Study Guide - Lecture Exam 2 PDF

**Chapter 19: The CVS: Blood Vessels** **3/4. Compare arteries, veins, capillaries.** **(i) Elastic Arteries (conducting arteries): with *elastin* in all three tunics; *Aorta* and its major branches; Act as *pressure reservoirs* that expand and recoil as blood ejected from heart.** **(ii) Muscula...

**Chapter 19: The CVS: Blood Vessels** **3/4. Compare arteries, veins, capillaries.** **(i) Elastic Arteries (conducting arteries): with *elastin* in all three tunics; *Aorta* and its major branches; Act as *pressure reservoirs* that expand and recoil as blood ejected from heart.** **(ii) Muscular Arteries (distributing arteries): Deliver blood to body organs; *more smooth muscle; a*ctive in *vasoconstriction. (iii)* Arterioles: *Smallest* arteries; lead to capillary beds; *control flow into capillary beds* via vasodilation and vasoconstriction. (iv) Veins: compared to arteries: Have thinner walls; larger lumens; lower BP; lack internal and external elastic membranes; venous valves prevent backflow of blood.** **(v) Capillaries: Their walls consist of just a thin tunica intima; Functions: Exchange of gases, nutrients, wastes, hormones, between blood and interstitial fluid; *Three structural types:*** **All have *intercellular clefts*, which allow passage of fluids and small solutes. (i) Continuous capillaries: (*least permeable and most common*) Abundant in skin, muscles, and CNS (blood brain barrier) (ii) Fenestrated capillaries: large fenestrations (pores) increase permeability. Occurs in areas of active filtration, absorption, or secretion (kidney, small intestine).** **(iii) Sinusoid capillaries (sinusoids): Most permeable (allows large molecules and even blood cells to pass); Larger fenestrations; larger intercellular clefts; large lumens.** **Occurs in limited locations (liver, bone marrow, spleen).** **Capillary beds: Capillary beds consists of two types of vessels: (i) Vascular shunt: short vessel that directly connects terminal arteriole and postcapillary venule. (ii) True capillaries: Branch off metarteriole and return to thoroughfare channel; Precapillary sphincters (cuff of smooth muscle fibers) at the root of each true capillary at the metarteriole regulate blood flow into true capillaries (constrict / relax); Blood may go into true capillaries or to shunt depending on needs of tissues.** **7. Describe blood flow, blood pressure, and resistance.** **Blood flow: Volume of blood flowing through vessel, organ, or entire circulation in given period (Equivalent to cardiac output (CO) for entire vascular system). Blood pressure (BP): Force per unit area exerted on wall of blood vessel by blood. Pressure gradient provides driving force that keeps blood moving from higher to lower pressure areas. Resistance (peripheral resistance): Opposition to flow. Measure of amount of friction blood encounters with vessel walls. Three important sources of resistance: (i) Blood viscosity (remain relatively constant): thickness of blood. Increased viscosity = increased resistance. (ii) Total blood vessel length (remain relatively constant): Longer vessel = greater resistance encountered. (iii) Blood vessel diameter: Greatest influence on resistance; smaller the vessel, more resistance.** **Blood flow (F) is directly proportional to blood pressure gradient (∆ P); If ∆ P increases, blood flow speeds up. Blood flow (F) is inversely proportional to peripheral resistance (R). If R increases, blood flow decreases.** **8. Blood pressure differs in the arteries, capillaries, and veins.** **Arterial Blood Pressure: (i) Systolic pressure: Pressure generated by ventricular contraction; (ii) Diastolic pressure: During diastole; (iii) Pulse pressure: Difference between systolic and diastolic pressure. (iii) Mean arterial pressure (MAP): MAP is calculated as: MAP = diastolic pressure + 1/3 pulse pressure** **Capillary Blood Pressure: Low capillary pressure is desirable because: High BP would rupture fragile, thin-walled capillaries.** **Venous Blood Pressure: Functional adaptations important to venous return: (i) Muscular pump: contraction of skeletal muscles \"milks\" blood toward heart; valves prevent backflow. (ii) Respiratory pump: pressure changes during breathing move blood toward heart. As we inhale, abdominal pressure increases, squeezing the local veins and forcing blood towards heart. At the same time pressure in chest decreases, allowing thoracic veins to expand and speed up blood entry to right atrium. (iii) Sympathetic venoconstriction: under sympathetic control pushes blood toward heart** **9. Describe how blood pressure is regulated.