Physiology and Respiration Flashcards Preview

Biology > Physiology and Respiration > Flashcards

Flashcards in Physiology and Respiration Deck (61):

Digestive System

  1. Absorption: Movement of a fluid or dissolved substances across a membrane
  2. Assimilation: Conversion of nutrients into fluid or solid parts of an organism

A image thumb


  1. Peristalsis: Continuous segments of smooth muscle (longitudinal & circular) rhythmically contracting & relaxing, causing food to move unidirectionally along alimentary canal from mouth to anus. 
  2. Circ. muscles contract behind food to constrict gut & prevent food from being pushed back towards mouth, whilst long. muscle contract perp. to food location, moving food along gut. 
  3. Contractions controlled unconsciously by enteric nervous system rather than brain. 
  4. Segmentation (peristalsis in stomach/small intestine) contractions move chyme bidirectionally allowing for greater mixing of food with dig. juices


Label Cross-Section of Small Intestine/Ileum. 

  1. Serosa: Protective outer coat composed of layer of cells reinforced by fibrous connective tissue.
  2. Muscle layers: Layer of long. muscle (peristalsis) & inner layer of circ. muscle (segmentation)
  3. Sub-mucosa: Layer composed of connective tissue separating muscle layer from mucosa; contains blood and lymph vessels. 
  4. Mucosa: Highly folded innermost layer with epithelium on its inner surface that absorbs nutrients from intestinal lumen.

A image thumb

Digestive Enzymes

A image thumb

Villi Features (MR SLIM)

  1. Microvilli: Ruffling of epithelial membrane further increases surface area
  2. Rich blood supply: Dense capillary network rapidly transports absorbed products
  3. Single layer epithelium: Minimises diffusion distance between lumen and blood
  4. Lacteals: Absorbs lipids from the intestine into the lymphatic system
  5. Intestinal glands: Exocrine pits (crypts of Lieberkuhn) release digestive juices
  6. Membrane proteins: Facilitates transport of digested materials into epithelial cells


Digestion of compounds

  1. Triglycerides:
    1. Triglucerides digested into fatty acids and monoglycerides by lipase. 
    2. Absorbed into villus epithelial cells by simple diffusion or fac. diff. (by carriers).
    3. Fatty acids re-combine with monoglycerides to produce triglycerides, which prevents diffusion back into lumen of small intestine.
    4. Triglycerides merge with cholesterol to form fat droplets, coated by phospholipids & protein = lipoproteins
    5. Lipoproteins released through plasma membrane (exocytosis) on inner side of villus epithelium cells.
    6. Lipoproteins enter lacteal & are carried away in lymph or enter blood capillaries in villi.
  2. Starch:

    1. 1,4 bonds in amylose & amylopectin (starch) broken by amylase in saliva into mixture of maltose (2-glucose) & maltotriose (3-glucose) fragments.
    2. Amylase can’t break 1,6-bonds in amylopectin, forms dextrins (1,6 fragments). 
    3. Microvilli membranes in small int. contain maltase, glucosidase & dextrinase to digest maltose, maltotriose & dextrins into glucose & complete dig. of starch. 
    4. Glucose abserbed to villus capillary, which carries blood to venules in sub-mucosa of small intestine wall. 
    5. Hepatic portal vein then takes venule blood to liver, where excess gluc. absorbed by liver cells & assimilated to glycogen for storage. 

  3. Proteins: 


William Harvey's Heart


  1. William Harvey discovered the circulation of blood, with arteries & veins belonging to same blood network.
  2. Showed that valves in the veins/heart ensure unidirectional flow of blood
  3. Predicted existence of capillaries.
  4. Showed that blood wasn't consumed by body (proposed by Galen)
  5. Showed that Galen's theories were false.



  1. Arteries: Carry blood at high press. from ventricles to body tissues.

  2. Artery Wall composed of several layers: 
    1. Tunica externa: Tough outer layer, has collagen that prevents artery ruptures.
    2. Tunica media: Thick layer, has smooth muscle & elastic fibres made of elastin.
    3. Tunica intima: Smooth endothelium forming artery lining.
  3. Tunica Media tissue:
    1. Elastic Fibres: Store EPE by stretching at systolic press. & use EPE at diastolic press. to propel blood along artery & maintain high press. 
    2. Smooth Muscle Fibres: Rigidify arterial wall to handle high blood press., without rupturing; & determine lumen diameter by contracting/relaxing, which affects press. between pumps & helps maintain blood press. throughout cardiac cycle.

    3. Both tissues contribute to wall toughness, needed to withstand constantly changing & intermittently high blood press. without forming outward bulge or bursting.

  4. Arterial Flow:

    1. Heart expels blood upon ventricular contraction & flows through arteries at high press. in pulses.

    2. Circ. (smooth) muscle in arterial wall form ring that contracts, which dec. lumen diameter --> inc. pressure of blood entering arteries to systolic levels --> blood exerts press. onto arterial wall, forcing elastic fibres in wall to stretch & expand, thus storing elastic PE. 

    3. When circ. muscles dilate (further along artery), lumen diameter inc. --> dec. blood press. in arteries to diastolic levels --> artery returns to norm. size (elastic recoil) using EPE, which propels blood along artery, saving energy & preventing diastolic press. becoming too low.

A image thumb


  1. Veins: Veins collect blood from body tissues & return it at low press. to heart atria.
  2. Vein flow: 
    1. Venous wall thinner as it contains less smooth muscle (and elastic fibres), so lumen is wider --> dec. press. --> allows more blood to enter vein at once. 
    2. Blood continuously progresses along arteries (not via periodic pulses)
    3. Flow usually assisted by gravity. But when it's not, press. also exerted onto venous walls by (dec. its press. and inc. flow) :
      1. Periodic contraction of skeletal muscles adjacent to veins. 
      2. Bulges of arteries parallel to vein 
  3. Valves: Gates that ensure unidirectional blood circulation using press. changes caused by arterial bulges & skeletal muscle contractions to prevent backflow of blood.

    1. If blood starts to flow backwards, caught in valve flaps → fill with blood, blocking vein lumen.

    2. When blood flows towards heart, flaps pushed to sides of vein (valve opens) & blood flows freely.



  1. Capillaries: Narrowest blood vessels that exchange materials between cells in body tissues & blood travelling at low press.
  2. Capillaries Structure:
    1. Small diameter, inc. body cap. for capill., which dec. diff. distance & allows for optimal exchange of nutrients.
    2. Capill. wall made of single endothelium layer → short diffusion distances.
    3. Also surrounded by basement membrane that is permeable to necessary materials.
  3. Capillary Flow: 
    1. Branching: Artery → arteriole → capillary 
      (network) → (pool into) venules → vein.
    2. Extensive branching + lumen narrowing 
      inc. total vol. of vessels  dissipate high arterial blood press.  blood flows through capill. slowly & at low press. to allow for max. material exchange. 
    3. Hydrostatic press. at arteriole end of capill. > blood osmotic press. → forces nutrients from blood into plasma, which
      leaks from capill. pores at body tissues.

    4. Hydrostatic press. at venule end of capill. < blood osmotic press. → forces
      waste from tissues (e.g. CO2 + urea) to enter bloodstream. 

  4. Capillaries structure & permeability varies depending on its location in body & specific role, as well as in time:
    1. Capillary wall maybe continuous with endothelial cells held together by tight junctions to limit perm. of large molecules.
    2. In absorption-specialised tissue (e.g. intestines, kidneys), capillary wall fenestrated → leaks out tissue fluid (plasma containing nutrients).
    3. Sinusoidal capillaries have open spaces between cells, so permeable to larger molecules & cells (e.g. in liver)
    4. Permeabilities change over time as capill.
      repair & remodel in response to current
      needs of tissues that they perfuse.


