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Chapter 21: GI Physiology
Sketch the anatomy of the digestive system, noting the role of each structure in the
gastrointestinal tract and accessory organs.
Alimentary canal- food passes through Oral cavity: contains salivary amylase Pharynx: common passageway for air + food Esophagus: hollow muscular tube (skeletal → smooth muscle) that transports food + liquids Stomach: minimal absorption, protein digestion Small intestine: duodenum, jejunum, ileum; receives secretions from accessory organs i.e. pancreas, liver, gallbladder Large intestine: colon, rectum Accessory organs: assist in digestion, food does not physically enter these organs Teeth tongue salivary glands: secrete amylase digestive enzyme in mouth for chemical breakdown to begin Liver: secrete into duodenum Gallbladder: storage of bile Pancreas: secrete into duodenum
List and describe the general processes involved in processing ingested food.
- Ingestion: occurs in the oral cavity
- Secretion: enzymes and mucus production help break down food and move it down the alimentary canal
- Digestion: occurs through mechanical and chemical processes, chewing food with teeth and tongue and muscle contractions help increase the food’s surface area for enzymes to chemically break down into smaller pieces.
- Absorption: nutrients move from lumen to ECF where they can enter the blood
- Motility: muscle contractions move food along the GI tract
- Excretion: undigested waste products are eliminated from the body in feces
3. Pancreatic amylase breaks down carbohydrates from
disaccharides to monosaccharides to be absorbed into the
bloodstream.
4. Trypsin - endopeptidase breaks down proteins into peptides.
5. Nuclease- breaks down nucleic acids
b. Large intestine: absorption of water, indirect digestion by bacteria
Compare the location, secretion, digestion, absorption, and motility that occur during each phase
of food processing.
- Cephalic Phase: oral cavity, salivary amylase + mucus, mechanical mastication and chemical digestion, salivary amylase, none, mastication, swallowing reflex
- Gastric Phase stomach, small intestine, large intestine, oral cavity- salivary amylase and mucus, stomach - gastrin, gastric acid, histamine, lipase, pepsinogen, pepsin, pancreas -chyme, lipase, trypsin, sodium bicarbonate, pancreatic amylase, liver - bile, none? none
- Intestinal Phase small intestines, sodium bicarbonate, pancreatic lipase, pancreatic amylase, chyme, nucleases, chemical breakdown of polymers into monomers, large intestine, water reabsorption
Map the processes and control pathways involved in the production of pepsin in the stomach.
G cells secrete Gastrin → parietal cells → gastric acid → chief cells → pepsinogen + gastric acid → pepsin
Chapter 22- Energy Storage & Metabolism
Explain how energy input and energy output in the body are quantified. Total body energy=energy stored + energy intake – energy output ● Law of mass balance: changes to the body’s energy stores result from the difference between the energy put into the body and the energy used. Direct calorimetry involves measuring the energy content of food that is consumed. The units for energy content are kilocalories. ● Proteins provide 4 kilocalories per gram- requires more energy to metabolize ● Carbohydrates provide 4 kilocalories per gram - easiest and first to be metabolized ● Fats provide 9 kilocalories per gram, making them useful for storing energy Define all terms associated with the conversions of biomolecules from one form to another. ● Glycolysis: the addition of water breaks glucose into two 3 carbon chains. ● Glycogenesis: glucose is converted to glycogen ● Glycogenolysis: breakdown of glycogen to release stored glucose ● Lipogenesis: synthesize fats from glucose, fatty acids, and amino acids ● Lipolysis: break fats down to release stored energy Lipase ● Gluconeogenesis: synthesizing glucose from non-carbohydrate precursors Create a map that summarizes the balance of nutrient pools and nutrient storage for carbohydrates, proteins, and lipids.
