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Flashcards by Brianne Schmiegelow, updated more than 1 year ago
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Created by Brianne Schmiegelow
over 8 years ago
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| Question | Answer |
| What is coprophagia? | Eating of feces Some species do this to recover the vitamin Bs that the colon can't absorb |
| What accounts for up to 10% of our caloric intake? | The absorption of small fatty acids in the large intestine that are produced by bacteria fiber digestion |
| How is the digestive system controlled? | Both neural and hormonal control |
| What is the Enteric NS? | Nervous system of the digestive system that controls glands, muscles, and motility |
| What determines the length of digestion in the stomach? | Amount and type of food Detected by stretch and chemoreceptors Carbohydrates - fast (<1hr) Proteins - intermediates Fats - slow (up to 6 hr) |
| What is CCK? | Hormone secreted by the small intestine when fat or acid-rich chyme from the stomach enters Causes the gallbladder to contract, sending stored bile to the small intestine Causes pancreas to release digestive enzymes Slows stomach emptying so chyme can be neutralized and emulsified a little at a time Stimulates satiety |
| What is secretin? | "first hormone" Release by small intestine is stimulated by the presence of acid Circulates and stimulates pancreas to secrete bicarbonate for neutralization (SI not as well protected as the stomach) and so the enzymes work best (neutral/alkaline) Slows down stomach emptying |
| What are the two types of incretins? What do they do? | GIP and GLP Stimulate insulin secretion Secreted in response to glucose in the small intestine |
| Who doesn't respond to GIP? | People with NIDDM because of lack of receptors |
| What does GLP do? | Inhibits acid secretion and stomach-emptying Increases satiety Increases insulin, decreases glucagon |
| Hormones don't play a role in ______ motility. Control is via _________ and _______. | Large intestine Enteric NS and ANS |
| What can stimulate/inhibit defecation? | Anxiety can do both! Coffee stimulates |
| What is the innate immune system? | System that provides an immediate, non-specific response Found in all plants and animals |
| What is the adaptive immune system? | System that is activated to specifically attack pathogens that evade/survive the innate response Specificity is carried into the future by immunological memory |
| What is immunological memory? | System that carries specificity into the future which enables faster, stronger attack next time that pathogen is seen How vaccinations work! |
| What are PAMPs? | Pathogen-associated molecular patterns Include LPS (lipopolysaccharide) from gram- membranes and peptidoglycan from gram+ walls and double-stranded RNA from viruses Trigger phagocytosis by the innate system |
| What are PRRs? | Pattern recognition receptors Receptors in innate system cells that recognize the PAMPs common to many microbes |
| What are neutrophils? | WBCs that are produced in the marrow Mobile, short-lived, and the 1st to arrive at infection sites (within minutes), biggest component of pus Attracted by cytokines and exit the bloodstream by diapedesis |
| What's the most abundant type of WBC? | Neutrophils |
| What are macrophages? | Derivatives of monocytes Mobile, long-lived phagocytes |
| What are organ-specific phagocytes? | Phagocytes that are often tethered and found in the liver, spleen, lymph nodes, lungs, and brain |
| Fever is part of innate immunity. How? | It is induced by pyrogens released by WBCs in response to PAMPs Increases body temp above the optimal growth temp for many microorganisms Leads to release of heat shock proteins |
| What are heat shock proteins? What is their role? | Family of proteins released in stressful conditions that cause production of inflammatory cytokines Cytokines increase metabolism which increases production and activity of phagocytes, speeds up multiplication of lymphocytes, increases antibody and cytokine production, and increases WBC release by marrow |
| What are interferons? | Polypeptides that are produced by virus-infected cells to boost immune activity Activate Natural Killer Cells Confers short-acting, non-specific resistance to viral infection on nearby cells |
| What are natural killer cells? (NKCs) | WBCs that are activated by interferons |
| What is the purpose of the complement system? | To help clear pathogens and bad cells from the body and to work with adaptive immunity |
