Unit 5: Body Systems

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+ Chemical Signalling // ERQ Practices: Pathways – Muscle contraction, Cell signalling, Depolarisation, Respiration, Photosynthesis

Last updated 8:28 AM on 8/24/26
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45 Terms

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Receptors as Proteins with Binding Sites for Specific Signalling Chemicals

Ligand = Signalling chemical; Bind reversibly to specific receptors on / in target cells → Specific cellular response via signal transduction pathway

  1. Binding of ligand to receptor

  2. Conformational change in receptor protein

  3. Activation of downstream signalling molecules

  4. Internalisation of receptor-ligand complex


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Cell Signaling by Bacteria in Quorum Sensing

Example of bioluminescence in marine bacterium Vibrio fischeri

  • When cells aggregate, inducer accumulates in confined environment → Concentrations of autoinducers increase → Luminescent system of ALL bacteria is activated → Emit light through bioluminescence

  • V. fischeri form symbiotic relationship with Hawaiian bobtail squid

    When squid hatches, capture V. fischeri from environment and house in specialised light organ

    • Bacteria produce autoinducers which accumulate to a certain point

    • Once threshold is reached, autoinducers enter cell and bind to LuxR protein → Activates lux operon → Production of luminescent protein (luciferase) → Emission of light

  • Light allows squid to match surrounding moonlight / Camouflage itself from predators by illuminating underside

  • Squid resets bacterial population by expelling 90% every morning; Remaining bacteria multiply / reach the quorum at night to produce light → Prevents overgrowth + Reduce risk to immune system


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Functional Categories of Signalling Chemicals in Animals & Differences (HINT: 4 types)

Hormones

  • Secreted by endocrine glans

  • Travel through bloodstream to reach target cells across body

  • Attaches only to specific receptor; Only specific cells respond

  • Takes time for secretion

  • Prolonged effect


Neurotransmitters

  • Released from one cell; When an electrical impulse reaches presynaptic nerve

  • Affect nearby target cell

  • Occurs at the synapse

  • Travels across the synaptic cleft to reach receptors on postsynaptic membrane

  • Results in an electrical impulse at the postsynaptic nerve cell


Cytokines

  • Glycoproteins

  • Functions include cell to cell messenger, enhance cell function, inflammation, cell proliferation, embryo development

  • Binds to cell membrane receptor; Triggers signals inside cells to activate proteins in cytoplasm → Sets of cascade reaction


Calcium Ions

  • Signalling molecules / second messengers

  • Participate in signal transduction pathways

  • Regulate cellular functions including nerve transmission, muscle contraction, hormone secretion, enzyme activity, and cell division

  • Released from intracellular stores

  • Enter cells via ion channels


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Chemical Diversity of Hormones and Neurotransmitters

Reasons for wide range of chemical substances as signalling chemicals

  • Diverse functions (Distance and duration)

  • Ability to bind to differently-located receptors / Interact with chemically-specific receptors

  • Different modes of action on target cells

  • Target various cells efficiently


Hormones = Amines, proteins, steroids chemical groups; For long-distance

  • Amines, proteins are hydrophilic → Cannot cross cell membrane; Must bind to receptors on surface

  • Steroids are hydrophobic → Easily cross cell membrane; Bind to intracellular receptors

Neurotransmitters = Amino acids, peptides, amines, nitrous oxide; For localised (across synaptic gap, ~20 mm)

  • Most are hydrophilic → Extracellular receptors


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Localised and Distant Effects of Signalling Molecules (& Contrasts)

Contrast between hormones transported by blood system and neurotransmitters that diffuse across synaptic gap

  • Neurotransmitters = Across synapses; Affect neighbouring cells

  • Oxytocin = E.g. Oxytocin affects reproductive system, social behaviour, stress response, etc.


