Biology Mechanisms

Human Anatomy and Physiology II

Glomerular filtration rate is the amount of pressure used to push out filtrate into the PCT. The hydrostatic “push” in the glomerulus is the most determining factor in GFR. Surface area is increased also because filtration can occur over the entire capillary bed not just at the arteriole side. Fenestrations allow smaller molecules like water, salt, and glucose to pass right through, but larger plasma proteins stay in the capillaries. 9. Describe how GFR is intrinsically auto-regulated via the myogenic mechanism (via arteriole constriction/dilation) and the tubuloglomerular feedback mechanism (via juxtaglomerular complex). Adjusting resistancen  Myogenic mechanisim: If you constrict the renal arterioles, you decrease GFR as to not damage the cells. This is done in response to an increased blood pressure.  Tubuloglomerular feedback: Macula densa detects changes in filtrate NaCl, which equate directly to filtrate flow rate. If GFR increases, then NaCl will also increase because there isn’t enough time for reabsorption. As a result, these cells release vasoconstricting chemicals that reduce the GFR into the afferent arteriole. 10. **Describe how GFR is regulated extrinsically via the sympathetic nervous system and the renin-angiotensin-aldosterone mechanism (outline this mechanism and know the functions of all hormones involved, as well as the physiological trigger and the physiological result of the mechanism). maintain blood pressure • SNS: Epi/norepi cause vasoconstriction (afferent arterioles) which decrease GFR • RAAS: granular cells of JGC work to increase sodium reabsorption via renin. Discuss the following concepts related to tubular reabsorption (obj. 11-14): 11. **Provide an overview of the differences in nutrient reabsorption (i.e. which nutrients—glucose, amino acids, water, sodium, etc.) among the various sections of the renal tubule. Explain why these processes are limited based on transporter saturation. Pulls nutrients from PCT through active and passive transport -Limited because they all need some type of transporter protein to reabsorb. -When those transporters are all saturated, the excess is excreted. • Na+ • Secondary active transport (into epithelial cell) • Na+/K+ ATPase pump (into interstitial space) • Other nutrients/ions (except water) • Via secondary active transport of Na+ • Water • As a result of osmosis 6

BIOL | 2222 | Human Anatomy and Physiology II | lecture notes | Glomerular filtration rate is 

BIOL 2222 Learning objectives Chapter 21—The Immune System: innate and adaptive body defenses Bhandari Fall 2019 1. Distinguish between nonspeciﬁc (innate) and speciﬁc (adaptive) immunity. Nonspeciﬁc (innate) immunity is present and fully functional since birth and speciﬁc (adaptive) immunity is only activated when surface and internal defenses are breached (acquired when you come into contact with an antigen or microbe later in life). 2. Nonspeciﬁc (innate) immunity: a. Deﬁne “surface barriers” and recall their helpful features. Surface Barriers: Skin- secretes a lot of oils and sweat that has its own PH so if it ever comes into contact with any pathogen, the sebum can ward it oﬀ. Mucous membranes- traps bacteria and pathogens coming their way. Internal Defenses: b. Outline the process of phagocytosis (including the role of opsonin). Phagocytosis is when monocytes turns into macrophages, target pathogens, look for surface molecules on the pathogen(sometimes hides its surface molecules), so opsonin compliments proteins on macrophages which enables them to bind and engulf the macrophages. Events of Phagocytosis: 1. Phagocyte adheres to pathogens or debris 2. Phagocyte forms pseudopods that eventually engulf the particles forming a phagosome 3. Lysosome fuses with the phagocytic vesicle, forming a phagolysosome 4. Lysosomal enzymes digest the particles, leaving a residual body. 5. Exocytosis of the vesicle removes indigestible and residual material. c. State the function of natural killer (NK) cells. Type of lymphocyte that enhances inﬂammation that induces apoptosis (shoot holes into cells to kill them) d. Fully explain the events that occur during an inﬂammation response (chemical alarm, vasodilation, phagocyte mobilization) and relate these events to the 4 signs of inﬂammation. A response to tissue injury. A lot of pain, redness, heat, and swelling because blood vessels end up dialating. The beneﬁts of this is to prevent antigen from spreading to healthy tissues, disposes of pathogens, and cell debris, red ﬂag to adaptive immunity and prep for repair. 1. Chemical alarm(from injured tissue/immune cells) – Histamine and Cytokines get released to amplify inﬂammatory response. When the chemical alarm starts leaving behind signals, a lot of blood ﬂow and platelets in that area, vessels dialate, capillaries get leaky, more and more leukocytes are attracted. 2. Vasodilation/ Capillary permeability - Exudate is a ﬂuid that has a lot of clotting factors and antibodies that gets sent over to the site of injury and once the CF comes into play, it forms a big ﬁbrin mesh. 3. Phagocyte mobilization- WBCs that are responsible for engulﬁng foreign particles are getting called into action. Neutrophils (chew up all foreign objects) arrive at the site ﬁrst, followed by macrophages. Macrophages(clean up whatever gets left behind) hold on to a piece of antigen and kick start the third line of defense where memories are being made with B cells and T cells. e. State the functions of (antimicrobial proteins) interferons and complement.

