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68 Cards in this Set
- Front
- Back
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Links Between Physical Activity and Chronic Diseases
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OBESITY
Coronary Artery Disease Diabetes type-2 Cancer Osteoporosis These chronic diseases are known as hypokinetic diseases. |
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Etiology >Pathology>
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Overweight / Obesity
In Childhood |
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Sedentary=
Caloric Imbalance= Genetic Predisposition= |
Health-Related Fitness /Mechanical Stressors
Malnutrition Fat Dispersion Obese Gene Theory Thermogenic Theory Type 2 Diabetes |
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Sedentary
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Health-Related Fitness
Cardiovascular Health Atherosclerosis Muscle Development Muscle Atrophy Metabolically inefficient Mechanical Stressors GH Production / Release Sleep Connection apnea |
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Caloric
Imbalance |
Malnutrition
Lack of / Excess calorie consumption Improper nutrition at critical periods lack of muscle development Adipose Accumulation Hypertrophic – large adipose cells Hyperplasticity – high number of adipose cells Hyperinsulinemia Overproduction of insulin by pancreas Fat Dispersion seeing adult fat distributions in pediatric populations |
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Genetic
Predisposition |
Obese Gene Theory
Ob gene effects leptin control / production Thermogenic Theory lack of brown fat cells produces body heat; difficult to burn off excess energy Type 2 Diabetes family correlation may have a connection with adipoplasia |
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Children exhibiting two or more of these etiological risk-
factors are prime for a metabolic melt-down!! |
are prime for a metabolic melt-down!!
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Potential Solutions
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Physical activity, clinical and community must focus on family intervention programs!
Emphasis on: family activities proper nutrition familial genetic risk-factors |
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Etiology
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The study of what causes a certain disease.
Most diseases are linked to one or a combination of: Genetic factors Environmental factors Self-regulation of behavior |
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Pathology
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Study of abnormal physiology of
disease based upon the development of the disease process |
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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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CHRONIC DISESEAS
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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 is Hyperplastic Greater number than normal of fat cells Hypertrophic Greater than normal size of fat cells Early childhood fat distribution is fairly evenly dispersed Current trends indicate that caloric imbalance is leading to fat dispersion in children that is more commonly found in adults. Abdominal dispersion Visceral adipose accumulation |
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Hyperplastic
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Greater number than normal of fat cells
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Hypertrophic
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Greater than normal size of fat cells
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Obesity Etiology
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Genetic theory
Fat cell Theory |
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Genetic theory
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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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Fat cell Theory
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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 4 – 11 years of age: Abnormal weight gain during these years is associated with adult obesity; lifelong risk 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 environmen |
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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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Insulin 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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nsulin Resistance / Hyperinsulinemia LEADS TO
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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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Higher insulin levels
Lower insulin sensitivity in a 75-g oral glucose tolerance test |
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Dyslipidemia
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(production of too much “bad” cholesterol; or free fatty acids [FFAs])
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Hypertension
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(high blood pressure
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Hypercoagulability
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(clotting)
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Insulin Resistance
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/ Hyperinsulinemia
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T2D
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Possibly greatest risk factor for getting T2D occurs in utero.