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Transmembrane Receptors in Plasma Membrane & Intracellular Receptors in Cytoplasm / Nucleus (& Difference)

Distribution of hydrophilic or hydrophobic amino acids in receptor

TRANSMEMBRANE RECEPTORS:

  • Consist cytoplasmic and extracellular domains (hydrophobic amino acids ~ IN cell / hydrophilic amino acids ~ OUTSIDE cell)

  • For signal transduction

  • Converts external signal into internal action; Ligand binding → Undergo conformational change → Initiate cascade → Activation of enzymes / Changes in gene expression / Change in cellular metabolism

  • Types include…

    1. Chemically gated ion channel = Multi-pass protein w/ central pore → Possess gates

    2. Enzymatic = Single-pass protein → Binds ligands extracellularly + Activates enzymes intracellularly

    3. G protein coupled receptors (GPCRs) = Multi-pass protein w/ intracellular binding site for G-protein → Bind with ligands → Activate G protein

INTRACELLULAR RECEPTORS:

  • Have hydrophobic regions to interact with lipid-soluble ligands

  • Act as transcription factors → Affect gene expression → Long-term change in cell’s function (E.g. growth, differentiation, metabolic regulation, etc.)


Whether signalling chemical penetrates the cell / remains outside based on size and polarity

  • Hydrophilic signalling chemicals bind to transmembrane receptors

  • Hydrophobic signalling chemicals diffuse through membrane + bind to intracellular receptors


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Initiation of Signal Transduction Pathway

Binding of ligand to receptor sets off a sequence of responses within the cell

  1. Reception

    Target cell detects ligand which binds to transmembrane receptor

  2. Transduction

    Signal is converted into new form that allows for response

  3. Response

    Transduced signal triggers cellular activity e.g. enzyme activity, gene expression changes, cytoskeletal changes


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Transmembrane Receptors for Neurotransmitters & Changes in Membrane Potential

  • Ligand binding causes ion channel to open → Positively-charged ions (Na+, K+) diffuse into cell → Generate action potential


Acetylcholine receptor = Found at neuromuscular junctions & neuron-neuron synapses

  • Chemically gated ion channel; Opens only when acetylcholine binds to it → Diffusion of ions (Na+ and Ca2+ into cell and K+ exit cell, along concentration gradient)

  • Results in depolarisation of membrane → Muscle contraction → Repolarization & return to resting potential


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Transmembrane Receptors that Activate G-Proteins

How GPCRs convey signal into cells

  1. Ligand binds

  2. Conformational change in receptor

  3. Activates associated G-protein

  4. Exchange of GDP (bound to G-protein) for GTP (guanosine di- / triphosphate)

  5. α subunit + GTP disassociates from the β and γ subunit of G protein

  6. Triggers cellular response; Interacts with other proteins / enzymes in cell; Transmit signal from activated receptor to downstream effector molecules

  1. GTP is hydrolysed to GDP and inorganic phosphate group / Ligand unattached from receptor

  2. α subunit + GTP comes back together with receptor & β and γ σ subunits


Many GPCRs are in humans

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Mechanisms of Action of Epinephrine Receptors

Roles of G protein and cAMP as second messenger

  • Epinephrine receptors = GPCRs; Use cAMP to relay signal inside cell → Fight-or-flight response

    Increased heart and breathing rate, dilation of airways, breakdown of glycogen to glucose, increased oxygen and glucose delivery to muscle cells, vasoconstriction of blood vessels

  • After G-protein activation…

    1. α-subunit + GTP binds with adenylate cyclase

    2. Converts ATP to cAMP

    3. Activates several protein kinase A (PKA)

    4. PKA phosphorylates enzymes and proteins e.g. phosphorylase in liver to break glycogen into glucose

    5. Inactivation occurs


Adrenaline terminates to prevent overstimulation + return to resting state in preparation for new signals and responses by…

  • Degradation of cAMP

  • Deactivation of G proteins

  • Receptor endocytosis / desensitisation


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Transmembrane Receptors with Tyrosine Kinase Activity

Kinase = Proteins that phosphorylates other substances using ATP

RTKs = Consist of three domains, single-pass protein; Composed of two α subunits (extracellular) and two β subunits (transmembrane) Occur in pairs

