digestive, metabolism, immune*

Digestion of Carbohydrates

1. Carbohydrates ingested as starch or sugars such as sucrose and lactose a.Starch digestion begins in mouth with salivary amylase; polysaccharides -> shorter chains b.No digestion in the stomach - too acidic c.Continues in intestines with pancreatic amylase; short chains à disaccharides and maltriose d.Brush border enzymes finish breaking down disaccharides (maltose, sucrose, lactose) to simple sugars (mainly glucose) 2. Monosaccharides absorbed across the epithelium via: oSecondary active transport with Na+ (Cl− follows) oFacilitated diffusion through GLUT carriers into interstitial fluid and then to villus capillary oWater follows NaCl through a paracellular route and is absorbed with glucose and NaCl doc

Digestion and Absorption of Proteins

1. Digestion of proteins a.Begins in stomach with pepsin and HCl to produce short-chain polypeptides b.Ends in duodenum and jejunum with pancreatic trypsin, chymotrypsin, elastase, and carboxypeptidase, and the brush border enzyme aminopeptidase. c.Final products aa, dipeptides and tripeptides 2. Absorption of Proteins a.Free amino acids cotransported with Na+ b.Dipeptides and tripeptides cross via secondary active transport using a H+ gradient. Hydrolyzed into free aa in the cytoplasm of the epithelial cells c.Free aa move by facilitated diffusion into interstitial fluid, then to the villi capillaries doc

Local Inflammation

1. Occurs when bacteria enter a break in the skin 2. Initiated by nonspecific mechanisms of phagocytosis a.Macrophages and mast cells release cytokines and chemokines to attract phagocytic neutrophils. b.Complement proteins are activated, which also attract phagocytic cells. c.More phagocytic cells arrive via extravasation from nearby venules. T lymphocytes are the last to arrive. doc 3. Mast cells degranulate and secrete heparin, histamine, prostaglandins, leukotrienes, cytokines, and TNF-α. a.These produce warmth, swelling, and pain (classic symptoms). b.They also recruit more leukocytes. 4.Neutrophils a.Kill microorganisms through phagocytosis b.Undergo programmed cell death and spill protein-digesting enzymes into the surrounding tissues, causing pus. c.Release granule proteins that draw monocytes to the area 5.Monocytes a.Enlarge into macrophages; phagocytose apoptotic neutrophils and release growth factors and other agents that will end inflammation and promote repair. 6. As inflammation progresses, B lymphocytes produce antibodies against bacterial antigens. a.Formation of antigen-antibody complexes amplifies phagocytosis by neutrophils, monocytes, and macrophages, a process called opsonization. 7.Symptoms of inflammation a.Redness and warmth due to histamine stimulated vasodilation b.Swelling - vasodilation c.Pain d.Pus - phagocytosis

Ulcers & Gastritis

1. Peptic Ulcers a.Peptic ulcers: erosions of the mucosa of the stomach or duodenum produce by HCl b.Helicobacter pylori: bacterium that reduces mucosal barriers to acid c.Treatment: combines proton pump inhibitors (PPI) (Prilosec, Nexium) and antibiotics. (ATPase molecules) 2. Acute Gastritis a.Inflammation of the submucosa caused by acid b.Histamine released as part of the inflammatory response can ↑ acid release. c.Prostaglandins are needed to stimulate protective alkaline mucus production. d.NSAIDs inhibit prostaglandin activity and can lead to gastritis. e.Tagamet and Zantac inhibit H2 receptors. 3. Duodenal Ulcers a.Protected by adherent layer of mucus with HCO3- secreted by Brunner's glands b.Acidic chyme neutralized by HCO3-

Vitamins and Minerals (1)

1. Vitamins are small organic molecules that serve as coenzymes or perform a specific function a.Must be obtained in the diet because: •The body cannot make them, or only makes a small amount (D, K, B) b.Two classes: •Fat-soluble - A, D, E, K •Water-soluble - Bs, C 2.Water-Soluble Vitamins a.Include B vitamins and vitamin C b.Cannot be stored in the body 3.Fat-Soluble Vitamins a.Include A, D, E, and K b.Can be stored in the body •Vitamin E: strong antioxidant; helps mitigate inflammatory response •Vitamin K: needed to make clotting factors •Vitamin D: needed for calcium absorption, tissue differentiation, and regulate gene expression •Vitamin A: involved in embryonic development, T cell activity, dim light vision, and epithelial cell development/function 4.Minerals a. Nonorganic molecules used as cofactors and in a wide range of processes b. Needed in large amounts: sodium, potassium, magnesium, phosphorus, calcium, and chlorine c. Needed in small amounts (trace elements): iron, zinc, manganese, fluorine, copper, molybdenum, chromium, and selenium

Allergies

1.Abnormal response to allergens (antigens) a.Also called hypersensitivity b.Two types: •Immediate hypersensitivity •Delayed hypersensitivity 2.Immediate Hypersensitivity a.Abnormal B cell response to allergen •Effects seen seconds to minutes after exposure •Can be caused by foods, bee stings, pollen, etc. b.Dendritic cells stimulate TH2 helper T cells to secrete IL-4 and IL-13, which stimulate B and plasma cells to secrete IgE antibodies c.The ab do not circulate in the blood but attach to mast cells and basophils. d.When re-exposed to the same allergen, these ab bind to it and stimulate the production of histamine, leukotrienes, and prostaglandin D, producing allergy symptoms. e.Can lead to anaphylactic shock 3.Delayed Hypersensitivity a.Abnormal T cell response that produces symptoms 24 to 72 hours after exposure b.Symptoms are caused by secretion of lymphokines, not histamine, so taking antihistamines has little effect. c.Example: contact dermatitis caused by poison oak, ivy, or sumac doc

Hypoglycemia

1.Abnormally low blood glucose levels 2.Can be from insulin overdose, (insulin-shock); may lead to coma 3.Can be an exaggerated response to increased insulin secretion after a carbohydrate-rich meal 4. Also called Reactive Hypoglycemia a.Most common in adults predisposed to developing type 2 diabetes b.These people should limit carbohydrate intake and eat frequent, small meals c.Symptoms: tremor, hunger, weakness, blurred vision, and mental confusion doc- reactive hypoglycemia

Esophagus

1.About 10 inches long 2.Passes through the diaphragm via the esophageal hiatus 3.Lined with nonkeratinized stratified squamous epithelium 4.Mouth, pharynx, and upper esophagus lined with skeletal muscles innervated by somatic motor neurons 5.Lower esophagus lined with smooth muscle controlled by autonomic nervous system 6.Lower esophageal sphincter opens to allow food to pass into stomach. It stays closed to prevent regurgitation. Upper 1/3 is skeletal: under our control Lower is smooth muscle- autonomic nervous system doc

Hormonal Regulation of Metabolism

1.Absorption of energy carriers from the intestines fluctuates a.Absorptive state - rise over four-hour period following a meal b.Postabsorptive (fasting) state - drops to zero between meals 2.Plasma levels of energy carriers stays within a homeostatic range due to the balanced influence of several hormones. doc

AIDS and HIV

1.Acquired immune deficiency syndrome (AIDS) has killed many millions of people worldwide, and millions more are currently infected. AIDS is caused by the human immunodeficiency virus (HIV), which preferentially infects and destroys helper T cells, particularly those in the gastrointestinal mucosa where up to 30% of helper T cells reside. 2.This results in decreased immunological function and greater susceptibility to opportunistic infections and cancer. Fig 15.3 HIV lifecycle: Retrovirus, RNA genome transcribed into cDNA, which integrates into the host genome and transcribed and translated to produce new virus. doc

Thyroxine

1.Acts on most cells in the body to increase rates of cellular respiration by decreasing intracellular ATP levels a.Due to production of uncoupling proteins b.Increases production of metabolic heat required for cold adaptation (calorigenic effects); Contributes to adaptive thermogenesis c.Increases basal metabolic rate (BMR) 2.BMR and Thyroxine BMR can be used to measure thyroid activity. 3.Thyroxine Balance a.Needed for proper growth and development of the CNS in children b.Needed for balance between anabolism and catabolism c.Both hyperthyroidism and hypothyroidism result in muscle wasting

Regulatory Functions of Adipose Tissue

1.Adipostat: mechanisms that defend a set amount of adipose tissue a.Changes in metabolism to match incoming kcal; Makes it difficult to lose weight; Negative feedback loop 2.Energy is stored in white fat as triglycerides. a.Hormones regulate fat storage and breakdown. b.Adipocytes secrete hormones that regulate hunger and metabolism. 3.Adipose Tissue Development a.Some appears in embryo but increases greatly after birth due to mitosis and differentiation of preadipocytes. b.Increase in circulating fatty acids increases the number of adipocytes. c.Nuclear receptor protein PPARγ is needed for preadipocyte differentiation 4.Endocrine functions of adipose tissue a.Adipokines: regulatory molecules secreted by adipocytes that affect hunger, metabolism, and insulin sensitivity b.Tumor necrosis factor α: made in obese people with large adipocytes o↓ ability of skeletal muscles to remove glucose from the blood in response to insulin oRelated to T2DM - promotes insulin resistance c.Adiponectin: reduced in obesity and T2DM oStimulates the use of glucose and fatty acids in muscle cells. oHelps increase insulin sensitivity and reduce the chance of developing T2DM. e. Leptin: Is an adipokine (regulates hunger, metabolism, and insulin sensitivity). Secreted in proportion to the amount of stored fat •Regulates appetite via feedback to hypothalamus •Regulates reproductive processes via hypothalamus. A woman with low body fat will not ovulate/menstruate. 5.Obesity a.Risk factor for cardiovascular disease, T2DM, gallbladder disease, cancers •Risk is greater if visceral fat is accumulated rather than subcutaneous fat. •High waist to hip ratio (apple shape versus pear shape) •Visceral fat is less sensitive to insulin b.Causes of obesity •Obesity in childhood is due to increasing number and size of adipocytes. •Obesity in adulthood occurs through increase in size alone. •When weight is lost, adipocytes get smaller but do not go away. •Critical to prevent childhood obesity. •1988 to 1994 - 36% increase in obesity •1982 to 1994 - 10-fold increase in T2DM c.Body Mass Index (BMI) Way to diagnose obesity BMI = weight in kg/height in m2 •BMI 19−25 = Healthy; 26−29 = Overweight; over 30 = Obese •60% of American adults are overweight or obese.

Adrenal Hormones

1.Adrenal medulla: secretes catecholamines in response to sympathetic stimulation 2.Adrenal cortex: secretes mineralocorticoids & glucocorticoids 3.Metabolic effects of catecholamines a.Similar to effects of glucagon •Stimulate glycogenolysis à release of glucose from liver •Lipolysis à release of fatty acids from adipose tissues b.Prepare body for increased energy demands in a fight/flight reaction doc 4.Metabolic effects of glucocorticoids a.Cortisol is released as part of general adaptation syndrome in response to stress (ACTH stimulation). b.Promotes lipolysis, ketogenesis, and gluconeogenesis to increase available energy c.Also promotes muscle proteolysis to increase circulating amino acids d.Helps compensate for prolonged fasting or exercise doc x2

Barrett's Esophagus

1.Affecting over 5% of the adults in the US; occurs when part of the normal stratified squamous epithelium of the esophagus is replaced by columnar epithelium. 2.Although a columnar epithelium is normal in the stomach and intestine, it is abnormal in the esophagus and so constitutes metaplastic tissue (metaplasia: the abnormal replacement of cell types). 3.Occurs because of injury to the esophageal mucosa by gastroesophageal reflux disease (GERD). 4.Barrett's esophagus increases the risk of esophageal adenocarcinoma.

Type 1 Diabetes

1.Also called insulin-dependent diabetes a.Beta cells are destroyed (autoimmune disease) and insulin is not made. b.Injections of insulin are required for sustaining life. 2.Autoimmune disease associated with MHC on chromosome 6 3.Environmental factors play a triggering role a.Viruses b.Bacteria c.Autoreactive T cells - helper and killer T cells - destroy the beta cells d.Autoantibodies attack the beta cells 4.Type 1 Diabetes and Fatty Acids a.Due to reduced insulin secretion, more fatty acids are also in the blood (not taken into and stored in adipose tissue). b.These are converted to ketone bodies in the liver. c.Increases in ketone bodies may produce ketoacidosis. d.Increased glucose and ketone bodies are secreted in the urine and act as osmotic diuretics, leading to dehydration. e.Excess dehydration, ketoacidosis, and electrolyte imbalance can lead to coma and death. 5.Type 1 Diabetes and Glucagon a.People with T1DM also have an abnormally high secretion of glucagon. b.Stimulates glycogenolysis in the liver, further raising blood glucose levels. c.It also stimulates the enzyme that converts fatty acids to ketone bodies.

