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DIABETES MELLITUS(DM)
DEFINITION
Diabetes mellitus(DM),commonly referred to as diabetes, is a
group of metabolic disorders in which there are high blood sugar
levels over a prolonged period.
Diabetes is due to either the pancreas not producing enough
insulin or the cells of the body not responding properly to the insulin
produced.
TYPES OF DIABETES MELLITUS
Type 1 DM
Type2DM
Gestational DM
TYPE 1 DIABETES MELLITUS
 It was previously termed as juvenile- onset diabetes due to
its occurrence in younger age.
 It was also known as insulin dependent DM.It constitutes
about 10% cases of DM.
 These patients require insulin replacement as treatment.
CAUSES:
Auto immune destruction of insulin producing beta cells in
the pancreas
TYPE 2 DIABETES MELLITUS
 It was previously called as maturity-onset
diabetes, or non-insulin dependent diabetes
mellitus(NIDDM)
 It comprise about 80%cases of diabetes
mellitus.
 It begins with insulin resistance, a condition in
which cells fails to respond to insulin properly.
CAUSES
 obesity
 lack of exercise
 genetics
GESTATIONAL DIABETES MELLITUS
 Woman without diabetes develops
high blood sugar level during
pregnancy.
 These woman's are prone to DM in
later life
CAUSES
Not enough insulin in the setting of
insulin resistance
 Acute complications:
 Ketoacidosis
 The hyperglycemic hyperosmolar nonketotic syndrome
 Hypoglycemia
 Late systemic complications:
 Microvascular complications
 Neuropathies
 Nephropathies
 Retinopathies
 Macrovascular complications
cardiovascular diseases
peripheral vascular diseases
 Foot ulcers
Complications of diabetes mellitus
 It occurs when ketone production by the liver exceeds
cellular use and renal excretion.
 Most commonly occurs in a person with type 1 diabetes, in
whom the lack of insulin leads to mobilization of fatty acids
from adipose tissue because of the unsuppressed adipose cell
lipase activity that breaks down triglycerides into fatty acids
and glycerol.
 The increase in fatty acid levels leads to ketone production
by the liver.
 Stress increases the release of gluconeogenic hormones and
predisposes the person to the development of ketoacidosis.
 DKA often is preceded by physical or emotional stress, such
as infection, pregnancy, or extreme anxiety.
 In clinical practice, ketoacidosis also occurs with the
omission or inadequate use of insulin.
DIABETIC KETOACIDOSIS (DKA)
CLINICAL FEATURES
 Anorexia
 Nausea
 Vomiting
 Deep and fast breathing
 Mental confusion
 Coma
 Excessive urination
 Dehydration
TREATMENT
 Fluid Replacement:
Provide fluids either by mouth or through
vein(intravenously) until you’re rehydrated and
it will helps in diluting the excess sugar in blood.
 Electrolyte replacement:
Electrolytes includes sodium potassium and chloride.
The absence of insulin lower the level of several electrolytes in blood.
To compensate the lost electrolyte, electrolyte replacement is necessary.
 Insulin therapy
Insulin reverses the processes that cause diabetic ketoacidosis .
Thus it is administered intravenously.
HYPERGLYCEMIC HYPEROSMOLAR
NONKETOTIC SYNDROME
 Hyperglycemic hyperosmolar nonketotic syndrome is characterised by
hyperglycemia (blood glucose >600mg/dl),hyperosmolarity(plasma
osmolarity>310mOsm/l)and dehydration,absence of ketoacidosis and
depression of sensorium.
 It is usually a complication of type 2 DM.
 It causes severe dehydration from sustained hyperglycemic diuresis.
 The loss of glucose in urine is so intensed that the patient is unable to
drink sufficient water to maintain urinary fluid loss.
 Thrombotic and bleeding complications are frequent due to high
viscosity of blood.
