualification for Admission into Diabetology Course

Qualification for Admission: Diploma Medical Course Completed. Or a short Medical Course with a Bachelor’s Degree or Master’s in any discipline.

Teacher for Diabetology Course

Dr. Sakulur Rahaman, MBBS, CCD (BIRDEM)

Dr. Disha, MBBS

Dr. Tisha, MBBS, PDT

Dr. Shamima, MBBS, PGT

What is Diabetes?

Diabetes is an endocrine disease. An increase in blood glucose due to a metabolic disorder is called diabetes. Insulin is a pancreatic hormone that reduces blood glucose. Diabetes occurs due to the deficiency or inactivity of insulin in our bodies.

What are the complications of Diabetes?

Complications of Diabetes are Diabetic Nephropathy, Diabetic Retinopathy, Diabetic Neuropathy, etc.

What is Diabetic Nephropathy?

Diabetes damages the Nephron of our Kidneys. This condition is called Diabetic Nephropathy.

What is Diabetic Retinopathy?

Diabetes damages the Nerves of the Retina. This condition is called Diabetic Retinopathy.

Location for Diabetology Course

Location: HRTD Medical Institute, Abdul Ali Madbor Mansion, Section-6, Block-Kha, Road-1, Plot-11, Metro Rail Piller No. 249, Mirpur-10 Golchattar, Dhaka-1216.

Subject for Diabetology Course

  • 1. Diabetic Related Anatomy, Histology & Cytology
  • 2. Antidiabetic Drugs & Pharmacology
  • 3. Diabetology-1 & Management of Diabetes
  • 4. Complications & Prevention of Diabetes 

Diabetology-for Post Diploma Training in Diabetology

Diabetes āĻ•āĻŋ? Diabetes āĻ•āĻŋ āϧāϰāύ⧇āϰ āϰ⧋āĻ— ?

āĻĻā§€āĻ°ā§āϘāĻĻāĻŋāύ āϧāϰ⧇ āϰāĻ•ā§āϤ⧇ glucose āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž normal āĻāϰ āĻšā§‡ā§Ÿā§‡ āĻŦ⧇āĻļāĻŋ āĻšāϞ⧇ āϤāĻžāϕ⧇ Diabetes āĻŦāϞ⧇āĨ¤

Diabetes āĻšāĻšā§āϛ⧇ āĻāĻ•āϟāĻŋ endocrine disease āĻ•āĻžāϰāύ insulin āύāĻžāĻŽāĻ• hormone āĻāϰ āĻ…āĻ­āĻžāĻŦ⧇ āĻ…āĻĨāĻŦāĻž āĻ…āĻ•āĻžāĻ°ā§āϝāĻ•āĻžāϰāĻŋāϤāĻžāϰ āϜāĻ¨ā§āϝ diabetes āĻšā§Ÿā§‡ āĻĨāĻžāϕ⧇āĨ¤

Endocrine disease āĻ•āĻžāϕ⧇ āĻŦāϞ⧇ ? Endocrinology & Diabetology āĻāϰ āϏāĻ‚āĻœā§āĻžāĻž –

Hormone āĻāϰ āϜāύāĻŋāϤ āĻ•āĻžāϰāύ⧇ āϝ⧇ āϏāĻ•āϞ āĻšā§Ÿ āϤāĻžāĻĻ⧇āϰāϕ⧇ Endocrine disease āĻŦāϞ⧇āĨ¤

āĻĻ⧇āĻšā§‡āϰ endocrine gland āϗ⧁āϞāĻŋ āĻĨ⧇āϕ⧇ hormone āύāĻŋāσāϏāϤ āĻšā§Ÿ āϤāĻžāχ āĻāχ āϰ⧋āĻ— āϗ⧁āϞāĻŋāϕ⧇ Endocrine disease āĻŦāϞ⧇āĨ¤

Endocrinology- āϚāĻŋāĻ•āĻŋā§ŽāϏāĻž āĻŦāĻŋāĻœā§āĻžāĻžāύ⧇āϰ āϝ⧇ āĻļāĻžāĻ–āĻžā§Ÿ Endocrine disease āϗ⧁āϞāĻŋ āύāĻŋā§Ÿā§‡ āφāϞ⧋āϚāύāĻž āĻ•āϰāĻž āĻšā§Ÿ āϤāĻžāϕ⧇ Endocrinology āĻŦāϞ⧇āĨ¤