GI Tract Layers

1.Also called tunics 2.There are four tunics: a.Mucosa: inner secretory and absorptive layer; may be folded to increase surface area -Muscle supports folding Folding increases surface area for absorption b.Submucosa: very vascular, to pick up nutrients; also has some glands and nerve plexuses -Connective tissue, blood vessels c.Muscularis: smooth muscle; responsible for peristalsis and segmentation; myenteric plexus for control by the ANS -Two layers: circular (diameter) and longitudinal (shorter): churn, mix, and polarize, and exposes to digestive enzymes, provides major nerve supply to GI tract d.Serosa: outer binding and protective layer -Connective tissue, simple squamous epithelium, responsible for things not moving around when exercising doc

Regulation of Hunger and Metabolic Rate

1.Animal Studies •Endorphins and serotonin play a role in suppressing eating. •Norepinephrine plays a role in stimulating eating. 2.Arcuate Nucleus of Hypothalamus a.Produces hormones involved in hunger Melanocyte-stimulating hormone decreases hunger. (produced by POMC neurons) One type of congenital obesity is associated with mutations in MSH receptors. Neuropeptide Y and Agouti-related protein (AgRP) increase hunger. b. The presence of circulating energy substrates stimulates the release of MSH and inhibits the release of neuropeptide Y and Agouti-related protein. •This suppresses appetite and increases metabolism. •This reverses when there is a reduction in circulating energy constructs. c. Regulated by hormones from the digestive organs and adipose tissue 3. Regulation by Digestive Tract Hormones a.Ghrelin: secreted by the stomach when it is empty •Acts on the hypothalamus to stimulate hunger •Stimulates the release of neuropeptide Y and Agouti-related protein •When the stomach fills, ghrelin release is reduced, as is hunger. •Dieters tend to increase their ghrelin production as they lose weight. •Short-term regulation b.Cholecystokinin (CCK) •Levels rise during and right after a meal •Suppresses hunger (promotes satiety) •Short-term regulation c.Polypeptide YY (PYY) •Reduces appetite •Stimulates release of MSH from arcuate nucleus 4.Regulation by Adipose Tissue Hormones a.Leptin: reduces hunger by inhibiting neuropeptide Y and Agouti-related protein and by stimulating MSH •The more adipose tissue you have, the more leptin you secrete. •This controls hunger for the long term. •Many obese people have reduced sensitivity to leptin. •Tends to maintain "normal" amounts of adipose tissue doc 5.Hunger regulation by insulin a.Insulin reduces hunger indirectly by increasing the storage of fat (which results in leptin production) b.May also inhibit the production of neuropeptide Y doc x2

Gallstones

1.Are hard mineral deposits in the gallbladder; cholesterol is the major component. 2.Produced when the liver cholesterol secretion is high enough for a supersaturated solution, and cholesterol crystals, together with mucus secreted by the gallbladder, can form a sludge. 3.Sometimes larger gallstones are produced that can block the hepatic, cystic, or common bile ducts and evoke the pain and nausea of biliary colic. doc

Defecation

1.As material passes to the rectum, pressure there increases, the internal anal sphincter relaxes, and the need to defecate rises. 2.The external anal sphincter controls defecation voluntarily. 3.During defecation, longitudinal rectal muscles contract to increase pressure as the anal sphincters relax. 4.Aided by contraction of abdominal and pelvic skeletal muscles

Pancreatic Islets

1.Beta cells: secrete insulin 2.Alpha cells: secrete glucagon 3.Delta cells: secrete somatostatin 4.Insulin is the main hormone regulating blood glucose levels, with glucagon playing a supportive role. Important in maintaining enough glucose for the brain while keeping levels below that which would damage tissues

Liver Functions: Bile Production & Secretion

1.Bile Production and Secretion a.The liver makes 250 to 1,500 ml of bile per day. b.Bile is composed of: oBile pigment (bilirubin) oBile salts oPhospholipids (lecithin) oCholesterol oInorganic ions c.Bilirubin a) Produced in spleen, liver, and bone marrow b) Derived from heme (minus iron) from hemoglobin c) Not water-soluble oCarried attached to albumin in the blood oNot directly filtered by kidneys or secreted into bile Breakdown of hemoglobin: When old rbc rupture the released hemoglobin is ingested my marcophages The chains of hemoglobins are broken into amino acids that are metabolized are used to build new proteins Iron is released from the heme of hemoglobin. The remaining structure is converted to biliverdin which is then converted into bilirubin. Iron is transported by transferrin in the blood to various tissues for storage or red bone marrow for making new hemoglobin Bilirubin in transported by albumin from blood to liver Liver make conjugated bilirubin which is excreted as part of the bile in the small intestine Intestinal bacteria convert bilirubin convert into biliribun derivatives which contributes to color of feces Some bilirubin derivatives are absored into the blood and excreted from the kidneys to the urine

Bone Deposition and Resorption

1.Bone Formation a.The skeleton serves as storage for calcium and phosphorus. b.Stored as hydroxyapatite c.Trapped in the bone matrix by osteoblasts in the process of bone deposition 2.Bone resorption by osteoclasts a.Hydroxylapatite is dissolved by cells called osteoclasts (bone resorption). b.Osteoclasts attach to bone matrix and forms a "ruffled membrane" c.Cells secrete H+ to dissolve calcium phosphate to return Ca2+ and PO43- to the blood doc 3.Bone Deposition and Resorption Balance a.Rates are determined by relative osteoblast and osteoclast activity. b.Growth occurs when osteoblast activity exceeds osteoclast activity. c.Bone mass begins to decline in persons in their 40s as osteoclast activity exceeds osteoblast activity. d.Calcium and phosphorus levels in the blood are maintained by intestinal absorption and urinary excretion. 4.Regulation of Osteoclasts Formation is also regulated by parathyroid hormone (PTH), calcitonin, and estrogen.

Intestinal Enzymes

1.Called brush border enzymes 2.Not released into lumen, but stay bound to plasma membrane with active sites exposed to chyme 3.Hydrolyze disaccharides, polypeptides and other substrates to simple molecules Carbs have to be broken down into monosaccharides, usually glucose doc Disaccharidase Sucrase: Digests sucrose to glucose and fructose; deficiency produces gastrointestinal disturbances Maltase: Digests maltose to glucose Lactase: Digests lactose to glucose and galactose; deficiency produces gastrointestinal disturbances (lactose intolerance) Peptidase Aminopeptidase: Produces free amino acids, dipeptides, and tripeptides Enterokinase: Activates trypsin (and indirectly other pancreatic juice enzymes); deficiency results in protein malnutrition Phosphatase Ca2+, Mg2+-ATPase: Needed for absorption of dietary calcium; enzyme activity regulated by vitamin D Alkaline phosphatase: Removes phosphate groups from organic molecules; enzyme activity may be regulated by vitamin D

Type 2 Diabetes

1.Called insulin-independent diabetes (95% of cases) a.Caused by very low target cell sensitivity to insulin (insulin resistance) 2.The tendency to develop type 2 diabetes is inherited, but the disease is most likely to occur in obese people. a.Adipokines promote insulin resistance b.Incidence in children is rising due to obesity 3. Type 2 Diabetes: Effects a.Skeletal muscles and liver cells do not take up glucose. b.Liver is not inhibited from releasing glucose. c.↑ production of β cells to compensate for loss of sensitivity may lead to β cell failure (a less severe case can degenerate into a more severe case). doc 4. Type 2 Diabetes and Obesity a.Rates of T2DM have tripled in the last 30 years to match obesity rates. b.A person with a BMI > 30 is 5x as likely to develop diabetes as one with a BMI < 25. c.Research showsT2 diabetics can ↓ the severity of the disease by losing weight. d.Weight reduction can also prevent the disease from developing. e.Adipose tissue releases pro-inflammatory adipokines that ↓ cell sensitivity to insulin f.Lean people release an anti-inflammatory adipokine that increases insulin sensitivity 5. T2DM and Exercise a.Exercise is beneficial in for diabetes in two ways: oBy ↑ caloric expenditure, helps lose fat cells which contribute to insulin resistance. oStimulates the production of GLUT4 in skeletal muscle independent of insulin and makes skeletal muscle more sensitive to insulin. This removes glucose from the blood. 6. Metabolic Syndrome Early in the progression of T2DM in obese subjects, there is ↑ release of insulin, but impaired glucose tolerance in spite of ↑ insulin and along with ↑ plasma triglyceride levels, low HDL levels, ↑ hypertension and risk for CVD and stroke, results in metabolic syndrome. 7. Effects of Type II Diabetes a.Although it does not usually lead to ketoacidosis, the increased amount of glucose in the blood does damage blood vessels, leading to blindness and tissue damage (gangrene). b.Increase kidney activity to excrete extra glucose leads to kidney failure. 8. Glycated hemoglobin test a.Also called hemoglobin A1c test b.Measures average blood glucose levels over several months (fasting is not required) c.More accurate test than glucose tolerance tests to determine blood glucose control d.A1c of 5% is normal e.5.7% to 6.4% is prediabetic f.Over 6.5% is diabetic

Pancreatitis

1.Can be acute or chronic. 2.Acute pancreatitis: caused by gallstones or provoked by reactions to some drugs. Symptoms appear rapidly, and most patients recover completely. 3.Chronic pancreatitis: due to chronic alcohol abuse. 4.Symptoms of both types of pancreatitis include abdominal pain, nausea, and vomiting, and diagnosis is aided by an abdominal ultrasound, which has the added virtue of visualizing gallstones that may be the cause of acute pancreatitis. 5.In pancreatitis, pancreatic enzymes can become abnormally activated in the pancreas and damage tissue.

Irritable Bowel Syndrome

1.Caused by complex factors that affect the neural regulation of the GI tract. 2.Can produce abdominal pain and discomfort with diarrhea, constipation, or alternating periods of each. 3.Alterations of the intestinal microbiota have been proposed as a root cause of IBS. For example, defective interactions of the intestinal microbiota with the enteric nervous system and with the brain, are believed to contribute to IBS.

Diabetes Mellitus

1.Characterized by chronic high blood glucose: Hyperglycemia 2.Results from inadequate secretion or action of insulin 3.Major cause of kidney failure and limb amputation; second leading cause of blindness; significant contributor to heart disease and stroke

Cirrhosis

1.Cirrhosis occurs when liver portal lobules are destroyed and replaced by fibrotic scar tissue and "regenerative nodules" of hepatocytes that lack the normal hepatic structure. 2.This tissue cannot remove bilirubin and toxic molecules from the blood and excrete them, causing jaundice and ill effects in many organs, including the brain (hepatic encephalopathy). 3.Disrupted blood flow through the liver sinusoids causes portal hypertension. 4.The most common causes of cirrhosis are hepatitis B virus and C virus, alcoholism, and nonalcoholic steatohepatitis. 5.Alcoholics with cirrhosis who stop drinking have a 65% chance of surviving 3 years but have no chance if they do not stop drinking.

Interactions Between Antigen-Presenting Cells and T Cells

1.Classes of MHC molecules a.Class 1 is made by all cells except RBCs. Class 1 MHC molecules & foreign ag are presented together to activate Killer T cells. b.Class 2 is made by antigen-presenting cells including B cells Class 2 MHC molecules and foreign antigens are presented together to TH cells c.Classes have different coreceptors •Killer T cells have CD8 for MHC-1; Helper T cells have CD4 for MHC-2 doc 2.T cell response to a virus (macrophage interactions) a.Virus phagocytosed by macrophages or dendritic cells b.Viral foreign antigens moved to the surface of the presenter cell c.Foreign antigen forms a complex with MHC-2 molecule e.Macrophages secrete interleukin-1, which stimulates helper T cell mitosis. f.TH cells secrete MCSF and γ IFN, which promote macrophage activity. g.TH cells secrete IL-2, which makes the macrophage produce TNF (against cancer) and activate cytotoxic T cell activity/mitosis. h.Interactions with B Cells •Activated TH cells promote humoral response of B cells by binding to foreign ag and MHC-2s •This stimulates mitosis of B cells, conversion to plasma cells, and production of ab. 3.Destruction of T Cells a.Activated T cells must be destroyed when the infection is over. b.Active T cells produce a surface receptor called FAS and later a protein called FAS ligand; binding of FAS to FAS ligand induces apoptosis. c.Helps maintain immunologically privileged sites - inner region of the eye and tubules of the testis -

Diarrhea

1.Diarrhea is the excretion of excessive fluid in the feces. 2.The most common cause is viral gastroenteritis (stomach flu), which causes intestinal inflammation and excessive fluid secretion into the lumen. 3.Certain bacteria (strains of E. coli, V. cholera, C. difficile) produce secretory diarrhea by releasing Enterotoxin. 4.Other bacteria (Salmonella, Campylobacter, Shigella) produce an inflammatory diarrhea by invading the mucosa causing damage and inflammation. 5.Osmotic diarrhea: lactose intolerance 6.The largest concern with diarrhea is dehydration due to fluid loss. And also loss of HCO3- (What do we remember about the consequences of the loss of HCO3- ?) Bicarbonate: HCO3-

Digestion of Fats

1.Digestion of Fats a.Begins in duodenum when bile emulsifies the fat and the pancreatic lipase, aided by colipase, breaks it into fatty acids and glycerol b.Pancreatic phospholipase A digests phospholipids into fatty acids and lysolecithin. Fat emulsification doc

Insulin and Glucagon: Postabsorptive State

1.During fasting, plasma glucose levels are constant due to liver glucose 2.Glucagon stimulates and insulin suppresses glycogenolysis 3.High glucagon and low insulin stimulate gluconeogenesis in the liver a.Formation of glucose from noncarbohydrate molecules b.Low insulin stimulates release of aa from skeletal muscle c.Glucagon and cortisol stimulate production of liver enzymes to convert aa to pyruvate and then to glucose 4.Skeletal muscle, heart, liver, and kidneys will switch to FFA for energy to "spare" glucose for the brain when insulin secretion is low. 5.Glucagon and Fat a.Stimulates hormone-sensitive lipase in adipose tissue •Converts stored triglycerides à fatty acids •FFA are released into blood to be used for energy by skeletal muscles instead of using glucose. b.In the liver, glucagon stimulates the conversion of FFA into ketone bodies to be used as an energy source.

Energy Sources

1.Energy reserves: molecules that can be used for energy a.Glycogen and fat good sources b.Proteins may be used in emergencies; source of proteins are body proteins, not dietary proteins 2.Molecules for energy also come from food we eat. 3.Once in the bloodstream, fatty acids, glucose, and amino acids are fuels. 4.Preferred Energy Sources a.Tissues have preferred energy sources. •Brain: glucose •Skeletal muscles at rest: fatty acids b.Various other organs can use ketone bodies, lactic acid, and aa doc

Introduction to Nutritional Requirements

1.Energy to form ATP comes from the carbohydrates, fats, and proteins we eat or from catabolism of our body tissues. 2.The energy value in food is measured as kilocalories. a.1 kilocalorie (1 Calorie) = 1,000 calories b.1 calorie = the amount of energy needed to raise 1 cubic cm water 1 degree C c.1g carbohydrate/protein = 4 kilocalories d.1g fat = 9 kilocalories

Regulation of Intestinal Function (1)

1.Enteric nervous system (ENS): neurons and glial cells that innervate the intestines a.Includes myenteric plexus and submucosal plexus b.Acts independently from CNS but with some feedback to CNS via vagus nerve (extrinsic afferents) c.Involved in regulation by the ANS d.Innervates interstitial cells of Cajal and smooth muscle to intrinsically regulate peristalsis doc 2.Paracrine Regulation a.Enterochromaffin-like cells in intestinal mucosa secrete serotonin and motilin in response to pressure (filling) and chemicals in the food. This stimulates muscle contractions. 3.Intestinal Reflexes a.Gastroileal reflex: increased gastric activity, increased ileum activity and movement of food through ileocecal valve b.Ileogastric reflex: distension of ileum causes a decrease in gastric motility c.Intestino-intestinal reflex: Over-distension of one portion of the intestine causes relaxation of other portions.

