Human Physiology, An Integrated Approach Test #4 Review PDF

Human Physiology, An Integrated Approach 8th Edition Test #4 Review Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Fig 19.1 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved F...

Human Physiology, An Integrated Approach 8th Edition Test #4 Review Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Fig 19.1 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 19.6(a) Glomerular Filtration Rate Filtration pressure depends on hydrostatic pressure, and is opposed by colloid osmotic pressure and capsule fluid GFR pressure. is determined by (a) Calculating glomerular filtration pressure Fil tratio n pressure Fil tratio n coefficien t PH –  – Pf luid = net filt ration pressure Fil tratio n pressure d epends 55 – 30 – 15 = 1 0mm Hg on hyd rostatic pressu re Effere nt and is opposed by colloi d art eriole osmot ic pre ssure and Slit surface Fil tratio n barr ier cap sul e fluid p ressur e are a per meabi lity Bo wm an’s capsule Glom erulus Afferent 15 mm Hg Pfluid art eriole 30 mm Hg  Net filt ration pre ssure = 10 mm Hg PH 55 mm Hg KEY PH = Hydrostatic pressure (bloo d pressure)  = Co lloid osm otic pressu re gra dient due to pro teins in plasma b ut not in B owman’s cap sul e Pf luid = Flu id pre ssure create d by fluid i n Bo wm an’s capsule Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Capillary Pressure Causes Filtration Glomerular Filtration Rate (GFR) – volume of fluid filtered per unit time – Influenced by ▪ Net filtration pressure – Renal blood flow and blood pressure ▪ Filtration coefficient – Surface areas of glomerular capillaries available for filtration – Permeability of filtration slits GFR is relatively constant (SBP 80-180 mm Hg) GFR is controlled primarily by regulating blood flow through the renal arterioles – Increased resistance in afferent arteriole, decreases GFR – Increased resistance in efferent arteriole, increases GFR – Decreased resistance in afferent arteriole, increases GFR – Decreased resistance in efferent arteriole, decreases GFR Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 19.6(c-e) Glomerular Filtration Rate (c) Resistance changes in renal arterioles alter renal blood flow and GFR. Bo wm an's capsule Effere nt art eriole Glom erular Glom erulus filtra tion r ate (GFR) Afferent arter iole Ar terial resistance Re nal bl ood flow (RB F) Flo w to oth er org ans (d) Vasoconstriction of the afferent arteriole increases (e) Increased resistance of efferent arteriole decreases resistance and decreases renal blood flow, capillary renal blood flow but increases PH and GFR. blood pressure (PH), and GFR. Increa sed PH Increa sed resistance De creased c apilla ry in effere nt art eriole blo od pre ssure ( PH) Increa sed GFR De creased GFR Increa sed resistance De creased R BF in affere nt art eriole De creased R BF Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 19.5 Reabsorption Reabsorption may be active or passive Transepithelial transport (transcellular transport) – Substances cross apical and basolateral membranes of the tubule epithelial cells Paracellular pathway – Substances pass through the cell–cell junction between two adjacent cells Active transport of Na+ – Creates electrical gradient – Anions follow Na+ creates osmotic gradient – H2O follows leaving behind higher concentration of cations – Cations follow down concentration gradients – Exchangers (NHE) and pumps (Na +-K+-ATPase) Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 19.8(a) Reabsorption- driven by sodium (a) Principles Governing the Tubular Reabsorption of Solutes Some solutes and water move into and then out of epithelial cells (transcellular or epithelial transport); other solutes move through junctions between epithelial cells (the paracellular pathway). Membrane transporters are not shown in this illustration. Tubule lumen Tubular Extracellular epithelium fluid 1 Na+ is reabsorbed by active transport. Na+ 2 Electrochemical gradient drives anion Anions reabsorption. Filtrate is similar to 3 Water moves by osmosis, following interstitial H2O solute reabsorption. Concentrations of fluid. other solutes increase as fluid volume in lumen decreases. K+, Ca2+ , 4 Permeable solutes are reabsorbed by urea diffusion through membrane transporters or by the paracellular pathway. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Reabsorption May Be Active or Passive Secondary active transport: symport with Na+ – Moves glucose, amino acids, and other organic molecules with sodium – Some transporters use H+ instead of Na+ Passive reabsorption: urea – Moves by diffusion following gradients created by Na+ active transport, etc. Endocytosis: plasma proteins – Receptor-mediated endocytosis – Digested by lysosomes – Amino acids returned to circulation Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Renal Transport Can Reach Saturation Saturation – maximum rate of transport that occurs when all carriers are occupied by (are saturated with) substrate Transport maximum (Tm) – the transport rate at saturation Renal threshold – the plasma concentration at which a substance first appears in the urine – Example: glucose ▪ Glucosuria or glycosuria – glucose in urine Peritubular capillary pressures favor reabsorption Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Fig 19.10 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Fig 19.10 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 19.6 Secretion Active movement of molecules from extracellular fluid into nephron lumen Important in homeostatic regulation: K+ and H+ Increasing secretion increases nephron excretion Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 19.7 Excretion Excretion = filtration – reabsorption + secretion Renal handling Clearance is a noninvasive way to measure GFR – Rate at which a solute disappears from the body by excretion or by metabolism ▪ Clearance of X = excretion rate of X (mg/min) / [X] plasma (mg/ml plasma) ▪ Expressed as volume of plasma (ml plasma/min) cleared of substance – Not how much X has been excreted Inulin and creatinine are used to measure GFR – Inulin, plant polysaccharide, freely filters, but is neither reabsorbed or secreted – Creatinine is breakdown product of phosphocreatine ▪ Production and breakdown is relatively constant ▪ Some secretion in urine so not 100% accurate Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Fig 19.14 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 20.1 Integrated responses to changes in blood volume and pressure Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 20.4 Osmolarity changes as fluid flows through the nephron Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 20.5(c) Vasopressin increases collecting duct permeability to water Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 20.6 Vasopressin Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved The Renin-Angiotensin Pathway Renin-angiotensin system (RAS) – Juxtaglomerular cells secrete the enzyme renin if blood pressure decreases – Renin converts angiotensinogen to angiotensin I – Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II – Stimuli 1. Granular cells are sensitive to blood pressure 2. Sympathetic stimulation form cardiovascular center 3. Paracrine feedback from macula densa cells Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 20.9(a) Aldosterone Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 20.10 (RAS) Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 20.11 Natriuretic Peptides Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 20.12 Disturbances in volume and osmolarity Osmolarity Decrease No change Increase Drinking Ingestion of Ingestion of Increase large amount isotonic hypertonic of water saline saline Volume Replacement Eating salt of sweat loss Normal without No change volume and with plain drinking water osmolarity water Incomplete Dehydration Decrease compensation Hemorrhage (e.g., sweat for dehydration loss or diarrhea) Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved pH Homeostasis Depends on Buffers, Lungs, and Kidneys Buffers systems include proteins, phosphate ions, and HCO3- – Moderate changes in pH by combining with or releasing H+ – Henderson-Hasselbalch equation Ventilation can compensate for pH disturbances – Corrects 75% of disturbances; can also cause them – Hypoventilation – Hyperventilation – Ventilation reflexes Kidneys use ammonia and phosphate buffers Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Figure 20.18 Intercalated cells function in acid-base disturbances (b) Alkalosis. Type B intercalated cells in collecting (a) Acidosis. Type A intercalated cells in duct function in alkalosis. HCO 3_ and K+ are collecting duct function in acidosis. H + is excreted; H+ is reabsorbed. excreted; HCO3_ and K+ are reabsorbed. Lumen of Type A Interstitial Lumen of Type B Interstitial collecting intercalated cell fluid collecting duct intercalated cell fluid duct [H+] high [H+] low H2O + CO 2 CO2 HCO 3_ + H+ H2O + CO2 Filtered K+ CA CA H+ + HCO3 _ HCO 3_ HCO 3 _ HCO3_ + H+ H+ ATP ATP acts as a – H+ Cl– buffer to Cl [H+] H+ ATP H+ K+ K+ ATP K+ High [K+] K+ reabsorbed H+ HCO3_ K+ excreted excreted in urine in urine Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Questions on Renal? Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 21.9(a) Gastric Secretions Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved The Pancreas Secretes Enzymes and Bicarbonate Endocrine portion (islets) – Secretes insulin and glucagon Exocrine portion – Secretes digestive enzymes (acini) and sodium bicarbonate (duct cells) – Enzyme secretion ▪ Brush border enteropeptidase converts trypsinogen to trypsin – Bicarbonate secretion ▪ Neutralizes gastric acid Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Figure 21.16(d) Digestion and Absorption: of Fats (d) Fat digestion and absorption Bile salts recycle Bile Lacteal Lymph to salts vena cava 3b 4 Cholesterol + triglycerides + protein Micelles Golgi 5 Capillary 2 Chylomicron apparatus 1 Emulsion Smooth Large fat ER droplets from stomach 3a Cells of small intestine Interstitial Lumen of small intestine fluid 1 Bile salts 2 Pancreatic lipase and 3a Monoglycerides and 3b Cholesterol is 4 Absorbed fats combine 5 Chylomicrons from liver colipase break down fats fatty acids move out transported with cholesterol and are removed by coat fat into monoglycerides and of micelles and enter into cells. proteins in the intestinal the lymphatic droplets. fatty acids stored in micelles. cells by diffusion. cells to form chylomicrons. system. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Carbohydrates Maltose Sucrose Lactose Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Figure 21.17 Digestion and Absorption of Carbohydrates Most carbohydrates in our diets are disaccharides and complex carbohydrates. Cellulose is not digestible. All other carbohydrates must be digested to monosaccharides before they can be absorbed. (a) Carbohydrates break down into monosaccharides. (b) Carbohydrate absorption in the small intestine Glucose Polymers Lumen of intestine Starch, glycogen Glucose or galactose Fructose enters Na+ Glucose enters with on GLUT5 and Na+ on SGLT and exits on GLUT2. Disaccharides Amylase exits on GLUT2. Maltose Sucrose Lactose Na+ Maltase Sucrase Lactase K+ Intestinal KEY mucosa ry 2 glucose 1 glucose + 1 glucose + illa SGLT 1 fructose 1 galactose p GLUT2 Ca Monosaccharides GLUT5 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 21.18 Digestion and Absorption of Proteins (a) Pr oteins ar e chai ns of amino acids. (c) Pe ptide absorptio n After digestion, proteins are absorbed mostly as free amino acids. Amino- Amino Peptide Carboxy- A few di- and tripeptides are absorbed. Some peptides larger than terminal end acids bonds terminal end tripeptides can be absorbed by transcytosis. H2 N COOH Proteins (b) En zym es fo r prot ein di gestion Endopeptidases include Peptides Endopeptidase pepsin in the stomach, and digests internal trypsin and chymotrypsin peptide bonds. in the small intestine. +H2 O Di- and tripeptides Amino acids Small peptides cotransport with H+ cotransport are carried intact on PepT1. with Na+. across the cell H2 N COOH by transcytosis. H+ H+ 2 smaller peptides H2 N COOH H2 N COOH Na+ Na+ Exopeptidases digest terminal peptide Peptidases bonds to release amino acids. Aminopeptidase Carboxypeptidase K+ +H2 O +H2 O ATP H2 N COOH H+ Na+ Na+ Amino acid Peptide Amino acid H2 N COOH H2 N COOH H2 N COOH Blood To the liver Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Energy Is Stored in Fat and Glycogen Glycogen (glucose polymer) – Stored in liver and skeletal muscles Fat is compact storage – Fats have more than twice the energy content of an equal amount of carbohydrate or protein – Energy in fats is harder and slower to access – Carbs and proteins vs alcohol vs fats Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 22.3 Metabolism Anabolic pathways synthesize larger molecules from smaller ones – Fed state, or absorptive state Catabolic pathways break large molecules into smaller ones – Fasted state, or postabsorptive state Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 22.5 Fasted-State Metabolism Glycogen converts to glucose – Glycogenolysis Proteins can be used to make ATP – Deamination of amino acids ▪ Ammonia (byproduct) converted to urea Lipids store more energy than glucose or protein – Lipids broken down through lipolysis – Glycerol feeds into glycolysis – Fatty acids undergo beta-oxidation (-oxidation) to produce acetyl CoA – Excess acetyl CoA become ketone bodies (ketones or keto acids) ▪ Strong metabolic acids lead to ketoacidosis Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 22.12 Lipolysis Triglycerides can be metabolized for ATP production. 1 Lipases digest Triglyceride Glucose triglycerides into glycerol and 3 fatty acids. 