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Exam 3 Bio 207
| Question | Answer |
|---|---|
| what is innate immunity | it is Inherited. Serves as a first line of defense against pathogens. Examples: epithelial membranes, high acidity in stomach, cells that can engulf/kill pathogens, fever |
| what is PAMPS (pathogen-associated molecular patterns) | Cells distinguish “self” from “nonself” using unique to the pathogens. Immune cells have toll-like receptors for PAMPs on their surface. So far, 10 distinct toll-like receptors have been identified. |
| PAMPS continued | These cells respond by secreting cytokines to recruit more immune cells or activate specific immune cells. |
| Phagocytosis | Three types of phagocytic cells: Neutrophils are the first to arrive at an infection. Mononuclear phagocytic cells (monocytes in the blood and macrophages in the tissues) arrive later. |
| phagocytosis continued | There are organ-specific phagocytes in the liver, spleen, lymph nodes, lungs, and brain. Some of these, called fixed phagocytes, are immobile in the walls of these organs. |
| phagocytosis | Neutrophils and monocytes squeeze through gaps in venule walls to enter tissue in a process called extravasation or diapedsis. Attracted to site by cytokines. |
| Phagocytosis | The pathogen becomes engulfed by pseudopods. The vacuole containing the pathogen fuses with a lysosome. The pathogen is digested. |
| Fever | Regulated by hypothalamus. A chemical called an endogenous pyrogen sets the body temperature higher.1.Produced as a cytokine by leukocytes. |
| Fever | 2.Toxins from some bacteria stimulate leukocytes to produce these cytokines.3.Along with fever, they also induce sleepiness and a fall in plasma iron concentration (which limits bacterial activity) |
| Interferons | Antiviral polypeptides produced by infected cells. Three types identified:Alpha, beta ,gamma. New antiviral drugs are being developed using interferons. |
| Adaptive Immunity | The acquired ability to defend against specific pathogens after exposure to these pathogens. Mediated by antigens and antibodies. |
| Antigens | Cell surface molecules that stimulate the production of specific antibodies. Foreign antigens illicit an immune response. The immune system can distinguish “self” from “nonself.” |
| Antigens | Antibodies bind to their specific antigens. Large molecules can have several antigenic determinant sites that stimulate the production of and binding to and antibodies |
| Haptens | Smaller, nonantigenic molecules that can become antigens when bound to other proteins. These are useful for creating antigens for research and diagnosis. |
| Immunoassays | Tests that use specific antibodies to identify specific antigens. Binding causes agglutination, which can be seen. Used to determine blood type and detect pregnancy. |
| Lymphocytes | Derived from stem cells in the bone marrow.These stem cells seed the thymus, spleen, and lymph nodes.The thymus is the site of new T lymphocytes through late childhood. |
| Lymphocytes | It degenerates in adulthood, and new T lymphocytes are made through mitosis in secondary lymphoid organs. The bone marrow and thymus are considered primary lymphoid organs. |
| T Lymphocytes | Lymphocytes that seed the thymus become T lymphocytes. These then seed the blood, lymph nodes, and spleen. T lymphocytes attack host cells that have become infected with a virus or fungus, transplanted human cells, and cancer cells. |
| T Lymphocytes | T lymphocytes do not produce antibodies. They must be in close proximity to the victim cell in order to destroy it. This is called cell-mediated immunity |
| B Lymphocytes | Lymphocytes that come directly from bone marrow to seed other organs (not the thymus) are called B lymphocytes. They combat bacterial and some viral infections. |
| B Lymphocytes | They secrete antibodies into blood and lymph so can be far from the victim. This is called humoral immunity or antibody-mediated immunity. |
| Chemotaxis | movement toward chemical attractants |
| Memory cells | these are visually indistinguishable from the original call and are important in active immunity |