Compare and contrast Type 1 and Type 2 diabetes mellitus. Diabetes mellitus is characterized by abnormally elevated plasma glucose concentrations (hyperglycemia). ● In Type 1 diabetes mellitus, the immune cells fail to recognize the beta cells of the pancreas as "self" cells and destroys them. Therefore, there is an insulin deficiency due to the beta cell destruction. Type I diabetes is a genetic condition that accounts for roughly 10% of diabetic patients. These patients must be treated with exogenous insulin. ● a) No insulin = no glucose metabolism. Ingested glucose remains in the blood. Glycogen and amino acids are converted to glucose even if the glucose pool is not empty. ● b) Amino acids are used in gluconeogenesis instead of protein synthesis. Proteins break down to refill the amino acid pool, resulting in the atrophy of muscle tissue. Likewise, fat stores are broken down to facilitate metabolism using fatty acids, resulting in little fat storage. ● c) Polyphagia is excessive eating. Neurons in the brain are insulin-sensitive. A lack of insulin is perceived as a starvation state by the brain, which initiates hunger despite high glucose concentrations in the blood. ● d) Because of excess glucose in the blood, glucose reabsorption in the proximal tubules of the nephron reach saturation. Excess glucose is therefore excreted in the urine (glucosuria). With more solute (glucose) in the collecting duct, the osmolarity of the filtrate is higher than normal and less water is reabsorbed. More water is therefore released in the urine, resulting in polyuria. ● e) High glucose concentrations in the blood and high volumes of urine released cause blood osmolarity (solute concentration) to increase. ● f) High blood osmolarity and dehydration increase thirst. Polydipsia is excessive thirst and over-consumption of water. ● g) Dehydration due to excess urine production causes blood volume to decrease, which causes low blood pressure. ● h) Excess ketone production from fat breakdown causes ketoacidosis. Ketones make blood more acidic. ● In Type 2 diabetes mellitus, the insulin receptors of the body's cells develop a resistance due to the production of insulin by the pancreas. This occurs when plasma glucose concentrations are consistently elevated due to an individual's diet. Thus, Type 2 diabetes is caused by a patient's lifestyle, although there is evidence of some genetic predisposition to the disease as well. Type 2 diabetes accounts for roughly 90% of diabetic patients.
Identify the specific components of the reflex pathway for metabolism during the fasted state. Stimulus - decreased plasma glucose Sensory receptor - alpha cells of the pancreas Integrating center - alpha cells of the pancreas Target - liver, muscle tissue, and adipose tissue Response - breakdown of glycogen, conversion of amino acids to glucose, breakdown of fats ● (These responses increase plasma glucose and utilize fatty acid metabolism) Lab 14- Sex Determination Create a flow chart summarizing the process of sexual differentiation in male and female embryonic development. Unless the SRY gene is present with the correct type and amount of hormones, a female system will develop in the presence of an X chromosome. If there is a Y chromosome, a male system will form and inhibit the female system from forming.
respond to androgens, which are hormones that direct male sexual development. The level of androgen insensitivity will vary an affected person's sex characteristics can vary from mostly female to mostly male. Fertility: infertile; females lack a uterus. Epidemiology: Complete androgen insensitivity syndrome affects 2 to 5 per 100,000 people who are genetically male. Partial androgen insensitivity is thought to be at least as common as complete androgen insensitivity. Mild androgen insensitivity is much less common. Treatment: estrogen replacement therapy from puberty onward Congenital Adrenal Hyperplasia (CAH) -characteristics/symptoms: Females with the classic form of CAH have external genitalia that do not look clearly male or female (atypical genitalia). They develop hypertension and the internal reproductive organs develop normally. -Females with the non-classic form of CAH due to 11-beta-hydroxylase deficiency have normal female genitalia. As affected females get older, they may experience hirsutism and irregular menstruation. Males with the non-classic form of this condition do not typically have any signs or symptoms except for short stature. Hypertension is not a feature of the non-classic form of CAH due to 11-beta-hydroxylase deficiency. ○ Mechanism: due to 11-beta-hydroxylase deficiency The CYP11B1 gene provides instructions for making an enzyme called 11-beta-hydroxylase. This enzyme is found in the adrenal glands, where it helps produce hormones called cortisol and corticosterone. Cortisol has numerous functions, such as maintaining blood sugar levels, protecting the body from stress, and suppressing inflammation. Corticosterone gets converted to the hormone aldosterone, which