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IB Biology HL > Chapter 6 > Flashcards

Chapter 6 Flashcards

Human physiology

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1
Q

Mouth

A
  • site of mechanical digestion
  • food is mixed w/ saliva
  • saliva contains amylase- beings digestion of starches
  • saliva also moistens mixture to help swallow
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2
Q

Peristalsis

A

A wave of contraction and relaxation of longitudinal and circular muscles of the alimentary canal, by which the contents are forced ahead
- longitudinal and circular muscles work antagonistically

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3
Q

Longitudinal and circular muscles of alimentary canal

A

Longitudinal:
- contracts to widen lumen of alimentary canal

Circular:
- contracts to constrict lumen of alimentary canal

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4
Q

Stomach

A
  • food is churned w/ acid
  • stomach acid kills bacteria
  • starts digestion of proteins
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5
Q

Small intestine

A
  • after stomach, food enters small intestine
  • first section = duodenum
  • acid passing from stomach needs to be neutralised so enzymes digesting fats and lipids, and further digesting carbs can function (their optimum pH is neutral to alkaline)
  • by end of small intestine, digestion has been completed
  • digested proteins have been absorbed from last section, the ileum
  • small intestine is where most of the absorption takes place
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6
Q

Large intestine

A
  • after small intestine (ileum), food now enters the large intestine
  • food is now a liquid mixture of undigested material and digestive juices
  • here water, along w/ vitamins made by bacteria that normally live in large intestine, are reabsorbed
  • anaerobic bacteria here also ferment undigested polysaccharides to produce energy
  • in the last parts of the large intestine, faeces is formed
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7
Q

Rectum

A

Faeces are stored here prior to egestion

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8
Q

Pancreas

A

secretes amylase (starch), lipase (lipids) and protease (proteins) into the small intestine

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9
Q

Liver

A

secretes bile to emulsify the lipids

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10
Q

Gall bladder

A

stores the bile

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11
Q

Structure of the small intestine

A
  • a muscular tube of approx. 6-7m in humans
  • lies between stomach and large intestine
  • divided into 3 parts: duodenum, jejunum and ileum
  • inner surface is covered w/ villi, that increases its SA 30-60 fold
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12
Q

Transverse section of small intestine - outside to the inside

A
  1. Serosa: outermost layer consisting of connective tissue that’s in contact w/ body cavities
  2. Longitudinal muscles: responsible for peristalsis
  3. Circular muscles: responsible for peristalsis
  4. Submucosa: connective tissue that supports mucosa and contains large veins and arteries that give rise to capillary bed of the mucosa
  5. Mucosa: innermost layer forming soft lining of tube comprising of epithelium, connective tissue and smooth muscle (villi form part of this layer)
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13
Q

Enzymes produced by the pancreas

A
  1. Amylase: breaks down starch into maltose
  2. Endopeptidase (trypsin): breaks down proteins into smaller polypeptides
  3. Lipases: break down lipases into glycerol and fatty acids
  4. Phospholipases: break down phospholipids to glycerol, fatty acids and phosphate

Once produced, pancreatic juice (w/ enzymes) is carried via pancreatic duct to duodenum
- where it’s released into lumen of small intestine

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14
Q

Enzymes of the small intestine

A
  • wall of small intestine contains some glands that produce enzymes that are immobilized in intestinal epithelial cells
  1. Nucleases: break down DNA and RNA
  2. Maltase: breaks down maltose into glucose
  3. Lactase: breaks down lactose into galactose and glucose
  4. Exopeptidases: remove a single AA from end of small polypeptides.
  5. Dipeptidases: break down a dipeptide into two AA
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15
Q

Digestion in the small intestine

A
  • movement of food along small intestine occurs by peristalsis
  • contraction of circular and longitudinal muscle of small intestine mixes food w/ enzymes.
  • enzymes (from pancreas and small intestine) digest most macromolecules in food into monomers in small intestine
  • these monomers are then absorbed into blood
  • variety of enzymes secreted by human body allows digestion of starch, glycogen, lipids and nucleic acids into their respective monomers
  • cellulose remains undigested, as enzyme cellulase (which breaks down cellulose) isn’t produced by humans
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16
Q

