Pathophysiology NUR 300
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Date Created: 09/19/15
AN EMIA MECHANISM CAUSES RETIC OTHER CHROMIC UNIQUE MISC COUNT LABS CYTIC SSx Acute Blood Loss lose it 7 lose RBCs trauma surg T need MCHC nml Normochromic Fast so less time Labs with slow return to nml from the body quickly OB normal MCV nml Nuuuuc tic to J c 39 39 takes 34 complications kidneys and more wks to replace lost RBCs amp manifestations Retic count takes a few days marrow Pt may have to increase low blood volume ampbe in shock CV III Chronic Blood lose it but occurs over slow GI bleed T need MCHC l Hypochromic Black tarry Recall pic from lecture of Loss several weeks really an ulcer normal MCV l lIicrocytic stools if slow GI bleeding ulcer iron deficiency anemia kidneys bc iron def bleed GI I bc iron is chronically amp See notes on means not depleted amp lost from marrow iron def enough nml the body instead of anemia Hb need 4 getting recycled heme ironHb 9 iron and bilirubin Sickle Cell destroy it inherited Inherited so T need MCV l lIicrocytic HandFoot Disease hemolytic from bad Hb genetic defect normal MCHC l because the Syndrome due which makes RBCs of gene that kidneys deformed shap to clotting in sickle when Hb is makes Hb amp will reduce small vessels in deoxygenated low HbS marrow size of RBC the hands and PaOZ hypoxemia then Hypochromic feet causes vessels to clog Homozygous because of the Splenic crisis ampRBC to break disease low Hb 1 due to abnml m may want to draw cells building up flow chart expand on Heterozygous and impairing how this relates to trait the spleen ssx Angina Ischemic Stroke Thalassemias Destroy It inherited Inherited T autosomal recessive many inheritance caused by different bad Hb kinds Some affect 3 chains while Cellulag Inium Ceuar changeadapted cell9apoptosis atrophy hypertrophy mm nerves cardiac because cells can t reenter cell cycle hyperplasia metaplasia dysplasia accumulations metaplasia one nml cell type another OR dysplasia nml cell messed up cell can lead to anaplasia if inflammation continues Ceuar injury9abnormal cell necrosis free radical hypoxia anaplasia electrolyte imbalance Anything that hurts us hurts cells K INTO cell Na OUT OF cell Neoplasia Benign well differenciated slow growth late in cell cycle grows by expansion encapsulated does NOT metastasize effects are local mass effect only causes tissue destruction if mass impinges on blood vessels ischemia only causes death if interferes with vital functions brain heart lungs Malignant poorly differenctiated fast growth early in cell cycle grows at periphery amp invasion9surrounding tissue not encapsulated does metastasize effects local amp systemic I r I amp causes tissue destruction by invasion usually causes death unless controlled Gene Types Genes that regulate DNA repair DNA sequences in nml cells that can fix or remove mutations that occur turned OFF in cancer cells Genes that control cell replication amp proliferation protooncogenes DNA sequences in nml cells that promote growth amp proliferation in nml cells only on for short amount of time continuously ON in cancer cells tumor suppressor genes quotantioncogenesquot DNA sequences in nml cells that inhibit growth amp proliferation mutations inactivate them turned OFF in cancer cells p53 suppressor protein inhibits angiogenesis BRCA1 inhibits estrogen receptor activity Genes that control healthy cell death apoptosis DNA sequences in nml cells that remove oldunwanted cells in regulated way turned OFF in cancer cells may be tumor suppressor genes Hematogoiesis amp Hemostasis Hematopoiesis making of RBCs WBCs amp platelets starts in bone marrow some mature in lymph tissue Hemostasis clot formation 1 Vessel Spasm 2 Formation of platelet plug vWF connect plts to subendothelium cluster defective plt plug9BLEEDING due to NSAIDs amp aspirin inhibiting this step OR prob wfactors 3 IntrinsicExtrinsic pathways9lnsoluble fibrin clot defective clotting cascade BLEEDlNG due to anticoagulants Natural anticoagulants heparin plasmin Drug anticoagulant heparin warfarin 4 Clot retraction 5 Clot dissolution Hygercoagulabiliy ncreased plt activity Anything that damages endothelial cells atherosclerosis DM smoking lncreased plt increased bone marrow production decreased plt destruction ncreased clotting cascade activity nherited disorders factor 5 Leiden mutation can t be turned off amp keeps clotting Acquired disorders blood ow stasis inactivity causing blood components squished together cancer sepsis crush injuries release tissue factor extrinsic system increased estrogen from pregOCP increases coag factor syn in liver Bleeding Disorders Decreased plt function Defective platelets vWF disease NSAIDSaspirin Decreased plt decreased bone marrow production increased plt destruction spleen takes old cells out of circulation SSx chronic bleeding in small vessels petechiae amp purpura bleeding from muc membranes Decreased clotting cascade activity lmpaired coag factor synthesis liver failure Vit K de ciencyHypocalcemia Clotting factor consumption late DIC nherited disorders hemophilia lowbad factor 89 or vWF disease DC p r U widespread bleeding throughout body secondary complication of other disorder Early DIC coag cascade is activated in vessels throughout body more clottinggtbleeding Late DIC more bleedinggtclotting plts amp coag factors used up RBC Disorders RBC Formation Decreased mature RBCS decreased blood flow increased 02 demands decreased 02 to tissues EPO secreted by kidneys bone marrow stimulated amp releases retiks amp RBCs RBCs mature amp eventually get phagocytosed in spleen which releases heme amp globin 9Heme9iron amp bilirubin iron reused by bone marrow or stored in spleenliver amp bilirubin conjugated by liver secreted Anemias low RBC countlow Hb concentraition see chart SSx depend more on how fast anemia develops rather than RBC countHb concentration General SSx fatigue weakness dyspnea HA angina decreased 02 carrying capacity amp hypoxia pale skin redistribution of blood to important areas tachycardia from high output failure from body trying to compensate amp maintain 02 delivery bone pain bone marrow being stimulated extra by body trying to compensate Newborn Hyperbilirubinemia immature liver amp shorter RBC lifespan liver can t conjugate the increased amount of RBCs coming in Newborn Hemolytic Disease hemolysis of fetal RBCs by maternal antibodies Rh mom sensitization mom s been exposed to Rh factor amp made Ab Rh fetus so moms body attacks babies WBC Disorders Lymphoma malignant proliferation of lymphoid tissue cells WBCs in the periphery that begins as solid tumors Hodgkin s Disease lymphoma from malignant proliferation of ReedSternberg cells quotowl eye cells SOME CARCINOGIC AGENT no specific cause increased risk if hx of mono EbsteinBarr virus9alters WBC DNA causing ReedSternberg cells Stage A painless lymph tissue enlargement in E area of the body Stage B disease spreads through lymph system SSx weight loss amp fatigue fever amp night sweats anemia pruritus if advanced liver lung CNS NonHodgkin s lymphoma from malignant proliferation of B or Tcells at any stage in periphery SOME CARCINOGENIC AGENT alters WBC DNA Starts with painless lymph tissue enlargement in my areas of the body noncontigouous spread invades other organs SSx depend on type of cell amp it s stage of development Leukemia malignant proliferation ofany blood cell that begins in the bone marrow No speci c cause increased risk wradiation chemotherapy genetic congenital disorder virus SSx depend on acute or chronic amp lymphocytic or myelocytic cells Acute Lymphocytic Leukemia ALL immature preB sT s in bone marrow mostly children Acute Myelocytic Leukemia MLL immature pm g 39 39 in bone marrow mostly adult linked wtoxins amp congenital disorders Chronic Lymphocytic Leukemia differentiated B sT s in bone marrow mostly elderly I39L I Chronic Myelocytic Leukemia 5 in bone marrow mostly adult linked wPhiladelphia chromosome9C9C22 trade places so oncogene keeps r 1 cell division turned on Pain Receptor spinal cord Spinal cord9brain Brain part of body Dermatomes regions of body supplied by single sensory neuron DRG Types Cutaneous exact sharp burning in ski Deep Somatic diffuse throbbing in mmZboneZtendon Neuropathic shooting stabbing burning paresthesias in nerves Viscera diffuse poorly localizeddefined in many but not all organs Referred sensation of pain at a site that s not directly stimulated or injured often cutaneous pain referred from visceral stimulus 2 different 1st order sensory nerves same spinal cord segment signals get mixed up Inflammation amp Healing Loca Manifestations 5 cardinal signs redness warmth swelling pain amp possible loss of fnx Exudate from increased vascular permeability Serousclearish watery thin Serosanguinouswatery w RBCs pink Hemorrhagic bloody PurulentSuppurative WBCs pus Systemic Manifestations Acute Phase Response fever inflammation increase increased erythrocyte sed rate amp CRP hypermetabolism muscle catabolism lethargy from lL l lL6 amp TNF Leukocytosis increased WBCs or quotleft shift increased immature WBCs from cytokines increasing hematopoiesis Leukopenia decreased WBCs from being used up when bone marrow can t keep up with demand Lymphadenitis nearby lymph nodes reacting amp making more cells Scar Formation severe acute inflammation or chronic inflammation Sepsis amp Septic Shock from widespread systemic reaction too many cells injured can t compensate Immunde Disorders APC9binds to CD4 Tcell through MHCTCR CD4 orchestrates response MHC Major Histamine Complex molecules receptors on immune cells that hold pieces of antigen amp bind Tcell receptorsMHCTCR complexidentify as SELF if can t bindFOREGN cell dies off CD4 Tcells orchestrates immune response by amplifying ceIImediated virus infected cell CD8 cells amp Tcells end viral infections kill intracellular bacteriafungiprotozoa reject graft tissue amp control malignant cells humoral virusbacteria in fluid Bcells amp antibodies kills bacteria neutralizes toxins MotherInfant Immunity IgG from mom baby long term immunity through placenta then decreases 36 months at 6 months baby starts making own AIDS acquired disorder where the human immunode ciency virus RNA infects CD4 helper Tcells amp patient eventually becomes unable to have effective immune response humoral amp cellmediated responses fail neither can occur without CD4 cells Window Period infection time person tests positive HVperson tests positive for HIV Ab 13 months 1 Primary Infection 24 weeks fast viral rep wpeaking viral loads as it infects cells CD4 decreases cells attacked then increases body tries to compensate SSx HIV Acute Clinical Syndrome HIV acute mono ssx like fever fatigue lymphadenopathy seroconversion person goes from testing to best time to initiate treatment 2 Latency Chronic Asymptomatic 810 years constant viral rep held in check by immune system slow replication amp low viral load CD4 slowly decrease body eventually can t replace cells SSx lymphadenopahty not too sick 3 Overt AIDS 23 years viral rep amp viral load increases steadily CD4 plummet virus very active amp killing lots of cells body can no longer replace them Diagnosed by CD4 cell count lt200uL OR AIDS defining illness AIDS Illness amp gt500 cells g no defining AIDS Illness amp lt200 cells Cardiovascular Disoders Blood Pressure BPC0 SVxHR x PVR Regulation ST Neural decreased BP increase baroreceptors9increase SNS ANS PNS ANSincrease SV increase C0 PNS9vasoconstriction9increase HRNCREASE BP decreased 02pH increased C029increase chemoreceptors9increase vasoconstriction 9increase HR9increase BP LT Neural Regulation of ECF by aldosterone RAAS renin kidney 9converts Ang to Angl Angl converts to Angll in lungs Angll stimulates aldosterone to hold in sodium AHD acts on kidneys to hold in water Atherosclerosis pastelike changes leading to clogginghardening of arteries Coronary Artery Disease atherosclerosis in coronary arteries leads to Chronic lschemic Heart Disease atherosoclerosis in coronary arteries9stenosis9 stabe anginapain when increased 02 demand amp silent myocardial ischemia Acute Coronary Syndromes heart attack plaque erodes thrombus embolism 9minor plaque disruption unstable angina painrest amp NonSTsegment elevation Ml 9major plaque disruption STSegment Elevation Ml HEART ATI39ACK 9necrotic myocardium releases enzymes Congestive Heart Failure decomp total heart failure RL failure compensatory mechanisms run out FrankStarling mechanism increase SV increase CO SNS increase HRvasoconstriction9increase CO RAAS increase aldosterone amp ADH9increase Na retention amp renal water retension increase blood volume venous return hypertrophy amp remodeling Cerebrovascular Accident CVAStroke embolism9brain Peripheral Vascular Occlusive Disease atherosclerosis in peripheral vesselsstenosis9ischemia legs superficial femoral amp popliteal Acute Arterial Occlusion acute blockage of peripheral artery mostly legs plaque erodes thrombus embolism quotheart attack in legs SSx Seven P s Pistol shot Pallor Polar Pulselessness Pain Parethesia Paralysis Heart Failure heart can t pump enough blood to meet body s demands High output v Low output High output failure rare caused by increased metabolic demand severe anemia hyperthyroidism not bad heart mm Low output failure caused by disorders that impair pumping ability CIHD ACS Systolic v Diastolic Systolic heart can39t pump impaired contractibility pressure overload Diastolic heart can t fill hypertrophy smaller chamber tachycardia less filling time Right Sided v Left Sided Right Sided restricted blood flow lungs from leftsided failure problems with tricuspid valve right sided MI pulmonary HTN manifestations from blood backup in veins Left Sided restricted blood flow systemic arteries CIHD problems with AVmitral valves left sided MI manifestations from blood backup in lungs amp decreased tissue perfusion Compensated v Decompensated Compensated asymptomatic Decompensated mechanisms are failingused up CO can t meet demand symptomatic Shock circulatory failure body suffocating on cellular level Cardiogenic heart failure causes poor perfusion body tried to compensate preloadafterload9worsens failure Hypovolemic reduced blood volume causes poor perfusion Septic systemic response infection causes diffuse quot39 puul perfusion 39 39venous return9decreased preload decreased CO SSx multiple organ dysfunction syndrome Respiratom Disorders Ventilation V getting air alveoli Perfusion Q getting blood9tissue VQ Mismatch hypoxic vasoconstriction Perfusion without ventilation Ventilation without perfusion fquot 39 Pulmonarv quot39 39 Asthma amp COPD Chronic Bronchitis amp Emphysema Asthma hyperresponsive airways that cause episodes of bronchoconstriction amp airway inflammation Trigger hyperresponsive airways allergic response mast cells coated wlgE activated releasing cytokines9bronchospasm amp mucous production9WBCs release own cytokines9inflammation obstruction Tx betaagonis1 activate beta receptors bronchodilation counteract bronchospasm leukotriene inhibitors decrease inflammation block receptors on WBCs that cytokines attach to corticosteroids suppress inflammation COPD Emphysema obstruction from loss of lung elasticity destruction of alveolar walls amp enlarged air spaces obstruction from dysfunctional elastin which usually helps hold airways open collapse on expiration barre chestedquot Chronic Bronchitis obstruction from continual airway irritation amp inflammation that causes excess mucus productive cough amp thick ainIvay walls obstruction from mucous amp narrowed airways plugged on inspiration amp expiration Both pursed lips increase back pressure to help hold airways open dyspnea without tachypnea short of breath BUT no tachypnea rapid breath because must allow extra time for gas exchange with clogged airways increased PaCOZ hypoxic drive SMOKNG 1 cause increased RV amp TLC ARDS Acute quot 39 Distress 39 nflammatory alveolar amp pulmonary capillary damage respiratory failure Causes major trauma inspiration amp near drowning shock pancreatitis radiation quotshock lungquot 9decreased lung compliance amp diffuse pulmonary hypoxic vasoconstriction rapid onset1224h 9diffuse bilateral consolidation white lung on xray dyspnea hypoxemia hypercapnia 9respiratory failure ungs can t exchange 02C02 at alveolarcapillary membrane Pa02 lt50 mm Hg PaCOZ gt 50 mm Hg except wCOPD C02 trapped from dec expiration Other Restrictive Disorders anything causing fibrous changes to lung difficult inflation decreased VC RV amp TLC dyspnea wtachypnea Pumonary Embolism Caused by DVT venous stasis hypercoagubility endothelial jury 9can lead to Pulmonary Hypertension usually secondary from either pulmonary congestion pulmonary vascular obstruction PE or hypoxic vasoconstriction Cor Pulmonale rightsided heart failure from increased pressure in pulmonary arteries increased backup Fluids amp Electrol es Diffusion particles Osmosis water Fluid Pressures from where Unit nhinriiun and I Normal Anatomy and Physiology 1 Define a Hematopoiesis how out bodies grown new RBC WBC and plts The process starts in bone marrow 2 Compare and contrast 3 a Pluripotent stem cells can differentiate into many types of stem cells lymphoid and myeloid Stem cells b Lymphoid stem cells can only differentiate into lymphocytes c Myeloid stem cells can only differentiate into myelocytes d Compare all three are considered llcommitted stem cells and always produce a copy of itself before producing daughter cells Alternative names functions and immature forms of platelets a Alternative names plts thrombocytes blood clotters b Functions key in forming plt plug and hemostasis c Immature forms Megakaryocytes i Gets broken up to make many platelets Patho physiology 1 2 5 quot N Define a phiia increase in normal range i Eosinophilia increased nonblood producing eosinophil b osis increase in normal range i Thrombocytosis high platelet count c penia decrease in normal range i Thrombopenia low platelet count Define and expand a Hemostasis the stoppage of blood flow i Vessel spasm ii Formation of platelet plug iii Formation of insoluble fibrin clot iv Retraction of clot v Clot disillusion State purpose and function of 5 steps of hemostasis a See table Describe a Von Willenbrand Factor i Helps with adhesion of plt s to endothelium ii Accompanied by factor 8 which activates fibrinogen to become fibrin cross linked fibrin The liviproduces most of the clotting factors and proteins CampC the intrinsic and extrinsic pathways a See flow chart Name the step of hemostasis where most anticoagulants exert their effect a Step 5 clot dissolution Plasmin is key to digesting the insoluble fibrin cross links 8 Connect the common final pathway of coagulation cascade to clot dissolution a The common final pathway ends with the production of fibrin as soon as fibrin clot is formed it begins to be broken down by natural anticoagulants formed in step 3 heparin and plasmin Step 5 ends in the total breakdown of fibrin by plasmin 9 Normal platelet count a 150400 x 103uL b Thrombocytosis high platelet count i Increased clotting potential for early DIC c Thrombocytopenia Low platelet count i Could indicate a bleeding disorder 10 Define and expand a Hypercoagulation conditions that lead to hyperactivite hemostasis and may cause clots to form inappropriately b Mechanisms i Increased platelet activity 1 Can be caused by anything that damaged endothelium such as atherosclerosis DM smoking or high cholesterol ii Increased clotting cascade 1 Inherited diseases a Factor 5 Leiden mutation 9 Factor 5 cannont be turned off therefor cascade keeps going a person makes too many clots 2 Acquired diseases a Blood flow stasis from bed rest postop inactivity or heart failure causes decreased blood flow and leads to pooling and therefore clotting b Cancer sepsis crush injuries cells are damaged and decreases blood flow c Increased estrogen pregnancy and oral contraceptives can increase coagulation factor in the liver 11 Analyze whether a cause of bleeding acts through increased platelet activity or increased cascade activity and how it affects the steps of hemostasis 12 Define a Bleeding disorders conditions that lead to hypoactive hemostasis and inhibit coagulation b Mechanisms i Decreased platelet function platelet plug cannot form 1 Defective plt receptors vWF diseases drugs ii Decreased activity of the Clotting cascade 1 impaired coagulation factor synthesis caused by liver problems 2 Vit K deficiency 3 Hypocalcemia Energy Balance Energy Input Energy in ingested food digested food energy trapped in ATP phosphate bonds ATP used to drive physiological functions Energy Output External work used to move objects or the body internal work posture shivering internal activities needed for life ion pumping heart pumping synthesis all activities ultimately become heat Basal Metabolic Rate Energytime caloriesday 2000calday are 2000kilocaloriesday Neutral Balance Energy inputoutput food energy external work internal work heat Positive Balance Energy inputgtoutput energy stored in adipose tissue weight gain Negative Balance Energy outputgtinput weight loss 1st from adipose tissue then 2nd muscle Hypothalamic Control oflntake Hypothalamus integrates multiple signals matching feeding to energy needs balance of hunger and satiety Neuropeptide Y Released by hypothalamus stimulates appetite Melanocortins Released by hypothalamus suppresses appetite neuropeptide Y and melanocortins alter brain activities that control food intake Leptins Secreted by adipose tissue proportional to T6 storage in adipose l fat stores signals satiety by releasing leptins leptins Jneuropeptide Y and melanocortins Digestive System Appetite Control Hormone s form the GI tract control hypothalamic release GhrelinPYY3 36 Ghrelin rises before eating stimulates appetite and falls after eating l neuropeptide Y release PW released during meals and signals satiety CCK The release of CCK signals satiety before digestion ahs occurred stop eating before the new calories available stimulating CCK with fat or protein early in eating may control food intake amount Social Control Social Cortex Family meals habits stress loneliness distractions etc caloric intake often strongly influenced by outside factors obesity Jexercise BMR biochemistry differences habit hormonal differences etc morbidity and mortality anorexia nervosa psychological start K imbalance Temperature Regulation 986 F 37 C Convulsions at 106 F death from protein denature at 110 F core temp is regulated shell variable Heat Balance Balance of inputoutput internal heat must be removed multiple heat exchange mechanisms Heat Exchange Radiation by electromagnetic waves sun fireplace Conduction transfer by contact from warm to cold Convection airwater currents l transfer Evaporation of water from skin removes heat sweat l evaporation dripping doesn tfitness Jsweat Na content l evaporation Heat Production Muscle contraction shivering is contraction without work all heat BMR sets lower limit of heat production Response to cold Hypothalamus Thermoreceptors control responses Jskin blood flow quotgoose bumps human 39 39 clothing outside sources Response to heat l skin blood flow l sweating adaptation fever WBC s release endogenous pyrogen reset hypothalamus asprin blocks prostaglandin production Principles of Endocrinology Circadian Rh hms Calcium Control Hormones Released from endocrine glands into blood go everywhere bind to receptors effects on different cells receptor dependent hydrophilic hormones bind to membrane receptors hydrophobic hormones bind to nuclear receptors after protein synthesis Plasma Hormone Concentrations Controlled by feedback mechanisms Hydrophilic hormones can change concentration rapidly minutes Hydrophobic hormones often partition into adipose tissue this buffer changes in plasma concentration hours Negative Feedback Concentrations vary minimally around a set point falling concentrations stimulate release mechanisms rising concentration inhibit release mechanisms Neuroendocrine Reflexes Neural activiation