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BIO 202- Final Exam Study Guide Washo.docx

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Department
Biology
Course
BIO 202
Professor
Washo
Semester
Fall

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1 BIO 202 –Anatomy & Physiology II: Review for Final Exam Blood Components of Blood: Plasma- a clear ECF (55% of blood). Plasma is 92% water and also contains a mixture of proteins, enzymes, nutrients, wastes, hormones, lipids, carbs, trace elements, and gases. Serum is plasma minus the clotting proteins. Proteins are the most abundant solute in plasma that are used for clotting, defense, and transport. There are 3 categories of plasma proteins: albumins (most abundant which contribute to viscosity and osmolarity and influence BP, blood flow, and fluid balance), fibrinogen (clotting), and globulins (immune system defenses). Formed elements- Erythrocytes (=RBCs), Leukocytes (=granulocytes which has cytoplasmic granules consist of neutrophils, eosinophils, & basophils; agranulocytes which have no cytoplasmic granules consist of lymphocytes like T-cells and B-cells & monocytes and macrophages) and Platelets. -Mean RBC count= 4.2-6.2 million/microliter -Mean WBC count= 5k-10k/microliter -Mean platelet count= 130k-360k/microliter Functions of Blood: Transports: -oxygen from lungs to organs/cells -oxygen from cells to lungs -nutrients from digestive system and storage -wastes to liver and kidneys -hormones Regulates: body temperature by transporting heat out of the skin Immunity: white blood cells Clotting: platelets Stabilizes: water balance Stabilizes: pH via buffers for acids & bases Viscosity and osmolarity: Viscocity- resistance to flow- “thickness/stickyness”. Blood is 4.5-5.5x more viscous than water; plasma alone is 2x more viscous than water; too many or too few RBCs changes the viscocity of blood and puts a strain on the heart. Osmolarity: Total molar concentration of dissolved particles in 1 L of solution due to transfer of nutrients and wastes between the blood and tissue fluids. If too high: bloodstream absorbs too much fluid from the tissues thus causing hypertension. If too low: bloodstream transfers too much fluid to tissues, resulting in edema and hypotension. Function of hemoglobin- consists of 2 alpha and 2 beta globin chains that are conjugated with a heme group that binds oxygen to ferrous ion (Fe2+). -can carry up to 4 oxygens *CompatibleABO & Rh types for blood donation: (RBC antigen=agglutinogenA& B; Plasma antibodies= agglutinins anti-A& anti-B) -YourABO blood type is determined by the presence or absence of agglutinogens (antigens) A& B on RBCS. -Blood type is (Rh+) if agglutinogens are present on RBCs, blood type is (Rh-) if agglutinogens are NOT present on RBCs.Anti-D agglutinins are not normally present in blood and form only in those that are exposed to Rh+ blood. If Rh- mother and Rh+ mother this is 2 mother-fetus mismatch; if mother is exposed to Rh+ agglutinogens its okay in 1 pregnancy but in second the mother’s anti-D antibodies will agglutinate fetal RBC causing hemolytic disease of the newborn. RhoGAM is given to pregnant Rh- women to prevent antibody formation. –blood type AhasAagglutinogens and anti-B agglutinins – blood type B has B agglutinogens and anti-A agglutinins –AB has both A& B agglutinogens and neither agglutinin –blood type O has neither agglutinogen, but both agglutinins –blood type O is the most common;AB the rarest •TypeA(anti-B) will react with RBC types B &AB •Type B (anti-A) will react with RBC types A&AB •Type AB will not react with any other RBCs •Type O (ant-A& anti-B) will react withA, B &AB Diseases and disorders: Polycythemia: an excess of RBCs. -1° polycythemia is due to cancer of erythropoietic cell line in the red bone marrow. -2° is RBC count up to 8 million/microliter-- dehydration from more RBCs due to less plasma, high altitude from extended stay at high altitude → RBC count rises up to 7-8 million RBCs/microliter, physical conditioning from endurance training where athletes have 6.5 million RBCs due to higher o2 requirements, and emphysema where there is less lung tissue but RBCs cannot correct for this but erythopoietin continues to be releses thus causing excess RBC production. *Dangers of polycythemia include increased blood volume, pressure and viscosity which can lead to poor circulation, heart strain, and clogged capillaries which in turn result in embolism, 3 stroke, or heart failure. Anemia – iron deficiency and pernicious anemia Iron-deficiencyAnemia: dietary iron deficient = less hemoglobin. Pernicious Anemia: inadequate vitamin B12 from poor nutrition or the lack of intrinsic factor which facilitates B12 absorption. Sickle cell =is a hereditary Hb defect. -recessive allele modifies Hb structure-- homozygous recessive for HbS have sickle-cell disease; heterozygous have HbS have sickle-cell trait -sickle-cell disease individual has shortened life-- death by age 2 with NO treatment though some live to age 50 with proper treatment. HbS turns to gell in low o2 concentrations. -HbS is indigestible to malaria parasites so gene perisists despite its harmful effects to homozygous individuals. Hemophilia- coagulation disorder: -genetic lack of any clotting factors affect coagulation -sex-linked