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PATHOPHYSIOLOGY GROUP 1 BALAMIENTO – BALMORES – BERNARDO – CABANTAC – CASTELLANO – CHAN - CORPUS.

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Presentation on theme: "PATHOPHYSIOLOGY GROUP 1 BALAMIENTO – BALMORES – BERNARDO – CABANTAC – CASTELLANO – CHAN - CORPUS."— Presentation transcript:

1 PATHOPHYSIOLOGY GROUP 1 BALAMIENTO – BALMORES – BERNARDO – CABANTAC – CASTELLANO – CHAN - CORPUS

2 PATHOPHYSIOLOGY Type II Diabetes Mellitus Pneumonia

3 TYPE II DIABETES MELLITUS PATHOPHYSIOLOGY An endocrine metabolic disorder –Primarily involves the pancreatic beta cell

4 TYPE II DIABETES MELLITUS PATHOPHYSIOLOGY With symptoms of hyperglycemia –increased peripheral insulin resistance –inadequate pancreatic insulin secretions –Increased hepatic glucose production Genetic and environmental factors

5 TYPE II DIABETES MELLITUS PATHOPHYSIOLOGY Genetic factors –T2DM among first-degree relatives  risk by 20 to 40% –The patient has strong family history greatly increases the risk of T2DM

6 TYPE II DIABETES MELLITUS PATHOPHYSIOLOGY increased peripheral insulin resistance inadequate pancreatic insulin secretions Increased hepatic glucose production

7 Increased Peripheral Insulin Resistance PATHOPHYSIOLOGY decreased insulin action on peripheral insulin-sensitive tissues Initially relative –Hypersecretion of insulin to normalize plasma glucose levels

8 Increased Peripheral Insulin Resistance PATHOPHYSIOLOGY Post-receptor defectsFFA Impaired PI-3-kinase signaling pathway Impaired translocation of GLUT4 Reduced transport of glucose intracellularly Elevated FFA levels Impairs skeletal muscle usage Enhances hepatic glucose production Impair beta cell function Increase hepatic glucose production (unsuppressed gluconeogenesis) Decreased glucose utilization

9 Inadequate Pancreatic Insulin Secretions PATHOPHYSIOLOGY Initially hyperinsulinemia Inadequate compensation progression Further dec in insulin secretion Increase hepatic glucose production Further progression Beta cell failure Ultimately Glucose toxicity Lipotoxicity Diabetes

10 Increased Hepatic Glucose Production PATHOPHYSIOLOGY Insulin resistance Failure of gluconeogenesis suppression Postprandial hyperglycemia Further reduction in glycogen storage

11 Symptoms PATHOPHYSIOLOGY hyperglycemia Dehydration [decrease skin turgor] hyperosmolarity Intracellular water depletion Trigger osmoreceptors (thirst center) Polydipsia [increased thirst]

12 Symptoms PATHOPHYSIOLOGY Renal excretion of glucose Glucosuria [ants around toilet seat] Exceeds renal threshold for glucose absorption Increase glucose levels in urine Promotes osmotic diuresis Nocturia or polyuria

13 Symptoms PATHOPHYSIOLOGY Eventual decline in insulin levels Fuel source shifts from carbohydrates to proteins and fats proteolysis Usage of gluconeogenic amino acids Depletion of glycogen stores Polyphagia Cells become hungry Increased appetite to compensate for depleted energy stores

14 Symptoms PATHOPHYSIOLOGY Obesity –central or visceral obesity is common more associated with insulin resistance –elevated free fatty acids lipid accumulation (liver and skeletal muscles)  intracellular accumulation of free fatty acid  toxic and potently inhibits insulin signaling pathway –adipokines adipokine secretion (leptin, adiponectin and resistin) dysregulation  food intake is abnormally increased and subsequent suppression of satiety

15 Symptoms PATHOPHYSIOLOGY Malaise –decreased glucose (main fuel source) utilization –Usage of fat as a fuel source requires body to use more energy patient constantly feels weak

16 Chronic complications PATHOPHYSIOLOGY Diabetic retinopathy Hypertension stage I Infection

17 DIABETIC RETINOPATHY PATHOPHYSIOLOGY nonproliferative diabetic retinopathy –retinal vascular microaneursysms, dot and blot hemorrhages, and exudates Several factors Retinal ischemiaNeovascularization

18 DIABETIC RETINOPATHY PATHOPHYSIOLOGY Damaged retinal pericytes –Endothelial supporting cells altered retinal blood flow Impaired retinal blood flow autoregulation Exudation secondary to increased permeability of retinal blood vessels in DM

19 DIABETIC RETINOPATHY PATHOPHYSIOLOGY

20 HYPERTENSION STAGE I PATHOPHYSIOLOGY Increased sympathetic nervous system activity hyperinsulinemia Increased sodium retention Increased cardiac output Increased peripheral vascular resistance [Landsberg] with anti-natruiretic effects on kidneys Prevents compensatory mechanism to decrease BP

21 HYPERTENSION STAGE I PATHOPHYSIOLOGY Vascular smooth muscle hypertrophy Mitogenic effects of insulin

22 HYPERTENSION STAGE I PATHOPHYSIOLOGY Modified ion transport Cell membrane defects Increased cytosolic calcium levels in insulin-sensitive tissues Increased responsiveness to vasoconstrictor agents

23 INFECTION PATHOPHYSIOLOGY Presence of fever  suggests ongoing infection Common among diabetic patients –Pneumonia –UTI –Skin and soft tissue infections

24 Pneumonia PATHOPHYSIOLOGY frequent pathogens –Gram-negative organisms, S. aureus and M. tuberculosis Mode of transmission –Aspiration (most likely) –Hematogenous spread –Direct extension

25 Pneumonia PATHOPHYSIOLOGY Inhalation of pathogens Enter the lower respiratory tract Phagocytosis by alveolar macrophages [Ljubic et. al.] enhanced adherence of pathogens in the respiratory epithelium in DM Impaired intracellular killing Release of cytokines

26 Pneumonia PATHOPHYSIOLOGY Decreased immune system function –Impaired neutrophil and macrophage functions Chemotaxis, adherence, phagocytosis and intracellular killing –Intracellular killing increased glucose levels  competes with usage of NADPH necessary for free radical production  decrease levels of free radicals (superoxide and hydrogen peroxide)

27 Pneumonia PATHOPHYSIOLOGY Release of cytokines Local leukocytosis Increased purulent secretions Alveolar capillary leakage Narrowing of air passageways Alveolar hypoxemia Rales Stimulation of respiratory centers Tachypnea

28 Pneumonia PATHOPHYSIOLOGY Release of cytokines Circumventricular organs (brain) Activation of ARA pathway Production of PGE2 Fever Acts on hypothalamus (ventromedial preoptic area and parvocellular portion of periventricular nucleus) Elevation of thermoregulatory set- point gen. circulation

29 Pneumonia PATHOPHYSIOLOGY Chest pain. –a reaction to the inflammation –pleuritic chest pain is the usual description

30 THANK YOU!!!


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