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Exam 2 Study Guide- Physiology

by: Sierra Mongeon

Exam 2 Study Guide- Physiology BIOS 213

Marketplace > University of Nebraska Lincoln > Biology > BIOS 213 > Exam 2 Study Guide Physiology
Sierra Mongeon
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This is the exam 2 study guide, and it is set up very very differently from the exam 1 study guide I posted earlier in the semester. I hope you find it helpful!
Human Physiology
Dr. Tony Zera
Study Guide
Physiology, University of Nebraska, Biology, Exam 2, Study Guide
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This 18 page Study Guide was uploaded by Sierra Mongeon on Friday March 11, 2016. The Study Guide belongs to BIOS 213 at University of Nebraska Lincoln taught by Dr. Tony Zera in Winter 2016. Since its upload, it has received 189 views. For similar materials see Human Physiology in Biology at University of Nebraska Lincoln.


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Date Created: 03/11/16
BIOS 213 Exam 2 Study Guide This study guide will be formatted differently than the last one (less questions, more condensed info). Happy studies! Review Exam 1 study guide and material – 25% of exam 2 will be exam 1 material -Renal system: function, ion movement, how the nephron works, pH balance etc. -Neuron anatomy -Refractory periods -ion equilibrium: what directions will ions move if allowed to freely diffuse? What does ion equilibrium mean? -Resting potential of a neuron is -70 mV -What does membrane potential mean? Main overarching concept: Antagonistic processes = fine control!! - renal system - nervous system - endocrine system - immune system Nervous System Graded potential vs. Action Potential 1. Graded potential a. No threshold b. Occurs on all cells c. Can be summed (summation) to produce a greater net effect d. Varying amplitudes (strengths) i. Strength of stimulus measured by AMPLITUDE (height) of GP e. Have no refractory period f. Is a SLOW change in membrane potential 2. Action Potential a. Memb. potential must reach threshold for AP to happen b. Occurs only in excitable cells (muscles, neurons) c. “All or none” – same amplitude (strength) every time i. Strength of stimulus measured by FREQUENCY of AP d. NO summation e. Have refractory periods i. Absolute= Na+ channels inactivated, no AP possible 1 ii. Relative = cell hyperpolarized, stronger than normal stim required f. Very fast change in membrane potential The Synapse: junction between neuron and another cell  Synapse types: axo-dendritic (axon  dendrite), axo-somatic (axon  cell body), axo-axonic (axonaxon)  Space btwn. cells = synaptic cleft  Electrical signal  chemical signal (neurotransmitters) NT  From pre-synaptic (sending) to post-synaptic (receiving) cell  What happens at synapse? o AP near end of axon causes depolarization of the axon terminal bouton of pre-synaptic cell. o Ca++ voltage gated channels open, Ca++ into cell which stimulates synaptic vesicles to fuse with cell membrane exocytosis o NT released into synaptic cleft, diffuse to post-synaptic cell, and bind to receptors on the membrane.  These receptors are often ligand-gated ion channels; when NT binds, they open and let ions diffuse according to their ion equilibrium o NT uptake/ degradation also occurs at synapse Neurotransmitters: small molecules released at synapse that bind to receptors and produce a graded potential in post-synaptic cell  The graded potential can be either excitatory or inhibitory depending on the characteristics of the receptor! o EPSP= excitatory post synaptic potential o IPSP = inhibitory post-synaptic potential o (Ex: ACh can have either effect, depending on whether it binds to a nicotinic or muscarinic receptor) o Excitatory = depolarizing; gets memb. closer to threshold o Inhibitory= hyperpolarizing; takes memb. away from threshold  Graded potentials = summation  Summation determines whether or not an AP will occur in post- synaptic cell  Mostly excitatory = AP  Mostly inhibitory = no AP  Summation of PSPs is required to produce an AP! (one PSP not strong enough)  Neural integration = combining info from different neurons. 