The Diabetes Mellitus is one of the hot topics in medical career, as it is widely seen among patients. But there are not just 2 types of diabetes,as you were taught in MBBS, there are 11! Below are our notes to Diabetes Mellitus to those preparing for NEET PG Exams after MBBS. Please do correct us if any, using the comments section below.

Contents

Definition

Diabetes Mellitus can be defined by the four criteria on basis of blood tests, which are given below:

  1. Fasting Blood Glucose (8 hrs) – 126 mg%
  2. Postprandial Blood Glucose – >200 mg% (after 2 hrs. of oral GTT: 75mg)
  3. Random Blood Glucose with symptoms – 200 mg%

Triad: Polyuria, Polydipsia and Weight Loss

  1. HbA1C > 6.5%

Best – American Diabetes Association (Average estimated glucose)

EAG – Estimated Average Glucose

Estimated Average Glucose: Conversion of % HbA1C into mg% of blood glucose is as follows:

  • 6.5 % – 126 mg%
  • 9.5 % – 226 mg%

Blood > Urine > PCT > Re-absorbs 1,5 Anhydroglucitol by Mannose-Fructose-1 receptor

1,5 Anhydroglucitol

It’s a serum used to find out hyperglycemia (at least 1 episode) in past 24 hrs.

 t1/2 = 24 hrs

Normally, glucose in urine is reabsorbed by PCT via SGLT2 while 1,5-Anhydroglucitol is reabsorbed from Fructose–Mannose-1 Receptor.

SGLT-2 is inversely proportional to FM-1

Therefore, in hyperglycemia, Increase of Glucose in urine leads to increase in activity of SGLT-2. This leads to Urinary loss of 1, 5-Anhydroglucitol which results in increased activity of FM-1. Finally, it results in decreased Serum level of 1, 5-Anhydroglucitol.

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Therefore, low serum level 1, 5- Anhydroglucitol is a surrogate marker of increased BG at least once in past 24 hrs.

Types of Diabetes Mellitus

There are 11 types of Diabetes Mellitus which are as follows:

  1. Type I DM
  2. Type II DM
  3. Type III DM
  4. Type IV DM
  5. Potential DM
  6. Protein Energy DM
  7. Acute Fulminant DM
  8. Tropical DM
  9. Double Diabetes
  10. MODY Diabetes
  11. LADA Diabetes

Difference between Type 1 and Type 2 Diabetes Mellitus Chart

The difference between Type 1 Diabetes Mellitus and Type 2 Diabetes Mellitus is give below:

Type I DM Type II DM
1.   Pathogenesis Antibody – Destruction of β cells pancreas. Insulin receptor resistance.
2.   Chromosome Chromosome 6 Chromosome 2
3.   Family History 5-15% 50-70%
4.   HLA Association ++++

Increase in HLA-DR3

Decrease HLA-DR2 (Protective)

Absent
5.   Weight Loss Gain
6.   Age of Onset Younger

<30 Years

Older

>30 Years

7.   Serum Insulin Low (Insulinopenia) Increases (Causes destruction of β cells
8.   Complications Diabetic Ketoacidosis Hyperosmolar Non-Ketotic Coma

Antibody in Type 1 Diabetes Mellitus

Usually questions asked:

  1. M/C – Antibody to inlet cells of pancreas.
  2. Anti- Insulin Antibody
  3. Anti – GAD (Glutamic Acid Decarboxylase) Antibody

Type I Diabetes Mellitus

Initial 1-3 Years after this, when insulin requirement is lesser than usual. (Honeymoon period of Type I Diabetes Mellitus).

Type III Diabetes Mellitus

Causes of Type 3 Diabetes Mellitus are given in the chart below:

Drug Induced Endocrine Defect Alzheimer’s Dementia
  1. Steroids
  2. Thiazides
  3. Clozapine
  4. Protein Inhibitors
  5. Phenytoin
  6. β-agonist
  1. Cushioning
  2. Hyperthyroidism
  3. Pheochromocytoma
  4. Acromegaly
  1. Brain Diabetes
  2. Insulin secretion to maintain its neuron (paracrine) > Decreased after 60 years > May lead to Memory Loss

Type IV Diabetes Mellitus

Gestational DM

Potential Diabetes Mellitus

If Single (15%) or both (40%) parents are diabetic, there’s increased chance in offspring, even though offspring may have normal Blood Glucose.

Acute Fulminant Diabetes Mellitus

  • Viral Infection – HIV / EBV (Mass destruction of β cells leading to Hyperglycemia)
  • Common in Pregnancy
  • Reversible – in about 80% cases

Protein Energy Diabetes Mellitus

  • Because of Insulin Deficiency (PEM), there is hyperglycemia
  • No need of Anti-Diabetic Drugs, but just nutritional support

LADA Diabetes Mellitus (Latent Autoimmune Diabetes of Adults)

  • Similar to Type I DM in Adults
  • Antibodies are more but less severe autoimmune DM as compared to DM 1
  • Decreased mass of β cell of pancreas

Treatment

Oral Hypoglycemic drugs:

  • Insulin for 2-3 Years
  • Type 2 (hence one and a half Diabetes)

MODY (Maturity Onset Diabetes of the Young)

  • Pathophysiology – Insulin secretion defect.
  • Similar to Type II in young.