Vessel Comparision

A image thumb

Heart Structure

  1. Heart has 2 sides, L & R, that pump blood to systemic & pulmonary circulations.

  2. Each side has 2 chambers: 

    1. Atrium is smaller chamber, collects blood from veins & transfers it to ventricle.

    2. Ventricle is large chamber, pumps blood out into arteries.

  3. Each side has 2 valves:

    1. Atrioventricular Valve between atrium & ventricle:
      1. Bicuspid on L
      2. Tricuspid on R
    2. Semilunar Valve between ventricle & artery:
      1. Aortic on L
      2. Pulmonary on R
  4. Blood Vessels:
    1. Vena Cava (inferior & superior): Returns deoxygenated blood from body into RA. 
    2. Pulmonary Artery: Sends deoxygenated blood to lungs from RV. 
    3. Pulmonary Vein: Returns deoxygenated blood from lungs into LA. 
    4. Aorta: Sends oxygenated blood around body from LV.


Heart Contractions

  1. Heart contractions are myogenic, meaning that cardiac muscle cells generate their own signal for contractions, rather than relying on motor neurone stimulation. 
  2. SAN: Small cluster of specialised cardiac muscle cells with extensive membranes in RA wall; have fastest rate of depolarisation. Initiate & control rate at which heart beats.
  3. Extensive SAN cell membranes depolarise
    upon contraction → activates adjacent cells, which also contract, etc. → electrical impulse to spread throughout atria walls.
  4. SAN initiates each heartbeat, as SAN cell membranes are first to depolarise in each cardiac cycle, & control rate of heartbeat depending on rate of depolarisation. 



  1. SAN regulated by medulla oblongata (in cardiovascular centre).

  2. Cardiovascular centre receives inputs from receptors monitoring blood press, its pH & [O2]
  3. Sympathetic nerves speed up rate of SAN depolarisation by releasing noradrenaline →
    inc. rate of myocardial contraction when low blood press, [O2] & pH → inc. rate of blood flow to tissues → inc. O2 delivered + CO2 taken
  4. Parasympathetic nerves slow up rate of SAN
    depolarisation by releasing acetylcholine → 
    dec. rate of myocardial contraction when high blood press, [O2] & pH → dec. rate of blood flow to tissues  dec. Odelivered + COtaken
  5. Adrenalin: Hormone secreted by adrenal glands → inc. rate of SAN depolarisation.
    • Secretion controlled by brain
    • Secreted when vigorous physical activity required for a threat or opportunity.
  6. Interference of pacemakers lead to irregular & uncoordinated contraction of heart muscle (fibrillation), which may only be re-established with controlled electrical current (defibrillation)
  7. Defective SANs require artificial pacemakers placed under skin with electrodes implanted in RA wall to initiate heartbeats in place of SAN.


Cardiac Cycle

  1. Deoxygenated blood returns from all parts of body (except lungs); enters RA via vena cava. AV valve is open; SL valve is closed. 
  2. SAN contracts + depolarises, sending elec. impulse → stimulates myocardium contraction
  3. Myocardium contractions spread signal throughout atrial walls → L & R atria contract 
  4. Atria contractions → inc. atrial press. > ventricular press. → Only AV valves open → 
    blood pumped to ventricles. 
    • Also spread signal to junction between atria & ventricles → stimulates AV node contraction + depolarisation.
    • Time delay exists between atria contraction & impulse transmission, allowing time for ventricles to fill.
  5. AV node sends impulses, via nerve fibres, down septum → spreading signal throughout ventricular walls → ventricles contract.
  6. Meanwhile, atrial press. dec. as ventricular press. inc. until < ventricular press. as blood continues to flow in them, but no blood pumped in → AV valves close to prevent backflow of blood & further inc. ventricle press.
  7. Ventricle contractions → inc. ventricular press. > aortic press. → SL valves open → Blood pumped into aorta.
  8. Meanwhile, vena cava feeding atria → inc. 
    atrial press, causing them to fill until atrial press. > ventricular press.
    • Occurs as ventricle contraction dissipates → ventricle press. dec. < aortic press. → SL & AV valves closed. 
    • AV valve re-opens once ventricle press.
      > atrial press. to repeat cycle.
  9. Cycle ensures delay between atria & ventricle
    contractions, resulting in 2 heart sounds due to
    closing of AV valves (1st), then SL valves (2nd)

A image thumb

Heart Disease

  1. Coronary Arteries: Surround heart & nourish cardiac muscle to keep heart working
    1. Blood pumped through heart is at high press, so can’t be used to supply cardiac muscle with O2 & nutrients
    2. If coronary arteries become occluded, One of the causes being atherosclerosis in coronary arteries. 
  2. Coronary Occlusion: Narrowing of arteries that supply blood containing O2 & nutrients to cardiac muscle → region of tissue nourished by blocked artery to die & cease to function.
    1. Caused by Atherosclerosis: Hardening & narrowing of arteries due to development of atheroma (fatty deposits) in artery wall adjacent to endothelium.
  3. Causes of atherosclerosis:
    1. Low Density Lipoproteins (LDL) accumulate in atheroma. 
    2. Phagocytes then attracted by signals from endothelium cells and smooth muscle.
    3. Phagocytes engulf fats & cholesterol by endocytosis & grow  artery wall bulging into lumen  dec. diameter of lumen 
      restricts blood flow → inc. arterial press. → stresses arterial wall → damage.
    4. Damaged region repaired with smooth muscle → dec. artery wall thickness → 
      forms lesions, which trigger blood clots if ruptured. 
  4. Consequences of atherosclerosis:
    1. May lead to coronary thrombosis, which causes CHD if in cor. arteries.
    2. Lack of O2 (anoxia) from blocked coronary arteries causes pain (angina), & impairs myocardial tissue’s ability to contract →
      heart beats faster to maintain blood circulation with some of its muscle out of action. Heart beats irregularly (fibrillation) & if fully blocked → heart attack.
    3. Coronary artery blockages usually treated by by-pass surgery or creating a stent.
    4. Coronary Thrombosis: Clot formation within coronary arteries.

      1. Coronary occlusion, damage to capillary epithelium, hardening of arteries, & atheroma ruptures all inc. risk. 

      2. Factors affecting risk of coronary thrombosis and heart attacks:


        High [blood cholesterol]

        High blood pressure



        Lack of exercise 

        But correlation doesn’t produce causation. 

  5. Factors associated with inc. risk of CHD:
    1. Age: Blood vessels become less flexible with advancing age
    2. Genetics: Having hypertension inc. chance of developing CHD. 
    3. Obesity: Being overweight places an additional strain on the heart
    4. Diseases: Certain diseases increase the risk of CHD (e.g. diabetes)
    5. Diet: Diets rich in saturated fats, salts and alcohol increases the risk
    6. Exercise: Sedentary lifestyles increase the risk of developing CHD
    7. Sex: Males are at a greater risk due to lower oestrogen levels
    8. Smoking: Nicotine causes vasoconstriction, raising blood pressure


Skin & Mucous Membranes

  1. Skin & mucous membranes form primary defence against pathogens causing infections.
  2. Skin:
    1. Thick outermost layer made of keratin, which is hard & tough, provides physical barrier to physical and chemical damage as well as direct entry to pathogens.
    2. Sebaceous Glands: Associated with hair follicles, secrete sebum, which maintains skin moisture and slightly lowers pH, which inhibits growth of bacteria & fungi.

