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"Never offer the devil a ride. He will always want to be in the driving seat…!"
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Pathology of Diabetes
Dr. Venkatesh M. ShashidharAssociate Professor of Pathology
Fiji School of Medicine
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Diabetes Mellitus
Disorder of metabolism (Carb, Prot & Fat)
Due to Absolute/relative deficiency of insulin. Characterized by hyperglycemia.
Clinically : Polyuria, Polydypsia, Polyphagia.
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Introduction Diabetes mellitus (sweet urine) 3% of world population, 100 million people Incidence is increasing alarmingly (40% in the
past decade, more in future. 259 m by 2025. Most Common non communicable disease High Morbidity & mortality. DM shortens life span by 15 years. Leading cause of blindness and Kidney dis. Pacific Islands – leaders in DM & Obesity…!
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World Statistics:
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Normal Pancreatic Islet:
ß cells ß cells (Insulin) αα cells cells (Glucagon)
δδ cells cells (Somatostatin) pp Cells pp Cells (pan prot)
ßß αα
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Insulin - Anabolic Steroid Transmembrane transport of glucose Liver, muscle & fat blood glucose Liver & skeletal muscle - glycogen Converts glucose to triglycerides Nucleic acid & Protein synthesis Diabetes Diabetes Increased catabolism. Increased catabolism. Hyperglycemia, protein synthesis, Liplysis,
wasting, weight loss.
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Blood Glucose & Hormones
Hormone Insulin Glucortocoids Glucagon Growth Hormone Epinephrine
Action Glucose Glucose Glucose Glucose Glucose
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Cellular Glucose Uptake
Insulin Requiring Striated Muscle Cardiac Muscle Fibroblasts FAT
Non-Insulin Requiring Blood Vessels Nerves Kidney Eye Lens
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Pathology in Diabetes:
Low glucose inside cell decreased cell metabolism (muscle,
liver)
High glucose outside Glycosylation damage (BV)Polyol products – osmotic damage*
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Classification Primary DM – (primary - no other disease)
Type I – IDDM / Juvenile – 10%. Type II – NIDDM /Adult onset – 80%. MODY – 5% maturity onset - Genetic Gestational Diabetes
Secondary DM – (secondary to other dis.) Pancreatitis/tumors/Hemochromatosis. Infectious – congenital rubella, CMV. Endocrinopathy, downs. Drugs – Corticosteroids.
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Pathogenesis of Type I DMGenetic Genetic
HLA-DR3/4HLA-DR3/4 EnvironmentEnvironment
Viral infe..?Viral infe..?
Insulin deficiencyInsulin deficiencyType I / IDDMType I / IDDM
Autoimmune InsulitisAutoimmune Insulitis
Ab to ß cells/insulin Ab to ß cells/insulin
ß cell ß cell DestructionDestruction
• PS Glomerulonephritis• Graves, Hashimoto thyroiditis.• Rheumatic heart disease• SLE, Collagen vascular disease• Rheumatoid arthritis.
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Progression of Type I
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IDDMIDDM
Genetic /Genetic /
ß cell defectß cell defect
Pathogenesis of Type II DMObesity /Obesity /
Life style ?Life style ?
ß cell ß cell
exhaustionexhaustion
Type II NIDDMType II NIDDM
Abnor. SecretionAbnor. Secretion
Insulin ResistanceInsulin Resistance
Relative Relative
Insulin Def.Insulin Def.
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“Things may come to those who wait, but only the things left by those who hustle.”
– Abraham Lincoln
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What type?
1. 56 year male obese2. 30 year female following
pregnancy3. 8 year old boy.4. 24 year female with Cushing’s
sy5. 68 Year male following
Carcinoma of pancreas.6. 34 year male with extensive
tuberculosis.
II NIDDM
II GDM
I IDDM
Sec IDDM
Sec IDDM
Sec IDDM
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Type-I Type-II
Less common Children < 25 Years Insulin- Dependent Duration: Weeks Acute Metabolic
complications Autoantibody: Yes Family History: No Insulin levels: very low Islets: Insulitis 50% in twins
More common Adult >25 Years Insulin Independent * Months to years Chronic Vascular
complications. No Yes Normal or high * Normal / Exhaustion 60-80% in twins
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Insulitis – Type I
InsulinitisInsulinitis
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Islets in Type II Diabetes:
Loss of ß cells, replaced by Amyloid deposits (hyalinization)Loss of ß cells, replaced by Amyloid deposits (hyalinization)
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Islets in Type II Diabetes:
Loss of ß cells, replaced by Amyloid deposits (hyalinization)Loss of ß cells, replaced by Amyloid deposits (hyalinization)
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Complications: Short term Complications: (metabolic)
Hypoglycemia Diabetic Ketoacidosis Non Ketotic hyperosmolar diabetic coma Lactic acidosis
Long term Complications:(Angiopathy) Microngiopathy - Retinopathy,
Nephropathy, Neurophathy, dermatopathy. Macroangiopathy – Atherosclerosis.
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Microangiopathy Pathogenesis:
Hyperglycemia chronic. Glycosylation of basement membrane
proteins Leaky blood vessels. Excess deposition of proteins –
glycosylation cycle. Thick and Leaky blood vessels. Narrow lumen Ischemic Organ damage...