Absorption of food molecules in the small intestine

A
  • actual absorption of food molecules takes place mainly in small intestine, over epithelium
  • SA is greatly increased by presence of villi
  • villi absorb all monomers produced by digestive processes in the small intestine
  • dense capillary network provides villus w/ a good blood supply
  • this creates a high-conc. gradient to maximise efficiency of removal of water-soluble products
  • lacteal absorbs fat-soluble products
  • this prevents blood from being clogged w/ absorbed fat
  • Nervous impulses from brain cause villus to sway in the intestine
  • pushes the chyme along and maximises contact w/ digested products for absorption
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17
Q

Absorption

A

taking in of digested food substances as well as minerals and vitamins from small intestine into the blood

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18
Q

What are the end products of digestion that are directly absorbed by the villi?

A
  • bases and phosphates from nucleic acids
  • fatty acids and glycerol
  • amino acids
  • monomeric carbohydrates eg. fructose, glucose, galactose and ribose
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19
Q

Absorption of contaminants

A
  • food may also contain some contaminants or poisons – including alcohol
  • Most contaminants pass directly into blood
  • liver detoxifies some of the compounds
  • but, if they can’t be broken down by the liver, they can be secreted from the body in the urine
  • most medical drugs are taken up directly into the blood and are broken down by the liver
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20
Q

Microvillus

A
  • hairlike folds in the membrane of the epithelial cells of the villus
  • where absorption takes place by means of (facilitated) diffusion, passive and active transport
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21
Q

Absorption into the blood

A
  • food molecules, minerals and vitamins are absorbed into the blood
  • to be absorbed into the blood, molecules need to pass into capillaries of the villus
  • fats are absorbed into the lymph, which circulates in the lacteal in centre of the villus
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22
Q

Process of absorption

A
  1. Substances to be absorbed move from lumen into epithelial microvilli
  2. Amino acids and monosaccharides move from microvilli into capillaries
    - monoglycerides move into the lacteals.
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23
Q

Four modes of absorption

A
  1. Simple diffusion:
    - occurs when molecules are small and are hydrophobic
    - they can pass through phospholipid bilayers
  2. Facilitated diffusion:
    - fructose, glucose and other hydrophilic monomers are moved by protein channels
    - this requires a concentration gradient
  3. Active transport:
    - needed when conc. are lower in the lumen of the small intestine
    - hence, movement needs to occur against a conc. gradient
    - glucose, amino acids and some mineral ions are transported in this way- requires ATP
    - cells of epithelium have many mitochondria that synthesise ATP for this
  4. Pinocytosis:
    - draws in small droplets of liquid surrounded by a small section of phospholipid membrane
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24
Q

Starch

A
  • important component of many human diets: pasta, rice, bread etc.
  • occurs as amylose and amylopectin
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25
Q

Digestion of starch

A
  • digestion of starch begins w/ chewing, amylase is present in saliva
  • once saliva and food have been mixed, amylase starts breaking down α-1,4 glycosidic bonds between glucose monomers in amylose and amylopectin
  • end products are maltose, a dimer of glucose connected by α-1,4 bonds, and maltotriose
  • other than α-1,4 bonds, amylopectin also has α-1,6 glycosidic bonds, but, these can’t be broken down by amylase.
  • even after initial catalytic breakdown by amylase, these starch molecules are too large to pass through membranes
  • they need to be broken down into monomers before they’re absorbed
  • what enters small intestine is a mixture of maltose, maltotriose and dextrins
  • 3 enzymes that are immobilised in epithelial cells of small intestine: maltase, glucosidase and dextrinase, break down these molecules into glucose
  • these are then absorbed by the villi
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26
Q

Transportation of absorbed food

A
  • all absorbed food is transported via hepatic portal vein from small intestine to liver, from where it enters general circulation
  • makes glucose available for use by all body cells
  • excess glucose is taken up by the liver and converted into glycogen
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27
Q