** **Main factors influencing blood pressure: (i) *Cardiac output* (CO = SV × HR); (ii) *Peripheral resistance* (PR) (*diameter of blood vessels)*; (iii) *Blood volume*; \[I\] Long-term renal regulation: Long-term controls alter blood volume; Low blood pressure leads to release of renin by kidneys; *Renin-angiotensin-aldosterone mechanism:* Angiotensin II acts in four ways to stabilize arterial blood pressure: (a) aldosterone (b) ADH, (c) sensation of thirst, (d) angiotensin II is a potent vasoconstrictor. \[II\] Short-term neural and hormonal controls** **Change blood pressure by altering *peripheral resistance* and *CO*: (a) Neural Controls: Drop in arterial pressure is detected by baroreceptors (stretch reflexes) located in carotid sinuses, aortic arch, walls of large arteries of neck and thorax; impulses from baroreceptors stimulate medullary cardiac and vasomotor centers. This increase heart rate, & force of contraction (SV) (increase CO) and vasoconstriction (increase PR); BP return to normal range. (ii) All these are reversed when BP increase; Cardiac centers: *Cardioaccelatory center* (Sympathetic stimulus: increases heart rate and increases force of heart contraction); *Cardioinhibitory center* (Parasympathetic: decreases heart rate); Vasomotor center: Control the diameter of blood vessels.** **(b) Hormonal control: Cause increased blood pressure \[most\];** **Cause lowered blood pressure \[Atrial natriuretic peptide\]** **\[I\] Primary or Essential Hypertension (90%;** n**o underlying cause identified; Risk factors include heredity, diet, obesity, age, diabetes mellitus, stress, and smoking; No cure but can be controlled); \[II\] Secondary hypertension (due to identifiable disorders such as hyperthyroidism and Cushing\'s syndrome; Treatment focuses on correcting underlying cause)** **Circulatory shock: Any condition in which blood vessels are inadequately filled and blood cannot circulate normally. If circulatory shock persists, cell die and organ damage follows. (i) Hypovolemic shock: results from large scale of blood or fluid loss (acute *hemorrhage*). (ii) Vascular shock: Blood volume is normal, but circulation is poor as a result of vasodilation (*anaphylactic* shock as a result of allergic reaction). (iii) Cardiogenic shock: Pump failure occurs when heart is so inefficient to sustain adequate circulation (*myocardial infarction*-heart attack).** **12/13. Explain blood flow regulation and capillary bulk flow.** **\[I\] Intrinsic controls (Autoregulation): are controlled intrinsically by *modifying the diameter of local arterioles* feeding the capillaries. (i) Metabolic controls: metabolic products (e.g., H+, CO2, lactic acid) directly cause vasodilation. (ii) Myogenic controls: Vascular smooth muscle contracts (constricts) when stretched and relaxes (dilates) when not stretched. High blood pressure may rupture fragile blood vessels; vascular smooth muscle prevents this by responding to stretch by vasoconstriction; \[II\] Extrinsic controls: act via the nerves (*sympathetic nervous system)* and *hormones* that act on arteriolar smooth muscle to maintain blood pressure.** **Fluid Movements: Bulk Flow: Fluid leaves capillaries through the clefts at arterial end; most returns to blood at venous end. Hydrostatic pressure in capillary "pushes" fluid *out* of capillary; Osmotic pressure in capillary "pulls" fluid into capillary. (i) At arterial end: NFP= (HP~c~ + OP~if~) -- (HP~if~ + OP~c~) = (35 + 1) -- (0 + 26) = 10 mm Hg (net outward pressure). (ii) At venous end: NFP = (HP~c~ + OP~if~) -- (HP~if~ + OP~c~) = (17 + 1) -- (0 + 26) = --8 mm Hg (net inward pressure)** **Chapter 20: Lymphatic System/Lymphoid Organs** **1. Describe functions of the lymphatic system/lymphoid organs. Lymphatic System: (i) Returns fluids that have leaked from the CVS back to blood (ii) Return leaked proteins to the blood. (iii) Carry absorbed fat from the intestine to the blood (lacteals)** **Consists of three parts: (i) Network of lymphatic vessels (lymphatics); (ii) Lymph: fluid in lymphatic vessels. (iii) Lymph nodes: cleanse lymph as it passes through them** **Lymphoid Organs and Tissues: (i) Provide structural basis of immune system. (ii) Structures include lymph nodes, spleen, thymus, tonsils, Mucosa Associated Lymphoid Tissue (MALT).** **2. Describe the structure and distribution of lymphatic vessels.