Biology 6 Test 3 Study Guide

Biology 5 Test 4 Study Guide

Chapter 19 – Urine Formation and Excretion

A. Kidneys a. General functions of the kidneys: fluid volume and pressure regulation, ion and pH balance, excretion, hormone production b. Kidneys  ureters  bladder  urethra (Fig. 19-1) c. Kidneys i. Function 1. Filters wastes from blood 2. Secretes blood hormones ii. Structure 1. Renal medulla makes up central portions 2. Renal cortex makes up outer portions. Origination of functional units called nephrons 3. Renal artery and vein transports blood to and from the kidney 4. Nephrons (Fig. 19-2) a. Ducts: glomerular (Bowman’s)capsule  proximal tubule  loop of Henle  distal tubule  collecting duct b. Kidney stones are mineralized deposits usually in the collecting ducts c. Blood supply: afferent arteriole  glomerulus  efferent arteriole  peritubular capillary system B. Urine Formation a. Urine formation and excretion = Glomerular filtration – tubular reabsorption + tubular secretion. (Fig. 19-3) b. Glomerular filtration i. Plasma flows from capillary through basal lamina through slits between podocytes. (Fig. 19-5) ii. Hydrostatic pressure in capillaries is greater than hydrostatic and osmotic pressure from glomerular capsule so fluid moves into it. (Fig. 19-6) iii. Regulation 1. Autoregulation a. GFR (glomerular filtration rate) is kept constant by myogenic response. Vasoconstriction and dilation of afferent arterioles give constant GFR (Fig. 19-8) b. Feedback from tubular flow can vasoconstrict afferent arterioles (Fig. 19-10) 2. Distal control a. Sympathetic nerves have tonic control over both afferent and efferent arterioles. b. Hormones can cause vasodilation and constriction (e.g. prostaglandins, angiotensin II) or change the size of slits between podocytes. c. Tubular reabsorption (Fig. 19-11) i. Transport of substances 1. Active a. Sodium is pumped into interstitial fluid by Na-K ATPase (Fig. 19-12) b. Na-glucose cotransporters are used too. (Fig. 19-13) c. Transcytosis of large proteins 2. Passive a. Diffusion of substances down their concentration gradients, including osmosis 3. Bulk flow – peritubular pressure is higher than interstitial pressure ii. Saturation – there is a maximum rate that a substance can move. This gives maximum reabsorption rate (Fig. 19-14) d. Tubular secretion i. Involves active transport. Substances such as hydrogen ion and potassium are pumped into the renal tubule e. Excretion i. Excretion measures the composition of the fluid being eliminated. ii. Clearance tells you the rate at which a substance is being eliminated. This is a better measure of renal efficiency. (Fig. 19-17) C. Urine Elimination a. Bladder structure (Fig.19-18) i. Inner wall is folded and can allow for expansion ii. Stretch receptors detect expansion and are sensory neurons iii. Parasympathetic neurons from micturition reflex control smooth muscle of the bladder. Motor neuron controls external sphincter b. Micturition i. Bladder at rest has motor neuron contracting external sphincter. ii. As bladder fills and stretches, receptors signal to micturition reflex center. This increases parasympathetic stimulation and decreases motor stimulation. iii. This causes smooth muscle contractions of bladder, leading to sense of urgency, and relaxation of external sphincter, allowing urination. iv. Reflex, especially motor neuron to sphincter muscle is under voluntary control so urination can be controlled.

