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week 12 notes for test 6 :)

by: Jennifer Fry

week 12 notes for test 6 :) PHYS 215

Marketplace > Ball State University > Science > PHYS 215 > week 12 notes for test 6
Jennifer Fry
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This 18 page Class Notes was uploaded by Jennifer Fry on Wednesday November 11, 2015. The Class Notes belongs to PHYS 215 at Ball State University taught by Zamlauski-Tucker in Summer 2015. Since its upload, it has received 26 views. For similar materials see Human Physiology in Science at Ball State University.


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Date Created: 11/11/15
Week 12 notes Physiology for test 6 11-9-15  Actions of Angiotensin II o It is a potent vasoconstrictor o In the kidneys, it constricts glomerular arterioles. This decreases the glomerular filtration rate (GFR), which in turn raises systemic arterial blood pressure. o Acts on the adrenal cortex, causing the release of aldosterone o Acts on the brain to increase the sense of thirst, and increase the desire for salt. > rise in blood pressure. o Increases the secretion of vasopressin and ACTH.  No Aldosterone/Too much Aldosterone o No aldosterone: ~8% sodium lost in the urine o Too much aldosterone: complete sodium reabsorption  Role of R-A-A system in disorders o Hypertension (high blood pressure)- can be caused by an abnormal increases in renin-angiotensin- aldosterone activity o Edema as a result of Heart failure-decrease cardiac output results in reduced blood pressure that triggers salt and fluid retention. In tissues not blood: water.  Drugs that Effect Na+ Reabsorption o Diuretics-cause “diuresis”; increased urinary output, can act by blocking Na+ reabsorption and thus, water is lost with the Na+ o ACE inhibitors-block ACE and thus the conversion of ANG I and ANG II  Transport maximum (Tm ) o The concentration of the substance that is just enough to achieve the maximum transport rate is called the transport maximum o Filtered load= plasma concentration *GFR of a substance o Tm for glucose ~ 375 mg/min  Glycosuria o The presence of glucose in urine is called glycosuria. This occurs when the plasma glucose level reaches 300 mg per 100 ml, but can occur at values as low as 150 mg per 100 ml. this plasma level is called the renal plasma threshold for glucose. o Glycosuria occurs most frequently in 2 conditions:  Diabetes mellitus- hyperglycemia occurs due to inadequate secretion or action of insulin. In this condition the plasma glucose level increses to a level above the renal plasma threshold.  Lowering of renal plasma threshold. This is usually a non- pathological condition and occurs most frequently during pregnancy. In this case glycosuria occurs even though the normal renal plasma threshold is not surpassed. o Phosphate reabsorption  Uptake is via a transport carrier in the proximal tubule  Phosphate intake is in excess of the bodies need.  Therefore, excess is eliminated bringing plasma levels to normal. o Chloride reabsorption  Chloride passes mainly between the cells.  Chloride is also taken up into the cell via a transporter that exchanges another anion for chloride o *E.C.** o Vasopressin is Antidiuretic Hormone (ADH)  ADH causes incorporation of more water channels into the membrane of the distal tubule and collecting duct so that more water can be reabsorbed, in turn reducing urine output.  ADH is synthesized in the hypothalamus but is stored and released from the posterior pituitary.  Urea o A waste product from the breakdown of proteins o The concentration of urea in the glomerular filtrate is equal to that in the plasma. o Urea becomes concentrated as water leaves and it is left behind o As the concentration of urea increases in the tubule, it can diffuse from the lumen into the peritubular capillary o Only 50% of all urea is reabsorbed   Inulin and PAH o Inulin is filtered in the glomerulus, but is not reabsorbed (125 ml/min) o PAH (para-aminohippuric acid) is filtered by the glomeruli and secreted in the proximal tubule (it is removed from all the plasma that moves through the kidneys, 625 ml/min)    Filtration Fraction o o 20% of plasma that enters the glomeruli is filtered  Tonicity o Isotonic- normal osmolarity (concentration of salts in water) is 300 milliosmols/liter (mosM) o Hypotonic- a solution with an osmolarity below the normal concentration o Hypertonic- a solution with an osmolarity greater than normal  Countercurrent system and the loop of Henle o The loop of Henle establishes medullary hyperosmolarity  The ascending limb of the loop of Henle transports solutes (NaCl) out of the tubule lumen with little or no water.  