    3. Skin also secretes lactic & fatty acids to lower pH, also inhibits microbial growth.

  3. Mucous Membranes: Thinner & softer membranes found in nasal passages, head of penis, & foreskin of vagina. Secretes mucus, tears, saliva, etc.
    1. Mucus: Sticky glycoprotein solution
      that traps pathogens & harmful particles (which are swallowed or expelled).
    2. Mucus has antiseptic properties as it contains lysosyme, which destroys cell walls & causes cells to lyse. 
    3. Mucous membranes maybe ciliated to aid in removal of pathogens (along with phy. actions like coughing / sneezing)


Blood Clotting

  1. Clotting: Mechanism by which broken blood vessels are repaired when damaged. Prevents blood loss from body & limits pathogenic access to bloodstream when skin is damaged.
  2. Blood clotting involves cascade of reactions, each of which produces catalyst for next reaction, stimulated by clotting factors released from damaged cells (extrinsic pathway) & platelets (intrinsic pathway)
  3. Clotting strictly controlled by catalysts as it occurs inside blood vessels & may cause blockages.
  4. Vessel lining injury triggers clotting factor release.
  5. Clotting factors:
    1. Activate platelets (blood-circulating cellular fragments) → structural change → form sticky aggregates, which adhere to damaged region to form plugs.
    2. Cause localised vasoconstriction to dec. blood flow through damaged region
    3. Catalyse prothrombin → thrombin (enzymes), which catalyses (soluble) fibrinogen → (insoluble) fibrin (proteins)
    4. Fibrin strands form fibre mesh in cuts, trapping more platelets & blood cells around platelet plug.
  6. Final clot initially a gel, but dries to form hard scab if exposed to air, prevents pathogen entry.



  1. Phagocytes provide 2nd line of defence:
    1. Phagocytes squeeze out through capillary wall pores & move to infection sites in response to chemicals released by damaged tissues. 

    2. Phagocytes surround & engulf pathogen, by forming int. vesicle with pathogen in it.

    3. Vesicle then fused to lysosome within & 
      pathogen digested using lysozyme.

    4. Large numbers of phagocytes attracted by infected wounds, resulting in pus.

    5. Phagocytes = non-specific & respond to infection always in same way.


Antibodies provide 3rd line of defence: 

  1. MHC: Chemical that body recognises as "self", is tolerated by immune system.
  2. Antigen: Chemical that body recognises as foreign, stimulates immune response.
  3. Antibodies: Y-shaped proteins made by B-cells specific to a given antigen. 2 functional parts:
    1. Hyper-variable region that binds to specific antigen, diff. between antibodies.
    2. Another region that helps prevent viruses from docking to host cells so that they can’t enter cells and opsonisation (PANIC):
      1. Precipitation: Soluble pathogens →
        insoluble for easier phagocytosis.
      2. AgglutinationClumping of cellular pathogens for easier removal
      3. NeutralisationAntibodies may occlude pathogenic regions.
      4. Inflammation: Trigger inflammatory response within body
      5. Complement ActivationActivates
        (complement) prots that cause lysis.
      6. PANI aids opsonisation & phagocytosis, whilst C causes lysis.
    3. Antibodies = specific & target response specific to given pathogen (so adaptive).

​Clonal Selection:

  1. Non-specific immune cells (macrophages) engulf & digest pathogens non-selectively.
  2. Some macrophages (dendritic cells) present antigen of pathogen to specific Helper T-cell. 
  3. Helper T-cell binds & is activated by antigen.
  4. Cytokines stimulate specific B cell that produces antibodies to specific antigen to divide & form clones (clonal selection).
  5. Most of clones develop into short-lived plasma cells that produce lots of specific antibody.
  6. Some clones differentiate into long-lived memory cells that provide long-term immunity.
    1. If 2nd infection with same pathogen occurs, memory cells react + vigorously
      to produce antibodies faster.

    2. Antibodies produced faster > pathogen reproduces → not enough to cause disease symptoms.

  7. Polyclonal Activation: Single pathogen stim.
    several diff. T + B lymph. to produce diff. 
    specific antibodies. (occurs as it has >1 antigen)


  1. Pathogen: Agent that causes disease – either a microorganism, virus or prion

  2. Pathogens are generally species-specific in that their capacity to cause disease is limited to a particular species.

  3. Polio, syphilis, measles = diseases caused by pathogens that specifically affect human hosts 
  4. Zoonoses: Animal diseases that can be transmitted to humans.
  5. Rabies (dogs), Bird flu (birds) & bubonic plague (rats) = diseases caused by zoonoses.
  6. Transmission of infectious diseases occur via:

    1. Direct Contact: Transfer of pathogens via physical contact or fluid exchange.

    2. Contamination: Ingestion of pathogens growing on, or in, edible food sources

    3. Airborne: Pathogens transferred in air via coughing & sneezing

    4. Vectors: Intermediary orgs that transfer pathogens without dev disease symptoms themselves (e.g. mosquitoes, rats).



Allergen: Env. substance that triggers localised
immune response (exposure region) despite not being harmful in practice

Anaphylaxis: Severe systemic allergic reaction; can be fatal if left untreated.

Allergic Reaction split into 2 parts:

  1. Allergen first enters bloodstream
  2. Specific B cell differentiates into plasma cells, which make antibodies that attach to mast cells
  3. When allergen re-enters bloodstream, it binds to antibodies in mast cells, which release 
    1. ↑ Permeability → swelling (due to + fluid leaking from blood) & pain (swelling causes compression of nerves)

    2. Vasodilation → redness + heat as blood closer to skin.

    3. Inflammation → ↑ leukocyte mobility to infected regions. 



  1. Human Immunodeficiency Virus (HIV): Retrovirus that infects & destroys helper T cells, causing patients to progressively lose ability to produce antibodies. 
  2. HIV = retrovirus, so has RNA genes & uses reverse transcriptase to make DNA copies of its genes once it exerts host helper T-cell.
  3. Following infection, virus undergoes period of inactivity during which infected helper T cells reproduce. 
  4. Eventually, virus becomes active again, destroying helper T-cells & begins to spread. 
  5. Anti-Retroviral drugs slow down rate of Helper T-cell destruction.
  6. AIDS: Acquired Immune Deficiency Syndrome when syndrome of conditions (due to HIV killing helper T-cells) present.
  7. With dec. in helper T-cell#, antibodies unable to be produced, resulting in lowered immunity, allowing opportunistic infections to strike, which usually kill patient if not managed.
  8. AIDS spreads by blood to blood contact:
    1. Sex contact, during which abrasions to mucous membranes of penis and vagina can cause minor bleeding.
    2. Infected blood transfusion
    3. “Sharing of hypodermic needles by intravenous drug users”.
  9. Reduced by: 
    1. Using latex protection (e.g. condoms) dec. risk of exposure through sex contact.
    2. Small minority immune to HIV infection. 
    3. HIV = global, but rather prevalent in poorer nations with poor education & health systems.



  1. Vaccine: Weak pathogen form containing
    enough antigens to stim. memory cell prod. but not enough to cause disease.
  2. When exposed to actual pathogen, memory cells trigger more potent 2º immune response, which prevents disease symptoms from dev.(individual becomes immune to pathogen)
  3. Length of immunity to infection after vacc. depends on how long memory cells survive for
  4. Memory cells may not survive lifetime & indiv. 
    may need booster shots to maintain immunity.
  5. Vaccination confers immunity to vaccinated individuals but also indirectly protects non-vaccinated individuals via herd immunity
  6. Herd Immunity: Immunity to pathogen given to unvacc. indiv. by lots of immune indivs that vac.


Monoclonal Antibodies

  1. Monoclonal antibodies: Artificial antibodies 
    made from a single B cell clone.
  2. Mouse injected with antigen & produces antigen-specific plasma cells.
  3. Plasma cells removed & fused (hybridised) with tumor cells capable of endless divisions
  4. Resulting hybridoma cell capable of synthesising lots of monoclonal antibody.