| Plasma cells | are protein factories that produce about 2,000 antibody protiens per second |
| Mast cells | are found in most tissues but are especially concentrated in the skin. bronchioles abd intestinal mucosa |
| Local Inflammation | Occurs when bacteria enter a break in the skin. Initiated by nonspecific mechanisms of phagocytosis by toll-like receptors. Macrophages and mast cells release cytokines to attract phagocytic neutrophils. |
| local inflammation | Complement proteins are activated, which also attract phagocytic cells. As inflammation progresses, B lymphocytes produce antibodies against bacterial antigens. |
| local inflammation | Formation of antigen-antibody complexes amplifies nonspecific response, a process called opsinization. |
| local inflammation | More phagocytic cells arrive via extravasation from nearby venules. T lymphocytes are the last to arrive. Neutrophils may spill protein-digesting enzymes into the surrounding tissues, causing pus. |
| local inflammation | Mast cells secrete heparin, histamine, prostaglandins, leukotrienes, cytokines, and TNF-α. These produce warmth, swelling, and pain (classic symptoms). They also recruit more leukocytes |
| Antibodies. | Also known as immunoglobulins. Five classes: IgG, IgA, IgM, IgD, and IgE Y-shaped. 2 long, heavy (H) chains joined by 2 shorter, light (L) chains The bottom (Fc) is constant across different antibodies |
| Antibodies (continued) | whereas the top (Fab) varies and allows antigen specificity. Everyone has 1020 antibody molecules. There are a few million different specificities. There should be an antibody for every antigen you might encounter |
| Antibodies extra fact: these genes mutate easily, making more combinations. | There are so many because: A large percentage of our genetic code is dedicated to making antibodies. Some genes code for light chains and some for heavy chains, and then these are combined in different ways to get even more. |
| The complement system | Complement is a group of plasma proteins activated by the binding of antibodies to antigens |
| How the complement system works | Part of the nonspecific defense system Activity is triggered by binding of antibodies to antigens (classic pathway) and by polysaccharides on bacterial membranes (alternative pathway). |
| How the complement system works | Binding of antibodies to antigens does not destroy the pathogen. This labels targets for attack by phagocytic cells and stimulates opsonization. Proteins are designated C1−C9. C1 serves as a recognition protein. C2, C3, and C4 serve as activators. |
| How the complement system works | C5−C9 attack by attaching to a cell membrane and destroying it. Classic pathway: more rapid and efficient; involves antibodies binding to antigens 1. IgG and IgM activate C1, which splits C4 into two fragments, C4a and C4b. |
| How the complement system works | 2. C4b binds to the cell membrane and becomes active, splitting C2 into C2a and C2b. 3. C2a attaches to C4b and cleaves C3 into C3a and C3b. 4. C3b converts C5 into C5a and C5b. |
| How the complement system works | 5. C5b and C6−C9 are inserted into the bacterial cell membrane, forming the membrane attack complex. 6. This creates a large pore in the membrane, causing influx of water into the cell = lysis. |
| Cytotoxic T Lymphocytes | Destroy body cells that harbor foreign antigens Usually from a pathogen (virus or fungus), but can be due to a malignancy (cancer) Cell-mediated destruction means the T cells must touch the target victim. |
| Cytotoxic T Lymphocytes | Secrete perforins to create large pore in cell Secrete granzymes to trigger apoptosis in cell |
| Helper T Lymphocytes | Improve ability of B lymphocytes to become plasma cells and enhance ability of cytotoxic T cells to kill targets Secretion of lymphokines |
| Regulatory T Lymphocytes | Inhibit response of B lymphocytes and cytotoxic T lymphocytes Previously called suppressor T lymphocytes People with genetic deficiencies in regulatory T lymphocyte production may develop autoimmune diseases and allergies. |
| Lymphokines | Cytokines specific to lymphocytes Many stimulate B cell or cytotoxic T cell activity. |
