Download MBBS Diabetes Mellitus Lecture PPT

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