Study guides for Exams 2, 3, and the Final
Study guides for Exams 2, 3, and the Final Bio 269
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This 56 page Study Guide was uploaded by Kelly Johnson on Friday January 15, 2016. The Study Guide belongs to Bio 269 at West Chester University of Pennsylvania taught by Giovanni Cassotti in Winter 2016. Since its upload, it has received 256 views. For similar materials see Anatomy and Physiology II in Biology at West Chester University of Pennsylvania.
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Anatomy and Physiology Exam 2 1. Cardiovascular II a. Know the pulmonary and systemic circuit and the names of the blood vessels that bring oxygenated and deoxygenated blood to and from each circuit. i. Arteries 1. Carry blood away from the heart 2. Normally oxygenated blood 3. Exception is the pulmonary artery a. Carries deoxygenated blood away from the heart to the lungs ii. Veins 1. Carry blood towards the heart 2. Normally deoxygenated blood 3. Exception is the pulmonary vein a. Carries oxygenated from the lungs to the heart b. Understand the architecture of heart, the names of the chambers, which chambers carry oxygenated and deoxygenated blood, and the names of the valves separating the chambers. i. Right atria ii. Left atria iii. Right ventricle iv. Left ventricle v. AV Valves 1. Tricuspid 2. Bicuspid vi. Semilunar Valves 1. Pulmonary (right) 2. Aortic (left) c. Know the layers of the heart wall. i. Pericardium ii. Epicedium 1. Covering the heart iii. Myocardium 1. Muscle of the heart iv. Endocardium 1. Innermost layer of the heart d. Understand what the coronary circuit and the types of coronary disease mean. i. Coronary Circuit 1. Blood that goes back to the muscles of the heart to oxygenate the muscle 2. Arteries arise from the aorta and venous blood empties into the right atrium 3. Blood vessels surrounding the heart ii. Coronary Diseases 1. Angina Pectoralis a. Temporary halt in blood delivery, vessels surrounding the heart, spasm of vessel 2. Myocardial Infraction (heart attack) a. Amitotic myocardium, non contractile scar tissue is formed due to stoppage of blood flow b. Prone to future heart attacks because fewer cells are doing more work e. Know the conductive pathway of the heart and the order in which action potentials move along the pathway and which chambers of the heart beat when. i. Muscle cells modified to conduct electrical information (myogenic pacemaker) ii. Autorhythmical cells are the conduction pathway of the heart (carry electro impulses) 1. SA node a. At the root of right atrium b. Start impulse 2. AV node a. Lies between Right atrium and right ventricle 3. Bundle of HIS (AV bundle) a. Receive impulse after Interatrial pathways 4. Bundle branch 5. Purkinje braches a. Impulse moves through gap junctions f. Understand the physiological mechanisms of how heart rate changes with respect to norepinephrine and acetylcholine. i. Excitation sequence 1. Spread of depolarization a. ECG 2. Heart rate fluctuations 3. Sympathetic a. Cardiac nerve (nodes and ventricles) b. Norepinephrine i. Up regulation c. Na+, Ca++ influx 4. Parasympathetic a. Vagus nerve (AV node) b. Acetylcholine i. Down regulate ii. K+ efflux g. Understand what pacemaker potentials are, and the ion movements that cause them. i. Membrane potentials 1. Repolarization causes efflux of K+ 2. Depolarization causes influx of Na+ and Ca++ a. An increase of heart rate is caused an increase of sodium 3. There is not resting membrane potential or hyperpolarization because the heart with stop a. Continuous ECG cycle h. Explain why action potentials in the ventricles look different that those of the atria and the physiological events that cause them. i. Atria 1. SA node fires 2. There is a small gap between depolarization (signal) and contraction ii. Ventricle 1. After AV node fires, the impulse has a longer pathway in which it has to travel before the ventricle contracts i. Explain what ions cause the refractory period in the heart and the importance of a long refractory period in cardiac muscle. i. The refectory period is cause by permeability of CA++, NA+, and K+ 1. Sodium is used to start the depolarization a. Voltage gates open 2. Calcium continues to influx with the high permeability keeping membrane positional positive 3. There is low permeability of potassium when membrane potential is positive ii. Long refractory period 1. 