  • Can activate MULTIPLE signal transduction pathways simultaneously

  • Initial signal becomes amplified


  1. Insulin binds to extracellular domain (α subunit)

  2. Receptors dimerize

  3. Autophosphorylate tyrosine residues on β subunits on intracellular domain

  4. Activates kinase

  5. Phosphorylation cascade occurs

  1. Mobilisation of glucose transporter vesicles containing GLUT4

    • GLUT4 = Facilitates glucose uptake into cells

    • Vesicles merge with plasma membrane → Increased active glucose cotransporters → More glucose enters cell from bloodstream → Lowers blood glucose levels → Provides energy for cell; Prevent hyperglycaemia


Insulin resistance = Cells do not respond effectively to insulin → Reduced glucose intake → Development of Type II diabetes

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Intracellular Receptors that Affect Gene Expression

Steroid hormones: Oestradiol, progesterone, and testosterone

  • Lipid soluble, steroid hormones pass through membrane and bind to intracellular receptors


Ligands bind to site on receptor → Activates receptor → Binds to specific DNA sequence → Promote gene transcription

  1. Upon binding, hormone-receptor complex undergoes conformational change → Activation

  2. Translocation to cell nucleus + Binds to hormone response elements (HRE)

  3. Promote / suppress transcription of target genes


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Effects of Hormones Oestradiol and Progesterone on Target Cells

For estradiol cells: Cells in hypothalamus secrete GnRH

  1. Oestradiol binds to oestrogen receptors within cells in hypothalamus → Secretes GnRH

  2. Stimulates release of LH & FSH from pituitary gland

  3. Stimulate ovaries to produce eggs + Production of estradiol from ovaries


For progesterone cells: Cells in endometrium

  1. Progesterone binds to progesterone receptors in endometrium cells

  2. Promotes gene transcription (nutrient storage and angiogenesis)

  3. Prepares endometrium for potential pregnancy (Induces thickening + Formation of additional blood vessels within)

  • During pregnancy, maintains integrity and functionality of endometrium; Otherwise, secretion decreases, uterus lining sheds


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Regulation of Cell Signalling Pathways by Positive and Negative Feedback

  • To regulate hormone levels + Maintain homeostasis


Difference between two forms of regulation + Brief outline of an example each

  • Positive feedback = Amplifies response; E.g. Release of oxytocin during childbirth

    Baby moves across cervix, activating stretch receptors in uterus → Brain signals oxytocin release → Oxytocin causes uterine muscle to contract → Contractions strengthen until baby is delivered

  • Negative feedback = Diminishes response; E.g. Insulin secretion

    During high blood glucose levels, β cells are stimulated to secrete insulin → Prompts cells to absorb glucose / Convert glucose into glycogen or fat in liver → Reduce blood sugar → Prevent hyperglycaemia


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Adaptations for Movement

Universal feature of living organisms; Range of organisms (Motile and sessile)

  • Motile = Organisms that have adaptations allowing movement within habitat, e.g. Three-toed sloth

    Three long toes → Hanging; Movement on ground is almost impossible

  • Sessile = Cannot move from place to place but can alter body in response to environmental stimuli e.g. Venus flytrap

    Pair of leaves with short and sturdy trigger hairs; When triggered, leaves close + Enzyme secretion → Trap and digest insects

    (When one hair is triggered, ~20 seconds wait for a second hair to be triggered as confirmation for “bug”)


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Sliding Filament Theory

Sarcomere contracts by sliding of actin and myosin filaments

  • Muscle → Bundle of muscle fibres → Single muscle fibre → Myofibrils → Sarcomere

  • Myofibrils = Composed of repeating sarcomeres units; Many of these make up one muscle fiber

  • Sarcomeres = Long fibrous proteins that are attached to each other end to end; Synchronised movement (One moves, all move) → Shortens muscle fibre / entire muscle

    • Striations of skeletal muscle = Alternating fibers of myosin and actin

      “I band” = Thin actin filaments = Light

      “A band” = Thick myosin filaments + actin filaments on outer edge = Dark

  • Actin = Round proteins linked in chain to form filament

  • Myosin = Long thin protein + Movable head; Linked together in bundles to form filament (Multiple heads)


  • In sarcomere, myosin remains stationary while the actin on both sides move towards the centre using movable heads on myosin

  • When sarcomeres contract, the actin filaments slide over the myosin fibers, resulting in sarcomere shortening