Dialysis tubing

A
  • partially permeable cellulose tubing that contains microscopic pores
  • allows water, small molecules and ions to pass through freely, but doesn’t allow movement of large molecules
  • used in separation techniques that enable removal of small molecules from macromolecules in solution based on differential diffusion
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28
Q

Dialysis

A

separation of smaller molecules from larger molecules in solution by selective diffusion through a partially permeable membrane

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29
Q

Dialysis tubing as a model for small intestine

A
  • used as a model of small intestine, w/ medium outside representing blood into which digested products are absorbed
  • tubing represents epithelium of small intestine
  • high conc. of glucose solution in the tubing is what is normally observed after a starchy meal has been fully digested
  • size of glucose molecules is small enough to pass through pores of tubing
  • they’ll diffuse from a region of higher conc. (in the tubing) to region of lower conc. (in beaker)
  • movement of glucose mimics absorption of glucose via epithelial cells- represented by dialysis tubing, into blood supply
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30
Q

Testing for presence of starch in dialysis tubing modelling absorption in small intestine

A
  • if starch solution was added inside tubing, and samples of water in beaker were tested for presence of starch at intervals of 10 minutes, a negative result would always be found
  • because starch molecules are too big to pass through pores of dialysis tubing
  • this is also observed in small intestine: starch and other complex undigested molecules are not absorbed
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31
Q

Shortcoming of dialysis tubing model

A

it can only account for absorption by diffusion or osmosis, and can’t be used to support absorption by active transport

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32
Q

Aorta

A

Main and biggest artery connecting the heart w/ the rest of the body

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33
Q

High pressure of blood flowing out of the heart

A
  • generated by contraction of ventricles

- is strong enough to convey blood to all tissues of the body

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34
Q

How do arteries cope w/ high pressure of blood?

A
  • aorta and all arteries in the body can cope w/ pressure that’s exerted on their walls because they’re elastic
  • walls contain elastic fibres (formed from elastin), which are stretched at every heartbeat when pressure is highest
  • when walls return to their normal shape, this recoil helps to propel blood forward
  • arteries also have muscular walls to help w/ propulsion of blood
  • muscle and elastic fibres present in wall of arteries assist in maintaining blood pressure between pump cycles
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35
Q

Layers of the arterial wall

A
  1. Tunica intima
  2. Tunica media
  3. Tunica adventitia
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36
Q

Tunica intima

A
  • innermost layer
  • in direct contact w/ blood in the lumen
  • includes endothelium that lines lumen of all vessels
  • hence, forms a smooth, friction-reducing lining.
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37
Q

Tunica media

A
  • middle coat

- mainly made of smooth (involuntary) muscle cells and elastic fibres arranged in roughly spiral layers

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38
Q

Tunica adventitia

A
  • outermost coat
  • is a tough layer consisting largely of loosely woven collagen fibres that protect blood vessel and anchor it to surrounding structures
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39
Q

Systolic blood pressure

A
  • when the heart contracts

- arteries experience the highest pressure

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40
Q

Vasoconstriction

A

when circular muscles surrounding arteries resist outward pressure and constrict

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41
Q

Diastolic blood pressure

A
  • when heart relaxes between beats

- pressure in arteries is at its lowest

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42
Q

Vasodilation

A

when smooth muscles surrounding arteries relax

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43
Q

Aterioles

A

Smaller forms of arteries

  • higher density of muscle
  • more susceptible to hormonal and nervous control of vasoconstriction and vasodilation
  • in both arteries and arterioles, tunica media is the thickest layer
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44
Q

Vasoconstriction and vasodilation

A
  • directly control flow of blood through the body
  • play a role in regulating body temp.
  • involved in slowing flow of blood when a person is severely wounded
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45
Q

Pulse

A
  • pulse or heart rate
  • no. of times the heart beats per minute
  • is the result of the alternate expansion and contraction of arterial wall as beating heart forces blood into system of arteries via the aorta
  • pulse can be felt when an artery lies near the surface of the skin
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46
Q