B Lymphocytes

1.Exposure to the specific antigen activates a B lymphocyte 2.Enters the germinal center of a secondary lymphoid organ 3.Undergo multiple cell divisions (cloning). a.Some become memory cells, which are used in a later infection by the same pathogen. b.Others become plasma cells, which produce 2,000 antibodies/second. doc

Anabolic Requirements

1.Food also supplies raw materials to build DNA, RNA, proteins, triglycerides, etc. a.Turnover rate - rate at which a particular molecule is broken down and resynthesized oProtein - 150g/day oFat - 100g/day b.Most fatty acids and amino acids can be produced by the body so dietary requirements are less c.A few cannot be produced by the body and therefore must be obtained in the diet. These are called essential nutrients. 2.Essential Nutrients a.There are nine essential amino acids b.There are two essential fatty acids: linoleic acid (an omega-6) and linolenic acid (an omega-3)

Digestive System

1.Food: Source of organic molecules to make ATP, build tissues, and serve as cofactors and coenzymes. a.Digestion breaks polymers (carbohydrates, fats, and proteins) into building blocks via hydrolysis reactions b.Absorption takes breakdown products into the bloodstream for uptake by cells 2.The digestive tract is open at both ends and is continuous with the environment Considered "outside" the body 3.One-way movement allows for specialization of function along the GI tract Building tissues-anabolic Hydrolysis reactions Hydrolysis: water causing breakdown of atoms -Carb: disaccharide- 2 molecules of glucose -Protein: peptide bond is broken, makes amino acid -Lipid: separation of fatty acids of glycerol More than 30 ft long, 1 direction, both ends communicate with external environment so therefore it is considered outside the body doc

Free Radicals and Antioxidants

1.Free radicals are molecules with unpaired electrons 2.Very reactive in the body-either oxidizing or reducing other molecules a.Reactive oxygen species (ROS): produced in electron transport chain; superoxide radical (O2•), hydroxyl radical (HO•) b.Reactive nitrogen species - nitric oxide radical (NO•) c.Serve a role in the immune response in phagocytic cells, vasodilation, and scar formation 3.Too many free radicals cause oxidative stress on cells by damaging proteins, DNA, and lipids. 4.This promotes: a.Cell death (apoptosis) b.Degeneration associated with aging c.Cancer malignancy d.Inflammatory diseases e.Cardiovascular & Neurological diseases 5.Protection from oxidative stress a.Enzymes (superoxide dismutase, catalase, glutathione peroxidase) prevent excess free radical buildup. Glutathione: tripeptide that reacts with free radicals to make them harmless; major antioxidant b.Nonenzymatic •Vitamin C and E pick up unpaired electrons. •Other molecules in fruits and vegetables are antioxidants. doc A balance in the number of free radicals must be maintained.

Stomach Functions and Structure

1.Functions a.Stores food b.Churns food to mix with gastric secretions c.Begins protein digestion d.Kills bacteria in the food (acid) e.Moves food into small intestine (chyme) 2.Stomach Structure a.Regions oFood is delivered from the esophagus to the cardiac region. oUpper region = fundus oLower region = body oDistal region = pyloric region; ends at pyloric sphincter b.Lining has folds called rugae. doc

GI Tract is One Long Tube

1.Gastrointestinal tract (GI tract, alimentary canal): 30 feet long, from mouth to anus Oral cavity -> Pharynx -> Esophagus -> Stomach -> Small intestines -> Large intestines -> Anus 2.Accessory organs: teeth, tongue, salivary glands, liver, gallbladder, pancreas Epiglottis prevents food from going into trachea and lungs Sphincter bwtn esophagus and stomach Plyoric valve between stomach and duodenum Stomach-chyme->small intestine: major site of digestive absorption Carb start digest in mouth Proteins may start to be digested in stomach doc

Bariatric (Weight Loss) Surgery

1.Goal to promote significant weight loss in obese people, who are prone to insulin resistance, hypertension, and T2DM: Type 2 diabetes 2. These surgical procedures produce long-term weight loss, reduced insulin resistance, improved blood glucose levels, and better insulin secretion within a few days after the surgery (even before much weight has been lost). 3. Evidence suggests that increased activity of the intestinal hormone GLP-1 which stimulates insulin secretion and alterations in the intestinal microbiome promote weight loss and reduce insulin resistance. Duodenum is bypassed 85% of stomach is removed but intersitial pathway is unaltered

Lactose Intolerance

1.Greatest prevalence among those with African, Asian, Hispanic, and Native American heritage. 2. Refers to an inability to digest the disaccharide lactose into glucose and galactose for absorption by the small intestine. 3.Digestion of lactose requires lactase, one of the brush border disaccharidases. Most people with lactose intolerance can produce lactase when they are babies and young children, but gradually lose this ability with age. 4.Accumulation of lactose in the intestine produces symptoms: abdominal gas and bloating, diarrhea, and nausea. Osmotic diarrhea Microbes lactose gas

Pancreas

1.Has endocrine and exocrine functions a.Endocrine: Islets of Langerhans cells (Pancreatic Islets) make insulin and glucagon. b.Exocrine: Acinar cells make pancreatic juice, which is delivered to the duodenum via the pancreatic duct. Alpha produce glucagon Beta cells produce insulin doc c.Bicarbonate formation oMade by cells lining the ductules oMade from CO2 from the blood i.First, carbonic acid is made. ii.This dissociates to form H+ and bicarbonate. iii.The bicarbonate is secreted into pancreatic juice, and H+ goes back into the blood. iv.Bicarbonate is countertransported with Cl−. oPeople with cystic fibrosis have trouble secreting bicarbonate because of defective chloride transporters, which can lead to destruction of the pancreas. doc d.Pancreatic Enzymes 1)Most are inactive (zymogens) until they reach the small intestine. Enterokinase activates trypsinogen à trypsin (to digest protein). a)Trypsin activates other enzymes. Trypsin is a protease doc x3

Immunological Tolerance

1.Immunological competence develops during early postnatal life - being able to distinguish self-ag from foreign ag 2.Immunological tolerance - continued tolerance of self-cells 3.In some instances, "self" cells are attacked by antibodies and autoreactive T cells: a.If cells in particular organs are never exposed to the immune system b.These lymphocytes are called autoreactive. 4.If lymphocytes begin attacking cells, there are mechanisms to stop this: a.In clonal deletion, these lymphocytes that recognize self-antigens are destroyed (apoptosis). b.In clonal anergy, these lymphocytes are prevented from becoming active. Regulatory T lymphocytes likely do this.

Appendicitis

1.Inflammation of the vermiform appendix. 2.The appendix does not function in digestion but contains lymphoid nodules and a population of commensal bacteria that helps to replenish a normal intestinal microbiota when needed. 3.Appendicitis: a medical emergency that produces pain in the lower right abdomen, nausea, and other symptoms that sometimes confuse the diagnosis. 4. A burst appendix spreads the inflammation to the surrounding peritoneal membranes, a condition called peritonitis that can produce circulatory shock and death. This can be prevented by an appendectomy, the surgical removal of the appendix.

Inflammatory Bowel Disease

1.Inflammatory bowel disease (IBD) includes Crohn's disease and ulcerative colitis. 2.Many genes associated with increased susceptibility to IBD, which involve altered immune responses to intestinal bacteria. 3.There is decreased mucus secretion by goblet cells and changes in tight junctions between epithelial cells that increase intestinal permeability. These can lead to erosions and ulcerations of the intestinal mucosa. 4.Crohn's disease is characterized by inflammation that can cause fibrosis, prolonged diarrhea with abdominal pain, fatigue, and weight loss. 5.The incidence of IBD has been rising in the United States and may be promoted by poor diet and the overuse of antibiotics, which cause a change in the intestinal microbiota that provokes an immune response against the changed bacterial population.

Regulation of Insulin and Glucagon Secretion

1.Insulin a.Plasma concentration of glucose and amino acids regulates secretion of insulin and glucagon •Fasting plasma glucose: 65 to 105 mg/dl •Absorptive state rises to 140 to 150mg/dl b.Insulin acts to remove excess glucose from the blood after a carbohydrate-rich meal c.Inserts GLUT4 carrier proteins in plasma membrane of target cells •Skeletal and cardiac muscle, liver, and adipose cells •Promotes production and storage of glycogen and fat, inhibits breakdown of fat and muscle proteins, stimulates use of glucose for energy ↑ blood glucose -> glucose enters pancreatic β cells -> ↑ ATP production -> closes K+ channels -> Depolarization/Hyperpolarization? -> opens voltage-gated Ca2+ channels -> Ca2+ triggers exocytosis of vesicles containing insulin. pancreatic beta cell- doc 2.Regulation of Glucagon Secretion a.After a carbohydrate-rich meal, ↑ plasma glucose inhibits α cells, and glucagon is not released. b.When glucose levels fall, the inhibition is lifted, and glucagon can be released again. 3.Action of Glucagon a.Prevents cellular uptake of glucose in the skeletal muscles, liver, and adipose tissue b.Promotes conversion of glycogen to glucose and release of glucose from liver. Glycogenolysis c.Promotes release of fatty acids from adipose tissue 4.Effect of Amino Acids a.Certain aa also stimulate insulin secretion to help move these aa into cells. b.If a high-protein, low-carbohydrate meal is eaten, both insulin and glucagon will be secreted to ensure proper glucose levels in the blood. 5.Oral Glucose Tolerance Test (OGTT) a.Tests ability of beta cells to release insulin and ability of insulin to reduce blood glucose levels b.The person drinks a glucose solution, and several blood samples are taken to measure glucose levels. •A healthy person will have normal glucose levels after 2 hours. •If levels stay high, the person has diabetes. 6.Effect of Autonomic Neurons a.Parasympathetic division is activated while eating and stimulates the release of insulin. b.The sympathetic division inhibits insulin secretion and stimulates glucagon secretion. Produces stress hyperglycemia 7.Effect of Intestinal Hormones a.Insulin begins to be secreted before glucose is even absorbed due to GIP and GLP-1 secreted by the intestines when carbohydrates are eaten. Where did we hear about this ? b.Helps prevent a sudden rise in blood glucose following absorption

Insulin and Glucagon: Absorptive State

1.Insulin action a.Skeletal muscles are the primary target. b.Intake of glucose for energy is primary goal. c.Muscles can also take in glucose and convert it to glycogen for later use. Once skeletal muscles make glycogen, they must use it for their own energy needs. They cannot release glucose back into blood. d.Promotes cellular uptake of aa for use in protein synthesis 2.Insulin Action: Energy Storage a.Glucose is taken into the liver and skeletal muscles to be converted to glycogen for storage. b.Limited "room" for glycogen; Once full, excess calories stored as fat. 3.Insulin and the Brain a.Insulin acts on the hypothalamus to inhibit conversion of glycogen -> glucose in the liver. b.When insulin levels drop, this inhibition is lifted, and the hypothalamus stimulates the liver to convert glycogen -> glucose and release it.

Antibodies

1.Introduction a.Also known as immunoglobulins (Ig) b.Five classes: IgG, IgA, IgM, IgD, and IgE 2.Antibody Structure a.Y-shaped protein •2 long, heavy (H) chains joined by 2 shorter, light (L) chains •The bottom (Fc) is constant across different antibodies, whereas the top (Fab) varies and allows antigen specificity. b.B lymphocytes have antibodies on the plasma membranes that are receptors for antigens. •When the antigen bonds to the antibody, the B cell is stimulated to divide and produce more antibodies doc 3.Diversity of Antibodies a.Everyone has 1020 antibody molecules. •There are a few million different specificities. •There should be an antibody for every antigen you might encounter. b.Mechanisms for antibody diversity •A large % of our genetic code is dedicated to making antibody light chains and heavy chains •Antigen-independent genetic recombination in the bone marrow - different combinations of light and heavy chains •Antigen-dependent cell division of lymphocytes in secondary lymphoid organs, somatic hypermutation, gene recombinations, class switch recombination doc

Jaundice

1.Is yellow staining of the sclera of the eyes, mucous membranes, and skin caused by elevated levels of blood bilirubin (hyperbilirubinemia). 2.May result from pre-hepatic, hepatic, or post-hepatic causes. 3.Pre-hepatic jaundice: an increase in free bilirubin due to increased hemolysis of red blood cells, providing more heme groups for conversion into bilirubin. 4.Hepatic jaundice: caused by hepatitis and cirrhosis, can raise bilirubin. 5.Post-hepatic jaundice, or obstructive jaundice: due to a blockage in the drainage of bile. 6.Because conjugated bilirubin cannot be excreted, it rises in the blood. The obstruction may result from a gallstone, pancreatic diseases, or stricture of the bile duct.