Therapeutic Use:

  1. Effective emergency treatment for rabies.

  2. Targets cancer cells body’s own immune cells fail to recognise as harmful.

Diagnostic Use:

  1. Pregnancy test via hCG presence in urine
  2. hCG produced by women during foetal dev, so
    monoclonal antibodies ind. hCG in urine.
  3. Pregnancy tests use a process called ELISA to identify substance via colour change:
    1. 1st set of hCG-specific monoclonal antibodies bound to enzyme "dye".
    2. 2nd set of hCG-specific monoclonal antibodies bound to dye substrate.
    3. hCG in urine binds to both monoclonal antibody sets → bringing enzyme
      + sub. together → changing dye colour.
    4. 3rd set of monoclonal antibodies bind any unattached enzyme-linked antibodies = control.


Antibiotics and Penicillin and Resistance

  1. Antibiotic: Chemical that kills/inhibits bacteria growth by targeting specifically prokaryote metabolic pathways, so don't kill human cells. 

  2. Processes targeted:

    1. Bacterial DNA Replication, Transcription and/or Translation

    2. Ribosome function

    3. Cell Wall formation.

  3. Viral diseases not killed by antibiotics as they lack metabolisms & rely on chemical processes (e.g. DNA trans.) of living host cell, which can’t be targeted as host cell also damaged.

  4. Antivirals: Drugs that target & inhibit viral enzymes & thus, don't damage host cell. 


  1. Penicillin: 1st antibiotic discovered, by Alexander Fleming.

  2. Discovery was accident: Unintended contamination of dish containing S. aureus stimulated Penicillium mould to grow on plate & halo of inhibited bacterial growth observed around mould.

  3. Fleming concluded that mould was releasing penicillin, which killed nearby bacteria.

  4. Medical applications of penicillin as an antibiotic later demonstrated by Sir Howard Florey & Ernst Chain:

    1. 8 mice injected with pathogenic bacteria & ½ subsequently injected with penicillin.

    2. Untreated mice died of bacterial infection whilst penicillin-treated mice survived – showing its antibiotic potential

    3. After finding penicillin chem. structure + extensive human-testing, synthetic derivatives created (e.g. methicillin) for use as antibiotics that offer benefits like:

      1. Greater tolerance

      2. Greater stability

      3. Broader spectrum


  1. Measures required to avoid antibiotic resistance in bacteria: 

    1. Doctors prescribing antibiotics only for serious bacterial infections.

    2. Patients completing courses of antibiotics to eliminate infections completely.

    3. Hospital staff maintaining high standards of hygiene to prevent cross-infection.

    4. Farmers not using antibiotics in animal feeds to stimulate growth.

    5. Pharmaceutical companies developing new antibiotic types. 


Alveoli and Pneumocytes


  1. Alveoli: Site of gas exchange.
    1. Have very thin epithelial layer to dec. diffusion distances for respiratory gases
    2. Surrounded by rich capillary network to inc. the cap for gas exchange with blood
    3. Roughly spherical in shape, inc. available SA for gas exchange
    4. Internal surface covered with layer of fluid, as dissolved gases diffuse better into bloodstream.
  2. Pneumocytes: cells that line alveoli & comprise of majority of inner surface of lungs. 2 types:
  3. Type I: Very thin & flat cells involved in gas exchange between alveoli & capillaries.
    1. Dec. diff. distance for O2 & CO2
    2. Connected by occluding junctions that prevent tissue fluid leakage into alveolar air space.
    3. Amitotic & unable to replicate, 
  4. Type II: Cuboidal cells that possess many granules that secrete pulmonary surfactant. 
    1. Surfactant create moisture lining on inner alveolar surface → dec. surface tension:
      1. As alveoli expands with gas intake, surfactant becomes more spread out across moist alveolar lining. → inc. surface tension & slows rate of expansion → all alveoli inflate at roughly same rate.
      2. Moisture prevents alveoli walls from adhering when air exhaled. 
    2. Mitotic & able to differentiate into type I cells if required.
    3. Also provides area from which CO2 can evaporate into air and be exhaled.



  1. Inhalation: (NOTE: AWM = Ab Wall Muscles)
    1. AWM relax, pushed outwards, causing diaphragm to contract, flattening;
    2. Ext intercostal muscles contract, pulling ribcage upwards and outwards.
    3. Int intercostal muscles relax, are pulled back to their elongated state.
    4. All of these cause thorax vol. to inc, which lowers press in thorax
    5. Air moves from high to low press, so air rushes into lungs.
  2. Exhalation: (NOTE: AWM = Ab Wall Muscles)
    1. AWM contract, causing diaphragm to relax & move upwards into dome shape.
    2. Ext. intercostal muscles relax, are pulled back to their elongated state. 
    3. Int. intercostal muscles contract, pulling ribcage downwards & inwards.
    4. All of these cause thorax vol to dec, which inc. press. in thorax.
    5. Air moves from high to low press., so air rushes out of lungs.


Lung Disease Causes and Consequences

  1. Lung Cancer: Uncontrolled lung cell production, leading to abnormal growth of lung tissue (tumour)
    1. Causes:
      1. Tobacco smoke contains many mutagenic chemicals, so incidence of lung cancer tends to inc. with no. of cigarettes smoked per day.
      2. Passive Smoking: Non-smokers inhaling tobacco smoke exhaled by smokers.
      3. Air pollution from diesel exhaust fumes, NOx from vehicle exhaust fumes & smoke from burning coal, wood or other organic matter.
    2. Consequences:
      1. Breathing difficulties, persistent coughing, coughing up blood, chest pain, loss of appetite, weight loss, general fatigue.
      2. Lung cancers usually too large & have metastasised upon discovery, so morality rates high.
      3. All/part of affected lung maybe 
        surgically removed, together with radiotherapy or chemotherapy, if lung cancer discovered early enough
      4. Most patients who do have lung parts removed still have breathing difficulties, fatigue & anxiety about possible return of disease.
  2. Emphysema: Alveolar walls lose their elasticity due to damage to alveolar walls

    1. Causes: 

      1. Phagocytes exist within alveoli produce elastase, which digests protein in pathogens. Also breaks down elastic fibres in alveolar wall, so inhibitor needed to prevent this. 

      2. Chemical irritants in cigarette smoke damage alveolar walls --> inc. no. of phagocytes in lungs --> produce more elastase --> breaks down more elastic fibres in alveolar wall. 

      3. Small proportion of emphysema cases due to hereditary deficiency of enzyme inhibitor for elastase (breaks down elastic fibres in alveolar wall) due to gene mutation.

    2. Consequences:

      1. Loss of elasticity results in abnormal enlargement of alveoli, leading to lower total SA for gas exchange

      2. Degradation of alveolar walls may cause holes to develop & alveoli to merge into huge air spaces

      3. Damage to alveoli irreversible, causing dec [O2] & inc [CO2] in blood

      4. Common symptoms of emphysema include shortness of breath, phlegm production, inc. susceptibility to chest infections, lack of energy. 


Measuring Change in Ventilation

Change in Ventilation

  1. Ventilation in humans changes in response to levels of physical activity, as body’s energy demands are increased
  2. ATP production (via cellular respiration) produces CO2 as waste product (& may consume oxygen aerobically).
  3. Changes in blood CO2 levels detected by chemosensors in arterial walls, which send signals to brain.
  4. As exercise intensity inc., so does demand for gas exchange, leading to inc. ventilation.