Hyperosmotic medullary interstitium while hyposmotic tubule fluid goes to the distal tubule. This is called the “single effect”.  The osmolarity of the intersitium rises progressively from cortex to medulla and papilla through multiplication of the “single effect”  The single effect in fluid processed by the loop segments located near the tip of the papilla occurs in fluid already subject to the single effect when the fluid was in loop segments located closer to the cortex.  Countercurrent exchange of solutes between ascending and descending vasa recta (the renal medullary capillaries) minimizes solute washout from the medullary interstitium. o The countercurrent system permits forming a concentrated urine  In the presence of ADH, water permeability increases  The hyposmotic fluid that enters the distal tubule (DT) from the thick ascending limb (TAL) looses most of its water by osmotic equilibration with the surrounding cortical intersitium along the cortical collecting duct (CCD).  It also continues loosing NaCl through reabsorptive transport along DT and CCD, until the tubule fluid becomes isosmotic with plasma, by the end of the CCD.  The small amount of isosmotic fluid that flows into the medullary collecting ducts losses more and more water to the hyperosmotic medullary and papillary interstitial and is finally excreted as hyperosmotic, highly concentrated urine. o The countercurrent system permits forming a dilute urine  In the absence of ADH, the hyperosmotic fluid that enters the DT from the loop of Henle, continues to be diluted by transport of NaCl via NaCl (thiazide sensitive) along the CD.  Water reabsorption is limited so that the tubule fluid becomes more and more dilute along DT, CNT and collecting ducts (CCD, OMCD and IMCD), until it is excreted as a large volume of hyposmotic urine. o Mechanism of hyperosmotic reabsorption in the TAL  There is apical Na-K-2Cl reabsorptive cotransport with K recycling through apical K-channels, and basolateral transport of Na via the Na-K-ATPase and the Cl via Cl- channels, in the water impermeable epithelium of the TAL.  A lumen positive electrical potential difference is generated by the luminal Na-K-2Cl cotransporter operating in parallel with channels that allow K to recycle into the lumen. The lumen positive potential drives passive paracellular reabsorption of more Na+ and of other cations (Mg++, Ca++)  The higher the delivery of Cl (Km= 50 mM), the higher the activity of the luminal Na-K-2Cl cotransporters and the higher the rate of hyperosmotic Na reabsorption at the TAL. o Mechanism for hyperosmotic reabsorption in the tAL (thin ascending limb)  Water abstraction along the early part of the thin descending limb (tDL) is driven by the high osmolarity (at least half due to urea) present in the medullary interstitium. In the deep nephrons, water reabsorption increases the tubule fluid osmolarity (up to 1200 mOsm/L) and the Na concentration (up to 300 mEq/L) by the bend of the loop.  Along the water impermeable tAL, Na diffuses from the tubule lumen into the medullary intersitium driven by its concentration gradient and some urea enters from the interstitium into the lumen; the osmolarity decreases as the fluid ascends along the tAL.  Operation of this passive mechanisms of Na reabsorption along the tAL is critically dependent on efficient medullary recirculation of urea. pH and Acid/Base Balance  What is pH? o Can be thought of as the power of Hydrogen concentration in a solution o Mathematical definition- negative log value of the hydrogen ion (H+) concentration, or  pH = -log [H+]   *E.C.