| Dendritic Cells | Originate in the marrow and migrate to most tissues (especially where pathogens might enter body) Engulf protein antigens, partially digest them, and display polypeptide fragments on surface for T cell to “see” |
| Dendritic Cells | Associated with histocompatibility antigens Secrete cytokines to attract lymphocytes |
| Histocompatibility Antigens | On surface of all body cells (except mature RBCs) Also called human leukocyte antigens (HLAs) Coded for by four genes on chromosome 6 called major histocompatibility complex (MHC) |
| Histocompatibility Antigens | Many versions of each gene are possible, so most people have different combinations. An organ transplant requires an MHC match |
| MHC | MHC genes produce two classes of cell surface molecules: class 1 and class 2. Class 1 is made by all cells except RBCs. Class 2 is made by antigen-presenting cells and B cells |
| MHC | Class 2 MHC molecules and foreign antigens are presented together to helper T lymphocytes. Class 1 MHC molecules and foreign antigens are presented together to activate cytotoxic T cells. |
| Active Immunity | When exposed to foreign antigens, immune cells respond by making many copies of themselves. This protects the body from future infections. This protection is called active immunity. |
| Active Immunity | After infection, it takes 5−10 days before antibodies are detected in the blood. This is the primary response. The person will get sick. Later exposure to the same infection results in maximum antibody production in less than 2 hours. |
| Active Immunity | (rapid response) This is the secondary response. The person will likely never get sick. |
| Clonal Selection Theory | Explains how the secondary immune response works: A person inherits lymphocytes specific to almost every pathogen, but there are few of each type. |
| Clonal Selection Theory | The primary response triggers a massive production of cells that can respond to that antigen. These cells respond much quicker after exposure a second time. |
| Immunological Tolerance | It is important to avoid attacking “self” cells. The immune system develops a tolerance for “self” antigens in the fetal period. In some instances, “self” cells are attacked: |
| Immunological Tolerance | If mutations occur in lymphocytes (usually good and adds to what the body can defend against) If cells in particular organs are never exposed to the immune system These lymphocytes are called autoreactive. |
| Immunological Tolerance | If lymphocytes do begin attacking cells,there are mechanisms to stop this: In clonal deletion, these lymphocytes are destroyed (apoptosis). In clonal anergy, these lymphocytes are prevented from becoming active. Regulatory T lymphocytes likely do this |
| Passive Immunity | Passing of antibodies from one individual to another Provides temporary protection: From mother to fetus From mother to child (in breast milk) Artificially via immunization (snake anti-venom) |
| Natural Killer Cells | Related to T lymphocytes but part of innate immunity without the ability to recognize specific antigens Can recognize malignant cells and cells infected with a virus Must be activated by pro-inflammatory cytokines from dendritic cells |
| Natural Killer Cells | Kill compromised cells in the same manner as cytotoxic T cells Cytokines released by natural killer cells activate both innate and adaptive immune cells. |
| Autoimmunity | Produced by failure of immune cells to tolerate “self” antigens Autoreactive T lymphocytes and autoantibodies are produced, causing inflammation and organ damage. |
| Autoimmunity | Common autoimmune diseases include rheumatoid arthritis, type 1 diabetes, multiple sclerosis, Grave’s disease, pernicious anemia, thyroiditis, psoriasis, and lupus |
| Autoimmunity | Several factors may cause autoimmune diseases: An antigen not normally exposed to the immune system becomes exposed. Hashimoto’s thyroiditis |
| Autoimmunity | A normally tolerated antigen is combined with a foreign hapten. This may occur when a drug such as aspirin combines with platelets, resulting in the destruction of platelets. Thrombocytopenia |