10x long that skeletal refractory period 2. You want a long refractory period because extra signals is not good or the heart beats will be irregular 3. Want a full contraction before next stimulus comes j. Be able to explain the sequence of events in a regular ECG. i. Electrocardiograph (ECG) 1. Spread of electrical conduction to the body 2. P, QRS, T waves 3. Depolarization a. Contraction and releasing of blood into next area 4. Repolarization a. Relaxation and filling with blood ii. P wave 1. The time it takes for atrial depolarization iii. QRS Complex 1. Ventricle depolarization 2. Atrial repolarization occurs at the same time iv. T wave 1. Ventricle repolarization k. Know what irregular ECG look like and what causes the events in each of them. i. Irregular Heart beats 1. Caused if SA node fire too early ii. The atria would not be fully filled and the force of contraction would be low 1. Autorhythmic cells will get beat back to normal 2. Heart waits until normal time allowing the atria to keep filling causing a harder force of contraction iii. Movies l. Explain the physiology that lead to different types of ectopic heartbeats i. AV node takes over the job and role of damaged SA node 1. Slower heart beat/rate 2. No P wave a. Atria does not depolarize causing ventricles to pump harder 3. Ventricles have a greater contractibility m. Know all of the events in the cardiac cycle. This means knowing each of the graphs shown in the lecture and just as importantly the timing of the events with respect to one another. i. Look at graphs and notes ii. Movies n. Understand what causes heart sounds and when the sounds occur with respect to different phases of the cardiac cycle. i. LUB 1. Turbulent blood flow ad a result of closure of AV Valves 2. Onset of Systole ii. DUB 1. Turbulent blood flow as a result of closure of aortic and pulmonary valve 2. Onset of diastole 3. Louder sound o. Know what heart murmurs are and what causes them. i. Irregular heart sounds (extra sounds other than lub/dub) 1. Common in children a. `Wall of atrium and ventricles are thin and you can hear blood sloshing around 2. Adults a. Irregular turbulent flow through valves i. Can be caused by a growth, and ventricles not filling completely b. Stenosis i. Narrow valve opening c. Regurgitation i. Leakage of blood though a valve ii. Movement back into atria iii. Needs surgery to fix 2. Cardiovascular III a. Know the correct sequence of blood vessels coming out of and go towards the heart. i. Arteries 1. Carry blood away from the heart 2. Normally oxygenated blood 3. Exception is the pulmonary artery a. Carries deoxygenated blood away from the heart to the lungs ii. Arterioles iii. Capillaries 1. Neither veins or arteries iv. Venules v. Veins 1. Carry blood towards the heart 2. Normally deoxygenated blood 3. Exception is the pulmonary vein a. Carries oxygenated from the lungs to the heart b. Know which blood vessels have high and which have low pressure. Also, know what is meant by systolic, diastolic pressure and be able to calculate pulse pressure. i. Pressure in vessels 1. Highest – Aorta 2. Lowest – Vena cava 3. Drop of blood pressure in arterioles because this is where vasodilation and vasoconstriction happen a. Control in pressure happens right before is goes into the tissues 4. Low pressure allows laminar flow in capillaries ii. Systemic Blood pressure 1. Systole a. High pressure in the atrial system (120 mmHg) b. Contraction of ventricles 2. Diastole a. Lowest pressure in the venous system (80 mmHg) b. Relaxing of ventricles 3. The difference between systolic and diastolic pressure is pulse pressure a. Decreases as you move away from the heart b. Systolic – diastolic = Pulse pressure 4. Mean arterial pressure a. MAP = diastolic pressure + (pulse pressure/3) b. c. Understand what is meant by cardiac output (C.O.) and what factors affect it. Be able to calculate C.O. i. Increasing preload pressure increasing heart rate and stroke volume ii. CO is the amount of blood that come out of the heart in one minute (volume) iii. SV is total amount of blood that come out of heart in one beat iv. CO = HR x SV d. Know Starlings Law of the heart. i. The greater the filling of the heart, the greater the amount pumped by the heart ii. Like an elastic band 1. The more you fill it, the more it contracts but only contracts as much as it needs e. Understand what factors affect blood pressure and the physiological mechanisms the body uses to regulate it. i. Blood pressure 1. Determines by cardiac output a. Exercise 2. Vascular resistance a. Total peripheral resistance b. Resistance to blood flow c. Vasoconstriction causes an increase in blood pressure 3. Blood Volume a. Closed circuit ii. Short Term Regulation 1. Neural control a. Happens in seconds b. Nervous system 2. Hormonal control a. Happens in minutes b. Endocrine system 3. Chemical Control a. Stimulus that declines Blood pressure i. Adrenal medulla ii. Releases norepinephrine iii. Increases heart rate b. Stimulus that increases blood pressure i. Atrial natriuretic peptide (ANP) ii. Decrease blood volume and pressure iii. ANP targets the kidneys to increase the amount of urine produced c. Vascular Resistance i. Altering blood flow by changing vessel diameter ii. Vasodilation and vasoconstriction 1. Allowing more blood to area is up regulation 2. The more blood that comes in the more that comes out a. Starlings Law b. Muscle pump iii. During exercise, some areas constrict while other dilate. 