Download MBBS (Bachelor of Medicine and Bachelor of Surgery) Latest Diabetes Mellitus Lecture PPT
Diabetes Mellitus
Diabetes mellitus (DM) comprises a group of
metabolic disorders presenting with
hyperglycaemia resulting from insulin deficiency or
decreased glucose utilization and increased glucose
production.
TYPES OF DIABETES MELLITUS.
TYPE- I DIABETES MELLITUS.
? Type I diabetes mellitus is due to pancreatic B-cell
destruction leading to insulin deficiency.
? It is more common in children, adolescents and young
adults usually below 30 years.
? Insulin is usually required for treatment i.e. patients
are insulin dependent.
? These subjects are genetically susceptible and are
prone to develop ketosis.
? Due to the above features, this diabetes is also
called brittle diabetes.
Type II Diabetes mellitus.
? Type II Diabetes Mellitus is characterized by
variable degree of insulin resistance, and impaired
insulin secretion.
? It is preceded by a period of abnormal glucose
homeostasis classified as impaired fasting glucose
(IFG) or impaired glucose tolerance (IGT).
? Typically, it develops with increasing age.
? However, age in no bar and can also occur in
obese children and adolescents.
Gestational Diabetes.
? Insulin resistance seen in late pregnancy may lead
to impaired glucose tolerance and even frank
diabetes called gestational diabetes mellitus.
? Most subjects revert to normal glucose
tolerance after delivery but have increased
risk (=~60%) of developing diabetes mellitus in
future (10-20 years).
METABOLIC CHANGES IN DIABETES
MELLITUS.
? Hyperglycemia--
1.overproduction of glucose by gluconeogenesis.
2.under utilization of glucose by the tissues due to insulin
deficiency.
? Lypolysis-- Low insulin : glucose ratio.
? KETOSIS and Hyperlipidemia- Acetyl-Co A diverted to other
pathway of its utilization LIKE .....
? Ketosis, cholesterol synthesis, and fatty acid synthesis.
? Excess ketone bodies produced by Liver , continued if not
treated leads to ketoacidosis.
LONG STANDING METABOLIC EFFECT.
AGEs( advanced glycation end products).
High glucose in tissue
leads to non enzymatic attachment of glucose and
its metabolites to several protein like Hb, albumin,
collagen etc. This process is called glycation.
Ultimately leads to the formation of advanced
glycation end product which causes cellular
dysfunction.one such glycated protein is HbA1c.
CATARACT--(polyol-pathway)--High glucose leads
to sorbitol accumulation causing cellular
dysfunction. Cataract is believed to be a result of
osmotic effect of sorbitol accumulation.
Clinical features of Diabetes Mellitus.
? Polyurea.
? Polydipsia.
.Polyphagia.
? Fatigue.
? Weight Loss.
DIAGNOSIS OF DIABETES
MELLITUS.
WHO guidelines
? FBG? 126mg%.
? PP-- 200%.
? RBG--> 200 mg% with symptomps of diabetes mellitus.
? Glycated Hb( HbA1c) > 6.5gm%.
DIFFERENT TYPES OF BLOOD GLUCOSE TESTS.
FBS
RBG
2-HourPP
HbA1c
OGTT
Diabetic profile.
Blood glucose.
4 types :FBS, PPBS, RBS, OGGT.
Urine Analysis.
Urine sugar/urine protein/urine microalbum/ketones.
HbA1C
Insulin
C-peptide
FASTING BLOOD SUGAR.
? Normal level
? 70---110mg/dl.
110mg/dl
126mg/dl
Diabetic
NORMAL BLOOD GLUCOSE
LEVEL
? FBG---70---110mg%.
? PP-----Less than 140 mg% after 75 mg
glucose load.
? HbA1c ?below 6.5 gm%.
INSULIN RESISTANCE
SYNDROME.
? Also known as Metabolic syndrome or the syndrome X,
characterised by the following....