Chapter Problems: 4-8, 10, 12, 14, 16abd, 17-21, 24-26

Chapter 20 – Water Balance

A. Fluid Balance a. Distribution i. Intracellular – inside cells (63% of fluids here). ii. Extracellular – outside cells (37% here). iii. Forces that allow movement (Fig. 20-1) 1. Osmotic pressure changes blood volume 2. Hydrostatic (blood) pressure b. Water i. Overall balance (Fig. 20-2) 1. Intake by drinking, eating, and metabolism 2. Output by urine, evaporation, feces. ii. Control by Kidneys (Fig. 20-4) 1. Water can be reabsorbed in parts of the nephron, such as loop of Henle, distal tubule, and collecting duct. Most of the control is at the collecting duct. 2. Role of vasopressin (antidiuretic hormone) a. Makes collecting duct more permeable to water. This makes your body gain water and makes urine more concentrated (Fig. 20-5) b. Vasopressin signals the production of aquaporins (Fig. 20-6) c. Vasopressin stimulation (Fig. 20-7) i. High plasma osmolarity – sensed by hypothalamic osmoreceptors (Fig. 20-7) ii. Low blood pressure – sensed by stretch receptors in atria iii. Low blood volume – sensed by baroreceptors in carotid artery and aorta. 3. Role of loop of Henle (Fig. 20-10) a. As water descends loop of Henle, it moves out due to high Osm in interstitial fluid. This is picked up by capillaries (vasa recta) b. As fluid ascends loop of Henle, solutes are pumped out, but water is not, so urine becomes diluted. iii. Water imbalances 1. Dehydration a. Output exceeds intake b. Symptoms are dry skin, mucous membranes, mouth. Can lead to hyperthermia. Affects older and younger people more. 2. Water intoxication a. Intake greatly exceeds output. b. Coma can result from swelling in the brain. B. Electrolyte Balance a. Sodium and potassium i. Vasopressin secretion and thirst reflex with high Na (Fig. 20-11) ii. Aldosterone 1. A steroid hormone synthesized in adrenal cortex 2. Enters principal cells in distal tubule and collecting duct. Triggers production of Na channels and pumps that retain Na and pump out K. (Fig. 20-12) iii. Renin 1. Low blood pressure triggers granular cells in kidney to produce renin 2. Renin activates angiotensin. Angiotensin is a vasoconstrictor, but also increases thirst and vasopressin production. (Fig. 20-13) b. Imbalances i. Sodium 1. Hyponatremia – low sodium concentration. Caused by prolonged sweating, vomiting, diarrhea, adrenal disease (low aldosterone), water intoxication. Results in swelling in the brain. 2. Hypernatremia – high sodium concentration. Caused by fever, diabetes. Results in CNS problems. ii. Potassium 1. Hypokalemia – low potassium. Caused by excess aldosterone production, diuretic drugs, kidney problems. Results in muscle weakness, paralysis, respiratory and circulatory problems. 2. Hyperkalemia – high potassium. Caused by similar conditions to hyponatremia. Results in circulatory and respiratory problems. C. Acid-Base Balance a. + - H2O  H + OH b. Sources of Hydrogen Ions (Fig. 20-18) i. Carbonic acid from respiration ii. Lactic acid from fermentation iii. Acids from lipid, protein, and nucleic acid breakdown c. Buffers i. Regulate pH by accepting/releasing hydrogen ions ii. Examples + - 1. Bicarbonate buffer: H + HCO3 ↔ H2CO3 + 2- - 2. Phosphate buffer: H + HPO4 ↔ H2PO4 d. Medullary Respiratory Center i. Regulates hydrogen ion by controlling breathing rate. Acts when buffers are overworked + - ii. Affects bicarbonate buffer reactions: H + HCO3 ↔ H2CO3 ↔ H2O + CO2 e. Kidneys (Fig. 20-20) i. Proximal tubule compensates for acidosis (Fig. 20-21) + - 1. H is secreted while HCO3 is reabsorbed. + - 2. Glutamine is broken down to NH4 and is secreted while HCO3 is absorbed. ii. Collecting duct can compensate for acidosis and alkalosis (Fig. 20-22) f. Imbalances i. Acidosis 1. Respiratory acidosis – when ventilation is hindered. E.g. obstruction of airways, decreased breathing. Results in CNS depression. 2. Metabolic acidosis – due to non-respiratory byproducts. E.g. kidney failure, diabetes. ii. Alkalosis 1. Respiratory alkalosis – due to hyperventilation. Caused by anxiety, poisoning, high altitude, fever. Results in overstimulation of nerves. 2. Metabolic alkalosis – loss of gastric juices by vomiting or antacids or other drugs.