Killer, Helper, and Regulatory T Lymphocytes

1.Killer (cytotoxic) T Lymphocytes a.Have surface molecules called CD8 b.Destroy body cells that harbor foreign antigens •Usually from a pathogen (virus or fungus), but can be due to a malignancy (cancer) •Transplant cells c.Cell-mediated destruction means the T cells must touch the target victim. •Secrete perforins to create large pore in cell •Secrete granzymes to trigger apoptosis in cell through the action of caspase enzymes 2.Helper T Lymphocytes a.Surface molecule is CD4 b.Improve ability of B lymphocytes to become plasma cells and enhance ability of cytotoxic T cells to kill targets •Secretion of lymphokines 3. Regulatory T Lymphocytes, T(reg) a.Surface molecules CD4 and CD25 b.Previously called suppressor T lymphocytes c.Inhibit response of B lymphocytes and killer T lymphocytes d.Activates the FOXP3 gene that codes for a transcription factor needed for development of T(reg) lymphocytes e.People with genetic deficiencies in regulatory T lymphocyte production may develop autoimmune diseases and allergies. doc- b cells and t cells work together 4.Lymphokines a.Autocrine regulators b.Cytokines specific to lymphocytes c.Called interleukins - see Table 15.7 d.Many stimulate B cell or cytotoxic T cell activity. e.Subtypes of helper T cells also produce lymphokines •TH1 - produces IL-2 and gamma interferon - activates killer T cells and stimulates NO production in macrophages •TH2 - produces IL-4, IL-5, IL-13 and others - stimulate B cells and humoral immunity, recruit eosinophils and induce IgE production •TH17 - secretes IL-17 - fights infections in skin, lungs, and mucous membranes; stimulates neutrophils 5.T Cell Receptor Proteins a.Antigen recognition proteins on the membranes of T cells •These cannot bind directly to antigens. •Antigen-presenting cells (APCs), such as dendritic cells and macrophages, help T cells bind to antigens. •Once activated, the T cells divide for form effector T cells and memory T cells 6.Histocompatibility Antigens a.On surface of all body cells (except mature RBCs); also called human leukocyte antigens (HLAs) b.Coded for by four genes on chromosome 6 called major histocompatibility complex (MHC) •Many versions of each gene are possible, so most people have different combinations. •An organ transplant requires an MHC match.

Lymphocytes and LymphoidOrgans

1.Lymphocytes a.Derived from stem cells in the bone marrow. b.These stem cells seed the thymus, spleen, and lymph nodes. •The thymus is the site of new T lymphocytes through late childhood. It degenerates in adulthood, and new T lymphocytes are made through mitosis in secondary lymphoid organs. •The bone marrow and thymus are considered primary lymphoid organs. c.T Lymphocytes •Lymphocytes that seed the thymus become T lymphocytes. These then seed the blood, lymph nodes, and spleen. •T lymphocytes attack host cells that have become infected with a virus or fungus, transplanted human cells, and cancer cells. •T lymphocytes do not produce antibodies. •They must be in close proximity to the victim cell in order to destroy it. •This is called cell-mediated immunity. d.B Lymphocytes •Lymphocytes that come directly from bone marrow to seed other organs (not the thymus) are called B lymphocytes. •They combat bacterial and some viral infections. •They secrete antibodies into blood and lymph so can be far from the victim. •This is called humoral immunity or antibody-mediated immunity. 2.Secondary Lymphoid Organs a.Lymph nodes, spleen, tonsils, and Peyer's patches (in mucosa of intestines) b.Capture and present pathogens to macrophages and house lymphocytes c.Lymphocytes migrate between lymphoid organs to sample blood & lymph. •The spleen filters blood for pathogens. •Other organs filter lymph for pathogens.

Mouth

1.Mastication: Chewing breaks food down into smaller pieces for deglutition and mixes it with saliva. 2.Saliva: contains mucus, an antimicrobial agent, and salivary amylase to start digestion of starch. 3.Deglutition a.Involves coordinated contraction of 25 pairs of muscles b.Three parts: i.Oral: voluntary; muscles of mouth and tongue mix food with saliva to form a bolus. ii.Pharyngeal: involuntary; initiated by receptors in the posterior oral cavity and oropharynx iii.Esophageal: automatic; controlled by the swallowing center of brain stem; bolus is moved down esophagus to stomach via peristalsis

Metabolic Rate & Caloric Requirements

1.Measured by amount of heat generated or amount of O2 consumed per minute Increased by exercise or eating 2.Body temperature is an important factor a.Influences reaction rates b.Control area of hypothalamus corrects deviations by directing physiological responses 3.Basal metabolic rate: O2 consumed by a relaxed, awake person, comfortable temperature, 12 to 14 hours after eating Affected by age, sex, body surface area, and thyroid activity 4.Energy Requirements Depend on physical activity Range: 1,300 to 5,000 kcal/day: Avg male = 2,900 kcal/d; Avg female = 2,100 kcal/d b.Excess calorie intake (regardless of source) = storage of fat; positive energy balance c.Weight is lost when fewer calories are consumed than needed; negative energy balance d.The body can adjust metabolic requirements which may make weight gain or loss difficult

Metabolic Syndrome

1.Metabolic syndrome refers to a group of symptoms associated with obesity. 2.Symptoms: Insulin resistance, type II diabetes, impaired glucose tolerance, hypertension, dyslipidemia. 3.These conditions promote cardiovascular disease development and lead to chronic kidney disease.

Treatments for Type II Diabetes

1.Metformin (Glucophage) is the most widely used drug used to treat type II diabetes. It inhibits hepatic gluconeogenesis. 2.The Sulfonylurea class of drugs closes ATP-gated K+ channels and stimulates insulin secretion. 3.The SGLT2 inhibitors inhibits the sodium-glucose transporter type 2 and decreases the renal reabsorption of glucose which increases glucose excretion via the urine. 4.Thiazolidinedione drug class (rosiglitazone and pioglitazone) act on PPAR-γ receptor to reduce inflammation and insulin resistance.

Fluid and Electrolyte Absorption

1.Most absorption occurs in small intestine, but some is left for large intestine. 2.Not all water is absorbed; about 200 ml is left per day to be excreted with feces. 3.Water is absorbed passively following an osmotic gradient set up by active Na+/K+ pumps. Aldosterone stimulates greater salt and water absorption here. 4.Some minor secretion of water occurs by osmosis.

Osteoporosis

1.Most common bone disorder affecting both men and women. It affects women 10 x more frequently than it does men. 2.Characterized by a loss of mineral and organic matrix which reduces bone density. 3.Reduced density results in fragile bones that fracture easily. 4.It is treated with: a.Bisphosphonates (Fosamax etc.) which disrupt osteoclast activity b.Denosumab prevents osteoclast development c.Roloxifene is an estrogen receptor modulator d.Teriparatide (Forteo) is a PTH derivative that increases bone mass doc

Regulation of Gastric Function

1.Motility and secretion are somewhat automatic. a.Contractions are stimulated spontaneously by pacemaker cells in stomach (intrinsic regulation). b.Secretion of HCl and pepsinogen occurs when proteins enter the stomach. Initiated and regulated by G cells (gastrin), D cells (somatostatin), and ECL cells (histamine) The presence of amino acids in the stomach stimulates Gastrin secretion from G cells. The secreted Gastrin then travels in the bloodstream to then stimulate ECL cells to secrete histamine which acts as a paracrine signal for the parietal cells to secrete HCl. doc 2.Three Phases of Extrinsic Gastric Regulation a.Cephalic phase: control by brain via vagus nerves oVagal ACh secretion onto cholinergic receptors stimulates parietal cells to secrete HCl. oVagus stimulates G cells to secrete Gastrin which stimulates ECL to secrete Histamine. The histamine in turn stimulates parietal cells to secrete HCl. (Fig 18.30) oLasts for the first 30 minutes of a meal Cephalic phase: taste or smell of food, tactile sensation food in the mouth, thoughts of food sends nervous impulses to the medulla oblangota, parasympathetic neuron via vagus nerve cause secretion of HCl and pepsin in the stomach. The parasympathetic stimulation results in secretion of gastrin in lower part of stomach. Further stimulates HCl and pepsin secretion in upper stomach b.Gastric phase: triggered by arrival of food into stomach oGastric secretion is stimulated by stomach distension and the chemistry of chyme. oAs pH drops, somatostatin is released. This inhibits gastrin secretion. oLarge amounts of proteins and polypeptides buffer pH, so secretion matches protein concentration. Gastric: food has entered and sitended the stomach. The distension activates a parasympathetic reflex via medulla oblandogtoa...secretion HCl and pepsin. Intestinal phase, chyme entered duodenum. Chyme contai c.Intestinal phase: ↓ of gastric activity when chyme enters small intestine oSlows movement of chyme into the duodenum to allow time for digestion and absorption oThe stretch when food enters the duodenum stimulates a neural reflex that inhibits gastric stimulation via the vagus nerve. oThe presence of fats stimulates the duodenum to secrete a hormone, generally labeled enterogastrone, which inhibits gastric function.

Digestive Tract

1.Motility: movement of food through the GI tract a.Ingestion: taking food into the mouth b.Mastication: chewing and mixing food with saliva c.Deglutition: swallowing d.Peristalsis: wave-like, one-way movement through tract e.Segmentation: churning and mixing while moving forward 2.Secretion a.Exocrine: digestive enzymes, hydrochloric acid, mucus, water, and bicarbonate b.Endocrine: hormones to regulate digestion 3.Digestion: breaking down into smaller units, physically and chemically 4.Absorption: passing broken-down food into blood or lymph 5.Storage and elimination: storage and elimination of undigested food 6.Immune barrier a.Tight junctions on simple columnar epithelium prevents swallowed pathogens from entering body. b.Immune cells in connective tissue of the tract promote immune responses Peristalsis: one part contracts when another part relaxes Segmentation: parts contract and relax at same time Digestive enzyme- most pancreas, small intestine, stomach, saliva Hydrochloric acid-stomach Bicarbonate from pancreas goes to duodenum? Exocrine goes in duct Endocrine go into circulatory system and go everywhere? Can't break down cellulose- undigested food

Digestive System Regulation

1.Neural and endocrine control mechanisms a.Modifies GI tract functioning b.Sight, smell, taste, or thought of food can stimulate salivation and gastric secretions to "prime" the digestive tract for food. c.Stimulation goes from brain to organ via vagus nerve; a conditioned reflex d.Short reflexes: do not involve the brain e.GI tract produces some hormones and is also the target for action 2.The first hormone to be described was Secretin. This hormone was identified by Bayliss & Starling in 1902.

Fatty Liver Disease

1.Nonalcoholic fatty liver disease: associated with obesity and the insulin resistance of prediabetes and T2DM and seems to be promoted by diets high in saturated fat and fructose. 2.It is benign unless it develops into nonalcoholic steatohepatitis(NASH), an inflammatory condition that promotes cirrhosis, cancer, and cardiovascular disease. 3.Alcoholic fatty liver disease can occur in moderate to heavy drinkers. 4.Alcohol oxidation occurs in the liver, where it is metabolized to acetyldehyde by alcohol dehydrogenase. Acetyldehyde is converted to acetate and then acetyl CoA, which is used to synthesize fatty acids. Other aspects of liver metabolism are also affected. 5.In addition, alcohol damages the intestine in ways that expose the liver to bacterial toxins from the intestine via the hepatic portal vein. 6.Alcoholic hepatitis is a potentially fatal condition, as is the increased risk of esophageal cancer in alcoholics.

Negative Feedback Control of Calcium and Phosphate Balance

1.PTH secretion controlled by plasma Ca2+ levels 2.PTH needed for activation of 1,25-dihydroxyvitamin D3 3.Kidneys help balance PO43- levels 4.Calcitonin stimulated by high blood Ca2+ and lower PO43- levels by inhibiting osteoclasts and stimulating excretion of excess in urine doc

Regulation of the GI Tract

1.Parasympathetic division (rest and digest) (extrinsic regulation) a.Stimulates esophagus, stomach, small intestine, pancreas, gallbladder, and first part of large intestine via vagus nerve b.Spinal nerves in sacral region stimulate lower large intestine. c.Preganglionic neurons synapse on submucosal and myenteric plexuses. 2.Sympathetic division (extrinsic regulation) a.Inhibits peristalsis and secretion b.Stimulates contraction of sphincters 3.Hormones: from brain or other digestive organs 4.Intrinsic regulation a.Intrinsic sensory neurons in gut wall help in intrinsic regulation via separate enteric nervous system b.Paracrine signals

Hormonal Regulation of Bone

1.Parathyroid Hormone a.When plasma calcium levels ↓, the parathyroid glands produce PTH. b.Mg+2 is needed to make PTH, so Mg+2 deficiency can lead to hypocalcemia. c.The role of PTH is to raise circulating Ca2+ & PO43- d.Regulates bone in three ways: •Stimulates osteoclasts to resorb bone, adding Ca2+ & PO43- to blood. This is the primary mechanism •Stimulates Ca2+ reabsorption in the kidneys. Inhibits reabsorption of PO43-, preventing calcium phosphate crystal formation in bone. •Stimulates kidneys to make the enzyme needed to convert 25-hydroxyvitamin D3 to its active form. This stimulates the absorption of Ca2+ & PO43- in intestine. doc 2.Calcitonin a.Secreted by the parafollicular cells (C cells) of the thyroid gland b.Inhibits resorption of bone by inhibiting osteoclast activity 3. Effects of Other Hormones a.People with hyperthyroidism are more prone to osteoporosis b.Leptin indirectly stimulates osteoblast proliferation c.Insulin promotes bone growth by suppressing an inhibition of osteoblast development; causes osteoblasts to secrete osteocalcin that stimulates insulin production doc x2

The Complement System (1)

1.Part of the nonspecific defense system •Activity is triggered by binding of antibodies to antigens (classic pathway) and by polysaccharides on bacterial membranes (alternative pathway). 2.Binding of antibodies to antigens does not destroy the pathogen. •This labels targets for attack by phagocytic cells and stimulates opsonization. 3.Complement is a group of plasma proteins activated by the binding of antibodies to antigens. •Proteins are designated C1 to C9. 4.Classic Pathway of Complement Action a.Complement-dependent cytotoxicity - rapid and efficient; involves antibodies binding to antigens to destroy cells b.IgG and IgM activate C1, which splits C4 into two fragments, C4a and C4b. c.C4b binds to the cell membrane becomes active, splitting C2 into C2a & C2b. d.C2a attaches to C4b and cleaves C3 into C3a and C3b. e. C3b converts C5 into C5a and C5b. f. C5b and C6−C9 are inserted into the bacterial cell membrane, forming the membrane attack complex - complement fixation g.This creates a large pore in the membrane, causing influx of water into the cell = lysis. 5.Effects of Complement Fragments a.Chemotaxis - attracting phagocytic cells b.Opsonization - phagocytes have receptors for C3b; forms a bridge between phagocyte and victim cell to facilitate phagocytosis c.C3a & C5a stimulate mast cells to release histamine to ↑ blood flow to the area.