can produce a rapid l in hormone release DiurnalCircadian Secretion Day nightaround a day rhythms on a 24hr cycle entrained by sleepwake or lightdark cycles night shift work put some pairs of hormones out of cycles l junk illness recent reports of l cancer risk possibly due to altered melatonin release Endocrine Disorders Hyposecretion or hypersecretion often related to endocrine or feedback cell receptors malfunction Target cell malfunction no response from normal hormone level Cell Responsiveness Controlled by the number of hormone receptors available on target cell Down Regulation Desensitization due to chronic elevated hormone level internalization or chemical modification of receptors type II diabetes has down regulation of insulin receptors Permissivness One hormone enhances the response of a second hormone TH l epinephrine receptor number on target cells Synergism 2 hormones I each other activity FSH and testosterone each help the other l sperm production Antagonism 1 hormone Jthe effect of another hormone progesterone J estrogen receptor number on the uterus Pineal Gland Release melatonin to help regulate circadian rhythms Biological Clocks Controlled by the superchiasmic nucleus in the hypothalamus Clock proteins in the SCN regulate their own production over a day Clock proteins control the neural output of the SCN which in turn controls some hormonal outputs like the cortisol External cues keep the SCN on 24hr rhythm Melatonin Release from pineal gland is controlled by light M release is high in dark controls lightdark hormonal fluctuations may help sleep lagain and free radicals and slow aging of the immune system link with puberty Plasma Calcium 90 of phosphate stored in bone 99 of CaZ quot stored in bone as Calcium Phosphate Ca2 25mM is plasma 107 M in cells regulated by parathyroid hormone Parathyroid Hormone Parathyroid hormone l reabsorption of Ca2 first from bone fluid in spaces and then from caphos necessary for life no parathyroid hormone hypocaicemia fatal Hypocalcemia Low blood Ca hyperactive nerve and muscle I Na entry larynx and diaphragm spasms no air Vitamin 0 Control of Ca2 absorption enhances parathyroid hormone activity Osteoporosis lestrogen linked parathyroid hormone vitamin D Ca2 all normal lbone density less effect when bones are thicker at menopause weight bearing work and exercise thickens bones Hygothalamus Pituita Growth HypothalamusPituitary Structure Hypothalamus at the base of the brainstalk connects hypothalamus to pituitary Posterior pituitary connected by neural axons anterior pituitary connected by HHypophyseal portal system Posterior Pituitary Hormones synthesized in the hypothalamus axon and nerve endings in posterior pituitary Vasopressin Secreted when l osmolarity I HZO reabsorption at collecting duct stimulates aquaporins insertions into comembrane Oxytocin Contracts uterus during childbirth causes milk ejection from mammary glands during lactation Hypothalamic ReleasingInhibiting Hormones Anterior pituitary hormone release control by hypothalamus releasinginhibiting hormones travel by portal system to anterior pituitary RH and H control released of 6 anterior pituitary hormones Portal System Connects capillary beds in hypothalamus to anterior pituitary small distance in very small amounts but with big effects Anterior Pituitary Hormone Release Input to the hypothalamus controls RH and H release input is neural and humoral balance of RH and H for particular anterior pituitary hormone controls anterior pituitary release Negative Feedback Anterior pituitary hormone release is regulated by negative feedback always to anterior pituitary sometimes to hypothalamus target gland hormone release inhibits anterior pituitary hormone release Growth Control Multiple factors all necessary for full growth Genetics provides base and maximum Nutrition most important nongenetic factor Proteins vitamins minerals essential for full growth calories needed Growth can catch up during puberty if lin childhood due to protein catabolism during diseaseinjury Growth Hormone Protein from anterior pituitary activates second messengers at many organ cell membranes 15min circulation time before metabolism by liver Non Growth Related Effects l liver glucose production l fatty acid release from adipose tissue conserves glucose for brain use during growth Growth Promoting Actions Hyperplasiahypertrophy of cells l protein synthesis Bone Growth Growth hormone stimulates bone thickness and length Bone Composition Outer layers have compact bone caphos hardenscollagen makes strong and flexible nner layers have spongy bone long bones epiphyses at both ends diaphysis in middle OsteoblastOsteoclasts Blast form new bone and secrete caphos Clast reabsorb bone creates spaces in boen Bone Length Growth Length growth occurs at epiphyseal plates clasts eat epiphyes blasts extend diaphysis fuse at puberty blasts catch clasts Control of Growth Hormone Release Hypothalamus releases both GHRH and GHIH diurnal highest an hour after sleep begins exercise physical stressamplow blood glucose I GH release GH Deficiency Children dwarfism occurs with lbone growth no effect on adults GH Excess Before puberty l proportional growthafter puberty acromegaly excess growth of face hands and feet Thyroid Thyroid Hormone l meta bolic activity in most tissue lTH poor mental health and physical function lcold resistance mental retardation in children I TH wasting nervousness l heat production tachycardia Thyroid Hormone Synthesis Protein thyroglobulin made by follicular thyroid cells exocytosis to colloid iodine added to tyrosines link DTeither DIT or MIT endocytosis digestion to T or T4 TH Secretion MIT and DIT recycled in follicular cells T and T4 secreted into blood number is iodines most secretion T4 TH Transport TampT4 circulate bound to protein T4 4000 bound 1 free free is active most T4 converted to T in circulation T more active TH Buffering As TH lost in urine or to cells other TH come off protein Tbinds weaker than T4 T lost faster TH Effects All l metabolic activity maximizes GH effects on protein synthesis and bone Calorogenic l heat production TH binds to nuclear receptors alters gene activity l cell activity l fatty acid metabolism PNa pump activity Sympathomimetic Function Required for full sympathetic response TH stimulated production of adrenergic receptors Heart TH l in adrenergic receptors I HR and force of contraction Neural Tissue Needed for CNS development in children TH required for full neural function response to catecholamines RAS function cortex and basal ganglia need TH Regulation of TH Secretion By thyroid stimulating hormones TSH from anterior pituitary TSH Regulation Jblood TH release of TSH from anterior pituitary TSH go to thyroid gland l thyroglobulin secretion endocytosis and T and T4 production Hypothyroidism Thyroid gland disease or JTSH production or autoimmune attack JBM R lethargy lmental and physical function Graves Disease Hyperthyroidism nervousness weight loss warmth I BMR exophthalmus bulging eyes cause is antibody TSI that bindsactivates TSH receptors l thyroid gland activity Hashimoto s Syndrome Autoimmune attack on thyroid gland Jfunction hypothyroidism need synthetic TH not rare Groiter Enlarged thyroid gland due to excess TSH or TSI may produce hypo from Jiodine or hyperthyroidism from I TSI Adrenal Gland Adrenal Medulla nner layer of adrenal gland similar to postganglionic sympathetic neuron Secretions Stored in granules epiNE 41 strong peripheral effects vitamin C stored and released with epiNE Effects of Catecholamines Epi l heart rate JTRC I CO NE l vasoconstriction exception in heart and skeletal muscle net effects is P l BP l metabolic rate Neural Control Release determined by baroreceptor activity lBP I EpiNE release I BP JEpiNE release Adrenal Cortex Outer layers of adrenal gland endocrine gland Secretions Released as made not stored All are steroid derivatives of cholesterol Mineralocorticoids aldosterone et al Glucocorticoids cortisol et al Androgens DHEA androstenedione ACTH Effects and Control ACTH form anterior pituitary when cortisol is low stress is high on top of diurnal rhythm ACTH causes I release of all adrenal cortex steroids except aldosterone Circulation of Glucocorticoids Most bound to globulin proteins only free form is active activity of steroids last lhr Glucocorticoid Effects Cortisol is quotstressquot hormone need to live bind to nuclear receptors to l protein synthesis Metabolism l protein catabolism free amino acids for damage repair l plasma glucoseplasma fatty acids glucose fatty acids provide energy for repair Permissive Actions Assists actions of glucagon and catecholamines vasoconstriction bronchiodilation Stress Something is only a stress if ACTH l ACTH l cortisol release Short term l energy availability amino acid availability catecholamines Long term stress harmful excess protein breakdown wasting pain Anti Inflammatory Effects Only at high glucocorticold levels Jswelling lhistamine Also blocks immune system apoptosis of WBC s Must use antibiotics to prevent infections NOT for ROUTINE USE Mineralocorticoids Aldosterone PNa reabsorption in kidney Adrenal Androgens Major effect in females nominor effects in males DHEA Sex drive and starts growth spurt at puberty in females estrogen caps females growth spurt no effect in males testosterone is 100x s stronger Androstenedione Little effect itself precursor to testosterone and estradiol Fuel Metabolism Insulin Diabetes AnabolismCatabolism Balance of buildup of large 39 39 with 39 39 39 t quot quot by activity and energy balance Essential Nutrients Some nutrients cannot be made in the body some amino acids and all vitamins must be in diet Nutrient Storage Glycogen storage in muscle and liver fat storage in adipose tissue body will consume muscle for amino acids during starvation Brain Glucose Supply Brain only uses glucose for energy liver glycogen maintains plasma glucose between meals fats cannot be made into glucose cannot supply energy to brain if no glucose available body converts protbiamino acids glucose Absorptive State Postmeal statequot several hours after eating many nutrients available from newly arrived meal absorption of carbs then protein then fats Post Absorptive State Between meals fasting used stored energy to supply tissues energy needs Islet Cells In pancreas secrete hormones into blood alpha cells secrete glucagon beta cells secrete insulin Secretion l plasma glucose 9 l insulin secretion leave capillaries through pores Insulin Effects All aimed at storing energy for future use Carbohydrate Seconds 4 number of glucose transporters by fusion of membrane transporter vesicles l glucose entry into cells brain and working skeletal muscle don t need insulin transporter vesicles Minutes l glycogen storage in liver and muscle Fats Hours l lipid storage Proteins Seconds l amino acid entry into cells Minutes l liver glycogen storage enzymes and protein synthesis Regulation of Insulin Secretion l plasma glucose l insulin release about 1hr lglucose causes linsulin release Sugar meal has rapid rise and fall in glucose 1 stays high Hypoglycemia after sugar meal as 1 stays high after sugar transport complete Starch meal takes longer to ingest glucose glucoseinsulin never get as high no hypoglycemia Glucagon Opposite of insulin glycogen breakdown liberates glucose from storage l lipid release and l glucose production by liver lplasma glucose l glycogen l plasma glucose Jglycogen Diabetes Mellitus Glucose in urine Type 10 autoimmune attack on beta cells Type II 90 obesity and age J number of receptors Hyperglycemia l plasma glucose hemoglobin alc test long term glucose indicator l blood osmolarity exceeds Tm for glucose Dehydration l urine volume loss of Na and K JBV9 lBP shock death Protein Metabolism Amino acids used for energy and to make glucose in liver negative protein balance and wasting Fat Utilization Use fats for energy in insulin dependent tissue most fa lI pli sma fatty acids and cholesterol l atherosclerosis Acidosis Fat metabolism l ketone bodies 4C keto acids l ketosis l acidosis l breathing rate and Jmental activity Coma Acidosis dehydration hyperosmolarity can call induce coma in diabetics and some comas lead to death Type I Diabetes Mellitus Juvenile diabetes Autoimmune attack immune attack gradually destroys beta cells over a few years gradual loss of insulin production hyperglycemia develops Type II Diabetes Mellitus Loss of insulin receptors associate with obesity in people below 40 symptoms like Type Obesity Prolonged elevated glucose constant insu lin production elevated insuli down regulation of insulin receptors lglucose entry and hyperglycemia reduce caloric intake helps Age n elderly peoplereceptor number or receptor availability not necessarily associated with obesity but l weight can l probability may take some insulin to maximize available receptors Cancer Incidence Males prostategtlunggtcolongtbladder Females breastgtlunggtcolongtuterine Incidence declining 2yr since 1992 Cancer deaths largest number with incidence deaths Males lung 100gtprostate 16gtcolon 45gtpancreas 100 Females lung 90gtbreast 22gtcolon 45gtpancreas 100 Types Separated by ability to spread Benign Localized produces problems if tumor crushes adjacent tissues or draws blood from adjacent tissues treat with surgery many benign tumors are not cancerous Malignant Has metastasized through lymph system surgery to remove large tumors chemo and radiation to kill metastasized cells Diagnosis Need biopsy for full diagnosis l use of MRI tumors often produce hormonal or protein markers Treatments Combination of treatments will vary with different cancers Surgery Remove tumor and some surrounding tissue to make sure all tumor removed Radiation Kills fast growing cells damages DNA and makes oxygen radicals side effects on bone marrow and GI tract Chemotherapy Kills fast growing cellsmultiple targersDNA and mitotic spindle main ones also bone marrow and GI tract side effects Biologic Therapy Shift hosttumor balance to host alter T cells antibody production cytokines to attack tumor Genetics Single cell generates tumor NOT inherited form parents even predisposition needs additional mutations Mutation DNA 39 39 lead to 39 39 cell r quot39 39 Tumor Viruses Only few cancers linked to viruses DNARNA viruses alter DNA in host cell only RNA virus cancer is a type of leukemia DNA viruses have several links cervical cancer liver cancer lymphomas during immune deficiency Cell Biology Uncontrolled growth due to cell changes 1 mutation not enough malignancy needs 510 p53 Mutations p53 pathway controls normal mitosis acts as tumor suppressor many tumors have p53 mutation mutation leads to genomic instability and resistance to apoptosis Environmental Signals Effects occur in cancer cells after mutations cytokines and paracrines later G protein and enzyme linked processes effect signals to genome that regulate mitosis loss of celltocell connections and contact inhibition Transcription Factors Control gene activation alteration in genes andor factors factors affect expression in tumor cells allowing tumor growth Apoptosis Regulation Programmed cell death often occurs after mutation caspases are enzymes controlling apoptosis attack DNA enzymes cytoskeleton Jcaspase activity in tumors target of new cancer treatments Angiogenesis Tumors draw blood from surrounding healthy tissues starves them Prevention Prevent the multiple mutations necessary to start tumor Smoking Cessation Stopping is the healthiest positive activity 400000 premature deathsyr from smoking Linked to lung larynx esophagus bladder and pancreatic cancers And cardiovascular and pulmonary disease 90 quitters do so on their own total quitting most successful Diet lfat intake Jcancer rate anticarcinogens in vegetables fruits and nuts fiber Jcolon cancer Sun Avoidance UV radiation l skin cancer acute sunburns even in childhood l risk of melanoma light skin l chance Chemoprevention New field durgs designed to Jmutation risk Antimutagenic antioxidant antiproliferaiton preventatives Often significant side effects Use of tamoxifen to lbreast cancer in high risk women may l cervical cancer risk balance risk Sex Differentiation Male Reproductive System Chromosomes 23 pairs 23mother 22x23father 22 x or y carry genes which code for proteins X and Y Chromosomes XX female XY male X chromosome is large many genes Y chromosome is small few genes SRY gene starts male development in utero Gonads in Embryo Gonadstestes and ovarie 7 h week with SRY gonadal medulla testes cortex regresses without SRY gonadal cortex ovaries medulla regresses Puberty Maturation of the reproductive system Males Hair pattern erectile function sperm musculature Females Hair pattern breast development and menses Onset l gonadotropin RH GnRH release from hypothalamus necessary kisspeptin stimulated l release of FSH and LH from pituitary leptin from adipose tissue may be necessary for menarche Pituitary Gonadotropins FSH and LH Need GnRH from hypothalamus for release controlled by negative feedback of gonadal hormones testosterone estrogen progesterone FSH Follicle stimulating hormone Female growthdevelopment of ovarian follicles Males develop mature sperm by activating sertoli cells LH Luteinizing hormone Female Ovarian maturation estrogen secretion ovulation Males testosterone secretion from Leydig cells Testes Seminferous tubules site of sperm production Sertoli cells assist sperm production Leydig cells testosterone production Spermatogenesis Formation of sperm cells from spermatocytes about 100million spermday Sperm Formation Spermatogonium mitosis one stays one migrates inward migrating cell spermatocyte remolded to sperm cell sertoli cells absorb most of spermatocyte cytoplasm Sperm Structure Head acrosome digestive enzymes nucleus 23 chromosomes midpiece mitochondria tail propulsion by microtubule rotation only need near ovum Temperature Max sperm production 32 C body is 37 C scrotum will rise in cold and descend in heat to maintain temp nondescended testicles usually sterile Semen Liquid holding sperm 3mlejaculate about 300000000 sperm lt20000 spermejaculate considered sterile accessory structures contribute fructose mucus clotting proteins bicarbonate to semen Erection Arteriole dilation venous compression 9 engorgement Parasympathetic neuron no production arteriole vasodilation Emission Mixing of prostatic fluid sperm and seminal vesicle fluid just prior to ejaculation sympathetic neuron controls emission Ejaculation Skeletal contraction expelling sperm Testosterone Steroid hormone released in utero and shortly after birth to create male reproductive system no further release until puberty tonic release thereafter Secretion From Leydig cells as made 98 bound to protein in circulation 2 free and active stimulates protein synthesis Secondary Sex Characteristics Male hair pattern penile and genitalia enlargement vocal cords thicken l mental acuity l sex drive l growth Anabolic Effects Growth spurt epiphyseal closure l musculature and kidney size Inhibin Released from sertoli cells inhibits FSH release all hormone FSH LN testosterone inhibin are tonic and stable after puberty Female Reproductive System Menstrual Cycle 2135 days variable 28 day average some regularirregular ovum prepared for release from follicle uterus prepared for implantation of embryo Ovarian Cycle Ovum growth release follicular change Follicular Phase Days 14 dominated by FSH stimulation several follicles enlarge form antrum one follicle outgrows others regress in size atrasia estrogen released from granulose and thecal cells surrounding ovum Ovulation 14 h day high estrogen stimulates kisspeptin release from hypothalamus Kisspeptin stimulates GnRH release stimulates the LH surge LH surge from anterior pituitary ruptures antrum Ovum released to abdomen fimbria sweep ovum into oviduct Ovum surrounded by granulose and tehcal cells and zoria pellucid gel Ovum moves down oviduct to uterus 5 days in transit Luteal Phase Days 1428 corpus luteum forms from remaining cells in ruptured follicle CL secretes progesterone and estrogen progesterone prepares uterus fro implantation Uterine Cycle Site of fetal growth changes will supply implanted embryo with energy until placenta develops Proliferative Phase Days 514 variable part of cycle estrogen dominated repair of uterine surface after menstruation l uterine lining thickness and blood supply Secretory Phase Days 1428 uterine lining greatly l vascularization and thickness progesterone dominates progesterone luterine contractions uterus secretes glycogen for embryo Menstruation Days 15 sloughing off of uterine lignin if no implantation Cervix Opening between vagina and uterus usually blocked with mucus prevents infection estrogen thins mucus and alkalizes secretions let sperm in lessens acid killing of sperm progesterone thickens mucus Indicators of Ovulation l basal body temperature by l progesterone thinning of cervical mucus Fertilization range 3 days 2 days before ovulation sperm lifetime to 1 day after ovulation fertilizable ovum Ovarian Hormones Estrogen and progesterone have multiple effects Estrogens Formed from 39 g and 39 quot from thecal cells thecal and granulose cells produce estrogen Effects ofEstrogens l follicular development inhibits FSH l cillary motion in oviducts l uterine muscle size thins cervical mucus kisspeptin release at ovulation l neural plasticity l sex drive Progesterone l secretions and size of uterus l breast development l cervical mucus inhibits LH release luterine 39 during p g l heat r 39 Relaxin Hormones from ovaries and placenta helps sperm penetrate ovum membrane l digestion of connective tissue softens pelvis and cervix for delivery Menopause About 400 cycles 1400 of 7 million oocytes developcycle only one ovum released the remainder undergo atresia decline and loss of estrogen and progesterone when oocytes gone Osteoporosis lestrogen linked PTH vit D Ca2 all normal lbone density less effect when bones are thicker at menopause weight bearing work and exercise thickens bones Cardiovascular Effects l cardiovascular disease after menopause JHDL l vascular reactivity with lestrogen l BP Hormone Replacement Designed to help lmenopause symptoms hot flashes Recent links slight l heart disease stroke breast cancer l caution balance riskbenefit Renal Filtration Reabsorgtion Renal Functions Filter waste from blood maintain blood volume maintain blood osmolarity uses filtration reabsorption secretion Nephron Functional unit of the kidneys has vascular system and tubular system all but cells and proteins in blood can be filtrated most reabsorbedremainderurine Vascular System 2 capillary systems 1 filtrating 1 reabsorption Afferent arteriole glomerulus filtration efferent arteriole peritubular capillaries reabsorption venules TubularSystem Sshaped Bowman s capsule glomerular capillaries have very wide pores only cells and proteins not filtered Glomerular Filtration From glomerulus into Bowman s capsule glomerular capillaries have very wide pores only cells and proteins not filtered Inulin Fructose polymer Filtered not reabsorbed or secreted used to measure glomerular filtration rate GFR inject in blood measure in urine proportional to amount of filtrate GFR 125mlmin 140 of total blood volume HydrostaticOsmotic Pressure H BP force filtrate into Bowman s capsule OP So much fluid is filtrated remaining proteins have higher than normal osmotic pressure Net Lots of filtration Control of GFR Afferent arteriole radius controls entry to golmerulus Afferent arteriole dilation I GFRafferent arteriole constriction JGFR sympathetic neuron constrict aff art JG FR Tubular Reabsorption Must recover most filtrate 125 filtered 124mlmin reabsorbed lmlmin urine 144Lday 125 filtered 123mlmin reabsorbed92mlmin urine 288Lday Excess urine loss in diabetes JBP9 shock death Transport Maximum Different carriers for different molecules TM is limit of transport due to limited number of carriers Glucosuria 3x s more carrier capacity than normal filtered load if G in