Diabetology- āϚāĻŋāĻ•āĻŋā§ŽāϏāĻž āĻŦāĻŋāĻœā§āĻžāĻžāύ⧇āϰ āϝ⧇ āĻļāĻžāĻ–āĻžā§Ÿ diabetes āϰ⧋āĻ— āύāĻŋā§Ÿā§‡ āφāϞ⧋āϚāύāĻž āĻ•āϰāĻž āĻšā§Ÿ āϤāĻžāϕ⧇ Diabetology āĻŦāϞ⧇āĨ¤Diabetology āĻšāĻšā§āϛ⧇ Endocrinology āĻāϰ āĻāĻ•āϟāĻŋ āĻļāĻžāĻ–āĻžāĨ¤

Hormone āĻ•āĻŋ? Hormone āĻāϰ āύāĻŋāσāϏāϰāĻŖ āĻĒāĻĻā§āϧāϤāĻŋ āφāϞ⧋āϚāύāĻž āĻ•āϰāĨ¤

Hormone āĻšāĻšā§āϛ⧇ āĻāĻ• āϧāϰāύ⧇āϰ biochemical āϝāĻž endocrine gland āϗ⧁āϞāĻŋ āĻĨ⧇āϕ⧇ āύāĻŋāσāϏāϰāϤ āĻšā§Ÿ āĻāĻŦāĻ‚ āĻĻ⧇āĻšā§‡ āϏāĻ‚āϘāϟāĻŋāϤ āύāĻžāύāĻžāĻŦāĻŋāϧ āĻŦāĻŋāĻ•ā§āϰāĻŋ⧟āĻžāϕ⧇ āύāĻŋ⧟āĻ¨ā§āĻ¤ā§āϰāύ āĻ•āϰ⧇āĨ¤

Hormone āĻāϰ āύāĻŋāσāϏāϰāĻŖ āĻĒāĻĻā§āϧāϤāĻŋ-āĻĻ⧇āĻšā§‡āϰ āĻĒā§āĻ°ā§Ÿā§‹āϜāύ⧇āϰ āĻ­āĻŋāĻ¤ā§āϤāĻŋāϤ⧇ āĻŦāĻž āĻ…āĻ¨ā§āϝ Hormone āĻāϰ āĻĒā§āϰāĻ­āĻžāĻŦ⧇ Hormone āύāĻŋāσāĻ¸ā§āϰāϤ āĻšā§ŸāĨ¤

Positive feedback mechanism āĻāϰ āĻŽāĻžāĻ§ā§āϝāĻŽā§‡ plasma āϤ⧇ hormone āĻāϰ āĻĒāϰāĻŋāĻŽāĻžāύ āĻ•āĻŽā§‡ āϗ⧇āϞ⧇ āĻāχ āĻĒā§āϰāĻ•ā§āϰāĻŋ⧟āĻžā§Ÿ gland āĻāϰ āĻ•ā§āώāϰāĻŖ āĻļ⧁āϰ⧁ āĻšā§ŸāĨ¤

Negative feedback mechanism āĻāϰ āĻŽāĻžāĻ§ā§āϝāĻŽā§‡ plasma āϤ⧇ hormone āĻāϰ āĻĒāϰāĻŋāĻŽāĻžāύ āĻŦ⧇āĻļāĻŋ āĻšāϞ⧇ āĻāχ āĻĒā§āϰāĻ•ā§āϰāĻŋ⧟āĻžā§Ÿ gland āĻāϰ āĻ•ā§āώāϰāĻŖ āĻļ⧁āϰ⧁ āĻšā§ŸāĨ¤