2  Spatial summation: many pre-synaptic neurons  one post- synaptic neuron. All pre-syn fire simultaneously, enough effect for an AP  Temporal summation: one pre-syn  one post-syn. Can also cause AP if stimulated frequently enough (builds up) Acetylcholine Receptors (AChR) 2 types: nicotinic and muscarinic 1. Nicotinic Receptor a. Found in skeletal muscle cells b. ALWAYS EXCITATORY (produce muscle contraction) c. Ligand-gated Na/K ion channel i. ACh binds  opens channel. Na+ in, K+ out (ion equilibrium) 1. Na+ in > K+ out 2. Cell becomes more positive (depolarizes) 2. Muscarinic Receptor a. Found in heart muscle b. ACh does not directly bind to ion channel! 2 steps: i. ACh binds to receptor, G-protein dissociates (activated) ii. G-protein subunit bind to channel and open it c. K+ channel only – K+ flows out = hyperpolarizes = inhibitory d. Vagus nerve – slows heart rate Inactivation of NTs Both involve enzymes! 1. Enzyme inactivation in/near the post-synaptic membrane a. Enzymes are integrated into cell membrane, NT binds and is split apart (inactivated) i. Example : ACh : Acetylcholinesterase (AChE) splits ACh into acetate and choline ii. Inhibitors of AChE – block enzyme so ACh can’t be broken down. 1. Irreversible= death (nerve gas, some insecticides) 2. Reversible inhibition of AChE used to treat myasthenia gravis (where muscle contractions are weak, not enough ACh) 3. Other inhibitors = botulinum toxin (Botox), pufferfish toxin (tetrodotoxin), curare b. The inactive parts are taken back into the cell to make new NT 2. Re-uptake into pre-synaptic cell, inactivation INSIDE pre- synaptic cell 3 a. Whole NT are taken out of synapse, enzyme in cell breaks them down b. Monoamine: MAO = monoamine oxidase. Breaks down NT like serotonin, dopamine. i. MAOI (MAO inhibitors) drugs to keep serotonin, dopamine in synapse longer. Used for depression/ other disorders. Types of NTs 1. ACh 2. Monoamines a. Dopamine  dopaminergic neurons in midbrain and forebrain i. Motor control: so you don’t constantly have tremors. Too little dopamine = Parkinson’s. 1. Treated with L-Dopa, which is converted to dopamine in neurons ii. Reward/ behavior- why addictive drugs are addictive! These are “pleasure neurons” b. Serotonin i. Mood, behavior, appetite. ii. LSD iii. Prozac and other antidepressants = SSRI (Serotonin specific re-upake inhibitors). Allow serotonin to stay in synapse and work longer, helps with depression. c. GABA i. Most prevalent NT in CNS ii. Inhibitory;hyperpolarizing iii. Motor control 1. Huntington’s disease = tremors Synaptic Modulation 1. Pre-synaptic = axon-axon. a. Axon of one neuron modifies axon of the next. Affects Ca+ +  amount of NT released. Example: Pain 2. Special neurons/nerves associated only with pain 3. 3 types pain receptors: chemical, thermal, mechanical 4. Substance P = the NT used by pain neurons. Amount released is modified (modulated); why in high stress situations, you stop feeling pain for a while. 5. Endogenous analgesics a. Our body’s own internal pain killers! Beta endorphins: released during strenuous exercise/childbirth, bind to opioid receptors i. Morphine 6. Referred pain: Pain attributed to location other than where actual damage is happening. 4 a. Pain neurons synapse with many other neurons in spinal cord, signal is re-routed. 7. Naked mole rats have no substance P, being used to study drugs to relieve chronic pain. Classic example of animal research to study human physiology. Autonomic Nervous System 1. 2 divisions that work in opposition a. both systems innervate same organs, but have opposite responses b. homeostasis dependent on the interaction between the two. Both are always on, but sometimes one takes over. (always on = tone) 2. Pre-ganglionic and post-ganglionic neurons a. Ganglion = ball of neurons outside CNS 3. Sympathetic = “fight or flight”, survival mode a. Thoracolumbar, diversity of receptors b. Increases heart rate, blood pressure, blood flow to muscles, mental activity (what would you need for survival?) c. Decreases blood flow to digestion, kidneys etc. i. Excitatory/inhibitory working together d. Main neurotransmitters = norephinephrine, epinephrine (also a hormone); adrenergic neurons. Fight or flight i. Adrenaline – adrenal medulla, works with neurons to stimulate organs. ii. Types of adrenergic receptors: 1. Alpha = constrict Arterioles a. Reduce blood flow to gut, kidneys 2. Beta = Bronchioles and Blood pressure a. Relax muscles in bronchioles = more airflow, increase heart rate  blood pressure b. Beta blockers = blood pressure med 4. Parasympathetic = “rest and digest” a. Opposite effects of sympathetic. Slows heart rate, increase blood flow to digestion, reproductive organs, kidneys. i. Vagus nerve  many organs ii. Acetylcholine = main NT (cholinergic neurons) 1. Muscarinic receptors Endocrine System Hormone = released into blood (systemic), by endocrine glands 1. Internal chemical messenger 5 2. Effects target cells (that have receptors), changes proteins made by cell (turns genes “on” or “off”, affects RNA) Differences between endocrine (ES) and nervous system (NS) 1. Larger quantity of NT released 2. NS has faster response time 3. ES effects last much longer 4. ES affects larger number of cells (long distance, whole body) 5. Examples of hormones =Table 11.1 in notes Basic principles of hormones: 1. Inactive pro/pre hormones are modified to produce active forms–many of these are peptides, part of peptide chain cleaved off a. Example: insulin, renin-angiotensin system 2. Response depends on concentration (titer) and how sensitive organs are to hormone (receptors) a. Negative feedback (when conc. Is low, more produced and vice versa) b. Released in pulses/cycles Example : circadian (daily rhythms) : blood glucose highest in am. Due to cortisol Tissues are regulated by multiple hormones (complex system), antagonistic processes and different hormones regulate different aspects of same process a. Example: male reproduction, FSH and LH b. Can have sequential effects (one hormone affects sensitivity of organs to next hormone) – a “chain” of events Multiple feedback mechanisms = amplification of endocrine signal (small amt. of hormone can produce great effects) Physiological vs. pharmacological: i. Physiological = normal body conc. ii. Pharmacological = higher than normal, abnormal effects 1. Example: anabolic steroids a. High concentration of testosterone  negative feedback loop, shuts down T production and excess T converted to estrogen. Feminizing effects. Types of hormones 1. Steroids and other lipids a. Diffuse through membranes, receptors inside cells (ligand binding), bind to receptors, hormone/receptor complex binds to DNA (DNA binding) b. Affects RNA  protein/enzyme synthesis c. Broken down by liver, or receptors stop being produced d. Sex steroids and thyroxine 1. Steroid = 4 carbon ring, made from cholesterol 6 e. Slower acting 2. Peptide/ Amino acids a. Polar, receptors on outside (membrane) b. Act via second messengers (like G proteins) c. Small amount of hormone = large effects (amplification) d. Fast acting e. Mode of action: i. Hormone receptor = hormone receptor complex (HRC) ii. HRC  G protein  dissociation iii. Activates adenylate cyclase  catalyzes prod of cAMP from ATP iv. cAMP  protein kinase, 1 cAMP + 1 Specific hormones: 1. Steroids a. Steroids of adrenal cortex i. Glucocorticoids : increase blood glucose, fight or flight/stress ii. Mineralcorticoids (aldosterone) : regulate mineral concentration in body b. Sex/Gonadal steroids i. Estrogen: growth of uterine lining ii. Progesterone: growth of lining to prepare for egg implantation iii. Testosterone: growth/ maintenance of male reproduction, increase metabolism, aggression c. Thyroxine i. Thyroid, involved in metabolic rate and heat production, iodine! 2. Polar (peptide) hormones a. Epinephrine (Adrenaline) and norephinephrine i. Adrenal medulla ii. Also act as neurotransmitters iii. Fight or flight response: increase heart rate/force of contraction, plasma glucose. iv. Effects similar to sympathetic nervous system integration of nervous and endocrine b. Insulin and Glucagon i. From pancreas ii. Metabolic functions, act in OPPOSITION to each other (antagonistic process) iii. Insulin = lower blood sugar, increase uptake of glucose and liipids into cells. iv. Glucagon= raise blood sugar, release glucose and fatty acids 7 c. ADH (osmoregulation) d. All hormones of pituitary and hypothalamus Hypothalamus  The integration center for data coming into brain.  