1. DIABETES MELLITUS

2. PRESENTED BY ,
PRIYANKA GUND

3. 1. INTRODUCTION
2. DEFINITION
3. SYNTHESIS , METABOLISM , ACTION OF
NORMAL INSULIN
4. CLASSIFICATION
5. SYMPTOMS
6. PATHOPHYSIOLOGY

4. 6. COMPLICATIONS
7. DIAGNOSIS
8. TEST FOR DIAGNOSIS OF DIABETES
MELLITUS

5. INTRODUCTION
 IT IS DISORDER OF ENDOCRINE PANCREAS.
 NORMAL STRUCTURE OF PANCREAS :-
TOTAL WEIGHT :- 60 – 100 gm
CELLS OF PANCREAS :- ISLET OF
LANGERHANS
 ISLET POSSESS NO DUCTAL SYSTEM & THEY
DRAIN THEIR SECRETORY PRODUCT DIRECTLY
INTO THE CIRCULATION.

6.  4 MAJOR TYPES OF CELLS

8.  2 MINOR TYPES OF CELLS

9. DEFINITION
 AS PER WHO,
“ DIABETES MELLITUS IS
DEFINED AS HETEROGENOUS METABOLIC
DISORDER CHARATERISED BY COMMON
FEATURE OF CHRONIC HYPERGLYCAEMIA
WITH DISTURBANCE OF CARBOHYDRATE
PROTEIN , FAT , METABOLISM.”

10.  ANOTHER DEFINITION,
“ DIABETES MELLITUS IS A
METABOLIC DISORDER CHRACTERISED BY THE
PRESENCE OF HYPERGLYCAEMIA DUE TO
DEFECTIVE INSULIN SECRETION , DEFECTIVE
INSULIN ACTION & BOTH.”

11. SYNTHESIS OF INSULIN
 OCCURS IN ROUGH ENDOPLASMIC RETICULUM
OF BETA CELLS IN ISLET OF LANGARHANS.
INSULUN SYNTHESIZED AS
PROTEOLYSIS
PREPROINSULIN
PEPTIC CLAVAGE
PROINSULIN
INSULIN C-PEPTIDE

12.  AT THE TIME OF SECRETION C-EPTIDE IS
DETACHED

13. METABOLISM OF INSULIN
 BINDING OF INSULIN TO RECEPTOR IS
ESSENTIAL FOR ITS REMOVAL FROM
CIRCULATION & DEGRADATION.
 INSULIN IS DEGRADED IN LIVER & KIDNEY
BY A CELLLULAR ENZYME CALLED INSULIN
DEGRADING ENZYME.

15.  CURRENT CLASSIFICATION BASED ON
ETIOLOGY :-
1. TYPE 1 DIABETES MELLITUS
2. TYPE 2 DIABETES MELLITUS
3. OTHER SPECIFIC TYPE OF DIABETES
MELLLITUS
4. GESTATIONAL DAIBETES MELLITUS

16. SINGS & SYMPTOMS
 INCREASED THIRST ( POLYDIPSIA )
 FREQUENT URINATION ( POLYURIA )
 EXTREME HUNGER ( POLYPHAGIA )
 WEIGHT LOSS
 PRESENCE OF KETONE IN URINE
 FATIGUE
 BLURRED VISION

17.  SLOW HEALING SORES
 HIGH BLOOD PRESSURE
 FREQUENT INFECTION

18. 1. TYPE 1 DIABETES MELLITUS :-
“ AN AUTOIMMUNE DISEASE THAT
OCCURS WHEN T CELLS ATTACK & DESTORY
MOST OF THE BETA CELLS IN THE PANCREAS
THAT ARE NEEDED TO PRODUCE INSULIN , SO
THAT THE PANCREAS MAKES TOO LITTLE
INSULIN OR NO INSULIN ”.

19.  TYPE 1 CLASSIFICATION :-
I. TYPE 1A – IMMUNE MEDIATED :-
“ IT IS CHARACTERISED BY
AUTOIMMUNE DESTRUCTION OF BETA CELLS
WHICH USUALLY LEADS TO INSULIN
DEFICIENCY ”.

20. II. TYPE 2B – IDIOPATHIC :-
“ IT IS CHARACTERISED BY
INSULIN DEFICIENCY WITH TENDENCY TO
DEVELOP KETOSIS BUT THESE PATIENTS ARE
NEGATIVE FOR AUTOIMMUNE MARKERS ”.

