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64 Cards in this Set
- Front
- Back
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Metabolic Syndrome
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Name for a group of risk factors that occur together and increase the risk for CAD, CVA, and NIDDM.
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FXNs of fat
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-main fxn is to store energy as fat
-cushions and insulates the body -surrounds internal organs-protection -source of hormones |
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Types of Adipose Tissues
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-white
-brown |
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Brown Fat
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found in newborns to generate heat
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Adipokines
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proteins produced and secreted from adipose tissue
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Adipokines
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-Resistin
-Leptin -TNF-a -Adiponectin |
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Leptin
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-Inhibits appetite
-Adipokine -key role in regulating energy intake, expenditure, and appetite -interacts with 6 receptors: LepRa-f |
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Binding of Leptin
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-Decreases appetite by down regulating endocannaboid
-mutant of leptin gene and/or defects in signal transduction/leptin deficiency results in overeating |
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Adipose Concentrations
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1. Expansion of adipose stores increases leptin and leptin decreases calorie intake by inhibiting hunger and stimulating satiety
2. Leptin stimulates thermogenesis to restore fat mass to setpoint |
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Leptin
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-Leptin circulates at levels proportional to body fat levels
-Higher leptin levels inhibit food intake and vice versa |
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Obesity and Leptin
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Obesity is associated with higher leptin plasma levels and a resistance to leptin
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Actions of Leptin
CV FXN |
-hyperleptinemia is associated with increased systolic/diastolic pressure (high leptin is also associated with hypotension)
-increased tubular reabsorption of sodium -modulates response to atherlosclerosis -increased sympathetic nerve activity -increased HR -poor prognosis after MI -may be a factor in reproduction (inhibits uterine contractions) -may be important for bone growth |
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Hyperleptinemia is associated with...
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increased:
-BP -lipotoxicity -inflammation -thrombogenesis -oxidative stress |
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Acrp30
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syn for adiponectin
adiponectin compoenent-related protein |
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apM1
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syn for adiponectin
Adipose Most abundant gene transcript |
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Adiponectin
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Complimentary/additive to leptin
-peptide/protein hormone -levels are inversely correlated with BMI -In Type 1 diabetes adiponectin lower -Wt loss, caloric restriction, and TZDs all increase adiponectin levels |
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TZDs
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thiazolidenediones (Avandia):used in the management of type 2 diabetes
-decrease in insulin resistance -adipocyte differentiation is modified -leptin levels increase (resulting in decreased appetite) -adiponectin levels rise |
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Effects of Adiponectin on Metabolism
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-increases glucose uptake
-increases insulin sensitivity -increases fatty acid oxidation/clearance -suppresses gluconeogenesis |
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Effects of Adiponectin on Endothelial Tissues
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-promotes endothelial cell survival
-anti-inflammatory |
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Adiponectin and Vessels
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-anti-atherogenic fxn
-possible role in regulating BP -cardioprotective: acts as a negative regulator of cardiac hypertrophy -protects from MI -high levels associated with lower risk of infarct |
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Resistin
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-peptide hormone
-produced in white adipose -levels elevated in fatties and insulin resistant pts -induces insulin resistance -high [resistin] increases risk for inflammation and atherosclerosis |
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Visfatin
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-peptide hormone
-produced in liver, white adipose, muscle, bone marrow, and lymphocytes -exerts insulinmimetic properties -lowers [glucose] in plasma -effects seen in liver, adipocytes, and myoctes -[plasma] increase with the development of obesity and are higher in NIDDM (the source of increase is from additional production from WAT) |
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Visfatin and Glucose Homeostasis
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-IV infusion of visfatin reduces [glucose] in plasma
-causes a direct hypoglycemic effect because there is no effect on insulin -binds to insulin receptor at a site other than insulin -stimulates the phosphorylation of the insulin receptor and of the insulin receptor substrates |
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Apelin (1)
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-Produced by WAT, heart, kidney, GI tract, brain, adrenal gland, and epithelium
-apelin-36 (original precursor) -now found as 13 and 17 which both have greater biologic activity than the -36 form -Vasodilator, natriuretic, stimulates cardiac contractility -operates mainly in a paracrine fashion -inactivated by ACE-2 |
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Apeline (2)
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-receptor found in brain and most tissues
-exerts vasodilator and natriuretic effects -stimulates cardiac contractility -low levels correlated with EF in patients with heart failure -treatment with exogenous apelin improves contractility in humans |
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Omentin
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-found in and secreted from visceral fat
-2 forms: 1. Omentin-1 (in plasma) 2. Omentin-2 -Levels decreased in obesity, PCOS, -Levels inversely correlated to BMI and waist size |
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Omentin (2)
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-appears to be inhibited by:
1. Hyperglycemia 2. Hyperinsulinemia 3. Dose-dependent decrease -infusion of recombinant omentin-1 enhances insulin-stimulated glucose uptake in fat cells through GLUT-4 |
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Myokines
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-factors secreted from skeletal muscle have endocrine fxns
-known targets: 1. Bone 2. Skeletal Muscle 3. Fat 4. Liver -appears to be associated with exercise and may contribute to the beneficial effects of exercise |
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FGF-2
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-osteogenic myokine that is released by exercise.
