The document discusses endocrine pancreas and its applied aspects of diabetes mellitus and hypoglycemia. It defines diabetes as a clinical syndrome of hyperglycemia due to insulin deficiency. There are two primary types of diabetes - type 1 diabetes which is caused by beta cell destruction and type 2 diabetes which involves resistance of target tissues to insulin. The stages of diabetes are also defined ranging from prediabetes to complicated diabetes. Causes, clinical features, complications and management of both hypoglycemia and diabetes are summarized.

1. Endocrine pancreas
(Applied aspects)

2. Applied aspects.
 Diabetes mellitus.
 Hypoglycemia.
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3. Diabetes mellitus.
 Diabetes – A clinical syndrome of hyperglycemia
due to deficiency of Insulin.
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TYPES .
PRIMARY DM – cause not
known.
IDDM
NIDDM
SECONDARY DM – due to
Pathological
conditions,
pancreatitis, cystic
fibrosis, Acromegaly,
Cushing syndrome etc.
STAGES.
•PRE-DIABETICS or Potential
diabetics. – Genetic
predisposition.
•Latent diabetics or chemical
diabetics – normal F& PP BSL
but increased after stress.
• Clinical diabetics – C/F
without complications.
• Complicated diabetics.

4. DIABETES MELLITUS
TYPES:
 1.PRIMARY D.M
IDDM
NIDDM
 2.SECONDARY D.M.
 STAGES:
 PREDIABETICS
 LATENT DIABETICS
 CLINICAL DIABETICS
 COMPLICATED DIABETICS

5. • INSULIN DEPENDENT D.M.:
 TYPE -1 D.M.,AUTOIMMUNE DISORDER
 <40 yrs OF AGE ,10-20%,LEAN
 POLYURIA,POLYDIPSIA
 POLYPHAGIA,WEIGHT LOSS
 KETOSIS AND ACIDOSIS
 PL.INSULIN-LOW OR UNDETECTABLE

6.  NIDDM:
 TYPE-2 D.M.
 OVER EATING AND UNDER ACTIVITY
 DECREASE IN INSULIN RECEPTORS
 >40yrs OF AGE,80-90%, MOSTLY
OBESE
 SYMPTOMS BEGIN GRADUALLY
 PL.INSULIN NORMAL OR ELEVATED
 KETOACIDOSIS –NOT COMMON

7. IDDM & NIDDM.
FEATURES IDDM NIDDM
DEFECT β cell destruction.–
insulin def.
Resistance of target
tissue.
Prevalence 10-20 % 80-90%
Age of onset < 40 yrs > 40 yrs.
Body wt Low High
Gene focus Chromosome 6 Chromosome 1
Family history Mild/moderate Strong.
Acute complication Ketoacidosis Hyperosmolar coma.
Plasma insulin Decreased or absent Normal
Ketonuria Present Absent
Treatment Insulin Oral hypoglycemic.
Mortality High Low.
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8. Pathophysiology of DM.
 Hyperglycemia. –
 Due to decreased peripheral utilization.
 Increased hepatic output of glucose.
 Hypertriglyceridaemia, ketosis .
 Less utilization turns it to FFA
 Excess FFA leads to formation ofTG & Ketoacidosis.
 Protein catabolism.
 Insulin --- Anabolic hormone.
 Promote protein synthesis & inhibit proteolysis.
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9. Hyperglycemia.
 Glycosuria. –
 Glucose in urine above 180 mg/100ml.
 Polyuria (osmotic diuresis), loss of electrolyte, cellular dehydration,
polydipsia, increased caloric loss, Polyphagia, loss of body weight.
CONDITION OF STARVATION IN THE MIDST OF PLENTY
 Impaired Phagocytic function.
 Hyperosmolar effect. (above 375 mOsm/kg) NONKETOTIC
HYPEROSMOLAR COMA
 Glycosylation of proteins.
 Hemoglobin (HbA1c )
 Tissue proteins – Diabetic Nephropathy, D. Neuropathy, D.
Retinopathy.
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10. GLYCOSURIA CONSEQUENCES-
 GLYCOSURIA
 POLYURIA
 LOSS OF ELECTROLYTES
 CELLULAR DEHYDRATION
 POLYDIPSIA
 POLYPHAGIA
 LOSS OF BODY WEIGHT-CONDITION OF
STARVATION IN THE MIDST OF PLENTY

11. GLYCOSYLATION OF HEMOGLOBIN-
HbA1C
CONDENSATION OF GLUCOSE WITH
N TERMINAL VALINEOF EACH BETA
CHAIN OF HB A
RATE OF PRODUCTION OF THIS IS
DIRECTLY RELATED TO EXPOSURE
OF RBC TO GLUCOSE

