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BIOL 2510 test 2 notes part 1

by: Laura Nall

BIOL 2510 test 2 notes part 1 BIOL 2510 - 012

Marketplace > Auburn University > Biology > BIOL 2510 - 012 > BIOL 2510 test 2 notes part 1
Laura Nall
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These are notes for the second anatomy 2 test. These notes are from the week of 2.15.16 and cover what will be on our next exam.
Human Anatomy and Physiology II
Jeffrey Goessling
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This 9 page Class Notes was uploaded by Laura Nall on Wednesday February 10, 2016. The Class Notes belongs to BIOL 2510 - 012 at Auburn University taught by Jeffrey Goessling in Winter 2016. Since its upload, it has received 164 views. For similar materials see Human Anatomy and Physiology II in Biology at Auburn University.


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Date Created: 02/10/16
Anatomy and Physiology 2 Test 2 notes Completing Chapter 22 – lungs and respiration: Transport of Respiratory gases ***Hb means hemoglobin*** O2 Transport:  Transported in blood in 2 ways: o 1.5% dissolved in plasma o 98.5% bound to Hb  Oxyhemoglobin – hemoglobin + bound to O2  Deoxyhemoglobin – hemoglobin without bound O2 Oxygen­hemoglobin dissociation curve:  Each Hb can bind 4 O2 o First O2 is bound  2 , 3 , 4  bind  Affinity (binding strength) of Gb to O2 increases with oxygen saturation  Oxygen­Hb dissociation curve o Relationship between Hb saturation and blood PO2  Key PO2 to remember o 100 mmHg = PO2 of lungs o 40 mmHg = PO2 of resting tissues o 20 mmHg = PO2 of exercising tissues Oxygen dissociation graph:  Y­axis: percent O2 saturation of hemoglobin  X­axis: PO2 (mmHg)  What factors alter the curve? o Temperature  Increased temperature makes the curve less steep  Decreasing temperature steepens the curve o Blood pH o PCO2 Effect of PCO2 and pH: Bohr effect  Bohr effect – lower pH, high PCO2 reduce Hb affinity for O2  Remember the logic: during exercise… o Increase temperature o Increase PCO2 o Decrease blood pH  As a result the curve will shift to the right, at a given PO2 more O2 unloading to tissues  where it is needed CO2 transport  Transported in blood in 3 ways o 10% dissolved in plasma o 20% bound to Hb  Carbaminohemoglobin – Hb + bound CO2 o 70% as bicarbonate ions from CO2 reaction CO2 transport: impairments  Hyperventilation o Breathing exceeding metabolic needs o Causes low PCO2, lower H+, respiratory alkalosis (blood pH too basic)  Hypoventilation o Breathing not meeting metabolic needs o Causes high PCO2, higher H+, respiratory acidosis (blood pH too acidic) Neural control of respiration  Respiratory centers in medulla o Dorsal respiratory group (DRG)  Integrate input from peripheral stretch and chemoreceptors  relay to  VRG o Ventral respiratory group (VRG)  Control rhythm of respiration  Inspiration: impulses via phrenic nerve to diaphragm and intercostal  nerves to external intercostals  Expiration: stop impulses = muscles relax and lungs passively recoil  Respiratory centers in pons o Pontine respiratory group  Transmit impulses to VRG to fine­tune breathing rhythms Neural control of respiration: chemoreceptors  Central chemoreceptors: throughout brainstem  Peripheral chemoreceptors: aortic arch and carotid sinus  These respond to changes in PCO2, H+, and PO2  High PCO2 and H+ stimulate chemoreceptors resulting in increased respiratory rate and  depth Question:  Decreasing the affinity of Hb for O2 causes ______ decrease in O2 binding. Question: a decrease in the affinity of Hb for O2 is described as a: ______ right shift. Pulmonary diseases and disorders   Pneumonia – inflammation of and fluid accumulation in alveoli o Cough, acute chest pain, fever, green or yellow sputum o Viral, bacterial, fungal, or parasitic infections  Infant respiratory disease syndrome (IRDS) o Premature birth  insufficient surfactant  Prevention/treatment  Antenatal steroids  Continuous positive airway pressure (CPAP), bubbler CPAP  Surfactant treatment  Asthma – inflammation of airways o Shortness of breath, wheezing, coughing o Causes: genetic, exercise, cold air, allergens o Treatment: inhalers containing steroids – reduce swelling  COPD – Chronic Obstructive Pulmonary Diseases o Difficulty breathing, hypoventilation, coughing, pulmonary infections o Treatment: inhalers containing steroids or bronchodilators  Chronic bronchitis – excessive mucus