recessive in males (inherited from mother) -hemophiliaAis missing clotting factor VIII (83%) -hemophilia B is missing clotting factor IX (15%) -physical exertion causes bleeding & excruciating pain-- transfusion of plasma or purified clotting factors; factor VIII now produced by transgenic bacteria DIC- coagulation disorder-- Disseminated Intravascular Coagulation -widespread clotting of blood within unbroken vessels -triggers by bacteria (septicemia) or if blood slows down or stops as in cardiac arrest Prevention of inappropriate coagulation: platelet repulsion, thrombin dilution, or natural anticoagulants Platelet repulsion: platelets do NOT adhere to prostacyclin-coating Thrombin dilution: normally diluted by rapidly flowing blood-- heart slowing in shock can result in clot formation Natural anti-coagulants: Antithrombin produced by the liver which deactivates thrombin before it can act on fibrinogen; Heparin is secreted by basophils and mast cells that interfere with formation of prothrombin activator. Genetics Gene: unit of information from sequence of DNAnucleotides that codes for a specific trait Alleles: alternative forms of the same gene In ABO genetics-- the alleles for blood type areA, B, and O: 2 A, or Aand O=typeA 2 B, or B and O=type B 2 O results in= type O Aand B results= type AB “codominant” In Rh bloodtype genetics-- the alleles for blood type are + and - + is dominant to -, so only one + is necessary to make a person Rh+ Two +, or + and - results in = type Rh+ Two - results in =type Rh- Clicker Questions: 1. You have all seen movies of people stranded in the ocean aboard lifeboats. The people are surrounded by water yet they cannot drink the seawater. The seawater would: 4 Increase the blood osmolality, and the tissues would become more dehydrated. 2. If skin and sclera turn yellow, there is an excess of ____ in the blood. Bilirubin 3. Aleukocyte count above 10,000 cells/ml of blood would indicate Infection 4. Someone with blood typeAB-positive could donate blood to which of the following blood types? AB+ only 5. Someone with blood typeAB-positive could receive blood from which of the following blood types? A+/-, B+/-,AB+/-, O+/- 6. Aperson with blood typeA-negative, can donate blood to someone with which blood types? AB-neg, AB+,A-neg, A+ 7. Awoman with blood typeAB marries a man with blood type O. What blood types may be seen in their offspring? A& B 8. Awoman with blood typeAmarries a man with blood type O. What blood types may be seen in their offspring? A& O 9. Awoman who is Rh-negative marries a man with Rh-positive blood. What blood types may be seen in their offspring? Both Rh-neg and Rh+ Heart Location: Located in thoracic cavity, specifically in mediastinum- (area between lungs) – superior to diaphragm – posterior to sternum – 2/3 of heart to the left of midsagittal plane due to the liver taking space on the right Pericardium: • Double walled membranous sac • Anchored to diaphragm at the bottom & connective tissue elsewhere • Allows heart to beat without friction, room to expand and resists excessive expansion Parietal Pericardium: – outer, tough, fibrous layer of connective tissue – folds over to become the visceral pericardium Visceral pericardium (a.k.a. epicardium of heart wall-outermost layer of heart) – inner, thin, smooth, moist serous layer covers heart surface Pericardial cavity– space between parietal & visceral – filled with pericardial fluid to reduce friction 5 Flow of blood through the heart: Superior/inferior vena cava (carrying deoxygenated blood from the body) → Right atrium → Right atrioventricular (AV) or tricuspid valve → Right ventricle → Pulmonary semilunar valve → Pulmonary trunk (1 part of pulmonary artery) → Lung (CO2 discharged, O2 absorbed) → Pulmonary veins (only veins that carry oxygenated blood) → Left atrium → Left atrioventricular (AV), bicuspid or mitral valve → Left ventricle → Aortic semilunar valve → Aorta Valve mechanics: AV valves hang open & SL valves are closed when the ventricles are relaxed → Ventricles fill with blood and then contract → Pressure & blood in the ventricles push the AV valves closed (chordae tendinae prevent cusps from bulging into the atria) → The same pressure and blood pushes SL valves open → Ventricles relax → Blood flows back down the pulmonary trunk and aorta; fills cusps to force SL valves closed Flow through the cardiac conduction system: “Explanation from textbook”: Action potentials originate in the SAnode and travel across the wall of the atrium from the SAnode to theAV node.APs pass slowly thruAV node to give the atria time to contract. They then pass rapidly along theAV bundle, which extends from the AV node thru the fibrous skeleton into the IV septum. TheAV bundle divides into right and left bundle branches, andAPs descend rapidly to the apex of each ventricle along the bundle branches.APs are carried by the purkinje fibers from the bundle branches to the ventricular walls. The rapid conduction from theAV bundle to the ends of the purkinje fibers allows the ventricular muscle cells to contract in unison, providing a strong contraction. Myogenic - heartbeat originates within heart, not brain Autorhymthic - depolarize spontaneously regularly – SAnode: pacemaker; initiates heartbeat; sets heart rate; signal spreads