PET 3323C Exam 4 Study Guide PDF

PET 3323C (Fall 2024 Semester) Exam 4 Study Guide Integumentary System (Lecture 12) 1. Know the layers of the skin, where is the epidermis, dermis and hypodermis? Which layer has vascularization? Epidermis is the outer layer, dermis is right underneath. The dermis is the layer tha...

PET 3323C (Fall 2024 Semester) Exam 4 Study Guide Integumentary System (Lecture 12) 1. Know the layers of the skin, where is the epidermis, dermis and hypodermis? Which layer has vascularization? Epidermis is the outer layer, dermis is right underneath. The dermis is the layer that is vascularized. The hypodermis is not considered a true part of the skin, it lies underneath and helps connect the skin to the muscle underneath. (Slides 3,7,12) 2. Immune cells in the epidermis – Dendritic cells (Slide 4) 3. Know the epidermis layers, features and cell types in each – Epidermis has 4 types of cells keratinocytes, melanocytes, dendritic cells, and tactile epithelial cells. (Slides 4-6) Know the different layers and features of each layer. E.g. stratum basale is composed of 10-25% melanocytes, stratum corneum is composed of dead keratinocytes, stratum lucidum found only in areas of thicker skin, stratum spinosum – prickle cell layer contains dendritic cells, stratum granulosum – has glycolipids (Slides 3, 7-10) 4. Know layers of the dermis and features of each (reticular layer) and (papillary layer) and what is distinct between them (Slides 12-14) Dermis is distinct from the epidermis (epi- = “upon” or “over”) and hypodermis (hypo- = “below”). It contains blood and lymph vessels, nerves, and other structures (e.g. hair follicles and sweat glands) Papillary layer made of loose, areolar connective tissue (collagen and elastin fibers – form a loose mesh, this superficial layer of the dermis projects into the stratum basale of the epidermis to form finger-like dermal papillae Collagen fibers run parallel to the skin surface 5. Factors that contribute to skin color – melanin (made by melanocytes gives skin either a dark or medium brown color, carotene gives a slightly yellowish color, hemoglobin color (reddish) only seen in very fair skin (Slide 16) 6. Location of apocrine and eccrine sweat glands (Slides 18-19) Eccrine (merocrine) glands: everywhere; abundant in palms, soles of feet, and forehead Apocrine (merocrine) glands: found in axillary and genital areas - Sweat contains fatty substances and proteins (yellowish, bacterial growth – body odor) Energy Balance & Thermoregulation (Lecture 13) Energy Balance 7. Factors that stimulate hunger and appetite, GHRELIN 8. Factors that signal satiety POMC/CART neuron activation in hypothalamus decreases appetite Hormonal satiety signals - CCK (cholecystokinin) and insulin Nutrient signals – blood levels of glucose, amino acids, fatty acids Neural satiety signals - Satiety signals are those arising from the GI tract and related organs during a meal (e.g. stomach stretching. 9. Hormone involved in long term regulation of food intake, LEPTIN 10. Most important determinants of basal metabolic rate (Slides 11-12)  Hormonal (thyroxine) most important hormonal factor (Slide 12) Other factors – size (surface area), age, gender, body temperature, stress Total Metabolic Rate = BMR + TEF + PA (Slide 10) Basal metabolic rate (contributes 70%), thermal effect of food (10%), physical activity (20%) Thermoregulation 11. Role of the hypothalamus in maintaining body temperature (Slide 15) It acts a thermostat – trying to keep body temperature at a specific set point, if temperature RISES it initiates HEAT RELEASE MECHANISMS, if temperature FALLS it initiates HEAT PRESERVATION MECHANISMS. 12. Mechanisms of cooling at the skin surface (Slides 14, 19) Skin blood vessels dilate increasing the amount of blood at your body surface, these capillaries get filled with warm blood, heat radiates from skin surface Sweat glands secrete sweat – which is vaporized (evaporated) by body heat, helping to cool body 13. Mechanisms of heat preservation (Slide 17) Skin blood vessels constrict decreasing the amount of blood at your body surface (diverting it toward your body core), these capillaries now carry less blood, lose less heat from skin surface Skeletal muscle shivering – activated by heat promoting center (hypothalamus) Thyroxine release 14. Voluntary mechanisms to increase body temperature (Slides 18-20) Alcohol causes vasodilation Hot shower – causes vasodilation Hot drink – increases core temperature 15. Purpose of sweating – the main function is to control body temperature. As water evaporates it cools the surface of the skin. (Slide 19) 16. What is the largest contributor to heat production during exercise? Skeletal