Download MBBS Diabetes Mellitus Lecture PPT

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metabolic disorders presenting with

hyperglycaemia resulting from insulin deficiency or

decreased glucose utilization and increased glucose

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production.
TYPES OF DIABETES MELLITUS.

TYPE- I DIABETES MELLITUS.

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? Type I diabetes mellitus is due to pancreatic B-cell

destruction leading to insulin deficiency.

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? It is more common in children, adolescents and young

adults usually below 30 years.

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? Insulin is usually required for treatment i.e. patients

are insulin dependent.

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? These subjects are genetically susceptible and are

prone to develop ketosis.

? Due to the above features, this diabetes is also

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called brittle diabetes.
Type II Diabetes mellitus.

? Type II Diabetes Mellitus is characterized by

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variable degree of insulin resistance, and impaired

insulin secretion.

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? It is preceded by a period of abnormal glucose

homeostasis classified as impaired fasting glucose

(IFG) or impaired glucose tolerance (IGT).

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? Typically, it develops with increasing age.

? However, age in no bar and can also occur in

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obese children and adolescents.
Gestational Diabetes.

? Insulin resistance seen in late pregnancy may lead

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to impaired glucose tolerance and even frank

diabetes called gestational diabetes mellitus.

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? Most subjects revert to normal glucose
tolerance after delivery but have increased
risk (=~60%) of developing diabetes mellitus in

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future (10-20 years).


METABOLIC CHANGES IN DIABETES

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MELLITUS.

? Hyperglycemia--

1.overproduction of glucose by gluconeogenesis.

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2.under utilization of glucose by the tissues due to insulin

deficiency.

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? Lypolysis-- Low insulin : glucose ratio.

? KETOSIS and Hyperlipidemia- Acetyl-Co A diverted to other

pathway of its utilization LIKE .....

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? Ketosis, cholesterol synthesis, and fatty acid synthesis.
? Excess ketone bodies produced by Liver , continued if not

treated leads to ketoacidosis.

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LONG STANDING METABOLIC EFFECT.

AGEs( advanced glycation end products).

High glucose in tissue

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leads to non enzymatic attachment of glucose and

its metabolites to several protein like Hb, albumin,

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collagen etc. This process is called glycation.

Ultimately leads to the formation of advanced

glycation end product which causes cellular

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dysfunction.one such glycated protein is HbA1c.

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CATARACT--(polyol-pathway)--High glucose leads

to sorbitol accumulation causing cellular

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dysfunction. Cataract is believed to be a result of

osmotic effect of sorbitol accumulation.

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Clinical features of Diabetes Mellitus.

? Polyurea.

? Polydipsia.

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.Polyphagia.

? Fatigue.

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? Weight Loss.

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DIAGNOSIS OF DIABETES

MELLITUS.

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WHO guidelines

? FBG? 126mg%.

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? PP-- 200%.

? RBG--> 200 mg% with symptomps of diabetes mellitus.

? Glycated Hb( HbA1c) > 6.5gm%.

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DIFFERENT TYPES OF BLOOD GLUCOSE TESTS.

FBS

RBG

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2-HourPP

HbA1c

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OGTT
Diabetic profile.

Blood glucose.

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4 types :FBS, PPBS, RBS, OGGT.

Urine Analysis.

Urine sugar/urine protein/urine microalbum/ketones.

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HbA1C

Insulin

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C-peptide
FASTING BLOOD SUGAR.

? Normal level
? 70---110mg/dl.

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110mg/dl

126mg/dl

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Diabetic
NORMAL BLOOD GLUCOSE

LEVEL

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? FBG---70---110mg%.

? PP-----Less than 140 mg% after 75 mg

glucose load.

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? HbA1c ?below 6.5 gm%.
INSULIN RESISTANCE

SYNDROME.

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? Also known as Metabolic syndrome or the syndrome X,

characterised by the following....

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? Insulin resistance indicated by blood glucose inspite

of insulin level in blood.

? Hypertension.