Stroke volume

A

amount of blood pumped out of the left ventricle of the heart during each contraction

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47
Q

Cardiac output

A

amount of blood the heart pumps through the circulatory system in a minute

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48
Q

Veins

A
  • transport blood back from tissues of the body and return it to atria
  • blood pressure is much lower- danger of backflow due to gravity- hence, they have valves that close to prevent backflow
  • blood flows more slowly
  • veins don’t need thick walls w/ lots of muscle fibres
  • blood flow is helped by pressure exerted by skeletal muscles
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49
Q

Valves

A
  • present in veins
  • ensure that blood flows in one direction only (towards the heart)
  • prevents backflow
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50
Q

Connection between arteries and veins

A
  • formed by a capillary network
  • nutrients and oxygen in blood need to reach every cell of the body
  • but, size and wall structure of arteries is too big for this
  • so, arteries form smaller arterioles that divide to form very fine blood vessels called capillaries
  • these vessels then fuse together to form venules, and many venules fuse to form veins
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51
Q

Capillaries

A
  • have walls that are only one-cell thick
  • no muscle fibres or other layers
  • allows for exchange of materials, oxygen and nutrients w/ cells in tissues
  • also allows waste products, eg. CO2 and urea, back into the capillaries to be transported by blood
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52
Q

Blood flow in capillaries

A
  • blood flows through tissues in capillaries
  • capillaries have permeable walls that allow exchange of materials between cells in the tissue and the blood in the capillary
  • capillaries connect arterioles to venules
  • blood flow is slowest in the capillaries, to allow time for exchange w/ tissues
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53
Q

Interstitial fluid

A

liquid part of blood that passes through capillary wall, to bathe tissue cells in

  • composed of. waters, sugars, salts, fatty acids, AA, coenzymes and hormones, and waste products from cells
  • tissue fluid w/ dissolved nutrients is in direct contact w/ tissue cells, exchange is greatly enhanced
  • after exchange has taken place, tissue fluid is mostly reabsorbed into capillaries
  • this ultimately drains into venules
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54
Q

Features of arteries

A
  • made of 3 layers (tunica externa, tunica media and tunica intima)
  • tunica media is thicker than in veins
  • thick layer of elastin and collagen fibres
  • no valves present
  • diameter can be greater than 10mm
  • have thicker walls w/ narrower lumens than veins
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55
Q

Features of veins

A
  • made of 3 layers (tunica externa, tunica media and tunica intima)
  • tunica media is thinner than in arteries
  • elastin and collagen fibres are relatively thin compared to artery
  • valves are present at intervals
  • diameter can be greater than 10mm
  • have thinner walls w/ larger lumens than to arteries
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56
Q

Features of capillaries

A
  • one layer of endothelial cells
  • no tunica media
  • no elastin and collagen fibres
  • no valves
  • diameter is between 2-10 micrometres
  • wall is one cell thick w/ a lumen of about 5 micrometres
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57
Q

Valves in the heart

A

Ensure that circulation of blood occurs in only one direction by preventing backflow

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58
Q

Structure of the heart

A
  • 2 ventricles
  • 2 atria
  • no. of valves
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59
Q

Double circulatory system

A
  • blood flows through heart twice before it’s distributed to tissues
  • there are two separate pathways that the blood follows
  • one path is to absorb oxygen and remove CO2 in the lungs
  • other path is to supply all the tissues w/ oxygen and to remove waste from the same time
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60
Q

Systemic circulation

A

circulation of blood from the heart to body tissues and back to the heart

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61
Q

Pulmonary circulation

A

movement of blood between the lungs and the heart

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62
Q

Movement of blood through the right side of the heart (pulmonary circulation)