muscle activity (contraction) Body Fluid and Electrolyte Balance (Lecture 14) 17. Compartments of body water (extracellular versus intracellular) (Slides 2-3) Two main compartments - Intracellular fluid (ICF) and Extracellular fluid (ECF). ECF is subdivided further into interstitial fluid (IF) and Plasma. ICF (intracellular) contains 1/3 of the water volume and the fluid inside cells. The ECF contains all fluid outside of the cells (IF that surrounds cells) and (Plasma – water within the closed circulatory system (blood vessels-veins-capillaries) 18. Extracellular compartments consist of plasma and interstitial fluid (Slides 2-3) 19. Ion composition of different body fluid type (Slides 4-5) ECF (Na+ and Cl- primary cations and anions, respectively) ICF (K+ primary cation and hydrogen phosphate (HPO42- the primary anion) Electrolytes – ions that dissociate in water Nonelectrolytes-don’t dissociate in water, e.g. glucose, lipids, creatine, and urea 20. Which route of fluid loss is the most regulated (variable) Kidney production of urine, kidneys can produce as little as 500 ml/day (minimum) or 1600-2000 ml/day (maximum) (Slides 6, 10) 21. Hypothalmic osmoreceptors respond to what changes in the body? (Slides 8-9) Decreased blood pressure, decreased blood volume, increased ECF osmolality 22. Action of ANP (Slides 12, 17) ANP – Atrial natriuretic peptide – released by atrial heart cells when sense too much fullness in the atria (stretching of atrial walls)  this stretch indicates BP is high. ANP targets the: 1) hypothalamus to inhibit ADH release, 2) kidney granular cells to inhibit renin release, and 3) adrenal cortex to inhibit aldosterone release. All these ADH, Renin, Aldosterone are BP increasing mechanisms). Ultimately more water and salt is lost through the kidneys + increase in blood vessel vasodilation  blood volume and blood pressure are decreased. IF BP DECREASED (Aldosterone and ADH released) – (increase blood volume and subsequently blood pressure). Other mechanisms activated include blood vessel baroreceptor inhibition that increases (SNS) activity causing vasoconstriction of systemic arterioles to increase peripheral resistance  directly increases BP. RAAS – through action of Ang-II causing vasoconstriction of systemic arterioles to increase peripheral resistance.  directly increases BP. (Slides 12, 17, 19) 23. Hormone that affects water resorption in the kidney ADH – (anti-diuretic hormone) ACTS TO MAINTAIN BLOOD PRESSURE AND BLOOD VOLUME AND AVOID DEHYDRATION -> so inhibits anything causing your body to lose WATER. This includes telling the kidney tubules to reabsorb water (Figure 12, 18-19) 24. Know the effect of the Renin-Angiotensin-Aldosterone System in the body and steps of activation (Slides 12, 16, 19) Aldosterone – Part of the RAAS system - which WORKS TO INCREASE BP). Steroid hormone released from the adrenal cortex that regulates salt reabsorption by the kidney. When aldosterone is released, the goal is to raise blood pressure  by increasing salt retention by the kidney – water automatically follows (so increase Na+ water) in the body and Blood volume and blood pressure goals up. ANG II – Angiotensin II – raises BP through various mechanisms that include sympathetic nervous system (SNS) stimulation (vasoconstriction) and increased production of aldosterone and actions on the kidney to retain water and salt. 25. Know the physiological responses if blood osmolality increases or decreases Increases  triggers thirst -> drink fluid RELEASE ADH (kidneys absorb water) Decreases  inhibits thirst -> not thirsty LESS/NO ADH RELEASED (large amount of dilute urine) 26. Major factors that determine where water goes – sodium, plays a role in ECF volume and distribution of body water, WATER FOLLOWS SALT, sodium (Na+) important for blood pressure (controlled by RAAS and ANP), Na+ also determines ECF osmolality, osmosis (Slide 15) 27. Physiological responses to high blood sodium or high blood pressure IF BP INCREASED or PLASMA Na+ INCREASED (ANP levels increase)  (decrease blood volume) to restore normal BP levels (Slide 17) Female and Male Reproduction (Lecture 15) 28. Sequential events that occur during uterine (menstrual) and ovarian cycles (Slide 4, 13- 14) Uterine Cycle: Menses phase (day 1-5): uterus sheds all but deepest parts of the endometrium a. Pre-ovulatory b. Occurs first part of follicular phase Proliferative phase (day 5-14): endometrium rebuilds a. Pre-ovulatory b. Occurs last part of follicular phase Secretory phase (day 15-28): endometrium prepares for implantation of an embryo a. Post-ovulatory b. Occurs the whole length of the luteal phase Ovarian Cycle: Follicular Phase a. Development of dominant follicle (LH and