Hormone āĻāϰ āĻ•āĻžāĻ°ā§āϝāĻĒāĻĻā§āϧāϤāĻŋ āφāϞ⧋āϚāύāĻž-

  • āϕ⧋āώ⧇ āĻ…āĻŦāĻ¸ā§āĻĨāĻŋāϤ Hormone receptor āĻāϰ āϏāĻžāĻĨ⧇ āϏāĻ‚āϝ⧁āĻ•ā§āϤāĻŋ (āĻŦāĻŋāĻļ⧇āώ āϧāϰāύ⧇āϰ āĻĒā§āϰ⧋āϟāĻŋāύ )
  • Hormone receptor complex āϏ⧃āĻˇā§āϟāĻŋ āĨ¤
  • āϕ⧋āώ⧇āϰ āĻ­āĻŋāϤāϰ cAMP āϤ⧈āϰāĻŋāϤ⧇ āωāĻ¤ā§āϤ⧇āϜāύāĻž āĻĒā§āϰāĻĻāĻžāύāĨ¤
  • cAMP āĻ•āϤ⧃āĻ• āĻŦāĻ‚āĻļāĻ—āϤāĻŋāϰ āĻ…āĻ™ā§āϘ āϏāĻŽā§‚āĻšāϕ⧇ āωāĻ¤ā§āϤ⧇āϜāĻŋāϤ āĻ•āϰ⧇ āĻ•āĻžāϰāϝ āϏāĻŽā§āĻĒāĻžāĻĻāύāĨ¤
  • cAMP- Cyclic Adenosine Monophosphate. cAMP is a derivative of Adenosine Triphosphate (ATP)

Pancreas āĻ•āĻŋ? Pancreas hormone āϗ⧁āϞāĻŋ āĻ•āĻŋ āĻ•āĻŋ?

Stomach āĻāϰ āύāĻŋāĻšā§‡ āĻāĻŦāĻ‚ duodenum āĻāϰ āĻĒāĻžāĻļ⧇ āĻĒāĻžāϤāĻžāϰ āĻŽāϤ āĻĻ⧇āĻ–āϤ⧇ āϝ⧇ āĻ…āĻ™ā§āĻ—āϟāĻŋ āĻĨāĻžāϕ⧇ āϤāĻžāϕ⧇ pancreas āĻŦāϞ⧇āĨ¤pancreas āĻĨ⧇āϕ⧇ āĻŦ⧇āϰ āĻšā§Ÿ āĻ•āĻŋāϛ⧁ enzyme āĻāĻŦāĻ‚ āĻ•āĻŋāϛ⧁ hormone .

Pancreatic hormone āϏāĻŽā§‚āĻš-

  • Insulin
  • Glucagon

Pancreas hormone āϗ⧁āϞāĻŋāϰ āĻ•āĻžāϜ āωāĻ˛ā§āϞ⧇āĻ– āĻ•āϰāĻž āĻšāϞ-

Pancreas hormones āĻāĻŦāĻ‚ āϤāĻžāĻĻ⧇āϰ āĻ•āĻžāϜ-

Insulin-āχāĻšāĻž āϰāĻ•ā§āϤ⧇ glucose āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž āĻ•āĻŽāĻžā§ŸāĨ¤

Glucagon-āχāĻšāĻž āϰāĻ•ā§āϤ⧇ glucose āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž āĻŦ⧃āĻĻā§āϧāĻŋ āĻ•āϰ⧇āĨ¤

Glucose āĻ•āĻŋ? Plasma glucose āĻ•āĻžāϕ⧇ āĻŦāϞ⧇?

Glucose āĻšāĻšā§āϛ⧇ āĻāĻ•āϟāĻŋ simple carbohydrate. Glucose āĻšāĻšā§āϛ⧇ āĻāĻ•āϟāĻŋ carbohydrate āϜāĻžāϤ āĻĒāĻĻāĻžāĻ°ā§āĻĨ āĨ¤ āχāĻšāĻžāϰ āϏāĻ‚āϕ⧇āϤ C6H12O6.

Plasma glucose- āϰāĻ•ā§āϤ⧇ āωāĻĒāĻ¸ā§āĻĨāĻŋāϤ glucose āϕ⧇ Plasma glucose āĻŦāϞ⧇āĨ¤

Fasting & Random āĻ…āĻŦāĻ¸ā§āĻĨāĻžā§Ÿ Plasma glucoseāĻāϰ normal value āωāĻ˛ā§āϞ⧇āĻ– āĻ•āϰ

Plasma glucose āĻāϰ normal value –

  • Fasting āĻ…āĻŦāĻ¸ā§āĻĨāĻžā§Ÿ <6.1 āĻŽāĻŋāϞāĻŋāĻŽāϞ/ āϞāĻŋāϟāĻžāϰ
  • Random āĻ…āĻŦāĻ¸ā§āĻĨāĻžā§Ÿ <11 āĻŽāĻŋāϞāĻŋāĻŽāϞ/ āϞāĻŋāϟāĻžāϰ

Insulin āĻ•āĻŋāĻ­āĻžāĻŦ⧇ āϰāĻ•ā§āϤ⧇āϰ glucose āĻ•āĻŽāĻžā§Ÿ āĻāĻŦāĻ‚ glucagon āĻ•āĻŋāĻ­āĻžāĻŦ⧇ āϰāĻ•ā§āϤ⧇ glucose āĻŦ⧃āĻĻā§āϧāĻŋ āĻ•āϰ⧇?