Passive Immunity

1.Passing of antibodies from one individual to another; person does not make their own antibodies 2.Provides temporary protection: a.From mother to fetus b.From mother to child (in breast milk - colostrum) c.Artificially via immunization (snake anti-venom) 3.Monoclonal antibodies a.Animals are injected with an antigen b.A single B lymphocyte that makes the desired antibodies is extracted c.The B cell is fused with a cancerous myeloma cell in vitro d.The hybridoma produces many clones that produce antibodies specific for the antigen

Intestinal Contractions and Motility

1.Peristalsis is weak. Movement of food is much slower due to pressure at pyloric end. 2.Segmentation is stronger and serves to mix the chyme. 3.Smooth muscle contractions occur automatically due to endogenous pacemaker activity a.Graded depolarizations called slow waves produced by pacemaker cells called interstitial cells of Cajal produce APs in muscle cells. b.Depolarization from the interstitial cells of Cajal opens voltage-gated Ca2+ channels in muscle cells à AP and contraction. c.Produces contractions needed for segmentation Pacemaker cells- not very strong, slower, doesn't travel far doc

Active Immunity & the Clonal Selection Theory

1.Primary response a.After infection, it takes 5 to 10 days before antibodies are detected in the blood. b.The person will get sick. 2.Secondary response a.Later exposure to the same infection results in maximum antibody production in less than 2 hours. b.The person will likely never get sick. doc 3.Clonal Selection Theory a.Explains how the secondary immune response works: •A person has lymphocytes to almost every pathogen, but there are few of each type. •When exposed to foreign ag, immune cells respond by making many copies of themselves. •Germinal centers in secondary lymphoid organs develop to produce the clones b.The 1⁰ response triggers a massive production of cells that can respond to that antigen. c.These cells respond much quicker after exposure a second time. 4.Active Immunity (Basis for vaccines) a.Development of the 2⁰ response b.Requires prior exposure to the antigen; protects from future infections c.Vaccines include an antigen but are not virulent. doc 5.Vaccines a.Stimulate a primary response and active immunity without making the person sick. b.Three ways to accomplish this: •Use a killed virus (Salk polio vaccine) •Use a live virus with attenuated virulence—that is, the virus either cannot replicate or cannot infect target tissues Sabin polio vaccine, MMR) •Use a genetically engineered recombinant virus (hepatitis B) c. Adjuvants - molecules that boost immune response when delivered with the vaccine antigens; found to be PAMPs doc

Autoimmunity

1.Produced by failure of immune cells to tolerate "self" antigens a.Autoreactive T lymphocytes and autoantibodies are produced, causing inflammation and organ damage. b.Common autoimmune diseases include RA, T1DM, MS, Grave's disease 2.Reasons why self-tolerance may fail a.An ag not normally exposed to the immune system becomes exposed. E.g. Hashimoto's thyroiditis b.A normally tolerated ag is combined with a foreign molecule. This may occur when a drug such as aspirin combines with platelets, resulting in the destruction of platelets. E.g. Thrombocytopenia c.Antibodies are produced aimed at other antibodies. E.g. inflammation in RA d.Ab produced against foreign ag cross-react with self ag and begin attacking self cells (can occur in the heart or kidneys after a strep infection).E.g. RA e.Self ag may be presented to T helper cells along with MHC-2 molecules. E.g. T1DM, Graves disease

1,25-Dihydroxyvitamin D3

1.Production begins in the skin in response to sunlight. a.Most don't produce sufficient levels of vitamin D3 and must get more in the diet. b.Forms vitamin D3 as a prehormone 2.An enzyme from the liver converts prehormone to 25-hydroxyvitamin D3 3.This must be activated by an enzyme produced in the kidneys after PTH stimulation to 1,25-dihydroxyvitamin D3 4.Raises circulating Ca2+ & PO43- levels in three ways: a.Increasing intestinal absorption b.Stimulating bone resorption by promoting the formation of osteoclasts c.Stimulating kidney reabsorption 5.Vitamin D3 and Bone Mineralization a.Vit D deficiency leads to decreased bone mineralization. b.Leading cause of rickets and osteomalacia c.Due to important role in Ca2+ & PO43- absorption in intestines d.Without this absorption, there will not be enough calcium for proper bone formation. doc

Pepsin and HCl Secretion (1)

1.Production of HCl a.Primary active transport of H+ via H+/K+ ATPase pumps on apical side. b.Parietal cells secrete Cl− as well as H+ into lumen while secreting HCO3- into the blood. H+ and HCO3- produced from H2CO3 catalyzed by CA. 2.Stimulation of HCl Secretion a.Gastrin: made in G cells; carried to parietal cells in blood; Also stimulates ECL cells to make histamine b.Histamine: also stimulates parietal cells via H2 histamine receptors Examples: Tagamet and Zantac block H2 receptors. c.Parasympathetic neurons and ACh: stimulate parietal and ECL cells Apical surface secretes H+ via H+/K+ ATPase pumps. Basolateral side secretes HCO3- in exchange for Cl-. doc Maintain acidic pH CO2 diffuses into parietal cell, and enzyme carbonicanhydrase catalyzes rxn between co2 and h2o to form carbonic acid, carbonic acid dissociates to bicarbonate ion and H+, bicarbonate ion is transported back into the blood stream, and ion exchange molecule in plasma molecule exchanges bicarbonate for Cl coming in, the H+ ion are actively transported into the duct of gastric gland, Cl- ions diffuse with the positively charged H+, K+ are counter transported into the parietal cell in exchange in H+ ion, the net result is production of HCl in parietal cells and its secretion into the duct of the gastric gland (lumen of stomach) Bicarbonate is sent into the plasma as a buffer and some of bicarbonate makes its way into the mucus that separatesa the lining of stomach from the lumen, to neutralize acid that comes close 3.Functions of HCl a.Drops pH to 2 b.Ingested proteins are denatured (allows enzymes access). c.Pepsinogen is converted to active pepsin (digests proteins). d.Serves as the optimal pH for pepsin activity 4.Function of pepsin: catalyzes the hydrolysis of peptide bonds in the ingested proteins doc activation of pepsin

Defense Mechanisms

1.Protect against disease-causing agents called pathogens 2.Make up the immune system 3.Two types: a.Innate (nonspecific) immunity - inherited b.Adaptive (specific) immunity - learned from exposure to specific pathogens; function of lymphocytes

Gastroesophageal Reflux Disease (GERD)

1.Reflux of the acidic gastric chyme produces symptoms such as heartburn, cough, and sore throat. 2.This can produce esophageal stricture, Barrett's esophagus and adenocarcinoma of the esophagus. 3. Risk factors for GERD include obesity, pregnancy, and hiatal hernia (upward protrusion of the stomach through the diaphragm). 4.GERD is commonly treated with H2 receptor blockers, and proton pump inhibitors (PPIs).

Large Intestine Structure (1)

1.Regions a.Through the ileocecal valve into the b.Cecum -> c.Ascending colon -> d.Transverse colon -> e.Descending colon -> f.Sigmoid colon -> g.Rectum -> h.Anal canal -> i.Anus doc 2.Mucosa - columnar epithelial cells with goblet cells, crypts, lymphatic nodules, but no villi 3.Outer surface forms pouches called haustra 4.Large Intestine Function a.Absorption of water, electrolytes, vitamin K, and some B vitamins b.Production of vitamin K and B vitamins via microbial organisms c.Storage of feces No digestion

Natural Killer (NK) Cells

1.Related to T lymphocytes but part of innate immunity without the ability to recognize specific antigens a.Can recognize malignant cells and cells infected with a virus b.Must be activated by pro-inflammatory cytokines from dendritic cells 2.Kill compromised cells in the same manner as cytotoxic T cells 3.Cytokines released by natural killer cells activate both innate and adaptive immune cells.

Gallbladder

1.Sac-like organ attached to the inferior surface of the liver 2.Stores and concentrates bile from the liver: Liver -> Bile ducts -> Hepatic duct -> Cystic duct -> Gallbladder -> Cystic duct -> Common bile duct -> Sphincter of Oddi into the duodenum doc

Growth Hormone (Somatotropin)

1.Secreted by anterior pituitary a.Stimulated by hypothalamic GHRH and inhibited by hypothalamic GHIH b.Release of GH follows a circadian rhythm, with ↑ release during sleep. c.Also stimulated by ↑ of aa & ↓ in glucose in plasma; fasting and exercise 2. Growth Hormone and IGF a.The liver releases IGF in response to growth hormone. b.These act as hormones by traveling to targets & also as autocrines c.IGF-1 stimulates mitosis in cartilage tissue and stimulates bone growth. d.IGF-2 supports IGF-1 actions but is more insulin-like. 3. Effects of Growth Hormone on Metabolism a.Has both anabolic and catabolic actions. Promotes: •Cellular uptake of amino acids for protein synthesis (anabolic) •Release of fats from adipocytes which reduces the use of glucose for energy (catabolic) doc 4.Growth Hormone and Growth a.Stimulates bone growth at epiphyseal plates (mediated by IGF-1 & IGF-2) Once the cartilage is converted to bone in the epiphyseal plates, no more height can be achieved. b.Excessive release of growth hormone in childhood = gigantism, increased height in normal body proportions c.Excess release of growth hormone in adults = acromegaly, which includes growth of soft tissues, elongation of the jaw, and deformities of the face, hands, and feet. d.Inadequate production of growth hormone can produce several forms of dwarfism. e.Most cases of dwarfism are caused by achondroplasia which is a mutation in fibroblast growth factor receptor 3.

Intestinal Microbiota

1.Several hundred different species of bacteria; aka microflora; mostly anaerobic a.Some are commensal. Bacteria benefit, host not harmed or benefitted. b.Others are mutualistic. Both bacteria and host benefit. c.An infant receives its initial colonies of bacteria from its mother during birth. 2.Benefits from Microbes a.Microbes make vitamin K and some B vitamins. b.They also make fatty acids from cellulose. Some of these are used for energy by large intestine epithelial cells. We can't absorb the fatty acids, but they help absorb electrolytes such as Na+, Ca+2, HCO3-, Mg+2, and iron. c.They outcompete harmful species of bacteria. d.Disruption of normal microflora can lead to inflammatory bowel disease. 3.Protection from Intestinal Bacteria a.Mucus from goblet cells prevents contact with epithelial cells. Beneficial to have microflora

Small Intestine Structure

1.Starts at the pyloric sphincter and ends at the ileocecal valve 2.Three sections: a.Duodenum - first 10 inches b.Jejunum - middle 2/5 c.Ileum - last 3/5 3.Mucosa and submucosa folded into plicae circulares; mucosa further folded into villi; and epithelial plasma membranes folded into microvilli; increase the surface area for absorption Total 3 meters Longest part of digestive tract Called small because smaller diameter than large intestine doc

Starvation

1.Starvation and malnutrition are the leading causes of diminished immune capacity worldwide. 2.Anorexia and bulimia nervosa: eating disorders affecting both young men and women and with serious physiological consequences similar to starvation and malnutrition. 3.During starvation there is lipolysis of the triglycerides stored in adipose tissues due to ↓ insulin, ↑ GH and ↑ SNS activity. 4. As adiposity decreases so does leptin secretion. 5. Leptin affects immune and reproductive systems. ↓ adiposity and leptin slow entry into puberty and menstrual cycles.

Adaptive Immunity

1.The acquired ability to defend against specific pathogens after exposure to these pathogens Mediated by antigens and antibodies, B cells and T cells 2.Antigens a.Cell surface molecules that stimulate the production of specific antibodies and combine with those antibodies •Foreign antigens elicit an immune response. The immune system can distinguish "self" from "nonself." •Antibodies bind to their specific antigens. •Large molecules can have several antigenic determinant sites or epitopes, that stimulate the production of and binding to antibodies. Immunoassays a.Tests that use specific antibodies to identify specific antigens b.Binding causes agglutination, which can be seen. c.Used to determine blood type and detect pregnancy d.ELISA: for detection of HIV, ab titers doc

Caloric Expenditures

1.Three components: a.Basal metabolic rate (BMR): energy used at rest, at about 28°C, 12 hrs after eating; 60% caloric expenditure b.Adaptive thermogenesis: energy expended to adapt to changes in ambient temperature and digestion/absorption of food; ~10% c.Physical activity: highly variable depending on activity levels 2.Adaptive Thermogenesis a.Cold promotes cutaneous vasoconstriction and shivering. Shivering requires a lot of energy. •Nonshivering thermogenesis: Brown adipose tissue has mitochondria that produce heat instead of ATP. •Thermic effect of food: Feeding increases metabolism 25 to 40%. b.Regulated by the brain via: •Sympathoadrenal stimulation of skeletal muscles and brown fat •TRH à TSH à thyroxine: falls in starvation in response to decreased leptin

Introduction: Tumor Immunology

1.Tumor biology is interrelated with functions of the immune system 2.Tumors are abnormal cells that dedifferentiate to an embryonic state. 3.Benign tumors are slow growing and limited to specific areas of the body. 4. Malignant tumors are fast growing and spread to other parts of the body. 5. Cancers arise when immune cells fail to stop the growth/spread of tumors. 6. Tumor Antigens a.Tumor antigens are due to dedifferentiated embryonic ag not recognized by the immune system; some ag provide the basis for diagnostic blood tests; some arise due to mutations from carcinogens; others are antigens from the virus that caused the tumor (human papillomavirus). b.Normally, over-expressed antigens may trigger an immune response. 7. Lymphocytes and Tumor Cells a.Lymphocytes provide immunological surveillance against cancer. b.Tumor cells can evade immune surveillance by suppressing immunity with secretions: •FAS ligand stimulates lymphocyte apoptosis.

Villi and Microvilli

1.Villi a.Columnar epithelium with goblet cells (mucus) b.Capillaries absorb monosaccharides and amino acids, and lacteals absorb fats. c.Intestinal crypts (Crypts of Lieberkuhn) with Paneth cells (secrete antibacterial molecules of lysozyme and defensin) and mitotic stem cells (divide by mitosis to replenish intestinal cells every 4 to 5 days) 2.Microvilli (brush border) - foldings of the apical surface of each epithelial cell doc Lysozyme and defensin protect small intestine from pathogens Most are bacteria are beneficial?