1. Heart, skeletal muscle, skin, etc. all increase the amount of blood flow 2. Kidney, abdomen, etc. all decrease blood flow to allow it to go other places a. Shunt 3. The brain does not vasconstrict and vasodilate iii. Long Term Regulation 1. Changes in blood volume a. Kidneys regulate the amount of fluid in blood 2. Renal Autoregulation a. Kidneys filter blood i. Filtrate (liquid) is left in the kidney but can be reabsorbed back into blood vessel 3. Angiotensin II (renin) a. Renin is a hormone that causes the production of Angiotensin II in the blood i. Angiotensin II is a potent vasoconstrictor causes blood pressure to increase b. Targets the pituitary gland i. ADH allows an increase in water reabsorption to increase blood volume and blood pressure will go up c. Targets the adrenal cortex i. Aldosterone allows an increased sodium reabsorption ii. Water follows salt iii. Increased blood volume and blood pressure will go up iv. Blood Pressure Regulation 1. Baroreceptors a. Nerve receptors that detect stretch i. Indirectly detects changed in blood pressure b. Most important receptors are in the aortic arch and carotid artery i. Detects change in blood pressure early 1. Possible stroke or heart attack c. Parasympathetic nervous system i. Decrease in heart rate to decrease blood pressure d. Sympathetic nervous system i. Decrease in heart rate and stroke volume allows for vasoconstriction 3. Lymphatics a. Hydrostatic and Osmotic pressures i. HP (Hydrostatic Pressure) a. 35 mmHg at highest point b. Arterial end of capillary 2. 17 mmHg at lowest point a. Venus end of capillary ii. OP (osmotic pressure) 1. Goes toward higher concentration in order to dilute iii. Net Filtration Pressure= Net HP Net OP 1. If HP is higher (arterial end) then fluid will go out of capillaries into interstitial fluid 2. If OP is higher (venus end) then fluid will go back into capillaries from interstitial fluid iv. 9/10 of fluid reenters, 1/10 comes back in through lymphatics 1. NO NET LOSS b. Anatomical components of the Lymphatic system i. Lymphatic Vessels 1. One way system toward the heart 2. Not in bones, teeth, and CNS (Brain and Spinal cord have cerebrospinal fluid) 3. Structure a. Contain minivalves where two cells meet i. Collagen fibers open the valves when pressure in interstitial fluid increases ii. Regulate fluid in lymphatic system b. Lacteals i. Run through villi ii. Face the lumen iii. Proteins and fats are absorbed/travel into body via lacteals c. Cancer travels via lymph and cannot be fought (metastasized) d. Lymph nodes i. Collections of tissue ii. House two types of cells 1. Macrophages 2. Lymphocytes spend most time in lymph nodes e. No pump i. Movement depends on muscle contraction and respiration pumps ii. Very slow circulation 4. Lymphatic cells and tissue a. House phagocytic cells (cells that engulf) and lymphocytes (T and B cells) used in defense i. Macrophages ingest antigens ii. Lymphocytes two types that aid in defense 1. T cells 2. B cells b. Tissue composed mostly of reticular connective tissue i. Looks like a spider web ii. Plays a role in immunity c. Lymphatic Organs i. Lymph Nodes 1. House lymph until it is needed to destroy antigens 2. Macrophages in nodes destroy microorganisms ii. Spleen 1. Filters blood 2. Constant Immune surveillance 3. Lymphocytes divide in spleen until they sense an antigen iii. Thymus 1. Home of tlymphocytes 2. Assist in making tcells immunocompetent iv. Tonsils 1. Bacteria enter blindending sacs (crypt) of tonsils through epithelium into lymphoid tissue to be destroyed a. Bacteria enter crypts b. Get caught c. Surrounding cells will destroy v. Peyer’s Patches 1. Part of the small intestine wall 2. Lymphoid tissue that destroys bacteria (in large numbers) that are trying to cross the wall of the small intestine and appendix 4. Immunology I a. Innate vs Adaptive i. Innate “ENLISTED” 1. Born with defenses 2. Interact with body systems through lymph and other body fluids 3. Surface Membranes a. Skin (stops bacteria from entering body) b. Mucosae (lines organs and acts as a protective layer) 4. Internal Defenses a. Phagocytes engulf other cells b. Fever line of defense c. Natural Killer Cells d. Antimicrobial proteins act to destroy microbes e. Inflammation needed for the process of healing ii. Adaptive “ARMY RANGER/ NAVY SEAL” 1. Acquired over time 2. Body must see antigen and