urine blood must have at least 3x s more G than normal Sodium Reabsorption Controls reabsorption of many other molecules Na pump only on basolateral side of tubular cells pump Na out create gradient for Na entry into cells ATP needed for energy tight junctions prevent flow in spaces between cells caffeine JNa reabsorption Cotransport Carriers for Na and cotransported molecule glucose amino acids bicarbonate Cl39 are cotransported with Na during reabsorption energy use is Na movement down gradient into cells HZO follows osmotically at proximal tubule variable HzOreabsorption at distal tubule and collecting duct Glucose Reabsorption Binds to carrier with Na on luminal side to enter tubular cell separate nonNa glucose carrier moves G into interstitial space Proximal Tubule Water Reabsorption 6070 of H10 reabsorbed in proximal tubule 180Lday filtered 1L of urine variable 500ml of urine minimum per day to remove toxins osmotic reabsorption of H10 follow solutes especially Na Renal Control Secretion Filtrate Dilution Renin Angiotensin System Maintain BP by PNa and H10 reabsorption Jrenal BP 9 release of renin from kidney G cells renin is a protease Production ofAngiotensin II Renin converts angiotensinogen inot angiotensin I Angiotensin converting enzyme ACE converts Alto A ACE is in the walls of lung capillaries Effects ofAngiotensin II Powerful vasoconstrictor I BP causes release ofaldosterone from adrenal cortex ACE Inhibitors Block production of angiotensin II used as treatment for hypertension few side effects but many produce fetal development problems TubularSecretion Extra removal from plasma carriers and pumps move material form tubular cells into filtrate most secretion is at proximal tubule organic acidsbases secreted poisons medicines dyes additives Renal Blood Flow PAH PAH is totally secreted from plasma appearance in urine proportional to renal blood flow RBF 2025 of cardiac output H Secretion Carbonic anhydrase in tubular cells makes H and HCOg39 H secreted in both proximal and distal tubules uses NaH Countertransport H into filtrate HCOg39 interstitial fluid net loss of H K Secretion K is reabsorbed in exchange for Na in proximal tubule the Na pump activity l tubular cell K which l secretion by proximal tubular cells since both K and H exchange with Na l one secretion Jother secretion Plasma Clearance Measure of kidney s ability to remove a substance from the plasma It is the volume of plasma from which an amount of material has been removed Glucose has zero clearance fa substance is filtered but not secreted or reabsorbed like inulin its plasma clearance is the GFR if a substance is both filtered an secreted its clearance is gtGFR If a substance PAH is filtered and entirely secreted plasma clearance is the renal blood flow 2025 of CO GFRRBF C inulin C PAH Filtration Fraction 20 Loop ofHenle Creates osmolic gradient in kidney medulla 300 mOsm at cortex 1200 mOsm in deep medulla filtrate at the end of the loop of Henley is 100mOsm plasma is 300mOsm Countercurrent Multiplication Descending limb of loop of Henley HZO permeable ascending limb is HZO impermeable H K Cl39 pumped out filtrate entering distal tubule always dilute NIOOOSom Urine Production Bladder Function Collecting Duct Goes through from cortex to medulla always dilute filtrate at cortical end responds to vasopressin no VP little HZO reabsorbed dilute urine Vasopressin From posterior pituitary released when plasma osmolarity high causes insertion of aquaporins in collecting duct membrane Aquaporins HZO channels HZO goes though osmotic pressures of solutes in medulla 1200mOsm draws HZO retain HZO urine up to 1200mOsm Diabetes Insipidus Either JVP production or lack of kidney response bad receptor excess water loss shock death Urine Buffering Filtrate pH must be 45 for H to enter filtrate bicarbonate and phosphate from filtration m ammonia from tubular secretion buffer urine Aldosterone Effects l number of active Na carriers on luminal side of CD tubular cells this PNa reabsorption in CD HZO follows osmotically K reabsorption is reciprocal to Na Secondary Hypertension Reduced renal artery flow lrenal BP 9 excess renin 9 I BP treat with ACE inhibitors to block Angil production diagnosis by determining RBF with PAH Renal Dysfunction Wide glomerular pores protein in urine edema due to low protein loss of concentratingdiluting loss of nephrons multiple causes acidosis by ex lack of ammonia reduced H quot excretion Sodium Dysfunction Excess Na retention leads to edema hypertension J filling excessive aldosterone leads to heart failure Bladder Function Storage of urine no changes after leaving the kidney Ureter Entry Ureter connects kidney to bladder Ureter passes inside bladder wall at an angle increased bladder pressure closes ureter prevents backflow Bladder Sphincters Around uretha the tube draining the bladder Internal urinary sphincter smooth muscle involuntary External urinary sphincter skeletal muscle voluntary Contorl ofMicturition Spinal reflex relaxation of internal sphincter when bladder pressure increases reflex relaxation of external sphincter follows cortex can overcome reflex relaxation of external sphincter Parasympathetic neurons l bladder body contraction Pelvic floor descends allowing urine flow Exercise after delivery maintains pelvic floor strength Fluid Balance Balance Concept The ECF is the pool of available material for cells input comes from ingestion or metabolic production output occurs from excretion or consumption balance must occur over the long run with inputoutput Negative Balance Outputgtinput net reduction in pool concentration Positive Balance nputgtoutput net increase in pool concentration Fluid Balance Balance of H10 in the body 60 of the body is HZO with adipose tissue causing variation Plasma 90 HZO soft tissues 7080 bone 22 and adipose tissue 10 Intracellular Fluid 2s of total body water K dominated with protein Extracellular Fluid oftotal body water Plasma 20 ofextracellularfluld wlth protelnl Int rstitial Fluid 80 of extracellularfluld wlth N0 protelnl Minor ECF Components Relatlvely small volumes lymph CSF sallva etc ECF Volume Regulation Regulatlon ofvolume needed for longterm BP control changes ln BP cause shlfts offluld between plasma and lnterstltlal fluld Blood Pressure Control Short term drop ln pressure causes Autotransfuslon Movement offluld from lnterstltlal fluld to plasmato malntaln BP changes ln baroreceptor actlvltyl Long term control ofvolume ls balance ofthlrstlntallte and lltldney fluld excretlon Salt IntakeThe lltldneys need 05g NaClday forfluld loss ln sweat and feces lntallte ls 105g NaClday excess excreted ln urlne Cl follows Na Salt Excretion Kldneys good at ellmlnatlng Na but lretentlon and lBP must balance 105gday lnput fltness reduces Na content ln s eninAngiotensinAldosterone System Long term control of Na excretlon controls BP everyone has thelr own set polnt for l ECF Osmolarity Control Needed to prevent swelllng or shrlnlltlng of cells total amount of materlal ln a volume regardless of composltlon produces lts osmolarlty Ions Na and K omlnate the osmolarlty oflntracellular fluld and lnterstltlal fluld other nonpenetratlng substances llllte protelnsl also contrlbute to osmolarlty water moves by osmosls lfthere are dlfferences ln lntracellular luld and lmel llal nulu 39H lunacellulal nulu and lmel llal nulu osmolarltyls 300m sml Tonicity The standard fortonlclty ls notthe number 0 s wollen dlssolved partlcles but the behavlor of cells ln the solutlon cells Shrum N quotquota39 swell ln hypotonlc solutlons ECF ls rarely hypotonlc H ertonicity Cell shrlnllts greaterthan 300m0sml CEquot 8 VP Dehydratlon low lntallte excess loss dlabetes asopressin Controls osmolarlty of urlne Ion concentra on vasopressln adds aquaporlns to collectlng duct to lwater nggg39ac mm Hypmonic lsomnic Hypo onic reabsorptlon Waterlnmke Fluld drlnlltlng food lntallte 39 a i balance a l lU llUlll lung xln meat feces and urine Osmoreceptors Receptors ln the hypothalamus that control VP release losmolarlty lvasopressln release 4 H20 retentlon Losmolarlty Lvasopressln release 4 H20 excretlon AcidBase Balance AcidsAclds are AH aclds dlssoclate lnto A and H strong aclds llllte HCl ln the stomach completely dlssoclate Bases Bases B can blnd H to become BH only slgnlflcant physlologlcal base ls ammonla NH becomes NHa ammonla buffers renal ltrate allowlng more H excretlon pH Measure of H ln a solutlon pH l0gH lH causes Lle Average blood pH740 Average cell pH70 Blood pH below 735 ls acldosls more commonl blood pH above 745 ls allltalosls Cells wlll have blgger pH shlfts than blood Acidosis E ectsAcldosls depresses the neurons especlally lnthe CNSl Allltalosls malltes neurons hyperexcltable Acldosls ln general Lenzyme actlvlty but few lncrease Acldosls causes lH excretlon and therefore decreased K excretlon 4 K causes cardlac and neutral problems Sources ofH Small amounts ln food such as cltrlc acldl most generated ln the body carbonlc aclds from C0 2sulfur and phosphorlc aclds from protelns metabollc aclds such as lactlc acl Control of H H ls controlled ln three ways chemlcal bufferlng resplratory control of C02 and renal control of H excretlon Buffersleferent buffers worllt ln dlfferent places buffers work by blndlng H convertlng A to AH thls removes H from the solutlon and pH 1St llne ofdefensel Extracellular Buffering Bicarbonate most important extracellular buffer HCOg bind H to form HzCOg which dissociates to HZO C01 hemoglobin in RBCs buffer H produced by C01 l venous blood Intracellular Buffering Protein in cells bind H in intracellular fluid in some cells especially muscle cells phosphate helps buffer intracellular fluid Urine Buffering I 39 39 base that also buffers renal filtrate Respiratory Control ofHquot Second line of H defense works with nonrespiratory sources of H I H or I COz l depth and frequency of respiration this reduces CO in blood reducing H back toward normal Kidney Control ofHquot 3rd line of defense Removes H from any nonrenal source in the body Hquot Excretion H ion pumps in the renal tubules secrete H into the filtrate urine pH is normally 60 but can be as low as 45 Acid Base lmbalances Pathological changes in the control of H quot result in pH changes These can be compensate by the respiratory and renal systems if not of renal or respiratory origins A system cannot compensate for its own problem renal problems require respiratory compensation respiratory problems require renal compensation RespiratoryAcidosis Abnormal CO retention form hypoventilation lung disease drugs nervemuscle disorders breath holding renal compensation l by H secretion RespiratoryAlkalosis JCOZ by hyperventilation fearanxiety aspirin poisoning conscious breathing JH secretion or removal of condition Metabolic Acidosis Most common acidbase disorder severe diarrhea loss of bicarbonate excess H quot production during fat use in diabetics exercise leading to lactate and H quot production kidney failure cannot excrete H or conserve HCOg Metabolic Alkalosis lin H for nonrespiratory reasons vomiting loses H quot in vomitus excess bicarbonate ingestion Jrespiratory rate and retain H in kidneys to compensate H retention PK loss andI 39 are 39 39 39 acids that buffer renal filtrate ammonia f quot 39 quot 39 39 vaertension Local Control Nonneural factors lP 9 lflow9 homeostatic tissue response9 l flow Autoregulation each organ controls local blood flow Metabolic Vasodilators Active tissues produce vasodilators ATP use9 l adenosine production adenosine is a strong vasodilator active hyperemia Endothelial Factors Paracrines local hormones released from endothelium affect VSM Nitric Oxide Hormonalneural activation I NO 9relaxes VSM9 l blood flow Endothelin Peptide constricts VSM lflow9 I BP stimulants of endothelin l gene activity that make endothelin Baroreceptors Stretch receptors in carotid sinus and aortic arch changes in BP after baroreceptor activity detects changes in BP Input to Medulla Baroreceptors send neurons to medulla in brain stem Control of VasoconstrictionDilation Cardiovascular control center CCC in medulla CCC controls sympathetic and parasympathetic output Homeostatic shortterm control of blood pressure 39 39 JBP9 J I input9 l I I 39 39 output9 I BPheartVSM l 39 39 I BP 9 lquot I input 9 l r I I 39 39 output9 JBPlower heart rate Resetting Body adjusts to own quotnormalquot BP adaptation to prolonged BP change occurs over days Hypertension Chronic elevated BP multiple causes several small changes causes large l in BP Cardiac Effects Hypertrophy against increased load diastolic pressure l oxygen use 9 heart attack when coronaries constrict with age I in systolic pressure l stroke risk Essential Hypertension Cause unknown treat symptoms effective reduces pathology Renal Hypertension secondary hypotension Jblood flow to kidneys cause l kidney renin release Renin converts angiotenisnogen to Angiotensin Al Angiotensin converting enzyme ACE in lung capillaries converts Alto Angiotensin II I BP U H strong 39 causes release from adrenal cortex Aldosterone PNa reabsorption and H10 reabsorption by kidneys more volume In Pregnancy Placental factor causes vasoconstriction preeclampsla is hypertension during pregnancy magnesium sulfate treatment lowers BP Drug Treatments Often used in combination varying side effects Diuretics PNa excretion lowers blood volume JBP ACE Inhibitors Block coversion of Angiotensin to Angiotensin II a Adrenergic Receptor Blockers Stops sympathetic constriction of VSM blocks NE effects fewer CaZ quot channels opens less Ca2 entry less force 6 Adrenergic Receptor Blockers Blocks NEEpi effects on hea rt less Ca2 entry lforce of cardiac contractions Calcium Channel Blockers JVSM contraction blocks tone side effects Shock Very low blood pressure loss of blood toxic vasodilation Reversible shock can recover from epinephrine I BP side effects significant Irreversible shock multiple organ failure due to low BP death results cannot recover from Digestion and Absorption The breaking down of food into absorbable units and their absorption Carbohydrate Digestion Must be reduced to monosaccharides to be absorbed Complex Carbohydrates Chains of sugars usually sugars Different complex carbs have different links between sugars starch is different than cellulose cannot digest sugar in fruit is often a monosaccharide fructose or glucose Enzymes Produced in the mouth and pancreas amylase converts starch to disaccharide disaccharides are in the wall of the small intestine disaccharides convert disaccharides to monosaccharide sucrose glucose fructose Lactose Intolerance Lactose milk sugar disaccharide of glucose and galactose if no lactase produced no digestion of lactose bacteria in large intestine use lactose as food source gas and diaherra produced Absorption Complete all sugars totally absorbed non diffusion use glucose transporters Sodium Dependence Glucose cotransported with Na into epithelia cells transport of glucose from epithelial cells to interstitial fluid sues a nonNa glucose transporter Protein Digestion Some in stomach some in small intestine Proenzymes Released in protected form acid then pepsin converts pepsinogen into pepsin enterokinase in small intestine wall converts trypsinogen into tyrpsin trypsin then converts other pancreatic proteases into active form Pepidases Both from pancreas and on small intestine wall convert peptides into amino acids some di and tri peptides absorbed Absorption Use amino acid transporters in mucosal wall some use Na Clquot or no cotransporter Sources ofProtein 50 food 25 digestive enzyme 25 mucosal cells no dietary protein in feces Infant Protein Absorption Newborns can absorb protein directly until tight junctions form IgG in colostrum provide protection Lipid Digestion Mouth and stomach lipases unimportant pancreatic lipases enter duodenum in active form Lipases Convert lipids to absorbable form lipases convert triglycerides into monoglycerides and free fatty acids Micelles Bile salts from liver emulsify monoglycerides and free fatty acids and cholesterol fats diffuse into mucosa at brush border Absorption Monoglycerides and free fatty acids cross and reform into triglyceride in mucosal cells triglyceride 39 39 Ifrom 39 enter lymph thru thoracic duct to blood Portal Vein Carriers water soluble foods directly to liver liver processes and detoxifies foods Fats lymph blood everywhere liver eventually Electrolyte Absorption Salts all HZO soluble portal vein small intestine has tight junctions salts use carriers channels and pumps to go thru cells Water 2000mlday ingestion 7000mlday secretions 200mlday in stool follows other absorption osmotically Sodium Most Na enters through cells energy gradient from Na pumps on basolateral side of mucosa as in kidney some Na entry through leaky tight junctions Potassium K enters down concentration gradient through channels K exchanged for Na last electrolyte absorbed during diarrhea K loss too fast for K reabsorption active transport of K in colon Bicarbonate Huge secretion by pancreas buffers acids in duodenum reabsorbed by concentration gradient in small intestine and Vitamins Water soluble B and Cvitamins rapidly absorbed rapid loss in urine must take in Band Cvitamin daily B11 absorption needs intrinsic factor from stomach Vitamins A D E K fat soluble micelles 99 lymph Minerals Caz 3080 absorbed vitamin D dependent Ca2 binding proteins and Ca2 ATPases I Cazentry GI Intro Mouth Esophagus GI layers Mucosa epithelia cells Submucosa longitudinal muscle submucosal plexus Muscularis circular and longitudinal smooth muscle myenteric plexus Serosa outer epithelial layer produces serosal fluid GI Innervation Plexuses neurons control local contractions longitudinal muscle propulsion of chyme circular muscle mixing food and secretions Parasympathetic Neurons dominates most of the time Activate plexuses I GI activity sympathetic neurons JGl activity Basic Electrical Rhythm Variable electrical baseline Ca2 and K channels openclose contraction when BER reaches threshold and APs occur Migrating Motility Complex Strong contraction migrates from stomach to end of small intestine starts as previous meal near complete digestion clears stomach and small intestine in anticipation of next meal GI Hormones Released in different areas both upstream and downstream effects Gastrin From stomach protein is strongest stimulus for release l stomach secretion ofacid and pepsinogen l small intestine illeocecal valve relaxation empties small intestine Initiates mass movement in large intestine that triggers defecation Cholecystokinin Secreted by duodenum into blood causes contraction of gall bladder and release of pancreatic digestive enzymes but inhibits stomach secretions Secretin Secreted from duodenum into blood l secretion of pancreatic bicarbonate into pancreatic duct bicarbonate neutralizes stomach acids in duodenum Mouth Little digestion here Almost no absorption only some medicine nitroglycerine absorbed by oral mucosa Secretions Bicarbonate neutralizes acids HzO amylase lipase mucase to coat food lysozyme antibacterial enzyme Swallowing Boluses formedcoated with mucus voluntary propulsion to pharynx reflex relaxation of upper esophageal sphincter bolus forced into esophagus Esophagus Tube to stomach sphincter at each end 59 seconds transit time to stomach no digestion or absorption Sphincters Upper esophageal sphincter relaxes upon swallowing peristaltic contractions behind bolus force it into stomach lower esophageal sphincter normally tightly closed relaxes to let bolus in Reflux Acid in esophagus thru lower esophageal sphincter loss of neural input most common cause acid irritates esophagus heartburn potential ulcer Gas In stomach Swallowed gas some burped out some absorbed some to colon most colonic gas is bacterial Stomach Pancreas Liver Stomach Holds contents kills pathogens starts protein digestion relaxes as food enters hold up to 1 liter Structure Lining has gastric pits cells produce secretions mucus coasts gastric pits prevents HCI killing cells Secretions Pepsinogen HCI separate H and Clquot pumps pH 12 mucus gastrin intrinsic factor for B11 absorption Motility Peristaltic waves 3min fundus to body to antrum forces food into antrum crushes boluses there forms chyme chyme is a mixture of food and secretions Emptying Pyloric sphincter separates antrum and duodenum squeezes shut as boluses are crushed only a small amount of chyme squirts through Ulcers Open sores in stomach cells exposed to acid kills cells no mucus covering Histamine Acid damage histamine more acid positive feedback loop Treatments Stop acid secretions neutralize acid H Pylori Bacteria Live in gastric pits gt50 of all ulcers hard to get due to mucus antibiotics can kill this Exocrine Pancreas Secretes bicarbonate solution to neutralize stomach acid and enzymes for digestion Duct System Carries solutions to duodenum duct cells secretes bicarbonate solution Alkaline Secretion Bicarbonate solution Pancreatic Aqueous Alkaline Solution PAAS almost entirely Na Bicarbonate 45x s more bicarbonate than plasma Regulation I H lower pH in duodenum causes secretin release into blood secretin from duodenum causes releases of Na Bicarbonate solution PAAS ex a negative feedback loop Enzymatic Secretions Proteases released in protected form lipase and amylase released in active form pancreas has trypsin inhibitor for protection Regulation Fat or protein in the duodenum causes CCK release CCK causes acinar cells to release enzymes enzymes carried to duodenum by PAAS parasympathetic neurons l enzyme release sightsmell response Liver release bile into duodenum to emulsify fats mostly undifferentiated cells 1000 s of metabolic reactions makes plasma proteins Blood Supply 2 sources merge at liver sinusoids hepatic artery supplies oxygenated blood from heart portal vein carries water soluble food from small intestine Bile Salts Major component of bile made by hepatocytes released into bile canaliculi on opposite side from blood bile salts from micelles 9095 of bile salts reabsorbed at ileum recycled Bilirbuin Metabolism Formed from heme of lysed RBC s fat soluble circulate bound to albumin released to liver cells modified to HZO soluble form most to bile feces provides color for both urine and feces jaundice is a bilirubin buildup usually a liver problem Gall Bladder Function Stores bile between meals when Sphincter of Oddi closed CCK relaxes Sphincter of Oddi and contracts the gall bladder bile enters duodenum Gallstones Calcium bilirubinate some or cholesterol stones most form in gall bladder with glycoprotein binding can block sphincter of Oddi gall bladder attack if gall bladder removed bild duct expands to hold bile Small Intestine Large Intestine Small Intestine Primary site of digestion and absorption Structure Duodenum jejunum ileum many folds l surface area 600 fold 9Lday presents 2 food7 secretions lZLday to colon 200ml in feces Villi Folds of small intestine wall tissue crypts of Lieberkuhn at base cells migrate upwards die by digestion cell replaced every 3 days fastest rate of mitosis here Microvilli Brush border Folds of cell membrane at the tips of villi cells site of absorption bound enzymes on surface enterokinase disaccharidases Mucus Secreted with HZO contains glycoproteins covers small intestine epithelium in C of L and upwards protection from digestive enzymes Motility Basic Electrical Rhythm BER higher at duodenum than at ileum moves chyme down small intestine peristaltic waves of longitudinal smooth muscle segmentation mixing contractions of circular smooth muscle Malabsorption lamino acid absorbance wasting ximuscle mass Jcarb and fat absorbance l stool and gas lvitamin absorbance Autoimmune Cronh s and allergic diseases Diarrhea Multiple causes most common small intestine motilitygtabsorption loss of H 20 and K potentially serious or fatal neuralheart problems dehydration leads to shock travel change in waterelectrolytes kill large intestine bacteria or e coliother bacteria in food Large Intestine Colon Handles absorption of H10 and Na and some K NO