    • Due to overlap, muscle appears lighter when contract


<p>Sarcomere contracts by sliding of actin and myosin filaments</p><ul><li><p>Muscle → Bundle of muscle fibres → Single muscle fibre → Myofibrils → Sarcomere</p></li><li><p><strong>Myofibrils</strong> = Composed of repeating sarcomeres units; Many of these make up one muscle fiber</p></li><li><p><strong>Sarcomeres</strong> = Long fibrous proteins that are attached to each other end to end; Synchronised movement (One moves, all move) → Shortens muscle fibre / entire muscle</p><ul><li><p>Striations of skeletal muscle = Alternating fibers of myosin and actin</p><p><strong>“I band”</strong> = Thin <strong>actin</strong> filaments = Light</p><p><strong>“A band”</strong> = Thick <strong>myosin</strong> filaments + actin filaments on outer edge = Dark</p></li></ul></li><li><p><strong>Actin</strong> = Round proteins linked in chain to form filament</p></li><li><p><strong>Myosin</strong> = Long thin protein + Movable head; Linked together in bundles to form filament (Multiple heads)</p></li></ul><p></p><ul><li><p>In sarcomere, myosin remains stationary while the actin on both sides move towards the centre using movable heads on myosin</p></li><li><p>When sarcomeres contract, the actin filaments slide over the myosin fibers, resulting in sarcomere shortening</p><ul><li><p>Due to overlap, muscle appears <strong>lighter</strong> when contract</p></li></ul></li></ul><p></p>
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Describe the Process of Muscle Contraction (ERQ Practice) (7 marks)

  1. Action potential in motor neuron triggers release of Ca2+ ions from sarcoplasmic reticulum

  2. Calcium ions bind to troponin on actin and cause tropomyosin to move → Expose bindings sites for myosin heads

  3. Actin filaments and myosin heads form a cross-bridge

  4. ATP hydrolysis breaks cross bridge and myosin heads to change orientation into a high energy configuration

  5. Myosin heads bind to actin filament before returning to original conformation

  6. Repositioning of myosin head moves the actin filaments as well towards the center

  7. Sliding of actin along myosin shortens the sarcomere, causing muscle contractions


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Role of Titin

Titin = Large protein (~27,000 AA)

  • Helps sarcomeres to recoil after stretching (Reset to original position; During contraction, a spring-like tension is present and released when relaxed)

  • Hold myosin fibers in place

  • Prevents muscle from overstretching


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Role of Antagonistic Muscles in Protein Relaxation

Needed because muscle tissue can only exert force when it contracts; If one bone is moved by one muscle, another muscle is required for the opposite movement

  • Contracting = Agonist

  • Relaxing = Antagonist


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Structure and Function of Motor Units in Skeletal Muscle

Motor Unit = A motor neuron are joined to a set of muscle fibres; Strength of contraction ~ Nerve impulse to # of motor units (Motor neuron to muscle fiber ratios range from 1:10 to 1:200)

Consists of…

  • Motor neuron = On one end is the cell body at brain stem or spinal cord; Motor end plate (nerve ending) is connected to muscle cell (at neuromuscular junction)

    • Connect to effectors; Carry response to stimulus

    • Controls set of muscle fibers

    • Neuromuscular junctions = Type of synapse particularly at muscle tissue to simulate contraction

  • Muscle fibres


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Skeletal Framework

Skeletons as anchorage for muscles and as levers

  • In body…

    • Bone = Lever / Joint = Fulcrum / Muscle contraction provides effort force on bone → Moves weight of body part (Load)

      • First-class lever = Contraction of neck muscle pulls on skull → Face rise

      • Second-class lever = Contraction of calf muscle causes ball of foot to pivot → Foot rise

      • Third-class lever = Contraction of bicep muscle acts on elbow jointForearm rises to lift object