Insulin stimulates the liver, muscles and fatty tissues to absorb and store extra blood glucose. So blood glucose is decreased. Glucagon stimulates the liver ,muscles and the fatty tissues to come out glucose in the blood. So blood glucose is increased.

Diabetes āĻ•āϤ āĻĒā§āϰāĻ•āĻžāϰ āĻ“ āĻ•āĻŋ āĻ•āĻŋ?

Classification of diabetes:

Diabetes Mellitus-

  • Type-1 Diabetes Mellitus
  • Type-2 Diabetes Mellitus

Gestational Diabetes

Juvenile diabetes (Childhood type 1 diabetes

Diabetes mellitus āĻ•āĻŋ? Diabetes mellitus āĻ•āϤ āĻĒā§āϰāĻ•āĻžāϰ āĻ“ āĻ•āĻŋ āĻ•āĻŋ?

Diabetes mellitus āĻāĻ•āϟāĻŋ metabolic disease.āĻĻā§€āĻ°ā§āϘāĻĻāĻŋāύ āϧāϰ⧇ āϰāĻ•ā§āϤ⧇ glucose āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž normal āĻāϰ āĻšā§‡ā§Ÿā§‡ āĻŦ⧇āĻļāĻŋ āĻĨāĻžāĻ•āϞ⧇ āϤāĻžāϕ⧇ Diabetes mellitus āĻŦāϞ⧇āĨ¤

Diabetes mellitus ⧍ āĻĒā§āϰāĻ•āĻžāϰ

Type-1 Diabetes Mellitus(DDM)

Type 2 Diabetes Mellitus(NIDDM)

Type-1 & Type 2 Diabetes Mellitus-

Type-1 Insulin dependent Diabetes Mellitus(DDM)āϕ⧇ Type-1 Diabetes Mellitus āĻŦāϞ⧇āĨ¤Type-1 Diabetes Mellitus āĻ insulin production āĻšā§Ÿ āύāĻž

Type-2 Diabetes Mellitus

Non Insulin dependent diabetes Mellitus (NIDDM) āϕ⧇ Type-2 diabetes Mellitus āĻŦāϞāĻž āĻšā§ŸāĨ¤ Type-2 diabetes Mellitus āĻ āϝāĻĨ⧇āĻˇā§āϟ āĻĒāϰāĻŋāĻŽāĻžāĻŖ insulin production āĻšā§ŸāύāĻžāĨ¤ āĻ…āĻĨāĻŦāĻž āĻĻ⧇āĻš āϕ⧋āώāϗ⧁āϞāĻŋ insulin response āĻ•āϰ⧇āύāĻžāĨ¤

Diabetes Mellitus āĻāϰ clinical features āωāĻ˛ā§āϞ⧇āĻ– āĻ•āϰ-

Clinical features of Diabetes Mellitus-

  • āϞāĻ•ā§āώāύāĻŦāĻŋāĻšāĻŋāύ
  • āϘāύ āϘāύ āĻĒā§āϰāϏāĻžāĻŦ āĨ¤
  • āĻ…āϤāĻŋāϰāĻŋāĻ•ā§āϤ āĻĒāĻŋāĻĒāĻžāϏāĻžāĨ¤
  • āĻ•ā§āϞāĻžāĻ¨ā§āϤāĻŋ āĻāĻŦāĻ‚ āĻ“āϜāύ āĻšā§āϰāĻžāϏāĨ¤
  • āϘāύ āϘāύ āĻ•ā§āώ⧁āϧāĻž āĨ¤

Diabetes Mellitus āĻāϰ investigation āϗ⧁āϞāĻŋ āĻ•āĻŋ āĻ•āĻŋ ?