| Autoimmunity | Several factors may cause autoimmune diseases: Antibodies are produced aimed at other antibodies. Cause of inflammation in rheumatoid arthritis |
| Autoimmunity | Antibodies produced against foreign antigens cross-react with self antigens and begin attacking self cells (can occur in the heart or kidneys after a strep infection). Rheumatic fever |
| Autoimmunity | Several factors may cause autoimmune diseases: Self antigens may be presented to T helper cells along with class 2 MHC molecules. May occur after viral infection of cells Occurs in diabetes type I Inadequate regulatory T cell activity |
| Immune Complex Diseases | Involve free antigen-antibody complexes that stimulate complement proteins and inflammation Usually self-regulating because complexes are removed via phagocytosis Complex formation may be prolonged or spread to other organs, leading to prolonged inflamm |
| Immune Complex Diseases last part:Rheumatoid arthritis and lupus | May result from infections from bacteria, viruses, or parasites Hepatitis B results in free complexes that cause damage to arteries due to inflammation. May also result from complexes formed by self antigens and autoantibodies |
| Allergies | Also called hypersensitivity Abnormal response to allergens (antigens) Two types: Immediate hypersensitivity Delayed hypersensitivity |
| external respiration | ventilation and the exchange of gases (oxygen and carbon dioxide) between air and blood in lungs |
| internal respiration | gas exchange between the blood and other tissues and oxygen utilization by the tissues |
| conduction zone | Air travels down the nasal cavity to Pharynx to Larynx to Trachea to Right and left primary bronchi to Secondary bronchi to Tertiary bronchi to(more branching)to Terminal bronchioles to Respiratory zone (respiratory bronchioles) to Terminal alveolar sacs |
| structure of the respiratory system | in conduction zone: trachea, primary bronchus, bronchial tree, terminal bronchioles in respiratory zone: air flow, terminal bronchiole, respiratory bronchiales, alveolar sacs, alveolus |
| conduction zone | Transports air to the lungs Warms, humidifies, filters, and cleans the air gets air to the respiratory zone Mucus traps small particles, and cilia move it away from the lungs. Voice production in the larynx as air passes over the vocal folds |
| Respiratory zone | is the region where gas exchange occurs |
| Alveoli | Air sacs in the lungs where gas exchange occurs 300 million of them Provide large surface area (760 square feet) to increase diffusion rate |
| visceral pleura | covers the lungs The parietal and visceral pleura are normally pushed together, with a potential space between called the intrapleural space. |
| parietal pleura | lines the thoracic wall The parietal and visceral pleura are normally pushed together, with a potential space between called the intrapleural space. |
| Gas exchange | Occurs via diffusion O2 concentration is higher in the lungs than in the blood, so O2 diffuses into blood. CO2 concentration in the blood is higher than in the lungs, so CO2 diffuses out of blood. |
| Ventilation | Air moves from higher to lower pressure. Pressure differences between the two ends of the conducting zone occur due to changing lung volumes. Compliance, elasticity, and surface tension are important physical properties of the lungs |
| Intrapulmonary pressure | pressure in the lungs Inhalation: Intrapulmonary pressure is lower than atmospheric pressure. Pressure below that of the atmosphere is called subatmospheric or negative pressure Exhalation: Intrapulmonary pressure is greater than atmospheric pressure |
| Intrapleural pressure | pressure within the intrapleural space (between parietal and visceral pleura) Lower than intrapulmonary and atmospheric pressure in both inhalation and exhalation |
| transpulmonary pressure | The difference between intrapulmonary and intrapleural pressure Keeps the lungs against the thoracic wall |
| Boyle's law | States that the pressure of a gas is inversely proportional to its volume An increase in lung volume during inspiration decreases intrapulmonary pressure to subatmospheric levels air goes in |