**  Physiological pH o Normal body pH is between 7.35-7.45 or ~7.4 o So, normal body pH is slightly basic o What pH range is compatible with life?  pH 6.8 or pH 8  Acid Disassociation Constant o Given a weak acid “HA”, its disassociation in water is subject to the following equilibrium:  HA+H2O <-> H3O+ + A-  HA <-> H+ + A- o Ka is the disassociation constant for acid  The stronger the acid, the higher the Ka  Ka=1, almost completely disassociated  Ka= 0, almost completely associated  pKa- the acidity constant is often represented by the inverse of its logarithm  Types of acids o Volatile-carbonic acid (can leave solution and enter the air) o Fixed acids- sulfuric and phosphoric (doesn’t leave solution) o Organic acids- lactic acid and ketone bodies  Buffers and buffer systems o Consist of a wear acid or base and a salt form of that acid or base o Prevent changes in pH by converting strong acids to weak acids and strong bases to weak bases o Neutralizes H+ as it moves from the point of origin to the lungs or the kidneys for excretion  Important Buffers in the Body o Protein buffers- slow adjustment of ECF o Hemoglobin buffer- intracellular buffer; has an immediate effect of ECF o Carbonic acid- bicarbonate buffer system  Prevent pH changes caused by organic and fixed acids  Cannot protect from changes resulting from abnormal levels of CO2  Only functions when respiratory system and respiratory control centers are working correctly.  Limited by the availability of HCO3- o Phosphate buffer system- plays a minor role in ECF major role in ICF  Controlling pH in the Body o There are 2 major processes; pH regulation and pH compensation o Regulation is a function of the buffer systems of the body in combination with respiratory and renal systems o Compensation requires further intervention of the respiratory and/or the renal system to restore normal body pH.  Regulation of the Lungs and Kidneys o The lungs remove CO2 (the respiratory acid) and there is a large amount to be removed (at least 12,000 to 13,000 mmols/day) o The kidneys excrete acids. This is critical even though the amounts (70-100 mmols/day) are smaller because there is no other way to excrete these acids and the amounts involved are still very large when compared to the plasma [H+] of only 40 mmols/liter. o The kidneys also reabsorb filtered bicarbonate. Bicarbonate is the predominant extracellular buffer against acids.  Respiration and Acid/Base Changes o Changes in pH due to pCO2 changes from alterations in ventilation (changes in pCO2 result in rapid changes in [H+] in all body fluid compartments) o Changes in alveolar ventilation are inversely related to changes in arterial pCO2 and directly proportional to total body CO2 production o paCO2 is proportional to [VCO2/VA]  paCO2 = 0.863 x [VCO2/VA]  VCO2= CO2 production by the body  VA= alveolar ventilation  Henderson-Hasselbach equation o Changes in arterial pCO2 cause changes in pH o pH = pKa + log {[HCO3] / (0.03 x pCO2)} o [H+] = 24 x (pCO2/ [HCO3])   Renal regulation o Remember, H+ leaves the proximal tubule cell by 2 mechanisms:  Via Na+ H+ antiporter (major route)  Via H+ ATPase (proton pump) o Filtered HCO3- cannot cross the apical membrane PT. Instead, it combines with the secreted H+ and is converted to CO2 and H2O by carbonic anhydrase. o CO2 is lipid soluble and easily crosses into the cytoplasm of the PT cell. In the cell, the reverse reaction takes place and HCO3- crosses the basolateral membrane via a Na+ HCO3- symporter. o The sodium pump keeps intracellular Na+ low maintaining the gradient for the H+ Na+ antiport at the apical membrane. The H+ Na+ antiport (secondary active transport) o Net effect reabsorption of one molecule of HCO3 and 1 molecule of Na+ from the tubular lumen into the blood stream for each molecule of H+ secreted.   