Exercise influences ventilation in 2 ways:

  1. Tidal Volume: Volume of air drawn in and expelled, allowing for more gas exchange.
    1. Count no. of times air exhaled or inhaled per min, breathing should be maintained at natural rate, which is as slow as possible without getting out of breath.
    2. Inflatable chest belt placed around thorax; air pumped in with bladder; differential pressure sensor in belt measures pressure changes inside belt due to chest expansions --> rate.
  2. Ventilation Rate: Number of times air is drawn in or expelled per minute, allowing for more continuous gas exchange
    1. 1 normal breath exhaled through delivery tube into pneumatic trough & vol. measured using bell jar with graduations. Unsafe for repeated inhaling/exhaling as [CO2] rises too high.
    2. Spirometers measure flow rate into & out of lungs & from these measurements, lung volumes can be deduced. 
  3. Variables:

    1. IV = Type/intensity of exercise or activity 

    2. DV = Ventilation parameter (ventilation rate or tidal volume)


  1. Nervous system consists of neurons that carry electrical impulses and CNS. 3 neuron types:
    1. Sensory: Conduct nerve impulses from receptors to CNS.
    2. Relay: Conduct nerve impulse within CNS
    3. Motor: Conduct nerve impulses from CNS to effectors.
  2. All 3 contain:
    1. Dendrites: Short branched nerve fibres, used to transmit impulses between neurons or CNS.
    2. Axons: Elongated nerve fibres, used to transmit impulses usually to effectors/from receptors.
    3. Cell Body: Contains nucleus and other organelles needed for cell metabolism.
  3. Some neurons are myelinated:

    1. Myelin Coat: Insulating fatty layer inc.
      conduction speed of elec. impulses along axon via saltatory conduction.

    2. Schwann Cells: Deposit myelin by growing round nerve fibre. 

    3. Nodes of Ranvier: Gap between myelin deposited by adjacent Schwann Cells. 

    4. Saltatory Conduction: Nerve impulse jumps between nodes of Ranvier in myelinated fibre, rather than sequentially.

      1. Faster than unmyelinated fibres.

      2. But needs + space in enclosed env. 

A image thumb


  1. Resting Potential (RP): V across membrane of neuron not transmitting nerve impulse. = -70mV
    1. Antiport Na/K pumps transfer 3Na+ out of neuron & 2K+ in.
    2. Membrane also more permeable to K+ ions than Na+, so K+ leaks back across membrane faster than Na+ 
    3. Above factors create [grad.] for both ions, [Na+] grad. steeper than [K+] grad. →
      unequal distribution of charge/ion on diff. sides of membrane → RP.
    4. Additionally, proteins inside nerve fibre are — charged → inc. charge imbalance.
  2. Action Potential (AP): Rapid change in membrane pot, occurs when neuron is firing. 
    Consist of 3 phases:

  3. Depolarisation: Rapid change in membrane pot. from — to +

    1. Na+ channels in axon membrane open due to local currents/signal initiated at dendrite

    2. Na+ diffuses into neuron (as conc. lower inside) until inside turns + relative to outside +30mV. Reverses imbalance.

  4. Repolarisation: Rapid change in membrane pot. back from + to —.

    1. Na+ channels close & K+ channels open in membrane

    2. K+ ions diffuse out of neuron (as conc. lower outside) until membrane pot. fallen to —70mV. 

    3. RP not restored yet as [gradients] of Na+ and K+ not re-established yet.

  5. Refractory Period: Period of time to restore [grad] after nerve impulse until neuron fired again. RP restored with antiport Na+/K+ pump.


Propagation of Impulse

  1. Depol. occurs when V-gated ion channels (so respond to changes in pot.) open & cause change in membrane pot.
  2. Thus, depol. at 1 axon part dec. [Na+] out axon & inc. [Na+] in axon → producing diff. [Na+] to neighbouring unpol. axon part → Na+ diffuses between regions (LC):
    1. Inside: Higher [Na+] in depol. part, so Na+ diffuse along inside axon to neighbouring part yet to be pol.
    2. Outside: Lower [Na+] in depol. part, so Na+ diffuse from pol. part back to depol. part.
  3. LC’s dec. [Na+] grad. in non-pol. part → pot. inc.
    from RP to TP (-50mV) → opens V-gated Na+ channels in neighbouring axon part’s memb
    → depolarisation.
  4. Hence, depolarisation spreads along length of axon as unidirectional ‘wave’ = propagated AP.


  1. Oscilloscopes: Sci instruments used to measure membrane pot. across axon membrane.
  2. Membrane potentials in neurons measured by placing electrodes on each side of membrane.
  3. Potentials displayed using oscilloscope or in graph (X = time (ms) and Y = membrane V (mV))
  4. Undershoot = refractory period.
    1. RP:  Before AP occurs, neuron should be in state of rest (approx. –70 mV)
    2. Depol:  Rising spike corresponds to depol. (approx. +30 mV)
    3. Repol:  Falling spike corresponds to repol. (approx. –80 mV)
    4. Ref. period:  Undershoot until membrane pot. back to RP (approx. –70 mV).

A image thumb

Synaptic Transmission

  1. Synapses: Physical gaps that separate neurons from other neurons or effector cells.
    1. AP reaches axon terminal → triggers opening of V-gated Ca2+ channels.
    2. Ca2+ diffuse into PESN & promote vesicles (with NT) to move to, & fuse with cell memb.
    3. NT’s released from axon terminal by exocytosis, cross synaptic cleft & bind to specific POSM receptors
    4. POSM ligand-gated Na2+ channels open → Na+ diffuses ↓ [Na+] grad. into POSN, → POSM reaches TP. 
    5. AP triggered in POSM & propagated along POSN.
    6. NT’s released into synapse either recycled (by reuptake pumps) or degraded (by enzymes).
  2. Summation: Agregation of AP's in POSN.
    1. Graded Potential: Change in membrane pot. caused by ligand-gated Na+ channels.

    2. Excitatory NT's (e.g. noradrenaline): cause POSN depol. by opening Na2+ channels.

    3. Inhibitory NT's (e.g. GABA): cause POSN hyperpol. by opening Cl¯ channels.

    4. Effect of all NT's acting on target POSN 
      determines whether TP reached.
      → synapses tend to have many PESNs. 

    5. 3 types of summation:

      1. Cancellation: Excitatory + inhibitory GP's cancel out → TP not reached
        → Na+ in POSN pumped out by Na/K pumps → POSM returns to RP. 

      2. Spatial Summation: Excitatory GP's generated from many PESN's at same time to reach TP.

      3. Temporal Summation: Excitatory GP's generated from single PESN in quick succession.

    6. Summation aids processing of info from different sources in body & helps in decision-making.



  1. Acetylcholine: NT produced at neuromuscular junctions, binds to muscle fibre receptors, triggers muscle contraction. Usually released within ANS to promote parasympathetic responses.
    1. Created in PESN by combining choline (from diet) with an acetate group (metabolic product). 
    2. Acetylcholine broken down into components by releasing synaptic enzyme AChE into synapse or embedding enzyme on POSM, as overstimulation can lead to fatal convulsions and paralysis. 
    3. Once broken down, choline recycled & re-coupled with another acetate group.
  2. Neonicotinoids: Synthetic compounds that bind to ACh receptors in insect cholinergic synapses & trigger a sustained response. 

  3. AChE can’t break down neonicotinoids →
    irreversible binding → perm. overstimulation of target cells → convulsions + paralysis.

  4. Neonicotinoid not as toxic to mammals as:

    1. Mammals use proportionally less cholinergic synapses than insects. 

    2. Neonicotinoids bind less strongly to ACh receptors in mammals than in insects. 

  5. Concern is that it may kill pollinators (e.g. bees and butterflies) and birds (due to loss of insects), so some countries (e.g. EU) have restricted use of neonicotinoid pesticides.