Responsible for lots of unconscious physiological regulation o Osmoregulation, breathing rate (pacemaker cells), heart rate, endocrine regulation (of pituitary) The Pituitary gland  “master” hormones – control many different things  anterior and posterior are very different!! (types of hormones, how they are released, what tissue they are made of) Posterior pituitary (PP) = derived from neural tissue.  Neural stimulation from hypothalamus  stimulates neurosecretory cells (like modified axon terminals with vesicles. These vesicles release a hormone instead of a NT)  Graded response  how much hormone is released. Operates very similar to neurons 2 key hormones released from PP o ADH – increase water reabsorption from collecting duct (see renal notes) o Oxytocin – involved in lactation and childbirth Anterior pituitary (AP)= derived from epithelial tissue  Releases trophic hormones (trophic = growth)  Release mechanism: o Hypothalamus  releasing factor hormone into portal vein. (This release is stimulated by a graded depolarization in hypothalamus from neural stim.) o Portal vein system : vein opens up into capillary bed, and then converges back into a vein. (Spreads out so it can contact more AP cells). Connects hypothalamus and AP o Releasing factor binds to receptors in AP  trophic hormones released into general circulation  Trophic hormones affect target tissues/other endocrine glands (Ex. Gonads)  This release mech subject to negative feedback regulation  Amplification of hormone signal: small amts of releasing hormone to start, results in each subsequent step having greater impact (effects are amplified/strengthened) Example: gonadotropins  sex steroids. o Small amount of GnRH  larger amt of FSH, LH  larger amt of sex steroids. 8 Endocrine disorders 1. Anabolic steroid misuse a. Higher than normal testosterone (T) concentration, negative feedback loop shuts down T production. b. T changed to estrogen (E) in liver, causes feminizing effects (breast tissue, shrinkage of testes, sterility) c. Masculinization in females d. Also causes high cholesterol….sex steroids are synthesized from cholesterol in body! 2. Disorders of Pituitary Function a. Inadequate growth hormone secreted during childhood. = Pituitary dwarfism: i. Recombinant growth hormone now available! (Recombinant = put gene into bacteria, grow bacteria, produce large quantities of product) b. Over-secretion of growth hormone i. In children = gigantism ii. In adults = acromegaly (thickening of bones, soft tissue) 3. Diabetes Mellitus a. Metabolic disease, problems maintaining homeostatic glucose levels. b. Insulin produced by beta cells in pancreas, Glucagon  alpha cells i. These hormones work to regulate blood glucose c. High blood sugar  insulin i. Glucose + fatty acids taken up into cells, synthesis of energy storage reserves. d. Low blood sugar  glucagon i. Releases glucose and fatty acids into blood to be used as energy (breaks down storage reserves) e. Insulin deficiency = diabetes mellitus f. Symptoms: high glucose in urine, frequent urination, insatiable thirst i. In extreme cases, ketoacidosis – can’t fully metabolize lipids, lipids become keto acids, lower blood pH g. Can be diagnosed with oral-glucose tolerance test (measures resting blood glucose, insulin production and how constant blood glucose stays) i. Normal blood glucose = 100 mg/dL ii. 200+ = diabetic h. Most commonly diagnosed with A1C glycosylated hemoglobin test : what % of hemoglobin has glucose attached? i. Greater than 6% = diabetic 9 i. 2 types diabetes i. Type 1 : insulin dependent 1. Autoimmune disease; destruction of beta cells, no insulin 10% of diabetics today 2. Early onset- children. 3. Prior to insulin discovery death. “wasting disease” 4. Insulin discovery saved lives! (Banting and Best, Toronto study) ii. Type 2 : Non-insulin dependent 1. 90% diabetics are this type. 2. Normal levels of insulin secreted, but reduced tissue sensitivity to it. (Due to adipose tissue hormones) 3. Usually appears in people 40+, but now happening in young people 4. Risks : Genetics, obesity, ethnicity (remember adipose tissue is a huge endocrine organ!) 