helps control blood pressure by maintaining proper salt and fluid levels in the body. CAH due to 11-beta-hydroxylase deficiency is caused by a shortage (deficiency) of the 11-beta-hydroxylase enzyme. When 11-beta-hydroxylase is lacking, precursors that are used to form cortisol and corticosterone build up in the adrenal glands and are converted to androgens. The excess production of androgens leads to abnormalities of sexual development, particularly in females with CAH due to 11-beta-hydroxylase deficiency. A buildup in the precursors used to form corticosterone increases salt retention, leading to hypertension in individuals with the classic form of CAH due to 11-beta-hydroxylase deficiency. Fertility: decreased among women compared to unaffected women
Epidemiology: CAH due to 11-beta-hydroxylase deficiency accounts for 5 to 8 percent of all cases of congenital adrenal hyperplasia. It is estimated that CAH due to 11-beta-hydroxylase deficiency occurs in 1 in 100,000 to 200,000 newborns. This condition is more common in Moroccan Jews living in Israel, occurring in approximately 1 in 5,000 to 7,000 newborns. The classic form of CAH due to 11-beta-hydroxylase deficiency appears to be much more common than the non-classic form. Treatment: hormone replacement Klinefelter Syndrome a. characteristics and symptoms: affects boys and men, intellectual disabilities, small testes that produce a reduced amout of testosterone (primary testicular insufficiency)breast enlargement (gynecomastia), decreased muscle mass, decreased bone density, and a reduced amount of facial and body hair. b. Mechanism: sex chromosome disorder that affects men more than women, some men acquire an extra copy of X chromosome (47,XXY). The shortage of testosterone can lead to delayed or incomplete puberty. c. fertility: infertile but can be assisted with reproductive techniques d. Epidemiology: affects boys and men; Klinefelter syndrome affects about 1 in 650 newborn boys. It is among the most common sex chromosome disorders, which are conditions caused by changes in the number of sex chromosomes. e. Treatment: no cure but testosterone replacement therapy can reduce some unwanted symptoms. Turner Syndrome a. Symptoms: affected females have a short stature and skeletal abnormalities. They do not undergo puberty unless stimulated by hormone replacement therapy, early loss of ovarian function due to cell death. b. Mechanism: sex chromosome disorder caused by a missing or defective X chromosome. The body only has half the copy of cells as it is supposed to have (n=23) also known as monosomy X. c. Epidemiology:This condition occurs in about 1 in 2,500 newborn girls worldwide, but it is much more common among pregnancies that do not survive to term (miscarriages and stillbirths). d. Fertility: fertility treatments and hormone replacement therapy e. Treatment: hormone replacement therapy - growth hormone and estrogen replacement therapy.
Map the common hormonal control and feedback pathways for reproductive function.
Sex steroids: estrogen ad progesterone; GnRH is under the influence of several hypothalamic neuropeptides, including one named kisspeptin. GnRH (Hypothealamus) → LH, FSH (Ant. Pit.) → Females: estrogens: ovary secretes estrogen and progesterone As estrogen levels rise, negative feedback inhibits the Ant. Pit. from releasing more FSH. High Estrogen levels create positive feedback and GnRH creates LH and FSH surge (day 14) Progesterone acts as negative feedback during the luteal phase, as levels rise, it decreases LH secretion by the Ant. Pit. gland. Males: androgens: testes secrete AMH (Sertoli cells), Testosterone (Leydig cells) and DHT. Diagram the ovarian and uterine stages of the menstrual cycle. Relate these stages to hormone secretion, follicle development, and endometrial thickness in the female body. Ovarian cycle a) Follicular phase - days 1-14 (variable) – FSH secreted, follicles develop, estrogen increases b) Ovulation – day 14 – estrogen causes GnRH increase (positive feedback), causes LH surge, causes ovulation c) Luteal phase – days 14-28 – corpus luteum produces estrogen and progesterone, which suppress GnRH, FSH, and LH (negative feedback) Uterine cycle a) Menstruation – days 1-7 – shedding of endometrium due to low estrogen/progesterone b) Proliferative phase – days 7-14 – high estrogen from follicles cause endometrium to thicken c) Secretory phase – days 14-28 – high estrogen and progesterone causes endometrium to thicken
● The mechanism for the generation and propagation of action potentials. ● The roles of sympathetic and parasympathetic innervation throughout the human body and the mechanism by which these neurons communicate with target cells. ● Principles of fluid flow in each of the organ systems. ● Electrical and mechanical events of the cardiac cycle. ● Mechanisms for maintaining adequate oxygen and carbon dioxide levels in the blood. ● The many functions of sodium and calcium in the human body. ● The role of sodium-potassium pumps throughout the human body.