** **The lymphatics vessels form one-way system in which lymph flows towards the heart. Lymph vessels (lymphatics) include:** **(1) Lymphatic capillaries: Transport of lymph begins in microscopic, blind-ended, lymphatic capillaries. These weave between the tissue cells and the blood capillaries. Lymphatic capillaries are remarkably permeable (take up proteins, cell debris, pathogens, and cancer cells). *From lymphatic capillaries, lymph flows through successively larger and thicker walled channels:* (2) Collecting lymphatic vessels: From lymphatic capillaries, lymph flows through larger and thicker walled channels. (3) Lymphatic trunks: Largest collecting vessels unite to form lymphatic trunks. (4) Lymphatic ducts: Lymph is eventually delivered to one of 2 large ducts in thoracic region: (i) Right lymphatic duct: drains right upper arm and right side of head and thorax. (ii) Thoracic duct : drains rest of body; Each empties lymph into venous circulation at junction of *internal jugular* and *subclavian veins* on its own side of body** **Lymph Transport: The lymphatic system lacks an organ that acts as a pump. Lymph propelled by: (i) Milking action of skeletal muscle. (ii) Pressure changes in thorax during breathing move blood toward lymphatic ducts by squeezing abdominal lymph vessels as thoracic lymph vessels expand. (iii) Valves to prevent backflow;** **3. Describe the basic structure/function of lymphoid tissue.** **Lymphoid cells (lymphocytes, macrophages); Lymphoid tissue (loose reticular connective tissue): 2 types: (i) Diffuse. (ii) Lymphoid Follicles: are solid, spherical bodies of tightly packed lymphoid cells; Functions: (i) Houses, and provides proliferation site for, lymphocytes. (ii) Surveillance vantage point for lymphocytes and macrophages; 1. Lymph nodes: i. *Cleansing the lymph:* Filter lymph. Macrophages destroy microorganisms and debris, preventing them from being delivered to blood. (ii) see above functions of lymphoid organs; 2. Spleen: i. see above functions of lymphoid organs. Ii. Cleanses blood (macrophages remove aged red blood cells, and debris);** **Chapter 21: The Immune System** 1\. Differentiate between the innate and adaptive defenses. **1. Innate Defenses (non-specific): i. Surface barriers** **(First line of defense): Skin; Mucous membranes; ii. Internal defenses (Second line of defense):** Phagocytes; Natural killer cells; Inflammation; Antimicrobial proteins; Fever. **2.** **Adaptive Defenses (specific) (Third line of defense**): i. Humoral immunity (B cells); ii. Cellular immunity (T cells) **2. Describe surface membrane barriers and their protective functions (First line of defense). \[skin, mucus membranes\]** **(i) Physical barriers: Keratin resistant to weak acids and bases, bacterial enzymes, and toxins; (ii) Secretions: \[Acid: Acidity of skin and secretions (vaginal, stomach); Enzymes: Lysozyme of saliva, respiratory mucus, and lacrimal fluid; Mucin: Thick sticky mucus that lines the digestive and respiratory passageways. Traps many microorganisms. Defensins: Antimicrobial peptides: inhibit growth; (iii) Respiratory system modifications: Mucus-coated hairs in nose; Cilia of upper respiratory tract sweep dust- and bacteria-laden mucus toward mouth** **3. Explain natural killer cells, fever, interferons, phagocytosis.** **Natural Killer (NK) Cells: Non-specific large lymphocytes that lyse and induce apoptosis (programmed death) of cancer cells and virus infected body cells. (ii) Attack cells that lack \"self\" cell-surface receptors; Fever: When leukocytes are exposed to foreign substances, they secrete *pyrogens,* that act on body\'s thermostat in hypothalamus, raising body temperature. Increases metabolic rate of tissue cells to speed up repair process; Interferons (antimicrobial proteins) enhance our innate defenses by an attacking microorganism directly or by hindering their ability to reproduce. (i) Virus enters cell. (ii) Interferon genes activated. (iii) Cell produces interferon molecules (cells infected with virus are killed). (iv) Interferon binds surrounding non-infected cells and stimulates cells to turn on genes for antiviral proteins. (v) Antiviral proteins block viral reproduction; Phagocytosis: (Neutrophils; Macrophage) (i) Phagocyte adheres to pathogens or debris. (ii) Phagocyte forms pseudopods that eventually engulf the particles, forming a phagosome. (iii) Lysosome fuses with the phagocytic vesicle, forming a phagolysosome. (iv) Lysosomal enzymes digest the particles, leaving a residual body. (v) Exocytosis of the vesicle removes indigestible and residual material.