Regulation of Pancreatic Juice and Bile Secretion

1.When chyme enters the duodenum, two hormones are produced: a.Secretin is produced in response to a drop in pH. (Stops with a rise in pH.) b.Cholecystokinin (CCK) is produced in response to the presence of partially digested proteins and fats in chyme. (Production stops when food leaves small intestine.) 2.Secretion of Pancreatic Juice a.Pancreatic production of trypsin, lipase, and amylase is stimulated by ACh from vagus nerve, CCK, and secretin. oACh and CCK use Ca2+ as a 2nd messenger. oSecretin uses cAMP as a second messenger. b.Bicarbonate production is stimulated by secretin. 3. Secretion of Bile a.The liver produces bile constantly, but the arrival of chyme into the duodenum stimulates increased production of bile. b.Happens when: oSecretin and CCK stimulate increased bicarbonate secretion into bile. oCCK (in response to the presence of fat in chyme) stimulates gallbladder contraction.

Liver: Hepatic Portal System

2.Hepatic Portal System a.Products of digestion absorbed in intestines are delivered to the liver via the hepatic portal vein. b.Veins from the pancreas, gallbladder, stomach, omentum, and spleen also join with the hepatic portal vein. c.After circulating through liver capillaries, the blood leaves via the hepatic vein to join regular venous circulation d.Portal system - a unique pattern of capillaries -> veins -> capillaries -> veins e.Total hepatic blood flow is about 25% of cardiac output; needed to maintain hepatic clearance ( the ability of the liver to remove substances from the blood). Portal system is a series

Innate Immunity

4. Activation of Innate Immunity a.Immune System needs to distinguish "self" from "nonself" using (PAMPs) unique to pathogens. •Immune cells have pathogen recognition receptors for PAMPs on their surface. •These cells respond by secreting chemokines to recruit more immune cells or activate specific immune cells. b.Complement System •Integrates innate and adaptive immune responses •Made of proteins in the plasma that are activated when antibodies bind to antigens •Complement proteins promote phagocytosis, lysis of target cells, and inflammation. c.Local inflammation •Tissue damage that causes necrosis 5.Fever a.Regulated by hypothalamus b.Chemicals called endogenous pyrogens sets the body temperature higher. •Produced as cytokines by leukocytes •Endotoxins from some bacteria stimulate leukocytes to produce these cytokines. •Along with fever, they also induce sleepiness and a fall in plasma iron concentration (which limits bacterial activity).

Interferons

6. Interferons a. Antiviral polypeptides produced by infected cells b. Three types identified •Alpha and beta - inhibit viral replication and assembly •Gamma - helps fight infections and cancer New antiviral drugs are being developed using interferons Effects of Interferons Interferons Stimulate Macrophage phagocytosis Activity of cytotoxic ("killer") T cells Activity of natural killer cells Production of antibodies Interferons Inhibit Cell division Tumor growth Maturation of adipose cells Maturation of erythrocytes

Choose an effective medication and mechanism of action that would reduce the signs and symptoms of seasonal allergies.

A medication that blocks the production of IgE.

Which of the following demonstrates a situation when the metabolic rate in A is greater than in B?

A single person in two different thermic states; A = exercise induced hyperthermia, B = surgically induced hypothermia

qUiZ

An enzyme that will digest proteins into amino acids is carboxypeptidase Amylases, the enzymes used to digest carbohydrates, are secreted by salivary glands and the pancreas Most products of fat digestion are absorbed by lymphatic lacteals Bile salts aid in the digestion of fats by emulsifying large fat droplets Micelles are tiny droplets of fatty acids, cholesterol, phospholipids, mono- and diglycerides, and bile salts.

Liver Functions: Bile Salts

Bile Salts Form micelles with polar groups toward water and nonpolar groups inward toward the fat oFats enter the micelle and are emulsified. oProvides a greater surface area for fat digestion by lipase doc Two to four polar groups Cholic acid Acid conjugated with amino acids to form bile salts Intestinal lumen: bile salts are combined together to form aggregates known as micelles. The non polar parts are located in the central region of the micelle away from water. The polar groups face water around the periphery of the micelle. Lecithin, cholesterol and other lipids of the small intestine entities Bile salt part polar, part nonpolar, all them to emulsify in chyme Emulsification: converted of larger fat globules by bile acids into a finer suspension of small fat globules. Which provide greater surface area for the fat to ingested by the ..enzyme The liver reductions of bile slats? from cholesterol is the major pathway of cholesterol breakdown. This amounts over half a gram of cholesterol converted into bile acids every day. No more than this is required because approx 95% of the bile acids released in the duodenum are absorbed in illume by means about specific carriers and hepatic circulation.

Phagocytosis of pathogens would be enhanced if

Both the number of monocytes and neutrophils in the blood increased

Morris has had a severe bout of diarrhea and is now dehydrated. Is his blood more likely to be in acidosis or alkalosis? Explain your reasoning.

Both the small intestine as well as pancreas produce bicarbonate. Bicarbonate in the small intestine helps neutralize the acidic chyme entering from the stomach into the small intestine. Whatever is not digested and absorbed in the small intestine moves on to the large intestine. The undigested matter in the large intestine has bicarbonate in it. When there is diarrhea there is reduced absorption of water from the large intestine and there is watery stool. This results in the loss of water as well as bicarbonate from the body leading to dehydration and acidosis. Acidosis is the result of the loss of bicarbonate from the body that then causes an imbalance between H+ and HCO3- levels. His blood is more likely to be in acidosis because of the loss of sodium bicarbonate from the body due to the diarrhea. Since bicarbonate is lost, this eventually leaves to acidosis of the blood because bicarbonate is a base. The body is losing base. Since diarrhea causes more feces to be eliminated, that causes the loss alkali and makes the blood acidic.

Regulation of Gastric Function: Phase of Regulation

Cephalic Phase 1.Sight, smell, and taste of food cause stimulation of vagus nuclei in brain 2.Vagus stimulates chief cells to secrete pepsinogen 3.Vagus stimulates gastric acid secretion mainly by stimulating ECL cells to secrete histamine, whichstimulates parietal cells to secrete HCl Gastric Phase 1.Distension of stomach stimulates vagus nerve; vagus stimulates acid secretion 2.Amino acids and peptides in stomach lumen stimulate acid secretion a.Direct stimulation of parietal cells (lesser effect) b.Stimulation of gastrin secretion; gastrin stimulates acid secretion (major effect) 3.Gastrin secretion inhibited when pH of gastric juice falls below 2.5 Intestinal Phase 1.Neural inhibition of gastric emptying and acid secretion a.Arrival of chyme in duodenum causes distension, increase in osmotic pressure b.These stimuli activate a neural reflex that inhibits gastric activity 2.In response to fat in the chyme, the duodenum secretes an enterogastrone hormone that inhibits gastric motility and secretion

The GI Hormones: Intestine

Cholecystokinin (CCK) Stimulus for Release: Fatty acids and some amino acids Primary Target(s): Gallbladder, pancreas, stomach Primary Effect(s): Stimulates gallbladder contraction and pancreatic enzyme secretion Inhibits gastric emptying and acid secretion Other Information: Promotes satiety Some effects may be due to C C K as a neurotransmitter Secretin Stimulus for Release: Acid in small intestine Primary Target(s): Pancreas, stomach Primary Effect(s): Stimulates HCO3- secretion Inhibits gastric emptying and acid secretion Gastric inhibitory peptide (G I P) Stimulus for Release: Glucose, fatty acids, and amino acids in small intestine Primary Target(s): Beta cells of pancreas Primary Effect(s): Stimulates insulin release (feedforward mechanism) Inhibits gastric emptying and acid secretion Glucagonlike peptide-1 (G L P-1) Stimulus for Release: Mixed meal that includes carbohydrates or fats in the lumen Primary Target(s): Endocrine pancreas Primary Effect(s): Stimulates insulin release Inhibits glucagon release and gastric function Other Information:Promotes satiety

Characteristics of the Lipid Carrier Proteins (Lipoproteins) Found in Plasma

Chylomicrons: Origin: intestine Destination: many organs Major Lipids: triglycerides, other lipids Functions: deliver lipids of dietary origin to body cells Very-low-density lipoproteins (VLDLs) Origin: liver Destination: many organs Major Lipids: triglycerides, cholesterol Functions: Deliver endogenously produced triglycerides to body cells Low-density-lipoproteins (LDLs) Origin: Intravascular removal of triglycerides from VLDLs Destination: blood vessels, liver Major Lipids: cholesterol Functions: Deliver endogenously produced cholesterol to various organs High-density lipoproteins (HDLs) Origin: liver and intestine Destination: liver and steroid-hormone-producing glands Major Lipids: cholesterol Functions: remove and degrade cholesterol

Describe three body systems that Lymphatic systems interacts with, and briefly explain how the interaction works.

Circulatory and Immune systems: The exchange happening at the capillaries is unequal in terms of the volume of material filtered from the capillaries and the volume of material reabsorbed from the interstitial fluid. There is extra fluid from the circulatory system entering the interstitial fluid and this extra fluid circulates through the lymphatic system as lymph, is exposed to any foreign material that may have found its way into the body in the various lymph nodes and other lymph organs. The lymphocytes present in the lymph nodes and lymph glands can they initiate an immune response against any foregn material that they detect in the lymph. Digestive system: The lipids that are digested in the small intestine, are reformed and along with proteins, form chylomicrons that are too large to be absorbed by the capillaries in the villi and are instead absorned by the lacteals in the villi. The lacteals are pat of the lymphatic system and the chylomirons from the small intestine eventually find their way into the circulatory system when the lymph joins the circulation. The lymphatic system interacts with the cardiovascular system when it drops chylomicrons into the blood just before it enters the right atrium and helps return body fluids to the blood. The lymphatic system interacts with the immense system by making and releasing lymphocytes that regulate and destroy foreign particles. The lymphatic system interacts with the circulatory system to help deliver hormones, oxygen, and nutrients to the body.

Liver Functions

Detoxication of Blood: Phagocytosis by Kupffer cells Chemical alteration of biologically active molecules (hormones and drugs, including alcohol) Production of urea, uric acid, and other molecules that are less toxic than parent compounds Excretion of molecules in bile Carbohydrate Metabolism: Conversion of blood glucose to glycogen and fat Production of glucose from liver glycogen and from other molecules (amino acids, lactic acid) by gluconeogenesis Secretion of glucose into the blood Lipid Metabolism: Synthesis of triglycerides and cholesterol Excretion of cholesterol in bile Production of ketone bodies from fatty acids Protein Synthesis: Production of albumin Production of plasma transport proteins Production of clotting factors (fibrinogen, prothrombin, and others) Secretion of Bile: Synthesis of bile salts Conjugation and excretion of bile pigment (bilirubin)

Compounds Excreted by the Liver into Bile

Endogenous (Naturally occurring): Bile salts, urobilinogen, cholesterol -High percentage reabsorbed and has an enterohepatic circulation* Lecithin -Small percentage reabsorbed and has an enterohepatic circulation Bilirubin -no enterohepatic circulation Exogenous (Drugs): Ampicillin, streptomycin, tetracyline -High percentage reabsorbed and has an enterohepatic circulation Sulfonamides, penicillin -Small percentage reabsorbed and has an enterohepatic circulation

Feeding and Fasting

Feeding moves metabolism towards anabolism and towards catabolism on fasting What is the determining factor? doc

Complement Fixation & Membrane Attack Complex

Fig 15.10 Formation of an ab-ag complex on the bacterial membrane results in splitting of C4. Leads to activation of other complement proteins, some of which attach to the membrane. doc Fig 15.11: The membrane attack complex. Activated proteins C5 through C9 assemble in the plasma membrane of a bacterial cell as a membrane attack complex. This forms a large pore that punctures the membrane and causes lysis of the cell. doc

Comparative Anatomy of Duodenum, Jejunum, and Ileum

Folds: Plicae and Villi Duodenal glands: Brunner's glands; secrete alkaline mucus Peyer's Patches: Aggregated lymphoid nodules doc Lymphoid nodules help function in immune

The GI Hormones: Stomach

Gastin (G cells) Stimulus for Release: Peptides and amino acids; neural reflexes Primary Target(s): E C L cells and parietal cells Primary Effect(s): Stimulates gastric acid secretion and mucosal growth Other Information: Somatostatin inhibits release

Stomach Has Gastric Pits

Gastric pits at base of folds lead to gastric glands that have several types of secretory cells: 1)Mucus neck cells secrete mucus to help protect stomach lining from acid. 2)Parietal cells secrete HCl & intrinsic factor (helps small intestine absorb vitamin B12). 3)Chief (zygomatic) cells secrete pepsinogen, the inactive form of a protein digesting enzyme 4)Enterochromaffin-like (ECL) cells secrete histamine and serotonin (paracrine signals). 5)G cells secrete gastrin (hormone). 6)D cells secrete somatostatin (hormone). 7)Also secretes the hormone ghrelin that signals the brain to regulate hunger Pepsinogen digests proteins? Serotonin: neurotransmitter Histamine has many roles in the body doc

Eric wants to determine his blood type, so he takes a few drops of blood from his finger and mixes it with various antibodies. His blood cells agglutinate when mixed with the anti-A antibody but not with the anti-B antibody. Therefore, which is true?

His plasma contains anti-B antibodies.

Choose the physiologic process that should not be compromised by disease of the liver.

Hydrolysis of lactose into lactase and sucrase

Sarah is a type 1 diabetic who forgot to bring her insulin today. By the end of the day, Sarah is not feeling well. She stops at the campus health center on her way back to her dorm, where they run a few tests on her blood. Which of these test results is likely?