21. PATHOPHYSIOLOGY OF TYPE 1
I. GENETIC SUSCEPTIBILITY :-
a. UNION IN IDENTICAL TWINS 50 %-
MUTATION OF GENE DUE TO INSULIN DEFICIENCY
BETA CELLS MAY HAVE TO WORK HARDER TO PRODUCE INSULIN
STRESS ON BETA CELL INCREASES
STIMULATES AUTOIMMUNE PROCESS
INCREASES BETA CELL STRESS

22. II. AUTOIMMUNE FACTOR :-
a. INSULITIS –
OCCURRENCE OF LYMPHOCYTIC INFILTRATE IN &
AROUND THE PANCREATIC ISLET .
b. DESTRUCTION OF BETA CELL –
GENERALLY INFLAMMATION PLAY VITAL ROLE IN
BETA CELL DESTRUCTION . BUT PRECISE FACTOR ARE
NOT KNOWN .
A PROTIEN BASED ENZYME FOUND IN BETA
CELL PRODUCES SPECIFIC LIPIDS THAT CAUSE
INFLAMMATION & LEAD TO DEATH OF BETA CELLS

23. III. ENVIRONMENTAL FACTOR :-
a. VIRAL INFECTION
b. EXPERIMENTAL INDUCTION WITH
CHEMICAL
c. GEOGRAPHIC

24. 2. TYPE 2 DIABETES MELLITUS :-
“THE BASIC METABOLIC
DEFECT IN TYPE 2DM IS EITHER DELAYED
INSULIN SECRETION RELATIVE TO GLUCOSE
LOAD OR THE PERIPHERAL TISSUES ARE
UNABLE TO RESPOND TO INSULIN ”.

25. PATHOPHYSIOLOGY OF TYPE 2
I. GENETIC FFACTOR :-
a. GENETIC COMPONENT HAS A STRONGER
BASIS FOR TYPE 2DM THAN TYPE 1DM .
b. UNION IN IDENTICAL TWINS 80% -
PERSONS WITH ONE PARENT HAVING TYPE
2DM IS AT AN INCREASED RISK OF
GETTING DIABETICS .

26. II. CONSTITUTIONAL FACTORS :-
a. OBESITY
STRESS THE MEMBRANOUS
NETWORK INSIDE THE CELL
WEAKEN THE INSULIN RECEPTOR
INCREASES BLOOD SUGER LEVEL

27. b. HYPERTENSION :-
OCCURS BECAUSE OF A NARROWING
IN THE ARTERIES CAUSED BY CONTINUED &
CONSISTENTLY HIGH BLOOD GLUCOSE LEVEL .

28. III. INSULIN RESISTANCE :-
a. LACK OF RESPONSIVENESS OF PERIPHERAL
TISSUE TO INSULIN SPECIALLY SKELETAL
MUCSLE & LIVER .
IV. IMPAIRED INSULIN SECRETION :-
a. IN CASE OF TYPE 2DM HAVE MILD
DEFICIENCY OF INSULIN BUT NOT ITS
TOTAL ABSENCE .

29. IV. INCREASED HEPATIC GLUCOSE SYNTHESIS :-
a. TYPE 2DM PART OF INSULIN RESISTANCE BY
PERIPHERAL TISSUE & LIVER .
b. INSULIN SUPRESS GLYCONEOGENESIS
DUE TO GF , CF , IR
GLYCONEOGENESIS IN LIVER IS NOT
SUPRESSED
INCREASES HEPATIC SYNTHESIS OF
GLUCOSE
HYPERGLYCAEMIA

30. 3. OTHER SPECIFIC TYPES OF DIABETES
MELLITUS :-
I. GENETIC DEFECT OF BETA CELL
II. GENETIC DEFECT IN INSULIN ACTION
III. DISEASE OF EXOCRINE PANCREASE
IV. DRUG OR CHEMICAL INDUSED
V. INFECTIN

31. 4. GESTATIONAL DIABETES MELLITUS :-
“ IT IS DEFINED AS ANY
DEGREE OF GLUCOSE INTOLERANCE WITH
ONSET OR FIRST RECOGNITION DURING
PREGNANCY ”.
DURING PREGNANCY THE PLACENTA
PRODUCES HIGH LEVELS OF VARIOUS OTHER
HORMONS.
ALMOST ALL OF THEM IMPAIR THE ACTION
OF INSULIN IN CELLS & RAISING BLOOD
SUGER.