nutrient absorption from small intestine some bacteria Structure Small intestine cecum ascending transverse descending and sigmoid colons rectum anus internal and external sphincters control anus appendix closed pouch of lymphoid tissue off cecum Gastroileal Reflex Food in stomach causes relaxation of cecum and allows ileum to empty gastrin relaxes illeocecal valve Absorption Active transportation of Na water follows FecesFiber Feces is minerals fiber bacteria and H20 bacteria grow even during starvation fiber is cellulose and related compounds fiber l colonic activity may Jcolon cancer Bacteria E coli and other types appear soon after birth bacteria quire nutrients from the colon mucosa may produce useful vitamins and essential amino acids can invade body after radiation poisoning Physiology Dynamic process of maintaining or moving to a control set point Functional anatomy Organization Each level builds on the next each has characteristics that the lower one doesn t Molecules Assembly of atoms proteins ca rbs lipids nucleic acids Cells Basic unit of life use energy have metabolism removes waste Tissues Collection of similar cells with the same local function Organs Collection of different tissues carries a distinct function for the body Systems Collection of organs controls major coordinated functions like respiration Homeostasis Maintain the normal physiological state Internal Environment Interstitial fluid surrounds every cellthe liquid around cells Negative feedback Event X causes a change away from the set point then point Y causes a return back to the original set point blood pressure ion concentration muscle reflexes Positivefeedback Event X causes a change to a new set and there is no return to original set point child birth Cell Structure Cytosol Liquid portion in cell high protein Protein clusters organized enzyme pathways enhanced metabolism Metabolism Thousands of reactions protein catalystsenzymes Structural proteins energy production enzymes use and storage of carbohydrates and lipids Protein synthesis Chains of connected amino acids mRNA from nucleus codes for protein manufacture on ribosomes Ribosomes Combo of proteins and RNA Free ribosomes make proteins for use in the cytosol Storage Glycogen is a polymer of glucose n muscle for use during contraction n liver to maintain blood glucose between meals Store calories for later energy Endoplasmic Reticulum Long chains of interconnected tubes in the cell Production of exported or organelle proteins Rough ER Ribosomes on surface site of protein synthesis New formed protein threaded into ER lumen as made new proteins move through ER to smooth ER Smooth ER Membranes manufactured fat membrane synthesis Produces vesicles that carry new protein to Golgi apparatus Produces new membrane and complex lipid molecules Golgi Apparatus Receives vesicles from smooth ER sit of protein modification directs vesicles to specific organellescell membranes docks proteins on vesicles and destination membrane ensure Protein Modification Modifies structure adds or deletes Fig 51 Emmosis Chaperon proteins ensure folding Exocytosis Vesicles from Golgi with export proteins merge with quot DW39S39DECELL membrane and dump contents Intracellular Ca triggers exocytosis which needs ATP Lysosomes Contain digestive enzymes Digest molecules down to useable sizes Proteins amino acids Complex carbohydrates monosacch rides Figure 5193 Endocylosis Endocytosis Occurs to balance exocytosis extracellular molecules bind to receptors and trigger membrane infolding phagocytosis eating Pinocytosis drinking v CVTOPLASM runumn has odd numberefe eumns Energydeuumn gmskemn Am LeHMar energy WHADM mm ammo whereaerVhas apumose unhkew x Adenosm w v nxvgen G umse NM unpamw 2 pwuvaxe 2w NADHt pwwama NAD 2 auaxe Makes may 2 w he mnermembrane WMaxe mmmuna CrmtAud Cycle Kerb vdeTCAum and we Wmvam a stem cm Wmvam 2 NAD 2 FAD co um mm 2 NADH MnomgmnmMmMembranuvmmomesrmm e eumn vanspnn wsiem on mner membrane NAD rezvded 2 SAWNADH and 1 SAWmun LVKDmasm MytmmbmesrPohmers ofmbuhn fnneH nabwhwand vanspnn aongneumnsmovmg veswdesorganeHesandzhmmosomes m n m H Hmm u m sperm Mmmfrmmemsrlgges Thmmamems sumpa vmerTmzkmamems mvosm pa vmer Formlwememsm musde mmramons andwhwe mm 22H 2 nvazeHmarrmsmeme 22H mersnna mdrme md amundbexween 22H ExvazeHmarr md bevond m 22H Phosphohprds Bazkbnne at membranes wumkumn Hvdmphnwan ew es an mass 23st vaophm ouxersmes at membran Hvumpmm KaHshvdmpmh mu Cholesterolr my waxy snmbmw due m smaH sue merspersed bexween hmd Dummy at phnsphnhmds Prevents close packing of fatty acid chains create flexibilityfluidity Proteins n membranes some mobilerestricted Receptors On outside Binds to solute either chemical or ion some activated by channel or enzymes Channels Only ions pass K Na Ca Clquot protein channels span the membrane openedclosed Enzymes Catalyzes reaction A98 some activated by receptors some always active Docking marker Acceptors Site of exocytosis recognize and bind to secretory vesicles Carriers carrier molecules Revolving proteins no ATPase Alternate open side 2 types Molecules move with gradient Co transport with ion usually Na use ion gradient for energy source 39 a Carbohydrate Protein Complexes Identify self to car39mm 39quot 0 gm immune system by the alignment of carbohydrates Basis of separation of cells into tissues during embryonic development limit normal tissue growth to confined region Intercellular Connections CAMs CellAdhesion Molecules Proteins that anchor cells to other cells or to basal lamina a non cellular surface maintain tissue integritycontrol cell migration Tight Junctions Block movement between moleculescreate tissue sidedness in skin intestines and kidneys Allow selective transportmolecules must go through the actual cell Desmosomes Cellular rivets hold moving cells together in skin and heart extremely strong Gap Junctions Channels between cells where only ions pass Electrical signal from one cell activates the next cell extremely large channels Membrane Transport Di usion Across Membrane Driven by chemical or electrical gradients simple diffusion channels and carriers Net diffusion always goes high low other diffusion can go in any direction Hydrophobicity Fats and gases cross easily fluidity allows larger red blood cells to go through smaller capillaries enhances oxygen transport Size Small objects pass easily over large ones RBCs being squished small causes 02 to escape Fick s Law of Di usion Q PAACAX MW Rate of diffusion Q P Permeability hydrophobicity A Area ACAX Concentration gradient MW Molecules weight size Ions Channels Different types for different ions Na K Clquot Ca2 allows ions to move by chemicalelectrical gradients Osmosis Diffusion of water moving from high concentration low solute concentration to low concentration high solute concentration semi permeable membranes lets water to cross nothing else Carrier Transport Protein molecules change shape in membrane and move molecules across Specificity Each carrier transport a specific molecule or type of molecule Saturation Only limited number of carriers in each cell When all carriers are being used the rate will be at maximum Facilitated Diffusion NO ATP USED Move down gradient high low Molecules bind to one side carrier revolves molecules leave on opposite side more bind on high concentration side now USES ATP Moves ions against their concentration gradient low high Moves ions from high affinity side to low affinity side affinitylikely to have binding NaK ATPase Moves Na out of cells 9 moves K in K high insideNa high outside Creates gradients that allow electrical signaling SecondaryActive Transport Carrier has two binding sites agonist and Na Energy of the Na gradient out to in drives secondary active transport Cotransport agonist in or counter transport agonist out Na transport some glucose and amino acids in ions drive secondary active transport in some tissues Membrane Potential Voltage Separation of charge all cells have a negative charge inside compared with the interstitial fluid opposite charges line up along the membrane Resting Membrane Potential Voltage across cell membrane where the cells are not activated determined by open ion channels K dominates at rest has most open channelsSome Na Concentration Na 150mM in extra cellular fluid and 15mM in intracellular fluid in muscle K 5mM in extra cellular fluid and 150 mM in intracellular fluid in muscle Protein 0mM extra cellular fluid and 65mM in intracellular fluid in muscle Intracellular concentrations of Na K and protein are different in different cells Permeability Determined by the number of open channels number of K or Na open channels determines ion diffusion different open number in different cell types produces different resting membrane potential Na KATPase Enzyme creates the gradients and restores them after ions diffuse across the membrane ion pump activity Equilibrium Potential Limits on KNa Only open channels determine membrane potential 60 70 90 Na Most K K All Few Na all Kquot Diffusion at Rest At rest K channels are openK diffuses out intracellular protein Aanions is trapped in the cell Na channels are mostly closed little Na diffusion PumpLeak Balance Balance between pump and diffusion activity since ions constantly diffuse down their gradients through channels a constant input of ATP energy into ion pumps is needed to maintain gradients Resting Membrane Potential Balance Membrane potential always negative at rest Membrane potential magnitude decrease less negative during depolarization Membrane potential magnitude increase more negative during hyperpolarization Depolarization Membrane potential is less negative from K channels closingNa channels opening membrane potential moves towards Na equilibrium Hyperpolarization Membrane potential is more negative from K channels openingNa closing membrane potential moves towards K equilibrium potential Graded Potentials Triggered by agonists or physical force Opens channels Size proportional to the size of the stimulus spreads to adjacent areas but decays rapidly over time and distance can only carry signals over short distances in receptors neurons muscles Action Potential Electrical signal long range activated by graded potentials Do NOT degrade over time and distance i39lran Voltageesored channels Open when membrane reached a particularyoltage llike 1520mvl above resting membrane potential all voltage gated channels open together causing action potential enters inactivated state soon after opening lrefractoiy periodl Action Potential Depolarization afThreshadr gated Na channels open enters down gradients to threshold from resting AP p39b quot I J Na channels open together enters 30 l lDEPoLARlZATloN rapid depolarization to 20 does not reach Na equilibrium se some K a e open RepalurizutianrVoltagergated Na channels close soon K channels still open K leaves membrane potentialfalls 39 anolta 39 K lnearer r90mVl K equilibrium potential Return to Resting Potentials Extra K channels close structure or Yypioal Neuron Dendmes Axon lenrinals Neural Structure Receive an d pass on signa s Dendritesr Receive neurotransmitter from other neurons many branches N0 ACTION POTENTIAL ONLV graded potentials 3 leg 3 CellBadya Cell organellesnucleus high I Schwann scells density of voltage gated Na channels at pun WEquot 5mm axon hillockr action potential starts here Nucleus Vewlon r ential away from cell body speed ofaction potential variable increase speed with diameterand myelin Meylin Nodes of Ronyierl Meylin surrounds axon and wraps layers of membrane increase action potential speed 39 rA er Touch neuronsr Myelin large Pain neuronsr No myelin small p r I ction pot g IUI All I otentials are 39 action potential r y A quotformation is passed bythefrequencylnotsizelofthe Synaptic Structuresr Neuralrneural synapses 39 r J 39 39 39 Receives action potentials down axon action potential opens Caz channels Ves39Eesr Co I 39 l at CaZ39 trigger merge neurotransmitterdump n 4 ed into cleft diffuses to poslrsvn membrane llUlll prersyn neuronwhen neurotransmitter n t u u u binds Excitatory Postsynaptic Potentials EPSPs Na enters when neurotransmitter binds and causes depolarization one EPSP is not enough to reach threshold Inhibitory Postsynaptic Potentials IPSPs K or Clquot channels opened by neurotransmitter K leaves or Clquot enters down their electrochemical gradient Membrane potential more negative less likely to reach threshold Grand PostsynapticAction Potential Sum of all EPSPs IPSPs does reach thresholdfire action potential most neurons are inhibited by IPSPs most of the time Axon Hillock At junction of cell body and the axon high density of voltage gated Na quot channels action potential starts here One way Conductance Neurotransmitter is only released from presynaptic neuron receptors only on postsynaptic neuron nfo goes in one direction Temporal Summation EPSPs from the same neuron close in time are additive they may M to reach threshold one neuron two events close together Spatial Summation EPSPs from different neurons are additive the M may reach threshold two neurons Convergence Multiple synapses into a single neuron anatomical basis for spatial summation Divergence An action potential in one neuron delivers it to all its divergent neurons at the same time Communication types Can be short or long combo of electrical and chemical activity Paracrines Local hormones released from one cell affects nearby cell Nitric oxide important in control of blood flow Neurotransmitters Specific each neuron ahs only ONE type of neurotransmitter Released locally and by exocytosis synapse celltocell Endocrine Hormone released from endocrine tissue broad effects because hormone is released into blood effects depend on target cell receptor Neurohormones Released from neurons into the blood Functions as other hormones receptor dependent Hydrophilic Hormones Cannot cross the membrane rely on membrane receptor activation membrane proteins produce second messengers Second messengers Made at membrane internal activation mechanism started by hydrophilic hormone only cells with receptors respond cAMP ATP cAMP activates kinasesadds phosphate to molecule kinase cascades amplify signal cGMP GTP cGMP activates kinases IPD Causes release of intracellular Ca2 stores Ca2 in sarcoplasmic reticulum Calcium Released from internal sacroplasmic reticulum by IP3 eneters across cell membrane through Ca2 channels binds to and alters protein activity Celltocell Ca2 signal produces coordinated cilia waves exocytosis Gap junctions depolarization causes cardiac and smooth muscle contraction in cells by opening CaZ G Proteins Timing proteins Bind to GTP increase activity until GTP GDP Regulate vesicle movement cytoskeleton growth visions 2nd messengers Unit Obiectives Cellular AdaptationI Iniuml and Death Normal Cell Biologv and thsiologv Review 1 P Basic anatomy and function of a Nucleus The large membranebounded organelle that contains the genetic material in the form of multiple linear DNA molecules organized into structures called chromosomes b Mitochondria Spherical or rodshaped organelles found within the cytoplasm of eukaryotic cells and are referred to as the llpowerhouse of the cell since they act as the site for the production of highenergy compounds eg ATP which are vital energy source for several cellular processes c Golgi Apparatus Packing Things Up d The Golgi apparatus or Golgi complex is found in most cells It is another packaging organelle like the endoplasmic reticulum ER e Ribosome A minute particle composed of protein and ribonucleic acid RNA that serves as the site of protein synthesis f Lysosome The purpose of the lysosome is to digest things They might be used to digest food or break down the cell when it dies g Receptors How cells communicate to work together and control growth Receive first messengers from extracellular matrix and transfer the message to second messengers to transmit message within cell h lon Pumps move ions across the cell membrane most important to us SodiumPotassium ATPase i Cell Membrane Define a Replication Occurs in the nucleus Multiplication of usable DNA for Protein synthesis 57 Transcription Transferring the DNA message onto mRNA Squot Translation Transferring of genetic code onto proteins Describe Genetic Expression a Different parts of the genome are expressed on each protein It is regulated by the nucleus of the cell Discuss ATP in terms of cellular energy and ion pumps a ATP degrades to ADT and to AM P In the breaking of bonds free energy is released The energy can be used to power ion pumps ie NaK pump Without the movement of sodium and potassium against the gradient Sodium builds up inside the cell and causes it to swell If the pump is not reactivated it can cause the cell to lyse Use the terms intracellular and extracellular to describe first and second messengers a First messengers from the extracellular matrix to bind to intramembranous receptors The message is then passed into the cell and transmitted by second messengers via intracellular matrix Pathoghysiology 1 Significance of unit in terms of illness and disease a Since we are a collection of cell illness is caused when a critical mass of cells become sick Normally cellular adaptation is how our bodies accommodate and fight against injury but when cells become sick they lose the ability to adapt and sometimes mutate causing illness or disease 2 Significance of Gene expression in cellular adaptation and cellular injury a Gene expression controls both cellular change in normal cells via atrophy metaplasia hypertrophy dysplasia hyperplasia and cellular accumulation eventually leading to planned cell death apoptosis However when a cell is damaged in can cased free radical disorders hypoxia anaplasia or electrolyte imbalance This eventually ends with unplanneduncontrolled cell necrosis 3 Change in size number type ofa cell is proportional to the stimulus Reverse or remove the stimulus reverse the adaptation not always 4 Describe the cellular changes that occur with a Atrophy Reduction in size i Stimuli from decreased demand or decreased nutrient supply ii Example decreased blood flow 9 atherosclerotic occlusive disorder b Hypertrophy increase in size i Stimuli from increased demand ii Example Skeletal muscle cardiac muscle neurons 1 Adapt to hypertrophy because body cannot make more of these cells They have to get bigger c Hyperplasia Increase in number i Stimuli from increased demand ii Example skin intestinal glands hepatic reproductive organ cells 1 Normally adapt to hyperplasia because body can produce more d Metaplasia change from 1 normal cell to another i Stimuli from chronic irritation and inflammation ii Example from ciliated columnar epithelium throat cells from smoking e Dysplasia cells are lmessed up i Stimuli from chronic irritation and inflammation ii Example cervical dysplasia 5 Examples of intracellular accumulations a Hemolytic anemia caused by blood bursting causing RBC s to lose hemoglobin Hemoglobin is converted to bilirubin which builds up in the sclera and skin 6 Compare and contrast Metastatic and dystrophic calcification a See table 7 Cellular Injury a Radiation b Chemical c Biological Agents Unit Objectives Integumentary Disorders Normal Anatomy and Physiology 1 The skin protects the body from external environment senses heat cold and many other things helps with heat regulation controls evaporation storage and synthesis excretion sweat absorption and water resistance 2 Epidermis is the skin with keratinocytes amp melanocytes The dermis is the connective tissue underneath the skin 3 Keratinocytes primary functions are the formation of a barrier against environmental damage such as pathogens heat UV radiation and water loss Melanocytes produce melanin 4 Sebaceous glands are found in great abundance on the face and scalp They secrete a waxy oil matter to lubricate the skin and hair 5 Skin disorders may look different on different types of skin Pathophysiology 1 Flat ampNonpalpable Macule 0 Small up to 1 cm ex freckle Patch 0 Large bigger than 1 cm ex birthmark Elevated palpable solid Plaque 0 Large bigger than 1 cm often from groupings ofpapules ex HPV Papule 0 Small up to one cm ex mole Wheal 0 Not determined by size irregular borders from skin edema ex hives Elevated palpable uid filled Vesicle 0 Small amp serous uid filled up to 1 cm ex genital herpes Bulla 0 Large amp serous uid filled bigger than 1 cm ex 2 101 degree burn Pustule 0 Not determined by size pusfilled ex acne 2 3 Different skin disorders may look different on patients with a different pigment of skin 4 Ultraviolet radiation can be from the sun UVA UVB UVC UV ray on the skin can cause crosslinks DNA so it can t be read properly burnt skill cells release vasoactive substances amp chemicals that damage more surrounding cells inhibits cutaneous immune cells melanocytes make more melanin like smoking 9premature aging of the skin 5 Sunburn is when the skin is warm amp red with underlying in ammation Second and third degree burns cause blistering problems with temp regulation and dehydration One bad burn greatly increases your risk for skin cancer 6 Effective sunburn prevention includes a cover up with clothes hat and sunglasses and using sunscreen It is recommended to use SPF 1530 and reapply every 2 hours Frequently missed areas to watch for include the tops of feet amp back of hands ears bald spots and neck 7 Basal cell Carcinoma Squamous Cell Carcinoma Malignant Melanoma Description Most common skin CA Second most common skin Rarest of skin CA most highly curable low CA curable not as easily as fatal highly meastatic metastatic potential basal cells medium metastatic potential if late dx Risk factors Highly associated with sun Highly associated with sun Moderately associated with exposure main risk factor exposure main risk factor also linked to arsenic tar amp coal occupation sun exposure FHx white with blondred hair lots of upper back freckles sz 3 blistering sunbirns before age 20 Hx3 2 yr as teen with outdoor job actinic keratoses Common areas Head neck Head nose forehead ears lips and hands Back arms legs Appearance Early smooth eshy palpable surrounded by small superficial vessels Late raised ulcer with central depression amp waxy borderring of pearls On dark skin similar but with same pigment as skin so often misdiagnosed Red papule or plaque often scaling crusting amp ulcerated highly irregular border no quotring of pearls or superficial vessels Black or dark brown papule plaque irregular border uneven surface may be scaling bleeding in amed Most from previou nevus that change asymmetry border irregularity color change amp variation diametergt 6mm 8 Ihave 16 risk so I am 2 times likely to get malignant melanoma Faciale Pedis 10 Tinea is caused by many different kinds of mycoses These fungi live off dead skin and cells amp digest keratin Candidiasis like to grow in warm moist skin folds 11 Superficial fungal infection appearances can look like red patches with well defined borders 12 Contact dermatitis may have symptoms such as a red rash not specifically localized and may have blister or wheals Candidiasis has red patches with 13 welldefined borders Impetigo Herpes Simplex Virus Herpes Zoster Common Names HSV cold sores fever blisters genital herpes Causes From staph or strep Herpes simplex virus I amp II Varicella zoster virus HVZ VZV chicken pox shingles From varicellazoster virus 14 Impetigo is easily transmitted by touch most common on the face In the early stage impetigo is a vesicle or bulla that ruptures to release serous uid and more bacteria Late stage its it honey colored crusting lesions that appear with vesicles or bullae that have not yet broken open HSV there is a primary where it makes antiviral antibodies Then the HSV lives in the dorsal root ganglia and come back out to reinfect the skin during a recurrent infection The face gets vesicles pustules ulcers and crusts that are more local VZV starts with exposure during childhood when you get the chicken pox This virus also lives in the dorsal root