Insulin is present and periferal tissues are partially responsive to it. Carbohydrate, proteins, fat metabolism are upset.
Insulin increases glucose transport into muscle, converts glucose into glycogen in the liver.
Insulin increases TG synthesis and fatty acid synthesis in liver, anabolises
protein and prevents protein breakdown, transports potassium into cells.
However since some glucose enters muscle cells, Ketogenesis does not usually occur.
Muscle cells depend on glucose primarily for resting anaerobic metabolism.
Amino acids enter Aerobic Krebs cycle and can provide energy only on exercise.
Brain cells however depend exclusively only on glucose for their function and as little as 6 g/hr.
Most of the glucose absorbed (80%) is stored as fat by Insulin. TG’s
stored are broken into glycerol and fatty acids.
Glycerol is converted into glucose for energy utilization.
Fatty acids enter Krebs cycle. Amino acids enter Krebs cycle for energy. Hence if there is absolutely no glucose entry into the cell in IDDM, the person should
not survive or should immediately go over to ketosis for energy utilization. Since
that does not occur, we can conclude that
Either Insulin is not totally
responsible for total glucose entry into cell and energy utilization (since at rest, neither fatty acids, glycerol nor amino
acids can support metabolism) OR
With Insulin deficiency as
in IDDM, some glucose is still entering the cells then you have a situation similar to NIDDM where some glucose still enters
Insulin resistant cells (and no Insulin deficiency exists).
Hence Insulin becomes not the only factor causing DM. In IDDM, the high
glucose is exerted in urine causing osmotic diuresis and increasing polyuria.
DIABETIC KETOACIDOTIC COMA
stressful situations the Acetyl CoA and fatty acids are converted to ketone bodies and these are utilized by the cells at
in prolonged starvation despite glucose deprivation, the body cells survive on ketone bodies.
production of ketone bodies results in acidosis and coma. After a few days even
brain cells start using ketone bodies and thus reduce ketonemia and acidosis causing recovery.
(hyperventilation, air hunger helps to blow out CO2, and reduces acidosis).
polyuria is compensated by thirst and when hypotension develops, the kidneys shut down in an attempt to conserve blood volume.
COMPLICATIONS OF DM
- Diabetic Retinopathy
is some evidence which suggests that Retinopathy is accelerated in Insulin treated cases with tight Blood Sugar control.
Retinopathy, Neuropathy and Nephropathy come after 10-20 years after diagnosis despite
treatment with Insulin very few patients go totally blind.
new vessel formations are actually collaterals to increase circulation to the ischemic areas.
haemorrhages and macular oedema usually resolve.Laser Photocoagulation is useful only before trouble startsand is of less use after established complications set in.
Laser photocoagulation itself causes some loss of vision.
is not common and occurs in 25% of Diabetics after 20 years only and few develop progressive disease .I
metabolism by kidney disease and Insulin sensitivity increases which actually stabilises
the blood sugar levels.
- Diabetic Neuropathy
It is symptomless in the majority .SymptomaticMotor neuropathies usually resolve within
Amputations are actually performed to save the patient from the torture of repeated constructive surgerys” states a popular medical text.
Insulin being discovered patients treated with Insulin still have a considerably
decreased life expectancy .Those diagnosed before 20 years of age have only a 70% chance of
living past the age of 50 years.
6. Macro vascular complications
Myocardial Infarctions and Periferal Vascular disease are largely dependent on other risk factors in addition to Diabetes.
12-18 months there is a natural remission with some recurrences in some patients.
of patients treated with radioiodine become hypothyroid. Opthalmoplegias in Thyrotoxicosis show spontaneous improvement
within 12-18 mths.
is often asymptomatic and is characteristic by a slow metabolism.
Functions of Thyroxine.
Increase in protein synthesis
Increase in BMR
Stimulation of carbohydrate,
(iv) Growth & Development , specially of Cartilage , CNS ,Hair , Teeth & Nails
(A) 90% of Adrenal Cortex has to be destroyed to cause Addison’s disease.
(B) Functions of Cortisol –BENEFICIAL
Endogenous Cortisol is beneficial
and its functions are Trauma, infection, stress, surgery , depression , Anxiety or any debilitating disease where there is
a 6-fold increase in cortisol levels. Endogenous cortisol is responsible for catabolism of proteins and fats and converts
it into glucose for instant energy.
They are responsible for rapid
resolution of inflammation by blocking. Interlenkins secreted by macrophages
and therefore increases the rate of healing and repair.
They dampen the inflammatory
response. Both these process are useful in connective tissue disease and allergies where inflammation is useful.
Endogenous cortisol blocks
the excess inflammatory response due to the Allergic AgAb destruction.
Endogenous cortisol increases
the RBC and WBC production.
(C) Exogenous Steroid Therapy causes
(1) Osteoporosis, Fractures and Avascular Necrosis
Blood Sugar and increases risk of Bacterial infections, Septicemia and TB.
(4) Depression and Psychosis.
(5) Menstrual Disorders (Amenorrhoea)
(6) Central Obesity and Proximal myopathy and wasting.
(7) Thrombotic tendencies.
(8) Suppression of immune responses – large doses of
exogenous steroids cause atrophy of lymphoid tissue and decrease in T cell and B cell immunoglobulins. This can cause fulminant infection and death.
(9) Suppression of Adrenal Axis – As little as 10 mg
of prednisone a day for 3 weeks can suppress the Adrenal axis for 1 year and during an operation, stress or disease, additional
dose of 100 mg IM may be needed. Therefore dose of steroids may have to be doubled
during infection, stress & fever.
HORMONAL BALANCE IN THE BODY
hormones break down TG and Proteins to raise Glucose. Anabolic hormones synthesize
proteins, TG and Glycogen from Glucose.
raises serum calcium by decalcifying bone via Acid Phosphatase and calcitonin reduces Serum Ca by depositing on bone via Alkaline