Blood glucose-Random

-Fasting

-2 hours after breakfast

Urine -RME

-Ketone body

GTT(Glucose Tolerance Test)

Diabetes Mellitus āĻāϰ treatment āϕ⧇ āϏāĻ‚āĻ•ā§āώ⧇āĻĒ⧇ 3D āĻĻā§āĻŦāĻžāϰāĻž āύāĻŋāĻ°ā§āĻĻ⧇āĻļ āĻ•āϰāĻž āĻšā§Ÿ- āĻŦā§āϝāĻžāĻ–ā§āϝāĻž āĻ•āϰ-

Diabetes Mellitus āĻāϰ treatment āĻ•āϰāϤ⧇ discipline, diet āĻāĻŦāĻ‚ drug āĻāχ āϤāĻŋāύ āĻĻāĻŋāϕ⧇ āϞāĻ•ā§āώ āϰāĻžāĻ–āϤ⧇ āĻšā§ŸāĨ¤āϤāĻžāχ āĻāϕ⧇ āϏāĻ‚āĻ•ā§āώ⧇āĻĒ⧇ 3D āĻĻā§āĻŦāĻžāϰāĻž āύāĻŋāĻ°ā§āĻĻ⧇āĻļ āĻ•āϰāĻž āĻšā§ŸāĨ¤

i) Discipline -āύāĻŋ⧟āĻŽāĻŋāϤ āĻŦā§āϝāĻžā§ŸāĻžāĻŽ āĻ“ āύāĻŋ⧟āĻŽāĻŋāϤ blood glucose check up

ii) Diet-Balance diet

iii) Drug -Metformin/Insulin āχāĻ¤ā§āϝāĻžāĻĻāĻŋ āĨ¤

Islets of Langerhans āĻ•āĻŋ? Insulin & Glucagon āϕ⧋āύ āϧāϰāύ⧇āϰ āϏ⧇āϞ āĻĨ⧇āϕ⧇ āύāĻŋāσāĻ¸ā§āϰāĻŋāϤ āĻšā§Ÿ?

Pancreas āĻāϰ āϞ⧇āĻœā§‡āϰ āύāĻŋāĻ•āĻŸā§‡ āĻŦāĻŋāĻ­āĻŋāĻ¨ā§āύ āĻ¸ā§āĻĨāĻžāύ⧇ āĻ›ā§œāĻŋā§Ÿā§‡ āĻĨāĻžāĻ•āĻž āĻ•āĻŋāϛ⧁ cell āĻĨ⧇āϕ⧇ insulin āĻāĻŦāĻ‚ glucagon āύāĻžāĻŽāĻ• āĻĻ⧁āχāϟāĻŋ hormone āύāĻŋāϏāϤ āĻšā§ŸāĨ¤āĻāχ hormone āĻĻ⧁āχāϟāĻŋ āϰāĻ•ā§āϤ⧇āϰ glucagon āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž āύāĻŋ⧟āĻ¨ā§āĻ¤ā§āϰāĻŖ āĻ•āϰ⧇āĨ¤ āĻŦāĻŋāĻœā§āĻžāĻžāύ⧀ Langerhans āĻāχ endocrine āϕ⧋āώāϗ⧁āϞāĻŋ āφāĻŦāĻŋāĻˇā§āĻ•āĻžāϰ āĻ•āϰ⧇āύ āĨ¤āϤāĻžāχ āĻāϰ āύāĻžāĻŽ āĻ…āύ⧁āϏāĻžāϰ⧇ pancreas āĻāϰ endocrine gland āϕ⧇ Islets of Langerhans āĻŦāϞāĻž āĻšā§ŸāĨ¤

Diabetes Mellitus āĻāϰ āĻ•āĻžāϰāύ āϏāĻŽā§‚āĻš āωāĻ˛ā§āϞ⧇āĻ– āĻ•āϰāĨ¤

āĻ•āĻžāϰāĻŖāϏāĻŽā§‚āĻš –

  • Insulin āĻāϰ production āĻ•āĻŽā§‡ āϝāĻžāĻ“ā§ŸāĻž āĨ¤
  • āĻĻ⧇āĻšāϕ⧋āώāϗ⧁āϞāĻŋ Insulin āĻ response āĻ•āϰ⧇ āύāĻžāĨ¤
  • āωāĻĒāϰ⧇āϰ āĻĻ⧁āχāϟāĻŋ āĻ•āĻžāϰāύ⧇āϰ āωāϭ⧟āϟāĻŋāχāĨ¤

Gestational Diabetes āĻ•āĻŋ? Gestational Diabetes āĻ•āĻ–āύ āĻļ⧁āϰ⧁ āĻšā§Ÿ āĻ•āĻ–āύ āĻļ⧇āώ āĻšā§Ÿ ?

