Title | BISC 305 Final EXAM Notes |
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Course | Animal Physiology |
Institution | Simon Fraser University |
Pages | 16 |
File Size | 397.3 KB |
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High yield summary notes for the final exam. Includes all the important information that you need to know including professor remarks not included in lecture slides....
BISC 305: FINAL EXAM NOTES NOTE: ALL CREDIT FOR IMAGES GO TO “PRINCIPLES OF ANIMAL PHYSIOLOGY” 3RD EDITION BY CHRISTOPHER D. MOYES AND PATRICIA M.SCHULTE.
Lecture 22: The Kidney Kidney Structure + Function ●
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6 roles in homeostasis ○ Ion, osmotic, blood, pH balance ○ Excretion of metabolic waste + toxin ○ Hormone production Kidney has 2 layers ○ Outer cortex ○ Inner medulla Urine leaves kidney via ureter , which empties into urinary bladder
Nephron ● ●
Functional unit of kidney Composed of ○ Renal tubule ■ Lined with transport epithelium ■ Different segments with specific transport functions ○ Vasculature ■ Glomerulus: ball of capillaries surrounded by Bowman’s capsule ■ Capillary beds surrounding renal tubule
Urine Production ●
4 processes: ○ Filtration: filtering blood at glomerulus into filtrate ○ Reabsorption: removing specific molecules from filtrate ○ Secretion: adding specific molecules to filtrate ○ Excretion: excreting urine from body
Filtration ●
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Liquid part of blood filtered into Bowman’s capsule ○ Water and small solutes can cross while blood cells and large macromolecules can’t Glomerular capillaries are very leaky ○ Podocytes with foot processes form filtration structure (contribute to leakiness)
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Mesangial cells control blood pressure and filtration within glomerulus
Reabsorption ● ● ●
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Initial filtrate is isosmotic to blood (same osmolarity) Most water/salt reabsorbed via transport proteins + energy Renal threshold: the limit of reabsorbing, ability of kidney to absorb certain molecule ○ Rate of reabsorption limited by # of transporters H2O + glucose primary molecules to reabsorb Glucose reabsorbed by secondary active transport
Secretion ● ● ● ●
Molecules removed from blood into filtrate Includes K+, NH4+, H+, drugs and water-soluble vitamins Requires transport proteins + energy K+ highly regulated ○ If too much K+ outside of cells ○ Irregular depolarization ○ Irregular muscle contraction
Tubule Regions ● ●
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Different regions have different transport functions + permeabilities (differences in epithelium) Proximal tubule: most of the solute and water reabsorption occurs here (other areas for “fine-tuning”) ○ Many solutes reabsorbed by N a+ cotransport WATER FOLLOWS SALTS Proximal tubule also carries out secretion
Loop of Henle ●
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THIN Descending limb is PERMEABLE to water ○ Water reabsorbed via aquaporins (can remove/add them) ○ Volume of urine decreases and becomes more concentrated THICK Ascending limb i s IMPERMEABLE to water ○ Ions reabsorbed ○ Urine becomes dilute Reabsorbed ions help to create osmotic gradient
Distal Tubule ● ●
Can reabsorb salts/water and secrete potassium Transport function affected by hormones ○ PTH: increase Ca2+ reabsorption ○ Aldosterone: increase K+ secretion
Countercurrent Multiplier ●
Loop of henle acts as countercurrent multiplier due to osmotic gradient facilitating reabsorption of water ○ Low osmolarity near cortex ○ High o smolarity deep in m edulla ■ RE: thin descending loop of henle is permeable to water, causing increased osmolarity going down, can reabsorb water
Glomerular FIltration Rate (GFR) ● ● ●
Capillaries are fragile so have to ensure pressure is well controlled GFR determined by pressure across glomerular wall 3 main forces: glomerular capillary and Bowman’s capsule hydrostatic pressure and oncotic pressure
3 Intrinsic Regulators for GFR ● ●
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Regulating blood flow into nephron, ball of capillaries is fragile so don’t want too much pressure, but want enough to get enough GFR (good filtration) Myogenic regulation [ arteriole stretch] ○ Constriction and dilation of afferent arteriole ○ Muscle cells can detect stretch and the higher blood pressure in afferent arteriole, cells contract to constrict the blood vessel, resulting in less pressure Tubuloglomerular feedback [ tubular stretch] ○ Juxtaglomerular apparatus: Juxtaglomerular cells in afferent arteriole ○ Macula densa cells detect stretch in distal tubule and can control diameter of afferent arteriole by sending signal to juxtaglomerular cells (via RAA pathway) Mesangial control ○ Mesangial cells can contract to alter the permeability of glomerulus (control how much filters through)