-Has an anabolic effect on bone. |
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Osteogenic Myokines
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-some myokines contribute to bone loss and atrophy
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Myostatin
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-negative regulator of bone growth
-derived primarily from skeletal muscle -concentrations elevated with stressful conditions -levels decrease with exercise -elevated levels suppress bone formation -mediated by glucocorticoids |
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Myokines and Adipose Tissue
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-Adipose tissue is a major site of TNFa production
-TNFa may lead to insulin resistance by inhibiting GLUT-4 translocation -IL-6 released from skeletal muscle may also enchance lipolysis and fat oxidation |
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IL-6
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-[IL-6] increases several fold with exercise
-increases glucose uptake and fat oxidation in skeletal muscle -may also help decrease hepatic glucose production and lipolysis of adipose tissue |
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IL-15 and Muscles
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-Anabolic factor in skeletal muscle that is independent of IGF-1
-modulates visceral but not sub-q fat mass -contributes to increased bone mineral content -highly expressed in skeletal muscle |
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Brain Derived Neurotrophic Factor
(BDNF) |
-secreted by the brain and muscles
-promotes growth/maintenance of neurons -fxns in learning and memory -also controls food intake, lowers blood glucose, and plays a role in insulin resistance -increased production from skeletal muscle with contractions -also appears to enhance fat oxidation |
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Action of Testosterone on Target Tissues
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-Differentiation of epididymis, vas deferens, and seminal vesicles
-Increased muscle mass -Pubertal growth spurt -Growth of penile seminal vesicles -Deepening of voice -Negative feedback on ant pituitary -Libido |
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Actions of DHT on Target Tissues
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1. Differentiation of penis, scrot, and prostate
2. Male hair pattern 3. Male pattern baldness 4. Sebaceous gland activity 5. Growth of prostate -DHT is 2x as potent as testosterone |
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Male Secondary Sex Characteristics
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-External genitalia: penis increases in length/width; scrot becomes pigmented and rugose
-Internal genitalia: seminal vesicles enlarge and secrete and begin to form fructose. Prostate/bulbourethral glands enlarge and secrete -Voice: larynx enlarges; vocal cords lengthen and thicken; voice becomes deeper -Hair growth: beard appears; hairline on scalp recedes; pubic hair grows w/male pattern (treasure trail); hair in armpits, chest, and taint; more body hair generally -Mental: more aggressive; interest in ladies -Body shape: shoulders broaden, muscles enlarge -Skin: sweat gland secretions thickens and increases |
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Exogenous Testosterone Use (1)
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-Decrease in LH/FSH release
-Decrease in sperm production and possible infertility -Increase in free estrogens: exogenous testosterone frees estrogens from binding proteins |
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Exogenous Testosterone Use (2)
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-Liver toxicity
-Dec HDL -HTN -Edema -Altered libido -Psychosis -Aggression -Acne |
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Exogenous Testosterone (3)
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-GI distress
-Electrolyte imbalances -Muscle cramps/spasms -Depressed immunity -Prostate hypertrophy/CA -Suppressed GnRH release -Shrinking of testes -Gynocomastia |
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Androgen Deficiency in Aging Males (ADAM)
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-Three Phases
1. Prepubertal phase: secretion of FSH/LH low due to inhibition of GnRH release 2. Puberty: increased secretion of GnRH stimulates FSH/LH which stimulates spermatogenesis and testosterone production 3. Senesance: production of sperm and testosterone decrease |
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Accessory Organs & Semen Production
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-Seminal vesicles: produce 60% of total ejaculate volume
-Prostate: 20% ejaculate -Bulbourethral gland: 10% -Sperm account for the last 10% |
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Seminal Vesicles
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-Supply fructose to nourish sperm
-Secrete prostaglandins to stimulate motility -Provides the bulk of semen (60%) -Provides the precursors for the clotting of semen -Pair that empty into the ductus deferens bilaterally |
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Prostate Gland
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-Secretes an alkaline fluid that neutralizes the acidic vagina