Arthropods have exoskeletons; Vertebrates have endoskeletons

<p>Skeletons as anchorage for muscles and as levers</p><ul><li><p>In body…</p><ul><li><p>Bone = Lever / Joint =<strong> </strong><span style="color: green;"><strong>Fulcrum</strong></span><strong> </strong>/&nbsp;Muscle contraction provides <span style="color: red;"><strong>effort force</strong></span><strong>&nbsp;</strong>on bone → Moves weight of body part (<span style="color: blue;"><strong>Load</strong></span>)</p><ul><li><p><strong>First-class lever</strong>&nbsp;= Contraction of <span style="color: red;">neck muscle</span> pulls on&nbsp;<span style="color: green;">skull</span>&nbsp;→ <span style="color: blue;">Face</span> rise</p></li><li><p><strong>Second-class lever</strong>&nbsp;= Contraction of <span style="color: red;">calf muscle</span>&nbsp;causes <span style="color: green;">ball of foot</span> to pivot → <span style="color: blue;">Foot</span> rise</p></li><li><p><strong>Third-class lever</strong>&nbsp;= Contraction of <span style="color: red;">bicep muscle&nbsp;</span>acts on <span style="color: green;">elbow joint</span> → <span style="color: blue;">Forearm</span>&nbsp;rises to lift object</p></li></ul></li></ul></li></ul><p></p><p>Arthropods have <strong>exoskeletons</strong>; Vertebrates have <strong>endoskeletons</strong></p>
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Synovial Joint + Example

Synovial joint = Where two bones need to move against each other; Allows wide range of motions

  • Ball and socket joints (Shoulder and hip) = Can move bones along several axes

    • Abduction (Out) and adduction (In)

    • Flexion (Backward; bending) and extension (Forward; straightening)

    • Rotation

  • Hinge joints (Ankle, elbow, knee) = Can only move along one axis

    • Flexion and extension


Roles of… (in Hip Joint)

  • Bone = Constituents of joint (E.g. Pelvis and femur in ball-and-socket hip joint)

    • Head of femur forms a “ball” that fits within the socket of the pelvis

  • Cartilage = Smooth protective connective tissue; Lines both pelvis and femur at hip joint to avoid bone on bone contact

  • Synovial fluid = Lubricating fluid; Reduces friction in hip joint

  • Ligaments = Tough connective tissue; Holds bones of hip joint in place while allowing range of motion

  • Muscles = Tissues that contract and relax; Controls movement of hip joint

  • Tendons = Connective tissue; Connects muscle (of hip joint) to bone


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Range of Motion ~ Goniometer

Range of motion = Distance and direction joint can move; Measured in degrees

  • Used to document change in joint movement after surgery, etc.


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Example of Antagonistic Muscles

Antagonistic muscle action → Facilitates internal body movements

Different orientations of muscle fibers in the internal and external layers of intercostal muscles mean that they move the ribcage in opposite directions; When one of the layers contract, it stretches the other, storing potential energy in the sarcomere protein titin.

  • External intercostal muscles contract → Pulls rib cage up and outInspiration (Thoracic cavity increase)

  • Internal intercostal muscles contract → Pulls rib cage down and inExpiration (Thoracic cavity decrease)

  • Contraction of one stretches the other → Stores PE in titin of other muscle fibers


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Reasons for Locomotion + Examples (FESM)

  • Foraging for food
    E.g. Honey bees; Fly to collect nectar and pollen

  • Escaping from danger
    E.g. Flying fish; Extend pectoral fins → Glide in water + Swim fast → Evade predator

  • Searching for a mate
    E.g. Loggerhead sea turtle; M & F swim back to “birth beach” to lay eggs

  • Migration
    E.g. Arctic tern; From Arctic breeding grounds → Antarctic region & back for food


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Adaptations for Swimming in Marine Animals

  • Streamlining → Allow dolphin to move through viscous water easily & fast

  • Adaptions of limbs to form flippers → Steering

  • Adaptation of tail to form a fluke → Up and down motion for propulsion

  • Changes to airways into blowhole at the dorsal surface of head → Allow periodic breathing between dives + Avoiding body leaving the water


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Pathogen

Broad range of organisms that cause infectious diseases; Typically reserved for:

  • Viruses (HIV, Measles, Smallpox, Influenza)

  • Bacteria (Salmonella, Cholera, Conjunctivitis)

  • Fungi (Athlete’s Foot)

  • Protists (Malaria - Plasmodium)


(No archaea !!)