  1. Body needs glucose to make ATP (via cell resp.), but amount needed fluctuates according to demand
  2. High [glucose] in blood damages cells (creates hypertonicity), so [glucose] regulated by 
    hormones released from pancreatic pits (but
    act mainly on liver).
  3. Diabetes: Metabolic disorder caused by high blood [glucose] over prolonged period

A image thumb

Hypothalamus Hormones

A image thumb

Sexual Reproduction

  1. One of earliest theories as to how animals reproduce sexually was 'soil and seed' theory proposed by Aristotle: 

    • Male produces ‘seed' that forms ‘egg' when mixed with menstrual blood (‘soil’)

    • ‘Egg’ develops into fetus inside mother according to info contained within male 'seed’ alone.

  2. ‘Soil + seed’ popular until debunked by William Harvey, who studied sexual organs of ♀ deer after mating to identify developing embryo.
  3. William Harvey shot deer at diff. stages of mating season & dissecting each deer to investigate sexual organs (e.g. uterus). 
  4. Unable to detect growing embryo until months after mating had occurred, rather than spontaneously after mating).
  5. He concluded that Aristotle’s theory was incorrect & that menstrual blood didn't contribute to fetal dev.
  6. Harvey unable to identify correct mechanism of sex. reproduction & incorrectly asserted that fetus didn't develop from mix of male & female ‘seeds’.

  7. Now known that fetus forms from combo of both ♂ + ♀ ‘seeds’ (gametes).


Sex Development

  1. Humans have 46 chromosomes in all diploid somatic cells: 

    • 22 autosomal pairs

    • 23rd pair are sex chromosomes (X or Y)

  2. ♀ possess 2 copies of X, while ♂ possess 1 X & shorter Y chromosome.

  3. Y contains gene (SRY), which codes for testis-determining factor (TDF), which causes embryonic gonads to form into testes.

  4. Without TDF protein/Y, embryonic gonads dev. into ovaries.

  5. ♂ & ♀ gametes produce diff. hormones to promote further dev. of sex characteristics:

    1. Testes produce test. to promote further dev. of male sex traits.

    2. Ovaries produce estrogen & prog. to promote dev. of female sex traits.

  6. Testosterone: Main ♂ reproductive hormone secreted by testes:

    1. Responsible for pre-natal ♂ gonad dev.

    2. Involved in sperm prod. following onset of puberty

    3. Aids in dev. of 2º sex traits (e.g. body hair, muscle mass, deepening of voice, etc.)

    4. Helps maintain ♂ sex drive (libido)

  7. Oest + Prog: Main ♀ reproductive hormones secreted initially secreted by mom’s ovaries,
    then placenta until ♀ reprod. organs (e.g. ovaries) dev. (in absence of test.).

    1. Promote pre-natal dev. of ♀ reprod.

    2. Aids in dev. of 2º sex traits (e.g. body hair, hip widening, breast dev.).

    3. Involved in monthly prep. of egg release after puberty (via menstrual cycle)


Male Reprod. System

Q image thumb

  1. ♂RS: Organs responsible for spermatogenesis + organs involved in semen synth. (used to transport sperm during copulation).


  1. Structures are organised according to the path taken by sperm (from production to release)

  2. Testes: responsible for spermatogenesis (♂ gamete) & test. prod. (♂ sex hormone)

  3. Epididymis: Site where sperm matures & devs
    motility – mature sperm stored here until ejac

  4. Vas Deferens: Long tube that conducts sperm from testes to prostate (connects to urethra) during ejac.

  5. Seminal Vesicle: Secretes fluid with fructose (to nourish sperm) & mucus (to protect sperm)

  6. Prostate Gland: Secretes alkaline fluid to neutralise vaginal acids (or else they die).

  7. Urethra: Conducts sperm/semen from prostate + urine to outside of body via penis.

A image thumb

Female Reprod. System

Q image thumb

  1. ♀RS: Includes organs responsible for oogenesis (female gamete) + organs involved in initially dev. & maintaining embryo during early preg. stages.
  2. Structures organised according to path taken by egg (from production to implantation or elimination)

  3. Ovary: Where oocytes mature prior to release (ovulation) – it also responsible for oest. + prog

  4. Fimbria (plural: fimbriae): Fringe of tissue adj. to ovary that sweep oocyte into oviduct

  5. Oviduct: Transports oocyte to uterus – also typical fertilisation site.

  6. Uterus: Organ where fertilised egg will implant & develop (to become an embryo)

  7. Endometrium: Mucous membrane lining of uterus - thickens in prep. for implantation or
    otherwise lost (via menstruation)

  8. Vagina: Passage leading to uterus by which penis can enter (uterus protected by muscular opening (cervix)).

A image thumb

  1. Menstrual cycle: Recurring changes that occur within ♀RS to make pregnancy possible.
  2. Each cycle lasts roughly 1 month & begins at puberty, before ending with menopause
  3. 2 key hormone groups that control & 
    coordinate menstrual cycle:
    1. Pituitary hormones (FSH + LH): Released from anterior pituitary gland & act on ovaries to develop follicles.
    2. Ovarian hormones (Oest + Prog): Made by ovaries & act on uterus to prepare for preg.

Menstrual Cycle Events:

  1. FSH secreted from ant. pit. & stim. follicle dev.

  2. Follicle: Single egg with surrounding cells that nourish & protect it. Secretes oestrogen.

  3. Oest. secreted inhibits FSH secretion (– feedback) to prevent other follicles growing.

  4. Oest. stim. endometrium thickening & ant. pit. gland to secrete LH (& some FSH) (+ feedback).

  5. Large LH surge → rupturing of follicle → 2º oocyte within follicle released (ovulation).

  6. Ruptured follicle dev into slowly degen. corpus luteum, which secretes prog (+ oest), which stim. endo. thicken. for pot. embryo implant.

  7. Both prog. & oest. inhibit LH/FSH secretion, which prevents any follicles from developing. 

  8. If fert. occurs, zygote/developing embryo will implant in endometrium & release hCG to maintain corpus luteum.

  9. If fertilisation doesn’t occur, corpus luteum eventually degen [oest + prog] ↓ and 
    endometrium can't be maintained anymore.

    1. Endometrium shed from body as menstrual blood (i.e. period)

    2. ↓[prog + oest] can't inhibit ant. pit anymore → FSH secreted again (cycle restarts).



  1. Stop normal menstrual cycle (with drugs delivered in form of nasal spray) by down regulating FSH + LH secretion → oest + prog.
  2. Hormone (FSH) injection → many follicles dev
    → follicles then treated with hCG to stim. maturation → superovulation. 

  3. Extract multiple eggs from ovaries 
  4. Sperm collected from sperm donor, then prepared (via capacitation).
  5. Fertilisation (external) of eggs + sperm, which are incubated to control conditions, then eggs analysed for successful fertilisation).
  6. Implantation of multiple healthy embryos into uterus (either patient or surrogate) following 
    PRO treat. to develop endometrium.
  7. Test for pregnancy after some weeks passed.


Small Pox

  1. Smallpox was 1st  human infectious disease to have been eradicated via vaccination.
  2. Smallpox targeted for eradication by WHO, via global vaccination programme
  3. Eradication of smallpox by vaccination was successful because:
    1. Smallpox easily ID'd due to overt clinical symptoms → limited pot. transmission.
    2. Transmission only occurred via direct contact + no animal vectors to sustain 
      infectious agent.
    3. Short lived infection period & virus was stable → didn’t mutate into alt. strains.
    4. Global cooperation & immunity was long-term so repeated booster shots unnec.


Elbow Joint


  1. Biceps: Bends arm (flexor)
  2. Triceps: Straightens arm (extensor)


  1. Humerus: Anchors muscle.
  2. Radius: Transmits forces from biceps through forearm. 
  3. Ulna: Transmits forces from triceps through forearm.