Pregnancy āĻ…āĻŦāĻ¸ā§āĻĨāĻžā§Ÿ āϕ⧋āύ āϕ⧋āύ āĻŽāĻšāĻŋāϞāĻžāϰ blood glucose āύāϰāĻŽāĻžāϞ āĻāϰ āĻšā§‡ā§Ÿā§‡ āĻŦā§‡ā§œā§‡ āϝāĻžā§Ÿ āϝāĻž āϤāĻžāϰ insulin control āĻ•āϰāϤ⧇ āĻĒāĻžāϰ⧇ āύāĻžāĨ¤ āĻ—āĻ°ā§āĻ­āĻžāĻŦāĻ¸ā§āĻĨāĻžā§Ÿ āĻāχ āϧāϰāύ⧇āϰ diabetes āϕ⧇ gestational diabetes āĻŦāϞ⧇āĨ¤ Gestational Diabetes āĻļ⧁āϰ⧁ āĻšā§Ÿ 3rd trimester āĻ āĻāĻŦāĻ‚ āĻļ⧇āώ āĻšā§Ÿ āϏāĻ¨ā§āϤāĻžāύ āϜāĻ¨ā§āĻŽā§‡āϰ āĻĒāϰ āĻĒāϰāχāĨ¤

Type-1 & TYPE-2 Diabetes mellitus āĻāϰ treatment āĻ•āĻŋ āĻ•āĻŋ āĻĻā§āĻŦāĻžāϰāĻž āĻ•āϰāĻž āĻšā§Ÿ āĻŦā§āϝāĻžāĻ–ā§āϝāĻž āĻ•āϰ-

Type-1 Diabetes mellitus āĻāϰ treatment āĻ•āϰāĻž āĻšā§Ÿ insulin āĻĻā§āĻŦāĻžāϰāĻž āĨ¤

TYPE-2 Diabetes mellitus āĻāϰ treatment āĻ•āϰāĻž āĻšā§Ÿ metaformin, gliclazide, glibenclamide, linagliptin āχāĻ¤ā§āϝāĻžāĻĻāĻŋ āĻĻā§āĻŦāĻžāϰāĻžāĨ¤

Diabetes mellitus āĻšāϞ⧇ āϘāύ āϘāύ āĻĒā§āϰāϏāĻžāĻŦ āĻšā§Ÿ āϕ⧇āύ?

Insulin āĻļ⧁āϧ⧁ glucose āĻāϰ āϰāĻ•ā§āϤ⧇āϰ āĻŽāĻžāĻ¤ā§āϰāĻžāχ āĻ•āĻŽāĻžā§Ÿ āύāĻžāĨ¤ āχāĻšāĻž āĻāĻ•āϟāĻŋ anti diuretic hormone āĻ“ āĻŦāĻŸā§‡āĨ¤ Diabetes mellitus āϰ⧋āĻ—ā§€āĻĻ⧇āϰ Insulin āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž āĻ•āĻŽ āĻĨāĻžāϕ⧇ āĻ…āĻĨāĻŦāĻž āĻ…āĻ•āĻžāĻ°ā§āϝāĻ•āϰ Insulin āĻĨāĻžāϕ⧇āĨ¤āĻĢāϞ⧇ Insulin āύāĻžāĻŽāĻ• hormone āϟāĻŋāϰ anti diuretic property āĻ•āĻŽā§‡ āϝāĻžā§ŸāĨ¤ āĻĢāϞ⧇ āĻĒā§āϰāϏāĻžāĻŦ⧇āϰ āĻŽāĻžāĻ¤ā§āϰāĻž āĻŦā§‡ā§œā§‡ āϝāĻžā§ŸāĨ¤ āĻ…āĻ°ā§āĻĨāĻžā§Ž āϘāύ āϘāύ āĻĒā§āϰāϏāĻžāĻŦ āĻšā§ŸāĨ¤

Diabetes Mellitus āĻšāϞ⧇ āĻ…āϤāĻŋāϰāĻŋāĻ•ā§āϤ āĻĒāĻŋāĻĒāĻžāϏāĻž āĻĒāĻžā§Ÿ āϕ⧇āύ?