ganglia and reactivated virus by stress illness steroids or chemo ravels along nerve They look like red skin lesion across the dermatome 15 Acne Vulgaris is a chronic in ammatory disorder of the pilosebaceous unit hair follicle sebaceous gland 16 During acne vulgaris cellular turnover amp sebum happened depending on how fast which causes a blockage in the punit which then causes and infection and in ammation Treatment includes topical creams such as steroidal and antibiotic oral steroids and hormones birth control helps retinoids and skin management 17 Atopic eczema Psoriasis Definition In ammatory skin disorder cause by hypersensitivity allergic reaction Tcell mediated autoimmune disease that causes thick scalingskinplagues Main cellular components Eosinophils Tcells amp histamine in ammation Tcells respond to an unk antigen amp produce cytokines that stimulate growth of keratinocytes amp dermal vessels cause Associations w other disorders Asthma amp allergic reactions Moderately associated with arthritis Location Usually starts in infants face later seen on exor surfaces trunk scalp Extensor surfaces Cyii inin fi39iamerit activatian by Ca binding ta Tmpurii39ri activatian spread directian Cardiac Activation Structures Activatian patnway nas autarnytnmic ceiis Avian Si39te of mai Heart beat i39rii39ti39ati39uri iri RGHT 39 39 no Heartbeatstartseisewheresnut usuaHy narmmi n ai L47 Depaiarizatian Fastest SA nade 70730 APsmi39ri AV nade 40750 APsmi39ri Bundie at HTSPurki39m39e bers 2040 APsmi39ri campiete AV biuck praduces separate atriai and ventricuiar amivatiun ienrricasAP p cantractian spreadsupward Bundle oin39s Off quV npde dawn tne septum 39 39 39 39 tnraugn gapiunctians w purki39m39e ipers Dazearizati39orisNa entry t tn n id Ca m i d p iittie Na i39ri u nce an AP 39 39 i 9 NF 2 i neart rate and strengtn ufcuntrami39uri id i micg 39 39 39 JHeartrate dnanges in membrane patentiai detected by different distancesta ieads ic c m 4 4 i need eiectricai shudlt ta resmurdi39riate APs P waveAtriai depaiarizatian start aratriai cantractian 1 was Comp2x7 Ventricuiar depaiarizatian masks atriai repaiarizatian E p atriai cantractipnstartaratriai fi39Hi39rig and ventrimiarmntrac ti un Twaves Ventricuiar repuiari39zati39uri end of ventricuiar mntracti39uri start of 7 ventricuiar fi39Hi39rig s airiai mmmtiian yainxnnan uf Car 1 Puma g3 contraction 1 ha M Cardiac Cycles Sequence of cantractian and reiaxatian 4 vaives 2 AV WWW W W amti39dpuimuriary keep pippd uwi39ng pne way Wastees Reiaxed neart time fur fi39Hi39rig end diastpiic vuiume130mi AtriaSystoes Cantracts rsts mmpietes ti39Hi39rig of ventricies Ventricular Systole Follows atrial contraction contraction spreads upwards pressure must be greater than aorta to open aortic valve Aortic Pressure Load left ventricle works against High BP puts greater load on heart Ejected Blood Volume 7090ml of blood ejectedbeat 65 of end diastolic volume Lower hear ratehigher ejected volume Heart Rate Dependence Max heart rate 220 dependant on age rates above 180 decrease filling time must be motivated to exceed 180 this can decrease cardiac output which is life threatening Arterial Pulse Arterial walls expand to hold blood rebounds during diastole creates pulse little drop in BP throughout arteries Heart sounds Closing of valves turbulent blood flow creates sounds low pressure AV mitral and tricuspid first then high pressure aortic and pulmonary valves different sound intensities Murmurs Nonlaminar nonsmooth flow sound when valves should be closed Valve Stenosis Stiff valve small opening turbulent flow as blood squirts though less rare Valve lnsufficiency Valve leaves don t properly mesh children with improper valve closure sometimes outgrow this murmur as growth alters valve alignment Cardiac Output Amount of blood pumpedmin Stroke Volume X s Heart Rate C0 70m at 70 beatsmins 5Lmin body has about 5L of blood circulation time 1 minute Starling s Law Stroke volume control I venous return stretches cardiac muscle l force I CO more actin myosin interaction less thick Z line contact les thinthin overlap more Ca1 release stronger contraction more SV more co Turbulent Neural lnfluences Both SV and HR changes Parasympathetic Dominate at rest cut vagus nerve to heart HR I 70100 immed exercise l parasympathetic output Jresting HR may go to 3040s Sympathetic I Ca channels opening faster depolarization causes increased HR more Ca1 causes more force causes increased SV Arteries Arterioles Blood Vessels 3 layers endothelium vascular smooth muscle connective tissue capillaries ONLY have endothelium Types ofBood Vessels Arteries arterioles capillaries veins each has a different function lymph vessels carry excess filtered fluid Physical Factors Some factors constant ex vessel length some factors variable flow pressureresistance Vessel Radius More important than variable factor Thickness of blood controlled by hematocrit RBCs in blood 45 males 42 females need large change to influence blood flow Above 48 RBC interation with arteriole walls greatly increases resistance Viscosity resistance 1radiusquot Small constriction causes large l resistance Jflowsmall dilation causes large Jresistance l flow Short blockages can compensate with increased velocity until greater than 80 closed Arterial Conductance High pressure blood enters aorta at 93mmHg large arteries expand to hold blood little change in BP 24mm wide momentum of moving blood caries blood forward to tissues Arterial Pressure Systolic P is 120mmHg diastolic P is 80mmHg Pulse pressure is Sys Dias 120 80 40mmHg Mean arterial pressure Dias 15PP 80 13 93mmHg Coronary Circulation Heart rate dependent Jdiastole at high HR Jfilling time and Jcoronary flow coronary flow only occurs during diastole HR gt 180 decreases cardiac output potential heart failure Atherosclerosis Multiple stages LDL low density lipoproteins lays down fatty streak 1WBCs and fibroblasts overgrow fatty streak 3 Caclium infiltrated hardens overgrowth Alcohol Effect Modest alcohol consumption can solubilize fatty streak can reverse atherosclerosis stage 1 biophysical effect not receptor effect no alcohol effect on other stages Arteriolar Flow Arterioles branch off arteries 30 microns wide 93mm Hg at artery end carries blood to capillaries 37mmHg at capillary end arteriole radius can go in either direction Tone Partial activation with m stimulus relax vasodilatation or constrict vasoconstrict arterioles have tone Perfusion Control Sympathetic neurons metabolites paracrines control arteriole smooth muscle NE adenosine NO whatever cell works the hardest produces the most adenosine and gets the most blood flow Capillaries Lymph Veins Capillary Blood Flow Very slow many capillaries spread flow out and decrease speed Capillary Pressure 37mm Hg at arteriole end down to 17mm Hg at venous end Capillary Fluid Exchange Balance of BP forcing fluid out and osmotic pressure from plasma proteins drawing fluid in fluid moves through capillary pores Filtration Dominates at high pressure end arteriolar BP gt osmotic pressure fluid forced out Reabsorption At venous end lower BP BP lt osmotic pressure fluid reenters Net fluid sweeps volume around capillary slightly more fluid filtered than reabsorbed outward BPinward plasma protein Lymphflow Return of excess filtered fluid to circulation Return ofFiltered Fluid Fluid enters closedended lymph vessels which merge with others lymph nodes are sties of large lymph vessel merger large lymph vessels have valves lymph enters vena cava BP0 at thoracic duct in chest Edema swelling Excess filtration broken capillaries low blood protein starvation alcoholism bacteria presence and destruction draws fluid osmotically parasites 9 filariasis 9block lymph flow 9 fatal Venous Flow Capacitance vessels hold largest blood volume Venous Pressure 17mm Hg at capillary end to O at vena cava during inspiration vessels in thorax may have negative pressure BP needs help getting blood up to heart Venous Valves Prevent backflow every lZinches in large veins valves can be seen on veins on back of hand Skeletal Pump Muscle contraction squeezes veins forces blood to heart Varicose Veins Ruptured valves column of blood slow return clots may form blood bypasses varicosities through other veins varicosities called varicose veins not life threatening only blood clots Red Blood Cells Platelet Plasma Liquid portion of blood water electrolyte metabolites hormones protein Plasma proteins Albumin highest draws fluid into capillary binds hydrophobic hormones Globulin many subgroups gamma globulins are antibodies Fibrinogen final protein for blood clot formation Erythrocytes RBC s Carry oxygen and CO no organelles only hemoglobin Hb sack of protein Production n bone marrow from stem cells 20ml of RBCday 50ml of bloodday low blood oxygen causes release of EPO from kidneys Shape Bioconcave disks 8 microns across spectrin net under membrane helps maintain shape fluidity of membrane allow squeeze through capillary membranemembrane squeeze increases gas transport Destruction RBC membranes lose cholesterol overtime rupture in spleen capillaries at 120 days life span if spleen lost liver ruptures RBCs Hemoglobin 2 alpha amp 2 beta chains has subunit protein globin Heme in center of chain iron in center of heme oxygen attaches to heme Cooperativity increase binding at lungs and release at tissues Fetal hemoglobin 2 alpha amp 2 gamma chains higher affinity for Oz than adult hemoglobin draws 02 from maternal blood replaced by 23 months postnatal Anemias Lack of oxygen altitude reduced RBC s bleeding no anemia with menses 50ml5days reduced delivery circulatory reduced use cyanide Sickle cell Single Hb mutation low oxygen 9 Hb forms stacks changes cell shape sickled cells hang up on branch points Survival value protection from malaria parasites lay eggs in RBC s growing malarial parasites rupture weakened RBC membranes before maturity Iron Deficiency Lack of iron9 Jamount of Hb NOT from using noniron cookware wrong form Platelets Pinched off parts of megakaryocytes in bone marrow Production Megakaryocytes stay in bone marrow platelets pinch off and enter circulation spleen kidneys and liver make thrombopoietin ThrP stimulates platelet formation ThrP binds to platelets in blood when platelets low I free ThrP Activation Activated by collagen and other proteins in connective tissue of blood vessels platelets adhere I ADP release more P s come and stick makes platelet plug Hemostasis Stoppage of bleeding Vasoconstriction Decreased BP at site of cut tone constricts small vessels Platelet Plug Exposure of collage platelet sticking ADP positive feedback prostacyclin from healthy blood vessel blocks platelet adherence Coagulation Blood clotting 2 systems both lead to fibrinogen soluble fibrin selfadhering Forms mesh that traps RBCs etc Intrinsic System Inside plasma collagen activated cascade needs Ca2 and all factors in pathway Extrinsic System Thromboplastin from damaged tissue starts cascade merges with IS halfway down stop bleeding Clot Removal Plasminogen trapped in clot cascade started by collagen plasmin Plasmin is an enzyme that slowly dissolves a clot over about 2 weeks White Blood Cells Innate Immuniy Cell types Leukocytes 5 types all have different defense functions Multilobe nuclei granulocytes neutrophils eosinophils basopihls stained by natural acid basic stains Singlelobed nuclei agranulocytes moncytes lymphocytes Whagocytes Phagocytosis of bacteria and dead cells order of attack resident macrophages neutrophils new monocytes macrophage migration ZNettrophils Rapid response move from blood to damaged tissue diapedesis squeeze through capillary pores attack bacteria r39 quotquot move into tissue and become macrophages resident macrophages wait for bacteria to come during infection vast movement of monocytes into infected area massive macrophage attack on bacteria 4Eosinophils Produce acids that kill parasites high in GI tract produce allergic responses 5Basophils Release histamine histamine causes inflammation I blood flow arteriolar dilation and I pore size allows diapedesis Defense Mechanisms Innate nonspecific immunity defense mechanisms not influenced by prior exposure acquired specific immunity B and T lymphocytes attack specific antigens Inflammation Nonspecific response occurs with any infection or injury Chemotaxis Chemical signals from damaged areas draw phagocytes Complement System Series of 9 factors C1C9 major bacteria killer Activation By antibodies or by the protein properdin this is opsonin tagging of surface carbohydrates on bacteria leads to pore formation in bacteria membrane Pore Formation C5C9 can form pores in membrane very local rapid inactivation pore allows osmotic lysis Na enters HZO follows cell swells and bursts ill feeling because bacterial toxins activation of pain receptors from partially digested protein of dead bacteria Histamine I blood flow brings phagocytes oxygen amino acids I capillary permeability opens pores for liquid and diapedesis Interferon Cytokin released from virus infected cells activate antiviral defenses in cells near virus infected cells many side effects Natural Killer Cells NonT cell lymphocytes no prior exposure needed for activation Activation Lipids and carbs on bacteria tumors transplants and by antibodies on cell surface forms pores by injecting perforin kills by lysis Adaptive Immuniy B Lymphoc es Antigens substances that activate B and T lymphocytes most foreign some selfantigens in autoimmune diseases Antigen Presentation Protein antigens Taken in and partially digested by macrophages part of antigen linked to MMC protein complex activate T cell attack on cells that have that protein or B cells produce antibodies B Lymphocytes Bind antigens full activation requires T helper cell contact antigen binding triggers cell proliferation into plasma B cell clone cells and memory cells Plasma cells Antibody factories make antibody to antigen that binds high ER for Ab production loses other organelles limited lifetime 1 week Memory cells B and T cells few cells have very long life provide immunity from antigens Primary Response Activation of B or T cells is slow short and weak Secondary Response Activation of memory cells is fast strong and long massive response upon 2nd exposure Immunoglobulins antibodies IgG gA IgD IgM IgE Yshaped proteins Variable Region arm tips of the yshaped protein can bind Z antigensAb must be same type of antigen Constant Region tall region activates some aspect of immune system when antigen bound Antibody Functions Activate complement system to kill bacteria labels cells for ingestion by phagocytes minor physiological function neutralized by binding used for lab testing Blood Types Based on surface carbohydrate genes code for enzymes that add carbohydrates transfusion reaction if mismatch ABO System A factor B factor AB has both factors 0 factor has neither Rh factor or 2 gene system Gene for factor Activator gene Non activator weak and reaction formely missed Rhogam given to Rh mothers of Rh children given after birthprevents transfusionproduce primary response Adaptive 39 Ti 39 Skin TLymphocytes protection against cellular changes attack cells with both a foreign antigen and selfantigen MHC cancer virusinfected cells transplants attacked Cytotoxic TCells Bind to cell and inject perforin form pore osmotic lysis follows Helper TCells Release cytokines that activate all B and T lymphocytes AIDS HIV attack on helper T cells decreased immune response opportunistic disease can now attack avoid multiple concurrent infections HIV needs broken skin to enter hard to get Helper TCell Cytokines Paracrines that regulate immune system I proliferaiton growth and function when cytokine structure known renamed an interleukin Major Histocompatibility Complex Previously known as HLA antigens MHC Class I Selfantigens on surface of all cells identify cells as self 36 out of 100 possible antigens on every cells others in foreign cells attacked MHC Class II Ingest and present antigens activated T cells Transplants Nonmatching MHC 1 cells are attacked by antibodies partial match has both self and foreign antigen triggering T lymphocyte attack Tyr to math MHC class 1 proteins T cells may attack suppress T cells more infections leukemia replace marrow fungus risk Tumors Benign tumors stay localized no infiltration of surrounding tissues malignant tumors have transformed cells cancer can infiltrate nearby tissues can metastasize to other parts of the body Allergies Immune reaction to a harmless substance allergens can produce responses Immediate Hypersensitivity Immune response in 20 minutes B cell mediated antibody production Stimuli Nonbacterial pollen bee strings penicillin mold dust IGE antibodiesmany in skin eyes lungs GI tract system designed to attack parasitic worms Chemical triggers histamine vasodilatation and capillary permeability I SRSA strong bronchiole contraction potentially lethal Symptoms Localized reaction Upper respiratory hay fever congestion edema sneezing runny nose Bronchioles lower inflammation constriction increased mucus difficulty breathing Anaphylactic Allergens spread by blood severe hypotension due to increased capillary permeability bronchoconstriction treat with epinephrine Delayed Hypersensitivity Immune response in 24hrs T cell mediated poison ivy some toxins stimulate T cells migrate to area of contact and produce rash Skin Mechanical barrier with defense mechanisms different layers 3 Epidermis Layers of epithelia cells dead cells outermost with dividing cells beneath No blood supply supplied by diffusion from the dermis desmosomes and keratin fibers hold cells together keratinized layer remains after death pathogen tight air tight fairly water tight prevents evaporation burns destroy the epidermis caused by hypertension and shock Dermis Connective tissue beneath the epidermis blood vessels nerve endings many cell types blood regulates heat loss Sweat glands sweat has variable Na content Sebaceous glands oil waterproof skin Hair follicles increased tough sensitivity Melanin absorbs UV light UV sensitive Langerhands cell present antigensUV resistant Granstein cells slow immune responses net UV light 4 skin cancer Hypodermis Adipose tissue insulates body from heat loss Lung Structure Breathing External Respiration Exchange of gases 0 and C02 between body and environment Internal Respiration Use of 02 by mitochondria Non respiratory Lung Functions Water and heat loss l venous returns acid base balance speech pathogen defense circulatory modification ACE and sense of smell Lung Structure Trachea bronchi bronchioles alveoli gt20 generations of bronchioles alveoli air sacks sites of gas exchange Type I Cells Epitheal cells I micron thick separate air form TraChea interstitial fluid Branch Type II Cells In alveoli Produce surfactant Jresistance to alveolar m Opening Lungs t Lung Mechanics Air flows from high pressure to low pressure Atomspheric Pressure 760 at sea level 600 at Denver 1 mile up Intra alveolar Variable exhale 1 2gtatm inhale 1 2ltatm Intrapleural Between lungs and thoracic wall always 4mmHgltatm lower pressure keeps lung always inflated Boyle s Law P x V constant JV l P l V JP Tidal Volume Normal breathing volume Inspiratory reserve volume extra amount you can inspire Expiratory reserve volume extra amount you can expire Inspiration Regular phrenic nerve form medulla sends AP to diaphragm diaphragm contraction increases thorax volume Jpressure decreased pressure causes inspiration Extra Inspiration External intercostals muscles contract expand thorax Expiration Normally passive as diaphragm relaxes Jvolume l pressure expiration Extra Expiration Internal intercostals muscles between ribs contract abdominal muscles contract also squeeze thorax Compliance Ease of lung expansion normally easy l brosis asbestosis of lungs J compliance Alveolar Surface Tension Adherence of H20 molecules creates surface tension on inside of alveoli surface tensions must be overcome to open alveoli Surfactant Several phospholipids mix with water and Jsurface tension also prevents edema in lungs first made at 36 h week of gestation glucocorticolds l surfactant production in premature infants Anatomical dead space Normal tidal volume is 500ml 150ml of mouth pharynx trachea bronchi bronchioles is dead space 350ml is normal alveolar inflation Long slow breathing minimizes dead space effectShort rapid breathing still must fill 150ml dead space Gas Exchange Partial Pressures Gas equivalent to concentration sea level 760mmHg 600 N2 160 02 C02 03mmHg gases independent of one another air in lungs is water saturated AlveolarAir P0 100mm Hg PCOZ 40 Venous blood P0 40 PCOZ 46 Diffusion Across Alveolar WaII Gases follow partial pressure gradient capillary gases match tissue it goes through 0101 enters pulmonary capillaries until PO is 100 C02 C01 leaves pulmonary capillaries until PCOZ is 40 Pulmonary Circulation Lower BP than aorta 1520mm Hg MAP of pulmonary artery quot quot 39 cj usiuu Ration quot quot and perfusion normally well matches 08 areas that have open alveoli get more blood flow as need for gas exchange I both blood flow and ventriculation l in new lung areas Tissue Gas Exchange Reverse of lungs Unload Ozload COZ opposite 01100mmHg arterial blood loses 02 to 40mm Hg tissue until capillary is 40mm Hg COZ 40mm Hg arterial blood receives CO from 46mmHg tissue until capillary is 46mmHg Oxygen Transport 15 carried by dissolved Oz985 carried by binding hemoglobin Oxygen Hemoglobin Binding Sigmodial curve cooperatively between 4Hb subunits Steep Region At tissues fall in P0 unloads 02 at lower PO even more 02 delivery Plateau Region At lungs all Hb is 02 bound no effect on extra 02 Cell that works the hardest gets more oxygen Bohr Effect COz acid shift HbOz curve to the right More 02 unloading at given POZ Carbon Monoxide 2 effects Binds Hb 200x s stronger than 01 less 02 available never dissociates must lyse RBC to lose CO shifts HbOz curve to left less 02 delivery Hypoxia Low blood oxygen Low 02 airhigh altitude or 02 deprivation high altitude ethnic groups higher Hb even at sea level sea level ethnic groups low 02 training I Hb lose when returned to sea level Hyperoxia Breathe high oxygen air no additional binding already full l dissolved 02 may lbreathing rate benefit only psychological Carbon Dioxide Transport 10 dissolved 30 bound to plasma portien and Hb 60 converted to biocarbonate by carbonic anhydrase carbonic anhydrase catalyzes HZO CO 9 HzCOg 9 HCO39 H tissueopposite for lungs Carbonic Anhydrase n RBCs tissues converts CO 9 bicarbonate at tissues as CO added Lungs reversal bicarbonate 9 CD then breathed out Hypcapnia Low COz hyperventilation JCOz in blood9 faint breathing into bag I COZ back to normal Hypercapnia High COz l breathing rate I COZ in blood strongest stimulus for increased respiration Regulation of Respiration Lung Diseases Medullary Control Centers Dorsal Respiratory Group DRG rhythmic discharge 9 phrenic nerve 9 diaphragm initiates normal breathing Ventral Respiratory Group VRG causes l inspiration expiration Pontine Control Centers Modify medullary centers Pneumotaxic center switches off inspiration Apneustic center prolongs inspiration normal inhibited lf PC damaged Hering Breuer reflex from lungs stops inspiration Chemical Control of Respiration Most powerful controller of rate l blood Oz 9 l brain CO 9 I H and HCOg H in brain increased DRG rate Peripheral Changes In carotid bodies and aortic bodies I H or I COZ or 402 will l rate of respiration little effect in normal range POZ lt 60mmHg l rate no help in CO poisoning Sleep Apnea Decreased DRG activity or airway obstruction in REM pharynegeal muscles relax and tounge blocks trachea lrestful sleep SIDS sudden infant death syndrome Exact cause unknown may be due to congenital DRG problem or cardiac arrhythmia baby sleep on back JSDSmother smoking during pregnancy I SIDS child abuse may have skewed SIDS statistics Pneumothroax Rupturing of thorax air enters intrapleural space pressure equalizes lung collapses on ruptured side decreased