Physiological conditions o Acidosis- an abnormal process or condition which would lower arterial pH if there were no secondary changes in response. o Alkalosis- an abnormal process or condition which would raise arterial pH if there were no secondary changes in response. o Simple (acid-base) Disorders- are those in which there is a single primary acid-base disorder. o Mixed (acid-base) Disorders- are those in which 2 or more primary disorders are present simultaneously. o Acidaemia- Arterial pH < 7.36 ([H+] > 44nM) o Alkalaemia- Arterial pH > 7.44 ([H+] < 36 nM)  Acid/Base Disorders o Respiratory acidosis- arterial pCO2 rises to a level higher than expected o Respiratory alkalosis- arterial pCO2 falls to a level lower than expected o Metabolic acidosis- a process or condition leading to an increase in acids in the blood o Metabolic alkalosis- a disorder which causes the plasma bicarbonate to rise to a level higher than expected.  Respiratory Compensation o Compensation for metabolic acidosis is hyperventilation to decrease the arterial pCO2  Maximum compensation can be calculated  Expected pCO2 = 1.5 [HCO3] + 8 mmHg o Compensation for metabolic alkalosis is hypoventilation to increase arterial pCO2  Maximum compensation can be calculated  Expected pCO2 = 0.7 [HCO3] + 20 mmHg  Renal Compensation o Chronic respiratory Acidosis – the kidneys responded by retaining bicarbonate  Response occurs because increased arterial pCO2 increases intracellular pCO2 in proximal tubular cells (PTC) and this causes increased H+ secretion from the PTCs  Acute respiratory acidosis is buffered by proteins o Respiratory alkalosis is compensated by a decrease in bicarbonate reabsorption by the kidneys 11-11-15  Digestive System o Motility- muscular contractions that mix and move the contents of the digestive tract o Secretion- release of digestive juices into the digestive tract o Digestion- the biological breakdown of complex food substances o Absorption- the movement of substances from the digestive tract into the blood or lymph  Food substances o Carbohydrates- neutral compounds of carbon, hydrogen, and oxygen such as sugars, starches, and cellulose o Proteins- any of numerous naturally occurring extremely complex substances that consist of amino-acids residues joined by peptide bonds o Fats- any substance of plant or animal origin that is nonvolatile, insoluble in water, and oily or greasy to the touch, lipids  Carbohydrates o End product of carbohydrate breakdown is monosaccharides (glucose, galactose, fructose) o Polysaccharides (starch or glycogen)  Broken down by amylase first, then maltase o Disaccharides  Have the ending “ose”  The enzyme that breaks them down will end in “ase”  Example lactose is broken down by lactase  Proteins o Broken down by enzymes that cleave between specific amino acid groups into peptides and amino acids o Examples of enzymes that cleave proteins  Chymotrypsin  Carboxypeptidase  Pepsin  Trypsin o Aminopeptidase- an enzyme that cleaves peptides into individual amino acids  Fats o Triglycerides (lipids)  Broken down by lipase into monoglycerides and free fatty acids   Components of digestive system o  The mouth o Motility-chewing o Secretions- in saliva  Amylase  Mucus  Lysozymes o Digestion- carbohydrates o Absorption- some medicines  Nitroglycerin  Pharynx and esophagus o Motility- swallowing o Secretion- mucus  Exocrine pancreas o Secretion  Trypsin- stored as trypsinogen until release  Activated by enterokinase and trypsin (itself)  Chymotrypsin- stored as chymotrypsinogen  Activated by trypsin  Carboxypeptidase- stored as procarboxypeptidase  Activated by trypsin  Amylase- secreted in its active form  Lipase- secreted in active form o Digestion- by these enzymes accomplishes digestion in the duodenum  Liver o Secretion- Bile  Bile salts  Alkaline secretion  Bilirubin o Digestion  Bile salts aid in fat digestion  Bile salts promote emulsification o Bile salts have both hydrophilic and hydrophobic domains (amphipathic). o On exposure to a large aggregates of triglyceride, the hydrophobic portion of bile salts go into the lipid, with the hydrophilic domains remaining at the surface. o Such coating with bile salts aids in breakdown of large aggregates or droplets into smaller and smaller droplets (micelles). o  Roles of the Liver o Metabolic processing of nutrients o Detoxification or degradation of body wastes and hormones o Synthesis of plasma proteins o Storage of glycogen o Activation of vitamin D (with the kidneys) o Removal of bacteria o Excretion of cholesterol and bilirubin  Small intestine o Motility- segmentation, migrating