Insulin āĻāĻ•āϟāĻŋ Anti diuretic hormone āĨ¤ Blood āĻ insulin āĻ•āĻŽā§‡ āϗ⧇āϞ⧇ āĻ…āĻĨāĻŦāĻž āĻ…āĻ•āĻžāĻ°ā§āϝāĻ•āϰ āĻĨāĻžāĻ•āϞ⧇ āĻĒā§āϰāϏāĻžāĻŦ⧇āϰ āĻŽāĻžāĻ¤ā§āϰāĻž āĻŦā§‡ā§œā§‡ āϝāĻžā§Ÿ āĨ¤ āĻāϤ⧇ blood volume āĻ•āĻŽā§‡ āϝāĻžā§ŸāĨ¤ Blood volume āĻŦ⧃āĻĻā§āϧāĻŋāϰ āϞāĻ•ā§āώ⧇ āĻ…āϤāĻŋāϰāĻŋāĻ•ā§āϤ āĻĒāĻŋāĻĒāĻžāϏāĻž āĻĒāĻžā§ŸāĨ¤

Homeostasis āĻ•āĻŋ? āωāĻĻāĻžāĻšāϰāύāϏāĻš āĻŦ⧁āĻāĻŋā§Ÿā§‡ āĻĻāĻžāĻ“āĨ¤

āĻĻ⧇āĻšā§‡āϰ āĻ…āĻ­ā§āϝāĻ¨ā§āϤāϰ⧀āĻŖ āĻ­āĻžāϰāϏāĻžāĻŽā§āϝ āϰāĻ•ā§āώāĻžāϰ āĻ•āϰāĻžāϕ⧇ Homeostasis āĻŦāϞ⧇āĨ¤ āĻĻ⧇āĻšā§‡āϰ āϏāĻ•āϞ āϕ⧋āώ āĻ•āϞāĻž āĻāχ āĻ­āĻžāϰāϏāĻžāĻŽā§āϝ āϰāĻ•ā§āώāĻž āĻ•āϰāϤ⧇ āϏāĻšāĻžā§ŸāϤāĻž āĻ•āϰ⧇āĨ¤

āωāĻĻāĻžāĻšāϰāĻŖ- āϰāĻ•ā§āϤ⧇ glucose āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž āĻŦā§‡ā§œā§‡ āϗ⧇āϞ⧇ Insulin āύāĻŋāσāϏāϰāĻŖ āĻŦā§‡ā§œā§‡ āϝāĻžā§Ÿ āφāĻŦāĻžāϰ āϰāĻ•ā§āϤ⧇ glucose āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž āĻ•āĻŽā§‡ āϗ⧇āϞ⧇ glucagon āύāĻŋāσāϏāϰāĻŖ āĻŦā§‡ā§œā§‡ āϝāĻžā§ŸāĨ¤ Insulin āĻāĻŦāĻ‚ glucagon āϰāĻ•ā§āϤ⧇ glucose āĻāϰ āĻ­āĻžāϰāϏāĻžāĻŽā§āϝ āϰāĻ•ā§āώāĻž āĻ•āϰ⧇āĨ¤

Feedback mechanism āĻ•āĻŋ? āϰāĻ•ā§āϤ⧇ glucose āĻāϰ āĻ­āĻžāϰāϏāĻžāĻŽā§āϝ āϰāĻ•ā§āώāĻžāϰ āϜāĻ¨ā§āϝ āϏāĻ‚āϘāϟāĻŋāϤ feedback mechanism āϟāĻŋ āωāĻ˛ā§āϞ⧇āĻ– āĻ•āϰāĨ¤

āϕ⧋āύ āĻ­āĻžāϰāϏāĻžāĻŽā§āϝ āϰāĻ•ā§āώāĻžāϰ āϜāĻ¨ā§āϝ āϝāĻ–āύ āĻāĻ•āϟāĻŋ āĻŦāĻ¸ā§āϤ⧁āϰ āĻŽāĻžāĻ¤ā§āϰāĻžāϕ⧇ āĻĒā§āϰāĻ­āĻžāĻŦāĻŋāϤ āĻ•āϰ⧇ āϤāĻ–āύ āϤāĻžāϕ⧇ feedback mechanism āĻŦāϞ⧇āĨ¤

glucose āĻāϰ āĻ­āĻžāϰāϏāĻžāĻŽā§āϝ āϰāĻ•ā§āώāĻžāϰ āϜāĻ¨ā§āϝ āϏāĻ‚āϘāϟāĻŋāϤ feedback mechanismāσ