Features

  1. Thin built
  2. HTN/CAD Risk low
  3. Mild Hyperglycemia
  4. Autosomal Dominant

Types

There are 26 types of MODY, most common types are given below:

Type Gene Defect Chromosome
MODY-3 HNF1 Alpha Chromosome 12
MODY-1 HNF4 Alpha Chromosome 20
MODY-2 Glucokinase Chromosome 7

Features

  1. Autosomal dominant
  2. Mild Hyperglycemia
  3. Age of onset – 20 to 30 Years.
  4. More risk of developing HTN/CAD but less as compared to type II DM.
  5. BMI – <25
  6. Auto antibodies – absent ( + only in case of LADA & Type I DM)

Treatment

  • MODY-3: Insulin
  • MODY-1, MODY-2 & rest: OHA followed by insulin

ADPKD

Autosomal Dominant Polycystic Kidney Disease caused involving Chromosome 16 and Chromosome 4.

RCAD – Renal Cyst and Diabetes, meaning ADPKD + MODY-5.

Acute Complications of Diabetes Mellitus

  1. Diabetic Ketoacidosis (Type 1) – Hyperglycemia

Precipitating factors include Non-compliance to treatment and Infection

  1. Hyperosmolar Non-Ketotic Coma (Type II)

Diabetic Ketoacidosis

Life threatening complication of Type I DM leading to excessive Ketone body formation.

Precipitating Factors

  1. Non compliance to Treatment.
  2. Infection
  3. MI
  4. Stroke

Clinical Features

  1. Fever – if infection is precipitating cause
  2. Acute epigastic pain repeated (Nausea/Vomiting)
  3. Dehydration
  4. Feeble Pulse, Hypotension
  5. Altered sensorium in severe cases because of hyposmolality of blood
  6. Similar to Pancreatitis

Lab Investigations

  1. Blood Sugar is Greater than 400 mg%
  2. Serum Osmolality is 320-350 mOsmol/l
  3. Urinary Ketones – More
  4. Arterial Blood Gas – Metabolic Acidosis (In Kidney) due to Ketonuria leads to less HCO3 absorption in PCT and High anion gap.
Metabolic Acidosis
High Anion Gap Normo (Chloromic 10±2)
DKA Renal Tubular Acidosis
Lactic Acidosis Cholera
Alcoholic Acidosis Ureterosigmoidostomy

 

  1. Na+ – Decrease in Pseudohyponatremia
  2. K+ Hyperkalemia (Potassium move from Extra-cellular fluid to Intra-cellular fluid due to decreased insulin)

Pseudohyponatremia in:

  1. Paraprotein Increases
  2. Cholesterol Increases
  3. Glucose Increases

Leading to:

  1. Multiple Myeloma
  2. Dyslipidemia
  3. Diabetic Ketoacidosis
  • Na comes lane from Autoanalyser due to defect.
  • Every 100 mg% increase in Glucose results in Decrease in 1.6mg/L in Na.

If,

Na+ is Increased (Normal in tests after Autoanalyser) > Excessive dehydration in diabetic Ketoacidosis

K+ is Decreased > Hyperkalemia (K+ in loss of GIT Contents) and severe dehydration

Difference between Diabetic Ketoacidosis and HyperOsmolar Non-Ketotic Hyperglycemic Coma (DKA vs HONK or HHS)

Diabetic Ketoacidosis Hyper-Osmolar Non-Ketotic Coma
1. Occurs in Type I Type II
2. S. osmolality 320-350 mosm >350 mosm
3. Blood Sugar >400 mg% >800 mg%
4. Expected fluid loss 4-6 L 8-10 L
5. Prognosis Less dangerous More dangerous

 

Treatment

  1. IV Fluids

Normal Saline (15-20ml/Kg/Hour for first 2-3 hrs followed by 200ml/hour till BG < 250 mg%)

  1. Insulin Infusion

I/V or Regular (plain)

0.15 IV/kg bolus dose followed by 0.1 IV/kg/hr flood glucose monitoring

Insulin Types: Regular, Ultra-short, Intermediate and Long Acting

  1. Potassium Replacement

10-20 mEq/hr K+ monitoring.

Treatment will eventually lead to hypokalemia from Hyperkalemia.

  1. Bicarbonate Replacement – No

Prognosis: 15-20% die even after best treatment

Complications

  1. Cerebral Edema (M/C of death in DKA)
  2. Arterial & Venous Thrombosis
  3. ARDS

Incretins

Substance released from stomach in response to oral glucose which potentiate or enhance the blood sugar lowering effect of stomach.

  • GIP – Gastric inhibitory peptide
  • GLP Agonist – Glucagon – A peptide

GLP Agonist-1

Eg. – Exanitide, Liraglutide

Side Effects
  1. Most common – Nausea/Vomiting
  2. Weight Loss – severe
  3. Bladder Cancer (Most dangerous)

Gliptans

Endogenous GLP-1 is converted to by-products through DPP 4. These Gliptan drugs prevent degradation of GLP-1 by inhibiting DPP 4, hence more availability of GLP-1 and decrease in blood sugar.

Examples: Sitagliptin, Saxagliptin, Vildagliptin, Linagliptin, Alogliptin

New Medications of Diabetes Mellitus

Given below are the newer drugs for DM:

  1. Gliptins
  2. Resveratrol – Anti-oxidant – decreases 20X doses antioxidant properly
  3. Colesevelam – bile and sequestrant
  4. Pramlintide (in both type 1 & 2) – Amylin analog – decreases glucagon levels in body causing hypoglycemia
  5. Fasiglifama free fatty acid Receptor Agonist. It’ll increase insulin secretion. FFAR-1 acts on beta cells.

Double Diabetes – Type I DM

Insulin requirement is increased in Insulin resistance (Type II DM). In patients of Type I DM, upon 5-8 years of onset, there is development of insulin resistance, i.e, feature of Type II DM, hence labelled as Double Diabetes.

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