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Diabetic Microangiopathy
Normal
Diabetic
Glucose Glycosylation BM damage leak ‘AGE’ deposition
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Neuropathy Sensory Motor (myelin) Peripheral Neuropathy
Bilateral, symmetric Progressive, irreversible Paraesthesia, pain, muscle
atrophy
Visceral neuropathy Cranial nerve – diplopia, Bell palsy GIT- constipation, diarrhoea CVS – orthostatic hypotension
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Neuropathy
Myelin loss in nerve
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Chronic Polyneuropathy
Claw foot – Dermopathy & Neuropathy
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Diabetic Amyotrophy
Painful muscle wasting
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Diabetic Neuropathic ulcer
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Neuropathic ulcer
Etiology: peripheral sensory
neuropathy, Trauma & deformity.
Factors: Ischemia, callus
formation, and edema.
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Neuropathic ulcers
FEATURES:Painless, surrounded by callus At pressure points. associated with good foot pulsesMay not be associated with gangrene
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Nephropathy Nodular Glomerulo
Sclerosis. Common morbidity &
mortality. Deposition of ‘AGE’
Advanced Glycosylation End-products as nodules.
Nephrotic syndrome Pyelonephritis End stage renal failure
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Diabetic Nephropathy
Microangiopathy, atherosclerosis & infections: Diffuse or nodular diabetic
glomerulosclerosis (Kimmelstiel Wilson Sy) Renal arteriolosclerosis & atherosclerosis Necrotizing renal papillitis. Pyelonephritis. End stage kidney.
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Nodular Glomerulosclerosis – KW lesion.
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Diabetic Glomerulosclerosis
Hyaline nodulesHyaline nodules
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Diabetic Glomerulosclerosis
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Normal Retina
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Non Proliferative Retinopathy Venous dilation and small red dots posterior retinal
pole - capillary micro-aneurysms. Dot and blot retinal hemorrhages and deep-lying
edema and lipid exudates impair macular function. Late generalized diminution of vision due to
ischemia and macular edema - common cause of visual defect (best detected by fluorescein angiography)
Cotton-wool spots (soft exudates) - microinfarcts due to ischemia. They are white and obscure underlying vessels. Hard exudates are caused by chronic edema. They are yellow and generally deep to retinal vessels.
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Proliferative Retinopathy Neovascularization - which grows into the vitreous
cavity. In advanced disease, neovascular membranes can
occur, resulting in a traction retinal detachment. Vitreous hemorrhages may result. sudden severe loss of vision can occur when there is
intravitreal hemorrhage. Poor visual prognosis if severe retinal ischemia,
extensive neovascularization, or extensive fibrous tissue formation.
Panretinal photocoagulation may diminish or eliminate proliferative retinopathy
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Retinopathy Non Proliferative
Microaneurysms, Dot blot hemorrhages Hard and soft exudates Cotton wool – infarcts Macular edema.
Proliferative. Neovascularization Large hemorrhages Retinal detachment.
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Diabetic Retinopathy
Neovascularization Cotton wool spots
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Diabetic Retinopathy
Dot blot – Hemorrhages (Microaneurysms)
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Diabetic Retinopathy
Pre retinal Hemorrhage - detachment
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Diabetic Retinopathy
Advanced fibrous plaques
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“The past cannot be changed, but the future can.. by actions in the present time.” --BK
Past is history, Past is history,
Future is mysteryFuture is mystery
Present is the gift…!Present is the gift…!
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Label the diagram.
1.
2.
3.
4.
5.
Hard dep.
Optic disc
Macula
Blot hem
Cotton wool
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Macroangiopathy Atherosclerosis
Dyslipidemia HDL Non-Enzymatic Glycosylation Platelet Adhesiveness
Thromboxane A2
Prostacyclin Endothelial damage Atherosclerosis MI, CVA, Gangrene of Leg (PVD), Renal
Insufficiency
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Atherosclerosis:
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Slide Show
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Diabetic Gangrene
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Fungal infections: Candidiasis
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Macrosomia
With Polycythemia
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Blood vessel calcification:
Amputated thumb
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Cataract
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Acanthosis Nigricans
Insulin resistance…
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Acanthosis Nigricans
Insulin resistance…
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Label the diagram.
1.
2.
3.
4.
Capillary
Nodule – AGE
Bowman caps
Hyaline arteriolo sclerosis in arteriole.
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Infections in Diabetes:
Decreased metabolism – low immunity. Decreased function of lymphocytes &
neutrophils – glycosylation. Glycosylation of immune mediators. Ab Capillary thickening – impaired inflammation. Ischemia & infarctions. Increased glucose (alone is not the cause*)
Diabetes State of immunosuppression.
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Laboratory Diagnosis:
Urine glucose - dip-stick –Screening Random or fasting blood glucose (<11) Fasting > 7mmol, Random >11mmol If Fasting level is between 7-11 then OGTT
HbA1c - for follow-up, not for diagnosis Fructosamine - for long term maintenance.
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Points to remember:
Disorder of metabolism – Insulin Type-I Children, Acute, Metabolic compl. Type-II Adults, Chronic, Vascular compl.
Angiopathy (micro/macro), Heart, Brain, Kidney, Retina, Skin, BV.
Increased Infections – know reasons. Hypoglycemia is more dangerous. Not hyper Glucose control is critical * FBS, GTT & HbA1C.
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Questions..
How – Ketoacidosis? How – hypoglycemia ? Angiopathy – Macro & Micro ? Infections in Types of retinopathy ? Diabetes insipidus ? Nephrotic / Nephritic syndrome ? Kidney damage in Diabetes ?
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The best gift of Nature to man is the briefness of his life…! Latin quote
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“It's not that I'm so smart, it's just that I stay with problems longer”--Albert Einstein