flow in good side danger of kinking of great veins if opening remains reclosed normal breathing on good side lung reinflates Asthma Episodic or chronic wheezing tightness in chest increased morbidity and mortality illnessdeath Airway Obstruction l mucus production response blocks airway reduces air flow Subcortical Structures memog Structures below the cortex that control different functions Basal Nuclei Collection of five structures on each side of the brain below cortex to the sides of the thalamus connected to each other and cortex Postural control is nonconscious feedback loops correct posture variations Decreased dopamine related to Parkinson s Thalamus Receives sensory input from opposite side directsedits input to cerebral cortex about 98 is blocked from reaching cortex Cortical focus allows information through thalamus autism type may be due to lack of thalamic editing Hypothalamus Monitors homeostatic functions temperature thirst milk release hunger reproductive urges circadian rhythms increases emotional feelings hypothalamus detects problems9 cortex decides how to fix it Limbic S tem Ring of structures underneath cortex detect emotions and memory formation hippocampus is a part of the limbic system Emotions Reproductive drive range fear motivation Cortical decisions few connections to the cortex limited cortical control of emotions Can t make emotions just go away takes time Cortical control is over responses limited input of limbic system to motor areas which means no compulsory action Neurotransmitters Norephinephrine dopamine and serotonin are NT in the limbic system Altered concentrations of NTs have been 39 39 with 39 r 39 anti 39 r use receptors for these NTs Excessive dopamine related to schizophrenia Memo Retention storage and ability to recall information memory traces are sequences of neural activations declarative memory facts events words language rules hippocampus and temporal lobe for storage procedural memory unconscious physical skills habits tasks cerebellum plays major role Short Term Memory Secondshours Alter activity in existing neurons in hippocampus can be erasedamp replaced Long Term Memory Creation of new synapses and memory traces make multiple copies of important memories over years retain youthful memories as you age transfer from hippocampus to cortex Working Memory In the prefrontal association cortex Compares newly acquired short term data and stored long term data determine relevance or new material organizes priorities Amnesia A amnesia is the inability to recall Retrograde Common RA caused by trauma loss of short term memory no long term memory formation of traumatic events NO long term loss nothing to recall later Anterograde Hippocampus damage can t form new long term memories NO loss of previous long term memory memory stuck on day of damage Cerebellum sleepspinal cord structure on back of brain stem controls coordinated and learned movements Balance Maintains balance and controls eye movements Coordination Connected to motor cortex receives quotmotor planquot afferent input gives current muscle positioncoordinates functions with aimquot As practice occurs motor cortex parietal lobe and cerebellum take over Planning is reduced initiation of activity is faster and smoother input to cortex Input to Cortex Allows cortex to know current position and movement cortex uses this information to plan future movements Brain stem Medulla oblongata pons and midbrain Interface between spinal cord and motor function to head and neck different centers in brain stem control heart rate breathing wakefulness ReticularActivating S tem RA52 Neural net awareness of surroundings cortical pain auditory visual input Output ot cortex and thalamus 9 all cortex controls consciousness and sleep Sleeg Low frequency activity in hypothalamus and thalamus sleep reason needed unknown EEG patterns Slow wave patterns in EEG give slow ware sleep its name EEG pattern during REM sleep in similar to being awake Slow Wave Sleep 4 stages each progressively deeper over about 75min cycle Circadian rhythm9 increase in adenosine 9 sleep Caffeine blocks adenosine response Sleep factor muramyl dipeptide strong sleep inducer Rapid Eye Movement Paradoxical Sleep 15mins long at the end a slow wave sleep cycle Paradoxical sleep hard to awaken most likely to wake self up high visual cortex low frontal high memory areas 9 dreams illogical New synaptic connection made increase in long term memory will make up missed REM sleep Spinal Cord Neural tissue encased in vertebral column 9 carries actions potentials between brain and body Gray matter in the middle cell bodies and interneuronswhite matter on the outside myelinated neuronal tracts Tracts Bundles of neural axons the carry action potentials ascending tracts carry action potentials towards the braindescending tracts carry action potentials from the brain to efferent neurons Dorsal Roots Entry points for afferent neuron to spinal cord bilateral afferent cell body in dorsal root ganglia Ventral Roots Carry efferent action potentials out of spinal cord cell body efferent neurons are in gray matter Re exes Neural response without a conscious imput Reflex arc Receptor afferent neuron CNS efferent neuron effector CNS portion may have 1 synapses Effectors are muscles and glands interneurons are between afferent and efferent neurons Monosynaptic reflex 1 synapse knee jerk Polysynaptic reflex multiple synapses Withdrawal Relfex Polysynaptic reflex multiple neurons between afferent and motor neurons Prolonged response and feedback very strong reflex but with potential CNS input Stretch Reflex Muscle length information Activation of afferent neuron produces reflex response through synapse to efferent neuron No control by upper CNS Afferent Nervous Svstem Pain Taste Smell Sensory Receptors sensation Connect an environmental signal to the body transduction is the conversion of a stimulus to a physiological signal Brian convert the physiological signal into a perceived sensation Stimulus Environment signal binds and changes a receptor signal now in body each receptor binds to one stimulus the best Sensation Conscious senses quot5 senses and timeUnconscious position temperature blood pressure changes Types of Receptors Must bind stimulus no dendrites on receptor cells modified nerve endings to interact with stimulus Physical Physical changes open ion changes changes membrane potential Touch receptors hair cells in ears photoreceptors ba roreceptors Chemical Taste smell chemoreceptor chemical binds receptors opens channel changes membrane potential Recegtor Potentials aka generator potentials types of local potentials Depolarization of receptor cells size of potential proportional to size of stimulus Receptor fields vary in size depend on number of afferent neurons Magnitude More stimulus greater resting potential in receptor cells without action potential release of neurotransmitter proportional to RP Frequency Dependence Continuous stimulus larger GPs more action potentials to CNS Action potential number translated by CNS as size of stimulus Adagtation Decrease AP number despite prolonged stimulus Phasic Receptors Adapt overtime ratevariable touch receptors adapt quickamp pain BP receptor adapt slow Tonic Receptors Virtually do not adapt there are few true tonic receptors smell Postural receptors in trunk are near tonic SensorySQeciticity Normal stimulus produces a response that the brain interprets different stimulus needs more strength for a response Brain still interprets as quotnormalquot response see quotstarsquot M Survival value protection from harm anticipation of pain activates pain areas of cortex Nociceptors pain receptors chemical and physical Fast pain Sharp localized passes quickly fastmyelinated afferents glutamate neurotransmitter Slow pain Diffuse dull long lasting slowunmyelinated afferents substance pain neurotransmitter Substance P Neurotransmitter unique to afferent slow pain neurons Opioid Receptors Natural analgesics block pain by binding to opiod receptors activated alters on channels and membrane potential 0 EnkephalinsEndorphins Peptides multiple types different sizes short half life 25secs Morphine effective for hours Chemical senses Molecular binding to receptors flavor combinatory of smell and taste Taste Molecules dissolve in saliva and reach taste bud receptors to be tasted Taste buds Receptors at taste pore tight junctions keep saliva away from rest of taste bud Surrounding epithelial cells basal cells receptor cells Neural Tracts Sensory neurson send taste information neurons to thalamus 9 parietal lobe quotwhatquot taste Neurons to limbic system quotlikequot the taste Taste receptors Salty Na sweet organic sugars acidsour H bitterbases or quinie cations poisons most sensitive umami glutamate messengers 39 39 quot r to actiimte H 20 soluble must be volatile enough to float on top ofcavity I 4 It I mum evenfew weeks unusual dendrites as receptors new neurons u r I I i r r Ada ption to one smell does not affect the other smells a muscle 4 amnion cornea clear nonrcellularfront ofeye llight passes through not refracted N 531 or bent LeIls ciliary badyr Lens refmcl light to focus on retina ciliary body has I claw muscles vlkeous hummir muscles relax for distance vision i u i i i a i i Aqueous Humarr Between cornea and lens lfront part of eyel constant wensW39wa productionand draina e Glaucoma sL dminageexcess production lretinal damagel 4 pressure his epic kiwi Betarblocksdecrease productioncholinergicagonistsincreasedraina e 39 Denim g m l 39 e e vir eaus HumarrGeHlke bulkofeyeyolumelbackpartl Between lensand ging min 512 253 retinas maintenance of eyeball shape lno refractionl 9 Lirlheee ui i uehindreiina b b iht n nosignal choroid 39g 39 Refractionr bending of light waves glycoproteins in lens refmcts lightfocus it on the retina Retimr Light passesthrough bipolarand ganglion cells to reach photoreceptor cells lbipolar and ganglion cells pulled back at fovea fovea has best color Visions dense in cone concentration Phatareceptars n 1 Conesr Color vision lbright lightl lfew receptors at alll o 1 1 m V i i L L L i cells Blpal r quotr r t d p p t t39 I p ganglioncellsl Edge effects centersurround onoff effect Ganglion relSr Reach threshold and quot 39 39 C y 39 39 39 39 ganicu late part ofthe lhalamus cortex nr39M n Al r retinal Cortex fills blind sport with expected image r My m imagesl Attamadutianr Change in lens thickness alters focus point lhickrnearhinrdistancel ciliaw muscles control focus Pres yapiur Hardening of lens oyerdecades reduces roundingoflensfor nearyision inevita le yapiurHyperapiur lna bility to focus on retina Myopia nearsighted eyeball too long focus in front of retina Hyperopia farsighted eyeball too short focus in back of retina RAM J r i 39p quot 39f 39 p39is 39 39 14 ecl i nrr L J gm Colarvisianes different opsinswith retinene shading of retinene limits frequency ranges peaks at warm n ed 2green 3blue i k i activation of remaining opsins more common in males because they have xv not XXrthe opsins lie on x Hear g and E9 m Outer eur little ampli cation direction detection i r 4 W39Bmemhrane e s t t i air waves 533 M Middle earAirliliedampliliessoundszox39s r i minimums Ear bones Malleus incus stapes hammer anvil whim stirrup Carry waves lrom tympanic membrane to oval window Eustachai39n Tube Drains middie earollluid equalizes air pressure between middle earand sinuses normally closed in 5mm unopenable tubes needed in eardrum vol Window Membrane connects middle to inner ear inner eur Fluid filled converts sound waves to electrical signals Eachea aka Organ ofCortl cspiral shaped tube o innerear 0 ol c part oi cochlea that transduces sound to action potentials vva e caiiieu A window vv 39 sound waves N0 APs came zunasnian mm Tnmnuzl Human Busiiur Membrane Vibrates to sound waves shape change over lengthhigh frequency at base low frequency at apex when vibrates imbedded hairs are pulled on Hair ceiis Rest on basilar membrane hairs imbedded in tectorial membrane Tectmi39a Membrane Much stillerthan basilar membrane less movement hair cellsquot produce GP gt neurotransmitter to allerent neurons APs to this by auditory nerve ndM 39g in Tirnbre avertones allow source distinction total signal iundamental ireduency overtones quot Ctlon p Deufness Loss oi hearing Conductive deafness Sound waves don t reach hair cells wax eardrum damage middle ear bone damage nearing 39 39 um iua a 39 39 Nerve deafness Damage to hair cells or auditory nerve need cochlear implant to treat H HUEWSV 1 i r Equilibriumvestibular apparatus detect changes in motion 39 39 39 39 39 39 39 iiuiu 39 39 iiirt pullson hair a iquotiuui DI iiaii 39 39 p39 39 h when hard rotating stops 253Osecs to reeduilibrate Linear 39 t39 39 39 39 39tL 39 a igai a a tonic signal know position of head Utri39Cesaccue Detectlinear acceleration u horizontal motions vertical motion Mismatch olsignals gt motion sickenss excess rides orloss space Efferent Nervous System Sxmgathetl39cstmcturepa of 39 39 39 39 p p39 quotinput from cord medulla hypothalamus no direct cortical control 4 V I i N i i s ii t i imulvirluhdm untl v s rnwnlmlhnir yaraivnaunavr xivrm mm quot quotgt Sympathetic responses Responds to emerge nces or highestress 39gh rorrfight response Designed to remove danger 1 blood flow to skeletal muscle and heart concurrent activation of motor units 1 activity of digestive and related functions Receptor typesr ALL bind NE from postrganglionic neurons Alphor Adrenergic receptors cause increase in tissue activity Alpha 1 increase IP39 increase Caz release from saroplasmic reticulum increase Caz Alpha 2 decrease cAMP9 decrease Caz pump9 net increase Caz Beta leadrenergic receptors increase Caz in heart open Caz39 channels increase heart activity Beta 27 increase cAMP increase Caz pump decrease Caz decrease blood vessel contraction and decrease lung bronchiole constriction more blood more air Porosymgothetic structurer part ofthe autonomic nervous system Two neurons se riesr all neurons use Ach as their r Pregonglionic Neuronsr Long neuronsr spinal cord to organ synapse at ganglia on organswith postrganglionic neuro Postgonglionic Neuronsr Short neuro nse travel from ganglia to cells Porosympothetic responses 1 heart rate quot 39 secretions l 39 39 contracts urinary b adder relaxes internalanal and urinary sphincters Agonistsontogonistsr Pharmaceuticals can mimic or antagonize autonomic NS Parasympathetic increase ordecrease digestive activity etc Sympathetic increase blood pressure in shock decrease blood pressure in hypertension tor neuronsr lp a motor neuron gets multiple inputs up to 10000 input from stretch receptors withdrawal reflexes cere bellum lea rned activities co rtex conscio us co ntro Both IPSPs and EPSPs to alpha motor neurons reach threshold most are IPSPs Neuromusculorjunction NM Motor neuron synapse with skeletal muscle fiber cell motor end plate very large na se Acetylcholine releosey Prersyna ptic AP Caz entry9 Ach release Ach binds to receptors on muscle membrane Endplote Potential EEPe much larger than EPSP Ach binds receptor increase Na entw threshold 1 motor neuron AP leadsto 1 muscle AP Control of motor neuron APs control muscle activation Acetylcholinesterose AchEr AchE degrades Ach to choline and acetic acid reuptake of choline diffusion away of acetic acid NM Poisonsr Inhibit diaphragmr can t breathe 1 Black Widow spider venom releases all Ach 2 Botulinum Toxin blocks Ach release most powerful known as Botox 3 Curarer blocksAch receptors Sarcomere gt Muscle Structure and EC Coup 39 g 39 2 t d to bone Cardiac smaller cells attached endrtorend Z n39e Z Musclefibersr single cellrfiber Runs length of muscle in skeletal muscle Tmcmlamem changes size thickness but no mitosis Thln maments Striotionsr Lines in skeletal and cardiac muscle d ue to filaments lined up In H zone 4 lt gt Dork Bondsrthicksome thin filaments 39band Aband Iband Light Bonds N0 thickallthin filaments Sorcomerer What one doesrthe all do Unit of contraction Z line to Z line Thin filaments are anchored to Z linesthickfilaments connect tothin filaments during contractions Thinfilomentse Actin polymer backboner double stranded helix Tropomyosinr longthin protein polymer runs along actin Troponinr bindsto tropomysoin hen M n Thickfilamentse Myosin polymer of filaments protein extension of myosin is cross bridge Cross bridge head can bind to actin and generate force reversible polarity TitubulesSarcoplasmic Reticulum TeT s are invaginations of muscle membranes carry AP s into muscle fiber interior SR develops from ER stores Ca Connected to TeT by voltage sensitive proteins AP down TeT opens Ca channels in SR ExcitationeContraction Coupling Electrical events leading to muscle contraction SkeletalAction Potential Starts at NMJ synapses NT binds to receptor opens Na channels and starts AP spread in both directions including down Tetubules Release ofCalciume At tetubule AP travels inward amp alters protein in tetubule leading to opening Ca channels in SR near TeT Ca released Ca pumps at far end of SR resequesters Ca and causes relaxation Tro onineCalcium Binding Ca binds to troponin on thin filament Tropomyosin Shift Ca bound torponin causes tropomyosin to shift into actin groove exposing AeM binding site ActineMyosin Binding AeM connect myosin already has ATP bound and converted to ADPePi still bound Force Generation ADPePi released myosin shape changes head twists leading to force development no sliding Pi released is key to force development Filament Sliding Filaments slide to decrease force on cross bridge head goes to lowest energy state force0 New ATP binds to myosin actin is released and process repeats as long as Ca is elevated Relaxation Cessation of APs stops Ca release from SR calcium pumps return released Ca to SR Tropomyosin reeblocks AM binding site muscle relaxes Skeletal Mechanics Motor unite motor neuron and muscle fibers it innervates Recruitment Small MUs first then larger allows gradation of force max force requires all MUs active simultaneously Asynchronous Recruitment For submaximal forces rotate activation of MUs mum Maintain forcee cannot simultaneously optimize force and rmquot continuous activity quotmquot quotquotquotquot 5mm Twitch Single muscle activation 1 neural AP9 1 muscle AP9 l A twitch each produces the next subemaximal force not enough Mm Ca reaches all troponin for full activation quotWquot JWVL Tetanus Summation of many twitches many APs enough Ca so mm that a myosin heads reach actin Figure 7 5 Pallems ul muscie lwuch summzuion and lelanus LengtheTension Relation Lemuscle length at which maximum force occurs resting skeletal muscle at L a length Falloff at Long Lengths Reduced overlaps of thick and thin filaments Falloff at Short Lengths Thick filaments compression against Z linethin filaments overlap amp interfere with each other reduced Ca release ForceeVelocity Relation Heavy loads can only be moved slowlylight loads are moved quickly Inverse Relation High force load9 low velocitylow force load9 high velocity Stretched Muscles Stretching before activation windup uses top of LeT curve betterforce maintenance also activating stretchereflexes reflex contraction of stretched muscle Power Curve From FeV cruve Power F x V AFOPOAVOPO At all others F x V is positive and must have a maximum 25 F has optimal power output Stretching active muscle can hold N 15 x F before yielding Muscle Metabolism and Control Muscle Energy Use Progressive use of energy resources Phosphocreatine Supports about 20secs of full activity PCr ADP 9 ATP Cr by creative kinase reaction ATP 9 ADP Pi by net reaction Pi inhibits myosin ATPase M x ADPx Pi 9 M ADP Pi Glycolysis 10 Rxs 2mins of energy use Glucose and glycogen in muscles 9 pyruvate 9 lactate NO OXYGEN USE Ozxidative Phosphorylation M of energy support Kerbs cycle and electron transport system Pyruvate 9 CO OXYGEN USED Fiber Types Variations in fiber type even within same muscle controlled by motor neuron most muscles are mixed Red Fibers aka slow oxidative High mitochondria levels slow myosin ATPase slow speed high energy capacity low energy use no fatigue White Fibers aka fast glycolytic Few mitochondria fast myosin ATPase fast speed Low energy capacity high energy use easily fatigued Hypertrophy Larger cells not hyperplasia more cells high intensity high force exercise needed for maximum effect Filament Number High intensity exercise causes microdamage to filaments disassembly of tangled filaments increases free myosin and causes pain free myosin causes increase in expression of filaments forming enzymes more filaments bigger cells T r 39 Filament r optimized by testosterone females with normal hormones cannot maximize muscle size males grow bigger than females because of their hormones Atrophy Reduction in size of muscle fibers not loss of number of fibers Young 48hr cycle 24 disassembly 24 assembly Elderly 72hr cycle risk Disuse Muscle immobilized loss of filaments easily reversible Denervation Motor neuron damage fiber loses filament not reversible loss of myotrophic factor from neuron electrical stimulation cannot prevent atrophy Stretch Reflex Muscle length information monosynaptic reflex knee jerk activation ofafferent neuron produced reflex response no control by upper CNS Muscle Spindles Stretch receptors in muscles groups of intrafusal fibers in connective tissue capsule Intrafusal Fibers Each fiber contains muscle secretion and stretch receptor section fibers activate afferent neurons from receptor secretion of fiber fibers also receive efferent gamma motor neuron to muscle section fiber Nuclear bag fibers Have larger central portion of receptor Dynamic Response Only detect change of length highest response when muscle rapidly stretch decreased response as stretch is sustained rapid adaptation Nuclear chain fibers Smaller set of receptors parallel to n bag fibers Static response Detects fibers length response proportional to position slow adaptation Gamma Motor Fibers Efferents to intrafusal fibers contract muscle portions of intrafus al fibers Coactivation Dual activation ofalpha and gamma motor neurons alpha motor neuron contracts muscle fibers gamma motor neuron contract intrafusal fibers keeps muscle spindles taut Reciprocal innervation Inhibition of paired muscle when stretch reflex occurs Afferent neuron 9 interneuron 9 lPSP to paired alpha motor neuron Golgi Tendon Organ Muscle force detectors receptors in tendon afferent input proportional to muscle force at very high forces GTO sends lPSPs to alpha motor neurons protective effectives Smooth Muscle Smooth muscle structure Small cells linked by desmosomes no stirations filaments parallel but not in register Filaments Thin Actin and tropomyosin NO troponinTM in groove in groove no AM blocking Dense Bodies Smooth muscle equivalent to 2 lines anchored to cell membrane also in interior thin filaments attach here and pull ends of cell Tone Force with no stimulus CaZ leaks in and partially activates smooth muscle important in BP maintenance holding cavity contents Organization Each ievei buiids on the next each has characteristics that the iower one doesn39t Molecules Assembiy of atoms proteins carbs iipids nucieic aci s Cells Basic unit of iife use energy have metaboiism removes waste Tissues Coiiection of simiiar ceiis with the same iocai function 0rgun51CoHection of different tissues carries a distinct function for the body System51CoHection of organs u z u 1 Jam ac uum point biood pressure ion concentration muscie refiexes controis major coordinated functions iike respiration u point V causes a return back to the originai set Pasitivefeedbuck Event X causes a change to a new set and there is no return to originai set point chiid birth 39 somesr Combo of proteins and RNA Free ribosomes make proteins for use in the cytosoi n n ains Lube in F exported or organeiie proteins Rough ERV Ribosomes on surface site of protein synthesis New formed protein threaded into ER iumen as hER made new proteins move through ER to smoot Smu t A quot Goigi apparatus Produces