? Insulin resistance indicated by blood glucose inspite
of insulin level in blood.
? Hypertension.
? Dyslipidemia((LDL + TG).
? Central obesity.
? Accelerated cardiovascular disease.
? Insulin resistance syndrome is due to post- receptor
signaling defect in target tissues, e.g. Skeletal muscle.
COMPLICATION OF DIABETES
MELLITUS.
Complication of DM.
Chronic
Acute
Diabetic ketoacidosis.and
Microvas--
Macro--MI, STROKE
Hyperglycemic non ketotic
retinopathy,neuropathy,neph.
hyperosmor.
? Alteration in blood sugar: hyperglycemia and
Hypoglycemia.
? Macrovascular( Larege blood vessels)
? Atherosclerosis involving :-
? coronary, cerebral and
peripheral arteries.
? Microvascular( small blood vessels):-
? affects basement membrane
of small blood vessels and capillaries involving
Eyes and Kidneys.
HYPERGLYCEMIA.
? High blood sugar
? DKA
? HHKs
? Dawn phenomenon-
? 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
rebound morning hyperglycemia that may lead to
insulin resistance for 12 to 48 hours.
ACUTE COMPLICATION
? Hypoglycemia
? Diabetic ketoacidosis.
? Hyperglycemic hyperosmotic non ketotic coma.
? HYPOGLYCEMIA:--
? Serum glucose < 55 mg/100ml.
? Brain damage develops when the brain is
deprived of needed glucose after a dramatic drop
in blood sugar.
HYPOGLYCEMIA
SIGN AND SYMPTOMPS.
? MILD:-
?
? Palpitation, pallor , tremors, anxiety
? Parasthesia,
? MODERATE:-
? confusion, cold extremities, blurred
vision.
? SEVERE:-
? Seizure, Loss of consciousness,can
result in death.
Otherscomplication.
? Cataract.
? Glucoma.
? Infection-Foot ulcer, osteomyelitis.
? Skin infection--candiasis and other fungal
infection.
DIABETIC KETOACIDOSIS.
? Diabetic ketoacidosis is the most dreaded acute
complication resulting from uncontrolled
diabetes mellitus, characterised by
? Severe hyperglycemia-Blood glucose is very high,
commonly 400- 500 mg %.
? Dehydration due to polyurea.
? Ketosis--due to increased production of ketone
bodies as a result of hyperglycemia.
? Ketone body test is positive in urine.
DKA: 4 main clinical features.
? 1.Hyperglycemia
? 2.Dehydration
? 3.Eectrolyte loss.
? 4.Metabolic Acidosis.
PATHOPHYSIOLOGY DKA.
NO insulin
Glucose stays in
Muscle not geting
Fat metabolism
blood
energy
Increased ketone in
Hyperglycemia
blood
Osmotic diuresis
Metabolic Acidosis
Electrolyte
polyurea
imbalance
Serum pH
polydipsia
Respiratory rate.
Dehydration
? Acidosis with increased anion gap---
? PH 6.8--7.3 and
anion gap of >15mEq/L.
? Hyperventilaton with fruity odour of breath---
? Acidisis stimulates respiration leading to
hyprventilation. Excretion of acetone (ketone
bodies) in the breath is responsible for fruity
odour in breath.
? Other symptomps include--
? Nausea
? vomiting
? pain abdomen
? letharginess
? Depression......etc.
? Hyperkalemia and hypontremia.
? It is acute medical emergency.
? Patient is admitted and treated with
intravenous insulin, fluids and electrolytes to
correct dehydration and electrolyte imbalance.
Glycated Hemoglobin.
? Glycated Hb(HbA1c)---Is formed by non-
enzymatic addition of N- terminal Valine of Hb
Beta chain due to persistent hyperglycemia.
? Its level in blood gives an estimate of blood
glucose over the preceding 6-8 weeks.
This post was last modified on 30 November 2021