CLINICAL FEATURES
 Excessive thirst
 Dry mouth
 Increased urination
 Warm, dry skin
 Fever
 Drowsiness
 Confusion
 Hallucination
PATHOGENESIS
TREATMENT
 Fluid replacement: In hyperosmolar hyperglycemia
the mean fluid loss is about 9L.
Thus rapid fluid replacement is preferred.
 Insulin therapy
Blood glucose level is reduced using insulin.
HYPOGLYCEMIA
 Hypoglycemia,also known as low blood sugar,
is when blood sugar decreases to below normal level.
 It may develop in patients with type 1 DM.
 The most common cause include the medications
of diabetes mellitus such as insulin and sulfonylureas.
 Other causes may include kidney failure,
certain tumors such as insulinoma, liver disease,
hypothyroidism, starvation etc.
CLINICAL FEATURES
 Heart palpitations
 Fatigue
 Pale skin
 Shakiness
 Anxiety
 Sweating
 Hunger
PATHOPHYSIOLOGY
TREATMENT
 Dietary therapy:
Provide 15g of fast-acting carbohydrates
such as fruit juice,candy,glucose tablet etc..
 Intravenous glucose therapy
 Alpha glucosidase inhibitor(acarbose, miglitol)
These drugs cause reversible inhibition of
pancreatic alpha amylase and membrane bound
intestinal alpha glucoside hydrolase enzyme.
This inhibition results in delayed glucose absorption.
MICROVASCULAR COMPLICATIONS.
Microvascular complications mainly include:
 Nephropathy
 Neuropathy
 Retinopathy
Diabetic nephropathy:
It is a progressive kidney disease involving damage to the
capillaries in the kidney’s glomeruli because of long standing
diabetes mellitus.
SYMPTOMS
 Albumin or protein in urine
 Ankle and leg swelling, leg cramps
 High blood pressure
 High BUN and serum creatinine
 Morning sickness, nausea and vomiting
TREATMENT
Lowers the blood pressure
o Angiotensin converting enzyme inhibitor
eg:captopril, enalapril,lisinopril,ramipril
o Angiotensin II receptor blocker
eg:telmisartan,candesartan
o Calcium channel blocker
eg: amlodipine,verapamil
Severe cases
o Dialysis
o Kidney transplantation
Diabetic neuropathy
Diabetic neuropathy is a type of nerve damage that can occur if you have
diabetes. High blood sugar can injure nerve fibers throughout your body,
but diabetic neuropathy most often damages nerves in your legs and feet
SYMPTOMS
 Numbness or reduced ability to feel pain or temperature changes
 Tingling or burning sensation.
 Sharp pains or cramps, muscle weakness
 Increases sensitivity to touch
TREATMENT
 Anti seizure medications
eg:gabapentin,pregabalin, carbamazepine
 Anti depressants
eg:amitriptyline, desipramine, imipramine
Diabetic retinopathy
Diabetic retinopathy is a diabetic complication
that affects eye. It is caused by damage to
the blood vessels of the light sensitive tissue at the back of the eye(retina)
SYMPTOMS
 Spots or dark strings floating in your vision
 Blurred vision
 Fluctuating vision
 Impaired colour vision
 Dark or empty areas in your vision
 Vision loss
TREATMENT
 Laser treatment
 Eye injections
 Eye surgery
PATHOPHYSIOLOGY OF MICROVASCULAR
COMPLICATIONS
MACROVASCULAR COMPLICATIONS
These mainly includes
 CARDIO VASCULAR DISEASE
 Coronary heart disease
 Hypertension
 Angina pectoris
 Stroke
 PERIPHERAL VASCULAR DISEASE
 Atherosclerosis
CORONARY HEART DISEASE
Coronary heart disease is a disease in which a waxy substance called
plaque builds up inside the coronary arteries. These arteries supply oxygen
rich blood to heart muscle.
SYMPTOMS
o chest pain
o Heart burn
o Tachycardia
o Dyspnoea
o sweating
TREATMENT
 Aspirin or other anti platelets to help prevent blood clots.