through both atria; located in roof of right atrium – AV node: electrical gateway to ventricles ; located in side wall of right atria; can take over pacemaker role if SAnode fails – AV bundle (Bundle of His): pathway for signals fromAV node – Right and left bundle branches: divisions ofAV bundle that enter interventricular septum and descend to apex – Purkinje fibers: upward from apex spread throughout ventricular myocardium 6 Cardiac rhythm: Systole = contraction; Diastole= relaxation Sinus rhythm – normal rhythm set by SAnode – adult at rest is 70 to 80 bpm Ectopic Foci – region other than SAnode sets rhythm – nodal rhythm - set byAV node; 40 to 50 bpm – intrinsic ventricular rhythm – AV bundle; 20-40 bpm (not enough to sustain normal functioning so artificial pacemaker is implanted) Arrythmia - abnormal cardiac rhythm; On ECG would be conduction failure atAV node – caused by number of things including bundle disease/degeneration Ventricular fibrillation (V-Fib) – uncoordinated contraction – ventricles spasm→ heart cannot pump→ cardiac arrest – defibrillation – strong electrical shock to depolarize myocardium and restore normal heartbeat Cardiac output: • Amount ejected by each ventricle in 1 MIN • CO= HR X SV • Resting values: CO = 75 beats/min x70 ml/beat = 5,250 ml/min, usually about 4 to 6L/min – this means that all of the body’s blood is circulated in 1 minute (*a RBC leaving the heart will return in 1 min) • Vigorous exercise increases CO to 21 L/min for a fit person and up to 35 L/min for world class athlete (*they have a lower heart rate, but a higher stroke volume) • Cardiac reserve: difference between CO maximum (during exercise) and resting CO – Heart disease = little or no cardiac reserve Effects of exercise: • Effect of proprioceptors: – HR increases at beginning of exercise due to signals from joints, muscles • Effect of venous return: – muscular activity increases venous return causes increased stroke volume (SV) 7 • Increased HR and increased SV cause increased CO • Effect of ventricular hypertrophy: – caused by sustained program of exercise – Increased SV allows heart to beat more slowly at rest, 40-60bpm – Incresed cardiac reserve, can tolerate more exertion Diseases & disorders: Pericarditis- – Inflammation of the pericardium – Painful friction between the two membranes when the heart beats Cardiac tamponade- – Abnormal accumulation of fluid in the pericardial cavity – Compresses the heart – Interferes with ventricular filling • The chamber of the heart most affected by cardiac tamponade is the right ventricle. Myocardial Infarction- • Heart attack - sudden death of heart tissue • Caused by interruption of blood flow from the narrowing or occlusion of an artery supplying the heart with blood • Usually fat deposits or blood clots are responsible • Lack of O →2ischemia • If O 2upply is not restored, necrosis (tissue death) of myocardium occurs • Responsible for ~1/2 of all deaths in United States * Anastomoses defend against interruption by providing alternate blood pathways Angina Pectoralis- • Heart pain due to temporary and REVERSIBLE myocardial ischemia Hypoxia → Myocardium undergoes anaerobic fermentation → Lactic acid is produced → Pain receptors are stimulated. CoronaryAtherosclerosis - • Fatty deposits form in a coronary artery • Due to abnormal uptake of plasma lipids (ie. cholesterol) by the cells of the blood vessel • Corrected by: – by-pass surgery – a blood vessel from elsewhere in the body is used to direct blood flow around the area of blockage – balloon angioplasty – balloon is inflated in the artery to push the fatty deposit up against the blood vessel wall – laser angioplasty – laser used to destroy fatty deposit Ventricular fibrillation(V-FIB) – uncoordinated contraction – ventricles spasm → heart can’t pump → cardiac arrest – defibrillation – strong electrical shock to depolarize myocardium and restore normal heartbeat Heart murmur- • sound of blood flowing backward due to valvular insufficiency -Valvcular stenosis-- cusps are stiffened -Mitral valve prolapse-- mitral valve cusps culge into left atrium 8 – an incompetent valve can eventually lead to heart failure – defective valves can be replaced: pig valve or artificial valve Congestive heart failure- • a weakness of the heart that leads to a buildup of fluid in the lungs and surrounding body tissues. Clicker Questions: 1. Complete cessation of a heartbeat is called Cardiac arrest 2. Ablockage in the ___________ would cause the most damage to the heart. Left coronary artery 3. The heart does not receive any signals from the nervous system. False 4. Repolarization of the ventricles produces the ______ of the ECG. T wave 5. Aheart rate of 45 bpm and no Pwave on an ECG indicates SAnode damage 6. In an angiogram, the blood vessels are injected with a dye so that they may be visualized. The angiogram is used to detect Atherosclerosis Blood Vessels Most common route: heart→ arteries → arterioles → capillaries → venules → veins 9 Portal system: blood flows thru 2 consectutive capillary networks before returning to the heart Shunts and anastomoses: Anastomoses= 2 arteries/veins merge Arteriovenous shunt: artery directly to vein i.e. fingers, toes, and ears. This reduces heat loss, blood bypasses cold exposed areas, areas are vulnerable to