Unit 2 Notes (1) PDF

Homeostasis Recall that homeostasis involves a stimulus-response model in which change in the condition of the external or internal environment is detected and appropriate responses occur via negative feedback. Recall that effectors are...

Homeostasis Recall that homeostasis involves a stimulus-response model in which change in the condition of the external or internal environment is detected and appropriate responses occur via negative feedback. Recall that effectors are either muscles or glands, and how they respond Homeostasis - the process by which an organism maintains a relatively stable internal environment, despite changing external environmental conditions. Stimulus Response Model: Positive feedback Loop: A less common system which causes a response to a change, which promotes the change. e.g. childbirth, blood clotting, milk production. Negative feedback Loop: A system which causes a response opposing the initial change, to return body conditions to normal. Most common type of feedback loop. Stimulus Change in internal or external environment from the stable state Sensory Receptors Cells that detect stimulus and alerts control centre. Control Centre (CNC) usually in the brain – hypothalamus, or transmission molecules Receives messages from receptors, coordinates a response by alerting effectors via the endocrine (hormone) or nervous system. Effectors A muscle or gland which responds to the signal from the CNC by doing something that will counteract the initial change. Muscles are stimulated by nervous impulses, and contract in response. Glands can be stimulated by nerve impulses or hormones, and secrete one or more products in response Response Appropriate state is maintained (back to original for negative feedback and promotion of change for positive feedback)  Recognise that sensory receptors (chemo, thermos, mechano, photo, noci) detect stimuli and can be classified by the type of stimulus. Exteroreceptors detect external stimuli – usually located close to the surface of the body and detect pain and pressure. Interoreceptors (or visceral receptors) detect internal states like blood pressure and blood chemistry. Chemoreceptors Detects a chemical stimulus (i.e. pH and oxygen concentration) Thermoreceptors Detect temperature Mechanoreceptors Detects a physical stimulus (i.e. pressure (touch), and sound) Photoreceptors Detects light (vision) Nociceptors Detects pain Identify cells that transport nerve impulses from sensory receptors to neurons to effectors. Neurons are nerve cells with structures which allow rapid transmission of information between cells. Three basic classes or neurons: Afferent (sensory) Transfer information from receptor cells (tissue and organs) to the central nervous system. Efferent (motor) Transmit information from central nervous system to effector cells (tissue and organs) Interneurons Connect neurons with the central nervous system. For all of these: - Information is received by dendrites. - Electrical impulse is passed on by the axon. - Neurons are separated by a small gap called synapse. - Information is passed on from one neuron to another via a chemical passenger (hormones) passing across the synapse. Recall that hormones are chemical messengers (produced mostly in the endocrine glands) that relay messages to cells displaying specific receptors for each hormone via the circulatory or lymphatic system. Hormones are signalling molecules produced in tiny amounts, usually produced by the endocrine glands. They circulate throughout the body in the circulatory and/or lymphatic systems (through blood). A hormone alters the activity of the target cell or tissue. They only target cells, which have that particular hormone’s specific receptor proteins, will be affected by the hormone. Non-target cells remain unaffected. Feature Nervous system Endocrine System Signals Electrical impulse Chemical impulse Pathways Transmission by neurons Transport by blood Speed of information Fast Slow Duration of Effect Short lived Long or short lived Type of Action and Voluntary or involuntary Always involuntary response Target Cells connected to neuron often distant – many cells can be affected.  Osmoregulation Identify and explain the various homeostatic mechanisms that maintain water balance in animals (osmoregulators and osmoconformers) in terms of: o Structural features (excretory system) o Behavioural responses o Physiological mechanisms o Homeostatic mechanisms (antidiuretic hormone (ADH) and the kidney Osmoregulation – the maintenance of osmotic pressure through regulation of water potential gradient within cell relative to the H2 O and electrolytes (ions, solute) in its surroundings. Osmoconformer Maintain internal conditions that are equal to the osmolarity (# of solute particles/L) of their environment. (change to match environment). Osmoregulator Keep body’s osmolarity constant regardless of environmental conditions (do not change to match environment). Osmoregulation Mechanisms: Structural Behavioural Physiological Contractile vacuole Seeking shade Production of dry faeces and concentrated urine Gills Habitats Fewer sweat glands Thirst and drinking behaviours Obtaining required water from food Fat storage