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? Dyslipidemia((LDL + TG).
? Central obesity.
? Accelerated cardiovascular disease.
? Insulin resistance syndrome is due to post- receptor

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signaling defect in target tissues, e.g. Skeletal muscle.
COMPLICATION OF DIABETES

MELLITUS.

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Complication of DM.

Chronic

Acute

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Diabetic ketoacidosis.and

Microvas--

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Macro--MI, STROKE

Hyperglycemic non ketotic

retinopathy,neuropathy,neph.

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hyperosmor.
? Alteration in blood sugar: hyperglycemia and

Hypoglycemia.

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? Macrovascular( Larege blood vessels)
? Atherosclerosis involving :-
? coronary, cerebral and

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peripheral arteries.

? Microvascular( small blood vessels):-
? affects basement membrane

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of small blood vessels and capillaries involving

Eyes and Kidneys.

HYPERGLYCEMIA.

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? High blood sugar
? DKA
? HHKs
? Dawn phenomenon-

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? Rise in blood sugar between 4 a.m. And 8 a.m.
? Not associated with hypoglycemia.
? SOMOGYI phenomenon----
? Combination of hypoglycemia during night with a

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rebound morning hyperglycemia that may lead to

insulin resistance for 12 to 48 hours.
ACUTE COMPLICATION

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? Hypoglycemia
? Diabetic ketoacidosis.
? Hyperglycemic hyperosmotic non ketotic coma.
? HYPOGLYCEMIA:--
? Serum glucose < 55 mg/100ml.

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? Brain damage develops when the brain is

deprived of needed glucose after a dramatic drop

in blood sugar.

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HYPOGLYCEMIA

SIGN AND SYMPTOMPS.

? MILD:-

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?
? Palpitation, pallor , tremors, anxiety
? Parasthesia,
? MODERATE:-
? confusion, cold extremities, blurred

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vision.

? SEVERE:-
? Seizure, Loss of consciousness,can

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result in death.
Otherscomplication.

? Cataract.

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? Glucoma.
? Infection-Foot ulcer, osteomyelitis.
? Skin infection--candiasis and other fungal

infection.

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DIABETIC KETOACIDOSIS.

? Diabetic ketoacidosis is the most dreaded acute

complication resulting from uncontrolled

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diabetes mellitus, characterised by

? Severe hyperglycemia-Blood glucose is very high,

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commonly 400- 500 mg %.

? Dehydration due to polyurea.
? Ketosis--due to increased production of ketone

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bodies as a result of hyperglycemia.

? Ketone body test is positive in urine.
DKA: 4 main clinical features.

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? 1.Hyperglycemia
? 2.Dehydration
? 3.Eectrolyte loss.
? 4.Metabolic Acidosis.
PATHOPHYSIOLOGY DKA.

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NO insulin

Glucose stays in

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Muscle not geting

Fat metabolism

blood

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energy

Increased ketone in

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Hyperglycemia

blood

Osmotic diuresis

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Metabolic Acidosis

Electrolyte

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polyurea

imbalance

Serum pH

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polydipsia

Respiratory rate.

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Dehydration
? Acidosis with increased anion gap---
? PH 6.8--7.3 and

anion gap of >15mEq/L.

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? Hyperventilaton with fruity odour of breath---
? Acidisis stimulates respiration leading to

hyprventilation. Excretion of acetone (ketone

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bodies) in the breath is responsible for fruity

odour in breath.
? Other symptomps include--

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? Nausea
? vomiting
? pain abdomen
? letharginess
? Depression......etc.

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? Hyperkalemia and hypontremia.
? It is acute medical emergency.
? Patient is admitted and treated with

intravenous insulin, fluids and electrolytes to

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correct dehydration and electrolyte imbalance.
Glycated Hemoglobin.

? Glycated Hb(HbA1c)---Is formed by non-

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enzymatic addition of N- terminal Valine of Hb

Beta chain due to persistent hyperglycemia.

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? Its level in blood gives an estimate of blood

glucose over the preceding 6-8 weeks.