frostbite. Venous anastomsis: 2 veins merge-- very common; alternate drainage of organs. Arterial anastomosis: alternative routes of blood flow; common around joints where movement can obstruct one pathway. Contrast arteries and veins: Arteries: more muscular than veins (smooth muscle) & thicker, can withstand great pressure from ventricular systole, perforated elastic tissue for expanding and recoiling, distribute blood among organs Veins: very porous, little smooth muscle/elastic tissue, exchange fluid w/ tissues at a specific site, thin walls, lower BP, expand easily, aid skeletal muscles in upward flow, collapse when empty, carry 54% of blood What tissues have few/no capillaries? -cartilage, cornea and lens of the eye Blood pressure: Highest in blood vessels closest to heart Diastolic: minimum BP between heartbeats Systolic: peak BP during ventricular systole Normal values: 120/80 Determined by? -cardiac output -blood volume -peripheral resistance: blood viscosity by RBCS and albumin (decreased viscocity with anemia, hypoproteinemia; increased viscosity with polycythemia, dehydration); vessel length with pressure and flow decline with distance; vessel radius is very powerful influence over flow-- radius is the most adjustable variable and controls resistance very quickly. Vasomotion is the change in vessel radius i.e. vasoconstriction, vasodilation. 10 Angiogenesis- local control of regulating BP and flow =growth of new vessels -regrowth of uterine lining, around obstructions, exercise, and malignant tumors -controlled by growth factors and inhibitors Causes and consequences of edema: Causes: -Increased capillary filtration: (increased capillary BP or permeability) >Poor venous return-- CHF, insufficient muscular activity >Kidney failure (water retention, hypertension) >Histamine makes capillaries more permeable >Increased age → increased capillary permeability -Reduced capillary reabsorption: not enough protein in blood (hypoproteinemia) → reduced osmosis from tissue >Cirrhosis: liver does not produce enough albumin >Famine: dietary protein deficiency >Protein excreted in urine-- burns, radiation sickness, kidney disease -Obstructed lymphatic drainage: lymphatic vessels usually absorb fluid from tissues & return it to bloodstream. Caused by obstructed lymphatic vessels or removal of lymph nodes. Consequences: -Circulatory shock: excess fluid in tissue spaces causes low blood volume and low BP -Tissue necrosis: oxygen delivery and waste remove become impaired -Pulmonary edema: suffocation -Cerebral edema: headaches, nausea, seizures, and coma Diseases & disorders: Hyper/hypotension: Hypertension: most common cardio problem >chronic resting BP greater than > 140/90 >30% ofAmericans over 50 y.o >50% ofAmericans over 74 y.o >Major cause of heart failure, stroke, & kidney failure >ventricles must work harder > myocardium enlarges → stretches and becomes less efficient strains by → endothelium tears → atheroscleosis >can weaken small arteries and cause aneurysms >arterioles in kidneys thicken → blood flow declines 1° Hypertension: due to obesity (need more bv → increases heart workload); sedentary (exercise controls weight, reduces emotional tension and stimulates vasodilation); diet (high cholesterol/fat → atherosclerosis; potassium and magnesium can reduce BP; now saying salt is unrelated maybe); nicotine (stimulant-- makes heart beat faster and harder thus promotes vasoconstriction → MI); & genetics (some are predisposed to HTN; more common in men from 18-54 y.o, but then becomes more common in women over 65 y.o.) 2° Hypertension: caused by another disease. Hypotension: chronic low resting BP >Causes: blood loss, dehydration, anemia Aneurysm: -weak point in blood vessel or heart wall 11 -bulging sac forms and pulsates with each heartbeat -can hemorrhage -can cause pain or death by exerting pressure on brain, nerve, air passages, or esophagus -can lead to neurological disorders, congestion of tissues, cough, difficulty breathing or swallowing Caused by: hypertension, artherosclerosis, congenital weakness of blood vessels, trauma, bacterial infections. *Dissecting aneurysm- blood pools between tunics causing degeneration of the tunica media Shock – all types: any state where cardiac output is insufficient to meet metabolic needs. -Cardiogenic shock: inadequate pumping of heart (MI) -Low venous return (LVR) Shock: 1) Hypovolemic shock- loss of blood volume (most common); from hemorrhage, trauma, bleeding ulcers, burns & dehydration 2) Obstructed venous return shock- tumor or aneurysm 3) Venous pooling (vascular) shock- long periods of standing, sitting or widespread vasodilation 4) Neurogenic shock- loss of vasomotor tone; caused from emotional shock to brainstem injury 5) Septic shock- bacterial toxins trigger vasodilation and increased capillary permeability 6) Anaphylactic shock- severe immune reaction causes generalized vasodilation and increased capillary permability TIA- transient ischemic attack: -dizziness, loss of vision, weakness, paralysis, headache -lasts from a moment to a few hours -often early warming of impending stroke CVA- cerebral vascular accident -brain infarction caused by ischemia-- atherosclerosis, thrombosis, ruptured aneurysm -effects range from unnoticable to fatal-- blindness, paralysis, loss of