and metabolism of fat. Homeostatic (ADH and Kidney) - Kidneys filter blood and remove excess water and salts (controlled by negative feedback loop which detects osmotic potential of blood) - ADH (anti-diuretic hormone) regulates level of water reabsorption in the collecting duct of the kidney (high ADH level = no urination, low ADH level = urination)  identify and explain the various mechanisms that maintain water balance in plants in terms of structural features (stomata, vacuoles, cuticle) and homeostatic mechanisms (abscisic acid); consider xerophytes, hydrophytes, halophytes and mesophytes in responses. Important features for osmoregulation in plants: Cuticle (epidermis) Stomata Vacuole Abscisic Acid (Plant hormone) Protecting internal tissue Opening and closing for Water storage and Controls plant organ gas exchange structural support size, root growth and stomatal closure Different Plant environment and their different osmoregulatory strategies: Hydrophyte Plants adapted to grow wholly or Large air spaces to allow floating partly submerged in water or wet water on surface. habits Can absorb water over whole surface. Broad leaves with high density of stomata on upper surface Plants adapted to growing in well- Mesophyte watered soil No specific adaptations Xerophyte Plants that can survive in an Leaf spines to reduce surface area environment with little liquid of to slow loss of water. water Few stomata Stomatal hairs to reduce transpiration. Halophyte Plants that grow in water of high Excretion of salt through gland salinity Modified leaf structure Osmoprotectants Removal of toxic ions Transport proteins Restricting entry of ions Sequestration of ions in vacuoles.  Thermoregulation Identify and explain the varying thermoregulatory mechanisms of endotherms and how they control heat exchange and metabolic activity in terms of o Structural features (brown adipose tissue, increased number of mitochondria per cell, insulation) o Behavioural responses (kleptothermy, hibernation, aestivation and torpor) o Physiological mechanisms (vasomotor control, evaporative heat loss, counter current heat exchange, thermogenesis/metabolic activity from organs and tissues) o Homeostatic mechanisms (thyroid hormones, insulin). Structural Thermoregulatory Features: Brown adipose tissue Fat cells with lots of mitochondria – oxidise fat to release heat. Mitochondria ATP synthesis releases heat Insulation Insulation (blubber traps in heat and resists cold. Behavioural Thermoregulatory Features: Kleptothermy Sharing of body heat Torpor Physiological state with low metabolism and low activity. Hibernation A long-term torpor that helps the animal survive cold and food scarcity. Aestivation Is summer torpor with low metabolism and activity during hot and dry summer periods. Physiological (bodily function) Thermoregulatory Features: Vasomotor Control Constriction (vasoconstriction) and dilation (vasodilation) of blood vessels. Evaporation Evaporation of sweat to reduce heat Counter current heat exchange Hot blood transfers heat to cooler blood in certain parts of bodies Thermogenesis Generation of heat through organs Homeostatic (hormonal) Thermoregulatory Features: Insulin TRH stimulates pituitary glands to release TSH. TSH regulates T3 AND T4 which regulate metabolism. Thyroid Hormones Stimulates brown adipose tissue to produce heat. Regulates metabolism by controlling the amount of glucose in the body by using the excess amount of glucose and converting and storing it as fat.  Infectious Diseases Identify the difference between infectious diseases (invasion by a pathogen and can be transmitted from one host to another) and non-infectious diseases (genetic and lifestyle diseases) Disease: abnormal condition of an organism which interrupts normal body functions Infectious: able to be passed from one individual to another (caused by pathogens and can be transmitted) - Pathogen: Biological disease-causing agent - Living (cellular) pathogens: parasites, bacteria, fungi, prokaryotes, protozoa - Non-living (acellular) pathogens: Viruses, prions Non-infectious: cannot not be passed for an individual (genetic and lifestyle diseases) Describe the following virulence factors which aid in pathogenesis: adherence and invasion factors, capsules, toxins, and lifestyle changes. Virulence: The ability of a pathogen to cause disease. Virulence Factors: Factors increasing a pathogen’s ability to cause disease. Adherence and invasion factors Proteins/carbohydrates on surface of pathogen which bind to the proteins on the surface of the host cell. Help overcome host’s defence mechanisms Capsules Coat bacteria and help then evade host’s immune system. Can protect bacteria from engulfment by macrophages. Toxins Exotoxins – toxic compounds produced by bacteria which cause disease (released outside bacterial cell) Endotoxins – toxins that a released when bacteria is destroyed Identify from given data and describe the following modes of disease transmission: direct contact, contact with body fluids, contaminated food, water and specific disease vectors Transmission: The passing of a pathogen. Modes of Disease transmission: Direct Contact Contamination Airborne Vectors Transfer via physical Ingestion of