Ms. Terkper's Digital Classroom

Human Systems — Ms. Terkper's Digital Classroom
Bio 20 — Unit D
Overview Digestive Respiratory Enzymes Circulatory Defence Blood Excretory Motor Indigenous Knowledge Practice
Biology 20 — Unit D

Human Systems

Ms. Terkper's Digital Classroom — Themes: Energy, Equilibrium, Matter & Systems

Focusing Questions

"How do specialized structures function in the overall biochemical balance of the living system? What conditions result if these structures do not function normally? How does knowledge of living systems and medical technology support the prevention and treatment of disorders?"

General Outcomes

20-D1:Explain how the human digestive and respiratory systems exchange energy and matter with the environment.
20-D2:Explain the role of the circulatory and defence systems in maintaining an internal equilibrium.
20-D3:Explain the role of the excretory system in maintaining an internal equilibrium through exchange of energy and matter with the environment.
20-D4:Explain the role of the motor system in the function of other body systems.

Key Concepts

Digestive SystemRespiratory SystemDigestive EnzymesGas ExchangeCirculatory SystemBlood CompositionImmune ResponseABO/Rh Blood GroupsRenal FunctionNephronADH & AldosteroneMuscle ContractionActin & Myosin

Unit Overview

Maintenance of metabolic equilibrium in organisms involves a number of physical and biochemical processes. The human organism is used as a model system to examine how energy and matter are exchanged with the environment through digestion, gas exchange, excretion, circulation and the function of the motor system. A defence system contributes to equilibrium by eliminating pathogenic organisms. This unit represents approximately 40% of the time allotted for Biology 20.

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Digestive System

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Respiratory System

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Enzyme Action & Factors

How Enzymes Work

Enzymes are biological catalysts — proteins that speed up biochemical reactions by lowering the activation energy. They are specific: each enzyme has a unique active site that fits a specific substrate (induced-fit model). Enzymes are not consumed in reactions and can be reused.

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Substrate binds to active site: The substrate molecule enters the enzyme's active site. The active site's shape is complementary to the substrate (like a lock and key, but the induced-fit model acknowledges slight conformational changes occur).
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Enzyme-substrate complex forms: Weak intermolecular bonds (hydrogen bonds, ionic interactions) hold the substrate in place. The enzyme stabilizes the transition state, lowering activation energy.
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Products released: Chemical bonds in the substrate are broken or formed. Products no longer fit the active site, so they are released. The enzyme returns to its original shape and is ready for another substrate.
General Enzyme Reaction
Enzyme + Substrate → [E-S Complex] → Enzyme + Products
Enzyme is regenerated; reaction rate greatly increased vs uncatalysed reaction

Types of Inhibition

Competitive Inhibition

An inhibitor molecule has a similar shape to the substrate and competes for the same active site. Binding blocks the substrate from entering. Effect can be overcome by increasing substrate concentration (more substrate molecules outcompete the inhibitor). Example: some antibiotics (sulfonamides) competitively inhibit bacterial enzymes by resembling their natural substrates.

Feedback (Non-Competitive) Inhibition

The inhibitor binds to an allosteric site (different from the active site), changing the enzyme's shape. This distorts the active site so the substrate can no longer fit. Used in metabolic regulation — the product of a pathway inhibits an earlier enzyme, preventing overproduction. Example: ATP inhibits phosphofructokinase in glycolysis when cellular energy is high.

Irreversible Inhibition

Inhibitor binds covalently and permanently to the enzyme (or active site), permanently inactivating it. Example: organophosphate pesticides irreversibly inhibit acetylcholinesterase (nerve agent mechanism). Cyanide irreversibly inhibits cytochrome c oxidase in the ETC.