create a defense system 3. Better trained/ more effective 4. Characteristics a. Specific recognition of pathogens (a disease causing microorganism, highly specific) b. Response is systematic c. Response has memory body remembers antigen d. Injected lymphocytes also offered protection (cell mediated) b. Skin and epithelial membranes acting as barriers i. Integument (SKIN) 1. Epidermis consists of five layers (more layers=more protection) 2. Keratin stops bacterial enzymes and toxins ii. Epithelium membranes 1. Acidic skin secretions a. Secretions from skin that are below a 7 pH b. Most bacteria cannot survive in such an acidic environment 2. Acid stomach secretions a. Can be as low as 2 pH 3. Saliva contains lysozymes a. Produces lysosomes that kill bacteria 4. Respiratory and digestive tract mucus a. Stops bacteria from reaching immune system c. Phagocytosis i. The use of macrophages (monocytes/neutrophils) to engulf and destroy ii. Steps 1. Engulf 2. Formation of vesicle phagosome (vacuole) formed to isolate antigen 3. Lysozome fusion lysozomes (digestive enzymes) fuse and release enzymes (creating a phagolysosome) 4. Digestion destroy the antigen 5. Exocytosis of broken down antigen iii. Antigen presenting cells(APCs) will destroy the antigen and then exocytose it to the other immune cells so that they can learn to destroy the same antigen d. Natural Killer (NK) Cells i. NonSpecific killers ii. Recognize the sugar groups present on the surface of target cells 1. If a cell in the body is not recognized, they will automatically kill it 2. Perforins are released cause pores to form on outside of antigen allowing fluid to enter, inflammation, and eventually lysis. e. Inflammation i. Signs 1. Redness, Heat, Swelling, Pain, Impairment of Function ii. Process 1. Receptors on cell surfaces release histamine 2. Histamine triggers vasodilation of capillaries (HEAT AND REDNESS) 3. Capillary permeability is also increased allowing fluid to enter (EDEMA) 4. Cell growth/Edema causes pain in the area iii. Purpose 1. Excess fluid helps to dilute harmful substances and bacteria that have already entered the area 2. Oxygen that is dissolved in plasma along with glucose that help provide energy and boost all activities 3. Proteins present (clotting proteins) in the area reduce blood lose iv. Phagocyte mobilization follows inflammation 1. When something breaks through the skin (nail in foot): a. Leukocytosis neutrophil count going to injured area increases 45 times b. Margination slowing down of blood cells as they adhere to blood vessel walls c. Diapedesis Squeeze through pores of blood vessel d. Chemotaxis follow chemical trail to injury site v. Final verdict 1. Inflammation is good in the short run, but over time it could over dilute f. Viruses i. About 1. Short life span 48 hours on average 2. Cannot replicate by self 3. Require the DNA or RNA of a host cell ii. Interferons 1. Body creates antimicrobial proteins (interferons) that fight the virus 2. Steps a. Virus enters host cell b. Uses DNA or RNA from host cell to replicate c. Inndcted cell then uses that DNA to create interferons d. 2 cell recognized interferons and begins to produce its own e. These antiviral proteins stop the virus from entering the cell, thus stopping replication g. Fever i. Iron and Zinc are needed to help the body 1. Gather in spleen and liver ii. Body temperature increases so that metabolic rate does also 1. Pyrogens (exogens) released and target hypothalamus 2. Hypothalamus releases prostaglandins that lead to muscle contraction 3. Muscle contraction (shivering) elevates temperature 5. Immunology II *Overview body must recognize antigen and prepare for it to take effect *Serum Plasma without clotting proteins **Antibodies are found in plasma a. Humeral immunity vs. cellular immunity i. Humeral 1. Protection from infection through body fluids 2. Antibodies made by B lymphocytes release into cell fluid ii. Cellular 1. Cells provide own defense a. T or B Lymphocytes b. Antigens i. What 1. Substances that are foreign to the body and provoke and immune response ii. How 1. Self vs. Nonselfrecognition a. Major Histocompatibility Complex (MHC) proteins on outside of cell are recognized i. MHC Class I on all Red Blood Cells ii. MHC Class II on all Antigen Presenting Cells b. If it recognizes a Class I or II, then it will leave the cell alone c. If neither Class I or II is identified, cell will be tagged for destruction c. Humeral Immunity and BCell cloning i. Humeral Immunity 1. Attached antigens (3) are made to recognize specific antigens and label them to be destroyed a. Antigenic determinants i. Surface appearance ii. Where antibodies attach 2. Steps a. Bcells make antibodies and clone themselves to deal with multiple antigens