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Offspring of mothers who get gestational diabetes or are hyperglycemic are more at risk
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T2D
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Extreme birth weights (high and low)
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are associated with T2D
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Risk of T2D rises greatly with
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weight gain in children
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/ 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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Metabolic markers indicating IR are:
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Acanthosis nigricans
Polycystic ovary syndrome |
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TYPE 1 DIABITES
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THEPANCREASE MAKES LITTLE OR NO INSULIN
LITTLE OR NO INSULIN ENTERS THE BLOOD STREAM GLUCOSE BUILDS UP IN THE BLOOD STREAM |
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TYPE 2 DIABETES
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THE PANCREASE MAKES THE INSULIN
INSULIN ENTERS THE BLOOD STREAM GLUCOSE CAN NOT ENTER THE BLOOD STREAM, GLUCOSE BUILDS UP IN BLOOD VESSELS |
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Stages of Prenatal Growth
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Zygote
Embryonic Fetal |
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Zygote Stage
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First 2 weeks after fertilization
Rapid mitosis (cell division) Result of totipotent stem cells Cells cluster – morula Development of what will be the entire fetal environment. |
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Embryonic Stage PART A
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Successful implantation into the endometrium
Hormonal action of blastocyst impairs maternal immune system to prevent antibodies from attacking blastocyst Stem cell proliferation and differentiation Pluripotent – potential to create differentiated cells or cells that will form specific tissues and eventually organs. |
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Embryonic Stage PART B
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Blastocyst structure differentiation (occurs by the end of the third week post conception and will continue to proliferate through embryonic stage!):
Ectoderm – forms skin, hair, sweat glands, tooth enamel, nervous tissue (including the brain) Mesoderm – muscles, bones, blood, circulatory system, teeth, connective tissues, and kidneys Endoderm – most of the internal organs (stomach, liver, intestines, lungs, heart, …) |
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Ectoderm
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Ectoderm – forms skin, hair, sweat glands, tooth enamel, nervous tissue (including the brain)
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Mesoderm
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– muscles, bones, blood, circulatory system, teeth, connective tissues, and kidneys
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Endoderm –
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Endoderm – most of the internal organs (stomach, liver, intestines, lungs, heart, …)
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Fetal Stage
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From weeks 9 to 40
Characterized by: Rapid growth Increased complexity of tissue and organ development No new anatomical features appear during this time Weight gain is of utmost importance during this time Low birth weight associated with increased risk of birth mortality and future health problems. |
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Fetal Stage
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Determinants of Intrauterine Growth and Birth Weight
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Fetal Stage
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Direct
Infant sex Ethnicity/race Maternal weight Pre-pregnancy weight Paternal height/weight Maternal birth weight Gestational weight gain Caloric intake General morbidity history Malaria Cigarette smoking Alcohol consumption / drug abuse Maternal exercise Tobacco chewing Prior low birth-weight infant |
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Indirect
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Maternal age
Socioeconomic status |
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What is the purpose of the endocrine system?
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The endocrine system is composed of glands that produce hormones for the purpose of regulating the function of an organ or tissue growth.
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What is the role of the hypothalamus?
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controls the release of hormones produced by the pituitary, thyroid and sex glands
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The hormones secreted by the hypothalamus into the pituitary gland
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growth hormone-releasing hormone (GHRH), somatotropin releasing – inhibiting factor (SRIF), thyrotropin – releasing hormone (TRH), corticotropin – releasing hormone (CRH), and gonadotropin releasinghormone(GnRH)
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neuroendocrines
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egulatory factors that determine the release of the hormones from the pituitary gland.
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What is the role of the pituitary gland?
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The pituitary gland is a primary gland in the regulation of anatomical and physiological growth. It is divided intotwolobes;theanteriorlobe(front)andtheposteriorlobe(back)
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. The anteriorlobe produces and secretes
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growth hormone (GH), thyrotropin (TSH), adrenocorticotropin (ACTH), follicle stimulating hormone(FSH),andluteinizinghormone(LH).
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The posteriorlobe does not secrete hormones directly related to the growth process.
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hormones directly related to the growth process.
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There are two primary hormones secreted by the posterior lobe of the pituitary gland; an anti-diuretic hormone called vasopressin and oxytocin.
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an anti-diuretic hormone called vasopressin and oxytocin.
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Vasopressin regulates
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the amount of water released in the urine. This controls the water balance in the body
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The oxytocin is associated with the end stage of the fetus development. The release of oxytocin
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causes the uterus to contractin the birthing process as well as signifies for the breast milk to be released after the delivery of the baby.
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The thyroid is another endocrine gland that
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that assists in the growth and maintenance of the body.
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The thyroid gland RELEASE AND SECRETES
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thyroxine (T4), triiodothyronine (T3), and calcitonin. The hormones from the thyroid gland are unique in that they are responsible for the stimulation of oxygen uptake and energy expenditure.
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the effects from GH are
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insignificant without T4 being present. It is the job of the T4 to facilitate other growth producing hormones performing their determined effects as well.
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Thyroid hormones stimulate
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oxygen up take and energy expenditure. Therefore,they promote the increase of oxygen consumption in the major O2 consuming tissues of the body (muscles, heart, and liver)by increasing mitochondrial oxidative metabolism.
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he endocrine system is a series of pathways from glands
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that secrete specific hormones and are then carried through the blood stream
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