motility complex o Secretions  Mucus  Salt o Digestion- in lumen by pancreatic enzymes and bile, carbohydrates and proteins are digested along with the completion of fat digestion o Absorption- all nutrients along with most electrolytes and water  The Brush Border o Epithelial cells that form the luminal surface of the small intestine o Plasma membrane contains 3 types of enzymes  Enterokinase- activates trypsinogen  Disaccharidases (maltase, sucrose, and lactase)- carbohydrate digestion  Aminopeptidases- hydrolyze small peptide fragments into amino acids  Large intestine o Motility- Haustral contractions, mass movement o Secretion- mucus o Absorption- salt and water, conversion of contents into feces  Autonomous smooth-muscle function o Pace setter cells- produce spontaneous, rhythmic, subthreshold fluctuations in membrane potential  Slow wave potentials  Basic electrical rhythm (BER)  Pacesetter potential o Slow wave potentials- not action potentials  Do not induce contractions without help  Spread to adjacent muscle cells via gap junctions (protein pores)  Bring the membrane closer to the threshold potential  Caused by cyclic changes in Ca and K currents  Rate is characteristic for each organ  Smooth Muscle Contraction o Depolarization caused by slow wave exceeds threshold for action potential and Ca2+ enters the cell o Voltage-gated Ca channels open o Ca inflow depolarizes the membrane, causing an action potential o Ca also initiates contraction by binding with calmodulin  Relationship between Slow wave and AP o Slow waves are always present in smooth muscle  In the “resting” state, only the slow waves occur o Stimulation from nerves or exposure to hormones may result in depolarization to threshold  As the muscle becomes active, action potentials begin to appear on the positive peaks of the slow waves and muscle contraction follows o The rate of slow waves will determine the frequency of contractions o The number of action potentials on each slow wave peak determines the strength of muscle contraction  The Enteric Nervous System o Intrinsic Nerve Plexus- relays information to and from the GI tract via the parasympathetic and sympathetic nervous systems  Relays information within the GI tract by local reflexes  Controls most functions of the GI tract o 2 parts:  Myenteric plexus- primary controls the motility of GI smooth muscles  Submucosal plexus  Primary controls secretion and blood flow  Receives sensory information from chemoreceptors and mechanoreceptors of the GI tract.  Extrinsic Nerves (parasympathetic) o In general, excitatory in the GI tract, increases smooth muscle motility and promotes secretion of digestive enzymes o Carried via vagus and pelvic nerves  Preganglionic fibers synapse in the myenteric and submucosal plexuses.  Cell bodies in the ganglia of the plexuses send information to the smooth muscle, secretory cells, and endocrine cells of the GI tract.  Vagus nerve carries information to the esophagus, stomach, pancreas and upper large intestine.  The pelvic nerve carries information to the lower large intestine, rectum and anus.  Extrinsic Nerves (sympathetic) o Inhibitory, decreases GI motility and secretion o Preganglionic cholinergic (acetylcholine secreting) fibers synapse in prevertebral ganglia o Postganglionic adrenergic fibers leave the prevertebral ganglia and synapse in the myenteric and submucosal plexuses o Direct postganglionic adrenergic innervation of blood vessels and some smooth muscles also occurs    Stomach o Motility- receptive relaxation; peristalsis o Secretion- gasric juice  HCl  Pepsin  Mucus  Intrinsic o Digestion- continuation of carbohydrate digestion beginning of protein digestion in the antrum of the stomach o Absorption of alcohol and aspirin  Function of stomach o Storage of Food in the body o Secretion of hydrochloric acid (HCl) and enzymes to begin protein digestion o Production of chime by mixing of the food in the antrum of the stomach  Stomach (protective mechanisms) o Protected from gastric secretion by the gastric mucosal barrier  Cells are almost impermeable to H+  Edges of cells form tight junctions, preventing the movement of acid between