b. Plasma cells make and secrete antibodies c. Memory cells are formed, but do not differentiate i. Do not act on primary infection, but only if the same antigen reappears later d. 1,0002,000 antibodies/second 3. Responses a. 1 response can take 36 days i. 23 days for recognition and symptoms ii. 45 days for antibody creation iii. IgM b. 2 response can take 12 days (cells are more familiar to antigen, and can create a response much faster) i. IgG ii. BCell cloning 1. Blymphocytes can differentiate into plasma or memory cells a. Plasma create antibodies (Largest amount) b. Memory create antibodies in a second response, do not release 2. Vaccines a. Dead antigen is injected b. The body will defend by creating memory cells d. Immunoglobulins 1. Structure a. 4 polypeptides (amino acids) b. Y or T shaped simplest shape c. Two binding sites d. Light chain short chain on outside e. Heavy chain center chain that is longer f. C (constant) region i. Majority of antibody ii. Same in all immunoglobulins of the same type iii. Differ between separate types of Igs g. V (variable) region i. End of antibody (closest to binding site) ii. Unique for antigen binding h. Do not uncoil due to disulfide bonds that hold them together 2. Types a. Monomers i. D, G, F ii. 2 antigen sites b. Dimer i. A ii. 4 antigen sites c. Pentamer i. M ii. 10 binding sites iii. Made during first wave of infection; takes longer, but is efficient e. Antibodies i. Function 1. Inactivate antigens and tag them for destruction ii. Strategies 1. Neutralization a. Antigen is made ineffective after being surrounded by antibodies b. Later destroyed by phagocytosis 2. Agglutination a. Only in RBCs b. Antibodies attach and cause clumping c. Later destroyed by phagocytosis 3. Precipitation a. Product of the antigen is bound to antibody b. Later destroyed by phagocytosis 4. Complement (Fixation) a. Plasma proteins bind to antigen but only after antibody binds to the antigen as well b. Pores form in antigen allowing H2O to enter c. Cell swells and lyses d. Cause of inflammation e. Can also lead to phagocytosis f. Humeral immunity **Active long term protection, memory B cells **Passive short term protection, no memory B cells i. Naturally acquired part of nature 1. Active body is challenged when antigen is encountered (Memory B) a. Infection, contact with pathogen 2. Passive antigen is never encountered, but it is passed between people a. Mother to child through placenta or breast milk ii. Artificially acquired human intervention 1. Active – manually insert pathogen, dead or attenuated (cannot make you sick or reproduce), forcing antibody production for that strain only a. Vaccines 2. Passive injection of immune serum a. Gamma globulin b. Antivenom g. Immunocompetence i. The process in which lymphocytes learn what an antigen looks like so that it can attack (become confident at immunity) ii. Lymphocytes are created by the bone 1. T cells leave the bone and travel to the thymus 2. B cells remain in the bone marrow a. Act as APCs b. Make plasma and memory cells iii. Cycle between blood and lymph h. Antigen Presenting Cells (APC) i. Mechanisms of Operation 1. Engulf antigens 2. Present fragments of antigen to cytotoxictcells 3. CytotoxicTcells destroy ii. Examples 1. Dendritic cells in connective tissue 2. Langerhans’ cells in the skin 3. Macrophages in lymph i. Cytotoxic and Helper T Cells i. Helper T (CD4) 1. Do not kill, the recognize MHC class II proteins 2. Do not want to kill macrophage 3. Process a. Release Interleukin I b. Stimulating release of Interleukin II c. Release of Interleukin II i. Stimulates/up regulates production of Cytotoxic T cells and B cells (plasma/memory) ii. Cytotoxic (CD8) 1. Double recognition a. See the MHC class II as well as the antigen b. Kill the cell and the virus c. Clone themselves so that it can destroy other infected cells i. PIRIFORINS CAUSE LYSING j. Clinical connections i. Organ Transplants 1. Must have to avoid attack: a. Same blood type b. Similar types of CT cells and NK cells i. CANNOT BE IDENTICAL 2. Immunosuppressant Therapy a. A large number of different drugs that help suppress cytotoxic t cells (adaptiveimmunosuppressant) and prevent inflammation (innateantiinflammatory) ii. Immunodeficiency 1. Present if any immune cells, phagocytes, or complement behave abnormally 2. HIV/AIDS a. Viruses destroy helper t cells b. Stop cell mediated and humeral immunity iii. Autoimmune diseases 1. Lose the ability to distinguish between self and nonself 2. Body produces antibodies against itself a. Destroys healthy selftissue 3. Examples a. MS body produces antibodies against white matter (axons destroyed, action potential halted) b. Type 1 Diabetes i. Only 5% of all diabetics ii. Insulin producing cells (beta