āϰāĻ•ā§āϤ⧇ glucose āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž āĻŦā§‡ā§œā§‡ āϗ⧇āϞ⧇ āĻāχ āĻ…āĻ¸ā§āĻŦāĻžāĻ­āĻžāĻŦāĻŋāĻ• glucose āĻāϰ āĻŽāĻžāĻ¤ā§āϰāĻž pancreas āϕ⧇ āĻĒā§āϰāĻ­āĻžāĻŦāĻŋāϤ āĻ•āϰ⧇ glucagon āύāĻŋāσāϏāϰāĻŖ āĻāϰ āϜāĻ¨ā§āϝāĨ¤Insulin hormone āϟāĻŋ fat cell āĻ glucose āĻ—ā§āϰāĻšāύ āĻŦ⧃āĻĻā§āϧāĻŋ āĻ•āϰ⧇ āĻāĻŦāĻ‚ glucagon hormone āϟāĻŋ āϞāĻŋāĻ­āĻžāϰ āĻšāϤ⧇ glucose āύāĻŋāσāϏāϰāĻŖ āϘāϟāĻžā§ŸāĨ¤

Diabetic Related Anatomy, Histology & Cytology

Diabetes mellitus is a metabolic disease that causes specific changes at the anatomical, histological, and cytological levels, primarily in the pancreas, kidneys, eyes, nerves, and skin. 

Anatomy

Anatomically, diabetes affects multiple organs due to prolonged hyperglycemia, leading to macrovascular and microvascular damage. Key affected anatomical areas include: 

  • Pancreas: The primary organ involved, responsible for producing insulin and glucagon in the islets of Langerhans.
  • Kidneys: Damage to the kidneys leads to diabetic nephropathy, a major cause of kidney failure.
  • Eyes: Microvascular damage affects the retina, causing diabetic retinopathy.
  • Peripheral Nerves: High blood sugar injures nerves throughout the body, most often in the legs and feet, a condition known as diabetic neuropathy.
  • Cardiovascular System: Damage to large and medium-sized arteries increases the risk of heart attack and stroke.
  • Skin: Changes in blood vessels and poor circulation can lead to various skin conditions like diabetic dermopathy. 

Histology

Histological changes refer to alterations at the tissue level, often visible under a microscope using stains like hematoxylin and eosin (H&E). 

  • Pancreas:
    • Type 1 Diabetes: Characterized by lymphocytic infiltrates in the pancreatic islets (insulitis), leading to the autoimmune destruction of insulin-producing beta cells.
    • Type 2 Diabetes: Histology often shows variable degrees of islet amyloidosis (amylin deposition as a pink, hyalinized tissue), reduced beta-cell mass, and a relative decrease in beta cells compared to alpha cells.
  • Kidneys: Histological features of diabetic nephropathy include thickening of the glomerular and tubular basement membranes, expansion of the mesangial matrix, and the formation of Kimmelstiel-Wilson nodules.
  • Skin: Diabetic dermopathy shows thickening of blood vessel walls, perivascular lymphocytic infiltrates, and hemosiderin deposits. In the plantar soft tissue, the dermis of diabetic patients has been found to be significantly thicker.
  • Placenta (in gestational diabetes): Shows increased placental weight, increased number of fetal capillaries, stromal villous fibrosis, and thickening of the syncytiotrophoblast basement membrane. 

Cytology

Cytology focuses on cellular changes, often observed using exfoliative techniques (collecting cells from surfaces). 

  • Oral Mucosa: Exfoliative cytology studies in diabetic patients reveal significant cellular alterations, including:
    • Increased nuclear area and nuclear-to-cytoplasm ratio.
    • Decreased cytoplasmic size (possibly due to dehydration).
    • Qualitative changes like binucleation, granular chromatin, prominent nucleoli, and cytoplasmic vacuolization (more pronounced in diabetic persons).
    • Altered keratinization and changes in cell surface sugar chains.
  • Other Cells:
    • Adipocytes (Fat cells): Enlarged subcutaneous abdominal adipocyte size is associated with insulin resistance and an increased risk of Type 2 diabetes.
    • Neurons: Advanced type 1 diabetes is associated with changes in dorsal root ganglion (DRG) neurons, specifically in acid-sensing ion channels (ASICs).
    • Mitochondria: In diabetic subjects, microscopic features of cheek cells revealed degenerated mitochondria with abnormalities such as loss of peaks and ruptured outer membranes

Antidiabetic Drugs & Pharmacology

Antidiabetic drugs manage blood glucose levels in patients with diabetes mellitus, primarily Type 2, through various mechanisms. These medications can be oral or injectable and are often used in combination to achieve optimal glycemic control. 

The primary classes of antidiabetic drugs and their pharmacology are detailed below. 

Oral Medications

HRTD Medical Institute

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