  1. Cartilage: Layer of smooth & tough tissue that covers ends of bones where they meet, to ↓ 
    friction, also absorbs shock & distributes load.
  2. Ligament: Hold humerus, ulna & radius in proper alignment.
  3. Synovial Fluid: Provides food, O2 & lubrication
    to cartilage & ↓ friction.
  4. Joint Capsule: Seals joint space & provides passive stability by limiting range of movement


Sarcomere Structure

A image thumb

Muscle Contraction

  1. Sliding of myosin filaments & actin filaments cause sarcomere contractions, which in turn cause muscle contractions.
  2. Motor neuron sends AP along sarcolemma, which releases acetylcholine, which allows AP to pass to sarcoplasmic reticulum → Ca2+ released upon stimulation.
  3. Ca2+ binds to troponin; causing troponin + tropomyosin to move, which exposes myosin binding sites on actin molecules;
  4. Myosin heads bind to actin, forming cross-bridges.
  5. ATP then binds to myosin heads → cross-bridges break & myosin head released.
  6. ATP hydrolysed into ADP + Pi at each cross-bridge → myosin heads bend; → actin pulled towards centre of sarcomere; → sarcomere shortens;
  7. Cycle of events repeated during muscle contraction, then Ca2+ reabsorbed & muscle relaxes.


Osmoregulators and Osmoconformers

  1. Osmoregulators: Animals that maintain constant int. [solute] even if their env. has diff. conditions.

E.g. Terrestial animals

  1. Osmoconformers: Animals whose int. [solute] is about same same as the environment's. 

E.g. Jellyfish



Malpighian Tubules

  1. In animals, excess AA broken down to N-waste, which must be excreted. Insects excrete uric acid.
  2. Insect's body cavity filled with fluid 
  3. [Solute] maintained by branches from posterior region of hindgut (Malpighian Tubules).
  4. Substances absorbed into tubules in hemolymph:
    • Na+ + K+ absorbed by AT.
    • Urea + AA's absorbed by diffusion.
    • H2O absorbed by osmosis.
  5. Tubules empty into hindgut, where some ions actively reabsorbed, & some water follows.

  6. Dehydrated uric acid paste excreted with faeces in a semi-solid form.


Draw Kidney + Annotate Nephron

Bowman’s Capsule: Cup-shaped structure with highly porous inner wall, which collects fluid filtered from blood.

PCT: Highly twisted section of nephron, with cells in wall having many mitochondria and microvilli projecting into tubule lumen.

Loop of Henlé: Consists of descending limb carrying filtrate deep into medulla of kidney and ascending limb that brings it back out to cortex.

DCT: Another highly twisted section, but with fewer, shorter microvilli and fewer mitochondria.

Collecting Duct: Wider tube carrying filtrate back through cortex and medulla to renal pelvis.

Blood Vessels (in order of where blood flows first):

  1. Afferent Arteriole: Brings blood from renal artery to kidneys
  2. Glomerulus: Tight, knot-like, high-pressure capillary bed - site of filtration.
  3. Efferent Arteriole: Narrow vessel restricting blood flow, helping to generate high pressure in glomerulus.
  4. Peritubular Capillaries: Low-pressure capillary bed that runs around convoluted tubules, absorbing fluid from them.
  5. Vasa Recta: Unbranched capillaries similarly shaped like loop of Henlé, with descending limb carrying blood deep into medulla and ascending limb bringing it back to cortex.
  6. Venules: Carry blood to renal vein.

A image thumb

Bowman's Capsule

  1. Blood is at high press. in capillaries, as efferent & afferent arteries are at diff diameters.
  2. Plasma forced out of capillaries into Bowman's Capsule.
  3. Ultrafiltration occurs through fenestrations in capillaries. Only fluid passes through basement membrane. Almost all large proteins remain in blood. Podocytes support capillaries.



PCT (Selective Reabsorption):

  1. Na+ moves by AT → Cl¯ to be absorbed (as it is attracted to Na+). 
  2. Co-transporter proteins move glucose using energy released by AT of Na+
  3. Movement of glucose → ↑  [solute] gradient inside tubule → H2O enters by osmosis.
  4. By the end of tubule, all glucose + AA's & most of H2O reabsorbed.
  5. PCT cells have many mitochondria to provide NRG for AT.

Loop of Henlé: U-shaped section of tubule that:

  • ↑[solute] in medulla by releasing Na+ into medulla from asc. limb→conc. urine prod.
  • Helps maintain correct H2O balance in body by drawing H2O from filtrate in loop.
  1. Na+ pumped out of filtrate to interstitial fluid by AT using protein pumps in asc. wall cells.

  2. Desc. limb wall cells H2O-permeable, but Na+-imperm, so H2O drawn out of filtrate as interstitial fluid [solute] ↑ going ↓ desc. limb.

  3. Asc. limb wall cells H2O-imperm, but Na+-perm, so H2O retained in filtrate, whilst Na+ diffuses into interstitial fluid.

  4. Counter current mechanism ensures [Na+] is greatest at lowest part of loop → H2O drawn out of descending limb along its entire length.

Collecting Duct: 

  1. ADH secreted by pituitary gland in response to stimuli from hypothalamus. 
  2. Hypotonic filtrate enters DCT, due to [solute] >
    [H2O] passed out of filtrate as it flows through loop of Henlé in medulla.

  3. Blood [solute] too low, hypothalamus detects this → pit. gland secrete ↓ ADH, → ↓ DCT + collecting tube permeability → ↓ H2
    reabsorbed →  high vol. of dilute urine prod. 
    → blood [solute] ↑

  4. Blood [solute] too high, hypothalamus detects 
    this → pit. gland secrete ↑ ADH → ↑ DCT + collecting tube permeability → ↑ H2O
    reabsorbed → low vol. of conc. urine prod.
    → blood [solute] ↑

  5. Animals in dry env. have long loops → ↑ medulla → ↑ H2O reabs. & short in humid env.


Types of N-waste

A image thumb

Kidney Problems + Treatments

  1. Haemodialysis: 
    1. Blood from patient's arm passed through machine, inside dialysis tubing.
    2. Tubing surrounded by dialysis fluid with measured [Na+ + glucose + H2O]
    3. Urea + excess salts diffuse through dialysis tube into fluid
      → excess H2O leaves blood by osmosis
    4. Blood returned to patient's vein, after its temp checked & gas bubbles removed.
    5. Dialysis fluid renewed regularly to ensure correct conc. of substances present in it.

A image thumb


  1. Urinalysis: Clinical procedure that examines urine for any deviation from normal composition.
  2. Urine produced by osmoregulation, excretion & metabolism, which may be affected by illness or drug abuse.

  3. Urine test strip contains 3 test areas designed to change colour to indicate + or – result after being dipped in urine, which is compared to results chart on testing kit.

A image thumb

Spermatogenesis + Oogenesis

Spermatogenesis: Sperm production, occurs in seminiferous tubules.

  1. Germinal epithelium cells divide by mitosis to produce more diploid cells.
  2. Diploid cells grow larger to form 1º spermatocytes.
  3. FSH (from PG) stim. 1º spermatocytes to divide by meiosis I → 2 2º spermatocytes (each)

  4. LH (from PG) stim. interstitial cells to prod. test. which stim. 2º spermatocytes to divide by meiosis II → 4 haploid spermatids (each).

  5. Test. from interstitial cells & nourishment from Sertoli cells associated to spermatids stim. 
    differentiation of spermatids into spermatozoa by:

    1. Developing tail

    2. Creating midsection with mitochondria

    3. Reducing their cytoplasm (↓ weight)

  6. Sperm stored & motility (ability to swim) developed in epididymis, then detach from Sertoli cells & pass along lumen of 
    seminiferous tubule;

Oogenesis: Ova production, begins in fetus ovaries.