32. COMPLICATIONS
 2 MAJOR GROUPS :-
I. ACUTE METABOLIC COMPLICATIONS :-
 DIABETIC KETOACIDOSIS
 HYPEROSMOLAR NONKETOTIC COMA
 HYPOGLYCAEMIA

33. II. LATE SYSTEMIC COMPLICATIONS :-
 ATHEROSCLEROSIS
 DIABETIC MICROANGIOPATHY
 DIABETIC NEUROPATHY
 DIABETIC RETINOPATHY

34.  KETOACIDOSIS :-
SEVERE LACK INSULIN
LIPOLYSIS IN ADIPOSE TISSUE
RELEASE OF FREE FATTY ACID IN PLASMA
OXIDATION IN LIVER
KETOACIDOSIS

36.  HYPEROSMOLAR HYPERGLYCAEMIC
NONKETOTIC COMA :-
INSULIN DEFICIENCY
HYPERGLYCAEMIA
GLYCOSURIA
DECRESED ANABOLISM
OSMOTIC DIURESIS
DEHYDRATION
& LOSS OF ELECTROLYSIS
DIABETIC COMA

37.  ATHEROSCLEROSIS :-
INSULIN DEFICIENCY
INCREASES BLOOD GLUCOSE
MORE IN SYNTHESIS
FAT DEPOSITION IN LARGE VESSELS
EVIDENCE OF THROMBOTIC STATE
ATHEROSCLEROSIS

38. ILL EFFECT :-
i. CORONARY ARTERY DISEASE
ii. SILENT MYOCARDIA INFARCTION
iii. GANGRENE OF TOE & FEET

40.  MICROANGIOPATHY :-
CHARACTERISED BY BASEMENT MEMBRANE
THICKING OF SMALL BLOOD VESSELS
HYPERGLYCAEMIA
INCREASED GLYCOSYLATION OF Hb
INCREASES BASEMENT MEMBRANE
OF VESSELS

41.  NEPHROPATHY :-
HYPERGLYCAEMIA
GLOMERULAR HYPERTENSION
RENAL HYPERPERFUSION
DEPOSITION OF PROTEIN
GLOMERULOSCLEROSIS
RENAL FAILUER

42.  NEUROPATHY :-
HYPERGLYCAEMIA
TRYGLYCERIDES SUGER AUTOXIDATION POLYOL PATHWAY
OXIDATIVE STRESS
ENDOTHELIAL DYSFUNCTION
DECREASES CAPILLARY FLOW
NERVE DYSFUNCTION
NERVE REGENERATION

44.  RETINOPATHY :-
DIABETES AFFECT ON BLOOD VESSELS IN
RATINA THE TISSUE WHICH LINES THE
INNER EYE .
CAUSES PERMENANT RETINAL BLOOD
VESSEL CHANGES LIKE OBSTRUCTION TO
INNER FLOW OF BLOOD , LEAKAGE &
ABNORMAL GROWTH .

45.  2 STAGES :-
I. NON – PROLIFERATIVE :-
FAT & PROTEIN FLUID LEAKAGE
DEPOSITED IN RATINA .
II. PROLIFERATIVE :-
ABNORMAL GROWTH OF BLOOD VESSELS
& TISSUE AROUND THE VESSELS IN RATINA .

47. A1C
( PERCENT )
FASTING PLASMA
GLUCOSE
( Mg/dL )
ORAL GLUCOSE
TOLERANCE
TEST
( Mg/dL )
DIABETES 6.5 OR ABOVE 126 OR ABOVE 200 OR ABOVE
PREDIABETES 5.7 TO 6.4 100 OR 125 140 TO 199
NORMAL ABOUT 5 99 OR BELOW 139 OR BELOW

48. TEST FOR DIAGNOSIS
 URINE TEST
 SINGLE BLOOD SUGER ESTIMATION
 SCREENING BY FASTING GLUCOSE TEST
 ORAL GLUCOSE TOLEANCE TEST

49. BIBLIOGRAPHY
BOOK NAME AUTHER NAME EDITION
TEXT BOOK OF
PATHOLOGY
HARSH MOHAN 7th EDITION
MEDICAL
PHYSIOLOGY
S.MANJUNATH 4th EDITION
MEDICAL
PHYSIOLOGY
K.SHAMBHULIGAM 4th EDITION
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