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Skin and Mucous Membranes as Primary Defense

Skin = Physical & chemical barrier to pathogens; 2 main layers

  1. Underneath Layer

    Sweat + Oil glands, Capillaries, Sensory neurones, Dermal cells

  2. Top Layer

    Mainly dead cells; New cells move up to replace the dead cells


  • CHEMICAL DEFENSES

    • Secrete antimicrobial peptides → Destroy pathogens

    • Sebaceous glands produce sebum → Maintains skin moisture + Lower pH → Inhibit bacterial growth

    • Lysozymes in sweat → Degrades bacterial cell walls

    • Non-harmful skin microbes inhibit pathogens by competitive exclusion

  • PHYSICAL DEFENSES

    • Continuous → Hard to find opening for pathogens to enter

    • Many layers + tough

    • Dry environment


Mucous membrane = Sticky mucus produce to trap pathogen; Produced by goblet cells

  • Cilia → Helps move pathogens up & out of respiratory tract

  • Found in trachea, nasal passages, vagina, urethra


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Sealing of Cuts in Skin by Blood Clotting

  • Pathogens can enter via cuts, abrasions, or other breaches → Evade immune system + Establish infections


Release of clotting factors from platelets causes a cascade of reactions

⇒ Rapid conversion of fibrinogen → fibrin by thrombin

⇒ Trapping of erythrocytes to form clot

  • Damaged blood vessel cells release clotting factors → Stimulate platelets to stick to damaged area → Forms platelet plug + Cause prothrombin to change into active form → Thrombin

  • Thrombin changes soluble fibrinogen → Insoluble fibrin protein

  • Fibrin fibres adhere to platelet plug + Form mesh which captures blood cells and platelets → Create a clot across wound site

  • In presence of air, clot dried to form scab → Shields healing tissues underneath + Stop blood leaking and entry of pathogen


Note: Fibrinogen and prothrombin are present in blood plasma at all times

<ul><li><p>Pathogens can enter via cuts, abrasions, or other breaches → Evade immune system + Establish infections</p><p></p></li></ul><p>Release of clotting factors from platelets causes a cascade of reactions </p><p>⇒ Rapid conversion of fibrinogen → fibrin by thrombin</p><p>⇒ Trapping of erythrocytes to form clot</p><ul><li><p>Damaged blood vessel cells release <strong>clotting factors</strong> → Stimulate platelets to stick to damaged area → Forms platelet plug + Cause <strong>prothrombin</strong> to change into active form → <strong>Thrombin</strong></p></li><li><p>Thrombin changes soluble <strong>fibrinogen</strong> → Insoluble <strong>fibrin</strong> protein</p></li><li><p>Fibrin fibres adhere to platelet plug + Form mesh which captures blood cells and platelets → Create a clot across wound site</p></li><li><p>In presence of air, clot dried to form scab → Shields healing tissues underneath + Stop blood leaking and entry of pathogen</p><p></p></li></ul><p>Note: Fibrinogen and prothrombin are present in blood plasma at all times</p>
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Innate VS Adaptive Immune System

Innate system (Up to macrophage)

  • Responds to broad categories of pathogens

    • Recognises “self” and “non-self” (e.g. pathogens, pollen, and dust) via antigens (lipoproteins)

  • Does not change during organism’s life; No memory

  • Rapid


Adaptive system (Starting from T-cells)

  • Responds in specific way to particular pathogen

  • Slower to activate

  • Builds up memory of pathogens encountered → Immune response becomes more effective (with age, too)

    • Memory cells = Type of white blood cell formed when first exposed to a pathogen; When exposed to pathogen a second time, memory cells are activated quickly

    • Vaccinations work by training immune system to recognise pathogens


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Infection Control by Phagocytes

Amoeboid movement from blood to infection site

  • Phagocyte = Type of white blood cell (leukocyte) that can move with amoeboid movement, i.e.