5. Symptoms/Long term effects a. Stem from hypertension! i. Blindness (high B/P damage of retina), vascular problems, kidney problems (blowing out the glomerulus with high B/P!) The Menstrual Cycle -Cyclic changes in secretion of gonadotropic hormones FSH and LH  secretion of estrogen and progesterone  changes in ovaries and uterus. -Hormonal integration: ovarian and pituitary hormones coordinate each other’s cycles. Figure 20.33 (next page). 10 Steps of the cycle: 1. Follicular phase: Bleeding is done, a new follicle is developing. FSH production decreases (so it doesn’t stim another follicle) and estrogen levels steadily increase. a. Near the end of this phase the follicle will mature into a Graafian follicle. The granulosa cells, otherwise known as follicular epithelium, secrete estrogen (estradiol). More of them = more estrogen. b. The uterine lining is in the proliferative phase, which means it is rebuilding itself after the menstrual bloodbath to prepare for possible implantation. 11 2. Ovulation: Right before ovulation, a surge in LH, FSH and estrogen occurs. This causes the egg to be released (ovulation). The LH and estrogen cause the ovulation, but the FSH surge causes another primary follicle to undergo development a. The uterus, seeing the opportunity for a potential baby, is stimulated to grow and differentiate the uterine lining in the secretory phase. 3. Luteal phase: The corpus luteum (the empty follicle) secretes progesterone and estrogen, which stimulate the uterine lining to go “Holy crap, there’s a baby on the way, let’s get everything ready!” However, more often than not, the uterus is let down and there is no baby. The corpus luteum regresses, and stops producing progesterone and estrogen, signaling to the uterus “better luck next time”, and the ovaries go back to cooking up a new egg. The unhappy uterus flies into a fit of rage, and tears up the lining it worked so hard to prepare, and then gets rid of it so it can try again. 4. The cycle begins again! Important points: A positive feedback response is what causes the LH surge before ovulation! estradiol acts on both pituitary and hypothalamus (makes pituitary more sensitive to GnRH, makes hypothalamus secrete more GnRH). GnRH  LH Birth Control 1. Birth control pills : contain estrogen and progesterone, simulates the luteal phase. Negative feedback prevents LH, ovulation doesn’t occur 2. Plan B (RU 486):Promotes abortion non-surgically, blocks progesterone receptors – progesterone antagonist. Pregnancy Tests  Detects hCG presence (hCG hormone only secreted by fetus, so only in pregnant woman) o Immunoassay: antibodies to hCG detect presence, change test strip color Autocrine/Paracrine regulation = LOCAL, hormones act within organs that produce them 1. Cytokines: regulate macrophages of the immune system. Produced by lymphocytes a. Stimulate reproduction/multiplication of immune cells 2. Growth factors: promote cell growth in any organ a. Example: nerve growth factors for repairing damaged nerves 12 3. Products from blood vessel epithelium: regulators of the smooth muscle layer of blood vessels, vasoconstriction/dilation 4. Prostaglandins: produced in many tissues, many functions a. immunity – promote inflammatory process b. reproduction- ovulation, uterine contractions during labor c. digestion – inhibit gastric secretions d. respiratory- bronchoconstrictors e. circulatory- vasoconstriction/dilation, blood clotting f. urinary- produced in renal medulla, cause vasodilationincreaseed renal blood flow g. Activity inhibited by NSAIDS (aspirin, ibuprofen) i. NSAIDS inhibit COX enzymes 1. COX 1 = general function, COX 2 = inflammatory, blood clotting function (why aspirin is good for your heart!) Immune System =body’s defense system! Functions: Recognize foreign substances and kill/remove them.  