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Presentation transcript:

Is there anything I haven’t covered that you would like to go over?????

Fate of Digestive End-Products Fats and Glycogen are the MAIN STORES for extra energy in the body You must convert fats & glycogen to GLUCOSE for metabolism!!!!!

Converting stored Glycogen to Glucose & vice versa Hormones Insulin & Glucagon control the rate of conversion When blood glucose is high INSULIN dominates When blood glucose is low GLUCAGON dominates

Insulin & Glucagon are synthesized in pancreatic islet cells Pancreas Small Intestine Pancreatic Duct Acini Cells Islet Cells Alpha Cells: secrete GLUCAGON Beta Cells: secrete INSULIN

The Liver Storage: Liver is a major storage site of glucose

Diabetes: chronically high plasma glucose levels Insulin secreted; excess glucose stored in muscle or fat Insulin not secreted or not effective Excess glucose remains in blood Can only be eliminated via kidney (VERY SLOW)

Muscle Cells uptake glucose from blood Insulin Resistance: Decreased Uptake Insulin Deficiency: Decreased Insulin Production

1) Excess glucose in renal filtrate (glucosuria) 2) Glucose in filtrate draws water away from renal ISF….huge increase in urine volume 3) Decreased blood volume & pressure 4) Circulatory system fails to compensate over time…anaerobic metabolism from dying tissues 5) Metabolic acidosis shuts down CNS 6) DEATH! Diabetes: Multisystem Pathophysiology

Amputation in Diabetes Hypovolemia = Root Cause Reduced Blood Flow Impared Healing Low Flow, High Tissue Glucose/Low O2 Rapid, Aggressive Infection Amputation to contain infection

Diabetes: chronically high plasma glucose levels Insulin secreted; excess glucose converted to glycogen Insulin not secreted or not effective Excess glucose remains in blood Can only be eliminated via kidney (VERY SLOW)

1) Excess glucose in renal filtrate (glucosuria) 2) Glucose in filtrate draws water away from renal ISF….huge increase in urine volume 3) Decreased blood volume & pressure 4) Circulatory system fails to compensate over time…anaerobic metabolism from dying tissues 5) Metabolic acidosis shuts down CNS 6) DEATH! Diabetes: Multisystem Pathophysiology

Reproductive Physiology 1)Menstrual Cycle 2)Pregnancy 3)Lactation

Menstrual Cycle: Generalizations and terms Two main phase: follicular & luteal Pituitary Gland secretes Luteinizing Hormone (LH) Follicle Stimulating Hormone (FSH) Ovary produces follicle containing an egg Follicle then Corpus Luteum secretes Estrogen, Progesterone, Inhibin Uterus prepares for egg fertilization & growth Spike in Progesterone leads to Body Temp spike

Menstrual Cycle: Step-by-step FOLLICULAR PHASE 1) Period: old uterine lining sloughed FSH is high > a follicle matures 2) Estrogen gradually increases inhibiting FSH ***ensures only one follicle*** LUTEAL PHASE 3) Estrogen levels peak causing spike in FSH & LH ***ovulation: egg leaves follicle*** Uterine wall thickens **Fertilization can now occur in a ~ 12 hour window** 4) Follicle converted to Corpus Luteum ** Secretes Progesterone & Inhibin ** Prepares Uterus for implantation ***If Fertilization DID NOT OCCUR within 12 hours after 3) then….5 5) Corpus Luteum and Egg dies, Uterine Wall sloughed Estrogen, Progesterone, Inhibin levels drop > FSH increase..back to 1)

Pregnancy…..stopping the menstrual cycle! Estradiol ~ Estrogen Corpus Luteum and later Placenta secrete Estrogen & Progesterone This prevents the breakdown of the uterine wall….thus preventing menstruation Estrogen & Progesterone Levels stay elevated due to Human Chorionic Gonadotropin (hCG) Pregnancy tests = hCG tests!

Parturition: Labor Mechanism that initiates labor is not well understood: 1)Progestrone & Estrogen drop after labor begins 1)Oxytocin initiates Uterine contractions… but inducing labor with artificial oxytocin doesn’t always work 3)Fetus may secrete a hormone…(CRH, corticotropin releasing hormone, controls adrenal gland) Labor IS well understood: Once labor begins uterus undergoes powerful contractions + Tissue in birth canal softens due to the peptide, RELAXIN = Which eject the baby from uterus and cause delivery

Lactation Mammary Gland Myoepitheleal cells Milk secreting cells Smooth Muscle cells Milk Ducts

Control of Lactation Suckling Mechanoreceptors Higher Brain Hypothalamus Ant. Pituitary Post. Pituitary PIH Prolactin Oxytocin HAPPY BABY! Milk Secretion Smooth Muscle Contration Oxytocin: Myoepithelial & Duct Muscle Contraction Crying baby PIH = prolactin inhibiting hormone Prolactin: Milk secretion in mammary gland

Hope you enjoyed Human Physiology Confocal image of retinal layers