** **4. Describe the inflammatory process.** **Inflammation: is triggered when body tissues injured by physical trauma, intense heat, irritating chemicals, or infection by viruses, fungi or bacteria. (i) Prevents spread of damaging agents. (ii) Disposes of cell debris and pathogens. (iii) Alerts adaptive immune system. (iv) Sets the stage for repair; The 4 Cardinal signs of acute inflammation are: (i) Redness (ii) Heat (iii) Swelling (iv) Pain (Sometimes (v) Impairment of function).** **Inflammation begins by release of inflammatory chemicals by injured cells or immune cells. (i) These chemicals dilate local arterioles (*heat, redness*): Locally increased temperature increases metabolic rate of cells to speed up repair process.** **(ii) The chemicals also make local capillaries leakier. Capillaries leak fluid (*exudate*) containing clotting factors and antibodies. That causes local *swelling* and *pain* (results from pressure of swelling on adjacent nerves endings and released bacterial toxins and inflammatory chemicals). Leaked clotting proteins form interstitial clots that wall off area to prevent injury to surrounding tissue and temporary fibrin patch forms scaffolding for repair. (iii) These chemicals also induce leukocytosis and chemotaxis; Leukocytosis: increased numbers of white blood cells in bloodstream; Margination: leukocytes cling to capillary walls; Diapedesis: Neutrophils squeeze out of capillaries; Chemotaxis: Neutrophils follow chemical trail.** **6/8. Describe adaptive immunity.** **3 primary traits of adaptive immunity: (i) It is specific (ii) It is systemic (iii) It has memory: after an initial exposure, it recognizes and mounts a faster and even stronger attacks on previously encountered pathogens; Adaptive immunity has two separate, overlapping arms: (i) Humoral (antibody-mediated) immunity; (ii) Cellular (cell-mediated) immunity: T cells directly kill cells (infected by viruses or bacteria, cancerous, foreign cells such as transplanted cells); Antigens are substances that can mobilize the adaptive defenses. They are targets of all adaptive immune responses.** **Lymphocytes: (i) Origin: Both B and T lymphocyte precursors originate in red bone marrow. (ii) Maturation: Lymphocyte precursors destined to become T cells migrate (in blood) to the thymus and mature there. B cells mature in the bone marrow. During maturation lymphocytes develop *immunocompetence* (be able to recognize its one specific antigen by binding to it) and *self-tolerance* (unresponsive to self-antigens, so that it does not attack the body's own cells). (iii) Seeding secondary lymphoid organs and circulation: where they are likely to encounter antigens. (iv) Antigen encounter and activation: When an immunocompetent but naive lymphocyte bind its antigen, that lymphocyte is activated. (v) Proliferation and differentiation: Activated lymphocytes proliferate and differentiate into effector cells and memory cells.** **9. Describe humoral immunity.** **When a B cell encounters its antigen, that antigen provokes the *humoral immune response*, in which antibodies specific for that antigen are made. An immunocompetent but naïve B cell is activated when antigens bind to its surface receptors. This leads to *proliferation and differentiation* into: (i) Plasma cells (antibody secreting effector cells): (ii) Memory cells: Provide immunological memory. Mount an immediate response to future exposures to same antigen; Primary immune response to antigen occurs after a delay (lag period: 3-6 days). Secondary immune response: Re-exposure to same antigen gives faster, more prolonged, more effective response.** **10. Compare active and passive humoral immunity.** ***1. Active humoral immunity: w*hen your B cells encounter antigens and produce antibody against them. (i) Naturally Acquired: response to bacterial or viral infection, during which time one may develop symptoms of the disease and suffer. (ii) Artificially acquired: response to vaccine of dead or attenuated pathogens. Their weakened antigens provide antigenic determinants. They spare us most of the symptoms and discomfort of the disease.