13. Hypertriglyceridaemia,
Ketosis .
 Hypertriglyceridaemia
– glucose converted to
FFA
 FFA toTG.
 Increase secretion of
VLDL & chylomicrons.
 Leads to
Hypercholesterolemia.
 Ketosis .
 Cellular dehydration.
 Ketoacidosis.
 Dyspnoea, Kussmaul
breathing.
 Breath acetone smell.
 Electrolyte loss
 Hypovolaemia &
hypotension.
 Coma & death
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14. Protein catabolism.
 Protein catabolism increased & anabolism
suppressed.
 Protein depletion.
 Muscle wasting.
 Negative nitrogen balance.
 Released large amount of amino acids
 Used for energy production.
.
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16. Clinical features
 Cardinal symptoms –
Polyuria, Polyphagia,
polydypsia, wt loss.
 Biochemical –
Hyperglycemia,
Glycosuria, ketosis,
ketonuria,
Ketoacidosis.
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17. Complications.
 Predisposition to infection.
– Phagocytic function, protein
depletion
 Acute complication – ketotic
coma, Non-ketotic Hyperosmolar
coma.
 Chronic complication.–
atherosclerosis., Hyperlipidemia,
hypercholesterolemia,
 Microangiopathy – D.
retinopathy, nephropathy,
neuropathy.
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18. Diagnosis.
 Urine examination for Glycosuria. – exclude
renal Glycosuria.
 Urine examination for ketone bodies. – other
causes starvation, fasting, high fat diet,
repeated vomiting.
 Blood glucose levels – fasting (70-110 mg%) &
postprandial (< 140 mg%)
 Glucose tolerance tests (GTT)
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19. Glucose
tolerance tests
(GTT)
 Prior test normal
carbohydrate diet for 3 days.
 Early morning fasting BSL &
urine taken.
 75 mg glucose dissolve in
300 ml of water given orally.
 BSL & urine tested ½ hrly for
next 3 hrs.
Plasma glucose conc. (mg%)
NORMAL IMPAIRED
GLUCOSE
TOLERAAN
CE
DM
Fasting
level.
< 110 110-126 ≥ 126.
Peak
post
prandial
level.
< 140 >140-<
200
≥ 200
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20. Management of Diabetes
Mellitus.
 Goals of therapy.
 Maintain blood glucose to normal.
 Maintain ideal body weight.
 Symptom free.
 Retard or prevent complications.
 Treatment modalities.
 Dietary management.
 Oral hypoglycemic agents.
 Insulin along with dietary management.
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21. Treatment modalities.
 Dietary management.
 Low energy wt reducing diet (for obese
NIDDM)
 Wt maintenance diet (Non obese NIDDM)
 Frequent small meals.
 Oral hypoglycemic agents.
 Sulphonylurea
 Biguanides.
 Insulin along with dietary
management.
 For IDDM.
 For newly detected Ketoacidosis.
 Emergencies with IDDM & NIDDM.
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22. Hypoglycemia.
 Blood Glucose level
below 45 mg %.
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23. Types & causes of
Hypoglycemia.
 Hypoglycemia in non-
diabetics.
 Postprandial hypoglycemia.
(Reactive)
 Post-absorption or fasting
hypoglycemia. – insulin
secreting tumors leading to
hyperinsulinaemia.
 Hepatic failure.
 Due to alcohol intake. – due
to decreased
Gluconeogenesis.
 Hypoglycemia in
Diabetics.
 Overdose of anti-
diabetic drugs.
 No intake.
 Mismatch between
insulin & food habits.
 Alcohol intake.
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24. Hypoglycemia signs & symptoms.
 CNS
 Neuroglycopenic symptoms –
tremors, hallucinations,
extreme nervousness,
convulsions, drowsiness.
 CVS
 Palpitation, tachycardia,
arrhythmias
 GIT – Nausea & vomiting.
 SKIN– sweating,
hypothermia.
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25. HYPOGLYCEMIC VS
HYPERGLYCEMIC COMA IN
DIABETICS
FEATURE HYPOGLYCEMIC
COMA
HYPERGLYCEMIC
COMA
CAUSE REGULAR DOSEOF
INSULINAND NO
FOOD
TOO LITTLE OR NO
INSULINWITH
REGULAR FOOD
INTAKE
PRECIPITATING
FACTOR
SEVERE
UNACCUSTOMED
EXERCISE
UNTREATED OR
HIDDEN INFECTION
RATE OF ONSET RAPID,DEVELOPS
WITH IN MTS
SLOW,HOURS OR
DAYS
SYMPTOMSAND
SIGNS
VOMITING
BREATHING
PULSE
NO OR OCCASIONAL
LABOURED,NO SMELL
BOUNDING
FREQUENT,ABDOMINA
L PAIN
KUSSMAULS
WEAK/FEEBLE