BIOL | 2222 | Human Anatomy and Physiology II | lecture notes | BIOL 2222 Learning objectives 

13) What are pseudogenes and why are they called nonfunctional vestigial genes?   like vestigial genes, it appears that they are only present simple because a commons ancestor had them 14) What characteristics of an isolated tropical ocean island make this island a great place to find one-of- a-kind endemic species?  there’s is no factors to cause a change in the species, so no genetic drift or influential forces to change the species   Chapter 23   The Evolution of Populations 15) What is the meaning of descent with modification in the modern definition of evolution?   the meaning of descent with modification is genetic variation. Organisms pass on their genetic information to their offspring and mutations occur cause this information to vary and change within the offspring within the offspring; some harmful others helpful; thus making way for modification in a species 16 When discussing genetic diversity, why are all new alleles the result of nucleotide variability? This is the result of mutation, but they cannot be predicted accurately on which segment it will take place within a DNA strand. Just one small change can impact a phenotype. Example is sickle cell disease 17) Explain how differences in diet could trigger the development of different types of organisms? certain foods have chemicals in them that over the course of time will change the body chemistry of and organisms; causing it to mutate and change. Take caterpillars for example for instance. They are raised on a diet of oak flowers resemble of flowers whereas their siblings raised on oak leaves resemble oak twigs 18) Cystic fibrosis is a genetic disorder in homozygous recessives that causes death during the teenage years. If 4 in 10,000 newborn babies have the disease, what are the expected frequencies of the dominant ( A1 ) and recessive ( A2 ) alleles according to the Hardy-Weinberg model?   √4/10,000 = .02 -1 =.98 A2= .02 A1= .98 P+Q=1 19) In a Hardy-Weinberg population with two alleles, A and a , that are in equilibrium, the frequency of the allele a is 0.5. What is the frequency of individuals that are homozygous for these alleles? .25 and .25   20) Why can’t you determine the allele frequency if you are only give the number of heterozygous organisms in a population?   With heterozygous you cannot determine allele frequency. w/o homozygous recessive or dominant it cannot be solved Use the following information to answer the question(s) 21-23) below. A large population of laboratory animals has been allowed to breed randomly for a number of generations. After several generations, 25% of the animals display a recessive trait ( aa ), the same percentage as at the beginning of the breeding program. The rest of the animals show the dominant phenotype, with heterozygotes indistinguishable from the homozygous dominants.   21) Why would you expect the two phenotypes to be equally adaptive under laboratory conditions? their equally adaptive and no outside influences 22) What is the estimated frequency of allele a in the gene pool?    little a little a = .25