 ACE inhibitors and beta blockers
 Statins to help lower cholesterol level
HYPERTENSION
Hypertension also known as high
blood pressure is a long-term
medical condition in which the
blood pressure in the arteries is
elevated.
TREATMENT
o Thiazide diuretics
o Calcium channel blockers
o ACE inhibitors
o Angiotensin receptor blockers
SYMPTOMS
Headache
Vertigo
Anxiety
Cushing syndrome
Moon face
palpitation
ANGINA PECTORIS
A condition marked by severe pain in the chest,
often also spreading to the shoulders ,arms and
neck owing to an inadequate blood supply
to the heart.
SYMPTOMS
Dyspnoea
Fatigue
Dizziness
Profuse sweating
Anxiety
TREATMENT
 Nitroglycerin which relieves pain associated with stable angina.
 Angioplasty
 Open heart surgery
 Coronary artery bypass graft
STROKE
A sudden disabling attack or loss of consciousness
caused by an interruption in the flow of blood to
the brain especially through thrombosis.
SYMPTOMS
 Weakness or numbness of the face arm or leg
on one side of the body
 Loss of vision
 Loss of speech
 Loss of balance
TREATMENT
 Aspirin
 Intravenous injection of tissue plasminogen activator
 Carotid endarterectomy
 Angioplasty and stents
 Surgical clipping
 Intracranial bypass
 Stereotactic radio surgery
ATHEROSCLEROSIS
Narrowing of artery characterised
by the deposition of fatty material
on their inner walls.
SYMPTOMS
o Chestpain
o Shortness of breath
o palpitation
o Difficulty In speaking
o blurred vision
o arrhythmia
TREATMENT
 Statins
 Antiplatelet drug
 ACE inhibitors
 Angioplasty
 Coronary artery bypass grafting
FOOT ULCER
Diabetic foot ulcer is the major complication of diabetic
mellitus.DM impairs the normal step in wound healing process. The
prolonged inflammatory phase is due to the delay in formation of
mature granulation tissue and a parallel reduction in wound tensile
strength.
PHYSICAL APPEARANCE
It looks like a red crater in the skin
mostly located in the side or bottom of foot
,or top or tip of a toe.
PATHOPHYSIOLOGY
TREATMENT
 Antibiotic
 Antiplatelet drug.
THANK YOU……

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Complications of diabetes mellitus

  • 1.
  • 2. DIABETES MELLITUS(DM) DEFINITION Diabetes mellitus(DM),commonly referred to as diabetes, is a group of metabolic disorders in which there are high blood sugar levels over a prolonged period. Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced. TYPES OF DIABETES MELLITUS Type 1 DM Type2DM Gestational DM
  • 3. TYPE 1 DIABETES MELLITUS  It was previously termed as juvenile- onset diabetes due to its occurrence in younger age.  It was also known as insulin dependent DM.It constitutes about 10% cases of DM.  These patients require insulin replacement as treatment. CAUSES: Auto immune destruction of insulin producing beta cells in the pancreas
  • 4. TYPE 2 DIABETES MELLITUS  It was previously called as maturity-onset diabetes, or non-insulin dependent diabetes mellitus(NIDDM)  It comprise about 80%cases of diabetes mellitus.  It begins with insulin resistance, a condition in which cells fails to respond to insulin properly. CAUSES  obesity  lack of exercise  genetics
  • 5. GESTATIONAL DIABETES MELLITUS  Woman without diabetes develops high blood sugar level during pregnancy.  These woman's are prone to DM in later life CAUSES Not enough insulin in the setting of insulin resistance
  • 6.  Acute complications:  Ketoacidosis  The hyperglycemic hyperosmolar nonketotic syndrome  Hypoglycemia  Late systemic complications:  Microvascular complications  Neuropathies  Nephropathies  Retinopathies  Macrovascular complications cardiovascular diseases peripheral vascular diseases  Foot ulcers Complications of diabetes mellitus
  • 7.  It occurs when ketone production by the liver exceeds cellular use and renal excretion.  Most commonly occurs in a person with type 1 diabetes, in whom the lack of insulin leads to mobilization of fatty acids from adipose tissue because of the unsuppressed adipose cell lipase activity that breaks down triglycerides into fatty acids and glycerol.  The increase in fatty acid levels leads to ketone production by the liver.  Stress increases the release of gluconeogenic hormones and predisposes the person to the development of ketoacidosis.  DKA often is preceded by physical or emotional stress, such as infection, pregnancy, or extreme anxiety.  In clinical practice, ketoacidosis also occurs with the omission or inadequate use of insulin. DIABETIC KETOACIDOSIS (DKA)
  • 8. CLINICAL FEATURES  Anorexia  Nausea  Vomiting  Deep and fast breathing  Mental confusion  Coma  Excessive urination  Dehydration
  • 9.
