Diabetic mellitus.pptxAs per WHO it is a heterogenous metabolic disorder characterized by chronic hyperglycemia with disturbance of carbohydrate fat and protein metabolism

As per WHO it is a heterogenous metabolic disorder characterized by chronic hyperglycemia with disturbance of carbohydrate fat and protein metabolism

1. DIABETES MELLITUS

2. DEFINITION As per WHO it is a heterogenous metabolic disorder characterized by chronic hyperglycemia with disturbance of carbohydrate fat and protein metabolism

3. PATHOGENESIS OF TYPE II DIABETES It is a multifactorial disease . Environmental factors play a role and includes: Sedentary lifestyle. Dietary habits and associated obesity particularly central or visceral obesity. Genetic factors

4. INSULIN RESISTANCE Insulin resistance is the decrease/failure of target (peripheral) tissues to insulin action. Main factors in the development of insulin resistance is obesity. The risk for diabetes increases as the body mass index (a measure of body fat content) increases. Central obesity > peripheral fat

5. β -CELL DYSFUNCTION It manifests as inadequate insulin secretion by the pancreatic β-cells (relative insulin deficiency) in association with insulin resistance and hyperglycemia.

6. PATHOGENESIS OF TYPE 1 DM

7. PATHOGENESIS OF TYPE 2 DM

8. HYPERTENSION

9. “Sustained increase in blood pressure” Systolic >140, Diastolic > 90 mm of Hg* Normal* < 130 <85 (120/80 +/- 10/5) Mild + 20, Moderate +40 Severe +80 Malignant - > 210/120

10. ETIOLOGICAL CLASSIFICATION Essential (Primary) Hypertension (95%) Unknown etiology. Life style, genetic, … Secondary Hypertension (5-10%) Renal – GN, RAS, Renin tumors Endocrine – Cushing, OCP, Thyrotoxicosis Myxdema , Pheochromocytoma, Acromegaly. Vascular – Coarctation of Aorta, PAN, Aortic insufficiency. Neurogenic – Psychogenic, Intracranial pressure, olyneuritis etc.

11. ETIOLOGY: Secondary - Known abnormal control. Renal disorders – Renin-Angiotensin. Sodium retention, ADH, Aldosterone. Cushings , Pheochromocytoma, Essential - Etiology is multifactorial. Increased peripheral resistance (sympathetic tone) stress, hormonal, neural. Genetic, familial, life style.

12. Pathogenesis of Renovascular HTN:  GFR Renin by JGA Angiotensin II Vasoconstriction  P. Resistance Sodium Retention  Blood Volume Aldosterone Hypertension

13. MALIGNANT HYPERTENSION: Rapidly progressive end organ damage. May complicate any type of HTN. Artery necrosis with thrombosis. Rapidly developing renal failure. Hypertensive encephalopathy. Left ventricular failure. less time  No hypertrophy …!

14. MORPHOLOGY: Large Blood Vessels – Macroangiopathy. Atherosclerosis and its complications. Small Blood Vessels – Microangiopathy. Hyperplastic arteriolosclerosis. (thick arterioles) Heart LVH, Hypertensive cardiomyopathy  IHD, MI. Kidney Benign nephrosclerosis. Eyes : Hypertensive retinopathy Brain : Haemorrhage , infarction, splinter hemorrhages & Lacunar infarcts.

15. PATHOGENESIS OF VASCULAR CHANGES. Arteriolosclerosis Rupture Aneurysm Rupture. Ischemia, Aneurysm, Rupture

16. Left Ventricular Hypertrophy: Left Ventricular Hypertrophy

17. Hyperplastic Arteriolosclerosis: Onion Skin Thickening Of arterioles. Narrow Lumen

18. Nephrosclerosis in HPTN: Artery Sclerosis Artery Sclerosis PCT hydropic deg.

19. Nephrosclerosis in HPTN: Artery Sclerosis Glom. Sclerosis Artery Sclerosis PCT hydropic deg.

20. Necrotizing arteriole: Malignant HPTN Fibrinoid Necrosis Thrombosis

21. Subarachnoid Haemorrhage: Cerebral Blood vessels Special features: Thin walled* End arteries* Cong. Aneurisms

22. Cerebral Infarction (Stroke) : Haemorrhagic Necrosis

23. Lacunar Infarct: Chronic hypertension Arteriolosclerosis of deep penetrating arterioles of brain stem. Single or multiple cavitary infarcts – lacunes. Lenticular nucleus, thalamus Slit Haemorrhages .

24. Benign Nephrosclerosis: Leathery Granularity due to minute scarring

25. CEREBRAL INFARCTION:

26. Renal Causes : Renal artery atherosclerosis Polycystic Disease Glomerulonephritis (A/C) Renal artery stenosis Renal vasculitis – SLE Renin producing tumors. Polycystic Kidney ->

27. Renal Artery stenosis - Atrophy Leathery Granularity Benign Nephrosclerosis

28. Normal Retina - Fundoscopy

29. HYPERTENSIVE RETINOPATHY: Arteriosclerosis cause the arteriole light reflex to become broad and dull – silver wire Generalized or focal retinal arteriolar constriction – pale. Superficial flame-shaped hemorrhages. Small white foci of retinal ischemia (cotton-wool spots). Yellow hard exudates, due to lipid deposition deep in the retina.

30. Hypertensive Retinopathy: Grade I – Thickening of arterioles. Grade II – Focal Arteriolar spasms. Vein constriction. (AV nipping) Grade III – Hemorrhages (Flame shape), dot-blot and Cotton wool (ischemia) and hard waxy exudates (lipid deposition). Grade IV - Papilloedema

31. Conclusions: Persistent increased blood pressure.. 95% Essential, 5% secondary - Renovascular Benign and Malignant types (>120 Diastolic) Vessel damage & Arteriolosclerosis Complicates - Atherosclerosis, Diabetes, IHD Ischemia or Infarction in end organs. Kidney, Brain, Heart & Eyes. Complications: Nephrosclerosis, renal damage, IHD, MI, Stroke & Retinopathy.