| Compliance | Lungs can expand when stretched. Defined as the change in lung volume per change in transpulmonary pressure: ΔV/ΔP Reduced by infiltration of connective tissue proteins in pulmonary fibrosis |
| elasticity | Lungs return to initial size after being stretched. Lungs have lots of elastin fibers. Because the lungs are stuck to the thoracic wall, they are always under elastic tension. |
| surface tension | Resists distension. Exerted by fluid secreted in the alveoli. Raises the pressure of the alveolar air as it acts to collapse the alveolus. |
| law of Laplace | Pressure is directly proportional to surface tension and inversely proportional to radius of alveolus. Small alveoli would be at greater risk of collapse without surfactant. |
| Boyle's lae | A decrease in lung volume during exhalation increases intrapulmonary pressure above atmospheric levels. Air goes out. |
| pulmonary ventilation (breathing) | Inspiration: breathe in Expiration: breathe out Accomplished by changing thoracic cavity/ lung volume |
| quiet breathing | inspiration: contraction of the diaphragm and external intercostal muscles increases the thoracic and lung volume decreasing intrapulmonary pressure to about -3 mmHg |
| forced ventilation (deep breathing) | inspiration: aided by contraction of accessory muscles such as the scalenes and sternocleidomastoid decrease intrapulmonary pressure to -20mmHg or lower |
| quiet breathing | expiration: relation of the diaphragm and external intercostals plus elastic recoil of lungs decreases lung volume and increase intraplumonary pressure to about +3mmHg |
| forced ventilation (deep breathing | expiration: aided by contraction of abdominal muscles and internalcostal muscles increases intrapulmonary pressure to +30mmHg or higher |
| spirometer | Subject breathes into and out of a device that records volume and frequency of air movement on a spirogram. Measures lung volumes and capacities Can diagnose restrictive and disruptive lung disorders |
| respiratory volumes 1.tidal volume 2.expiratory reserve volume 3.inspiratory reserve volume 4.residual volume | 1. amount of air expired or inspired in quiet breathing 2. amount of air that can be forced out after tidal volume 3. amount of air that can be forced in after tidal volume 4. amount of air left in lungs after maximum expiration |
| restrictive disorders | Restrictive: Lung tissue is damaged. Vital capacity is reduced, but forced expiration is normal. Examples: pulmonary fibrosis and emphysema |
| obstructive disorders | Obstructive: Lung tissue is normal. Vital capacity is normal, but forced expiration is reduced. Example: asthma |
| partial pressure | the pressure of an individual gas; can be measured by multiplying the % of that gas by the total pressure. O2 makes up 21% of the atmosphere, so partial pressure of O2 = 760 X 20% = 159 mmHg. |
| role of gas exchange | In the alveoli, the percentage of oxygen decreases and CO2 increases, changing the partial pressure of each |
| nitrogen narcosis | occurs if nitrogen is inhaled under pressure; results in dizziness and drowsiness |
| the bends | also called Decompression sickness: When a diver comes to the surface too fast, nitrogen bubbles can form in the blood and block small vessels. Can also happen if an airplane suddenly loses pressure |
| receptors 1. chemoreceptors | Automatic control of breathing is influenced by feedback from chemoreceptors, which monitor pH of fluids in the brain and pH, PCO2 and PO2 of the blood. Central chemoreceptors in medulla Peripheral chemoreceptors in carotid and aorta arteries |
| receptors 2.receptors that stimulate coughing | Irritant receptors: in wall of larynx; respond to smoke, particulates, etc. Rapidly adapting receptors: in lungs; respond to excess fluid |
| Hemoglobin | Most of the oxygen in blood is bound to hemoglobin. 4 polypeptide globins and 4 iron-containing hemes Each hemoglobin can carry 4 molecules O2. 248 million hemoglobin/RBC |
| hemoglobin forms | Oxyhemoglobin/reduced hemoglobin: Iron is in reduced form (Fe2+) and can bind with O2. Methemoglobin: Oxidized iron (Fe3+) can’t bind to O2. Abnormal; some drugs cause this. Carboxyhemoglobin: Hemoglobin is bound with carbon monoxide. |