BIOL | 1107 | Biology Mechanisms | exam | 13) What are pseudogenes and w

9. Recall the 3 types of antigen presenting cells (APCs) and state each of their roles in adaptive immunity. -APC’s(prevent body from destroying itself) eat antigens and present pieces on their surface attached to self MHC. This is how T cells get activated. -Dendritic cells (antigen scavengers) found in body’s entrances (skin, mouth, stomach) encounter an antigen and to the lymph node and tissues to activate an immune response. They are of hematopoietic origin. -Macrophages are activated into phagocytes by activated T cells -B-Lymphocytes enlist the help of helper T cells to activate themselves. 10. Humoral response: a. Recall the eﬀector cells and state their function. Plasma cells – secrete antibodies b. Outline the mechanism of clonal selection of a B cell.  -Antigens bind neighboring receptors and form cross-bridges on the surface of the B cell.  Endocytosis of that receptors-antigen cross-bridge occurs  -Plasma cells secrete antibodies that bind the original antigen and will circulate in search of the antigen.  -Memory cells stay behind to mount a faster response rate if the antigen comes in again. c. Describe why initial infection by a speciﬁc pathogen causes disease whereas one is "protected" during subsequent exposure to the same pathogen (immunological memory via memory cells). Primary response to antigen A occurs after a delay. Secondary response to antigen A is faster and larger. Mounts the response. d. Contrast active and passive humoral immunity.  Active humoral immunity involves naturally acquired antibodies so if you directly come in contact with an infection, your body is forced to make antibodies and ﬁght oﬀ on its own. With Artiﬁcally acquired, your injecting vaccines to prevent getting sick or antigens and oathogens from agtacking your body.  Passive also has naturally acquired in which antibodies are passed downj from the mother to the fetus. It doesn’t make memory cells and isn’t as robust. Eﬀects last only as long as those antibodies last (weeks to several months). With Artiﬁcally acquired, passive is used to treat tetanus, rabies, snake bites – things that can be fatal before your own humoral immunity kicks in. Keeps you from dying. e. Deﬁne the term antibody and explain how they are related to antigens. Recall the important structural features of an antibody. Antibodies are secreted by plasma cells and they clone themselves, speciﬁc to antigen. It latches on to antigens and destroys it. Classes: • IgG (primary antibody. Able to cross placenta into fetus) • IgA (mucous, saliva, tears and breast milk) • IgD (part of B cell receptor) • IgM (produced upon ﬁst antigen invasion) • IgE (protects against parasitic worms, mediates allergic reactions and inﬂammation) f. Explain all mechanisms by which antibodies help to destroy pathogens.  Neutralization: block the pathogen from secreting toxins (phagocytosis)  Agglutination: clump foreign cells (phagocytosis)  Precipitation: soluble antigens clump (phagocytosis)  Complement ﬁxation: triggers complement (cell lysis). Shows the complement fragments of antigens to phagocytes. They opsonize it which results in inﬂammation and lysis.  The stem region of the antibodies are used to activate the complement proteins, which causes the cells to be marked for phagocytosis via opsonization, further enhancing the inﬂammatory response at that site.

BIOL | 2222 | Human Anatomy and Physiology II | lecture notes | 9. Recall the 3 types of antig