sensation, loss of speech Clicker Questions: 1. In cold conditions, it is crucial to keep vital organs of the body warm. Acirculatory adaptation to conserve body heat is Arteriovenous shunt 2. If all of the arteries of the body dilated at once, what would happen? Blood pressure would decrease 3. How does drinking alcohol affect blood pressure? It depends on when BP is measured 4. Which of the following should occur if you had hypertension? ANF would be released Respiratory Conducting verses respiratory divisions: Conducting division: passages serve only for airflow, nostrils to bronchioles Respiratory division: alevoli and distal gas-exhchange region. Upper verses lower respiratory tract: 12 Upper: is larynx and above- organs in head and neck; nose through larynx. Lower is trachea and below- organs of the thorax, trachea through lungs. Pleurae- 2 membrane layers - visceral and parietal layers • Visceral pleura– inner moist serous membrane; folds over • Parietal pleura – outer layer – adheres to mediastinum, diaphragm, rib cage – pulmonary ligament extends from base of each lung to diaphragm • Pleural cavity– space between pleurae; contains pleural fluid • Functions: – reduction of friction – creation of pressure gradient • lower pressure assists in inflation of lungs – compartmentalization • prevents spread of infection Pneumothorax: -Presence of air in pleural cavity. The loss of negative intrapleural pressure allows lungs to recoil and collapse. Resistance to airflow-The greater the resistance, the slower the air flow. Pulmonary compliance is the distensibility of the lungs. Decreased in disease with pulmonary fibrosis (TB). Bronchiolar diameter is the primary control over resistance to airflow: -Bronchoconstriction: triggered by airborne irritants, cold air, parasympathetic stimulation, histamine -Bronchodilation: sympathetic nerves, epinephrine Tidal volume -air inhaled or exhaled in one quiet breath (500 ml) Vital capacity: -amount of air that can be exhaled with maximum effort after maximum inspiration; assess strength of thoracic muscles and pulmonary function Primary stimulus of respiration= pH of CSF -Respiratory acidosis when pH is less than 7.35 caused by failure of pulmonary ventilation→ hypercapnia. -Respiratory alkalosis when pH is greater than 7.35 → hypocapnia. Hypercapnia/hypocapnia– what effects will they cause and how will the body compensate? Hypercapnia- (PCO2) is greater than > 43 mmHg. “Too much oxygen.” -CO2 easily crosses brain-blood barrier, in CSF the CO2 reacts with water and releases H+, central chemoreceptors strongly stimulate inspiratory center. -Corrected by hyperventilation. Pushes reaction to left by “blowing off” CO2 - CO2 (expired) + H2O ← H2CO3 ← HCO3- + H+ Hypocapnia- (PCO2) is less than < 37 mmHg. “Not enough oxygen.” -Corrected by hypoventilation, pushes reaction to right. - CO2 + H2O → H2CO3 → HCO3- + H+ -Increased H+ will lower pH back to normal *pH imbalances can have metabolic causes-- DM: fat oxidation causes ketoacidosis, can be compensated for by Kussmaul respiration (deep rapid breathing) 13 Apnea-temporary cessation of breathing Dyspnea-labored breathing Tachypnea-accelerated respiration Hyperventillation- increase in excess of metabolic demands. CO2 expelled too fast, this increases blood pH; often due to anxiety! Diseases and disorders: Ondine’s curse-automatic respiratory functions do not work so much remember to take each and every breath. Need to use ventilator while sleeping. Results from damage to brain stem i.e. tramua or poliomyelitis. Emphysema- COPD -alveolar walls break down, much less respiratory membrane for gas exchange, lungs fibrotic and less elastic, air passages collapse and obstruct outflow of air, air becomes trapped in lungs. Asthma- COPD - allergen triggers histamine release, intense bronchoconstriction Pneumonia: -alveoli filled with fluid -caused by: stretococcus pneumoniae, other bacteria, viruses, fungi, and protozoa Tuberculosis: -fibrosis of lungs -Mycobacteria infect lungs → lung forms tubercles around the invaders Decompression sickness: - “Bends” N2 bubbles in joints, bones, muscles, pulmonary capillaries Clicker Questions: 1) TheAdam’sApple is an area of the thyroid cartilage of the larynx that is usually more prominent in men. What could be a logical cause of the size difference? Testosterone stimulates the growth of the cartilage 2) Atracheostomy is the surgical creation of an opening in the trachea to bypass the upper respiratory tract if it becomes obstructed. What could be a complication of this procedure? Membranes of the respiratory tract dry out 3) The muscles used for respiration (inhalation & exhalation) are: Skeletal muscle 4) In pleurisy, the pleural membranes can become dry and inflamed. Each breath results in painful friction between the parietal and visceral pleura. This is similar to : Pericarditis 5) When you inhale, does your chest expand because your lungs inflate, or do your lungs inflate because your chest expands? Chest expands first 6) Which of these values should be the highest? Vital capacity Lymphatic & Immune Systems Function: 14 -Protect body from infections and disease -Maintain fluid balance -- absorbs plasma protein and tissue fluid and returns it to the bloodstream, 2-4 L/per -- interference with lymphatic