| fetal hemoglobin | Adult hemoglobin (hemoglobin A) can bind to 2,3-DPG, but fetal hemoglobin (hemoglobin F) cannot. Fetal hemoglobin therefore has a higher affinity for O2 than the mother, so oxygen is transferred to the fetus. |
| myoglobin | Red pigment found in skeletal and cardiac muscles Similar to hemoglobin, but with 1 heme, so it can only carry 1 oxygen molecule Higher affinity to oxygen; oxygen is only released when PO2 is very low |
| chloride shift | H+ in RBCs attach to hemoglobin and attract Cl−. The exchange of bicarbonate out of and Cl− into RBCs is called the chloride shift |
| acidosis | when blood pH falls below 7.35 Respiratory acidosis: hypoventilation Metabolic acidosis: excessive production of acids, loss of bicarbonate (diarrhea |
| alkalosis | when blood pH rises above 7.45 Respiratory alkalosis: hyperventilation Metabolic alkalosis: inadequate production of acids or overproduction of bicarbonates, loss of digestive acids from vomiting |
| hypernea | Exercise produces deeper, faster breathing to match oxygen utilization and CO2 production |
| reverse chloride shift | In pulmonary capillaries, increased PO2 favors the production of oxyhemoglobin. This makes H+ dissociate from hemoglobin and recombine with bicarbonate to form carbonic acid: H+ + HCO3− to H2CO3 |
| reverse chloride shift | In low PCO2, carbonic anhydrase converts carbonic acid back into CO2 + H2O: H2CO3 to CO2 + H2O CO2 is exhaled |
| myoglobin | Stores oxygen and serves as go-between in transferring oxygen from blood to mitochondria |
| alkalosis | Respiratory component of blood pH measured by plasma CO2 Metabolic component measured by bicarbonate |
| kidney functions | Regulation of the extracellular fluid environment in the body, including: Volume of blood plasma (affects blood pressure) Wastes Electrolytes pH |
| kidney structure | Urine made in the kidneys pools into the renal pelvis, then down the ureter to the urinary bladder. It passes from the bladder through the urethra to exit the body. Urine is transported using peristalsis. |
| kidney structure | The kidney has two distinct regions: Renal cortex Renal medulla, made up of renal pyramids and columns Each pyramid drains into a minor calyx to major calyx to renal pelvis. |
| Nephron | functional unit of the kidney Each kidney has more than a million nephrons. Nephron consists of small tubules and associated blood vessels. |
| Nephron tubules | Glomerular (Bowman’s) capsule surrounds the glomerulus. Together, they make up the renal corpuscle. Filtrate produced in renal corpuscle passes into the proximal convoluted tubule. Next, fluid passes into the descending and ascending loop of Henle. |
| Nephron tubules | After the loop of Henle, fluid passes into the distal convoluted tubule. Finally, fluid passes into the collecting duct. The fluid is now urine and will drain into a minor calyx. |
| two types of nephron | Juxtamedullary: better at making concentrated urine Cortical |
| Glomerular corpuscle | Capillaries of the glomerulus are fenestrated. Large pores allow water and solutes to leave but not blood cells and plasma proteins. Fluid entering the glomerular capsule is called filtrate |
| glomerular corpuscle | Filtrates must pass through: 1.Capillary fenestrae 2.Glomerular basement membrane 3.Visceral layer of the glomerular capsule composed of cells called podocytes with extensions called pedicles |
| glomerular corpuscle | Slits in the pedicles called slit diaphragm pores are the major barrier for the filtration of plasma proteins. Defect here causes proteinuria = proteins in urine. Some albumin is filtered out but is reabsorbed by active endocytosis |
| Ultrafiltrate | Fluid in glomerular capsule gets there via hydrostatic pressure of the blood, colloid osmotic pressure, and very permeable capillaries. |
| Filtration Rates | Glomerular filtration rate (GFR): volume of filtrate produced by both kidneys each minute = 115−125 ml. 180 ml/ day Total blood volume filtered every 40 minutes Most must be reabsorbed immediately |