  1. Germinal epithelium cells divide by mitosis to produce more diploid cells.

  2. Diploid cells grow & undergo meiosis I to produce 1º oocytes, surrounded by follicle cells (1º follicle).
  3. 1º follicle dev. arrested until puberty, where FSH is produced, which stim. follicle Meiosis I.
  4. Meiosis I produces 1 large (2º oocyte) + 1 small (polar body) haploid cell.
  5. Meiosis II then arrested until ovulation, where 
    the 2º oocyte is released into the oviduct.
  6. At fertilisation, 2º oocyte completes meiosis II to become mature ovum & expels polar body.

A image thumb

Fertilisation, Pregnancy, Parturition

  1. 2º oocyte releases chem. signals, which attract sperm to it – generally meet in fallopian tube.
  2. Sperm passes through follicle until it reaches zona pellucida (to which it binds to).
  3. Acrosome reaction: Acrosome vesicle fuses with zona pellucida & releases digestive enzymes, which digest through zona pellucida.
  4. Membs of sperm & oocyte fuse (fert.) & sperm nucleus enters egg → stim. cortical reaction.
  5. Fertilisation stimulates release of Ca2+ in egg, which stimulates meiosis II.
  6. Cortical Reaction: Cortical granules fuse with oocyte membrane, releasing contents (enzymes → zona pellucida hardening)
    → prevents polyspermy.
  7. Once oocyte nucleus undergoes meiosis II, prod. ovuum + polar body (which is expelled)
  8. Ovuum nucleus fuses with sperm nuclei to form zygote.
  9. Zygote moves down oviduct & divides by mitosis until it forms blastocyst, which sinks into uterus endometrium (implantation). 
  10. Blastocyst secretes hCG, which stim. corpus luteum in ovary to keep secreting PR + OES, which stim. continued dev. of endometrium to supply blastocyst until it becomes an embryo.

  11. Continues until placenta made, which prod. PR + OES; so corpus luteum breaks down. Amniotic sac containing fluid now surrounds embryo.

    1. Shock absorber

    2. Allows skeleton to develop without added strain of gravity

    3. Prevents tissue dehydration,

    4. Effective barrier to infection.

  12. Placenta:

    1. Structure: 

      • Made of maternal and fetal tissue; embedded in endometrium;

      • Maternal blood flows in intervillous spaces, foetal blood flows in capillaries in placental villi.

      • Chorionic villi ↑ SA for exchange of mom & fetal blood;

    2. Function:

      • Placenta produces hCG to maintain corpus luteum; which keeps [PR + OES] high to maintain pregnancy;

      • Site of exchange of: (table)

      • Connected to fetus via umbilical cord; which prevents mom & fetal blood mixing; & prevents damage from high press. in maternal arteries;

  13. High [PR] due to placenta inhibit oxytocin secretions by PG & myometrium contactions.

  14. At end of preg, foetus signals placenta to stop secreting PR & engages its head in cervix.

  15. [PR]↓ → oxytocin secreted, which stim.
    endometrium fibre contractions.

  16. Stretching (pressure changes) detected by receptors → stim. PG to secrete + oxytocin 
    → stims + & stronger myometrium contractions (+ feedback).

  17. Cervix muscle fibres relax in response to myometrium contractions → dilation.

  18. Myometrium contractions → amniotic sac bursts → amniotic fluid flows out

  19. Child born through vagina when cervix is correct size.

  20. Contractions continue after birth & placenta ejected. 

  21. Breastfeeding encourages oxytocin prod, in turn encouraging bonding with newborn baby. - Also has antibodies. 

A image thumb

Aerobic Respiration


  1. Occurs in cytoplasm of cell; regardless of aerobic or anaerobic conditions
  2. Hexose undergoes phosphorylation; to form hexose diphosphate; using 2 ATP (which form 2ADP + 2Pi);
  3. Hexose biphosphate lyses to form 2 Triose Phosphate (TP) molecules.
  4. TP oxidised, so releases 2 hydrogen atoms, which reduces 2NAD+ to form 2NADH + H+;
  5. Hexose diphosphate converted into 2 pyruvates;
  6. Net gain of 2 ATP (per glucose);
  7. Following reactions occur in mitochondria only under aerobic conditions.

Link Reaction:

  1. Pyruvates move into mitochondria
  2. Pyruvate decarboxylated & oxidised (oxidative decarboxylation)
  3. Decarboxylation removes CO2 from Pyruvate to form an Acetyl group.
  4. Oxidation removes H from Pyruvate, which reduces NAD+ into NADH + H+ 
  5. Acetyl group reacts with Coenzyme A to form Acetyl CoA; which enters Krebs cycle;

Kreb’s Cycle + ETC:

  1. Acetyl CoA from Link Reaction releases an acetyl group.
  2. Acetyl joins to 4-C molecule to form 6-C molecule
  3. 6-C undergoes oxidation + decarboxylation (oxidative decarboxylation) to form 5-C molecule; which is converted to 4-C molecule by oxidative decarboxylation;
  4. Oxidation releases H, which is accepted by NAD+ (reducing it) to form NADH + H+
  5. Decarboxylation releases 1 CO2 molecule per reaction.
  6. 4-C molecule converted back into original 4-C molecule & cycle repeats;
  7. 1 ATP molecule made during this step (per pyruvate) by combining ADP + P (substrate lvl phosphorylation);
  8. 3NADH + H+ + 1FADH2 & 2CO2 are end-products of Krebs cycle; of which:
    • NADH + H+ & FADH2 carry e¯ to ETC on inner mitochondrial membrane (cristae); 
    • CO2 is removed from cell.
  9. As e¯ passed between carriers in ETC, H+ move (against their conc. gradient) into & accumulate in intermemb space; creating H+ grad across membrane;
  10. ATP synthesised by flow of H+ back across membrane (chemiosmosis) through ATP synthase; to matrix.
  11. O2 reduced by ETC (added H+) to prod. H2O; which carries e¯ along ETC & allows NAD+ to be regenerated; which allows more ATP prod
    (hence ↑ yield). 


Aerobic vs. Anaerobic

Anaerobic respiration:

  1. Glucose converted into 2 pyruvate molecules;

  2. Glucose loses hydrogen (oxidation), which reduces NAD+ into NADH; 

  3. Less ATP yield than in aerobic respiration;

  4. Pyruvate converted to CO2 + CH3COOH in yeast (fermentation); 

  5. Pyruvate converted to Lactic acid in humans;

Aerobic respiration:

  1. Pyruvate fully oxidised; by Link reaction + Krebs cycle;
  2. NADH passes e¯ to ETC; 
  3. H+ gradient generated (chemiosmosis); which is used by ATP synthase to produce ATP;
  4. O2 needed as terminal e¯ acceptor; forms H2O

A image thumb


Small size ↑ SA:Vol ratio:

  1. + Space for ETC (+ other processes)

  2. Large SA:Vol allows rapid uptake and release of materials.


  1. Contains enzymes of Krebs cycle (making process faster).

  2. Contains 70S ribosomes to synth. proteins, so some proteins don’t need to be imported.

Inner membrane:

  1. Forms dynamic cristae to ↑ SA

  2. Contains ETC, as well as ATP synthase that make lots of ATP.

Narrow intermembrane space: Allows for short diffusion distance for H+ ions in ETC:

  1. [H+] gradient rapidly established

  2. Chemiosmosis therefore more efficient.

Electron tomography: Extension of TEM used to produce images of active mitochondria.

  1. e¯ beam passed at diff angles through sample.
  2. Info collected & used to assemble 3-D image of the target (e.g. mitochondria).
  3. Used to determine that cristae are dynamic, which further inc. SA for reactions + ETC.
  4. Cristae may also split off & form vesicles & re-form elsewhere (presumably where + active).

A image thumb