| How does the complement system work? | When activated, the system initiates an enzyme cascade that results in the formation of MACs to kill pathogenic cells |
| What are MACs? | Membrane attack complexes Large pores formed by complement proteins that perforate and lyse pathogenic cells |
| What are antigens? | Molecules that can elicit an immune response Immune system can distinguish self from non-self antigens and NORMALLY only makes antibodies against nonself |
| What are lymphocytes? | A class of WBCs that include T cells, B cells, and natural killer cells Produced by the thymus, spleen, and lymph nodes |
| What are T cells? | Cells produced by the thymus that provide cell-mediated immunity Constitute 65-85% of lymphocytes in blood Attack infected host cells, cancer cells, and foreign cells |
| What are B cells? | Lymphocytes that secrete antibodies into blood and lymph which provide humoral immunity Have antibodies on their surface that are receptors for antigens When bound to the antigen, they are stimulated to divide and secrete antibodies |
| What happens when B cells divide? | Some become plasma cells, some become memory cells |
| What are plasma cells? | Cells derived from B cells that produce about 2000 antibodies per second Provide active immunity |
| What are memory cells? | Cells derived from B cells that provide a rapid, strong antibody response to subsequent exposures to an antigen |
| What is the complement cascade? | A process triggered by the binding of B cells to antigens B cells and their products serve as signals for MACs and phagocytes to carry out killing |
| What are antibodies? | Proteins called immunoglobulins 5 types, basic structure is a "Y" |
| What are the 5 types of antibodies? | IgG, IgE, IgM, IgA, and IgD |
| What is Fab? | The variable region of antibodies at the tips of the "Y" arms that binds antigens and confers antibody specificity |
| What is Fc? | The stem part of the "Y" that is constant among different antibodies Activates other parts of the immune system |
| How many antibody molecules does each person have? | 10^20 (With a few million different specificities) |
| What is antigen specificity based on? | Shape An antibody binds to an antigen that fits into its binding pocket |
| What is opsonization? | Labeling of a pathogen for phagocytosis or complement attack Antibodies do this because they can't kill on their own |
| What do antibodies use opsonization on? | Gram negative bacteria, viruses, and host cells recognized as non-self |
| What are MHCs? | The Major Histocompatibility Complex 4 gene complex on Chromosome 6 Produce cell surface proteins that display self peptides normally made by a cell or non-self peptides normally originating from a pathogen Are on the surface of all the body's cells EXCEPT mature RBCs |
| What forms the basis for histocompatibility typing? | MHC genes have multiple alleles, creating many possible MHC types Basis of organ compatibility |
| What do MHCs produce? | 2 types of antigen-presenting proteins: Class 1 and Class 2 |
| What are class-1s? | Antigen-presenting molecules produced by MHCs in all cells except RBCs Display peptides normally made by a cell on the cell's surface Interacts with CD8 coreceptor on killer Ts which (normally) recognize these peptides as self and leave them alone |
| What happens if a killer T's antigen is presented by a class-1 protein? | The killer T takes out the cell with the help of the complement system because it indicates it's a bad self cell Killer Ts have to have found a class 1 with a foreign antigen to bind to the cell |
| What happens if killer Ts respond to self antigens? | They are (normally) deleted or inactivated |
| What are class-2s? | Antigen-presenting proteins produced by MHCs that are expressed by professional antigen-presenting cells |
| What are pro APCs? | Professional antigen-presenting cells Include macrophages, dendritic cells, and B cells Phagocytize antigens then digest them into small pieces (epitopes) which are presented by class-2s on their surface |
| What do pro APCs have on their surface? | Class-1 and Class-2 proteins |
| Which cells can activate a killer or helper T that has never seen its antigen before? How? | Dendritics When a naive helper T binds to its antigen and a class-2 MHC, a dendritic cell activates it with ILs which leads to secretion of antibodies, memory cells, and plasma cells |
| What is CD4? | A coreceptor on helper Ts that interacts only with class-2s on dendritic cells |