production, inflammation of  airways  Emphysema – destruction of alveoli Chapter 23 Digestive system – Part 1 Functions of the digestive system: 1. Ingestion: take in food 2. Digestion: break down food into component nutrients 3. Absorption: absorb nutrient molecules into blood 4. Defecation: expel indigestible remains Digestive system: early observations  “Gastric experiments” starring: o Alexis St. Martin – the fistulated man o William Beaumont – “The Father of Gastric Physiology”  Experiments and Observations on the Gastric Juice, and the Physiology of Digestion  published in 1838 Length of the GI tract: 9 m (30 ft), 6m of it the SI Surface area is as large as a studio apartment Two main divisions  Alimentary Canal (GI tract) o Mouth, pharynx, esophagus, stomach, small intestine, large intestine, rectum  Accessory Organs o Teeth, tongue, salivary glands, gall bladder, liver, pancreas  **figure in book that labels all parts of the digestive tract; he literally talked about this for 10 minutes so you should probably be somewhat familiar with it Digestive System Processes 1. Ingestion – taking in solids and liquids via oral cavity 2. Propulsion – movement of food through the GI tract (24­36 hours) a. Deglutition (AKA swallowing) – to move from oral cavity to esophagus b. Peristalsis – wave­like alternation of contraction and relaxation of smooth  muscles to move food through the GI tract 3. Mechanical digestion  a. Mastication (chewing) – increases surface area and mixes food with saliva b. Churning – in stomach to mix food with gastric juices c. Segmentation – rhythmic constriction of small intestines to mix food and expose  all surfaces for absorption 4. Chemical digestion – enzymes to break down complex food molecules into their  component nutrients 5. Absorption – passage of digested food (and vitamins and minerals and water) from the GI tract into the blood and lymph (mostly occurs in the small intestines) 6. Defecation – elimination of indigestible substances from body via feces Serous Membranes of Digestive System  Parietal peritoneum  Visceral peritoneum  Mesentery – double layer of serous membranes extending from body wall to digestive  organs o Provides pathway for blood vessels, lymphatic vessels, and nerves o Holds organs in place o Stores fat o Omentum   Retroperitoneal: o Organs have lost direct dorsal mesentery contact  Most of large intestine, part of small intestine Layers of the GI tract 1. Mucosa a. Secretes mucus, digestive enzymes, and hormones b. Absorb the end products of digestion into blood  c. **Protest against infectious diseases i. MALT (=mucosa associated lymphoid tissue) – protects against ingested  microbes d. 3 sublayers i. Simple columnar epithelium ii. Lamina propria – areolar Ct iii. Muscularis mucosae – smooth muscle 2. Submucosa a. Thick areolar CT b. Contains blood and lymphatic vessels, nerve fibers, small glands 3. Muscularis externa a. Important for segmentation and peristalsis b. 2 layers i. Inner circular layer – smooth muscle that controls lumen diameter ii. Outer longitudinal layer – smooth muscle that controls tract length 4. Serosa = visceral peritoneum a. Outermost layer b. Replaced by adventitia in the esophagus Control of GI Tract Activity  In­house, intrinsic o Enteric neurons  Submucosal nerve plexus – controls activity of glands and mucosal  smooth muscles  Myenteric nerve plexus – controls GI tract motility (circular and  longitudinal muscle) o Some control over segmentation and peristalsis  Extrinsic o Sympathetic NS inputs = decrease secretion and motility o Parasympathetic NS inputs = increase secretion and motility Substrates & Digestion  3 major classes of food macromolecules o Carbohydrates o Proteins o Lipids   How is each class digested? o By what? Where?   ­ase = enzyme  ­ose = sugar  Lactase, maltase, sucrose = enzymes hat break down lactose, maltose,  sucrose, respectively  Peptidase = enzyme that breaks down peptides  Lipase = enzyme that breaks down fats Carbohydrates  Start to end: polysaccharides and oligosaccharides into monosaccharides (=simple  sugars)  Digested by: amylase, brush boarder enzymes (dextrinase, glucoamylase, amylase,  lactase, maltase, sucrose)  Enzyme location: saliva, pancreas, small intestine  Location of digestion: mouth, small intestine Proteins  Start to end: proteins into amino acids  Digested by: pepsin, pancreatic enzymes (trypsin, chymotrypsin, carboxypeptidase),  brush boarder enzymes (aminopeptidase, carboxypeptidase, dipeptidase) o Pepsin is the main protease, HCl causes pepsinogen to cleave and produce pepsin  Protein  large polypeptides  small polypeptides, small peptides  amino acids (some  dipeptides and tripeptides)  Enzyme location: stomach, pancreas, small intestine  Location of digestion: stomach, small intestine Lipids  Start to end: unemulsified fats into monoglycerides and fatty acids  “pre­treatment” by: bile salts (~detergent) to make fat soluble in water  Digested by: lipases (lingual, gastric, pancreatic)  Enzyme location: mouth, stomach, pancreas  Location of digestion: mouth, stomach, small intestine Functional Anatomy of the GI tract  Oral cavity o Ingestion, mastication (chewing), deglutition (swallowing), digestion (mechanical and chemical) o Palatine tonsils – lymph nodes o Palate – roof of the mouth o Uvula – projection off soft palate o Lingual frenulum – secures the tongue to the floor of the mouth o Labial frenulum – joins lip to gum o *Defensins*   Antimicrobial peptides produced by oral mucosa  Tongue  o Skeletal muscle o Mixes food and forms bolus o Chewing, swallowing, speaking o 4 types of papillae:   1. Filiform – keratin, most numerous, *no taste buds  2. Fungiform – scattered, contain taste buds  3. Circumvallate – in row at back of tongue, contain taste buds  4. Foliate – postero­lateral; contain taste buds but function in taste only in  early infancy/childhood  Salivary glands o Saliva:   Cleanses mouth  pH 6.57­7  secretes salivary amylase (carbohydrate digestion) and lingual lipase (fat  digestion)  micro­organism defense  1. Defensins – anti­microbial proteins  2. IgA antibodies – causes phagocytosis by WBCs and prevent  pathogens from adhering to mucous membranes  Lysozymes – enzyme that damage bacterial cell walls o Glands:   Parotid  Submandibular  Sublingual   Control of salivation o Stimulated via parasympathetic nervous system o Strong activation of sympathetic NS  1. Release of epi / norepi  2. Vasocontriction & decrease in blood delivery to the salivary glands  3. Decrease in salivation   Teeth o 20 baby (milk) teeth – fall out by age 13 o 32 permanent teeth in adults o Crown  Exposed part of tooth above gumline  Outer surface covered with enamel – consists of hydroxyapatite  Protects teeth against abrasion and acid  Interior consists of dentin – bulk of tooth; calcified, protein­rich o Root  Portion of tooth embedded in jaw bone  Outer surface covered by cement – calcified CT  Interior mostly dentin  Periodontal ligament  Esophagus o Extend from pharynx to stomach o Enters abdominal cavity through esophageal hiatus (a hole in diaphragm) o Joins stomach at the gastro­esophageal sphincter (aka cardiac sphincter)  Allows food to pass into stomach, but prevents stomach acid from entering esophagus o Function: moves food to stomach via peristalsis  Stomach – gross anatomy o 6­10 inches long o 4 regions   Cardiac region  Fundus  Body  Pyloric region o Sphincters  Gastroesophageal sphincter  Pyloric sphincter – controls emptying into intestine o Bolus becomes chyme (creamy paste) o Rugae – mucosal folds  Stomach – microanatomy o Surface epithelium (mucous cells) – secretes viscous and alkaline mucus, protects  stomach lining from acidity o Mucosa has   Gastric pits (openings for gastric glands)  Gastric glands – secrete gastric juices o 4 glandular secretory cells:  1. Mucous neck cells – secretes thin, acidic mucus  2. Parietal cells – HCl and Intrinsic Factor (glycoprotein needed for  Vitamin B12 absorption in the small intestine)  3. Chief cells – secretes pepsinogen and small amount lipase  4. Enteroendocrine cells – produce chemical messengers (5)   A. gastrin – stimulates HCl secretion and stomach motility  B. histamine – stimulates HCl secretion  C. endorphins – suppress appetite  D. serotonin – causes contraction of stomach muscles  E. somatostatin – inhibits stomach secretion and motility o Regulation of gastric secretion   Three sites of stimuli. Inhibit or enhance secretion  Cephalic phase: before food enters stomach o Smell, taste, site, thought of food o Vagus nerve stimulates stomach  Gastric phase: 3­4 hours, food in stomach o Stimulation   Stretch receptors   Chemical changes cause G cells to release gastrin  Partially digested proteins, caffeine,  increased pH o Inhibition   Low pH inhibits gastrin secretion  Empty stomach, stress adrenal responses


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