Foreign= non-living material (viruses, chemicals), injured/abnormal cells (cancer), living pathogens (bacteria) 2 types: Innate immunity (non-specific) -No prior exposure to pathogen. We are born with some immunity. Very general. Fast (instant) action) Two components: 1. Non-cellular = first line of external defense (skin, stomach acids) 2. Cellular = “cell mediated”, first line of internal defense a. Phagocytosis= engulfment and digestion of invader. Phagocytes bind to lipopolysaccharides (LPS), compounds only found on cell walls of bacteria. b. Phagocytes= macrophages (macs) and related cells (neutrophils, monocytes etc.) 3. All phagocytes are leukocytes  white blood cells (WBC) or modified WBC. 4. Found in lymph nodes (immobile/anchored, remove foreign things as lymph/blood flows by) or circulating around blood a. Can move to the site of infection by chemotaxis (response to chemical signal) 5. Macs release pyrogens (cause fever), interferons (proteins that interfere with viral replication) and cytokines a. Cytokines= autocrine/paracrine, part of local inflammation process 13 i. Coordinate response, have effects like blood vessel dilation, attract other macrophages to site of infection ii. produce fever, sleepiness, lower iron conc. Acquired immunity (adaptive, specific) -Responding to a specific pathogen. Slow acting, but more efficient when exposed to same pathogen again. -Components: antibodies and antigen-specific defense cells -antigenic determinant: part of a molecule that induces antibody production and to which the antibodies bind 1. B cells (B lymphocytes) a. B cell exposed to antigen, binds to it b. Signals replication of itself into memory cells and plasma cells. “sounds the alarm” i. Memory cells: are able to bind to antigens just like the “parent” cells and initiate same response. 1. Immunologcial memory: Population of memory cells is maintained, so it can recognize the same pathogen again. Why you usually don’t get sick with the same thing twice. ii. Plasma cells: produce antibodies (antibody factories). 1. Antibodies react with the same antigen that induced their production c. Humoral immunity: humor=fluid, antibodies travel through body fluid d. Antibodies = Y shaped proteins, immunoglobulins. Allow B cell to kill at a distance. i. Structure: 4 polypeptide chains (2 long, 2 short) ii. Variable (V, Fab) and constant (C, Fc) regions. It’s the V regions that give antibodies their specificity and diversity!! (C regions don’t change much) iii. Factors in the diversity of antibodies 1. Encoded by different genes (several hundred V and C genes) stitched together in lots of different ways. Random combination. 2. Somatic mutations can occur (good mutations, allow for variance) iv. Function: 1. Bind to antigen, marks it as something to be destroyed. Binding activates complement proteins 2. Complement proteins: 1 part produces hole (pore) in bacterial cell wall, other part attracts macrophages (of innate immunity) to site of infection. a. This is an example of phys. integration 14 e. Primary and Secondary responses: i. Primary: First exposure! 1. slow production of B cells (memory cells mostly), low antibody conc. (titer) 2. Latent period 5-10 days, weak immune response (why you get sick) ii. Secondary: second/subsequent exposures! Recognizes pathogen from first time. 1. Faster response, rapid B cell production (because memory cells were formed in primary response) 2. high antibody titer, very active immunity iii. These responses are the basis behind why vaccines work! 1. Vaccine induces primary response with a weakened, less toxic form of the antigen (reduced virulence, sufficient antigenicity) that is injected into body. 2. Needed for very bad diseases- you don’t have time to wait for your primary response with the real thing! 3. History: a. cows, anthraxPasteur b. smallpox/cowpoxEdward Jenner f. Clonal selection theory- explains primary and secondary response i. Pre-existing B lymphocytes before you’re ever exposed to pathogens (at birth) ii. Foreign antigen causes reproduction of one of the pre-existing clones (primary response) iii. clone copies=memory cells 2. T Cells (T lymphocytes) a. Direct contact with pathogen- does not produce antibodies. Cell mediated immunity (not humoral immunity like B cells) b. Macrophage presents foreign cell to T cell because T cell cannot bind to free antigen!! c. Types of T cells: i. Killer (cytotoxic) : kills foreign cell ii. Helper/suppressor: modify and control activity of T and B cells (such as differentiation of B cell into plasma and memory cells) by secreting cytokines d. MHC complex (major histocompatibility complex) i. Prevents attacks to person’s own body by labeling normal body cells as “self”, helps macrophages find foreign cells and present them to T cells 15 1. Body doesn’t destroy its own cells 2. Foreign invaders identified and destroyed ii. Group of 4 genes with many allelesvariety of antigens on body cells. 