cells) destroyed 1. Inhibits glucose release iv. Allergies 1. Anaphylaxis a. Localized overreaction of histamine release causing fluid build up b. Antihistamine is used to reverse effects c. Innate and Adaptive i. Mast cells overproduce IgE 1. IgE oversensitive to antigens 2. Release histamine any time and antigen binds ii. Increase in B cells in mucus membranes 2. Anaphylactic Shock a. System wide b. Travels through blood stream c. Blood pressure decreases with vasodilation d. Bronchioles constrict e. Effect is reversed by epinephrine Final Exam: The Specifics a. Digestion I 1. Know the anatomy of the alimentary tract and the 6 functions of the tract. a. Alimentary tract (mouth to anus) b. Gastrointestinal (GI) tract (stomach to anus) c. Anatomy i. Mouth (oral cavity) 1. Salivary glands a. Parotid b. Sublingual c. Submandibular ii. Pharynx iii. Esophagus iv. Stomach v. Small intestine 1. Duodenum- first loop, smallest part 2. Jejunum 3. Ilium vi. Large intestine (colon) 1. Cecum- beginning of the ascending colon a. Vermiform appendix- projection from cecum 2. Ascending colon 3. Transverse colon 4. Descending colon 5. Sigmoid colon vii. Rectum viii. Anus ix. Other 1. Liver – produces bile salts 2. Pancreas- produces enzymes d. Functions i. Ingestion via the mouth ii. Motility 1. Entire tract is lines with smooth muscle 2. Stomach will stretch up to 5x when we eat 3. Stomach muscle contracts 24/7 to keep muscle tone (ensures that muscle will not get stuck in a stretched position a. Propulsive i. One directional ii. In esophagus and large intestine iii. peristalsis b. Mixing i. Two directional ii. Assists to break down food iii. Stomach and small intestine c. Digestion i. Mechanical 1. Physical breakdown a. Mouth = chewing b. Stomach = churning c. Small intestine = segmentation ii. Chemical 1. The existing form of nutrients are unable to pass across the membrane a. Carbs -> monosaccharides b. Proteins -> Amino acids c. Fats -> monoglycerides and fatty acids d. Secretion i. Nothing is able to be digested without something being secreted into the lumen of the digestive tract ii. Secretions 1. Mouth (saliva) a. Salivary glands moisten, lubricate, and begin carbohydrate breakdown 2. Stomach (HCl and pepsin) 3. Liver (bile salts) a. Breaks down fats and assists in neutralizing stomach acid b. Creates bile 4. Pancreas (enzymes) a. Break down fats, carbs, and protein) b. Also neutralizes acidic pH as it enters the small intestine 5. Small intestine 6. Gallbladder a. Stores bile iii. Absorption 1. 80% occurs in the duodenum 2. Other 20% is done in the rest of the small and large intestines iv. Elimination of wastes 1. Fecal matter 2. Know the microanatomy of the small intestine and the function of villi and microvilli. a. Microanatomy i. Lumen-center ii. Mucosa 1. Epithelial layer a. Single layer, allows for absorption 2. Lamina Propria a. Layer of connective tissue b. Houses capillaries, lacteals, and lymph 3. Muscularis mucosae a. Thin layer of smooth muscle iii. Submucosa 1. Lies under the mucosa 2. Connective tissue filled with arteries and veins 3. Contains nerve cells iv. Muscularis external 1. Longitudinal Muscle a. Outer layer that changes in length 2. Circular Muscle a. Inner layer that changes in width v. Serosa 1. Holds it together a. Epithelium layer b. Connective tissue c. Blood Vessels, lymph, etc. 3. Understand where along the alimentary tract you might find villi and why. a. Location i. Villi are present in the small intestine 1. Longest villi are in the duodenum which increases the amount of the absorption the occurs here 2. Shortest villi are in the ilium ii. Not present in the stomach or esophagus 1. Esophagus is lined by flat epithelium 2. Stomach is also lines by flat epithelium and contains small divots a. Only allows for alcohol absorption iii. Large intestine has no villi 1. Absorbs sodium and water b. Anatomy i. Each villi is made up of a collection of nerve and epithelial cells ii. Each villi has one lacteal 1. Lacteal is surrounded by blood vessels iii. Villi are surrounded by microvilli (small hair like extensions of the apical membrane) c. Function i. Villi and microvilli serve to aid in absorption ii. Since most nutrient absorption occurs by diffusion, they help to increase surface area b. Digestion II 1. Know the process of deglutition and the anatomy of the upper digestive tract. a. Deglutition i. The process of swallowing 1. When food reaches the soft palate, the uvula is moved upwards, so that the nose is closed off. 2. The epiglottis also seals off the trachea in order to ensure food moving out of the pharynx and into the esophagus. 