Vasopressin [ADH] ● ● ● ● ●
Extrinsic regulator of GFR, peptide hormone produced in hypothalamus and released by posterior pituitary gland Increases water reabsorption from collecting duct by INCREASING number of aquaporins Stimulated by increased plasma osmolarity Inhibited by increasing blood pressure Molecular mechanism: ○ GPCR pathway leading to phosphorylation, resulting in insertion of aquaporins in membrane
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Alcohol inhibits release of ADH, resulting in LESS aquaporins, thus dilute urine (don’t reabsorb as much water, that’s why danger of dehydration) Vasopressin regulates permeability of aquaporins in collecting duct, which determines f inal osmotic concentration of final urine
Aldosterone ●
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Mineralocorticoid hormone (steroid) that controls ion excretion, produced by adrenal cortex ○ Can diffuse to nucleus to activate transcription factor, different mechanism than ADH (slower) Targets distal tubule and collecting duct cells Stimulates Na+ r eabsorption and K+ excretion Aldosterone controls K+ levels in blood (stimulated by increases in circulating K+)
Renin-Angiotensin-Aldosterone (RAA) Pathway ● ●
Juxtaglomerular cells secrete renin enzyme when blood pressure or GFR lower than normal Secretion of renin can be controlled by: ○ Juxtaglomerular cells release renin in response to LOW B.P. (Via baroreceptors) ○ Macula densa cells in distal tubule respond to decrease blood flow by sending signal to juxtaglomerular cells to release renin
Atrial Natriuretic Peptide (ANP) ● ● ●
Increases urine output and lowers blood volume + pressure Antagonist to RAA pathway, increases excretion of Na+ Increases GFR
Thirst ● ●
Detected and controlled by hypothalamus Osmoreceptors monitor body fluid concentrations
Lecture 23: Digestion 1 ● ●
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Assimilation: p rocesses of nutrient uptake, digestion and absorption taking place in G I (gastrointestinal) tract Diets provide energy ○ Caloric equivalent: energy content of gram of specific molecule (e.g. protein/carb = 4 kcal/gram) Some energy spent digesting food (have to expend energy to break down food): ○ Specific dynamic action (SDA): increased metabolic rate during digestion ○ Heat increment (energy released as heat): importance source of thermal energy
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Vitamins: group of unrelated molecules with diverse functions, many participate as cofactors for enzymes, obtained in diet or from GI tract bacteria ○ Fat soluble: vitamins D, E, A, K ○ Water soluble: vitamins B, C Minerals: metallic elements participating in protein structure (e.g. calcium), most absorbed by specific transporters along GI tract Amino acids: used to build proteins, 8 essential (obtained from diet), deficiency can lead to development defects ○ Protein quality: amino acid profile of dietary protein ■ Animal tissue provides HIGHER protein quality than plant tissue (animal has similar amino acid profile to you when eaten, some plants lack specific amino acids) Digestive enzymes: enzymes that convert macromolecules into forms that can be absorbed and processed ○ Lipases: break down triglycerides/phospholipids into fatty acids ○ Proteases: break down proteins into shorter polypeptides ○ Amylase: break down polysaccharides into oligosaccharides ○ Nucleases: break down DNA into nucleotides Most digestion occurs extracellularly (GI tract lumen) Symbiotic organisms aid digestion in many animals (e.g. bacteria and fungi) ○ Enterosymbionts: in gut, live within lumen of GI tract ○ Exosymbionts: actively cultivated outside body ○ Endosymbionts: g row in interstitial spaces or within host cells Nutrient transport (across plasma membranes) ○ Some polar molecules require protein carriers ■ Facilitated diffusion: d own concentration gradient ■ Active transport: against concentration gradient (via N a+ dependent cotransporters) ○ Some nutrients transported via v esicles: ■ Uptake ● Pinocytosis: nutrients in solution ● Phagocytosis: particulate nutrients ■ Expulsion ● Exocytosis Carbohydrate breakdown and absorption ○ Maintenance of glucose levels is crucial ○ Polysaccharides (e.g. glycogen, starch) and disaccharides (e.g. sucrose, lactose) are broken down into monosaccharides (e.g. glucose) ○ Mouth: ■ Salivary amylase can digest glycogen/starch into oligosaccharides ○ Small intestine: ■ Pancreatic amylase can digest glycogen/oligosaccharides/starch into disaccharides (which then digested into monosaccharides such as glucose, which can be used as fuel) Carbohydrate Transport (absorbing glucose) ○ LOW glucose levels in gut lumen