drainage can lead to severe edema Lymph-clear fluid; similar to plasma but contains much less protein. Flows at low pressure and speed. Lymphatic capillaries-closed at one end; tethered by protein filaments; endothelial cells overlapped-- this allows bacteria and cells entry to lymphatic capillary; and creates valve-like flaps that open when interstitial fluid pressure is high, and close when its low and valve open up; closed down to prevent blackflow Mechanisms of flow: -Lymph flows at low pressure and speed. -Valves prevents backward flow. -Moved along primarily by rhythmic contractions of lymphatic vessels (stretching of vessels stimulates contraction) -Flow is aided by skeletal muscle pump. -Thoracic pump aids flow from abdominal to thoracic cavity. -Rapidly flowing bloodstream in subclavian veins, draws lymph into it. -Exercise significantly increases lymphatic return Route of lymphatic flow: lymphatic capillaries→ collecting vessels→ lymphatic trunk→ collecting ducts (right lymphatic duct or thoracic duct) → subclavian vein. Functions of: lymph nodes, tonsils, thymus & spleen Lymph nodes: -only organ that filters lymph -fewer efferent vessels, slows flow thru node: reticular cells, macrophages phagocytize foreign matter -lymphocytes respond to antigens -common sites for metastaic cancer Tonsils: -covered by epitelium, pathogens get into crypts and encounter lymphocytes -pharyngeal (on wall of pharynx); palatine (2 of them), can see them and can be removed; lingual (2 of them), root of tongue Thymus: -contains developing t-lymphocytes -secretes hormones (thymopoietin & thymosins) -very large in fetus, after age 14 begings involution -in elderly, mostly composed of fatty and fibrous tissue -cortex gives off trabeculae, divide parenchyma into lobules of cortex and medulla Spleen: -blood production in fetus -blood reservior -RBC disposal -immune reactions: filters blood, quick to detect antigens Non-specific defenses: -broadly effective, no prior exposure -external barriers -inflammation, fever 15 -From Textbook: external barriers, leukocytes and macrophages, antimicrobial proteins, immune surveillance, inflammation and fever; guard equally against a broad range of pathogens and their effectiveness does not depend on prior exposure, present from birth. External Barriers: Skin: toughness of keratin; dry and nutrient-poor; defensins: peptides, from neutrophils attack microbes; lactic acid (acid mantle) is a component of perspiration Mucous membrane: stickiness of mucus; lysozyme: enzyme destroys bacterial cell walls Subepithelial areolar tissue: tissue gel-- viscous barrier of hyaluronic acid; hyaluronidase-- enzyme used by pathogens Inflammation: -defensive response to tissue injury -limits spread of pathogens, then destroys them; removes debris, initiates tissue repair *Cardinal signs*: -erythemia (caused by hyperemia); -edema (caused by increased capillary permeability and filtration); -heat (caused by hyperemia); -pain (caused by inflammatory chemicals i.e. bradykinin, prostaglandins which are secreted by damaged cells, puts pressure on nerves Fever: -defense mechanism: can do more good than harm -promotes interferon activity -accelerating metabolic rate and tissue repair -inhibiting pathogen reproduction -Pyrogen: secreted by macrophages, stimualtes anterior hypothalamus to secrete PGE which resets body thermostat higher - 102° F. Fever greater than 105° may cause delirium, 111°-115° lead to coma-death. Stages of fever: onset, stadium, defervescence Types of non-specific WBCs: Neutrophils – phagocytize bacteria – create a killing zone • degranulation: lysosomes discharge into tissue flui.- triggers • respiratory burst: toxic chemicals are created (O 2 H O2, 2ClO) Eosinophils – phagocytize antigen-antibody complexes, allergens, inflammatory chemicals – enzymes block excess inflammation, limit action of histamine – antiparasitic effects: aggregate and release enzymes Other Leukocytes: Basophils – aid mobility and action of WBC’s by the release of: • histamine (vasodilator) increases blood flow to infected tissue • heparin (anticoagulant) prevents immobilization of phagocytes Lymphocytes – natural killer (NK) cells, nonspecific defense, large cells lyse host cells infected with viruses or cancerous Monocytes 16 – circulating precursors to macrophages Interferons- antimicrobial proteins: -Polypeptides secreted by cells invaded by viruses -Antiviral effect: generalized protection, interferons diffuse to neighboring cells and stimulate them to produce antiviral proteins; activates natural killer cells and macrophages which destroy infected host cells -Anticancer effect: stimulates destruction of cancer cells Mechanisms of complement action: group of proteins in blood that must be activated by pathogens to exert their effect. • Pathways of complement activation – classical pathway – alternate pathway • *Mechanisms of action:* – Enhanced inflammation-stimulates release of inflammatory chemicals – Opsonization- promotes phagocytosis – Cytolysis- membrane attack complex (MAC) • MembraneAttack Complex= Complement proteins form a ring in plasma membrane of enemy cell causing cytolysis Specific Immunity: -Specificity and memory • Humoral immunity: antibody mediated. From book: employs antibodies that do not directly estroy pathogen but tag them for destruction by mechanisms. Effective against extracellular viruses, bacterias, yeasts, protozoans, and noncellular pathogens such as toxins, venoms, and allergens. Only works against extracellular stages of infectious microorganisms. • Cellular immunity: cell-mediated. From book: employs lymphocytes that directly attack and destroy foreign cells or diseased host cells. Way to rid body of pathogens that reside in human cells where they are inaccessible to antibodies i.e. intracellular viruses, bacteria, yeasts, and protozoans.Also acts against parasitic worms, cancer cells, and cells of transplanted tissues and organs. Antigens: -Triggers an immune response -Complex molecules i.e. proteins, polysaccharides, glycoproteins, glycolipids -Antigentic determinants-epitopes Antibodies (you don’t need to know the 5 specific types): • By amino acid sequences of C region of antibody • IgA: monomer in plasma; dimer in mucus, saliva tears, milk, intestinal secretions, prevents adherence to epithelia • IgD: monomer; B cell membrane, antigen receptor • IgE: monomer; tonsils, skin, mucous membranes; stimulates release of histamines, attracts eosinophils • IgG: monomer; 75-85% circulating, crosses placenta to fetus, secondary immune response, binds complement • IgM: monomer; B cell membrane, antigen receptor; pentamer in plasma, 1° immune response, agglutination Humoral verses cellular specific immunity. What types of WBCs in each? What types of 17 pathogens does each protect against? >Humoral is antibody mediated. • Recognition- B cells recognize antigen, divide repeatedly, differentiate into plasma cells, produce antibodies specific to that antigen. Capping and endocytosis: antigen binds to several receptor sites on membrane of B cell. Receptor sites are drawn together into a cluster (looks like a worm).Antigen is taken into B cell by receptor-mediated endocytosis.Antigen is fully internalized. Display, clonal selection & plasma cell differentiation: 1) Immunocompetent B cells exposed to antigen.Antigen binds only to B cells with complementary receptors. 2) B cell displays processed antigen fragments. Helper T cell binds to B cell and secretes helper factor. 3) Helper factor stimulates B cell to divide repeatedly and form a clone. 4) Some cells of the clone become memory B cells. Most differentiate into plasma cells. 5) Plasma cells synthesize and secrete antibodies. • Attack- plasma cells release antibodies, bind to antigen, render it harmless, ‘tag it’for destruction Neutralization: antibodies mask pathogenic region of antigen Complement fixation: antigen binds to IgM or IgG, antibody changes shape, initiates complement binding; primary defense against foreign cells & bacteria Agglutination: Antibody has 2-10 binding sites, binds to multiple enemy cells immobilizing them Precipitation: similar process, antibody binds antigen molecules not cells; creates antigen- antibody complex that precipitates, phagocytized by eosinophil • Memory- some B cells differentiate into memory cells >Cellular is cell-mediated. • Lymphocytes attack and destroy foreign cells and diseased host cells • Cytotoxic (CD8) T cells - carry out attack • Helper (CD4) T cells - promote cytotoxic T cell action and coordinate other defenses • Suppressor T cells - limit attack • Delayed-hypersensitivity T cells – allergic reaction • Memory T cells - descended from cytotoxic T cells Recognition • Role of MHC-I proteins – found on nearly all body cells – display antigens produced by host cells – stimulate attack by cytotoxic T cells • Role of MHC-II proteins – found only on antigen presenting cells – stimulate helper T cells • MHC restriction: T cells in thymus develop receptors for either MHC-I or MHC-II proteins • T CellActivation: CD4 and CD8 proteins – CAMs that bind T cell to target cell – Linked to 2nd messenger system that triggers clonal selection: activated T cell enlarges, multiples, forms clone of identical T cells – Clonal selection requires costimulation helper T cells binds to macrophage macrophage releases interleukin-1 stimulates helper T cell to release and synthesize receptors for interleukin-2 18 causes large population of activated T cells Attack phase: role of helper T cells which secrete lymphokines and coordinate humoral and cellular immunity Memory: memory T cells- following clonal selection some, cells become memory cells. T cell recall response-- upon reexposure to same pathogen, memory cells launch a quick attack Primary verses secondary immune response: Primary – Complement fixation: antigen binds to IgM or IgG,Antibody changes shape, initiates complement binding; primary defense against foreign cells, bacteria Secondary – IgG: monomer; 75-85% circulating, crosses placenta to fetus, secondary immune response, binds complement – Hypersensitivity (Allergy) Excessive immune reaction against antigens that most people tolerate - allergens MHC: Major histocompatibility complex: family of genes on chromosome 6 that code for MHC proteins on theAPC surface that each as identification tags. When anAPC encounters an antigen, it internalizes via endocytosis, digests it and displays epitopes in grooves of the MHC proteins-- this is known as antigen processing. Immunological disorders: -Allergies & asthma -Autoimmune diseases 2 types of hypersensitivity: allergy & autoimmunity Allergy: excessive immune reaction against atnigens that most people tolerate-- allergens. Type 1 (acute) hypersensitivity- anaphylaxis occurs in sensitized people, allergen caps IgE on mast cells, basophils; release inflammatory chemicals, cause local edema, mucous hypersectretion, congestion; hives, water eyes, runny nose are typical Asthma (most common chronic illness in children)- inhaled allergens, histamines, bronchiole constriction Anaphylactic shock: bronchiolar constriction, dyspnea, vasodilation, shock, death; treatment=epinephrine Type III (immune complex) hypersensitivity: widespread antigen-antibody complexing complexes trigger intesnse inflammation, involved in acute glomerulonephritis and in systemic lupas erythematosus What can cause a failure of self-tolerance? Autoimmune Diseases Failure of self tolerance: 19 – Failure of cross-reactivity/antigenic mimicry • foreign antigens may be similar to self-antigens – abnormal exposure of self-antigens - barrier breach • Blood-testis barrier – changes in structure of self-antigens • induction by viruses – failure of clonal deletion in the thymus – mutations – heredity Production of autoantibodies Immunodeficiency: SCID- severe combines immunodeficiency disease – hereditary lack of T and B cells – vulnerability to opportunistic infection – “Bubble–boy” AIDS: – Invades helper T cells, macrophages, neutrophils and brain cells by “tricking” them to internalize the viruses by receptor mediated endocytosis – Retrovirus - reverse transcriptase uses viral RNA as template to synthesize DNA: • new DNAinserted into host cell DNA • may be dormant for months to years Clicker Questions: 1) If the right lymphatic duct was blocked, where might you see lymphedema? The right arm 2) Should tonsils routinely be removed if they become infected? No 3) In what situation would we derive the most benefit from inflammation? Alaceration to the arm 4) If parasitic worms infest the body, which type of white blood cells will be prevalent? Eosinophils 5) If you are vaccinated for polio, what type of immunity is produced? Artificial active immunity 6) The humoral immune response would be most effective against which of the following? Bacteria 7) Which type of cells help to control type I allergic reactions? Eosinophils Endocrine Posterior pituitary hormones and their general actions Stores and releases OT andADH which are produced in hypothalamus, transported down to 20 posterior love by hypothalamo-hypophyseal tract and the posterior pituitary secretes them. Nerve signals trigger release of these hormones. OT- labor contractions and milk release (lactation-ejection); synthetic forms of OT are used to induce labor in pregnant women. ADH- promotes water retention by the kidneys in response to low blood pressure Anterior pituitary hormones and their general actions Tropic hormones target other endocrine glands. Gonadotropins target gonads i.e. FSH & LH TSH a.k.a. Thyrotropin ACTH a.k.a. Corticotropin PRL GH a.k.a. Somatotropin Pituitary-gonadal axis, pituitary-adrenal axis, and pituitary-thyroid axis: principle hormones and target organs shown, most hormone production declines with age. Hormone Actions: FSH- Ovaries—stimulates development of eggs and follicles Testes—stimulates production of sperm LH- Females—stimulates ovulation → progesterone secretion Males—stimulates testosterone secretion ACTH- regulates milk synthesis, effect on adrenal cortex of the adrenal glands and secretion of glucocorticoids; regulates secretion of insulin from the pancreases PRL- Female—milk synthesis in mammary glands Male—increases LH sensitivity, thus increases testosterone secretion ADH- targets kidneys to increase water retention, reduce urine—which prevents dehydration; ADH also functions as a neurotransmitter. OT- Female—labor contractions, lactation (OT stimulates ejection of milk while PRL stimulates the production of milk) Male—possible roles in sperm transport & emotional bonding Both—surges during sexual arousal and orgasm by the propulsion of semen and uterine contractions GH- pituitary produces at least 1000x more GH than any other hormones. GH targets liver to produce somatomedins (insulin-like growth factors) which increase mitosis and cellular differentiation for tissue growth—protein synthesis, lipid metabolism, carbohydrate metabolism, electrolyte balance via promotes Na+, K+, Cl- retention, Ca2+ absorption. During childhood, GH involved with bone/cartilage/muscle growth. During adulthood, GH involved with osteoblastic activity, appositional growth affecting bone thickening and remodeling. Levels of GH: HIGHER during first 2 hours of deep sleep, after high protein meals, after vigorous exercise; LOWER after high carbohydrate meals. Declines with age→ less protein synthesis =Aging. At age 30 there is 10% bone, 30% muscle, and 20% fat and at age 75 there is 8% bone, 15% muscle, and 40% fat. Negative feedback: Increases target organ hormone levels inhibit release of tropic hormones. Pituitary disorders: Hypo-pituitarism: -Pituitary dwarfism which is in childhood with DECREASED GH. -Panhypo-pituitarism which is complete cessation of pituitary secretion, causes broad range of disorders including infertility
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