  • 10. TREATMENT  Fluid Replacement: Provide fluids either by mouth or through vein(intravenously) until you’re rehydrated and it will helps in diluting the excess sugar in blood.  Electrolyte replacement: Electrolytes includes sodium potassium and chloride. The absence of insulin lower the level of several electrolytes in blood. To compensate the lost electrolyte, electrolyte replacement is necessary.  Insulin therapy Insulin reverses the processes that cause diabetic ketoacidosis . Thus it is administered intravenously.
  • 11. HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME  Hyperglycemic hyperosmolar nonketotic syndrome is characterised by hyperglycemia (blood glucose >600mg/dl),hyperosmolarity(plasma osmolarity>310mOsm/l)and dehydration,absence of ketoacidosis and depression of sensorium.  It is usually a complication of type 2 DM.  It causes severe dehydration from sustained hyperglycemic diuresis.  The loss of glucose in urine is so intensed that the patient is unable to drink sufficient water to maintain urinary fluid loss.  Thrombotic and bleeding complications are frequent due to high viscosity of blood.
  • 12. CLINICAL FEATURES  Excessive thirst  Dry mouth  Increased urination  Warm, dry skin  Fever  Drowsiness  Confusion  Hallucination
  • 14. TREATMENT  Fluid replacement: In hyperosmolar hyperglycemia the mean fluid loss is about 9L. Thus rapid fluid replacement is preferred.  Insulin therapy Blood glucose level is reduced using insulin.
  • 15. HYPOGLYCEMIA  Hypoglycemia,also known as low blood sugar, is when blood sugar decreases to below normal level.  It may develop in patients with type 1 DM.  The most common cause include the medications of diabetes mellitus such as insulin and sulfonylureas.  Other causes may include kidney failure, certain tumors such as insulinoma, liver disease, hypothyroidism, starvation etc.
  • 16. CLINICAL FEATURES  Heart palpitations  Fatigue  Pale skin  Shakiness  Anxiety  Sweating  Hunger
  • 18. TREATMENT  Dietary therapy: Provide 15g of fast-acting carbohydrates such as fruit juice,candy,glucose tablet etc..  Intravenous glucose therapy  Alpha glucosidase inhibitor(acarbose, miglitol) These drugs cause reversible inhibition of pancreatic alpha amylase and membrane bound intestinal alpha glucoside hydrolase enzyme. This inhibition results in delayed glucose absorption.