Not many glucose transporters to absorb glucose, physically removed to ensure glucose is “trapped” within enterocyte (otherwise glucose would leave, going down its concentration gradient) ○ HIGH glucose levels in gut lumen ■ Transporters move to apical surface to absorb extra glucose Proteins are broken down into dipeptides and amino acids, which can then be absorbed by epithelial cells ○ Slide 20 Lipids are more difficult to digest/import because of their h ydrophobicity ○ GI tract secretes bile, which emulsifies large lipids into smaller droplets, which can then diffuse across cell membrane into epithelial cell ○ Lipids go through smooth ER for packaging, since lipophilic, they get a protein coat to ensure that lipid doesn’t diffuse into any cell in body when travelling through bloodstream ○ Lipids carried in blood as lipoprotein complexes ■
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Finding + Consuming Food ● ● ● ● ●
Digestion physiology matches chemical + physical nature of diet Animals detect food via sensory receptors (gustatory + olfactory) Simple animals (e.g. sponges ) ingest food by phagocytosis ○ Nutrients taken up directly Cnidaria have primitive gut, takes up bigger molecules which can digest via digestive enzymes, then absorb Teeth: many vertebrates have toothlike structures ○ Chewing breaks up food to smaller chunks to i ncrease surface area for digestive enzymes to more efficiently “attack” (digest) ○ Teeth shape reflects diet
Digestive Systems ●
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Surface area: ○ Nutrients hydrolyzed in GI tract lumen and taken up by epithelial cells lining the gut ○ Net uptake of nutrients is based on the surface area (i.e. exposed epithelial cells) ○ Increase surface area via: ■ Increasing gut length ■ Increasing surface “undulations”: circular folds, villi and microvilli Specialized compartments: increases efficiency of digestion ○ Functional specialization (pH, enzymes, types of cells) ○ Sphincters controls passage of food between compartments ○ Ruminants: modification in some mammals allowing to digest plant material (i.e. cellulose) Salivary glands: exocrine gland that secretes saliva, which contains enzymes to initiate digestion
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Stomach: c ontains columnar epithelial cells on surface ○ Tight junctions: prevent leakage across epithelium ○ Mucous neck cells: secrete mucous ○ Parietal cells: secrete HCl ○ Chief cells: secrete pepsin (protease) ○ Enteroendocrine cells: detect if food is in gut and secrete hormones into blood Intestines: most nutrients absorbed here Exocrine secretion into intestines ○ Bile: solution of digestive chemicals + liver waste products ■ Produced in liver ■ Stored in gallbladder ■ Contains: ● Phospholipids: aids in uptake of lipids ● Bile salts: emulsify salts ○ Pancreas s ecretes enzymes (e.g. proteases, amylase etc.) Activation of proenzymes ○ Pancreas secretes proenzymes into small intestine via pancreatic duct ○ Membrane-bound enterokinase i n small intestine activates trypsinogen to trypsin, which activates other proenzymes into the active enzymes (small intestine mucous walls ensure body doesn’t get digested) ○ Procarboxypeptidase -> carboxypeptidase ○ Trypsinogen -> trypsin ○ Chymotrypsinogen -> chymotrypsin
Lecture 24: Digestion 2 Regulation of Feeding + Digestion ● ●
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Nerve signals (e.g. CNS) and hormones control digestive functions Control of appetite ○ 3 gut hormones control appetite by binding hypothalamus receptors: ■ Leptin: secreted by white adipose tissue when lipid content is high ● suppresses a ppetite ■ Peptide YY (PYY): secreted by colon when full, ● suppresses a ppetite ■ Ghrelin: secreted by stomach when empty, ● stimulates appetite ○ Hypothalamic neurons release neurotransmitters in response to gut hormones ■ NPY STIMULATES appetite ■ POMC INHIBITS appetite Control of Secretions ○ Gastric: i ngestion + sight/taste/smell of food leads to secretion of enzymes for digestion (e.g. gastric acid + pepsinogen)
Intestinal: acidic gastric secretions produce VIP/secretin/CCK into bloodstream, which act on target organs (e.g. pancreas, liver, gallbladder), which secrete things that aid in digestion (e.g. HCO3-, bile and digestive enzymes) Control of gut motility ○ Smooth muscle contractions move food along GI tract (control via nerves + hormones) ○ Optimal speed: want to minimize amount of indigestible material in GI tract but also want to maximize time for digestion and assimilation (if too slow, wasting energy) ○ Myenteric plexus: nerve network between smooth muscle layers that controls gut motility (receives CNS signals) ■ Motor neurons and interneurons within nerve network are part of enteric system ○ Peristalsis: contractile waves that move food down GI tract, controlled by intrinsic myogenic activity (pacemaker cells) Control of smooth muscle motility ○ acetylcholine activates GPCR transduction pathway, leading to activation of calcium channels (in membrane AND in sarcoplasmic reticulum), resulting in increased intracellular calcium concentration ○ Increased calcium in muscle cell results in more activated cross bridges and more forceful contraction ○