    • Squeeze out of capillaries

    • Leave bloodstream to move to body tissues

Phagocytes recognise pathogens → Engulf them via endocytosis → Digest them using enzymes from lysosomes

  • Phagocytosis = Engulfing of molecules with non-self antigens

    • Foreign particles are placed inside vesicle + Digested by enzymes in lysosome


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Lymphocytes

Lymphocytes = Cells in adaptive immune system; Cooperate to produce antibodies

  • Two types → B-lymphocyte (B-cell) & T-lymphocyte (T-cell)

    • B cells = Each individual has a large number of these cells that each make a specific type of antibody

  • Circulate in blood & contained in lymph nodes of the lymphatic system


Antibodies = Y-shaped proteins with a variable region at the tip of the ends acting as a binding site for a specific antigen

NOTE: Some pathogens have multiple antigens and require multiple antibodies for them to be “disabled”

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Antigens

Antigens = Recognition molecules; Trigger antibody production

  • Most antigens are glycoproteins / other proteins usually located on the outer surface of pathogen

  • In the case of the surface antigens of erythrocyte…

    • If the blood is transfused to an incompatible receiver / different blood group, antigens may stimulate antibodies production → Clumping / Agglutination


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Activation of B-lymphocytes by Helper T-lymphocytes

There are many B-cells and Helper T-cells but each are antigen specific

B-cells = Produce antibodies + Become memory cell ONLY when activated

  • Activation = Requires both…

    1. Direct interaction with the specific antigen

    2. Contact with a helper T-cell that has been activated by the same type of antigen


<p>There are many B-cells and Helper T-cells but each are antigen specific</p><p>B-cells = Produce antibodies + Become memory cell ONLY when activated</p><ul><li><p><strong>Activation</strong> = Requires both…</p><ol><li><p>Direct interaction with the specific antigen</p></li><li><p>Contact with a helper T-cell that has been activated by the same type of antigen</p></li></ol></li></ul><p></p>
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Multiplication of Activated B-cells (Plasma B-cells)

Multiplication of B-lymphocyte by mitosis → Form clones of antibody-secreting plasma cells

  • Relatively small number of B-cells respond to a specific antigen

  • Therefore, to produce enough antibodies, activated B-cells first rapidly divide by mitosis to produce lots of plasma B-cells


Plasma B-cells = Capable of producing same type of antibody; Have…

  • Large amount of cytoplasm + rough ER, ribosomes, and Golgi → Produce large amounts of antibody proteins


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Immune Response (FULL)

  1. Macrophage engulfs pathogen and presents its antigen

  2. Helper T-cell imprints pathogen antigen(s)

~~~~~~~~~~~~

  1. B-cell has a random antibody that binds to the pathogen antigen BY CHANCE

  2. B-cell also engulfs pathogen and presents its antigen on the surface

~~~~~~~~~~~~

  1. Helper T-cell with imprint binds to the B-cell with antigen in order to activate it

  2. B-cell differentiates into plasma B-cells and divide

  3. Plasma B-cell produces lots of antibodies to bind to pathogen and neutralise it by marking them for destruction


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Immunity (Memory Cells) & Primary / Secondary Immune Response

Immunity = Consequence of retaining memory cells; Ability to eliminate an infectious disease from body

  • Due to long-term survival of lymphocytes (memory cells) capable of making specific antibodies needed to fight the infection


Memory (B/T) cells = Formed after initial infection / vaccination; Remain in body long-term

  • Provide rapid and robust response to subsequent exposures to same pathogen → Secondary immune response


Primary immune response = Takes time (B/T cells must be activated)

Secondary immune response = Faster + Produce more antibodies than first exposure

<p>Immunity = Consequence of retaining memory cells; Ability to eliminate an infectious disease from body</p><ul><li><p>Due to long-term survival of lymphocytes (<strong>memory cells</strong>) capable of making specific antibodies needed to fight the infection</p></li></ul><p></p><p><strong>Memory (B/T) cells </strong>= Formed after initial infection / vaccination; Remain in body long-term</p><ul><li><p>Provide rapid and robust response to subsequent exposures to same pathogen → <strong>Secondary immune response</strong></p></li></ul><p></p><p>Primary immune response = Takes time (B/T cells must be activated)</p><p>Secondary immune response = Faster + Produce more antibodies than first exposure</p>
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Transmission of HIV in Body Fluids

HIV = Human immunodeficiency virus; Gradually attacks immune system

  • Leads to AIDS

  • Transmission must involve body fluids, e.g.

