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30 Cards in this Set
- Front
- Back
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Etiology
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The study of what causes a certain disease.
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Most diseases are linked to one or a combination of:
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Genetic factors
Environmental factors Self-regulation of behavior |
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Pathology
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The disturbance away from the normal function of an organ caused by disease.
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Chronic Disease
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An abnormal physiological state that creates organs and tissues in the body to malfunction to a point that is detrimental to a normal functioning body.
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Common chronic diseases
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Obesity
Coronary artery disease Diabetes Type 1 Type 2 Certain cancers |
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Obesity
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BMI that corresponds to >120% of ideal body weight.
Body fat percent >30% Imbalance between caloric intake and expenditure. Childhood obesity |
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Childhood obesity is
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Hyperplastic
Greater number than normal of fat cells Hypertrophic Greater than normal size of fat cells |
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Current trends indicate that caloric imbalance is leading
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to fat dispersion in children that is more commonly found in adults.
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obesity
Genetic theory |
Obese gene product leptin may function to control body fat stores by regulating satiety and energy expenditure. Genetic alterations in the obese gene production of leptin may result in adipose accumulation.
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obesity
Fat cell Theory |
Individuals with hyperplastic fat cells are overweight due to number of fat cells.
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Thermogenic theory
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Obese individuals have fewer brown fat cells, the mitochondria rich fat cells responsible for heat production; difficult time burning off excess energy.
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Diabetes-associated theory
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Excess food intake stimulates hyperinsulinemia and promotes high blood glucose levels
Excess blood glucose is stored in the liver as glycogen or in the adipose cells as triglycerides Enhances hypertrophy and hyperplasia in the fat cells of the already obese person |
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Pathophysiology of obesity
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Disturbance of the normal function of specific organs due to increased accumulation of adipose tissue
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The number of fat cells predisposes an individual to becoming obese.
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1 year of age:
normal weight gain is associated with increased size of fat cell, but not indicative of obesity in adulthood However, high amounts of weight gain may be associated with adult obesity |
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The number of fat cells predisposes an individual to becoming obese.
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4 – 11 years of age:
Abnormal weight gain during these years is associated with adult obesity; lifelong risk |
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The number of fat cells predisposes an individual to becoming obese.
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Adult obesity:
Associated with increased fat cell size, but when they reach a finite capacity adipogenesis occurs. |
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Genetics or Environment?
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30 – 40% of reason for being obese is attributed to genetics
60 – 70% attributed to environment |
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Pima Indian Study
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Two groups of Pimas: Mexico & Arizona
Genetically the same; environment not the same Pima Indians in Mexico have significantly lower BMI’s; lower incidences of obesity and T2D Average BMI’s 24.9 kg/m2 for Pima Indians in Mexico 33.4 kg/m2 for Pima Indians in Arizona |
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Metabolic Predictors for Weight Gain
3 metabolic predictors |
Low resting metabolic rate (RMR)
High FFM results in in greater RMR Respiratory Quotient (RQ) CHO to fat oxidation ratio RQ of .7 indicates a low level of CHO metabolism at rest Ratio of 1.0 suggests that more CHO is being burned at rest as opposed to fat; not good Sedentary lifestyle Fewer calories being burned |
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Patterns of Body Fat Distribution & Risk
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High risk distributions:
Abdominal distribution High visceral adipose accumulation Lower risk distributions: Hips & lower body |
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Disorders associated with obesity
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nsulin resistance
T2D Hypertension Dyslipidemia CAD Cancer Stroke |
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Disorders associated with obesity
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Osteoarthritis
Asthma Sleep apnea Breathing difficulties Psychological distress |
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Insulin Resistance
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Hyperinsulinemia
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Obese individuals typically have:
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Higher insulin levels
Lower insulin sensitivity in a 75-g oral glucose tolerance test Leads to: Diabetes Dyslipidemia (production of too much “bad” cholesterol; or free fatty acids [FFAs]) Hypertension (high blood pressure) Hypercoagulability (clotting) CAD |
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Insulin Resistance / Hyperinsulinemia
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Decrease in insulin sensitivity associated with onset of puberty
Normal pancreatic β-cell compensation though by increased insulin production |
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African American & Hispanic children may have a more difficult time
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difficult time regulating insulin
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Bogalusa Heart Study indicated that
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AA girls had higher insulin levels and insulin : glucose ratios
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Hispanic children have lower
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adiponectin production; secreted by adipose tissue and thought to have a role in energy production and insulin sensitivity
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Possibly greatest risk factor for getting T2D occurs
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in utero.
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Metabolic markers indicating IR are:
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Acanthosis nigricans
Polycystic ovary syndrome |