new membrane and compiex iipid moiecuies Proteinsgt amino aci s Compiex carbohydratesgt monosacchrides ATPV ceiiuiar energy AT gtADP P XATP 9 X7PADP whereas XVP has a purpose uniike just X Adenosin u l l y y Giucose NAD ZADPNADH 2 pyruvate ZATP NADH pyruvate NAD iactate Makesenergyr A P M u 1 i n ui riuuuLLiuiIl permeabie inner membrane is highiy impermeabie TAquot gt mitochondria Micmtubulesr Poiymers oftubuiin for ceii stabiiity anu chromosome mummy Hm Wm Lu membrane 2 ATPgiucose without oxygen membrane has iarge in H4 theinneri i n neuron 39 g 39 s CiiiarFiageHa In the iungs oviducts dynein drives MTtwists propeis mucus ovum fiageiia in sperm Phasphulipids Backbone of membranes fiuidity within Hydrophobicr Moiecuies can cross easiiy Hydrophiiici Outer sides of membrane Water moiecuies don39t cross by diffusion excp H10 Hydrophobic taiishydrophiiic head Chulestemly High water soiubiiity dueto smaH size Interspersed between iipid portions of phosphoiipids Prevents ciose packing of fatty acid chains create fiexibiiityfiuidity Pmteinsy n membranes some mobiierestri e Receptors On outside Binds to soiute either chemicai or ion some activated by channei or enzymes Waur 0 H up mm Balm had ii WW 2 395 H mm Chunnelsy Oniy ions pass K Na Ca Ci39 protein channeis span the membrane openedciosed e Enzymesr Cataiyzes reaction AgtB some activated by receptors some aiways ac r u 1 u A tiv r iock seiective transportmoiecuies must gothrough the actuai ceH in kimintestines and kidneys Aiiow Gap Junctionsr Channeis between ceiis where oniy ions pass Eiectricai signai from one ceii activates the next ceii extremeiy iarge channeis Fick s Law of Diffusion Q PAACAX MW Rate of diffusion Q P Permeabiiity hydrophobicity A Area ACAX Concentration gradient MW Molecules weight size Carrier Transportr Protein molecules change shape in membrane and move molecules across Facilitated Diffusionr NO ATP USED Move down gradient high low Molecules bind to one side carrier revolves molecules leave on opposite side more bind on high concentration side now Active Transport USES ATP Moves ions against their concentration gradient low 9high Moves ions from high affinity side to low affinity side affinityzlikely to have binding NarK ATPasee Moves Na out of cells 9 moves K in K high insideNa high outside Creates gradients that allow electrical signaling SecondaryActive Transportr Carrier has two binding sites agonist and Na39 Energy of the Na39 gradient out to in drives secondary active transport Cotransport agonist in or countertransport agonist out Na transport some glucose and amino acids in ions drive secondary active transport in some tissues Resting Membrane Potentialr Voltage across cell membrane where the cells are not activated determined by open ion channels K dominates at rest has most open channelsSome Na Permeabilityr Determined by the number of open channels number of K or Na open channels determines ion diffusion different open number in different cell types produces different resting membrane potential Equilibrium Potentialr Limits on K39Na Only open channels determine membrane potential r70 790 Na Most K K All Few Na Resting Membrane Potential Balancer Membrane potential always negative at rest Membrane potential magnitude decrease less negative during depolarization Membrane potential magnitude increase more negative during hyperpolarization Depolarizationr Membrane potential is less negative from K channels closingNa channels opening membrane potential moves towards Na eduilibrium Hyperpolarizatione Membrane potential is more negative from K channels openingNa closing membrane potential moves towards K eduilibrium potentia Graded Potentialsr Triggered by agonists or physical force Opens channels Size proportional to the size of the stimulus spreads to adjacent areas but decays rapidly overtime and distance can only carry signals over short distances in receptors neurons musc es Action Potentialr Electrical signal long range activated by graded potentials Do NOT degrade overtime and distance Vo tagerGated Channelsr Open when membrane reached a particularvoltage like 1520mV above resting membrane potential all voltage gated channels open together causing action potential enters inactivated state soon after opening refractory period AP Phases Depolarization of Threshold gated Na channels open enters down gradients to threshold from rest39ng AP Spiker Al voltage gated Na channels open together enters rapid depolarization to 20 does not reach Na eduilibrium because some K are open Dendritese Receive neurotransmitterfrom other neurons many branches NO ACTION POTENTIAL ONLY graded potentials slmuuruatypluluunn Meylin Nodes of Ranvier7 Meylin surrounds axon and wraps layers of W WW membrane increase action potential speed Refractory Periodr After voltage gated channels close they are x 39 quot quot 4 unopenable for some time Touch neuronsr Myelin large Pain neuronsr No myelin small 9quot LO m K m M Presynaptic neurone End of axon synaptic knob terminal button Receives action potentials down axon action potential opens Ca channels Vesicles Contain neurotransmitter I Ca triggers merger with cell membrane neurotransmitter dumped into cleft diffuses to postsyn membrane Temporal Summation EPSPs from the same neuron close in time are additive they may M to reach threshold E neuron two events close together Spatial Summation EPSPs from different neurons are additive the M may reach threshold two neurons Inhibitory Postsynaptic Potentials IPSPs K or Cl39 channels opened by neurotransmitter K leaves or Cl39 enters down their electrochemical gradient Membrane potential more negative less likely to reach threshold Axon Hillock At junction of cell body and the axon high density of voltage gated Na quot channels action potential starts here Excitatory Postsynaptic Potentials EPSPs Na enters when neurotransmitter binds and causes depolarization one EPSP is not enough to reach threshold Paracrines Local hormones released from one cell affects nearby cell Nitric oxide important in control of blood flow Hydrophilic Hormones Cannot cross the membrane rely on membrane receptor activation membrane proteins produce second messengers Second messengers Made at membrane internal activation mechanism started by hydrophilic hormone only cells with receptors respond cAMP ATP cAMP activates kinasesadds phosphate to molecule kinase cascades amplify signal G Proteins Timing proteins Bind to GTP increase activity until GTP GDP Regulate vesicle movement cytoskeleton growth visions 2nd messengers Calcium Released from internal sacroplasmic reticulum by IP3 eneters across cell membrane through CaZ quot channels binds to and alters protein activity Celltocell Ca2 signal produces coordinated cilia waves exocytosis Gap junctions depolarization causes cardiac and smooth muscle contraction in cells by opening Ca2 Afferent neurons Carry info to the CNS both conscious and unconscious info is carried Efferent neurons Carry info from the CNS to the body somatic nervous system neurons activate skeletal muscles The autonomic nervous system supplies neural imput sympatheticparasympathetic to organs Parasympathetic Dayto daySympathetic Emergences Glial Cells Nonneural support cells in the CNS have cancer potential because are capable of mitosis Astrocytes Starshaped hold neurons in proper physical positions control neural growth and blood vessel growth in the brain Blood vessels form bloodbrainbarrier tight capillaries small pores btw cells Repair brain injuries and form scar tissue degrade neurotransmitters glutamate and GABA and control extracellular K Ependymal Cells Lines the brain s ventricles and secrete cerebrospinal fluid absorbs shock Cancer potential Neural cells do not divide and can t form cancers Plasticity No mitosis of neurons they make new synapses between existing neurons practiced motor activity enlarges controlling area of brain if cortical input reduceddamaged areas receive input from adjacent areas Language control Connections of sounds and symbols with objects Broca s area in frontal lobe Speech formation deficit difficulty forming words spoken or written know what you want to say though Wernicke s area Temporal lobe comprehension of auditoryvisual info Deficit can form sounds but contain no content don t know what you are saying or others are Hemispheres Right side visualspatial relations aesthetics Left side Analytical processing and language Basal Nuclei Collection of five structures on each side of the brain below cortex to the sides of the thalamus connected to each other and cortex Postural control is nonconscious feedback loops correct posture variations Decreased dopamine related to Parkinson s Thalamus Receives sensory input from opposite side directsedits input to cerebral cortex about 98 is blocked from reaching cortex Cortical focus allows information through thalamus autism type may be due to lack of thalamic editing Limbic S tem Ring of structures underneath cortex detect emotions and memory formation hippocampus is a part of the limbic system Emotions Reproductive drive range fear motivation Cortical decisions few connections to the cortex limited cortical control of emotions Can t make emotions just go away takes time Cortical control is over responses limited input of limbic system to motor areas which means no compulsory action Short Term Memory Secondshours Alter activity in existing neurons in hippocampus can be erasedamp replaced Long Term Memory Creation of new synapses and memory traces make multiple copies of important memories over years retain youthful memories as you age transfer from hippocampus to cortex Working Memory In the prefrontal association cortex Compares newly acquired short term data and stored long term data determine relevance or new material organizes priorities Cerebellum sleepspinal cord structure on back of brain stem controls coordinated and learned movements Balance Maintains balance and controls eye movements Coordination Connected to motor cortex receives quotmotor plan afferent input gives current muscle positioncoordinates functions with aimquot As practice occurs motor cortex parietal lobe and cerebellum take over Planning is reduced initiation of activity is faster and smoother input to cortex Sleeg Low frequency activity in hypothalamus and thalamus sleep reason needed unknown Slow Wave Sleep 4 stages each progressively deeper over about 75min cycle Circadian rhythm increase in adenosine 9 sleep Caffeine blocks adenosine response Sleep factor muramyl dipeptide strong sleep inducer Rapid Eye Movement Paradoxical Sleep 15mins long at the end a slow wave sleep cycle Paradoxical sleep hard to awaken most likely to wake self up high visual cortex low frontal high memory areas 9 dreams illogical New synaptic connection made increase in long term memory will make up missed REM sleep Withdrawal Relfex Polysynaptic reflex multiple neurons between afferent and motor neurons Prolonged response and feedback very strong reflex but with potential CNS input Stretch Reflex Muscle length information Activation of afferent neuron produces reflex response through synapse to efferent neuron No control by upper CNS Types of Recegtors Must bind stimulus no dendrites on receptor cells modified nerve endings to interact with stimulus Physical Physical changes open ion changes changes membrane potential Touch receptors hair cells in ears photoreceptors ba roreceptors Chemical Taste smell chemoreceptor chemical binds receptors opens channel changes membrane potential Recegtor Potentials aka generator potentials types of local potentials Depolarization of receptor cells size of potential proportional to size of stimulus Receptor fields vary in size depend on number of afferent neurons Magnitude More stimulus greater resting potential in receptor cells without action potential release of neurotransmitter proportional to RP Phasic Receptors Adapt overtime ratevariable touch receptors adapt quickamp pain BP receptor adapt slow Tonic Receptors Virtually do not adapt there are few true tonic receptors smell Postural receptors in trunk are near tonic Slow pain Diffuse dull long lasting slowunmyelinated afferents substance pain neurotransmitter Substance P Neurotransmitter unique to afferent slow pain neurons Olfactory adaptation Unusual Receptors primarily tonicmost adaption in CNS brain can overcome adaptation Adaption to one smell does not affect the other smells Lens Ciliary body Lens refract light to focus on retina ciliary body has muscles parallel to lens muscle contraction allow lens to round up focus near muscles relax for distance vision Choroid Highly pigmented layer behind retina absorbs light no reflection no signal Refraction bending of light waves glycoproteins in lens refracts light focus it on the retina Photoreceptors Rods black and white and shades of grey most photoreceptors Cones Color vision bright light few receptors at all Rods cones produce receptor potentials not action potentials both converge on bipolar cells Bipolar Cells Generated potentials activated by rodsamp cones NO action potentials synapse w ganglion cells Edge effect centersurround onoff effect Ganglion cells Reach threshold and fire action potentials that leave eye for CNS carry visual info to lateral ganiculate part of the thalamus9 cortex Color Vision 3 different opsins with retinene shading of retinene limits frequency range peaks at red 2green 3blue Color blindness One opsin is missing out ofthe three Cannot distinguish certain wavelengths with equal activation of remaining opsins more common in males because they have XY not XXethe opsins lie on X Ear bones Malleus incus stapes hammer anvil stirrup Carry waves from tympanic membrane to oval window Eustachain Tube Drains middle ear of fluid equalizes air pressure between middle ear and sinuses normally closed in unopenable tubes needed in eardrum Basilar Membrane Vibrates to sound waves shape change over lengthhigh frequency at base low frequency at apex when vibrates imbedded hairs are pulled on Hair cells Rest on basilar membrane hairs imbedded in tectorial membrane Tectorial Membrane Much stifferthan basilar membrane less movement hair cells produce GP 9 neurotransmitterto afferent neurons APs to CNS by auditory nerve LinearAcceeratione Hair cells imbedded in gel with otoliths acceleration pulls on hair cells gravity constant 9 tonic signal know position of head Utriclee saccule Detect linear acceleration U horizontal motionS vertical motion Mismatch of signals9 motion sickenss excess rides or loss space Sympathetic responses Responds to emergences or highestress Fighteore ight response Designed to remove danger 1 blood flow to skeletal muscle and heart concurrent activation of motor units 1 activity of digestive and related functions Receptor types ALL bind NE from posteganglionic neurons Iphae Adrenergic receptors cause increase in tissue activity Alpha 1 increase IP39 increase Ca release from saroplasmic reticulum9 increase Ca Alpha 2 decrease cAMP9 decrease Caz pump net increase Ca Beta 17 adrenergic receptors increase Ca in heart open Ca channels increase heart activity Beta27 increase cAMP9 increase Ca pump decrease Ca decrease blood vessel contraction and decrease lung bronchiole constriction more blood more air Parasympathetic responses 1 heart rate 1 GI contractions and secretions I pancreatic secretions contracts urinary bladder relaxes internal anal and urinary sphincters Acetylcholine release Preesynaptic AP9 Ca entry Ach release Ach binds to receptors on muscle membrane AcetylcholinesteraseAchE AchE degrades Ach to choline and acetic acid reuptake of choline diffusion away of acetic acId Sarcomere Sarcomeree What one doesethey all do Unit of contraction Z line to Z line Thin filaments are anchored to Z lines thick filaments connect to thin filaments during contractions ii Thin filaments Actin polymer backbone double stranded helix 1quotquot6 1quotquot0 Tropomyosine long thin protein polymer runs along actin mnmar immem Troponine binds to tropomysoin Thickfilamentse Myosin polymer of filaments protein extension of myosin is cross Hzone bridge Cross bridge head can bind to actin and generate force reversible polarity mm mm quotmm TitubulesSarcoplasmic Reticulum TeT s are invaginations of muscle membranes carry AP s into muscle fiber interior SR develops from ER stores Ca Connected to TeT by voltage sensitive proteins AP down TeT opens Caz channels in SR TroponineCalcium Binding Ca binds to troponin on thin filament Tropomyosin Shift Ca bound torponin causes tropomyosin to shift into actin groove exposing AeM binding site Force Generation ADPPi released myosin shape changes head twists leading to force development no sliding Pi released is key to force development Filament Sliding Filaments slide to decrease force on cross bridge head goes to lowest energy state force0 New ATP binds to myosin actin is released and process repeats as long as CaZ quot is elevated Motor unit motor neuron and muscle fibers it innervates Twitch Single muscle activation 1 neural AP 1 muscle AP 1 twitch each produces the next submaximal force not enough Ca2 reaches all troponin for full activation Tetanus Summation of many twitches many APs enough CaZ so that all myosin heads reach actin Falloff at Long Lengths Reduced overlaps of thick and thin filaments Stretched Muscles Stretching before activation windup uses top of LT curve better force maintenance also activating stretchreflexes reflex contraction of stretched muscle Power Curve From FV cruve Power F x V AFOPOAVOPO At all others F x V is positive and must have a maximum 25 F has optimal power output Stretching active muscle can hold quot 15 x F before yielding Phosphocreatine Supports about 205ecs of full activity PCr ADP ATP Cr by creative kinase reaction ATP ADP Pi by net reaction Pi inhibits myosin ATPase M x ADP x Pi M ADP Pi Glycolysis 10 Rxs 2mins of energy use Glucose and glycogen in muscles pyruvate lactate NO OXYGEN USE Red Fibers aka slow oxidative High mitochondria levels slow myosin ATPase slow speed high energy capacity low energy use no fatigue Hypertrophy Larger cells not hyperplasia more cells high intensity high force exercise needed for maximum effect White Fibers aka fast glycolytic Few mitochondria fast myosin ATPase fast speed Low energy capacity high energy use easily fatigued Golgi Tendon Organ Muscle force detectors receptors in tendon afferent input proportional to muscle force at very high forces GTO sends PSPs to alpha motor neurons protective effectives Nuclear bag fibers Have larger central portion of receptor Dynamic Response Only detect change of length highest response when muscle rapidly stretch decreased response as stretch is sustained rapid adaptation Nuclear chainfibers Smaller set of receptors parallel to n bag fibers Static response Detects fibers length response proportional to position slow adaptation Dense Bodies Smooth muscle equivalent to 2 lines anchored to cell membrane also in interior thin filaments attach here and pull ends of cell Tone Force with no stimulus CaZ leaks in and partially activates smooth muscle important in BP maintenance holding cavity contents Myosin Light Chain Kinase Ca2 activated adds phosphate to myosin light chains activate myosin ATPase for shortening and force Multi Unit SM Each cell individually active NO APs or gap junctions get average force large blood vessels eye muscles Visceral single unit SM One contracts all contracts use APs linked by gap junctions phasic activity stomach random contractions small intestine Must shorten to empty cavity Latch Removal of Pi from light chain when AM attached decreased M detachment rate Maintains force with little energy use allows BP maintenance with low energy use allows upright position Intercalated Disks Strong connections between cells desmosomes for strengthgap junctions for electrical activation spread SA Node In RIGHT atrium depolarizes to threshold starts AP fastest depolarizer no stable baseline membrane potential the intermodal pathway connects the SA node to the AV node premature beats occur if heartbeat starts elsewhere not usually harmful AVNode Electrical connection from atria to ventricles delays AP spread allows ventricular filling to be complete AV block produces separate atrial and ventricular activation Purkinje Fibers Branch off of septum ofventricular muscle activated by bundle ofHIS through gap junctions Ventricular Muscle Apex cells activated first by Purkinje fibers gt then muscle cell to cel through gap junctions gt contraction spreads upward forcing blood into aorta and pulmonary artery no pacemaker activity Pacemaker Cells aka autorhythmic No stable baseline potential SA and AV nodes some cells of Bundle of HIS and purkinje fibers a P wave Atrial depolarization start of atrial contraction QRS Complex Ventricular depolarization masks atrial repolarization 39r of atrial contraction start of atrial filling and ventricular contractIon T wave Ventricular repolarization end ofventricular contraction start of ventricular filling Q 5 mi mnrmumu Hzlaxnrmnuf Diastole Relaxed heart timeforfilling end diastolic volume l30ml mm m Limit vermin VentricularSystole Follows atrial contraction contraction spreads upwards pressure must be greater than aorta to open aortic valve Aortic Pressure Load left ventricle works against High BP puts greater load on heart Starling s Law Stroke volume control 4 venous return stretches cardiac musclegt 4 forcegt TCO more actin myosin interaction less thick Z line contact les thin thin overlap more Ca release stronger contraction more SV more CO Cardiac OutputAmount of blood pumpedmin Vessel Radius More important than variable factor Thickness of blood controlled by hematocrit RBCs in blood 45 males 42 females need large change to influence blood ow Above 48 RBC interation with arteriole walls greatly increases resistance Viscosity resistance 1radiu5 Small constriction causes large Tresistance Lflowsmall dilation causes large Lresistance 4 flow Coronary Circulation Heart rate dependent Ldiastole at high HR gt Lfillingtime and Lcoronary flow coronary flow only occurs during diastole HR gt 180 decreases cardiac output potential heart failure Atherosclerosis Multiple stages LDL low density lipoproteins lays down fatty streak ZWBCs and fibroblasts overgrow fatty streak 3Caclium infiltrated hardens overgrowth Alcohol E ect Modest alcohol consumption can solubilize fatty streak can reverse atherosclerosis stage 1 biophysical effect not receptor effect no alcohol effect on other stages Filtration Dominates at high pressure end arteriolar BP gt osmotic pressure fluid forced out Reabsorption At venous end lower BP BP lt osmotic pressure fluid reenters Return ofFiltered Fluid Fluid enters closed ended lymph vessels which merge with others lymph nodes are sties of large lymph vessel merger large lymph vessels have valves lymph enters vena cava BP0 at thoracic duct in chest Edema 5welling Excess filtration broken capillaries low blood protein starvation alcoholism bacteria presence and destruction draws uid osmotically parasites gt filariasis gtblock lymph ow gt fatal Varicose Veins Ruptured valves column of blood slow return clots may form blood bypasses varicosities through other veins varicosities called varicose veins not lifethreatening only blood clots Plasma proteinsAlbumin highest draws fluid into capillary binds hydrophobic hormones Globulin many subgroups gamma globulins are antibodies Fibrinogen final protein for blood clot formation Erythrocytes RBC 5 Carry oxygen and CO no organelles only hemoglobin Hb sack of protein Production n bone marrow from stem cells 20ml of RBCday 50ml of bloodday low blood oxygen causes release of EPO from kidneys Platelets Pinched off parts of megakaryocytes in bone marrow Platelet Plug Exposure of collage gt platelet sticking gt ADP positive feedback prostacyclin from healthy blood vessel blocks platelet adherence Coagulation Blood clotting 2 systems both lead to fibrinogen soluble gt fibrin self adhering Forms mesh that traps RBCs etc Intrinsic