Enzyme Activity Simulator

Relative Activity

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Circulatory System

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Defence System (Immune Response)

Lines of Defence

First Line — Non-Specific Physical Barriers
  • Skin: Physical barrier; low pH (slightly acidic, ~5.5) inhibits bacterial growth; sebaceous glands secrete antimicrobial fatty acids; keratin layer is waterproof and impermeable to pathogens
  • Mucous membranes: Line respiratory, digestive, urinary tracts; trap pathogens in mucus; cilia sweep particles up and out
  • Secretions: Saliva, tears, gastric acid (pH 1.5–3.5) kill many pathogens
Second Line — Non-Specific Internal Defences
  • Phagocytes (macrophages, neutrophils): Engulf and digest pathogens; macrophages also present antigens to T cells
  • Inflammation: Damaged cells release histamine → vasodilation, increased capillary permeability, recruitment of phagocytes to infection site
  • Fever: Elevated body temperature inhibits pathogen reproduction and enhances immune cell activity
  • Interferons: Proteins released by virus-infected cells; warn neighbouring cells to produce antiviral proteins
  • Complement proteins: Cascade of plasma proteins that lyse pathogens or mark them for phagocytosis (opsonization)
Third Line — Specific Adaptive Immunity
  • Lymphocytes (B cells and T cells): Recognize specific antigens; mount targeted responses; retain immunological memory
  • Cell-mediated immunity (T cells): Killer T cells directly destroy infected cells; helper T cells coordinate immune response
  • Humoral immunity (B cells): B cells produce antibodies that neutralize or tag antigens

Key Immune Cells — Click to Expand

Notable Pathogens & Society's Response (Alberta Context)
PathogenTypeDisease / EffectImmune Mechanism ExploitedTechnology / Societal Response
Staphylococcus aureusBacteriumSkin infections, pneumonia, sepsis; MRSA strains are antibiotic-resistantProduces toxins that destroy phagocytes; protein A blocks antibody bindingAntibiotic stewardship programs; hand hygiene campaigns; MRSA surveillance in Alberta hospitals
Smallpox virusVirus (Variola)Historically devastating; 30% mortality; last natural case 1977Attacked cellular immune response; pockmarked scars = immune battlegrounds in skinJenner's smallpox vaccine (1796) — first vaccine ever; WHO eradication declared 1980. First demonstration of herd immunity.
Escherichia coli O157:H7BacteriumHemolytic uremic syndrome; kidney failure; 2000 Walkerton, ON outbreak killed 7Shiga toxin destroys kidney endothelial cells; resists stomach acidMunicipal water treatment standards strengthened; Alberta beef industry E. coli testing protocols
HIVRetrovirusAIDS; destroys helper T cells (CD4+); leaves body unable to fight other infectionsSpecifically infects and destroys helper T cells, collapsing entire adaptive immune responseAntiretroviral therapy (ART); no cure but viral load suppression; pre-exposure prophylaxis (PrEP); significant stigma-reduction efforts
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Blood Groups, Transfusion & Compatibility

ABO Blood Group System

Blood type is determined by specific antigens (glycoproteins) on the surface of red blood cells. The immune system naturally produces antibodies against the antigens it does not have. This is called the ABO system.

Blood TypeAntigens on RBCAntibodies in PlasmaCan Donate ToCan Receive From
AA antigensAnti-B antibodiesA, ABA, O
BB antigensAnti-A antibodiesB, ABB, O
ABBoth A and B antigensNeither (no antibodies)AB onlyA, B, AB, O (Universal Recipient)
ONeither A nor BBoth Anti-A and Anti-BA, B, AB, O (Universal Donor)O only

What Happens in a Transfusion Reaction?

If incompatible blood is transfused, the recipient's antibodies bind to antigens on the donated red blood cells → agglutination (clumping). Agglutinated RBCs cannot carry oxygen and block capillaries → haemolysis (bursting of RBCs) → kidney damage, potentially fatal. This is why blood type matching before transfusion is critical.

Rh Factor

The Rh (Rhesus) factor is another antigen on red blood cells. People with the Rh antigen are Rh+ (positive); those without are Rh- (negative). Unlike ABO, Rh- people do not naturally have anti-Rh antibodies — they only develop them after exposure to Rh+ blood.

Rh Incompatibility in Pregnancy (Erythroblastosis Fetalis)

If an Rh- mother carries an Rh+ fetus: during first pregnancy, small amounts of fetal blood may enter maternal circulation. Mother's immune system produces anti-Rh antibodies. In a second Rh+ pregnancy, maternal antibodies cross the placenta and destroy fetal RBCs, causing hemolytic disease of the newborn. Prevention: Rh- mothers receive Rho(D) immune globulin (RhoGAM) during pregnancy/delivery, which destroys fetal RBCs before the mother's immune system can respond, preventing sensitization.