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Metabolic Transitions Between Meals ● ●
Postprandial period: immediately after meal, nutrients absorbed into blood Hormones control postprandial levels of nutrients: ○ Pancreatic beta-cells secrete insulin to stimulate glucose uptake ○ Pancreatic alpha-cells secrete glucagon to stimulate glucose release by liver
Starvation Response ●
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Metabolism reorganization to ensure long-term survival: ○ Conserve glucose to protect glucose-dependent tissue ○ Muscle shifting to lipid metabolism ○ After lipid + glucose stores depleted, PROTEIN BREAKDOWN ACCELERATED ■ Amino acids converted to fatty acids + carbohydrates ○ Structural degradation occurs because no protein stores in body (have to degrade skeletal muscle, B AD) Early starvation: use glycogen stores early Late starvation: protein breakdown starts (once lipid + glucose stores depleted) ○ Muscle tissue breaks down, skeletal musculature degrades
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Digestive system degradation + rebuilding
Can reduce energetic costs in between meals E.g. pythons eat infrequently, digestive organ mass increases right after eating big meal, then gradually degrades, smooth muscle + nerves retained Dormancy: ○ Hypometabolism: metabolic rate decreased allowing animal to survive adverse conditions ■ Torpor: short sleeps ■ Hibernation: longer sleeps (e.g. bears) ■ Estivation: avoiding dry/hot climate to avoid dehydration (e.g. desert animals) ○ ○
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Lecture 25: Locomotion 1 ● ●
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Locomotion is the act of moving, integrates anatomy with physiological system (mode of locomotion is constrained by e nvironment) Invertebrates: move by crawling except arthropods ○ Simple muscles work with a fluid-filled internal chamber (hydrostatic skeleton, pressure on fluid provides structure) ○ Nematodes: muscle layers alternate contractions to produce undulations ○ Earthworm: peristaltic waves of contraction (muscle contractions alternate) Fish: muscles composed of homogenous fibre types (either red [slow] or white [fast]) Central pattern generator: area of CNS that controls timing of muscle contraction ○ Alternating sequence of motor neuron activation Tetrapods (and humans) have heterogenous fibre types within muscle fibres due to many complex movements (transition to land) Muscle activity requires lots of ATP energy, metabolic efficiency: ○ Glycolysis: 2 ATP per glucose ○ Aerobic metabolism: 36 ATP per glucose Oxidative phosphorylation: allows for steady-state activity ○ HIGH mitochondrial content in oxidative muscles Glycolysis: high-intensity activity ○ Uses large quantities of glucose and produces lactic acid, which results in muscle exhaustion (ion disturbances + pH imbalances) ○ Exhaustion recovery: must replenish energy stores (e.g. glycogen, ATP) AND reestablish ion gradients (Ca2+ distribution + pH) ○ Lactate produced by glycolysis is removed during recovery, converted back into glucose by liver (gluconeogenesis) Postexercise oxygen recovery: rates of oxygen consumption remain elevated even after exercise is done Metabolic Transitions During Exercise ○ Respiratory Quotient (RQ): the ratio of CO2 production to O2 consumption
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■ This can determine type of fuel being used for activity Metabolic Transitions During Migration ○ Initially S almon are FAT, energy expenditure is mostly from fat (conserve glycogen stores) ○ During migration, less fat is used, more p rotein is utilized as fuel (digest muscle) ○ Near end of migration, Salmon are SKINNY, glycogen is now used for spawning Metabolic transitions controlled by hormones Glucose main fuel for low-moderate activity (insulin/cortisol) During sustained activity, glycogen stores become depleted, triglycerides are mobilized and utilized Both glucose and fatty acids can be used as metabolic fuel sources Oxygen delivery to muscles important ○ Small animals can use diffusion (low metabolic rates) ○ Large animals use cardiovascular system (use blood to carry oxygen) Rate of oxygen delivery depends on ○ Capillary density ○ Blood flow (vascular tone) ○ Hemoglobin oxygen affinity Rate of O2 diffusion out of RBC depends on ○ Partial pressure gradient for Oxygen ○ Diffusion distance August Krogh Model of Capillary Geometry: capillaries flow straight ○ Problem: hypoxic regions (deprived of oxygen supply) Actual c apillary geometry ○ Capillary tortuousity: Capillaries are NOT straight tubes, actually weave back and forth in muscle to ensure no hypoxic regions Angiogenesis: synthesis of additional blood vessels ○ Triggered by persistent regional hypoxia ○ More capillaries increase perfusion (blood flow) Myoglobin: oxygen-binding heme protein in aerobic muscle, functions as oxygen storage and for oxyg...