System Inside plasma collagen activated cascade needs Ca2 and all factors in pathway Extrinsic System Thromboplastin from damaged tissue starts cascade merges with IS halfway down stop bleeding Whagocytes Phagocytosis of bacteria and dead cells order of attack resident macrophages neutrophils new monocytes macrophage migration Neutrophils Rapid response move from blood to damaged tissue diapedesis squeeze through capillary pores attack bacteria r39 quotquot move into tissue and become macrophages resident macrophages wait for bacteria to come during infection vast movement of monocytes into infected area massive macrophage attack on bacteria 5Basophils Release histamine histamine causes inflammation I blood flow arteriolar dilation and I pore size allows diapedesis Complement System Series of 9 factors C1C9 major bacteria killer Histamine I blood flow brings phagocytes oxygen amino acids I capillary permeability opens pores for liquid and diapedesis Interferon Cytokin released from virus infected cells activate antiviral defenses in cells near virus infected cells many side effects B Lymphocytes Bind antigens full activation requires T helper cell contact antigen binding triggers cell proliferation into plasma B cell clone cells and memory cells Plasma cells Antibody factories make antibody to antigen that binds high ER for Ab production loses other organelles limited lifetime 1 week Memory cells B and T cells few cells have very long life provide immunity from antigens Primary Response Activation of B or T cells is slow short and weak Secondary Response Activation of memory cells is fast strong and long massive response upon 2nd exposure Antibody Functions Activate complement system to kill bacteria labels cells for ingestion by phagocytes minor physiological function neutralized by binding used for lab testing Helper TCells Release cytokines that activate all B and T lymphocytes Helper TCell Cytokines Paracrines that regulate immune system I proliferaiton growth and function when cytokine structure known renamed an interleukin MHC Class I Selfantigens on surface of all cells identify cells as self 36 out of 100 possible antigens on every cells others in foreign cells attacked MHC Class II Ingest and present antigens activated T cells Immediate Hypersensitivity Immune response in 20 minutes B cell mediated antibody production Delayed Hypersensitivity Immune response in 24hrs T cell mediated poison ivy some toxins stimulate T cells migrate to area of contact and produce rash Dermis Connective tissue beneath the epidermis blood vessels nerve endings many cell types blood regulates heat loss Sweat glands sweat has variable Na content Sebaceous glands oil waterproof skin Hair follicles increased tough sensitivity Melanin absorbs UV light UV sensitive Langerhands cell present antigensUV resistant Granstein cells slow immune responses net UV light 4 skin cancer Type I Cells Epitheal cells I micron thick separate air form interstitial fluid Type II Cells In alveoli Produce surfactant Jresistance to alveolar opening Atomspheric Pressure 760 at sea level 600 at Denver 1 mile up Intra alveolar Variable exhale 12gtatm inhale l2ltatm Intrapleural Between lungs and thoracic wall always 4mmHgltatm lower pressure keeps lung always inflated Boyle s Law P x V constant xiV I P I V IP Inspiration Regular phrenic nerve form medulla sends AP to diaphragm diaphragm contraction increases thorax volume lpressure decreased pressure causes inspiration Alveolar Surface Tension Adherence of H10 molecules creates surface tension on inside of alveoli surface tensions must be overcome to open alveoli Surfactant Several phospholipids mix with water and lsurface tension also prevents edema in lungs first made at 36 h week of gestation glucocorticolds l surfactant production in premature infants Anatomical dead space Normal tidal volume is 500ml 150ml of mouth pharynx trachea bronchi bronchioles is dead space 350ml is normal alveolar inflation Long slow breathing minimizes dead space effectShort rapid breathing still must fill 150ml dead space Diffusion Across Alveolar WaII Gases follow partial pressure gradient capillary gases match tissue it goes through 0101 enters pulmonary capillaries until PO is 100 C02 C01 leaves pulmonary capillaries until PCOZ is 40 Oxygen Transport 15 carried by dissolved Oz985 carried by binding hemoglobin Oxygen Hemoglobin Binding Sigmodial curve cooperatively between 4Hb subunits Steep Region At tissues fall in P0 unloads 02 at lower POZ even more 02 delivery Plateau Region At lungs all Hb is 02 bound no effect on extra 02 Cell that works the hardest gets more oxygen Carbon Monoxide 2 effects Binds Hb 200x s stronger than 01 less 02 available never Carbon Dioxide Transport 10 dissolved 30 bound to plasma portien and Hb 60 converted to biocarbonate by carbonic anhydrase carbonic anhydrase catalyzes HZO CO 9 HzCOg 9 HCO39 H tissueopposite for lungs Hypcapnia Low COz hyperventilation JCOZ in blood9 faint breathing into bag I COZ back to normal Hypercapnia High COz l breathing rate I COZ in blood strongest stimulus for increased respiration Medullary Control Centers Dorsal Respiratory Group DRG rhythmic discharge 9 phrenic nerve 9 diaphragm initiates normal breathing Ventral Respiratory Group VRG causes l inspiration expiration Chemical Control ofRespiration Most powerful controller of rate l blood Oz 9 l brain CO 9 I H and HCOg H in brain increased DRG rate SIDS sudden infant death syndrome Exact cause unknown may be due to congenital DRG problem or cardiac arrhythmia baby sleep on back JSDSmother smoking during pregnancy I SIDS child abuse may have skewed SIDS statistics Pneumothroax Rupturing of thorax air enters intrapleural space pressure equalizes lung collapses on ruptured side decreased flow in good side danger of kinking of great veins if opening remains reclosed normal breathing on good side lung reinflates Emphysema Cigarette smoke coal tar most common causes Decreaed a Antitryspin Lungs have digestive enzymes for defense alphaantitryspin protects lung tissue from digestion inhibit alphaAT production and enzymes digest alveoli Jnumber of alveoli and l size of reaming alveoli Surface Area Progressive lin surface area may need pure 02 to fill Hb irreversible right heart enlarges and fails Nephron Functional unit of the kidneys has vascular system and tubular system all but cells and proteins in blood can be filtrated most reabsorbedremainderurine Glomerular Filtration From glomerulus into Bowman s capsule glomerular capillaries have very wide pores only cells and proteins not filtered Inulin Fructose polymer Filtered not reabsorbed or secreted used to measure glomerular filtration rate G FR inject in blood measure in urine proportional to amount of filtrate G FR 125mlmin 140 of total blood volume Glucosuria 3x s more carrier capacity than normal filtered load if G in urine blood must have at least 3x s more G than normal Sodium Reabsorption Controls reabsorption of many other molecules Na quot pump only on basolateral side of tubular cells pump Na out create gradient for Na entry into cells ATP needed for energy tight junctions prevent flow in spaces between cells caffeine JNa reabsorption Cotransport Carriers for Na and cotransported molecule glucose amino acids bicarbonate Clquot are cotransported with Na during reabsorption energy use is Na movement down gradient into cells HZO follows osmotically at proximal tubule variable HZO reabsorption at distal tubule and collecting duct Glucose Reabsorption Binds to carrier with Naquot on luminal side to enter tubular cell separate nonNaquot glucose carrier moves G into interstitial space ReninAngiotensin System Maintain BP by I Naquot and H10 reabsorption Jrenal BP 9 release of renin from kidney IG cells renin is a protease Effects ofAngiotensin ll Powerful vasoconstrictor I BP causes release of aldosterone from adrenal cortex ACE Inhibitors Block production of angiotensin II used as treatment for hypertension few side effects but many produce fetal development problems RenaBlood Flow PAH PAH is totally secreted from plasma appearance in urine proportional to renal blood flow RBF 2025 of cardiac output Loop ofHene Creates osmolic gradient in kidney medulla 300 mOsm at cortex 1200 mOsm in deep medulla filtrate at the end of the loop of Henley is 100mOsm plasma is 300mOsm Vasopressin From posterior pituitary released when plasma osmolarity high causes insertion of aquaporins in collecting duct membrane Aquaporins H10 channels H10 goes though osmotic pressures of solutes in medulla lZOOmOsm draws H10 retain H10 urine up to lZOOmOsm Urine Buffering Filtrate pH must be 45 for Hquot to enter filtrate bicarbonate and phosphate from filtration ammonia from tubular secretion buffer urine Aldosterone Effects l number of active Naquot carriers on luminal side of CD tubular cells this I Naquot reabsorption in CD H10 follows osmotically K reabsorption is reciprocal to Naquot Ureter Entry Ureter connects kidney to bladder Ureter passes inside bladder wall at an angle increased bladder pressure closes ureter prevents backflow Bladder Sphincters Around uretha the tube draining the bladder Internal urinary sphincter smooth muscle involuntary External urinary sphincter skeletal muscle voluntary Intracellular Fluid 23 of total body water K dominated with protein Extracellular Fluid 15 of total body water Plasma 20 of extracellular fluid with protein Interstitial Fluid 80 of extracellular fluid with NO protein Blood Pressure Control Short term drop in pressure causes Autotransfusion Movement of fluid from interstitial fluid to plasma to maintain BP changes in baroreceptor activity Long term control of volume is balance of thirstintake and kidney fluid excretion Tonicity The standard for tonicity is not the number of dissolved particles but the Shrunk Normal S quotEquot behavior of cells in the solution cells swell in hypotonic solutions ECF is rarely CE 6 G hypotonic Osmoreceptors Receptors in the hypothalamus that control VP release loncnncenlra nn l osmolarity l vasopressin release I Hzo retention iquot 39 equotquot39quot Josmolarity Jvasopressin release I Hzo excretion Hypertonil Isotonic Hypotonic pH Measure of Hquot in a solution pH logH I H causes JpH Average blood pH740 Average cell pH70 Blood pH below 735 is acidosis more common blood pH above 745 is alkalosis Cells will have bigger pH shifts than blood Acidosis Effects Acidosis depresses the neurons especially in the CNS Alkalosis makes neurons hyperexcitable Acidosis in general Jenzyme activity but few increase Acidosis causes I H excretion and therefore decreased K excretion I K causes cardiac and neutral problems Respiratory Control oth Second line of Hquot defense works with nonrespiratory sources of H l H or I C01 l depth and frequency of respiration this reduces C01 in blood reducing H back toward normal Kidney Control ofH 3rd line of defense Removes Hquot from any nonrenal source in the body MetabolicAkalosis Jin H for nonrespiratory reasons vomiting loses Hquot in vomitus excess bicarbonate ingestion Jrespiratory rate and retain H in kidneys to compensate Hquot retention I K loss AcidBase lmbalances Pathological changes in the control of Hquot result in pH changes These can be compensate by the respiratory and renal systems if not of renal or respiratory origins A system cannot compensate for its own problem renal problems require respiratory compensation respiratory problems require renal compensation RespiratoryAcidosis Abnormal COZ retention form hypoventilation lung disease drugs nervemuscle disorders breath holding renal compensation l by H secretion Metabolic Vasodilators Active tissues produce vasodilators ATP use l adenosine production adenosine is a strong vasodilator active hyperemia Endothelial Factors Paracrines local hormones released from endothelium affect VSM Nitric Oxide Hormonalneural activation I NO relaxes VSM l blood flow Baroreceptors Stretch receptors in carotid sinus and aortic arch changes in BP after baroreceptor activity detects changes in BP Input to Medulla Baroreceptors send neurons to medulla in brain stem Cardiac Effects Hypertrophy against increased load diastolic pressure l oxygen use heart attack when coronaries constrict with age I in systolic pressure l stroke risk of hypertension a Adrenergic Receptor Blockers Stops sympathetic constriction of VSM blocks NE effects fewer CaZ quot channels opens less Ca2 entry less force 6 Adrenergic Receptor Blockers Blocks NEEpi effects on hea rt less Ca2 entry lforce of cardiac contractions Complex Carbohydrates Chains of sugars usually sugars Different complex carbs have different links between sugars starch is different than cellulose cannot digest sugar in fruit is often a monosaccharide fructose or glucose Enzymes Produced in the mouth and pancreas amylase converts starch to disaccharide disaccharides are in the wall of the small intestine disaccharides convert disaccharides to monosaccharide sucrose glucose fructose Protein Digestion Some in stomach some in small intestine Proenzymes Released in protected form acid then pepsin converts pepsinogen into pepsin enterokinase in small intestine wall converts trypsinogen into tyrpsin trypsin then converts other pancreatic proteases into active form Pepidases Both from pancreas and on small intestine wall convert peptides into amino acids some di and tri peptides absorbed Lipases Convert lipids to absorbable form lipases convert triglycerides into monoglycerides and free fatty acids Micelles Bile salts from liver emulsify monoglycerides and free fatty acids and cholesterol fats diffuse into mucosa at brush border Portal Vein Carriers water soluble foods directly to liver liver processes and detoxifies foods Fats lymph blood everywhere liver eventually Vitamins Water soluble B and C vitamins rapidly absorbed rapid loss in urine must take in Band Cvitamin daily B11 absorption needs intrinsic factor from stomach GI layers Mucosa epithelia cells Basic Electrical Rhythm Variable electrical baseline Ca2 and K channels openclose contraction when BER reaches threshold and APs occur Migrating Motility Complex Strong contraction migrates from stomach to end of small intestine starts as previous meal near complete digestion clears stomach and small intestine in anticipation of next meal Gastrin From stomach protein is strongest stimulus for release l stomach secretion ofacid and pepsinogen l small intestine illeocecal valve relaxation empties small intestine Reflux Acid in esophagus thru lower esophageal sphincter loss of neural input most common cause acid irritates esophagus heartburn potential ulcer Secretions of the mouth Bicarbonate neutralizes acids HZO amylase lipase mucase to coat food lysozyme anti bacterial enzyme Stomach Secretions Pepsinogen HCl separate H and Clquot pumps pH 12 mucus gastrin intrinsic factor for B11 absorption Unit obiectives Neoplasia Normal Anatomy and Physiology 1 Describe and relate to permanent cells stable cells and labile cells a Cell Cycle 2 Examples of a Permanent Cells b Stable Cells c Labile Cells 3 Define a Metaplasia change of one cell to another cell type b Dysplasia change of one cell to many different types cells are quotall messed upquot c Apoptosis Programmed cell death Cell suicidequot 4 Define a Apoptosis see apoptosis vs necrosis table 5 Describe how genes relate to cell and tissue function and size a Genes control cell function Depending on what part of the genome is being expressed a cell will express different functions If for whatever reason the sequence is changed a cell will begin to express different functions Reasons could include viral infections radiation exposure chemical changes physical agents or nutritional imbalance Metaplasia and dysplasia can be caused by increased demand Patho physiology 1 Recognize that cancer is not one disease 2 Define a Proliferation is the process of new cell growth and reproduction It is an inherent system to replace dead or dying cells when old cells die new cells are formed to replace them and continue normal function b Differentiation the process by which cells become more specialized 3 Discuss the relationship between proliferation and apoptosis and Proliferation and necrosis in determining tissue or tumor size a Part of normal cell function is programed cell death apoptosis a balance is met when old cells die and are replaced by new cells This keeps tissue size at a relatively constant size However this can be altered by states of hypertrophy such as in skeletal muscles The same can happen in relation to necrosis They sit on a balanced beam This balance beam can be swayed depending on the amount of proliferation or cell death planned or necrotic If there is too much proliferation the tissue will get bigger but if there is more cell death the tissue will get smaller 4 Examples of well vs poorly differentiated cells a Poorly differentiated malignant neoplasms b Well differentiated Benign Neoplasms c For differences and characteristics refer to table for objective 9 5 Discuss the relationships among DNA cells and tissues including the concepts of proliferation and differentiation a 6 Define a Neoplasia meaning new growth or new cells This contrasts with hyperplasia because hyperplasia is the increase in size of cells while neoplasia is the formation of new cells 7 Differentiate between Metaplasia dysplasia and anaplasia a Metaplasia change of one cell to another cell type b Dysplasia change of one cell to many different types cells are quotall messed upquot c Anaplasia Cancerous 8 Malignancy is a spectrum a TNM system 9 Compare and contrast benign and malignant neoplasms according to the 7 characteristics a See table 10 Define a Metastasis the development of a secondary tumor in a location distant from the primary tumor b Immune Surveillance hypothesis states that the immune system plays a central roll in the early detection and resistance of tumors c Metastatic routes i Mass growth benign ii Invasion of healthy tissue malignant 11 Pathogenisis of metastasis a Lymphatic route the tumor cells lodge first in the lymph nodes that receive drainage from the area If the cells survive the cells can grow and spread throughout the body b Homological route cancer cells enter the venous blood via peripheral veins or veins that drain the area Since blood from the GI tract pancreas and spleen is routed through the portal vein the liver is a common site of metastatic neoplasms Angiogenesis means the formation of new blood vessels and new metastasis cannot form without new and sustained blood flow 13 Etiological factors of neoplasms a Heredity b Immunologic mechanisms c Oncogenic viruses d Chemical carcinogens e Hormones 14 Discuss 4 types of genes that could be mutated to transform a normal a Refer to table Unit Objectives Male Genitourinary Disorders Normal Anatomy and Physiology 1 Equot 539quot F 5 6 Prostate stores and secretes a slightly alkaline uid milky or white in appearance Testesproduce sperm and produce androgens primarily testosterone Scrotum keep the testes at a tempslightly lower than the rest of the body Penisreporductive intomittent organ that additionally serves as the urinal duct in placental mammals Glansvascular structure located at the tip of the penis sensation Corpus spongiosummass of spongy tissue surrounding the male urethra within the penis that prevents the urethra from pinching closed during an erection maintaining the urethra a viable channel for ejaculation Corpus cavernosumspongelike regions of the erectile tissue which contain most of the blood in the penis during penile erection Dartos muscle fat free layer of smooth muscular fiber outside external spermatic fascia below the skin that regulates the temperature of the testicles Cremasteric muscle muscle that covers the testes that raises and lowers the testes in order to regulate the temperature of the testes Ductus deferens transfer sperm from the epididymis in anticipation of ejaculation Seminal vesiclelocated postinferior to the urinary bladder they secrete a significant proportion of the uid that ultimately becomes semen Inguinal canal a passage in the anterior abdominal wall which in men conveys the spermatic cord The urinary system in males travels from the bladder through the urethra The male reproductive system using the prostate to secrete the alkaline milky uid through the urethra When you are looking at the penis from the underside you are looking at the ventral side when you are viewing the penis from the topside you would be viewing the penis from the dorsal side Somatic nerves relays any senses that the male reproductive system senses up to the brain The PNS affects the vascular endothelium releasing nitric oxide NO acts on smooth muscle to relax and vasodialate and increases arterial blood ow to corpora C amp S in the male reproductive system The SNS causes muscular contractions stops NO release amp increases its breakdown after ejaculation it opens the venous channels amp lets blood out and brings the penis to the detumescence in the male reproductive system Nitric oxide relaxes vascular smooth muscle Hyperplasia is an abnormal proliferation of cells Pathophysiology 1 Hypospadias amp epispadias are congenital disorders where the urethral meatus is in an unusual location and are often associated with other congenital disorders Hypospadias is when the urethral meatus in on the Equot F 539quot 9 Uquot 9 HO O H H H N H W 14 ventral side of the penis it is more common and easily corrected with surgery Epispadias is when the urethral meatus is on the dorsal side of the penis less common and surgery is more difficult Erectile dysfunction is the inability to achieve and maintain an erection sufficient to permit satisfactory sexual intercourse Mechanisms include problems with the nerves amp CNS problems with hormones problems with drugs or chemicals and problems with vessels An increase blood pressure for erectile dysfunction increased the risk for Treatment for erectile dysfunction includes drugs like Viagra levitra and cialisthat helps the breakdown of NO so the male could get an erection Priapism is an abnormally prolonged amp painful erection that lasts grater than 3 hours This is an emergent situation because there is too much blood in the penis and it cannot get out which eventually can lead to impotence Cryptorchidism is failure of one or both testes to move down form the abdomen into the scrotal sac also known as undescended testes 30 of premature boys get it and 5 of fullterm boys get it Consequences of cryptorchidism include the testes can t be palpated in scrotal sac ofbaby boy may descend over neXt 6 months and increases the risk of infertility in affected side testicular torsion neoplasm s and inguinal hernia Inguinal hernia is the outpouchingof peritoneum amp intestines through a weakening at the inguinal canal Ifincarcerated it can lead to an emergency The hernia can t be reduced Decreased blood supply to bowel ischemia necrosis Inguinal hernias are almost always seen in males due to the Causes ofinguinal hernia include crytorchidism congenital weakness injurytrauma and heavy lifting Manifestations ofinguinal hernia include swelling or palpable mass pain which can be acute or chronic and may be radiate to groin or may be visceral and Gi symptoms such as bowel obstruction TX is always surgical to reduce hernia and reinforce inguinal r1ng Testicular torsion is the twisting of the testes on the spermatic cord leading to vascular occlusion It is an emergent condition because it can cause the male to be sterile Signs and symptoms of testicular torsion include edema from venous occlusion and an increase in hydrostatic pressure acute pain from arterial occlusion ischemia necrosis and testicular elevation from cremastericampdartos muscle contraction Treatment for testicular torsion include a manual detorsion with pain control surgical detorsion and it must be detorsedwithing 6 hours from onset of symptoms Benign Prostatic Prostate cancer hyperplasia
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