Blood Compatibility Checker
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Excretory System & Renal Function

Excretory System Overview

The excretory system removes metabolic waste products (primarily urea from amino acid catabolism, uric acid, CO2, excess water and ions) from the blood, maintaining plasma composition, water balance, pH, and blood pressure.

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Kidneys (paired): Main excretory organs. Filter blood, reabsorb useful substances, secrete additional waste, produce urine. Located retroperitoneally on either side of the vertebral column in the posterior abdomen.
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Ureters: Muscular tubes carrying urine from each kidney to the urinary bladder via peristaltic contractions.
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Urinary bladder: Muscular reservoir that stores urine (capacity ~400–600 mL). Stretch receptors trigger the micturition reflex. Transitional epithelium allows stretching.
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Urethra: Carries urine from bladder to exterior. Two sphincters: internal (involuntary smooth muscle) and external (voluntary skeletal muscle). Shorter in females (~4 cm) than males (~20 cm) — hence higher UTI risk in females.

Metabolic Wastes Excreted

WasteSourceExcretion route
UreaAmino acid catabolism (deamination) in liver; ammonia converted to urea (ornithine cycle)Kidneys (major); sweat (minor)
CO2Cellular respiration (Krebs cycle)Lungs (respiratory system)
WaterMetabolic water + dietary water + cellular reactionsKidneys, lungs, skin
Uric acidNucleic acid catabolismKidneys; excess causes gout (joint deposits)
CreatinineCreatine phosphate breakdown in musclesKidneys (useful marker of kidney function)
Bile pigments (bilirubin)Haemoglobin breakdown (haem group)Liver → bile → intestines; gives faeces brown colour

Nephron — The Functional Unit of the Kidney

Each kidney contains approximately 1 million nephrons. Each nephron performs filtration, reabsorption, secretion, and water conservation. Click each part to learn its function.

ADH (Antidiuretic Hormone / Vasopressin)

Source: Hypothalamus (produced), released by posterior pituitary gland.
Stimulus: High plasma osmolarity (dehydration); sensed by hypothalamic osmoreceptors. Also released by low blood pressure, pain, stress, and alcohol/caffeine (inhibit ADH → increased urination).

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Dehydration detected → hypothalamus releases ADH
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ADH acts on collecting duct: Increases water permeability by inserting aquaporin channels into tubule cell membranes
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More water reabsorbed from filtrate back into blood → small volume of concentrated urine produced
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Negative feedback: Blood osmolarity returns to normal → ADH secretion decreases → less water reabsorption → more dilute urine

Aldosterone

Source: Adrenal cortex (zona glomerulosa).
Stimulus: Renin-angiotensin-aldosterone system (RAAS) activated by low blood pressure/volume → kidneys release renin → angiotensinogen → angiotensin II → adrenal cortex releases aldosterone. Also stimulated directly by high K+ in plasma.

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Low blood pressure/volume detected by juxtaglomerular cells → renin released
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Angiotensin II formed (via ACE in lungs) → stimulates adrenal cortex
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Aldosterone released: Increases Na+ reabsorption in distal tubule; water follows Na+ osmotically → blood volume and pressure rise
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K+ is excreted in exchange for Na+ reabsorption. ACE inhibitors (blood pressure drugs) block angiotensin II formation, reducing aldosterone and blood pressure.
Kidney Failure Technologies: Dialysis Comparison
FeatureHemodialysisPeritoneal DialysisKidney Transplant
How it worksBlood removed, filtered through dialysis membrane (semipermeable), waste diffuses into dialysate, clean blood returnedDialysate solution infused into peritoneal cavity; peritoneum acts as natural membrane; waste diffuses across, fluid drainedFunctional donor kidney surgically implanted (usually lower abdomen); donor may be living or deceased; patient's own kidneys usually left in place
Frequency/time3 sessions/week, 3–5 hours each; done in dialysis centreDaily (continuous ambulatory peritoneal dialysis, CAPD) or overnight (CCPD); can be done at homePermanent; follows normal kidney schedule once functioning
AdvantagesEfficient; medically supervised; good for high-risk patientsMore flexible; home-based; fewer dietary restrictions; gentler on cardiovascular systemBest long-term quality of life; most similar to normal kidney function; no machine dependence
Disadvantages/risksAccess-site infections; AV fistula required; cardiovascular stress; dietary restrictions strictPeritonitis risk; less efficient; requires manual dexterityLifelong immunosuppressants required; organ shortage; surgical risks; rejection
Alberta contextAlberta Kidney Care provides dialysis centres across the provinceCAPD program allows Albertans in remote communities to avoid travelAverage wait time in Alberta: 4–8 years. Living donors (often family members) reduce wait time significantly.
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Motor System