1)What is a nucleic acid? Give two examples of nucleic acids. 2) How does the number centromeres at anaphase compare to the number of centromeres at metaphase? 3) What does GTP do in for a G-protein receptor? 4) What does adding a phosphate to a compound do in signal transducon? 5) If a heterozygous is crossed with a homozygous dominant, what is the probability of a homozygous dominant? A A A AA AA a Aa Aa The probability of being AA is 50% 6) If a heterozygous is crossed with a homozygous dominant, what is the probability of a heterozygous? The probability of being Aa is 50% 7)What is the connecon between telophase and cytokinesis? 8)At which phase of cellular reproducon does a cell achieve a “N” number of chromosomes? 9) At which phase of cellular reproducon does a cell achieve a “c” amount of DNA? 10) What is the overall purpose of meiosis? Chapter 11 Cell Communicaon 11) Explain yeast signal transducon and describe how ligands combine with membrane receptors in other types of yeast cells. What is the funcon of this process and how does it demonstrate cell communicaon? 12) Explain why a neurotransmier that opens gated ion channels would be considered a signal molecule. 13) Explain what it means to say that a GTP bound G-protein receptor with GTP bound to it is in its acve state It is turned on using phosphorylaon 14) Describe why testosterone is funconal as a transcriponal factor that controls the acvity of certain genes. What is a transcriponal factor? 15) Why are steroid receptors oﬅen found inside the nucleus of a target cell? Steroids are small hydrophobic molecules. Binding to the receptor transducon happens which leads to transcripon. 16) What signal is transduced and how does it lead to the physical form of the signal changing from one form to another. Transducon is taking a message and transforming a message to a form that can be recognized inside the cell 17) Explain how GTPase acvity is associated with the hydrolysis of GTP to GDP. Give an example of this in cellular communicaon. GTPase phosphorylates compounds 18) What is a protein kinase and how does the addion of a phosphate inﬂuence cellular behavior? Protein kinase phosphorylates compounds, giving them energy. 19) Explain the concept of a second messenger and why is cAMP considered one of the most common second messengers. GTP will turn on the producon of cAMP. cAMP is a messenger and binds to receptors inside of the cell turning things on. 20) Describe the role of transcripon factors in the control gene expression. What is transcripon and why would the cell need to control gene expression? Gene instrucons are copied to form RNA, in order to copy the instrucons you need RNA polymerase. Transcripon factor is a signal that binds to the gene and says “start here” so the RNA polymerase knows which gene to copy. Chapter 12 The Cell Cycle 21) What are the roles of DNA and protein in the formaon of chromosomes? DNA is a sequence of double nucleodes that make up a nucleic acid; RNA is a single nucleode. A chromosome is DNA. In S phase DNA is copied 22) Explain how G1 and the normal growth of a cell is analogous to the normal growth of a child. G1 is during interphase, the cell grows and cytoplasmic organelles are replicated. It spends most of its me in G1. Go is when the cell does not replicate. G1 grows up to do adult things (sex). 23) What is cytokinesis and how could a cell that fails to experience cytokinesis end up with mulple nuclei? the cytoplasmic division of a cell at the end of mitosis or meiosis, bringing about the separaon into two daughter cells. You duplicate the DNA but you dot divide the cell. Cytokinesis occurs by cleavage furrow. Mitosis is giving birth and is complete with cytokinesis (two disnct cells) 24) A is a cleavage furrow? How is a groove in the plasma membrane between daughter nuclei formed? Cytokinesis: divided into cleavage furrow and cell plate. 25) Why would the number of centromeres in a cell during anaphase result in half the number of chromosomes in the daughter cells? Give an example of this. When chromosomes line up in metaphase you have # and in anaphase you have 2x #. 26) Why would you expect a cell to spend twice as long in the S phase of the cell cycle when compared to cells with half the amount of DNA? 27) Why would the failure of a cell to enter the S phase of the cell cycle suggest that the cell is in Go? G o cells that don’t want to have ‘kids’ or divide 28) Describe the events would occur in a plant cell in the process of cytokinesis. Plant cells are ridged and cannot be squeezed in the middle. 29) Explain how adding phosphates to other proteins by cyclin-dependent kinase (Cdk) can be used to control cellular acvity. There are chemicals (Cdk) that move the cycle along. Cdk is a chemical that phosphorylates the system to move things along. Cdk helps the cell move onto the next stage 30) Explain how MPF is used to trigger the cell's passage past the G2 checkpoint into mitosis. MPF promotes mitosis, makes mitosis happen. Causes the cell to go from G2 to mitosis, it is a

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