3. The lower and upper esophageal sphincters, normally closed, open to allow food to pass through. ii. When swallowing ,foot must go down the right tube b. Mastication i. The process of chewing done by the teeth 1. Incisors and Canines a. 55 lbs of force b. Cut and tear 2. Premolars and molars a. 200 lbs of force b. Grind ii. Grinds and breaks down food iii. Stimulates saliva production and causes saliva to mix with the bolus c. Anatomy i. Bolus ii. Hard Palate- front of the roof of the mouth iii. Soft Palate- back of the roof of the mouth, terminates in the uvula iv. Tongue v. Uvula- ending part of the soft palate, seals of nose when swallowing vi. Pharynx- vii. Epiglottis- normally open, closes to prevent food from entering airway viii. Glottis ix. Larynx- voice box x. Trachea-airway xi. Esophagus 1. Food travels through the esophagus to reach the stomach 2. Average of 9 seconds to pass through a. Just transit time 3. NO nutrient absorption occurs, no villi or microvilli 2. Know the importance of the esophageal sphincters. a. Upper Esophageal Sphincter i. Ensures that breathing ends or begins ii. Closed most of the time iii. Only opens when a signal is sent to the medulla for no more information to be sent from the dorsal respiratory group (stops inspiration, allows bolus to enter the esophagus) b. Lower Esophageal Sphincter (Cardiac Sphincter) i. Usually closes so that stomach acid does not enter esophagus 1. Prevents acid reflux (backflow of acid, heartburn) ii. Acid can erode the wall of the lower esophagus iii. Close to heart, also called cardiac sphincter 3. Know the anatomy of the stomach and how and when the stomach empties its contents. a. Anatomy i. Made up of three chambers with no distinct separation 1. Fundus- first 1/3 2. Body- middle 1/3 3. Antrum- distal 1/3 ii. Pyloric Sphincter 1. Between the antrum and duodenum 2. Pylorus is the opening iii. Like the cardiac sphincter, this is closed until food needs to pass through iv. Rugae 1. Waves/folds along the lining of the stomach 4. Understand the neural influence on the stomach and how motility is regulated. a. Motor functions i. Receptive Relaxation 1. Before food is eaten, food stimulus causes the stomach to relax and produce acid in preparation ii. Food Storage 1. The stomach can expand to hold up to 1.5L of food iii. Gastric peristalsis 1. Contractions travel in waves down stomach to push/ mix food iv. Slow emptying 1. Sphincter opens slowly to allow some contents to exit 2. Allows SI time to get its job done b. Gastric motility i. Slow waves 1. How muscles react when there is no food in the stomach 2. Ensures muscle tone when resting ii. Peristalsis Signals 1. Spike potentials 2. Vigorous depolarization cause by an increase in PS stimuli, ACh 3. An increase in stretch leads to an increase in contraction 4. HYPERPOLARIZATION= Norepinephrine increases sympathetic iii. Regulation 1. Stomach- occurs in and effects the stomach a. Volume of Chyme i. Partially digested food combined w/ alimentary secretions (saliva and stomach secretions) ii. The more volume, the more stretch and the more contractions b. Presence of protein i. The higher protein concentration, the stronger the contractions ii. Most protein breakdown occurs in the stomach iii. Gastrin released from the antral mucosa cells effect the stomach 2. Duodenum- occur in the small intestine but effects the stomach a. Distention of the duodenum i. As chyme leaves the stomach, the duodenum expands ii. This down regulates the stomach so that the duodenum has more time to breakdown chyme b. Acidity of the Duodenal chyme i. Hydrochloric acid is released and the pH drops ii. Down regulates stomach c. Presence of proteins, sugars, and fats i. When levels are detected, hormones are released from the duodenal mucosa help down regulate gastric emptying 1. Gastric Inhibitory Protein (GIP) 2. Secretin 5. Know how motility is regulated in the small and large intestine. a. Small intestine i. Control of Motility 1. An increase in segmentation is caused by an increase in parasympathetic nerve signals 2. Controlled by hormones a. Upregulation of PS i. Gastrin 1. In stomach, downregulated to stop HCL production and digestive enzymes 2. In SI, upregulates smooth muscle contraction and blood circulation ii. Cholecystokinin (CCK) 1. Released by and upregulates duodenum iii. Insulin 1. Increases in pancreas after a meal iv. Secretin 1. Released by duodenum b. Down regulation of PS i. Glucagon 1. Converts glucagon to glucose after you have eaten b. Large Intestine i. Motility is regular, every 30 minutes or so ii. Mass movements- the colon contracts to move chyme 1. Coincides with ileum contraction 2. Elicits poop feeling as pressure grows 3. Often happens after eating 6. Be able to describe segmentation in the small intestine. a. Segmentation i. Pieces of chyme are separated by small areas of smooth muscle that