1. HAMDARD PUBLIC SCHOOL
2022-2023
BIOLOGY
INVESTIGATORY PROJECT
By: Gaurav
11thB-2

2. This is to certify that GAURAV Of Class XI-b2 has successfully completed
His BIOLOGY project on the topic Diabetes MELLITUS as prescribed by MR.
ABUSHAMA During the academic year 2022-2023 as per the guidelines by cbse.
Name of examiner: name of teacher:
Signature: Signature:

3. I would like to express my special thanks of gratitude
to my teacher Mr. Abushama, who gave me the
golden opportunity to do this wonderful project of
Biology on “Diabetes Mellitus”, Who also helped me
in completing my project. I came to know about so
many new things I am really thankful to them.
Secondly I would also like to thank my parents and
friends who helped me a lot in finalizing this project
within the limited time frame.

4. DIABET
ES
MELLIT
I
4

5. A metabolic disorder of Multiple
aetiology characterized by chronic
hyperglycemia with disturbances of
carbohydrate, fat and protein metabolism
resulting from defects in Insulin
secretion, insulin action or both.
5

6. PREDISPOSING FACTORS
1. Heredityis the most common
predisposing factor.
2. Obesity, where adipose tissues are more
resistant to actions of insulin as compared
to normal (non- obese).
6

7. TYPES AND STAGES OF DIABETES
MELLITUS
PRIMARY DIABETES
MELLITUS
2 TYPES
SECONDARY DIABETES
MELLITUS
INSULIN
DEPENDENT
DIABETES
MELLITUS
NON INSULIN
DEPENDENT
DIABETES
MELLITUS
• PANCREATITIS
• CYSTIC
FIBROSIS
• ACROMEGALY
• CUSHING
SYNDROME
TYPE I TYPE II
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8. 8

9. TYPE I VS TYPE II DIABETES MELLITUS
GENERAL
FEATURES
TYPE 1 TYPE II
DEFECT • Autoimmune disorder
• Antibody destroys the β- cells of Islets of
Langerhans
• Absolute deficiency of insulin
• Genetic disorder
• Decreased Insulin receptors
• Resistance to extrahepatic/
peripheral targeted tissues
PREVALENCE 10-20% of diabetic population 80-90% of diabetic population
AGE OF ONSET < 40 years > 40 years
BODY WEIGHT Low (lean and thin) High ( obese or normal)
GENE LOCUS Chromosome 6 Chromosome 1
• Why does Type 1 DM associated with low body weight as compared to type II DM?
Renal Glycosuria, Lipolysis
9

10. CONTD.. (CLINICAL COMPARISON)
CLINICAL FEATURES TYPE 1 TYPE II
DURATION OF SYMPTOMS WEEKS (rapid) MONTHS TO YEARS (slow)
PRESENTING SYMPTOMS
POLUDYPSI
DIFFERENT COMPLICATIONS
• Achanthosis nigricans –
patches on skin
• slow healing of wounds
COMPLICATIONS AT THE TIME
OF DIAGNOSIS
ABSENAT PRESENT (in 10-20% cases)
ACUTE COMPLICATIONS KETOACIDOSIS HYPEROSMOLAR COMA
Achanthosis
nigricans
10

11. BIOCHEMICAL FEATURES AND
TREATMENT
BIOCHEMICAL FEATURES
AND TREATMENT
TYPE 1 TYPE 11
PLASMA INSULIN DECREASED OR ABSENT NORMAL OR INCREASED
AUTOANTIBODIES PRESENT RARE
KETONURIA PRESENT ABSENT
TREATMENT INSULIN (oral hypoglycemics
not required)
ORAL HYPOGLYCEMICS
not required)
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14. SYNDROME X
14

15. SYMPTOMS AND SIGNS
POLYURIA
POLYDYPSIA
POLYPHAGIA
WEIGHT LOSS IN SPITE OF POLYPHAGIA
HYPERGLYCEMIA
GLYCOSURIA
KETOSIS
ACIDOSIS
DIABETIC COMA
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16. PATHOPHYISOLOGY OF DIABETES MELLITUS
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17. COMPLICATIONS OF DIABETES MELLITUS
NON- KETOTIC COMA
ACUTE KETOTIC COMA
ATHEROSCLEROSIS
CHRONIC
PRE- DISPOSING INFECTIONS
Prolonged DYSLIPIDEMIA
&
HYPERCHOLESTEROLEMIA
Tunica intima of blood vessels (
coronary, peripheral and cerebral
arteries
Microangiopathy Capillary basement
membrane becomes
thicker
• Diabetic Retinopathy
• Diabetic Neuropathy
• Diabetic Nephropathy
17
Deposition of lipid underneath the