1. Each individual has different cell antigens! This is why organ transplants are rejected (body recognizes the other person’s organ as foreign, attacks/kills it) 2. Solutions: transplants from genetically similar people, immunosuppressive drugs Local Inflammation: Coordination between Innate and Acquired immunity 1. Microbe enters body and causes cell damage, signaling macrophages to engulf. Non-specific complement proteins activated to destroy bacterial cell walls. a. Histamine released from damaged mast cells (special immune cell, found in body tissues). Functions of histamine: i. Make capillaries more leaky (so lymphocytes can squeeze through easier), increase blood flow ii. Due to increased blood flow, redness and warmth (inflammation) occurs at site of infection b. Fibrin fibrinogenblood clots, delays the spread of infection 2. Macrophages produce cytokines that attract other macrophages (neutrophils, monocytes) to the site of infection. The phagocytotic cells are attracted to the microbes once in the location (amplified defense) 3. Specific immunity kicks in! a. B cells antibodies, which enhance phagocytosis and activate complement proteins (which further stimulate phagocytotic cells) b. Macrophages present antibody-weakened pathogens to the T cells Immunological tolerance: body recognizes “self” and “not self”, tolerates its own antigens  Attacks non-self (foreign)  Clonal deletion/clonal inactivation (T/B cells): about 1 month after birth, any that would recognize and attack “self” antigens are inactivated/destroyed. 16 o Only lymphocytes left are those that recognize non-self antigens o When this malfunctions = autoimmune disease, body attacks self Tumor Immunology Tumor= mass of clones of a single cell whose division is malfunctioning, due to de-differentiation  Cells in embryo differentiate into specialized cells and cell division is regulated. De-differentiation by mutation causes cells to revert back to embryonic state, divide rapidly and uncontrollably.  Because the de-differentiated cell is present in the embryo before clonal deletion happens and has different antigens than the adult cell, it is recognized as foreign and killed. o Tumor cells occur in our bodies all the time, but our immune system protects us! Depressed immune function (AIDS)rare cancers Autoimmune disease  Failure of immune system to recognize and tolerate self antigens (sees them as foreign and attacks them)  67% affect women, many different diseases, 5-7% population Types: 1. Antibodies made against other antibodies of self a. Different antibody classes (each body tissue has slightly different antigens that distinguish it from other tissues). b. Example: rheumatoid arthritis- body attacks joints 2. Cross reactivity: antibodies against foreign antigens, but similar enough to body’s own that it attacks “self” thinking it is foreign. (cross reactivity was how smallpox vaccine came from cowpox) 3. Antigen not normally circulating in blood is now in blood a. This antigen not present during clonal deletion b. Organ damage: proteins/parts of organ now in blood, immune system attacks i. Example: eye, thyroid Passive immunity  Taking antibodies from a donor and injecting them into someone to strengthen immune response.  Short term-no memory cells, only antibodies  Used for children (before immune system developed)  Used for toxins that can kill before secondary response kicks in o Snake bites etc. o Anti-toxin, anti-serum, gamma-globulin shots 17 Antibodies in Research and Diagnostics  Specificity and sensitivity of antibodies mean they can detect small amounts of specific antigen in complex biological mixtures.  Histology (viewing things under a microscope)- allows for staining techniques, antibodies bind to specimen  Immunoassays o Clumping (blood tests, pregnancy tests)  Monoclonal antibodies used for studying very very specific antigen, usually cancer Allergies  Hypersensitivity to antigens, such as pollen in the air.  Types: o Immediate: B cell response, IgE antibodiesmast cellshistamine  Antihistamines o Delayed: T cell response to poison ivy, oak etc.  Corticosteroids 18


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