pathogens Certain pathogens can be Intermediatory association or exchange growing on or in edible transferred in the air via organisms that can of bodily fluids food/water sources. coughing & sneezing transfer pathogens without developing disease symptoms themselves Zoonoses: transmission of an animal disease to humans - Can only be transmitted directly from the animal to the human (e.g. rabies) Transmission + Spread of Diseases Recognise that the transmission of disease is facilitated by regional and global movement of organisms Transmission occurs through regional and global movement of organisms. Can be transmitted through: Environmental Factors Migration Transport Vectors Water supply, sanitation Probability of Movement of people Contribute to the facilities, food, climate. encountering new through transport (e.g. spread as they move diseases increases as planes, buses, etc) causes over large distances humans move: movement of disease into and interact with local different population organisms. - into previously densities. uninhabited lands Local organisms then because of population become vectors for growth disease. - into areas where they lack resistance to certain diseases. Identify the interrelated factors affecting immunity Interrelated factors affecting immunity: Persistence of pathogens within host, transmission mechanism, proportion of the population that is immune or has been immunised, mobility of individuals in the affected population Evaluate strategies to control the spread of disease: Community level management: Statergies to control spread of diseases Personal Temperature Contact Tracing Hygiene Screening (community) Measures (community)  Immune Response Understand how pathogens (bacterial and viral) can cause both physical and chemical changes in host cells that stimulate the host immune responses (introduction of foreign chemicals via the surface of the pathogens, production of toxins, recognition of self and non-self). Changes caused by bacterial and viral pathogens to host cells which stimulate immune responses: Physical Chemical Change in shape Release of different chemicals Change in proteins present on surface of cell. Change in concentration gradient Antigens: Carbohydrate/protein found on the surface of cells capable of binding with antibodies produced by the immune system They are capable of stimulating an immune response by allowing the body to distinguish between self (body cells) and non-self (pathogens): Self-Antigens Non-self Antigens (Immunogens) Have unique and distinctive surface molecules Antigens which elicit an immune response, also known called MHC (major histocompatibility molecules) as immunogens. Due to their lack of MHC. which allow then to be identified as body cells. Immune system does not react to these due to self-tolerance. While pathogens have antigens, they are non-self and hence lack MHC, triggering an immune response as Disease where body attacks its own cells is they are seen as foreign. known as autoimmune disease. Immune Response to Viruses When virus invades the body, it inserts its genome (DNA or RNA) into a host cell, hiding itself from the body’s immune system. In response, the cell will display viral proteins on its MHC molecule so that the body knows which cells have been infected and can destroy them. Viral Protein MHC Infected cell Toxins Pathogens may also secrete toxins to attack the host and will cause chemical changes in the host. These toxins are also recognised as foreign and trigger immune response Antibody: A specific protein (immunoglobulin) produced by lymphocytes in response to a particular antigen, with which it binds. Lymphocytes: Specialised white blood cells which enter the blood stream from bone marrow and detect foreign molecules in the body. Recognise that all plants and animals have innate immune responses (general/non-specific) and that vertebrates also have adaptive (specific) immune responses. Recall that the innate immune response in vertebrates comprises surface barriers (skin, mucus and cilia), inflammation and the complement system Lines of Defence: 1st Line: Surface Barriers – barriers to entry of pathogens - Skin – physical barrier to entry of pathogen - Ciliated epithelium – mucus lining to trap foreign particles and cilia lining to sweep them away from lungs. - Secretion that deters microbes – enzymes and toxic metabolites in tears, sweat and saliva which kills microbes. Acidic environment of stomach. 