    • Blood, semen, rectal fluids, vaginal fluids, breastmilk

  • Mechanisms of HIV transmission include…

    • Unprotected sex, birth, breastfeeding, blood transfusion, contaminated needles, (rarely) across placenta

  • HIV positive mothers can reduce the risk by…

    • Taking antiretroviral medications during pregnancy

    • Avoid breastfeeding


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Infection of Lymphocytes by HIV with AIDS as a Consequence

Only certain types of lymphocytes are infected and killed

Reduction in these lymphocytes limits the ability to produce antibodies and fight opportunistic infections

  • HIV infect helper T-cells → Cannot activate B-cells → Unable to produce antibodies and fight off other infections → AIDS (Acquired immune deficiency syndrome)

  • HIV is monitored by measuring T cell count and viral load

  • Antiretroviral therapy (ART) can be used to control HIV → Allow immune system to recover


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Antibiotics

Antibiotics = Chemicals that block processes occurring in bacteria BUT not in eukaryotic cells

  • Stop chemical pathways unique to prokaryotes → Eukaryotic cells are unaffected

  • Affects…

    • Cell wall and membranes

    • Protein synthesis

    • DNA/RNA synthesis

Antibiotics fail to control infection with viruses because…

  • Viruses have no metabolism; Cannot be affected


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Evolution of Resistance to Several Antibiotics in Strains of Pathogenic Bacteria

Careful use of antibiotics is necessary to slow the emergence of multi-resistant bacteria

  • Antibiotic resistance occurs when bacteria mutate and no longer respond to drugs; Accelerated by overuse and misuse of antibiotics

    • Can be developed via mutations or horizontal gene transfer (Resistance spreads between bacteria of same and different species)


E.g. MRSA = Superbug

  • Threat to public health; Lead to longer illness, more hospital stays, increased mortality


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Zoonoses

Zoonoses = Infectious diseases that can be naturally transferred from vertebrate animals to humans

  • Highly prevalent; ~60% emerging infectious diseases globally are zoonoses → High economic burden (Healthcare costs + Loss of productivity)


Examples:

  • Tuberculosis

    • Primarily human disease, can be transmitted through infected animals, especially cattle

    • Transmitted via inhalation of aerosols

  • Rabies

    • Viral disease spread through the bite of an infected animal

  • Japanese encephalitis

    • Mosquito-borne viral infection

    • Reservoirs of virus = Pigs & wild birds

  • COVID-19

    • Caused by SARS-CoV-2 virus

    • Reservoirs of virus = Bats

    • Spread through human via intermediate host at a wildlife market

    • Primarily spreads through respiratory particles released by infected person


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Vaccines and Immunisation

Vaccines contain antigens, or nucleic acids with sequences that code for antigens → Stimulate the development of immunity to a specific pathogen without causing disease

  • Vaccines introduce antigens / genetic instructions to produce antigens into body, which simulates an infection → Triggers immune system to produce T-cells and antibodies + Memory cells which recognise and fight pathogen in future exposure

    • Live vaccines use a weakened form of the pathogen

    • Inactivated vaccines contain the “killed” version of the pathogen

    • mRNA vaccines use mRNA to instruct cells to produce a protein that triggers an immune response

  • Immunisation = Process of developing immunity without disease symptoms


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Herd Immunity and Prevention of Epidemics

Members of a population are interdependent in building herd immunity

  • Herd immunity = Occurs when large portion of community become immune to disease, preventing spread from person to person

    • Protects those who cannot be vaccinated e.g. immunocompromised patients and newborns

If a sufficient % of a population is immune too a disease, transmission is greatly impeded

  • For highly contagious diseases, e.g. measles, ≥95% of population must be immune to stop spread


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Evaluation of Data related to COVID 18 (% Change VS Difference)

Percentage change = Two values over time

Difference/Original * 100

Percentage difference = Two values at the same time

Difference/(Average of two values)*100