A
  1. Blood enters the heart through the inferior and superior vena cava
    - oxygen-poor blood from body tissues flowing into RA
  2. As atrium contracts, blood flows from RA into RV through open tricuspid valve
  3. When ventricle is full, it begins to contract
    - increased pressure of blood against tricuspid valve forces it shut
    - this prevents blood from flowing back into the atria
  4. As ventricle contracts, blood leaves the heart through the pulmonary artery and flows to lungs where it’s oxygenated
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63
Q

Movement of blood through the left side of the body (systemic circulation)

A
  1. Pulmonary vein carries oxygen-rich blood from the lungs into left atrium of the heart
  2. As atrium contracts, blood flows from left atrium into left ventricle, through open bicuspid valve
  3. When ventricle is full, it begins to contract
    - increased pressure of blood against bicuspid valve causes it to close
    - prevents blood from flowing back into atrium, while ventricle contracts
  4. As ventricle contracts, blood leaves the heart through aortic value, into the aorta and to the body
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64
Q

Myogenic

A

The heart muscle can generate its own contractions

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65
Q

Sinoatrial node

A
  • group of specialised muscle cells in the wall of the RA
  • SA node initiates each heartbeat and it sets the heart rate
  • called the pacemaker
  • fires at regular intervals to cause hear to beat w/ a rhythm of 60-70 bpm for a healthy, resting heart
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66
Q

Propagation through the heart of the electrical signal initiated in SA node

A
  1. SA node sends out an electrical signal that stimulates contraction as it’s propagated through walls of the atria
  2. Signal then passes via inter-atrial septum to reach the atrioventricular node (AV)
  3. From AV node, signal is relayed via bundle of His located in inter-ventricular septum to the top of each ventricle
  4. At the top of the ventricles, signal spreads from the bundle of His to the ventricles via the Purkinje fibres located in its wall
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67
Q

Cardiac cucle

A

The complete sequence of events in the heart from the start of one beat to the beginning of the following beat

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68
Q

Pressure and volume change during the cardiac cycle

A
  1. Atrial contraction begins
  2. Atria eject blood into ventricles
  3. Atrial systole ends; AV valves close
  4. Isovolumetric contraction
  5. Ventricular ejection occurs
  6. Semilunar valves close
  7. Isovolumetric relaxation occurs
  8. AV valves open; passive ventricular filling occurs
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69
Q

Isovolumetric contraction

A

used to refer to an event occurring at the beginning of systole, during which ventricles contract w/ no corresponding volume change

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70
Q

Cardiovascular centre of medulla oblongata

A

Signals sinoatrial node to speed up the heart or slow it down

  • BP, pH and CO2 conc. of blood are all monitored by cardiovascular centre
  • determines whether impulses should be sent along the cardiac accelerator nerve or vagus nerve to the heart
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71
Q

Cardiac accelerator nerve

A

nerve that stimulates the heart to beat faster

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72
Q

Vagus nerve

A

nerve that reduces the heart rate

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73
Q

How does heart rate increase due to increased activity?

A
  • increased activity = more respiration
  • greater need for oxygen
  • increased production of waste products e.g CO@
  • increased CO2 in the blood will decrease pH
  • decrease in pH is sensed by cardiovascular centre
  • it will then send impulses along cardiac accelerator nerve to SA node to increase HR
  • as heart pumps faster, more oxygen is sent o body tissues and more CO2 is removed
  • once activity stops, heart can slow down
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74
Q

Fitness

A

speed at which heart slows down after activity

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75
Q

Epinephrine

A
  • another factor that influences SA node
  • the ‘fight or flight’ hormone secreted by the medulla of the adrenal glands
  • strong emotions eg. fear or anger, cause it to be released
  • it’s carried to all parts of the body, including the heart
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76
Q

How does epinephrine increase the HR?

A
  • stimulates the SA node to emit electrical signals at a faster rate
  • increasing conduction speed of impulses generated by both SA and AV nodes
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77
Q

Why is epinephrine called the ‘fight or flight’ response?

A
  • speeds up the HR to prepare the body for either of those two actions
  • it triggers a rise in HR
  • also increases muscle strength, BP and sugar metabolism
  • all of these prepare the body for immediate action
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78
Q

Why does our body need fats?