2nd Line: Innate Immunity (non-specific) 3rd Line: Adaptive Immunity (specific) Innate Immune Response to Infections Adaptive Immune Response to Infections General/ non-specific responses produced when Targets specific pathogens the body detects pathogens, or the toxins secreted by them. Does not create immunological memory (no Creates immunological memory memory cells) Same response every exposure. Modified response each exposure, making it highly specific. Plants and most invertebrate are confined to innate immune responses. Undergone by vertebrates, which have the ability to undergo both innate and adaptive immune responses. Present in all organisms and is always working Recall that the innate immune response in vertebrates comprises surface barriers (skin, mucus and cilia), inflammation and the complement system. Innate Immune Response to Infections - Non-specific, rapid, fixed response, no immunological memory, involves inflammation and the complement system. - Animals recognise and respond to pathogens just like plants. In vertebrates, they do this through the identification of pathogen associated molecular patterns (PAMPs). - In vertebrates this involves specialised white blood cells called leukocytes. Leukocytes Immune cells found in the blood and tissue which have pattern recognition molecules called TLRs on their surface which enable them to identify PAMPs. Their ability to recognise the presence of foreign pathogens enables them to form an innate immune response. Vasodilation (widening of blood vessels) increases the number of leukocytes that can reach damaged tissue. Prostaglandins Lipid compounds with hormone like effects which stimulate vasodilation and vasoconstriction. When pathogens are present, they increase blood flow. They cause pain, fever and inflammation. Inflammation is the accumulation of fluid, plasma proteins and leukocytes that occurs when tissue is damaged (tissue becomes, red, hot and painful) Complement System Protein cascade (proteins which work complementary to each other and activate on another) which punches hole in the membrane of pathogen Increases permeability of the pathogen’s membrane and helps the ability of macrophages (phagocyte ->white blood cells which engulf pathogen to destroy it) Describe the inflammatory response (prostaglandins, vasodilation, phagocytes) and the role of the complement system. Inflammation Response: 1. Pathogens break first line of defence and enter body tissue. 2. Physical and chemical changes occur in host. 3. TLR’s do not react to MHC, detect antigens, and start immune response. 4. Prostaglandins stimulate vasodilation. 5. Vasodilation allows leukocytes to reach damaged tissue. 6. Complement system proteins cascade and punch holes in the membrane of the pathogen (increasing permeability) 7. Macrophages do phagocytosis (engulf pathogen and destroy it) 8. Macrophage digests pathogen and produces PAMPs Explain the adaptive immune responses in vertebrates – both humoral (fluids) and cell-mediated The adaptive Immune Response Is Specific The specific immune response recognizes specific antigens, responds antigenic determinants, distinguishes self from non-self, and remembers the antigens it has encountered. Specific responses include the humoral immune response, which involves antibody production by B cells, and the cell-mediated immune response, mediated by T cells. Both the Humoral and Cell-mediated responses require specific receptors to bind to each antigen. Cell mediated adaptive immune response: T – Cells Cytotoxic T- Lymphocytes (CTLs) T-Helper Cells Activated by signal of pathogen from TCR Recognises foreign antigens & secrete cytokines (special chemicals) which activate B-lymphocytes and CTLs. They rapidly increase in numbers (proliferate) Use receptors called TCRs to detect pathogens Gain ability to induce apoptosis (cell death) Activated by antigen presenting cells, they proliferate and help other T and B - lymphocytes Migrate through blood to reach site of infection, and secrete pore forming proteins to create holes in pathogen’s membrane Humoral Adaptive Response: B-Lymphocytes Part of humoral adaptive immune response. B-cells are activated by receptors called BCRs to recognise an antigen. Produce antibodies to keep memory of encountered disease. Slower and less effective response than cell-mediated response through direct contact of antigen. Antibodies Produced by B-lymphocytes Binds to antigens. After binding they: neutralise bacterial toxins, block viral entry into cells, promote phagocytosis. Soluble in blood or membrane bound B-lymphocytes. Interpret long-term immune response data Initial exposure No antibodies, never seen the specific antigen Primary immune response During 1st exposure, the body slowly produces antibodies to kill of pathogen Secondary exposure T and B Memory cells can circulate the body for years and up to decades before dying Secondary immune response Memory cells immediately become CTLs and B-lymphocytes Skips Th cells involvement for a more rapid production of a greater concentration of antibodies Recall examples of physical defence strategies (barriers and leaf structures) and chemical defence strategies (plant defensins and production of toxins) of plants in response to the presence of pathogens Physical Chemical Ligma Toxins - Terpenoids Waxy Cuticle - Phenolic - Alkaloids Thorns Trichome Defensins - Enzymes -> catabolic (break down pathogens) Analyse the differences + similarities between passive and active immunity for both naturally and artificially acquired immunity Natural Immunity Non-deliberate contact with an antigen Passive – provided with antibodies. Antibodies passed from mother to offspring (placenta or breast milk) Active – produce your own antibodies. Natural exposure to antigens Artificial Immunity Deliberate exposure to an antigen Passive – provided with antibodies. Antibodies present in serum injection. Active – produce your own antibodies. Vaccines containing inactivated or weakened pathogens.