Three Types of Muscle Tissue

Sliding Filament Theory — Actin and Myosin

Muscle contraction is explained by the sliding filament theory (Huxley & Hanson, 1954). Thick myosin filaments "walk" along thin actin filaments using ATP as energy, shortening the sarcomere (the functional unit of a myofibril). The filaments themselves do not shorten — they slide past each other.

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Nerve impulse arrives at neuromuscular junction: Acetylcholine (ACh) released from motor neuron terminal → binds to receptors on muscle cell membrane → action potential generated.
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Calcium release: Action potential travels into T-tubules → stimulates sarcoplasmic reticulum to release Ca2+ into cytoplasm.
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Tropomyosin moves: Ca2+ binds to troponin (on actin filament), causing tropomyosin to shift and expose myosin-binding sites on actin.
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Cross-bridge formation: Myosin head (already energized from ATP hydrolysis → ADP + Pi) binds to exposed actin site.
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Power stroke: Myosin head pivots, pulling actin filament toward centre of sarcomere. ADP and Pi released. Sarcomere shortens → muscle contracts and generates force.
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Detachment: New ATP molecule binds to myosin head → myosin detaches from actin. ATP hydrolyzed → myosin head re-cocked. Cycle repeats as long as Ca2+ and ATP are present.
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Relaxation: When nerve impulse stops, Ca2+ pumped back into sarcoplasmic reticulum (active transport, requires ATP). Tropomyosin covers actin sites. Cross-bridges cannot form → muscle relaxes.

ATP's Role in Muscle Function

  • Cross-bridge cycling: Each power stroke consumes one ATP (myosin ATPase). A single step requires 1 ATP; a whole-body sprint burns millions of ATP per second.
  • Ca2+ reuptake: SERCA (sarcoplasmic/endoplasmic reticulum Ca2+-ATPase) pumps Ca2+ back — consumes ATP.
  • Na+/K+ pump: Restores membrane potential after action potential — consumes ATP.
  • Heat production: Only ~25% of ATP energy produces mechanical work; ~75% released as heat. Muscle activity is the body's primary heat source; shivering is rapid muscle contraction specifically for heat generation.
  • Rigor mortis: After death, ATP production stops. Myosin heads remain bound to actin (cannot detach without ATP) → muscles stiffen (rigor). Resolves after 24–48 hours as proteins begin to decompose.

Pathologies of the Motor System

ConditionDescriptionTreatment
Muscle atrophyLoss of muscle mass from disuse, immobilization, or denervation. Muscle fibres shrink (decrease in myofibril number/size).Physical rehabilitation, resistance training, electrical stimulation
Muscle fatigueTemporary inability to produce force after prolonged activity. Causes: lactate accumulation, depleted creatine phosphate/ATP, ionic imbalance (K+, Ca2+ disturbance).Rest, hydration, nutrition (carbohydrate replenishment)
Muscle strainOverstretching or tearing of muscle fibres or the muscle-tendon unit. Grades I–III based on severity of tear.RICE protocol (Rest, Ice, Compression, Elevation); physiotherapy; surgical repair for Grade III
TendonitisInflammation of a tendon (connective tissue connecting muscle to bone). Often overuse injury. Example: Achilles tendonitis in runners.NSAID anti-inflammatories, physiotherapy, eccentric exercise programs, corticosteroid injections
Anabolic steroidsSynthetic androgens increase muscle protein synthesis; increase lean body mass and strength. Side effects: liver damage, cardiovascular disease (LDL increase, HDL decrease), hormonal disruption, mood effects ("roid rage"), adolescent growth plate closure.Banned in competitive sport; no medical treatment for misuse except supportive care
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Indigenous Knowledge & Human Systems

Traditional Knowledge of Health, Healing & the Human Body

Alberta's First Nations, Métis and Inuit peoples developed sophisticated observational understanding of human and animal physiology long before Western medicine. These knowledge systems are recognized directly in the Alberta Biology 20 Program of Studies.