A

Body needs fats for:

  • energy
  • insulation
  • starting material for certain hormones and anti-inflammatory compounds
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79
Q

Atheromas

A
  • fatty deposits caused by high blood conc. of low density lipoprotein (LDL) in arterial walls next to endothelial cells
  • LDL consist of cholesterol and fats
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80
Q

Myocardial infarction

A
  • coronary artery is blocked
  • cells in that part of the heart will die
  • results in a myocardial infarction (heart attack)
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81
Q

Angina

A
  • build up of plaque takes time
  • initially, the restricted flow of blood in such an artery will cause pain to heart cells
  • this is because, heart cells have been deprived of oxygen and nutrients
  • pain is known as angina
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82
Q

Coronary artery

A

an artery supplying the heart w/ oxygen and nutrients

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83
Q

Plaque formation

A

building up of fatty deposits in arteries

  • leads to atherosclerosis
  • increase in cardiovascular disease
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84
Q

Causes of plaque formation

A
  • high blood conc. of LDL
  • diabetes causing high blood glucose conc.
  • smoking and stress causing high blood pressure
  • diets containing high levels of trans fats
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85
Q

Skin

A
  • outermost layer of the body
  • has pores for sweating, hair follicles and sebaceous glands that produce sebum (oils)
  • this keeps skin supple and at a slightly lower pH
  • oil and low pH both act as growth inhibitors for certain bacteria
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86
Q

Mucous membranes

A

Made of a surface layer of epithelial cells over a deeper layer of connective tissue

  • produce mucous for protection and lubrication
  • mucous contains glycoproteins and lysozymes, enzymes that attack bacterial cell walls
  • both have antiseptic properties
  • mucous also forms a barrier, trapping organisms that can be killed by WBC found in mucous membranes
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87
Q

Openings into the body

A

A potential entry point for pathogens

  • nose and mouth give access to nasal passages, sinuses, lungs and gastrointestinal tract
  • eyes, vagina, urethra and head of penis are entry points too
  • in these places, mucous membranes help protect the body
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88
Q

Physsical barriers

A
  • form a primary defence against pathogens that cause infectious disease
  • skin and mucous membranes act as physical barriers
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89
Q

Blood clotting

A
  • a cascade of reactions triggered by exposure to air
  • release of clotting factors from platelets triggers production of thrombin
  • thrombin catalyses conversion of soluble fibrinogen into insoluble fibrin
  • blood becomes thicker and starts to gel
  • after a while, a soft scab forms
  • scab hardens and forms a protective layer under which the skin can heal itself
  • scab prevents entry of pathogens into the body
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90
Q

Thrombus

A

a blood clot that forms in a vessel and remains in place where it was formed
- if it happens in the coronary arteries, it’s a coronary thrombus

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91
Q

Process of atherosclerosis

A
  • atherosclerosis narrows lumen of arteries and slows down blood flow
  • this increases chance of a clot occluding in a coronary artery
  • leads to certain parts of the heart not receiving any oxygen and nutrients
  • this causes that part of the heart to die, resulting in a heart attack
  • when a blood clot reduces amount of blood reaching heart muscles, it causes angina- heart muscles don’t get enough oxygen-rich blood
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92
Q

Factors that increase risk of clot formation

A
  • smoking
  • obesity
  • hypertension
  • diabetes
  • atherosclerosis
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93
Q

Causes of coronary artery thrombosis

A
  • starts when plaque in artery walls rupture the lining of the walls
  • clot that began at the site of the rupture can grow larger w/ time
  • eventually it will completely block the artery

CAT= formation of a clot within the coronary artery

94
Q

Immune system can be divided into

A
  1. Non-specific immune system involving phagocytes

2. Specific immune system made up of lymphocytes and antibodies

95
Q

When is the body’s second line of defence activated?