-Triggers the clotting of semen to keep them in the vag -Single gland found around the urethra at the neck of the bladder -Major source of prostaglandins |
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Bulbourethral Gland
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-Secrete mucus for lubrication
-Pair which both empty into the urethra, one on either side, just before the urethra enters the penis -10% ejaculate |
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Components of Male Sexual Response
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1. Erection
2. Ejaculation |
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Sexual Response Cycle
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-4 phases
1. Excitation 2. Plateau 3. Orgasm 4. Resolution |
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Excitement Phase
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-Initiated by either physical/psychological stimuli
-Includes erection and heightened sexual awareness -Spinal reflex that can be initiated or facilitated by higher brain centers |
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Plateau Phase
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-Intensification of initial responses
-ANS activity -Characterised by steadily increasing HR, BP, RR, and muscle tension |
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Orgasmic Phase
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-Ejaculation and other responses that are collectively experienced as intense physical pleasure
-Experience in female similar to that of males except that there is no female counterpart to ejaculation and they do not become refractory to further orgasms |
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Resolution Phase
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-Return of genitalia and body systems to pre-arousal state and physical relaxation
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Erectile Tissue
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-Consists of three components:
-Two corpora cavernosa -One corpus spongiosum |
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Erectile Response
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-Flaccid State: blood flow into cavernous spaces is limited by contraction of helicine arteries
-Erect State: relaxation of helicine arteries by NO allow blood to flow into cavernous spaces to induce engorement and erection |
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Female Plateau Phase
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-Further vasocongestion of lower 1/3 of vagina
-Tenting effect: uterus raises upward lifting the cervix; enlargement of the upper 2/3 of the vagina for ejaculatory deposition |
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Male Ejaculation Phase
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-Consists of two components
1. Emission: semen enters urethra, SNS stimulation of smooth muscles causes contraction of accessory glands 2. Explusion: filling of the urethra triggers SNS nerve impulses which activate skeletal muscles at the base of the shaft 2-6ml of semen |
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Path of Semen
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Ductus (vas) deferens-Ejaculatory Duct (ampulla)-Urethra (Penis)-outside
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Female Orgasmic Phase
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-SNS stimulates contraction of pelvic muscles, contraction of lower 1/3 of vagina, vaginal secretions may rapidly increase
-no immediate refractory period -no ejaculation |
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Erectile Dysfunction
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-Failure to achieve an erection despite appropriate stimulation
-Pathophysiology: 1. psychological 2. nerve damage 3. flow disturbance 4. diabetes 5. medications |
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TX for ED
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-PO phosphodiesterase inhibitors which enhance the effects of NO on the penis smooth muscle
-Additional options: prostagladin E HRT Penis pump Vascular surgery Penile implants Psychological counseling and sex therapy |
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Phosphodiesterase Inhibitors MOA
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-cGMP activates myosin phosphotase in smooth muscle and promotes relaxation
-Phosphodiesterase degrades cGMP -Inhibitition of phosphodiesterase means that cGMP can continue to relax the arteries that feed blood into penis to facilitate erection |
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Vasectomy
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-Surgical cut of vas deferens prevents migration of sperm out of penis
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Desotrogestrel and Etonogesterel
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-Produces semen with low sperm counts, resulting in infertility
-Not yet available -Results in acne, increased body wt, decreased HDL -contains synthetic progestin |
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Intra Vas Device
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-Silicone plug that blocks the vas deferens
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