Hyperglycemia

Types of Antibodies (immunoglobulins)

IgG: Main form of antibodies in circulation: production increased after immunization; secreted during secondary response IgA: Main antibody type in external secretions, such as saliva and mother's milk IgE: Responsible for allergic symptoms in immediate hypersensitivity reactions IgM: Function as antigen receptors on lymphocyte surface prior to immunization; secreted during primary response IgD: Function as antigen receptors on lymphocyte surface prior to immunization; other functions unknown

Comparison of Active and Passive Immunity characteristic-active immunity-passive immunity

Injection of person with-Antigens-Antibodies Source of antibodies-The person inoculated-Natural—the mother; artificial—injection with antibodies Method-Injection with killed or attenuated pathogens or their toxins-Natural—transfer of antibodies across the placenta; artificial—injection with antibodies Time to develop resistance-5 to 14 days- Immediately after injection Duration of resistance-Long (perhaps years)-Immediately after injection When used-Before exposure to pathogen-Before or after exposure to pathogen

Summary of Events in Local Inflammation

Innate (Nonspecific) Immunity: -Bacteria enter a break in the skin. -Resident phagocytic cells—neutrophils and macrophages—engulf the bacteria. -Nonspecific activation of complement proteins occurs. Adaptive (Specific) Immunity: -B cells are stimulated to produce specific antibodies. -Phagocytosis is enhanced by antibodies attached to bacterial surface antigens (opsonization). -Specific activation of complement proteins occurs, which stimulates phagocytosis, chemotaxis of new phagocytes to the infected area, and secretion of histamine from tissue mast cells. -Extravasation (diapedesis) allows new phagocytic leukocytes (neutrophils and monocytes) to invade the infected area. -Vasodilation and increased capillary permeability (as a result of histamine secretion) produce redness and edema.

endocrine regulation of metabolism hormone, blood glucose, carb metabolism, protein metabolism, lipid metabolism

Insulin: Decreased bg ↑ Glycogen formation ↓ Glycogenolysis ↓ Gluconeogenesis ↑ Protein synthesis ↑ Lipogenesis, ↓ Lipolysis ↓ Ketogenesis Glucagon: increased bg ↓ Glycogen formation ↑ Glycogenolysis ↑ Gluconeogenesis No direct effect ↑ Lipolysis ↑ Ketogenesis Growth hormone: increased bg ↑ Glycogenolysis ↑ Gluconeogenesis ↓ Glucose utilization ↑ Protein synthesis ↓ Lipogenesis ↑ Lipolysis ↑ Ketogenesis glucocorticoids (hydrocortisone) increased bg ↑ Glycogen formation ↑ Gluconeogenesis ↓ Protein synthesis ↓ Lipogenesis ↑ Lipolysis ↑ Ketogenesis epinephrine: increased bg ↓ Glycogen formation ↑ Glycogenolysis ↑ Gluconeogenesis No direct effect ↑ Lipolysis ↑ Ketogenesis thyroid hormones no effect on bg ↑ Glucose utilization ↑ Protein synthesis No direct effect

Some Cytokines that Regulate the Immune System

Interleukin-1 (IL-1): Induces proliferation and activation of T lymphocytes Interleukin-2 (IL-2): Induces proliferation of activated T lymphocytes Interleukin-3 (IL-3): Stimulates proliferation of bone marrow stem cells and mast cells Interleukin-4 (IL-4): Stimulates proliferation of activated B cells; promotes production of IgE antibodies; increases activity of cytotoxic T cells Interleukin-5 (IL-5): Induces activation of cytotoxic T cells; promotes eosinophil differentiation and serves as chemokine for eosinophils Interleukin-6 (IL-6): Stimulates proliferation and activation of T and B lymphocytes Granulocyte/monocytemacrophage colonystimulating factor (GM-CSF): Stimulates proliferation and differentiation of neutrophils, eosinophils, monocytes, and macrophages

quiz

Intrinsic factor is secreted by the parietal cells and is required for the absorption of vitamin B12 Enterochromaffin-like (E C L) cells secrete histamine Bicarbonate secretion occurs mainly in the small intestine Which cells secrete somatostatin? D cells Chief cells of the stomach secrete none of the above Which is NOT an accessory gland to the digestive system? Enteric nervous system Food moves through the digestive tract by peristaltic contractions of smooth muscle Lipids converted to chylomicrons are transported into the lacteals (lymph vessels) in the villi because they are too large to be absorbed by the capillaries in the villi.

Which accurately describes the metabolic actions of cortisol during fasting?

It is permissive of gluconeogenesis and lipolysis, and reduces sensitivity of muscle and adipose tissue to insulin.

Phagocytosis

Phagocyte-location Neutrophils-blood and all tissues Monocytes-blood Tissue macrophages (histiocytes)-all tissues (including splee, lymph nodes, bone marrow) kupffer cells-liver alveolar macrophages-lungs microglia-central nervous system Phagocytosis in Tissues •extravasation or diapedesis: Neutrophils and monocytes squeeze through gaps in venule walls to enter tissue. •Attracted to site by a process called chemotaxis by cytokines called chemokines •The pathogen becomes engulfed by pseudopods; the vacuole containing the pathogen fuses with a lysosome; the pathogen is digested. doc

Structures and Defense Mechanisms of Nonspecific (Innate) Immunity: internal

Phagocytic cells: Ingest and destroy bacteria, cellular debris, denatured proteins, and toxins interferons: Inhibit replication of viruses complement proteins: Promote destruction of bacteria; enhance inflammatory response endogenous pyrogen: Secreted by leukocytes and other cells; produces fever natural killer (NK) cells: Destroy cells infected with viruses, tumor cells, and mismatched transplanted tissue cells mast cells: Release histamine and other mediators of inflammation, and cytokines that promote adaptive immunity

digestive tract

Physiologist view doc

Endocrine Regulation of Calcium and Phosphate

Plasma concentrations are controlled by three factors: a.Bone formation and resorption b.Intestinal absorption c.Urinary excretion 2.These processes are regulated by calcitonin, parathyroid hormone, estrogen, and vitamin D3.

Role of Calcium

Role of Calcium in the Body a. Blood clotting b. Cell signaling c. Second messenger d. Neurotransmitter release e. Muscle contraction 1)Hypocalcemia results in increased permeability to Na+ and other ions. 2)This results in increased muscle excitability, muscle spasms, and cardiac abnormalities. 3)Hypocalcemia can result from loss of parathyroid function or from calcium, vitamin D, or Mg+2 deficiencies.

Characteristics of the Major Digestive Enzymes Enzyme: Site of Action, Source, Substrate, Optimum pH, Product(s)

Salivary amylase: Mouth, Saliva, Starch, 6.7, Maltose Pepsin: Stomach, Gastric glands, Protein, 1.6 to 2.4, Shorter polypeptides Pancreatic amylase: Duodenum, Pancreatic juice, Starch, 6.7 to 7.0, Maltose; maltriose; and oligosaccharides Trypsin, chymotrypsin, carboxypeptidase: Small intestine, Pancreatic juice, Polypeptides, 8.0, Amino acids; dipeptides; and tripeptides Pancreatic lipase: Small intestine, Pancreatic juice, Triglycerides, 8.0, Fatty acids and monoglycerides Maltase: Small intestine, Brush border of epithelial cell, Maltose, 5.0 to 7.0, Glucose Sucrase: Small intestine, Brush border of epithelial cells, Sucrose, 5.0 to 7.0, Glucose + fructose Lactase: Small intestine, Brush border of epithelial cells, Lactose, 5.8 to 6.2, Glucose + galactose Aminopeptidase: Small intestine, Brush border of epithelial cells, Polypeptides, 8.0, Amino acids, dipeptides, tripeptides

Liver Functions (4)

Secretion of Glucose, Triglycerides, and Ketone Bodies a.The liver helps balance blood glucose levels by removing glucose and storing it as glycogen (glycogenesis) and triglycerides (lipogenesis) or by breaking down glycogen (glycogenolysis) and releasing it into the blood. b.The liver can also make glucose from amino acids (gluconeogenesis) and convert fatty acids into ketones (ketogenesis). Production of Plasma Proteins a.Plasma albumin and most plasma globulins, clotting factors and angiotensinogen are produced by the liver. b.Albumin provides colloid osmotic pressure and transport c.Globulins provide transport and blood clotting d.Clotting factors I, II, II, V, VII, IX, X Most plasma globulins Exception of immunoglobins or antibodies Albumin makes 70% of total plasma protein and contributes to osmotic pressure of the blood The globulin transport cholesterol and triglycerides, transfer of steroids and thyroid hormones, inhibit of trypsin activity and blood clotting 1,2,3,5,7,9 and angiotensin are all produced by liver

Comparison of T and B Lymphocytes

Site where processed B Lymphocytes: Bone marrow T Lymphocytes: Thymus type of immunity B Lymphocytes: humoral (secretes antibodies) T lymphocytes: Cell-mediated subpopulations B Lymphocytes: memory B cells and plasma cells T lymphocytes: cytotoxic T cells, helper T cells, regulatory T cells presence of surface antibodies B Lymphocytes: Yes-IgM or IgD T lymphocytes: not detectable receptors for antigens B lymphocytes: present-are surface antibodies T lymphocytes: present-are related to immunoglobulins life span B lymphocytes: short T lymphocytes: long tissue distribution B lymphocytes: high in spleen, low in blood T lymphocytes: high in blood and lymph percentage of blood lymphocytes B lymphocytes: 10% to 15% T lymphocytes: 75% to 80% transformed by antigens into B lymphocytes: plasma cells T lymphocytes: activated lymphocytes secretory product B lymphocytes: antibodies T lymphocytes: lymphokines immunity to viral infections B lymphocytes: Enteroviruses, poliomyelitis T lymphocytes: most others immunity to bacterial infections B lymphocytes: streptococcus, staphylococcus, many others T lymphocytes: tuberculosis, leprosy immunity to fungal infections B lymphocytes: none known T lymphocytes: many immunity to parasitic infections B lymphocytes: trypanosomiasis, maybe to malaria T lymphocytes: most others

Diabetic patients who have surgery, become sick, or are under other physiological stress are told to monitor their blood sugar carefully because they may need to increase their insulin dose temporarily. What is the physiological basis for this advice?

Stress causes release of hormones like cortisol, epinephrine, and growth hormone. They all increase circulating plasma glucose levels. When this happens in healthy people the glucose homeostasis pathway is able to maintain normal glucose levels. Cortisol stimulates the action of glucagon, and promotes lipolysis, and ketogenesis, as well as gluconeogenesis. Cortisol also inhibits secretion of insulin. When this happens in diabetics, there is further increase in glucose levels and this may require careful monitoring and appropriate adjustments in insulin doses. Diabetes is caused by the lack of insulin secretion or action of insulin. Insulin helps break down glucose and it can become dangerous if glucose builds up in the body which can lead to hyperglycemia. When diabetic patients are stressed, they need more insulin than usual to help break down the glucose. This is because when the body is stressed it creates more glucose or energy to prepare itself for the stressfull event.

Flow of Blood and Bile in a Liver Lobule

Substances secreted in the bile may be absorbed by the intestinal epithelium an recycled to the liver via the hepatic portal vein. doc The flow of blood and bile in a portal lobule: Blood flows from a portal vein to the central vein. Bile flows within hepatic plates from the center to the periphery. doc Bile is produced by hepatocytes and secreted into thin channels called bile canaliculus. Each hepatic plat this bile canaliculus are drained at periphery at porto olobul by bile ductulus which in turn drain into hepatic duct that carry bile away from liver. Blood travels on sinusoids and bile travels in the opposite direction. Bile can hepatic plates. Blood and bile don't mix in portal. In addition to the normal costumes of bile, a wide variety of exogenous compounds including drugs are secreted into the liver into bile ductures. The liver can clear blood of particular compounds by removing them from the blood and excreting them into the intestine with the bile. Molecules are cleared from the blood by secretion. In the bible are eliminated in the feces analogous to renal clearance of blood to excretion in urine. Many compounds released with bile into the intestine, and are not eliminated with feces. Some of these are absorbed are absorbed in the small intestine and enter hepatic portal and then blood. They go carried back to liver where then can secreted by parasites into the bile. Antidote hepatic circulation For example, a few grams of bile salts released in the intestine recirculate six to 10 times a day with only one point five grams of salt per day excreted in the feces

Which of the following statements regarding the loop of Henle is true?

The descending limb of the loop of Henle is impermeable to solutes

What you see is a figure of a beta cell of the pancreas that is secreting insulin in response to a rise in glucose levels. Describe what happens when glucose levels increase that result in the secretion of insulin. Then, explain with all needed detail what would happen if the glucose levels were not increased but extracellular potassium levels were to increase.

The increase in extracellular glucose levels results in the transport of glucose into the beta cells through the GLUT 2 transporters. This results in increased ATP production in the cell following the entry of glucose into glycolysis, TCA Cycle and ETC. The increase in ATP then causes the closing of the ATP-gated K+ channel, resulting in depolarization of the cell. When the ATP-gated K+ channels close, there is less efflux of K+ ions from the beta cells, leading to more positive membrane potential on the inside of the beta cell. This depolarization results in the opening of the voltage-gated Ca+2 channels, which allow the influx of Ca+2, which triggers the fusion of vesicles with the plasma membrane. This results in exocytosis of insulin stored in the vesicles. The insulin moves into the extracellular fluid and then into the blood vessels. When there is no increase in plasma glucose levels, but an increase in extracellular K+ levels, this will result in depolarization of the beta cells. The normal gradient is for K+ to leave the cells. But if extracellular K+ is elevated, then less K+ will leave the cells making the interior of the cell more positive ⇒ depolarization. This will lead to exocytosis of vesicles filled with insulin ⇒ insulin secretion. This is a strategy to increase insulin secretion as a treatment option for type 2 diabetics

Liver Function: Detoxification of Blood

The liver can remove hormones, drugs, and other substances in three ways: 1)Excreted into bile 2)Phagocytized by Kupffer cells lining sinusoids 3)Chemically altered by hepatocytes oAmmonia is converted into urea, porphyrins into bilirubin, and purines into uric acid oUrea is returned to the blood to be filtered by the kidneys. oSteroids and xenobiotics are altered and then secreted into bile. Liver has ability to recognize what is known as pathogen associated molecular patents which enable them to scavenge blood born bacteria. Anything in the body or in the circulation that doesn't belong- foreign, infectious, pathogen. Molecular patters on surfaces of bacteria can be taken and recognized by the parasites. In addition, the liver can also remove hormones, drugs, and bio active molecules from the blood by excreting these compounds in the bile. Ammonia is toxic molecule produced as a result deamination of amino acids in the liver and by the actual bacteria in the intestine. The ammonia conc in portal vein blood is 4 to 50 times greater than blood. Ammonia is removed by liver. The liver can convert the ammonia into the less toxic urea molecules which are secreted by the liver into the blood and excreted by the kidneys in the urine. Steroid hormones and other drugs are inactivated in their passage through the liver by modifications of their chemical structure The liver has enzymes that convert these nonpolar molecules are more polar molecule by hydroxidation by highly polar groups such as sulfate and lurchonic acid. Derivatives of steroid hormones and drugs are less bio active and because of their increased water solubility are more easily excreted by the kidneys in the urine

Which of the following statements regarding phagocytosis is TRUE?