Observing Animal Excrement for Health Assessment

The Alberta Biology 20 curriculum (Outcome 20-D1.4s) specifically references the traditional practice of Aboriginal peoples and ranchers observing the excrement of game and farm animals to assess their health. This is a sophisticated application of understanding excretory system function: urine and fecal composition reflect kidney function, hydration status, diet, metabolic state, and the presence of parasites or pathogens.

  • Cree hunters assessed bison and caribou health from droppings before harvesting — avoiding animals showing signs of disease, parasites, or starvation (indicated by changes in fecal colour, consistency, frequency).
  • Blackfoot people monitored elk and deer through urine markings during the rut — strong urine odour and deep colouration indicating good health and reproductive fitness.
  • Modern veterinary equivalence: Fecal egg counts for parasites, urinalysis for renal function, fecal flotation tests — all validate the observational approach developed by indigenous people over millennia.
  • Alberta ranchers: This knowledge persists in contemporary ranch management; experienced ranchers assess cattle health from manure colour, consistency, and frequency — traditional ecological knowledge and veterinary science aligned.

Traditional Respiratory Remedies

The curriculum (Outcome 20-D1.4s) notes research into cultural contributions to understanding respiration and healing, including traditional remedies for respiratory illness. Many First Nations peoples developed plant-based respiratory treatments that modern pharmacology has validated:

  • Yarrow (Achillea millefolium): Used by numerous First Nations including Cree and Blackfoot for colds, fever, and respiratory infections. Contains azulene (anti-inflammatory) and camphor (bronchodilator).
  • Sweetgrass (Hierochloe odorata): Smudging with sweetgrass reduces airborne microorganism levels. Research at University of Alberta has begun confirming antimicrobial properties.
  • Wild bergamot (Monarda fistulosa): Used by Plains peoples for respiratory conditions; contains thymol and carvacrol — compounds now used in commercial antiseptic mouthwashes (thymol is the active ingredient in Listerine).

Understanding of Nutrition and Digestive Health

Traditional diet knowledge encoded understanding of macronutrient balance: bison provided complete protein (all amino acids) + fat-soluble vitamins; berries provided carbohydrates and antioxidants; organs (liver, kidney) provided iron, zinc, B12. Fermentation was used across cultures to pre-digest foods (e.g., fermented fish, bannock leavened with natural yeasts), reducing digestive load and increasing bioavailability of nutrients — knowledge now understood through enzyme biochemistry.

Contributions from Various Cultures to Understanding Digestion & Respiration

Ancient Egyptian Medicine

Ebers Papyrus (~1550 BCE) documents treatments for digestive disorders. Egyptian physicians understood the stomach as a "cooking vessel" processing food. First recorded descriptions of intestinal parasites and their treatments.

Traditional Chinese Medicine

Detailed understanding of circulatory system in Huang Di Nei Jing (~200 BCE) — 2,000 years before Harvey's description of blood circulation. Acupuncture points mapped along meridians corresponding to major nerve and vascular pathways now understood anatomically.

Inuit Physiology Knowledge

Inuit understanding of thermoregulation (motor system heat production) enabled survival in extreme cold. Knowledge of brown fat in marine mammals and how high-fat diets support aerobic metabolism for heat generation predates scientific discovery of adaptive thermogenesis.

Islamic Golden Age Medicine

Ibn Sina (Avicenna, ~1020 CE) described pulmonary circulation in Canon of Medicine — 400 years before Vesalius. Ibn al-Nafis correctly described how blood flows through the lungs for oxygenation, contradicting Galen's 1,400-year-old claim of interventricular pores.

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Interactive Practice & Review

Knowledge Check Quiz

12 questions covering all four human systems.

Bio 20 — Unit D

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Structure Match

Match each structure on the left to its correct system and function on the right.

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Vocabulary Flashcards

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