FSH) b. Pre-ovulation (estrogen levels peak right before LH and FSH surge c. Surge in LH and FSH right before ovulation Luteal Phase c. Ovulation of ovum d. Corpus luteum forms (releases estrogen + progesterone) (shrinks and degenerates before end of luteal phase e. Estrogen levels decline but remain elevated f. Progesterone levels increase g. Both estrogen and progesterone decline (relieving inhibition of FSH and LH) h. FSH and LH start to rise (to start follicular phase again) 29. Ages when sperm or oocyte production stops (Slide 5 and 15) Males (around 70 years of age) (Slide 15) Females – before birth, ovulation stops at menopause (40-50 years of age) 30. Know the female sex hormones, which are dominant in the follicular and luteal phases of the ovarian cycle and pregnancy (which structures produce which hormones) (Slides 9, 11-12) A. Hormones Estrogen peaks at the highest during the follicular phase and is mid-level in the luteal phase. Progesterone is only high in the luteal phase and is made by the corpus luteum, which forms right after ovulation. LH is highest in follicular phase and peaks right at ovulation. – stimulates ovulation, kept at low levels by estrogen (negative feedback on LH – lower estrogen levels), put estrogen levels elevate right before ovulation (higher estrogen levels – positive feedback effect on LH) causing sudden LH surge (at ovulation)  FSH levels are highest in the follicular phase (drives follicle development) and peak at ovulation. B. Follicular phase (ovarian cycle) Uterine cycle – menses followed by proliferative phase Mid-Cycle Events (14 days) occur simultaneously during ovulation (mid-cycle) - Mid cycle (ovulation, estrogen levels peak right before, LH and FSH peak during ovulation, prostaglandins are released which facilitate oocyte release from the Graafian follicle, the uterine cycle shifts to the secretory phase. C. Luteal phase (ovarian cycle) Corpus luteum – structure that forms at site of ovulation that produces progesterone and estrogen Secretory phase of menstrual (uterine) cycle (continue building the uterine lining adding spiral arteries) in preparation for potential pregnancy What happens to the corpus luteum if pregnancy does not occur/or does occur? – if pregnancy does not occur the corpus luteum will degenerate in ten days. If pregnancy does occur the corpus luteum produces hormones until the placenta takes over the role of making progesterone (about 3 months). 31. Know about the hormonal regulation of pregnancy (Slide 10, 25-26) Right after ovulation after fertilization Progesterone levels go up and estrogens are still midlevel, FSH and LH go down as normal. Corpus luteum will remain around 3 months. LH maintains the corpus luteum Human chorionic gonadoptropin (hCG) is made by early forming cells that will make up the placenta. hCG is produced around day 7 after ovulation and goes up rapidly. LH levels decline as hCG levels increase, hCG now maintains the corpus luteum Progesterone made by corpus luteum for 3 months and then the placenta (3 months and remainder of pregnancy) 32. Role of male sex hormones in spermatogenesis (Slide 17) Regulation of spermatogenesis requires both FSH and testosterone Hormones Testosterone – has major role in spermatogenesis and produced by interstitial cells (Leydig cells) near the seminiferous tubules LH – stimulates the Leydig cells to make testosterone FSH – is released by pituitary gland-> FSH increases # of LH receptors on Leydig cells causing them to produce more testosterone to maintain spermatogenesis. GnRH - hypothalamic hormones that directly act on the anterior pituitary to control the release of gonadotropins – Hypothalamic hormone = gonadotropin releasing hormone (GnRH) released and goes to anterior pituitary, which then produces LH and FSH (with direct action on gonads Hormones involved in regulating spermatogenesis – FSH and testosterone required for spermatogenesis regulation, FSH binds to receptors on Sertoli cells to initiate  spermatogenesis. FSH increases LH receptor # on Leydig cells (causing more testosterone to be produced -> maintaining spermatogenesis Fetal Development (Lecture 15) 33. General timing of fertilization and implantation (Slides 21-23) – The sperm could be present before ovulation and fertilize the egg when it is ovulated – resulting in pregnancy. A blastocyst (fertilized egg) forms and it takes 6 days to move to the uterus. It starts dividing on its path down the fallopian tube. 3 days post fertilization – the ovum divides into 16 cells (morula), 4 days it becomes a 58-cell blastocyst, 4 ½ days it becomes a 107- cell unilaminar blastocyst, and after 9 days post-fertilization the blastocyst implants into the endometrium.