The microbe engulfed by the phagocyte is killed by lysosomal enzymes.

How does the immune system recognize a foreign cell?

The presence of pathogen-associated molecular patterns

Comparison of Immediate and Delayed Hypersensitivity Reactions characteristic-immediate reaction-delayed reaction

Time for onset of symptoms-Within several minutes-Within 1 to 3 days Lymphocytes involved-B cells-T cells Immune effector- IgE antibodies- Cell-mediated immunity Allergies most commonly produced- Hay fever, asthma, and most other allergic conditions- Contact dermatitis (such as to poison ivy and poison oak) Therapy-Antihistamines and adrenergic drugs-Corticosteroids (such as cortisone)

Enzymes Contained in Pancreatic Juice Enzyme, Zymogen, Activator, Action

Trypsin: Trypsinogen, Enterokinase, Cleaves internal peptide bonds Chymotrypsin: Chymotrypsinogen, Trypsin, Cleaves internal peptide bonds Elastase: Proelastase, Trypsin, Cleaves internal peptide bonds Carboxypeptidase: Procarboxypeptidase, Trypsin, Cleaves last amino acid from carboxyl-terminal end of polypeptide Phospholipase: Prophospholipase, Trypsin, Cleaves fatty acids from phospholipids such as lecithin Lipase: None, None, Cleaves fatty acids from glycerol Amylase: None, None, Digests starch to maltose and short chains of glucose molecules Cholesterolesterase: None, None, Releases cholesterol from its bonds with other molecules Ribonuclease: None, None, Cleaves RNA to form short chains Deoxyribonuclease: None, None, Cleaves DNA to form short chains

An older technique to treat ulcers that is not used any longer is abdominal vagotomy, which is the surgical cutting of the vagus nerve to the stomach. By what mechanism might this procedure help to heal ulcers and reduce the incidence of new ulcers?

Ulcers are erosions of the mucosa of the stomach or deuodenum produced by HCl. The vagus nerve helps produce acid for digestion. If the vagus nerve was cut, that would mean a decrease in acid, which would likely decrease the ulcers (since ulcers are caused by the erosion of acid.) Stimulation of HCl Secretion a.Gastrin: made in G cells; carried to parietal cells in blood; Also stimulates ECL cells to make histamine b.Histamine: also stimulates parietal cells via H2 histamine receptors Examples: Tagamet and Zantac block H2 receptors. c.Parasympathetic neurons and ACh: stimulate parietal and ECL cells Vagus is a parasympathetic nerve and is part of the autonomic nervous system controlled upregulation of the digestive processes.

Regulation of Gastric Function What is(are) the enterogastric hormone(s)?

What is(are) the enterogastric hormone(s)? A signaling molecule produced by the duodenum that inhibits gastric function a)GIP—glucose-dependent insulinotropic peptide—stimulates insulin secretion and inhibits gastric function b)Somatostatin c)CCK—cholecystokinin—secreted by the duodenum in response to chyme d)GLP-1—glucagon-like peptide-1—secreted by the ileum- is an insulin stimulator

quiz digestive

Which enzyme helps digest proteins into peptides? Trypsin The first organ to receive the blood-borne products of digestion is the liver Which of the following statements about the liver are NOT true? Its cells cannot regenerate when damaged

quiiizz

Which is a G I hormone? Secretin Generally, increased parasympathetic signaling stimulates_ the G I tract, and increased sympathetic signaling __inhibits__ it. Which digestive hormone is also made by neurons and acts as a neurotransmitter in the brain? cholecystokinin (C C K) Which digestive hormone targets beta cells of the pancreas? Gastric inhibitory peptide (GIP) Which digestive hormone inhibits gastric emptying and acid secretion? cholecystokinin (C C K) secretin gastric inhibitory peptide (G I P) More than one of the above

quiz 2

Which is the correct order of structures that food passes through? pyloric valve → duodenum → jejunum → ileum Which layer of the G I tract Peyer's patches? Mucosa Which is the correct order for substances that are absorbed from the lumen of the digestive tract? apical side of epithelial cell → basolateral side of epithelial cell → interstitial fluid → blood Bicarbonate secretion occurs mainly in the small intestine

Stomach Defenses

a.Acid and pepsin could damage the stomach lining. b.Defenses that help prevent this: oAdherent layer of mucus with alkaline bicarbonate oTight junctions between epithelial cells oRapid epithelial mitosis that replaces epithelium every three days

Regulation of Contraction

a.Autonomic nerves influence enteric nervous system to stimulate or inhibit cells of Cajal. b.ACh from parasympathetic system interacts with mAChR to increase amplitude and duration of slow waves. doc

Small Intestine Functions

a.Complete digestion of carbohydrates, proteins, and fats b.Absorption of nutrients oSugars, lipids, amino acids, calcium, and iron absorbed in duodenum and jejunum oBile salts, vitamin B12, water, and electrolytes in ileum oVery rapid due to villi and microvilli doc

Absorption of Fats

a.Fatty acids, monoglycerides, and lysolecithin move into bile micelles and are transported to brush border. b.The fat molecules then leave the micelles and diffuse into the epithelial cells of the villi. c.Inside the epithelial cells, they are regenerated into triglycerides and together with cholesterol, and phospholipids are combined with proteins to form chylomicrons. d.Chylomicrons are secreted by exocytosis into the central lacteal of the villus doc

Liver

a.Largest abdominal organ; immediately beneath the diaphragm, on the right b.Has amazing regenerative abilities due to mitosis of hepatocytes c.Hepatocytes form hepatic plates separated by capillaries called sinusoids oFenestrated capillaries with no basement membrane oVery permeable, allowing of proteins, fat, and cholesterol d.Hepatic damage due to alcohol or viral hepatitis causes liver fibrosis that can lead to cirrhosis of the liver. Many lobes doc

Digestion and Absorption in the Stomach

a.Proteins begin digestion in the stomach. b.Starches begin digestion in the mouth, but salivary amylase is not active at pH 2, so this stops in the stomach. c.Alcohol and NSAIDs (aspirin) are the only common substances absorbed in the stomach (due to high lipid solubility).

Transport of Lipids in Blood

a.The lymphatic system drops chylomicrons into the blood just before it enters the right atrium. b.They pick up an apolipoprotein (ApoE), which allows them to bind to receptors on the capillary endothelium within muscles and adipose tissue. oHere they are digested by lipoprotein lipase, which releases FFA for use as fuel or for storage by fat cells. oThe remaining particles with cholesterol released and travel in the blood to the liver. c.Cholesterol and triglycerides made in the liver are combined with other apolipoproteins to form very-low-density lipoproteins (VLDLs) to deliver triglycerides to organs. d.Once triglycerides are removed, they are low- density lipoproteins (LDLs), which transport cholesterol to organs. e.Excess cholesterol is returned to the liver on high-density lipids (HDL). f.HDL binds to receptors in the blood vessel walls and capture phospholipids and free cholesterol, reducing cholesterol amounts. g.Once the HDL is full, it travels to the liver and unloads the cholesterol. Hdl good kind of cholesterol

In an experimental situation focused on the development of a new vaccine, mice were injected with a viral antigen. Their plasma was removed in order to detect the presence of antibodies. This is an example of

active immunity.

Type 1 vs. Type 2 Diabetes

age 1= under 20 years 2=over 40 years development of symptoms 1= rapid 2= slow percentage of diabetic pop 1= 5% 2= 95% development of ketoacidosis 1= common 2= rare association with obesity 1=rare 2=common beta cells of islets (at the onset of disease) 1= destroyed 2= not destroyed insulin secretion 1= decreased 2= normal or increased autoantibodies to islet cells 1= present 2= absent associated with partiular MHC antigens 1=yes 2= unclear treatment 1= insulin injections 2= diet and exercise; oral stimulators of insulin sensitivity

Specific immune responses are mediated by

antibodies.

Digestion refers to the

breakdown of food into particles small enough to cross epithelial cells.

osteoporosis

can be limited by estrogen-replacement therapy

Catabolism during fasting

doc

Consequences of Uncorrected T1DM

doc

Homeostasis of Body Weight

doc

Hormonal Interactions in Metabolic Regulation

doc

Impact of vaccines on infectious disease incidence

doc

Interaction Between Antigen-Presenting Cells and T Cells and B Cells

doc

Macrophages, Helper T Cells and Interactions with B Cells

doc

Tumor Immunology

doc

You go see a scary movie. By the end of the movie your heart is racing thanks to high levels of epinephrine in your bloodstream. You ate nothing during the movie, but your blood glucose level is likely

elevated due to the action of epinephrine on blood glucose regulation.

Short reflexes of the digestive system are integrated in the ________ nervous system.

enteric

Anorexia nervosa is excessive thinness usually caused by hyperthyroidism.

false

Blood from the digestive organs enters general circulation and eventually reaches the liver for processing.

false

Emily suffers from chronic "heartburn." Emily's helpful aunt suggests that the cause is that Emily's cat often sits on her stomach following a large meal and the "heartburn" is due to pressure of the stomach against the heart. Indeed, this is the typical cause of heartburn.

false

Leptin stimulates and ghrelin inhibits appetite and hunger.

false

Neural regulation of the digestive processes is carried out exclusively by the enteric nervous system.

false

The calorigenic effect of thyroid hormones refers to their effect in increasing the rate at which the body synthesizes protein and fat.

false

The hormone that stimulates secretion of bicarbonate by the pancreas is also the hormone principally responsible for stimulating contraction of the gallbladder.

false

The pH of the contents of the stomach lumen is considerably higher than that of interstitial fluid.

false

Levels of ________ could not be measured in a blood sample.

glycogen

Most absorbed nutrients first enter the blood of the ________ system.

hepatic portal

You are a pediatrician. You have a young patient who does not seem to be growing. You suspect that there might be stress in the home. You decide to perform a blood test for cortisol and expect to find

high plasma cortisol levels have led to overall state of catabolism.

Rugae, plicae, and villi are all structures that

increase surface area.

Following diagnosis with pancreatic cancer, Neil had a large portion of his pancreasremoved. Which of the following hormones will now be found in lower amounts?

insulin

Which condition is matched to its correct abnormal immune response?

lack of response; H I V

The ________ is a significant site of absorption of water and electrolytes, but NOT of nutrients.

large intestine

Which leukocytes are mainly responsible for specific immune responses?

lymphocytes

A cell's __________ is recognized as "self" and is not targeted by the immune response for destruction.

major histocompatibility complex (M H C) membrane proteins

Which are phagocytic?

monocytes neutrophils macrophages eosinophils

Which is the sequence of layers from the lumen to the outer wall of the digestive tract?

mucosa, submucosa, muscularis externa, serosa

Physical barriers are the first line of defense against invading pathogens. Which is a physical barrier?

mucous membranes lining the G I and respiratory tracts

Endocrine Regulation of Calcium and Phosphate hormone, effect on intestine, effect on kidneys, effect on bone, associated diseases

parathyroid hormone (PTH) -no direct effect -stimulates Ca2+ reabsorption; inhibits PO43- reabsorption -stimulates resorption -osteitis fibrosa cystica with hypercalcemia due to excess PTH 1,25 dihydroxvyvitamin D3 -stimulates absorption of Ca2+ and PO43- -stimulates reabsorption of Ca2+ and PO43- -stimulates resorption -osteromalacia (adults) and rickets (children) due to deficiency of 1,25- dihydroxyvitamin D3 Calcitonin -none -inhibits resorption of Ca2+ and PO43- -stimulates depostion -none

In a routine examination, some blood is taken and analyzed. The results show a high IgM level for the mumps antigen. This would indicate the

person is just coming down with mumps.

Match the type of immunity to its description.

present at birth innate Secreted lysozyme kills bacteria. innate Antibodies in breast milk protect a newborn baby from pathogens. Adaptive NK cells cause apoptosis of viral-infected cells. innate

Which of the following is NOT a function of the kidneys?

regulate body temperature

Secretion refers to the

release of substances into the lumen of the gut.

The immune system

removes dead or damaged cells protects against pathogens removes abnormal cells produced during cell replication

Kit had her gallbladder removed last month and has been experiencing some changes to herdigestion. One thing that she has noticed is that

she has trouble digesting high protein foods such as egg whites.

Structures and Defense Mechanisms of Nonspecific (Innate) Immunity: external

skin: Physical barrier to penetration by pathogens; secretions contain lysozyme (enzyme that destroys bacteria) digestive tract: High acidity of stomach; protection by normal bacterial population of colon respiratory tract: Secretion of mucus; movement of mucus by cilia; alveolar macrophages genitourinary tract: Acidity of urine; vaginal lactic acid

Digestion is almost completely finished in the

small intestine.

Which of the following statements concerning the micturition reflex is FALSE? A full bladder

stimulates parasympathetic nerve activity to stimulate contraction of the detrusor muscle inhibits sympathetic nerve activity to the internal urethral sphincter causing the internal sphincter to relax inhibits somatic motor neurons that innervate skeletal muscle in the external urethral sphincter causing the external sphincter to relax causes a sensation of fullness that initiates a conscious desire to urinate before the micturition reflex actually occurs

Absorbed lipids are initially transported by the lymphatic system.

true

Chronic long-term stress could lead to weakening of cardiac and skeletal muscle tissues.

true

Due to the route of fat absorption and transport in the body, fat-soluble toxins could have agreater effect on the body and brain than water-soluble toxins which are filtered first by the liver.

true

Excess use of antibiotics can kill the normal intestinal microflora and open a niche for pathogenic bacteria.

true

Fevers increase neutrophil activity and interferon production

true

Inhibiting the actions of helper T lymphocytes may impair humoral immunity.

true

The release of epinephrine during exercise contributes to an increase in nutrient levels in the blood.

true

Three enzymes important for protein digestion are trypsin, chymotrypsin, and pepsin.

true