Diabetes Mellitus
Diabetes mellitus (DM) comprises a group of
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metabolic disorders presenting withhyperglycaemia 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 areprone 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 glucosehomeostasis 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 frankdiabetes 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 ofosmotic 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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OGTTDiabetic 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-peptideFASTING BLOOD SUGAR.
? Normal level
? 70---110mg/dl.
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110mg/dl
126mg/dl
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DiabeticNORMAL 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 inspiteof 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, STROKEHyperglycemic 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 involvingEyes 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 toinsulin 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 isdeprived of needed glucose after a dramatic drop
in blood sugar.
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HYPOGLYCEMIASIGN 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 getingFat metabolism
blood
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energy
Increased ketone in
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Hyperglycemiablood
Osmotic diuresis
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Metabolic Acidosis
Electrolyte
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polyureaimbalance
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 bloodglucose over the preceding 6-8 weeks.