1 G L Y Glycerol 2 2 Glycerol becomes a C glycolysis substrate. O L Y O S C I S HO Fatty acid Pyruvate Cytosol 3 -oxidation chops 2-carbon acyl units 3 off the fatty acids. CO2 Acetyl CoA 4 Acyl units become Acyl unit CoA acetyl CoA and can be used in the 4 citric acid cycle. CoA CITRI C ACI D CYCLE Mitochondrial matrix Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 22.15 Insulin in the fed state Eat a meal Distension Presence KEY Nutrient digestion of GI tract of carbohydrates and absorption wall in GI lumen Stimulus Sensor Input signal Stretch Integrating center receptors Plasma Plasma Endocrine amino glucose Output signal cells of small acids Target intestine Sensory – Tissue response neuron input Systemic response  cells of pancreas GLP-1 and GIP CNS Parasympathetic *  Cells output of pancreas Insulin Liver Muscle, adipose, and other cells Glucose Glycolysis transport Glycogenesis Lipogenesis Protein synthesis Plasma Negative glucose feedback Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 22.18 Endocrine response to hypoglycemia Gluca gon he lps main tain a dequat e plasma gluco se levels by pro motin g glycog enolysis and gluco neogen esi s. Plasma glu cose – + – Plasma  Ce lls  Ce lls am ino ac ids of pan creas of pan creas Gluca gon Insulin Lac tate, pyruvate, Liver Muscle, am ino ac ids adi pose, and oth er cel ls Fat ty acids Prolon ged hypogl ycemia Glycogen olysis Gluco neogen esi s Keton es Negat ive Plasma For use by brai n and glu cose per iphera l tissues feedba ck Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 22.17(a-b) Glucose transport in fed and fasted states FASTED STATE FED STATE Adipose and Resting Skeletal Muscle (a) In the absence of insulin, there are no GLUT4 transporters (b) In the fed state, insulin signals the cell to insert GLUT4 in the membrane. transporters into the membrane, allowing glucose to enter cell. Extracellular fluid Glucose Glucose 1 Insulin binds to receptor Insulin receptor 4 Glucose 3 Exocytosis enters cell Adipose or 2 Signal muscle cell Secretory transduction vesicle cascade GLUT4 transport protein GLUT4 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 22.17(c-d) Glucose transport in fed and fasted states FASTED STATE FED STATE Liver Hepatocytes (c) In the fasted state, the hepatocyte makes glucose and (d) In the fed state, the glucose concentration gradient reverses, transports it out into the blood, using GLUT2 transporters. and glucose enters the hepatocyte. ECF Insulin Glucose high Glucose low GLUT2 Low insulin GLUT2 Glucose low Glucose high ATP Signal cascade ADP Glycogen stores and gluconeogenesis P Hepatocyte Hexokinase-mediated conversion of glucose to glucose 6-phosphate keeps intracellular [glucose] low. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Diabetes Mellitus Is a Family of Diseases Diabetes mellitus (DM) - abnormally elevated plasma glucose concentrations or hyperglycemia Complications of diabetes affect blood vessels, eyes, kidneys, and nervous system Type 1 diabetes mellitus - insulin deficiency from autoimmune destruction of beta cells Type 2 diabetes mellitus - insulin-resistant diabetes Diagnosing diabetes – Blood glucose after 8 hrs fasting ▪ Prediabetes: 100 – 125 mg/dL or Diabetes: >125 mg/dL – Glucose tolerance test (after 2 hrs) ▪ Prediabetes: 140 – 199 mg/dL or Diabetes: >200 mg/dL Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 22.20 Acute pathophysiology of type 1 diabetes mellitus Untreated type 1 diabetes is marked by tissue breakdown, glucosuria, polyuria, polydipsia, polyphagia, and metabolic ketoacidosis. FAT METABOLISM GLUCOSE METABOLISM PROTEIN METABOLISM Me al a bso rb ed Plas ma Plas ma Plas ma fa tty a cid s a mino ac id s g lu co se No insulin released G lu co se up tak e Am in o a cid Pro te in F at F at G lu co se utilizat ion u pta ke by (mu sc le an d a dip ose ) b rea kd own , b rea kd own st or ag e mo st c ells e spe cia lly mus cle L iv er Plas ma Plas ma fa tty a cid s K eto ne G ly co ge no lysis a mino ac id s Br ain in ter pr ets p rod uc tio n G lu co ne og en es is a s sta rv atio n Sub st rat e Sub st rat e fo r fo r ATP ATP pr od uc tion p rod uc tio n H ype rg lyce mia Poly ph ag ia Tissu e Tissu e los s METABOLIC ACIDOSIS DEHYDRATION los s Exc ee ds ren al th re sh old fo r glu co se K eto ac ido sis G lu co su ria O smo larit y O smo tic d iure sis a nd p oly uria Ve nt ila tion Me tab olic a cido sis Thir st Poly dips ia U rine De hy dra tio n a cidific atio n ADH se cre tio n a nd h ype rk ale mia Blo od v olu me At tem pt ed c om pe ns atio n L ac tic a cid a nd b y ca rd io va sc ular p rod uc tio n Blo od p re ssu re c on tro l c en ter An ae ro bic Circ ula to ry If co mp en sa tion me ta bo lis m fa ilu re fa ils Co ma o r d ea th Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Good luck with your test! It has been my pleasure teaching and interacting with you this year. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved