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BSC 182- Week three notes

by: Summer Schuler

BSC 182- Week three notes BSC 182

Summer Schuler
GPA 3.58
Human Physiology & Anatomy 2
Betsy Wargo

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Hey guys! Here are the notes from the last week of class. We have our first exam this Tuesday! I will be posting a study guide for that tonight. WEEK THREE NOTES START AT SLIDE #127 & GO TO THE END...
Human Physiology & Anatomy 2
Betsy Wargo
Class Notes
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This 149 page Class Notes was uploaded by Summer Schuler on Sunday September 6, 2015. The Class Notes belongs to BSC 182 at Illinois State University taught by Betsy Wargo in Fall 2015. Since its upload, it has received 27 views. For similar materials see Human Physiology & Anatomy 2 in Biological Sciences at Illinois State University.

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Date Created: 09/06/15
Endocrine Hormones System Overview Acts with nervous system to coordinate amp integrate activity of body cells Influences activities Response slower but longer lasting than nervous system Diffused pathway bloodstream9 slow response Hormones are systemic Endocrine System 39 Pinealgland Hypothalamus Pituitary gland ExoeXItcrIne Glands Thyroid gland leavmg the body to the skrn Parathyroid glands on dorsal aspect 0r caVItles ofthyroid gland Nonhormonal substances Thymus sweat saliva Have ducts to carry secretion Adrenal glands to membrane surface Endoinsidecrine Glands Pam39eas fluids bloodcirculatory pathways tissues Gonads Ovary female Produce hormones oTestis male No ducts Chemical Messengers Hormones longdistance chemical signals travel in blood or lymph Autocrines chemicals that exert effects on same cells that secrete them Paracrines locally acting chemicals that affect cells other than those that secrete them Autocrines and paracrines are local chemical messengers not considered part of endocrine system Chemistry of Hormones Two main classes Amino Acidbased hormones nonsteroidal Hydrophilic Amino acid derivatives peptides and proteins Steriods lipids oils amp fats Hydrophobic Synthesized from cholesterol Gonadal and adrenocortical hormones Mechanisms of Hormone Action Though hormones circulate systemically only cells with receptors for that hormone affected Target Cells the one that has the receptor Tissues with receptors for specific hormone Hormones alter target cell activity Mechanisms of Hormone Action Hormones act at receptors in one of two ways depending on their chemical nature and receptor location 1 Watersoluble hormones all amino acid based hormones except thyroid hormone Act on plasma membrane receptors Use second messengers Cannot enter cell Mechanisms of Hormone Action 2 Lipidsoluble hormones steroid and thyroid hormones Act on intracellular within the cell receptors that directly activate genes Can enter cell Intracellular Receptors and Direct Gene Activation Steroid hormones and thyroid hormone 1 Diffuse into target cells and bind with receptors within the cell 2 Receptor hormone enters nucleus binds to specific region of DNA 3 Prompts DNA transcription to produce mRNA 4 mRNA directs protein synthesis 5 Promote metabolic activities or promote synthesis of structural proteins or proteins for export from cell Target Cell Specificity Target cells must have specific receptors to which hormone binds for example Some hormones have only a few target cells ACTH receptors found only on certain cells of adrenal cortex Some hormones have many different target cells Thyroxin receptors are found on nearly all cells of the body Control of Hormone Release Blood levels of hormones Controlled by negative feedback systems Negative feedback systems turn off production of something when we have enough Vary only within narrow desirable range Endocrine gland stimulated to synthesize and release hormones in response to Humoral Stimuli 9 something in body s fluid is triggering a response Neural Stimuli neurons stimulate a release Ca 29 parathyroid hormones Hormonal Stimuli 9 hormones stimulate hormones Humoral Stimuli a Humoral Stimulus Hormone release caused by altered Changing blood levels of ions levels of certain critical ions or and nutrients directly stimulate nutrients secretion of hormones Capillary low Ca2 in blood Thyroid gland posterior view Example Ca2 in blood parathyroid glands Declining blood Ca2 concentration j stimulates parathyroid glands to secrete PTH parathyroid hormone 39 Parathyroid PTH causes Ca2 concentrations to glands sPTll rIse and stimulus IS removed Neural Stimuli Nerve fibers stimulate hormone release Sympathetic nervous system fibers stimulate adrenal medulla to secrete catecholamines Fight or flight norepinephrine Goes from a neurotransmitter to a hormonecan be either gtgt Adrenal gland or posterior pituitary gland b Neural Stimulus Hormone release caused by neural input CNS spinal cord sl Preganglionic sympathetic bers I Medulla of adrenal gland Hormonal Stimuli Hormones stimulate other endocrine organs to release their hormones Hypothalamic hormones stimulate release of most anterior pituitary hormones Anterior pituitary hormones stimulate targets to secrete still more hormones Hypothalamicpituitarytarget endocrine organ feedback loop hormones from final target organs inhibit release of anterior pituitary hormones c Hormonal Stimulus Hormone release caused by another hormone a tropic hormone Hypothalamus 7quot Anterior pituitary gland Nervous System Modulation Nervous system modifies stimulation of endocrine glands and their negative feedback mechanisms Example under severe stress hypothalamus and sympathetic nervous system activated 9 body glucose levels rise Nervous system can override normal endocrine controls Onset of Hormone Activity Some responses are almost immediate Some especially steroids hours to days Some must be activated in target cells Duration of Hormone Activity Limited Ranges from 10 seconds to several hours Effects may disappear as blood levels drop Some persist at low blood levels The Pituitary Gland and Hypothalamus Pituitary gland hypophysis has two major lobes Posterior pituitary Neurohypophysis Neural tissue Anterior pituitary Adenohypophysis Gland Less than Below Grow Gland that grows below the hypothalamus Glandular tissue Pituitaryhypothalamic Relationships Posterior pituitary lobe Extension of hypothalamic neural tissue Neural connection to hypothalamus hypothalamic hypophyseal tract Nuclei of hypothalamus make oxytocin amp antidiuretic hormone Neurohormones are transported to and stored in posterior pituitary quotpbthalah nus J Supraoptic nucleus lnfundlbulum connecting stalk Inferior Hypothalamic hypophyseal hypophyseal artery tr act lt Axon terminals Posteriorjobe of pltultary Posterior Pituitary and Hypothalamic Hormones Oxytocin and ADH Each composed of 9 amino acids Almost identical differ in 2 amino acids Oxytocin Strong stimulant of uterine contraction Released during childbirth Hormonal trigger for milk ejection Acts as neurotransmitter in brain ADH Vasopressin Prevents urine formation Regulates water balance Release also triggered by pain low blood pressure and drugs Inhibited by alchoholdiuretic High concentrations 9 vasoconstriction tightening of blood vessels Kidneys Extra notes from Lecture 1 Hypothalamus is the only place you see a releasing hormone RH Pituitary Gland Posterior Neural Stimulation tractneurons that connects the 2 hypothalamus pituitary Anterior Hormonal stimulation portalblood vessel connects the 2 hypothalamus pituitary Extra notes from Lecture 1 Paracrine nearby Autocrine Self Comparing Hormones Steroidal Cholesterol Insoluble in water Can diffuse thru plasma membranes Internal receptors StimulatesInhibits DNA Non Steroidal Amino Acids Water soluble Target cells have external receptor Stimulates a quot2nd messenger system Pituitaryhypothalamic Relationships Anterior Lobe Vascular connection to hypothalamus Hypophyseal portal system Carries releasing and inhibiting hormones only place we release releasing GHgTSHTACTH hormones is from the hypothalamus quot quotquotquota Always goes to the anterior pituitary regulate hormone secretion Hypothalamic neurons synthesize GHRH GHlH TRH 39 CRH GnRH PIH Hypophyseal portal system Pri ary capillary plexus Hypophyseal portal veins Secondary capillary plexus Anterior Pituitary Hormones Growth hormone GH Thyroidstimulating hormone TSH or thyrotropin Adrenocorticotropic hormone ACTH Folliclestimulating hormone FSH Luteinizing hormone LH Prolactin PRL Growth Hormone GH GH release chiefly regulated by hypothalamic hormones Growth hormone releasing hormone GHRH Stimulates release Growth hormone inhibiting hormone GHIH somatostatin Inhibits release Ghrelin hunger hormone also stimulates release Homeostatic Imbalances of Growth Hormone Hypersecretion In children results in gigantism In adults results in acromegaly Hyposecretion In children results in pituitary dwarfism Thyroidstimulating Hormone Thyrotropin Produced by thyrotropic cells of anterior pituitary Stimulates normal develoEment and secretory activity of t yroid l TRH t Anterir ituitar y H Release triggered by thyrotropinreleasing hormone w l W from hypothalamus t T5 Inhibited by rising blood levels Thy Ian OHMmid hormones that act on f Thyroid PItUItary and hypothalamus e e A w hormonee l Taret cells J Adrenocorticotropic Hormone Corticotropin Secreted by corticotropic cells of anterior pituitary Stimulates adrenal cortex to release corticosteroids Adrenocorticotropic Hormone Corticotropin U HYOthalamus H Regulation of ACTH release Triggered by hypothalamic corticotropin releasing hormone CRH in daily rhythm CRH H Anterior pituitary H l ACTH Internal and external factors such as fever hypoglycemia and StFESSOFS can J Adrenal Crtex U alter release of CRH e w u a Corticosteroids l Taret cells J Gonadotropins Folliclestimulating hormone FSH and luteinizing hormone LH Secreted by gonadotrophs secrets the gonadotropinsgonad nourishing cells of anterior pituitary FSH stimulates gamete egg or sperm production LH promotes production of gonadal hormones Absent from the blood in prepubertal boys and girls Gonadotropins Hythalamus I Regulation of gonadotropin release F GnRH Triggered by gonadotropinreleasing hormone GnRH during and after Ameri ituitary puberty Wquot 39 quot FSH d LH Gn IS abbrevratlon for gonadotropln F an Gnads J Suppressed by gonadal hormones F Estrogen feedback r m Target cells Prolactin PRL Secreted by prolactin cells of anterior pituitary Stimulates milk production Role in males not well understood Prolactin PRL Regulation of PRL release Primarily controlled by prolactininhibiting hormone PIH dopamine Blood levels rise toward end of pregnancy Suckling stimulates PRL release and promotes continued milk production Hypersecretion causes inappropriate lactation lack of menses infertility in females and impotence in males Thyroid Gland I b 39 39939 e 39 Isthmus of 5 W39 W thyroid gland Two lateral lobes connected by a ili f Trache Composed of follicles that produce thyroglobulin Colloid lled follicles Follicular cells Parafollicular cells produce the hormone calcitonin Parafollicular cells Thyroid Hormone TH Actually two related compounds T4 thyroxine T3 triodothyronine Both made from the follicle Hormones that are released into the bloodstream Affects virtually every cell in the body Thyroid Hormone Vajor metabolic hormone Increases metabolic rate Regulation of tissue growth and development Development of skeletal and nervous systems Reproductive capabilities Maintenance of blood pressure Transport and Regulation of TH H Hypothalamus H Negative feedback regulation of TH release TRH Rising TH levels provide negative Anterior pituitary feedback inhibition on release of TSH 2 TSH Hypothalamic thyrotropinreleasing Thymid g39and hormone TRH can overcome negative Thyroid hormones feedback during pregnancy or exposure t0 COId 1 Target cells J Calcitonin Produced by parafollicular cells Also called extrafollicular cells Antagonist to parathyroid hormone PTH At higher than normal doses Helps to keep Ca2 in bones Stimulates Ca2 uptake and incorporation into bone matrix Parathyroid Glands Four to eight tiny glands embedded in posterior aspect of thyroid Contain oxyphil cells function unknown parathyroid cells secrete parathyroid hormone PTH PTH most important hormone in Ca 2 homeostasis Parathyroid Hormone Functions Stimulates osteoclasts to digest bone matrix and release Ca2 Enhances reabsorption of Ca2 and secretion of phosphate by kidneys Promotes activation of vitamin D by kidneys increases absorption of Ca2 by intestinal mucosa Negative feedback control rising Ca2 in blood inhibits PTH release Homeostatic lmbalances of PTH Hyperparathyroidism excessive PTH due to tumor Bones soften and deform Elevated Ca2 Depresses nervous system contributes to formation of kidney stones Hypoparathyroidism following gland trauma or removal or dietary magnesium deficiency Results in tetany muscle tightenscontracts and won t release Muscle becomes unfuntionable respiratory paralysis and death Adrenal Suprarenal Glands Paired pyramidshaped organs atop kidneys Structurally and functionally are two glands in one Adrenal medulla nervous tissue part of sympathetic nervous system right next toon top of kidneys Adrenal cortex three layers of glandular tissue that synthesize and secrete corticosteroids right next toon top of kidneys Adrenal Cortex Three layers of cortex produce the different corticosteroids Zona glomerulosa 3 Mineralocorticoids g Sodium amp potassium ions Target and cause a release of the 53369 minerals in our system ltonex 7 3 Zona fasciculata Glucocorticoids Some level of control over our glucose levels Zona reticularis Gonadocoritcoids Gonads ovariestestes The hormones they produce estrogentestosterone gtgt Manufactured out of cholesterol Medth g V b jk lt 0 I 39 c l I 39 LCapsule Zona glomerulosa quot2 Zona fasciculata I 1quot quot 39 Zona llquot v reticularis Adrenal medulla Mineralocorticoids Regulate electrolytes Na and K in extracellular fluid Aldosterone most potent mineralocorticoid Causes water retention by kidneys Where sodium goes water goes Elimination of K Aldosterone Release triggered by Decreasing blood volume and blood pressure Rising blood levels of K Bloating during menstruation is caused from this It caused sodium levels to increase which causes water levels to increase No fluid 9 no blood pressure Lots of fluid high blood pressure Mechanisms of Aldosterone Secretion Reninangiotensinaldosterone mechanism decreased blood pressure stimulates kidneys to release renin 9 triggers formation of angiotensin 2 a potent stimulator of aldosterone release ACTH causes small increases of aldosterone during stress Atrial atria of the heart upper chamber natriuretic peptide ANP blocks renin and aldosterone secretion to decrease blood pressure when stressed Removes water from the system Glucocorticoids Keep blood glucose levels relatively constant IVIaintain blood pressure by increasing action of vasoconstrictors Cortisol hydrocortisone Only one in significant amounts in humans Can attribute to blood pressure changes vasoconstriction Cortisone Corticosterone Glucocorticoids Cortisol Released in response to ACTH Patterns of eating and activity Stress Prime metabolic effect is glucogucoseneo newgenesiscreation of9 New source of glucose Formation of glucose from fats and proteins Promotes rises in blood glucose fatty acids and amino acids quotSavesquot glucose for brain Enhances vasoconstriction 9 rise in blood pressure to quickly distribute nutrients to cells Gonadocorticoids Sex Hormones Vost weak androgens male sex hormones converted to testosterone in tissue cells some to estrogens IVIay contribute to Onset of puberty Appearance of secondary sex characteristics Sex drive in women adrenal glands produce testosterone for our sex drive Estrogens in postmenopausal women Adrenal Medulla Medullary chromaffin cells synthesize epinephrine 80 and norepinephrine 20 9stimuation of the medulla Effects Vasoconstriction Increased heart rate Increased blood glucose levels Blood diverted to brain heart and skeletal muscle Adrenal Medulla Responses are brief Epinephrine stimulates metabolic activities bronchial dilation and blood flow to skeletal muscles and heart Norepinephrine influences peripheral vasoconstriction and blood pressure Pineal Gland Small gland hanging from roof of third ventricle secretes melatonin derived from serotonin IVIeIatonin may affect Timing of sexual maturation and puberty Daynight cycles Physiological processes that show rhythmic variations body temperature sleep appetite Pancreas Triangular gland partially behind stomach Has both exocrine and endocrine cells Acinar cells exocrine produce enzymerich juice for digestion Pancreatic islets islets of Langerhans contain endocrine cells Alpha on cells produce glucagon Beta 3 cells produce insulin Glucagon Major target liver Causes increased blood glucose levels Effects Release of glucose to blood Glycogenolysis breakdown of glycogen to glucose Gluconeogenesis Synthesis of glucose from lactic acid and noncarbohyd rates Insulin Effects of insulin Lowers blood glucose levels Enhances membrane transport of glucose into fat and muscle cells Inhibits glycogenolysis and gluconeogenesis Participates in neuronal development and learning and memory Not needed for glucose uptake in liver kidney or brain Homeostatic Imbalances of Insulin Diabetes mellitus DIVI Due to hyposecretion type 1 or hypoactivity type 2 of insulin Blood glucose levels remain high 9 nausea 9 higher blood glucose levels Glycosuria glucose spilled into urine Diabetes Mellitus Signs Three cardinal signs of DIVI Polyuria huge urine output Glucose acts as osmotic diuretic Polydipsia excessive thirst From water loss due to polyuria Polyphagia excessive hunger and food consumption Cells cannot take up glucose are quotstarvingquot Homeostatic Imbalances of Insulin Hyperinsulinism Excessive insulin secretion Causes hypoglycemia Low blood glucose levels Anxiety nervousness disorientation unconsciousness even death Treated by sugar ingestion Ovaries and Placenta Gonads produce steroid sex hormones Same as those of adrenal cortex Ovaries produce estrogens and progesterone Estrogen Maturation of reproductive organs Appearance of secondary sexual characteristics With progesterone causes breast development and cyclic changes in uterine mucosa Placenta secretes estrogens progesterone and human chorionic gonadotropin hCG Testes Testes produce testosterone Initiates maturation of male reproductive organs Causes appearance of male secondary sexual characteristics and sex drive Necessary for normal sperm production Maintains reproductive organs in functional state Other Hormoneproducing Structures Adipose tissue Leptin appetite control stimulates increased energy expenditure Resistin insulin antagonist Adiponectin enhances sensitivity to insulin Other Hormoneproducing Structures Enteroendocrine intestinal hormones cells of gastrointestinal tract Gastrin stimulates release of HCI Secretin stimulates liver and pancreas Cholecystokinin CCK stimulates pancreas and gallbladder Other Hormoneproducing Structures Heart Atrial natriuretic peptide AN P decreases blood Na concentration blood pressure and blood volume decreases Kidneys Erythropoietin signals production of red blood cells Renin initiates the reninangiotensinaldosterone mechanism Results in increased blood pressure amp volume Blood Composition Blood Fluid connective tissue Plasma nonliving fluid matrix not just water Formed elements living blood quotcellsquot suspended in plasma Erythrocytes gtgt red blood cells or RBCs Leukocytes gtgt white blood cells or WBCs Platelets gtgt Little fragments that are circulating around Blood Composition Spun tube of blood yields three layers Plasma on top Erythrocytes on bottom WBCs and platelets in Buffy coat Plasma of total blood Buffy Boat 9 leukocytes 3 platelets Willi oft tal blond Hematocrit Percent of blood volume that is RBCs Erythrocytes l i b oftotal blood 47 i 5 for males 42 i 5 for females Physical Characteristics and Volume Color varies with 02 content High 02 Bright red scarlet Low 02 Darkred pH 735 745 Average volume S 6 Lfor males 4 S L for females Functions of Blood Functions include Distributing substances Delivering 02 and nutrients to body cells Transporting metabolic wastes to lungs and kidneys for elimination Transporting hormones from endocrine organs to target organs Functions of Blood Regulating blood levels of substances Maintaining body temperature by absorbing and distributing heat Maintaining normal pH using buffers alkaline reserve of bicarbonate ions Maintaining adequate fluid volume in circulatory system Functions of Blood Protection Preventing blood loss Plasma proteins and platelets initiate clot formation Preventing infection Antibodies Complement proteins WBCs Blood Plasma 90 water Over 100 dissolved solutes Nutrients gases hormones wastes proteins inorganic ions Plasma proteins most abundant solutes Remain in blood not taken up by cells Proteins produced mostly by liver Albumin 60 of plasma proteins smallest protein but largest percentage Functions Substance carrier things that don t get along in a watery environment Blood buffer Major contributor of plasma osmotic pressure Globulins Globe Three subcategories Alpha Transport molecule carry stuff around that wouldn t normally be compatible with a watery environment Beta Transport molecule Gamma Antibodies Transport molecules carry those compounds that do not circulate well in a watery plasma environment Fats cholesterol etc Formed Elements Only WBCs are complete cells RBCs have no nuclei or other organelles Starts off with a nucleus but as it matures it gets rid of it We need every little bit of area in a red blood cell specifically for hemoglobin Hemoglobin carries oxygen Platelets are cell fragments lVIost formed elements survive in bloodstream only few days lVIost blood cells originate in bone marrow and do not divide Erythrocytes Biconcave discs Anucleate No nucleus essentially no organelles 15 um Top View D i a m ete rs a rge r t h a n s o m e ca pi a ri e s Filled with hemoglobin Hb for gas transport Major factor contributing to blood viscosity thickness Erythrocytes Structural characteristics contribute to gas transport Biconcave shape flexibility huge surface area relative to volume gt97 hemoglobin not counting water No mitochondria do not consume 02 they transport Erythrocyte Function RBCs dedicated to respiratory gas 02 transport Hemoglobin binds reversibly with oxygen Hemoglobin Structure Globin composed of 4 polypeptide chains Two alpha and two beta chains Heme pigment bonded to each globin chain Gives blood red color Heme39s central iron atom binds one 02 Each Hb molecule can transport four 02 Each RBC contains 250 million Hb molecules Hemoglobin Hb 02 loading in lungs Oxygen binds with hemoglobin Produces oxyhemoglobin ruby red 02 unloading in tissues Oxygen detaches from hemoglobin Produces deoxyhemoglobin or reduced hemoglobin dark red C02 can also be carried on hemoglobin At a site separate from where oxygen binds Hematopoiesis The process of making blood Blood cell formation in red bone marrow In adult found in Axial skeleton Girdles collar bone scapula pelvic girdle Proximal epiphyses expanded ends of the bone of humerus and femur Hematopoiesis Hematopoietic stem cells Hemocytoblasts Starting point for blood cells Give rise to all formed elements Hormones and growth factors push cell toward specific pathway of blood cell development Committed cells cannot change Erythropoiesis Red Blood Cell Production Stages Myeloid stem cell transformed into proerythroblast In 15 days proerythroblasts develop into Basophilic erythroblasts then polychromatic erythroblasts then orthochromatic erythroblasts where we get rid of the nucleus then into reticulocytes more mature than everything else Blasts amp pros always come first Cytes always come after blasts Reticulocytes enter bloodstream in 2 days mature into RBC Regulation of Erythropoiesis Too few RBCs leads to tissue hypoxia not enough oxygen gtgt We want to keep red blood cell levels appropriate Too many RBCs increases blood viscosity Can effect blood pressure Hormonal Control of Erythropoiesis Hormone Erythropoietin EPO Direct stimulus for erythropoiesis Always a small amount in blood to maintain basal rate High RBC or 02 levels depress production Released by kidneys some from liver in response to hypoxia Hormonal Control of Erythropoiesis Causes of hypoxia Decreased RBC numbers hemorrhage or increased destruction Insufficient hemoglobin per RBC iron deficiency Reduced availability of 02 high altitudes Dietary Requirements for Erythropoiesis Nutrients amino acids lipids and carbohydrates Iron Available from diet 65 in Hb rest in liver spleen and bone marrow Vitamin 312 and folic acid necessary for DNA synthesis for rapidly dividing cells developing RBCs Fate and Destruction of Erythrocytes Life span 100120 days No protein synthesis growth division Old RBCs become fragile Hb begins to degenerate Get trapped in smaller circulatory channels especially in spleen Macrophages engulf dying RBCs in spleen Fate and Destruction of Erythrocytes Heme and globin are separated Iron salvaged for reuse Heme degraded to yellow pigment bilirubin Liver secretes bilirubin in bile into intestines Globin metabolized into amino acids Released into circulation Erythrocyte Disorders Anemia something is missing from the blood9symptom not a diagnosis Blood has abnormally low OZcarrying capacity Clinical sign Not a disease itself Blood 02 levels cannot support normal metabolism Accompanied by fatigue pallor shortness of breath and chills Causes of Anemia Three groups Blood loss Low RBC production High RBC destruction Symptoms of Anemia Red In severe Central anemia Fatigue Eyes Dizziness Yellowing Fai mng 3km Blood vessels Pa9n988 Low blood pressure Coldness Yellowing Hurt Palpitations Respiratory Shortness Ratp39d heart of breath a e Chest pain Muscular Angina Weakness Heart atack Intestinal Spleen Changed Enlarge stool color ment Causes of Anemia Blood Loss Acute hemorrhagic anemia Rapid blood loss Treated by blood replacement Chronic hemorrhagic anemia Slight but persistent blood loss Hemorrhoids bleeding ulcer If primary problem is treated it typically goes away Causes of Anemia Low RBC Production Irondeficiency anemia Caused by hemorrhagic anemia low iron intake or impaired absorption lVIicrocytic hypochromic red blood cells are smaller and pale RBCs Iron supplements to treat I 0 Causes of Anemia Low RBC Production Pernicious anemia Autoimmune disease destroys stomach mucosa Lack of intrinsic factor needed to absorb 312 Deficiency of vitamin B12 RBCs cannot divide 9 macrocytes Treated with B12 injections or nasal gel Also caused by low dietary BlZ vegetarians Causes of Anemia Low RBC Production Renal anemia Results from kidney damage Lack of erythropoeitin Often accompanies renal disease Treated with synthetic erythropoeitin Causes of Anemia Low RBC Production Aplastic anemia Destruction or inhibition of red marrow by drugs chemicals radiation viruses Usually cause unknown All cell lines affected Anemia clotting and immunity defects Treated shortterm with transfusions longterm with transplanted stem cells Causes of Anemia High RBC Destruction Hemolytic bloodbreaking anemia Being destroyed after we make them Premature RBC lysis Caused by Hb abnormalities I Incompatible transfusions Infections Causes of Anemia High RBC Destruction Usually genetic basis for abnormal Hb Hemoglobin Globin abnormal Fragile RBCs lyse prematurely Causes of Anemia High RBC Destruction Thalassemias Typically Mediterranean ancestry One globin chain absent or faulty o RBCs thin delicate deficient in Hb Many subtypes Severity from mild to severe UV V3 3 39 G i Causes of Anemia High RBC Destruction Sicklecell anemia 463 Hemoglobin S quot5 am One ammo and wrong In a globln Q I J 2 beta chain mg C RBCs are crescentshaped when the unload 02 or when blood 02 low RBCs rupture easily and block small x vessels Poor 02 delivery pain Sicklecell Anemia Black people of African malarial belt and descendants Malaria Kills 1 million each year Sicklecell gene Two copies 9 Sicklecell anemia One copy 9 Sicklecell trait milder disease better chance to survive malaria Erythrocyte Disorders Polycythemia vera True overproduction of cells Bone marrow cancer 9 excess RBCs Severely increased blood viscosity egfi 7 quotquot ii 3 quot Secondary polycythemia 39 w Less 02 available andor EPO 3 production increases 9 higher RBC count Blood doping artificially increase the number of our blood cells Leukocytes Make up lt1 of total blood volume Function in defense against disease Can leave capillaries via diapedesis Move through tissue spaces by ameboid motion and positive chemotaxis positive chemical movement Leukocytosis WBC count over 11000mm3 Normal response to infection Leukocytes Two Categories Granulocytes Visible cytoplasmic granules grainy cells Neutrophils eosinophils basophils Agranulocytes No visible cytoplasmic granules Lymphocytes monocytes Memory tools ever let monkeys eat bananas 6040830 Nanna lost my Easter bow Granulocytes Granulocytes Larger and shorterlived than RBCs Lobed nuclei Cytoplasmic granules stain specifically with Wright39s stain All phagocytic to some degree Neutrophils Vost numerous WBCs Granules stain lilac hot purple Contain hydrolytic enzymes or defensins 39 J P a 36 lobes in nucleus Twice the size of RBCs a Neutrophil Multilobed nucleus pale red and blue cytoplasmic granules Very phagocytic first to arrive to help clean up quotbacteria slayers Eosinophils Redstaining granules Bilobed nucleus Granules lysosomelike Release enzymes to digest parasitic worms Role in allergies and asthma b Eosinophil Bilobed nucleus red cytoplasmic granules Role in modulating immune response Basoph s Rarest WBC s Bilobed nucleus Large purplishblack granules contain histamine Histamine inflammatory chemical that acts as vasodilator to attract WBCs to inflamed sites Are functionally similar to mast cells BEN s Granny Basophil Eosinophil Neutrophil GrainyGranny c Basophil Bilobed nucleus purplishblack cytoplasmic granules Agranulocytes Agranulocytes Lack visible cytoplasmic granules Have spherical or kidneyshaped nuclei Lymphocytes Second most numerous WBC Large darkpurple circular nuclei with thin rim of blue cytoplasm Mostly in lymphoid tissue eg lymph nodes spleen few circulate in blood Crucial to immunity I J d Lymphocyte small Large spherical nucleus thin rim of pale blue cytoplasm Lymphocytes Two types T lymphocytes T cells act against virusinfected cells and tumor cells B lymphocytes B cells give rise to plasma cells which produce antibodies Monocytes Largest leukocytes Abundant paleblue cytoplasm Dark purplestaining U or kidneyshaped nuclei e Monocyte Kidneyshaped nucleus abundant pale blue cytoplasm Monocytes Leave circulation enter tissues and differentiate into macrophages Actively phagocytic cells crucial against viruses intracellular bacterial parasites and chronic infections Activate lymphocytes to mount an immune response Leukopoiesis All leukocytes originate from hemocytoblasts Lymphoid stem cells 9 lymphocytes Vyeloid stem cells 9 all others Progression of all granulocytes Myeloblast 9 promyelocyte 9 myelocyte 9 band 9 mature cell Granulocytes stored in bone marrow 3 times more WBCs produced than RBCs Shorter life span die fighting microbes Leukopoiesis Progression of agranulocytes differs Vonocytes live several months Share common precursor with neutrophils lVIonoblast 9 promonocyte 9 monocyte Lymphocytes live few hours to decades Lymphoid stem cell 9 T lymphocyte precursors travel to thymus and B lymphocyte precursors Figure 1711 Leukocyte formation Stem cells Hematopoietic stem cell hemocytoblast 3 39 Myeloid stem cell Lymphoid stem cell Committed J I i l 1 cells Myeloblast Myeloblast Myeloblast Monoblast B lymphocyte T lymphocyte 0 0 0 0 precursor precursor Developmental P pathway Promyelocyte Promyelocyte Promyelocyte romonocyte Eosinophilic Basophilic Neutrophilic myelocyte myelocyte myelocyte Eosinophilic Basophilic Neutrophilic b 3 has Granular Agranular leukocytes leukocyte v v Eosinophils Basophils Neutrophils Monocytes B lymphocytes T lymphocytes a 39 1 b c d e f 0 Some become Some become Some become Macrophages tissues Plasma cells Effector T cells Leukocyte disorders Leukopenia Abnormally low WBC count Leukemias all fatal if untreated Cancer 9 overproduction of abnormal WBC s Myeloid leukemia Involves myeloblast descendants neutrophil eosinophil basophil monocyte Lymphocytic Lymphoid leukemia involves lymphocytes Acute leukemia derives from stem cells primarily affects children Chronic leukemia more prevalent in older people Leukemia Cancerous leukocytes fill red bone marrow Other cells compromised Fewer functional RBCs anemia Fewer functional platelets bleeding Immature nonfunctional WBCs in bloodstream Death from internal hemorrhage overwhelming infections Treatments Irradiation antileukemic drugs stem cell transplants Infectious Mononucleosis Higth contagious viral disease EpsteinBarr virus High numbers atypical agranulocytes lVIonocytes and lymphocytes Symptoms Tired achy chronic sore throat low fever Runs course with rest Platelets Cytoplasmic fragments of megakaryocytes Bluestaining outer region purple granules Platelets Form temporary platelet plug that helps seal breaks in blood vessels Circulating platelets kept inactive until needed Age quickly degenerate in about 10 days Platelets Formation regulated by thrombopoietin Derive from megakaryoblast Stem cell Developmental pathway 44 Hematopoietic stem Megakaryoblast Megakaryocyte Meakaryocyte Platelets cell hemocytoblast stage I megakaryocyte stage IIIlll stage IV Hemostasis Fast series of reactions for stoppage of bleeding Requires clotting factors and substances released by platelets and injured tissues Three steps 1 Vascular spasm 2 Platelet plug formation 3 Coagulation blood clotting Hemostasis Vascular Spasm Vasoconstriction of damaged blood vessel Triggers Direct injury to vascular smooth muscle Chemicals released by endothelial cells and platelets Pain reflexes Vost effective in smaller blood vessels Hemostasis Platelet Plug Formation Positive feedback cycle Damaged endothelium exposes collagen fibers Platelets stick to collagen fibers Swell become spiked and sticky release chemical messengers Process encourages more vascular spasm and more platelet formation Positive feedback Hemostasis Coagulation Reinforces platelet plug with fibrin threads Blood transformed from liquid to gel Series of reactions using clotting factors Coagulation Intrinsic pathway Uses factors present within blood intrinsic Causes clotting outside of the body Blood in a glass test tube Extrinsic pathway Typically triggered with tissue damage Bypasses several steps of intrinsic pathway Faster Both Extrinsic and Intrinsic pathways merge together to create a common pathway that results in coagulation Coagulation Clotting9 Fibrinogen ogeninactive dissolved plasma protein fibrin insoluble creates mesh Plasminogen becomes active form of plasmin helps us break down the clot Thrombin converts soluble fibrinogen to fibrin Fibrin strands form structural basis of clot Fibrin causes plasma to become a gellike trap for formed elements Thrombin with Ca2 activates another clotting factor which Crosslinks fibrin Strengthens and stabilizes clot Clot Retraction Stabilizes clot Actin and myosin in platelets contract within 30 60 minutes Contraction pulls on fibrin strands squeezing serum from clot Draws ruptured blood vessel edges together Fibrinolysis Removes unneeded cots after healing Begins within two days continues for several Plasminogen in dot is converted to plasmin by tissue plasminogen activator more clotting factors and thrombin Plasmin is a fibrindigesting enzyme Disorders of Hemostasis Thromboembolic disorders undesirable clot formation Bleeding disorders abnormalities that prevent normal clot formation Disseminated intravascular coagulation DIC Involves both types of disorders Thromboembolic Conditions Thrombus clot that develops and persists in unbroken blood vessel May block circulation leading to tissue death Embolus thrombus freely floating in bloodstream Embolism embolus obstructing a vessel Eg pulmonary and cerebral emboli Pulmonary embolism deep vein thrombosis Risk factors atherosclerosis inflammation slowly flowing blood or blood stasis from immobility Petechiae Bleeding Disorders Thrombocytopenia Not enough clotting cells 39 39 D not bla h 39tl Not enough CIrculatIng platelets pressg rie W39 Not palpable Petechiae appear due to spontaneous widespread hemorrhage Due to suppression or destruction of red bone marrow Treated with transfusion of concentrated platelets Bleeding Disorders Impaired liver function Inability to synthesize procoagulants Causes include vitamin K deficiency hepatitis and cirrhosis Impaired fat absorption and liver disease can also prevent liver from producing bile impairing fat and vitamin K absorption Bleeding Disorders Hemophilia includes several similar hereditary bleeding disorders Hemophilia A most common type 77 of all cases factor 8 deficiency Hemophilia B factor 9 deficiency Hemophilia C mild type factor 11 deficiency Symptoms include prolonged bleeding especially into joint cavities Memory tools A8 same vowel sound B9 benign C11 Disseminated lntravascular Coagulation DIC Widespread within blood vessels Widespread clotting event in blood vessels that aren t necessarily damaged Clotting causes bleeding Widespread clotting blocks intact blood vessels Severe bleeding occurs because residual blood unable to clot Occurs As pregnancy complication In septicemia with incompatible blood transfusions Transfusions Wholeblood transfusions used when blood loss rapid and substantial Packed red cells plasma and WBCs removed transfused to restore oxygencarrying capacity Transfusion of incompatible blood can be fatal Human Blood Groups RBC membranes bear 30 types of glycoprotein antigens Anything perceived as foreign generates an immune response Promoters of agglutination called agglutinogens can create a glutinogen response IVIismatched transfused blood perceived as foreign May be agglutinated and destroyed can be fatal Presence or absence of each antigen is used to classify blood cells into different groups Blood Groups Antigens of ABC and Rh blood groups cause vigorous transfusion reactions Other blood groups IVINS Duffy Kell and Lewis usually weak agglutinogens Type O is the universal donor ABO Blood Groups Types A B AB and 0 Based on presence or absence of two agglutinogens A and B on surface of RBCs Blood may contain circulating antiA or antiB antibodies Antibodies seek out and attach to nonself markers AntiA or antiB form in blood at about 2 months of age adult levels by 810 years of age Antigen is on the red blood cell Antibody is in the plasma Anti j H Type A Blood iii 1quot quot a Type A Blood has antigen A on the cell surface It has antibody B circulating in the plasma Will attach to any type B antigen B antigens would be foreign nonself to this individual There will be NO reaction between the Type A antigen on the surface and the AntiB antibody in the plasma Type B Blood Type B Blood has antigen B on the cell surface It has antibody A circulating in the plasma Will attach to any type A antigen A antigens would be foreign nonself to this individual There will be NO reaction between the Type B antigen on the surface and the AntiA antibody in the plasma Type AB Blood Type AB blood has both antigen A and B displayed on the surface There will be NO ABO antibodies circulating in the blood if there were there would be an agglutination response which could be fatal Because there are NO antibodies in the bloodstream this blood type is considered a Universal Recipient You can put any blood cell into this environment and not have an agglutination reaction because there are no antibodies in the host plasma Type 0 blood Annsan AntiA4 Type 0 blood has NO antigens on the cell surface Because of this ANY antigen is considered nonself so the plasma will have BOTH antiA and antiB antibodies Type 0 blood is considered a Universal Donor because the Type 0 blood cell with no antigens can safely go into any other blood type With no antigens on the surface there will be no interaction with any of the antibodies found in the host Rh Blood Groups 52 named Rh factors C D and E are most common Rh indicates presence of D antigen 85 Americans Rh Rh Blood Groups An individual with no D antigen on the blood cell surface will NOT have circulating Rh antibodies but they CAN make them following exposure to antigen D Second exposure to Rh blood will result in typical transfusion reaction Homeostatic Imbalance Hemolytic Disease of the Newborn Also called erythroblastosis fetalis Only occurs in Rh mom with Rh fetus Rh mom exposed to Rh blood of fetus during delivery of first baby baby healthy Mother synthesizes antiRh antibodies Antibodies are lgM type huge and can not cross the placenta Second pregnancy or second exposure Antibodies formed are lgG type tiny and CAN cross the placenta Destroy RBCs of Rh baby Homeostatic Imbalance Hemolytic Disease of the Newborn Baby treated with prebirth transfusions and exchange transfusions after birth RhoGAIVI serum containing antiRh can prevent Rh mother from becoming sensitized Transfusion Reactions Occur if mismatched blood infused DononsceHs Attacked by recipient39s plasma agglutinins Agglutinate and clog small vessels Rupture and release hemoglobin into bloodstream Result in Diminished oxygencarrying capacity Diminished blood flow beyond blocked vessels Hemoglobin in kidney tubules 9 renal failure Transfusion Reactions Symptoms Fever chills low blood pressure rapid heartbeat nausea vomiting Treatment Preventing kidney damage Fluids and diuretics to wash out hemoglobin


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