Chapter Problems: 1-8, 11-17, 19, 20, 23c-e, 24-28, 30

Chapter 24 – Immunity

A. Cells of the Immune System a. Cell types (Fig. 24-4) i. Granulocytes – have granules. Some release chemicals, others are phagocytic ii. Agranulocytes – no granules. Some release chemicals, others are phagocytic, lymphocytes are used in specific defense. b. Phagocytosis i. Steps: chemotaxis, adherence, ingestion, digestion, excretion. ii. Some will hold on to antigens to activate specific defenses. These are antigen- presenting cells (Fig. 24-5) B. Innate Immunity a. Barriers i. Skin – dead cells forming a protective barrier ii. Mucous membranes – lining of digestive, urinary, and respiratory systems 1. Secretions: enzymes, acid etc. to kill pathogens 2. Mucus: traps organisms and is moved to the stomach or out the nose. Moved by ciliary action. b. White blood cells i. Phagocytes eat pathogens ii. Natural Killer Cells kill our own cells that are infected c. Inflammatory Response i. Caused by direct damage to tissue. Symptoms include swelling, redness, pain. ii. Mechanism 1. Damaged tissue releases chemicals that lead to vasodilation and leaky vessels. E.g. histamine released by mast cells in connective tissue. 2. White blood cells migrate to site of damage by squeezing vessels. Some cells fight infection, platelets help clot broken vessels. 3. Abscess forms with pus from concentration of cells and debris. 4. Repair – scab forms. Epidermis regenerates. Scar tissue replaces irreplaceable cells. d. Fever – raising of body temperature i. Reduces growth rate of pathogen ii. Stimulates phagocytes. iii. Stimulates interferon, proteins that prepare other body cells against attack by pathogens e. Complement System i. Components – made of proteins that activate and work with one another. Activation through cascades. ii. Pathways of action 1. Opsonization – enhancement of phagocytosis by coating bacteria. 2. Inflammation – stimulates mast cell release of histamine and a chemoattractant for macrophages. 3. Cytolysis – membrane attack complex (MAC) forms and creates pores in membrane of pathogen. (Fig. 24-8) C. Adaptive Immunity a. Overview i. Three steps: recognize, destroy, remember ii. Two systems: humoral (B-cell mediated) and cell-mediated (T-cell mediated). Lymphocytes are made in red bone marrow and stored in lymph nodes. iii. Antigen: a foreign molecule that is part of the pathogen and that the immune system recognizes. Usually a carbohydrate or protein. iv. Antibodies 1. Produced by plasma B-cells and recognize specific antigens. 2. Each B-cell makes one kind of antibody. Every newly formed B-cell will make a different kind (out of 100s million types). This gives the immune system the ability to recognize almost any antigen. 3. Y shaped (Fig. 24-12) a. Made of two heavy and two light chains. Each has a constant (C) and variable (V) region. b. V regions make up the antigen binding sites. c. Fc domain is stem formed from heavy C regions d. 5 Classes – IgG, M, A, D, E 4. Functions (Fig. 24-13) a. Opsonization – coats pathogen for better phagocytic recognition. b. Agglutination – clumping of pathogen. Eases phagocytosis of small sized objects. c. Neutralization – surrounds pathogen or toxin preventing it from attaching or entering cell. d. Complement – activates complement proteins. e. Inflammation – complement will induce inflammation. f. Cytotoxicity – coated pathogen will be recognized by cytotoxic lymphocytes. b. Humoral Immunity i. Clonal Selection (Fig. 24-10) 1. 108 antibodies. Each B cell makes one type of antibody. Binding of an antigen to the one cell that has the correct antibody. Makes it divide. 2. Activated B cell will produce memory and plasma cells. 3. Memory cells remain in body for a long time in case of subsequent exposure to antigen. 4. Plasma cells produce antibodies (2000/sec) ii. Immune Response (Fig. 24-11) 1. Initial exposure triggers primary response. May not me protective. 2. Second exposure triggers stronger secondary response. Usually more protective. c. Cell-Mediated Immunity i. Communication 1. Cell-cell contact via receptors. E.g. CD4 and CD8 receptors. 2. Chemicals – uses cytokines ii. Clonal selection – a T cell will become activated by being bound by an antigen presenting cell and differentiate into the cell types below. (Fig. 24-15) 1. Helper – produce cytokines and bind other cell types 2. Cytotoxic – destroys cells on contact. Binds to cells with MHC presenting antigen. 3. Memory – long-lived. d. Vaccination (Fig. 14.16) i. Tricks the immune system into an immune response. This makes it easier to fight an infection on secondary response. ii. Mothers’ milk contains antibodies to help baby fight infections. This is passive immunity and does not stimulate an immune response. e. Immune Dysfunction i. Overactive: 1. Allergies: an immune response against a harmless antigen. Histamine is often involved. (Fig. 24-19) 2. Transplant rejection: foreign tissues are rejected because they contain nonself antigens. 3. Autoimmune diseases: when the immune system attacks own body. E.g. multiple sclerosis (neural), rheumatism (joints), Lupus (DNA). ii. Underactive: bubble-boy David Vetter was missing B cells and T cells D. HIV and AIDS a. HIV (Human immunodeficiency virus) i. Retrovirus that attacks CD4 Helper T cells. ii. Life cycle involves insertion of the virus into the host cell’s DNA. b. AIDS epidemiology i. 33 million infected, 25 million dead. Transmission by bodily fluids only. ii. Stages of disease 1. Acute phase – initial infection launches immune response. Flu-like symptoms that pass in a few weeks. 2. Asymptomatic phase – prophage produces very little viral particles 3. AIDS – immune system depressed. High viral titer. Opportunistic infections usually causes death. c. Avoiding the immune response i. Latent infection (asymptomatic phase)- very little or no RNA and protein made. ii. High mutation rate- reverse transcriptase is very error-prone. iii. Immune suppression- infects the immune system itself. d. Therapies (show movie again) i. Many drugs (AZT, protease inhibitors) block specific parts of the HIV life cycle. ii. Cocktails (combination of drugs) work the best iii. Vaccine – problem of developing because of high mutation rate of HIV.