ARISHA IBRAHIM

ROLL NO. 105

2nd YEAR MBBS

“DIABETES MELLITUS”

LAY OUT Definition

Types

Etiology

Sign/symptoms

Complications

Ketoacidosis

Diagnosis

Treatment

References

Acknowledgements

DEFINITION “It is a metabolic syndrome of impaired Carbohydrate,Lipid & protein metabolism characterized by “Hyperglycemia” either due to insufficient insulin or defective insulin receptors leading to Polyuria, Polydipsia & Polyphagia.”

TYPES OF DM1) Type 1 DM

2) Type 2 DM

Type 2 is further classified as:

• Non-Obese Type 2 DM

• Obese Type 2 DM

TYPE 1 DM

Due to Insulin deficiency also called :

Insulin Dependent DM (IDDM)

Juvenile onset DM

TYPE 2 DM

Due to combined insulin resistance & decrease insulin secretions also known as :

Noninsulin Dependent DM (NIDDM)

Adult onset DM

SUB TYPES OF NIDDMNON-OBESE TYPE

2 DM

Do not show the early phase of insulin release in response to raised Plasma glucose but B cells do respond to other Insulinogenicstimuli.

OBESE TYPE 2 DM

Insulin Resistance cause Hyperplasia of B cells .Hyperinsulinemiacause Down Regulation of insulin receptors. Obesity is of Abdominal type (Apple Like ).

ETIOLOGYOF

TYPE 1DM TYPE2 DM

• Autoimmune Diseases

• Idiopathic

• Environmental Factors

Mumps

Rubella

Viruses

• Nutrients

Cow milk

• Mutation of insulin receptor Gene (19)

• Auto antibodies to insulin receptor

• Obesity

• Hemo-chromatosis

FACTORS CAUSING INSULIN RESISTANCE

Obesity

Excess Glucocorticoids

Excess Growth Hormone

Lipodystrophy

Ploycystic Ovary Disease

Mutation in Insulin Receptor

Contraceptive agents

B cell Adenoma

Other causes

16

17

SIGN/SYMPTOMS

o Glucosuria

o Polyuria

o Poydipsia

o Polyphagia

o Weight Loss

o Hyperlipedemia

COMPLICATIONS OF DM

EARLY

Ketoacidosis

Coma

Late Complications

Macrovascular

Microvascular

A. MACROVASCULAR

• Atherosclerosis of

Coronary Vessels

• Cerebral Accidents

(stroke)

B. MICROVASCULAR Diabetic Retinopathy

Diabetic Cataract

Diabetic Nephropathy

Proteinuria + Hypertension + Edema

( KIMMELSTEL-WILSON SYNDROME)

Diabetic Neuropathy

Diabetic Gangrene

EARLY Complications

• Diabetic Ketoacidosis

DKA

• Common

in Type 1

• Hyperosmolar

Hyperglycemic

Nonketotic

syndrome

HHNS

• Common

in Type 2

DKAInsulin + Glucagon

Hormone Sensitive Lipase

Lipolysis + Fatty acid oxidation

KETONE BODIES

(8-15mmol/l)

Ketonemia

Ketonuria

Ketoacdisis

Coma

HHNSBlood

glucose+Cellular

dehydration

Hyperosmolarity

(340mOsm/l)

Brain cells shrinkage

Coma

SIGN/SYMPTOMSDKA

1. Hyperglycemia

2. Nausea

3. Air Hunger

4. Fruity Breath Odor

5. Hypotension

6. Tachycardia

7. Abdominal Pain

8. Fatigue

HHNS

1. Altered Consciousness

2. Hyperthermia

3. Motor & sensory impairment

4. Seizures

5. Dry skin & Mucous Mem.

6. Hypotension

7. Extreme thirst

8. Hperglycemia

CLINICAL FEATURES OF DKA

DIAGNOSISDKA

• Metabolic Acidosis

• Blood Glucose is relatively low 350mg/dl

• Ketone bodies in Urine

• Low Bicarbonate & Blood ph

HHNS• No acidosis

• Blood glucose level is up to 800-1000 mg/dl

• Altered Level of Consciousness

• No fruity smell of Breath

MANAGEMENTDKA

Intravenous Fluids

Administration of Potassium

Administration of Sodium Bicarbonate

Insulin

Mannitol /Hypertonic saline 3% to treat Cerebral Edema

HHNS

Intravenous Fluids to treat Dehydration

Electrolyte Replacementspecially K+

Insulin to lower blood Glucose level

INSULIN SHOCK & HYPOGLYCEMIA

Type 1 DM

Insulin therapy/Missing meals/ Excersise

Sign/symptoms

• Blood Glu (50-70mg/100ml) CNS excites

• Hallucinations

• Trembling/sweating

• Blood Glu (20-50mg/100ml)

• Clonic Seizures/Unconsciousnes

• Coma

DIAGNOSIS

• low blood Glucose level

• No rapid deep breathing

TREATMENT

• Iv Glucose

• Glucagon

• Epinephrine

DIAGNOSTIC TEST FOR DMo GLUCOSURIA

To detect Glucose in Urine

by a Paper Strip Method

o FASTING BLOOD GLUCOSE LEVEL

Normal : 60-110 mg/dl

Impaired: 110-126 mg/dl

Abnormal: >126 mg/dl

o RANDOM BLOOD GLUCOSE LEVEL

Normal : 110-140 mg/dl

Impaired : 140-200 mg/dl

Abnormal: >200 mg/dl

o GLUCOSE TOLERANCE TEST (GTT)

• Indicate Milder or Early DM

Standard Oral GTT

Intravenous GTT

FASTING

2Hrs

Normalmg/dl

100

<140

Impairedmg/dl

100-125

140-199

Diabetesmg/dl

>126

>200

o GLYCOSYLATED HAEMOGLOBIN HbA1c

• Normally it contains 4-6% of

total Hb

• In case of DM its is >7%

TREATMENT OF DM

Non pharmacological Therapy

Pharmacological Therapy

NON PHRAMACOLOGICAL THERAPY

DIET1. TYPE 1 DM :

Fat + Cholesterol+ Carbohydrate

2. TYPE 2 DM : (Cont’d)

“Caloric” Restriction

( Cont’d)

• ARTIFICIAL

SWEETNERS

Aspartate

Saccharin

Acesulfame

• NUTRITIVE SWEETNERS

Fructose

Sorbitol

ACTIVITYExercise should start slowly in patients to enhance Insulin sensitivity

PHARMACOLOGICAL THERAPY

o INSULIN both for DM Type 1 & 2

o Drugs Inc. Insulin sensitivity :

Thiazolidinedione

Metformin

Troglitazone

o Drugs Inc. Insulin Release :

Sulfonylureas

(Glyburide & Tolbutamide)

o α- Glucosidase Inhibitors

REFERENCESo Harrison’s Principles Of Internal

Medicine (17th Edition)

o William’s Book Of Endocrinology

(11th Edition)

o Guyton & Hall Physiology

(12th Edition)

o Medical Biochemistry By Mushtaq

Ahmad (7th Edition)

o Textbook Of Medical Biochemistry By MN.Chatterjea (8th Edition)

o Wikipedia

ACKNOWLEDGEMENTS• ALLAH ALMIGHTY

• Prophet (SAW)

• My Parents

• HOD of Biochemistry

“Dr. Khawaja Muhammad Fayyaz”

• My Sister

Dr. Sidra Zafar

• My Friends