** **2. Passive *humoral immunity* Instead of being made by our plasma cells, ready-made antibodies are introduced into your body. As a result, your B cells are not challenged by antigens, immunological memory does not occur. (i) Naturally acquired: Antibodies passed from mother to fetus via placenta; or to infant in her milk. (ii) Artificially acquired: Injection of exogenous antibodies. Prevent rapidly fatal diseases before active immunity can be established. (Antivenom, rabies, tetanus). Provide immediate protection but their effect is short lived.** **Antibody targets and functions: Antibodies themselves cannot destroy antigens; they can inactivate antigens and tag them for destruction; forms antigen antibody complexes.** **Defensive mechanisms used by antibodies: (i) Neutralization: masks dangerous parts of viruses and bacterial exotoxins; Prevent these antigens from binding to receptors on tissue cells (ii) Agglutination: bind cell bound antigen; Cross-linked antigen antibody complexes agglutinate; (iii) Precipitation: Soluble molecules are cross-linked; Complexes precipitate; (iv) Complement fixation: Antibodies attached to cells such as bacteria activate the complement system. The complement system: (i) leads to cell lysis. (ii) enhances inflammation. (iii) promote phagocytosis.** **Chapter 22: The Respiratory System** **1-5. Describe the four processes of respiration and anatomy.** **(i) Pulmonary ventilation (breathing): movement of air into (inspiration) and out (expiration) of lungs. (ii) External respiration: O~2~ diffuses from the lungs to the blood and CO~2~ diffuses from blood to the lungs. (iii) Transport of respiratory gases: O~2~ is transported from lungs to the tissue cells of the body, and CO~2~ is transported from tissue cells to the lungs. (iv) Internal respiration: O~2~ diffuses from blood to tissues cells and CO~2~ diffuses from tissue cells to blood** **Respiratory zone: Site of gas exchange; respiratory bronchiole, alveolar ducts, and alveoli. (ii) Conducting zone: Conduits to gas exchange sites; from the nose to respiratory bronchioles. Functions: makes air moist, warm, filter and clean. Respiratory mucosa: Pseudostratified ciliated columnar epithelium; Mucous secretions contain lysozyme and defensins; Cilia move contaminated mucus; *Respiratory membrane*; The alveolar and capillary walls and their fused basement membranes; Majority of alveolar walls is made of a single layer of squamous epithelium (type I alveolar cells). Scattered among the these cells are cuboidal type II alveolar cells secrete that surfactant (reduce surface tension of alveolar fluid); Alveoli have 3 significant features: (i) Surrounded by fine elastic fibers and pulmonary capillaries (ii) Alveolar pores connect adjacent alveoli that equalize air pressure throughout lung. (iii) Alveolar macrophages keep alveolar surfaces sterile.** **6/7/8. Relate Boyle's law to pulmonary ventilation** **Intrapulmonary (intra-alveolar) pressure: Pressure in alveoli; Fluctuates with breathing; Always eventually equalizes with atmospheric pressure; Intrapleural pressure: Pressure in pleural cavity; Fluctuates with breathing; Always a negative pressure ( -4 mm of Hg).** **Boyle\'s Law: At constant temperature pressure (*P*) varies inversely with volume (*V*). (1) Inspiration: Inspiratory muscles contract (diaphragm descends; rib cage rises). Intrapulmonary volume increases. Intrapulmonary pressure drops (to --1 mm Hg). Air (gases) flows into lungs down its pressure gradient until intrapulmonary pressure is 0 (equal to atmospheric pressure). (i) Normal quiet inspiration: It is an active process (diaphragm and external intercostal muscles are activated). (ii) Forced Inspiration: Occur during vigorous exercise, COPD accessory muscles (scalene, sternocleidomastoid, pectoralis minor) further increase in thoracic cage size. (2) Expiration: Inspiratory muscles relax (diaphragm rises; rib cage descends due to recoil of costal cartilages). Elastic lungs recoil passively, intrapulmonary volume decreases. Intrapulmonary pressure rises (to +1 mm Hg). Air (gases) flows out of lungs down its pressure gradient until intrapulmonary pressure is 0. (i) Normal quiet expiration: normally passive process. (ii) Forced expiration: active process - uses abdominal (oblique and transverse) and internal intercostal muscles.** **Factors that influence pulmonary ventilation: (i) Airway resistance: determined by the diameters of the conducting tubes; sympathetic nervous system causes relaxation of this smooth muscle which results in bronchodilation and decreased resistance; Conditions such as asthma and COPD obstruct or narrow airways that increase airway resistance and decrease air flow. (ii) Alveolar surface tension: Surfactant a detergent like complex is produced by type II alveolar cells. Surfactant decreases the cohesiveness of water molecules. As a result, the surface tension is reduced. (iii) Lung compliance: The distensibility of lungs is called lung compliance. Chronic inflammation or infection can cause scar tissue that can cause reduced lung compliance.** **11. Describe how oxygen is transported in blood.** **Molecular O~2~ is carried in blood in two ways: (i) Only 1.5% dissolved in plasma (ii) 98.5% loosely bound to each Fe of hemoglobin (Hb) in RBCs (4 O~2~ per Hb); The hemoglobin-O~2~ combination is called Oxyhemoglobin (HbO~2~); Hemoglobin that has released O~2~ is called reduced hemoglobin/ deoxyhemoglobin) (HHb); As O~2~ binds, Hb affinity for O~2~ increases. ; As O~2~ is released, Hb affinity for O~2~ decreases** ***Fully saturated* (100%) if all 4 heme groups carry O~2~; *Partially saturated* when 1-3 hemes carry O~2~. The rate at which Hb reversibly binds or releases O~2~ is regulated by: Po~2,~ Temperature, Blood pH, and Pco~2~** **\[I\] Influence of Po~2~ on Oxygen-hemoglobin dissociation curve: (i) At high Po~2~, \[lungs\] large changes in Po~2~ cause only small changes in Hb saturation (notice the curve is flat here); At high altitude (or lung disease), there is less O~2~ in lungs; (ii) At low Po~2~, large changes in Po~2~ cause large changes in Hb saturation (notice the curve is steep here. Hb properties ensure that oxygen is delivered where it is most needed); In metabolically active tissues (e.g. exercising muscle), the Po~2~ is even lower \[II\] Effect of temperature, P~CO2~, and blood pH on the oxygen-hemoglobin dissociation curve: (1) Increases in temperature, H^+^, and Pco~2~: (i) decrease its affinity for O~2~ (Enhance O~2~ unloading from blood) (ii) Shift O~2~-hemoglobin dissociation curve to right. (2) Decreases in these factors (i) Decreases oxygen unloading from blood. (ii) shift curve to left. All these factors tend to be higher in systemic capillaries, where oxygen unloading is the goal. As cells metabolize glucose and use O~2~, they release CO~2~, which increases Pco~2~ and H^+^ levels in capillary blood. Both declining blood pH (acidosis) and increasing Pco~2~ weaken the Hb-O~2~ bond, a phenomenon called Bohr effect. This enhances oxygen unloading where it is need most.** **12. Describe carbon dioxide transport in the blood.** **CO~2~ transported in blood in three forms: (i) 7 -10% dissolved in plasma (ii) 20% bound to hemoglobin (carbaminohemoglobin). (iii) 70% transported as bicarbonate ions (HCO~3~^--^)** **(1) In plasma CO~2~ combines with water to form carbonic acid (H~2~CO~3~), which quickly dissociates to H^+^ and HCO~3~^--^. Although this reaction also occurs in plasma, it is much faster in RBCs, where carbonic anhydrase reversibly catalyzes reaction; Once generated, HCO~3~^--^ moves quickly from the RBCs into the plasma, where it is carried to the lungs. To counterbalance the rapid rush of these anions from the RBCs, chloride ions (Cl^-^) move from plasma into the RBCs. This ion exchange process is called chloride shift; (2) In lungs the process is reversed. HCO~3~^--^ moves into RBCs (while Cl^-^ move out) and binds with H^+^ to form H~2~CO~3.~ Carbonic anhydrase then split H~2~CO~3~ into CO~2~ and water; CO~2~ diffuses into alveoli.** **Influence of CO~2~ on Blood pH:** **Slow, shallow breathing increased CO~2~ in blood drop in pH** **Rapid, deep breathing decreased CO~2~ in blood rise in pH** **13. Briefly describe the control of respiration.** **Respiratory centers in the *brain stem* control breathing with input from *chemoreceptors* and *higher brain centers.*** ***Control of respiration* primarily involves neurons in the *medulla* that supply the respiratory muscles; these influence the breath rate and depth; changing levels of O~2'~ CO~2~ and H^+^** **are detected by chemoreceptors.** **Homeostatic Imbalances: 1. Chronic obstructive pulmonary disease (COPD): Exemplified by chronic *bronchitis* and *emphysema;* Irreversible decrease in ability to force air out of lungs; History of smoking in 80% of patients; Dyspnea - labored breathing (\"air hunger\"); Coughing and frequent pulmonary infections; Most develop respiratory failure (hypoventilation) and respiratory acidosis, hypoxemia; 2. Lung cancer: Leading cause of cancer deaths in North America; 90% of all cases are the result of smoking; Overwhelms defenses (nasal hairs, mucus, cilia); Cilia are paralyzed, allowing accumulation of pathogens.**