| What do activated helper Ts do? | Stimulate other cells with ILs |
| What are NKCs? | Natural killer cells Lymphocytes that can kill virus-infected and tumor self cells that are opsonized and lack class-1 MHC antigens |
| How do intracellular microbes and tumors become resistant to killer T actions? What kills them then? | They down-regulate class-1 molecules NKCs recognize these cells and attack them with MACs, granzymes, and perforins |
| What is affinity maturation? | When a B cell binds to an antigen, it undergoes programmed point mutations of its variable region genes at a rate 10^6x higher than normal If the new Bs bind longer and tighter to the epitope, they will divide more and survive longer, so this fine-tunes the shape of the Fab antigen pocket (binds epitope better) The better-fit Bs become plasma and memory cells |
| What is immunological tolerance? | The ability to produce antibodies against non-self while tolerating self BEGINS at about 1 month of life |
| Where does T cell tolerance first develop? B cell? | Thymus Marrow |
| What is AIRE? | Autoimmune regulator A transcription factor in the thymus that causes the thymus to express peptides produced by most other tissues, creating a profile of self-antigens |
| What happens to new Ts that bind to the selfs produced by AIRE? | They are deleted! |
| Why do dendritics migrate to the cortex of the thymus? | To help present self-antibodies to developing Ts for potential deletion in the event that they bind to selfs |
| What happens to B cells in marrow that bind selfs? | They undergo receptor editing, meaning they reshuffle gene expression to make new receptors If it still bind self, they will undergo apoptosis |
| What is peripheral tolerance? | Outside the thymus, naive T cells that recognize self-antigens undergo apoptosis (clonal deletion), usually in the lymph nodes And/or Ts, Bs that bind selfs are inactivated and circulate without function until they die (ANERGY) |
| What are autoreactive Ts? | Killer Ts that attack self-antigens |
| Which self-antigens are normally hidden from the blood? What happens if the body has exposure to these? | Lens protein in the eye, those in joints, etc. Exposure results in production of autoantibodies and attack from autoreactive Ts |
| What is FAS? | A surface receptor on killer Ts that increases during infection |
| What is FAS ligand? | Produced by killer Ts a few days after an infection begins Binds to FAS and triggers apoptosis of the killer Ts |
| What are Tregs? | Suppressor T cells Cells that shut down immune attack after a disease to deter autoimmunity Secrete cytokines that suppress other immune cell activity |
| What happens if you have a deficiency of Tregs? | Severe autoimmunity, immunopathology, and allergy |
| What is the primary antibody response? | On first exposure to a pathogen, there is a latency of 5-10 days before specific antibodies are made, then antibody levels decline after a few weeks Induced by vaccines |
| What is the secondary antibody response? | A response caused by subsequent exposure to the same antigen that causes much more rapid and sustained antibody production |
| What is passive immunity? | Protection produced by transfer of antibodies from a donor to a recipient Used to treat snakebite, rabies, tetanus, and hepatitis |
| How does passive immunity occur with babies? | Occurs naturally before and after birth (most in breastmilk) Some antibodies from the mother pass the placenta to the fetus during pregnancy and provide passive immunity |
| What is colostrum? | Produced by a mother during the first 2-3 days of nursing Contains her antibodies and gives her immunity to the infant |
| When does a specific immune response develop? When do vaccines take? | 1 month 15 months |
| What happens when you have an autoimmune disease? | Autoreactive T cells are formed and B cells produce autoantibodies |
| What happens in Hashimoto's? | Antibodies attack thyroglobulin which is normally hidden from immune surveillance |
| What happens in thrombocytopenia? | Platelets are destroyed because they combine with the victim's medications An example of a self-antigen that is otherwise tolerated with a foreign antigen that is not |
| What happens in rheumatoid arthritis? | Antibodies are produced that are directed against other antibodies |
| What happens in Type I diabetes to make it autoimmune? | Self-antigens are presented to a helper T by a class-2 molecule causing them to be activated |
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