| Regulation of Filtration Rate | Vasoconstriction or dilation of afferent arterioles changes filtration rate. Extrinsic regulation via sympathetic nervous system Intrinsic regulation via signals from the kidneys; called renal autoregulation |
| Reabsorption | 180 ml of water is filtered per day, but only 1−2 ml is excreted as urine. This will increase when well hydrated and decrease when dehydrated. A minimum 400 ml must be excreted to rid the body of wastes = obligatory water loss. |
| Reabsorption in the Proximal Tubule | The osmolality of filtrate in the glomerular capsule is equal to that of blood plasma. Na+ is actively transported out of the filtrate into the peritubular blood to set up a concentration gradient to drive osmosis |
| Secretion | Kidneys must also remove excess ions and wastes from the blood. Sometimes called renal plasma clearance Filtration in the glomerular capsule begins this process. |
| Excretion Rate | Excretion rate = filtration rate + secretion rate – reabsorption rate Used to measure glomerular filtration rate (GFR), an indicator of renal health |
| Secretion of Drugs | Membrane carriers specific to foreign substances transport them into the tubules. Called organic anion transporters (OATs) or organic cation transporters Very fast; may interfere with action of therapeutic drugs |
| Reabsorption | 85% of reabsorption occurs in the proximal tubules and descending loop of Henle.This portion is unregulated |
| secretion | Secretion finishes the process when substances are moved from the peritubular capillaries into the tubules |
| Juxtaglomerular Apparatus | Located where the afferent arteriole comes into contact with the distal tubule. A decrease in plasma Na+ results in a fall in blood volume. Sensed by juxtaglomerular apparatus Granular cells secrete renin into the afferent arteriole. |
| Juxtaglomerular Apparatus | This converts angiotensinogen into angiotensin I. Angiotensin-converting enzyme (ACE) converts this into angiotensin II |
| Acid-base regulation | Kidneys maintain blood pH by reabsorbing bicarbonate and secreting H+. Urine is thus acidic. Proximal tubule uses Na+/H+ pumps to exchange Na+ out and H+ in. Some of the H+ brought in is used for the reabsorption of bicarbonate. |
| acid-base regulation | Bicarbonate cannot cross the inner tubule membrane so must be converted to CO2 and H2O using carbonic anhydrase. Bicarbonate + H+ tocarbonic acid Carbonic acid (w/ carbonic anhydrase) to H2O + CO2 |
| Urinary Buffers | Nephrons cannot produce urine with a pH below 4.5. To increase H+ secretion, urine must be buffered. Phosphates and ammonia buffer the urine. Phosphates enter via filtration. Ammonia comes from the deamination of amino acids. |
| Diuretics | Used clinically to control blood pressure and relieve edema (fluid accumulation) Diuretics increase urine volume, decreasing blood volume and interstitial fluid volume. Many types act on different portions of the nephron. |
| acid-base regulation | CO2 can cross into tubule cells, where the reaction reverses and bicarbonate is made again. This diffuses into the interstitial space. |
| type of diuretics | Potassium-sparing diuretics: Aldosterone antagonists block reabsorption of Na+ and secretion of K+. |
| Acute Renal Failure | Ability of kidneys to regulate blood volume, pH, and solute concentrations crashes in a matter of hours/days. Usually due to decreased blood flow through kidneys due to: Atherosclerosis of renal arteries |
| Glomerulonephritis | Inflammation of the glomerulus Autoimmune disease Many glomeruli are destroyed, and others are more permeable to proteins. Loss of proteins from blood reduces blood osmotic pressure and leads to edema. |
| Renal Insufficiency | Any reduction in renal activity Can be caused by glomerulonephritis, diabetes, atherosclerosis, or blockage by kidney stones Can lead to high blood pressure, high blood K+ and H+, and uremia = urea in the blood. |
| Acute Renal Failure | Inflammation of renal tubules Use of certain drugs (NSAIDs) |
| Renal Insufficiency | Patients with uremia are placed on a dialysis machine to clear blood of these solutes. |
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