pathophysiology group 1 balamiento – balmores – bernardo – cabantac – castellano – chan -...
Post on 01-Apr-2015
220 Views
Preview:
TRANSCRIPT
PATHOPHYSIOLOGY
GROUP 1BALAMIENTO – BALMORES – BERNARDO
– CABANTAC – CASTELLANO – CHAN - CORPUS
PATHOPHYSIOLOGY
• Type II Diabetes Mellitus
• Pneumonia
TYPE II DIABETES MELLITUSPATHOPHYSIOLOGY
• An endocrine metabolic disorder– Primarily involves the pancreatic beta cell
TYPE II DIABETES MELLITUSPATHOPHYSIOLOGY
• With symptoms of hyperglycemia– increased peripheral insulin resistance– inadequate pancreatic insulin secretions– Increased hepatic glucose production
• Genetic and environmental factors
TYPE II DIABETES MELLITUSPATHOPHYSIOLOGY
• Genetic factors– T2DM among first-degree relatives
• risk by 20 to 40%
– The patient has strong family history• greatly increases the risk of T2DM
TYPE II DIABETES MELLITUSPATHOPHYSIOLOGY
• increased peripheral insulin resistance
• inadequate pancreatic insulin secretions
• Increased hepatic glucose production
Increased Peripheral Insulin ResistancePATHOPHYSIOLOGY
• decreased insulin action on peripheral insulin-sensitive tissues
• Initially relative– Hypersecretion of insulin to normalize plasma
glucose levels
Increased Peripheral Insulin ResistancePATHOPHYSIOLOGY
Post-receptor defects FFA
Impaired PI-3-kinase signaling pathway
Impaired translocation of GLUT4
Reduced transport of glucose intracellularly
Elevated FFA levels
Impairs skeletal muscle usageEnhances hepatic glucose
productionImpair beta cell function
Increase hepatic glucose production (unsuppressed gluconeogenesis)
Decreased glucose utilization
Inadequate Pancreatic Insulin Secretions
PATHOPHYSIOLOGYInitially
hyperinsulinemia
Inadequate compensation
progression
Further dec in insulin secretionIncrease hepatic glucose production
Further progression
Beta cell failure
UltimatelyGlucose toxicity
Lipotoxicity
Diabetes
Increased Hepatic Glucose Production PATHOPHYSIOLOGY
Insulin resistance
Failure of gluconeogenesis suppression
Postprandial hyperglycemia
Further reduction in glycogen storage
Symptoms PATHOPHYSIOLOGY
hyperglycemia
Dehydration[decrease skin turgor]
hyperosmolarity
Intracellular water depletion
Trigger osmoreceptors (thirst center)
Polydipsia[increased thirst]
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
Symptoms PATHOPHYSIOLOGY
Eventual decline in insulin levels
Fuel source shifts from carbohydrates to proteins and fats
proteolysis
Usage of gluconeogenic amino acidsDepletion of glycogen stores
Polyphagia
Cells become hungry
Increased appetite to compensate for depleted energy stores
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
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
Chronic complications PATHOPHYSIOLOGY
• Diabetic retinopathy
• Hypertension stage I
• Infection
DIABETIC RETINOPATHY PATHOPHYSIOLOGY
• nonproliferative diabetic retinopathy– retinal vascular microaneursysms, dot and
blot hemorrhages, and exudates
Several factors Retinal ischemia Neovascularization
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
DIABETIC RETINOPATHY PATHOPHYSIOLOGY
HYPERTENSION STAGE I PATHOPHYSIOLOGY
Increased sympathetic nervous system activity
hyperinsulinemia
Increased sodium retentionIncreased cardiac output
Increased peripheral vascular resistance
[Landsberg]with anti-natruiretic effects on kidneys
Prevents compensatory mechanism to decrease BP
HYPERTENSION STAGE I PATHOPHYSIOLOGY
Vascular smooth muscle hypertrophy
Mitogenic effects of insulin
HYPERTENSION STAGE I PATHOPHYSIOLOGY
Modified ion transport
Cell membrane defects
Increased cytosolic calcium levels in insulin-sensitive
tissues
Increased responsiveness to
vasoconstrictor agents
INFECTION PATHOPHYSIOLOGY
• Presence of fever suggests ongoing infection
• Common among diabetic patients– Pneumonia– UTI– Skin and soft tissue infections
Pneumonia PATHOPHYSIOLOGY
• frequent pathogens– Gram-negative organisms, S. aureus and M.
tuberculosis
• Mode of transmission– Aspiration (most likely)– Hematogenous spread– Direct extension
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
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)
Pneumonia PATHOPHYSIOLOGY
Release of cytokines
Local leukocytosisIncreased purulent secretions
Alveolar capillary leakageNarrowing of air passageways
Alveolar hypoxemia
Rales
Stimulation of respiratory centers Tachypnea
Pneumonia PATHOPHYSIOLOGYRelease of cytokines
Circumventricular organs (brain)
Activation of ARA pathway
Production of PGE2Fever
Acts on hypothalamus (ventromedial preoptic area and parvocellular portion of
periventricular nucleus)
Elevation of thermoregulatory set-
point
gen. circulation
Pneumonia PATHOPHYSIOLOGY
• Chest pain.– a reaction to the inflammation– pleuritic chest pain is the usual description
THANK YOU!!!
top related