  • 19. MICROVASCULAR COMPLICATIONS. Microvascular complications mainly include:  Nephropathy  Neuropathy  Retinopathy Diabetic nephropathy: It is a progressive kidney disease involving damage to the capillaries in the kidney’s glomeruli because of long standing diabetes mellitus. SYMPTOMS  Albumin or protein in urine  Ankle and leg swelling, leg cramps
  • 20.  High blood pressure  High BUN and serum creatinine  Morning sickness, nausea and vomiting TREATMENT Lowers the blood pressure o Angiotensin converting enzyme inhibitor eg:captopril, enalapril,lisinopril,ramipril o Angiotensin II receptor blocker eg:telmisartan,candesartan o Calcium channel blocker eg: amlodipine,verapamil
  • 21. Severe cases o Dialysis o Kidney transplantation Diabetic neuropathy Diabetic neuropathy is a type of nerve damage that can occur if you have diabetes. High blood sugar can injure nerve fibers throughout your body, but diabetic neuropathy most often damages nerves in your legs and feet SYMPTOMS  Numbness or reduced ability to feel pain or temperature changes  Tingling or burning sensation.  Sharp pains or cramps, muscle weakness  Increases sensitivity to touch
  • 22. TREATMENT  Anti seizure medications eg:gabapentin,pregabalin, carbamazepine  Anti depressants eg:amitriptyline, desipramine, imipramine Diabetic retinopathy Diabetic retinopathy is a diabetic complication that affects eye. It is caused by damage to the blood vessels of the light sensitive tissue at the back of the eye(retina) SYMPTOMS  Spots or dark strings floating in your vision  Blurred vision  Fluctuating vision
  • 23.  Impaired colour vision  Dark or empty areas in your vision  Vision loss TREATMENT  Laser treatment  Eye injections  Eye surgery
  • 25. MACROVASCULAR COMPLICATIONS These mainly includes  CARDIO VASCULAR DISEASE  Coronary heart disease  Hypertension  Angina pectoris  Stroke  PERIPHERAL VASCULAR DISEASE  Atherosclerosis
  • 26. CORONARY HEART DISEASE Coronary heart disease is a disease in which a waxy substance called plaque builds up inside the coronary arteries. These arteries supply oxygen rich blood to heart muscle. SYMPTOMS o chest pain o Heart burn o Tachycardia o Dyspnoea o sweating
  • 27. TREATMENT  Aspirin or other anti platelets to help prevent blood clots.  ACE inhibitors and beta blockers  Statins to help lower cholesterol level HYPERTENSION Hypertension also known as high blood pressure is a long-term medical condition in which the blood pressure in the arteries is elevated.
  • 28. TREATMENT o Thiazide diuretics o Calcium channel blockers o ACE inhibitors o Angiotensin receptor blockers SYMPTOMS Headache Vertigo Anxiety Cushing syndrome Moon face palpitation
  • 29. ANGINA PECTORIS A condition marked by severe pain in the chest, often also spreading to the shoulders ,arms and neck owing to an inadequate blood supply to the heart. SYMPTOMS Dyspnoea Fatigue Dizziness Profuse sweating Anxiety
  • 30. TREATMENT  Nitroglycerin which relieves pain associated with stable angina.  Angioplasty  Open heart surgery  Coronary artery bypass graft STROKE A sudden disabling attack or loss of consciousness caused by an interruption in the flow of blood to the brain especially through thrombosis. SYMPTOMS  Weakness or numbness of the face arm or leg on one side of the body  Loss of vision  Loss of speech  Loss of balance
  • 31. TREATMENT  Aspirin  Intravenous injection of tissue plasminogen activator  Carotid endarterectomy  Angioplasty and stents  Surgical clipping  Intracranial bypass  Stereotactic radio surgery
  • 32. ATHEROSCLEROSIS Narrowing of artery characterised by the deposition of fatty material on their inner walls. SYMPTOMS o Chestpain o Shortness of breath o palpitation o Difficulty In speaking o blurred vision o arrhythmia
  • 33. TREATMENT  Statins  Antiplatelet drug  ACE inhibitors  Angioplasty  Coronary artery bypass grafting
  • 34. FOOT ULCER Diabetic foot ulcer is the major complication of diabetic mellitus.DM impairs the normal step in wound healing process. The prolonged inflammatory phase is due to the delay in formation of mature granulation tissue and a parallel reduction in wound tensile strength. PHYSICAL APPEARANCE It looks like a red crater in the skin mostly located in the side or bottom of foot ,or top or tip of a toe.