18. HYPERGLYCEMIA AND ITS CONSEQUENCES
• Increased blood glucose level
• Absence of Insulin
• Characteristic feature of
Uncontrolled Diabetes Mellitus
• Decreased peripheral utilization
of glucose
• Increased hepatic output of
glucose to carry out
glycogenolysis and
gluconeogenesis.
18

19. 1. GLYCOSURIA
OSMOTIC
DIURESIS
POL
YURIA
POL
YDYPSIA
LOSS OF ELECTROLYTE
Na+, K+, PO4
3-
LOSS OF BODY WEIGHT
POLYPHAGIA
CELLULAR
DEHYDRA
TION
19

20. 2. IMPAIRED PHAGOCYTOSIS
Hyperglycaemia impairs
all aspects of leucocytic phagocytic function, i.e.
adherence,
diapedesis, phagocytosis and intracellular killing.
Because of
impaired phagocytic function, the diabetics are more
prone
to infections as compared to the non-diabetics.
20

21. 3. GLYCOSYLATION OF PROTEINS
Glycosylation of tissue proteins
Occurs when the blood glucose levels
remain elevated for a prolonged duration
(years). Glycosylation leads to irreversible
changes in the chemical structure of tissue
proteins. These chemical changes have
been implicated in producing long-term
complications of diabetes mellitus, such as:
• Diabetic nephropathy,
• Diabetic retinopathy,
• Diabetic neuropathy and so on.
Glycosylation of haemoglobin.
Glycosylated haemoglobin refers to the
glucose-derived products of normal
hemoglobin(HbA).
• Among the glycosylated hemoglobins, the
most abundant form is HbA1C, which is
produced by condensation of glucose with N-
terminal valine of each β chain of hemoglobin
A (HbA).
• Normally, HbA1C concentration is about 3–
5% of the
total haemoglobin.
• During sustained hyperglycemia, as in
diabetes mellitus, the concentration of
HbA1C may be elevated to 10–20% of the
total hemoglobin.
• Determination of HbA1C has become an 21

22. 4. HYPERTRYGLYCERIDAEMIA
INCREASED ACTIVITY OF HORMONE
SENSITIVE TG LIPASE
22
INC. CHOLESTEROL SYNTHESIS
INC. TG SYNTHESIS
INC. FFA PRODUCTION
INCREASED LIPOLYSIS
INSULIN DEFICIENCY

23. 5. KETOSIS
INCREASED PLASMA
KETONE BODIES LEVEL
CELLULAR
DEHYDRATION
Rapid Deep Respiration
(Dyspnea, KUSSMAUL breathing)
Acetone smell in patient’s
breathe
Acidic urine due to ketonuria
Electrolyte loss
Hypovolemia and Hypotension
Coma and death
23

24. EFFECT ON PROTEIN CATABOLISM
INSULIN
PROMOTES PROTEIN SYNTHESIS
(-) PROTEIN
ANABOLISM IS
SUPPRESSED
(-) CATABOLISM
INCREASED
INHIBITS PROTEOLYSIS
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Protein depletion in
the body
Muscle Wasting
Negative
Nitrogen balance

25. HYPOGLYCAEMIA IN DIABETICS
Hypoglycaemia in diabetics is more common in diabetics than in non-
diabetics. About 4% deaths of IDDM are said to be due to hypoglycaemia.
OVERDOSE OF
ANTIDIABETIC
DRUGS ( INSULIN)
MISMATCH B/W INSULIN
ADMINISTRATION AND
FOOD HABITS
HEAVY EXERCISE
ALCOHOL INTAKE
INTAKE OF TOO LITTLE
OR NO FOOD
25

26. HYPOGLYCAEMIA
NEUROGLYCOPENIC
SIGNS
CNS becomes excitable
• Hallucination
• Extreme nervousness
• Tremors
• Confusions
• Drowsiness
• Convulsions
• Palpitation
• Tachycardia
• Sinus Arrhythmia
SYMPTOMS
26
CVS
GIT
DERMATOLOGICAL
• Vomiting
• Nausea
• Sweating
• Hypothermia

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30. MADE BY: GAURAV
SUBJECT TEACHER: MR.ABUSHAMA