cells o Lining of stomach is replaced every 3 days o Peptic ulcer- breakdown in the barrier and erosion of the stomach wall  Gastric Secretion o Gastric mucosa- 2 areas  Oxyntic mucosa- lines the body and fundus  Pyloric gland area- lines the antrum o Gastric pits- foldings in the gastric mucosa containing gastric glands  Gastric Secretory Cells o Surface epithelial cells- line the walls between the pits and secrete thick mucus o Mucus cells- line the gastric pits and gland entrance, secrete watery mucus o Chief cells- line the gastric gland and secrete pepsinogen o Parietal cells- line the outer wall of the gastric pits, secrete HCl and intrinsic factor o All arise from gastric stem cells  Receptive relaxation o Empty stomach has deep folds and holds about 50 mL o As food fills the stomach the folds get smaller and flatten as the stomach relaxes o Full stomach holds about 1 L o Over eating leads to discomfort from over-distending the stomach  Vomiting o Coordinated by a vomiting center in the medulla o Achieved by contraction of the diaphragm and abdominal muscles o Deep inspiration and closure of the glottis o Diaphragm descends down onto the stomach while contraction of the abdominal muscles compresses the abdominal cavity o As the stomach is squeezed, the contents move upward through the relaxed sphincters and esophagus and out the mouth o Excessive vomiting can lead to dehydration, circulatory problems and metabolic alkalosis  Small Intestine Absorption (Carbohydrate Absorption) o Remember, disaccharides must first be converted into monosaccharides (glucose, galactose and fructose) o Glucose and galactose are taken up by secondary active transport o Fructose is taken up by facilitated diffusion  Small Intestine Absorption (Protein Absorption) o Absorbed as amino acids by secondary active transport o Absorbs amino acids from  Food  Digestive enzymes  Cellular protein last during mucosal turnover  Plasma proteins that leak from the capillaries  Fat Absorption o Micelle comes into contact with the epithelial surface cells o Monoglycerides and fatty acids passively diffuse through the cell membrane (lipid bilayer) o The monoglycerides and fatty acids are synthesizes back into triglycerides inside the cells o Triglycerides aggregate to form chylomicrons which are extruded from the cell by exocytosis o Chylomicrons enter the lymph system because they cannot enter the blood vessels  Vitamin Absorption o Vitamin B12 requires intrinsic factor for absorption o Fat soluble vitamins  Vitamin E is absorbed passively. The vitamin is cleaved by esterases located in the stomach lining.  It is then packaged into very low-density lipoproteins (VLDL) by the addition of lipid-like substances o Water soluble vitamins  Believed to be taken up passively or via transporters  Iron Absorption o In the U.S. adults ingest up to 20 mg of iron daily. Of this amount, about 0.5 to 1.0 mg in men, 1.0 to 1.5 mg in women o Iron is taken up by active transport into intestinal epithelial cells o Iron in food may exist primarily as inorganic (ferrous) iron and a smaller portion as ferric iron o After uptake by the intestinal call, iron is stored as protein-bound ferric iron eventually transferred from the cell. o Iron needed for production of red blood cell is transported in the blood by transferrin  Calcium Absorption o Absorption of calcium occurs mainly in the duodenum o Vitamin D facilitates active transport of calcium o Vitamin D must first be activated in the liver and kidneys, which is enhanced by parathyroid hormone o A decrease in calcium concentration results in the secretion of parathyroid hormone  Large Intestine and Bacteria o Slow colonic movement so bacteria have time to grow o Colon does not secrete antibacterial agents o Surviving bacteria thrive and help the body by  Synthesizing vitamin K  Preventing the growth of potentially harmful bacteria  Promoting colonic motility  Maintaining colonic mucosal integrity  Diarrhea o Helpful in elimination of harmful material o Harmful if excessive loss of intestinal contents results in:  Dehydration  Loss of nutrients  Metabolic acidosis


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