are contracted, with areas of relaxed muscle in between ii. Contractions alternate to propel chyme iii. LOOKS LIKE PULSITILE LAMINAR FLOW 7. Understand how the ileocecal valve operates. a. Function i. Sphincter separates the ileum and the cecum ii. Serves to stop fecal backflow into the small intestine b. Operation i. Normally remains closed ii. Opens when pressure changes iii. Allows chyme to exit the ileum and enter the cecum as pressure in ileum exceeds that in the cecum 8. Know the anatomy of the large intestine and how it empties during defecation. a. Anatomy i. Sections 1. Cecum 2. Ascending 3. Transverse 4. Descending 5. Sigmoid ii. Tenia coli 1. Long bands of smooth muscle that support the colon 2. Three bands iii. Haustra 1. Pouches (act like the fabric of an umbrella) 2. Change in position as fecal matter is formed and moved iv. Rectum 1. Ending portion of sigmoid colon v. Anus b. Defecation i. Controlled by anal sphincters 1. Internal- smooth muscle we cannot control 2. External- skeletal muscle we can control ii. Act of defecation 1. As musculature of the abdomen contracts and lowers, pressure is placed on the colon wall (external pressure↑, internal will ↑) 2. Fecal matter will stretch the colon and sensory neurons send a message to the motor neurons in the cerebral cortex of the brain 3. Internal sphincter is then triggered and you release external c. Digestion III 1. Know the pH of secretion in different parts of the alimentary tract. a. Saliva- neutral to slightly acidic, about 1L per day (6-7 pH) b. Gastric- very acidic, about 1.5L per day (1-3.5 pH) c. Pancreatic- Basic, about 1L per day (8.0-8.3 pH) d. Bile – Basic, about 1L per day (7.8 pH) e. Small intestine- basic to combat gastric secretions, about 2L per day (7.5-8.0 pH) f. Large intestine- basic to combat gastric secretions, about .2L per day (7.5-8.0pH) *** We drink 1.5L per day *** Most fluid is absorbed 2. Know the phases of digestion and what secretions are produced in each phase. a. Cephalic Phase i. Any event before food hits the stomach ii. Senses are activated before tasting food iii. Secretions 1. Saliva 2. Esophageal Mucus 3. HCl b. Gastric Phase i. Events that occur in the stomach ii. Gastric pits- continuation of flat epithelium, top portion iii. Gastric gland- from constriction down iv. Secretions 1. HCl by parietal cells a. Aid to break down peptides b. Distend stomach increases HCl release 2. Gastrin a. Caused by protein and HCl release b. Increases HCl release (BENFICIAL POSITIVE FEEDBACK) 3. Pepsinogen a. Stored in chief cells as zymogen granules b. Not released until food enters the stomach c. It is pepsin in an inactive form that will activate in a low enough pH i. Between 1-3.5 pH (only enzyme to work in an acidic environment) d. Effect is nullified once buffers are added in the SI c. Intestinal Phase i. Events that occur in the intestines ii. Inhibition of gastric secretions 1. Goal= give the duodenum time by down regulating the stomach a. Decrease PS stimulation b. Local reflex action c. Release of secretin, GIP and CCK **Mucus is produced all the time by goblet cells, and it increases when eating. Protects inner layer of stomach from mechanical injury, self-digestion by pepsin, and neutralizes pH. 3. Know the functions of saliva. a. Produced by parotid, sublingual, and submandibular glands b. Glands increase production in cephalic phase c. Composition (99.5% water, .5% protein & electrolytes) i. Water softens food ii. Amylase begins carbohydrates breakdown iii. Mucus lubricates iv. Lysozyme kills bacteria 4. Understand what secretions the stomach produces and when they are produced in detail. a. SEE QUESTION 2 i. HCl ii. Pepsinogen/ Pepsin iii. Mucus 5. Understand the physiological mechanisms of inhibitors of stomach secretions. a. Gastric Inhibitory Peptide (GIP) i. During the intestinal phase it is released from the duodenal mucosa as fats and sugars enter ii. Downregulates gastric motility and secretions (HCl and Pepsin) b. Secretin i. Released by the duodenal mucosa when acidity increases in duodenum ii. Downregulates gastric motility and gastrin release, which stops HCl and pepsin release. iii. Upregulates pancreatic secretions c. Cholecystokinin (CCK) i. Released by the duodenal mucosa when lipids and protein are present ii. Downregulates gastric motility in stomach(HCl and Pepsin decrease) iii. Upregulates gallbladder and pancreatic secretions 6. Know the anatomy of the pancreas; what cells produce the secretions and what those secretions do. a. Anatomy i. Inferior to the stomach ii. Pancreatic duct 1. Empties into the duodenum iii. Acinar cells 1. Deep cells 2. Secretions a. Proteolytic enzymes (break down protein into peptides)
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