A
  • despite body’s primary defence systems, eg. skin and mucous membranes, pathogens can enter our body and cause disease
  • when this happens, body’ s second line of defence by immune system, is activated
96
Q

Phagocytes

A

Types of WBC that can engulf a pathogen

- once in the phagocyte, enzymes secreted by the lysosome will digest the pathogen

97
Q

How do phagocytes work?

A

Phagocytes squeeze past leaky endothelial cells of capillaries

  • invade tissue where an infection has occurred eg. a small wound in skin
  • this is amoeboid movement
  • this is non-specific immunity to diseases- phagocytes can responds equally well to a variety of organisms
98
Q

Pathogen

A

A disease-causing organism or virus

99
Q

Specific immune system

A

Recognises proteins and other molecules on surface of pathogens as foreign

100
Q

Antigen

A

any molecule that enters the body and triggers an immune response

101
Q

Lymphocytes (B)

A
  • special type of WBC that produces antibodies
  • each type of lymphocyte will produce one type of antibody, specific for a particular antigen
  • small no. of each type of lymphocyte in the body
  • some antibodies produced by lymphocytes are carried on their cell surface membrane w/ antigen binding site projecting outwards
102
Q

What happens in the early stages of an infection?

A
  • there aren’t enough lymphocytes bearing correct antibody to mass produce a specific antibody against pathogen
  • but specific antigens will trigger lymphocytes that produces specific antibody to divide by mitosis to produce plasma cells
  • plasma cells give rise to large quantities of same antibody, enabling body to control the infection
103
Q

What are the two ways in which antibodies work?

A
  1. Bind to the antigen, allows phagocytes to recognise pathogen
  2. Bind to proteins in the coat of a virus, prevents virus from entering other (human) cells
104
Q

Specific immunity

A
  • once an infection has been overcome, no. of plasma cells that produce specific antibodies will decrease
  • but, some of the lymphocytes triggered by infection will become memory cells
  • so, if same pathogen invades body again, response will be much faster
  • antibody production in response to an infection = specific immunity
105
Q

Memory cells

A

cells that ‘remember’ how to respond to that infection, so if same pathogen invades body again, response will be much faster

  • some lymphocytes activated by an infection act as memory cells
  • can quickly reproduce to form a clone of plasma cells if a pathogen carrying specific antigen is encountered again
106
Q

Define specific immunity

A

antibody production in response to an infection

107
Q

Process of antibody production by B lymphocytes

A
  1. Antigens bind only to B cells that have corresponding antigen binding site and activate them
  2. Activated B cells divide by mitosis to form plasma cells (cell clones)
  3. Clone of plasma cells secrete same type of antibodies
  4. Specific antibody molecules are secreted by plasma cells
108
Q

Antibody

A

A large protein w/ variable regions produced by your own body that will bind to an antigen

109
Q

Antibiotic

A

any substance produced by a microorganism that can inhibit the growth of other microorganisms

110
Q

Why can antibiotics be used to treat only bacterial infections?

A
  • block processes that occur in prokaryotic cells but not in eukaryotic cells
  • thus, antibiotics can be used to treat bacterial infections in humans and animals (as they’re eukaryotes) without harming their body cells
111
Q

How do antibiotics work?

A
  • antibiotics don’t have an effect on human cellular processes
  • drugs target bacterial cell wall and membrane formation, ribosome function or DNA replication, transcription and translation
  • none of these directly kill the bacteria, but it slows down/stops growth and prevent cellular division
112
Q

Why are antibiotics ineffective on viruses?

A
  • viruses aren’t affected by antibiotics
  • they aren’t living and don’t have their own metabolic processes
  • they infect living cells and use/ abuses cell’s own metabolic processes to spread viral infection
113
Q

Development of resistance

A
  • resistance quickly develops to new antibiotics
  • natural selection favours spread of resistance
  • so, if a mutation causing resistance to an antibiotic occurs in a bacterium, after several generations a strain of bacteria will evolve w/ genes that confer resistance to that antibiotic
114
Q

T- helper cell

A
  • antigen presenting cell, a special type of WBC that traps the antigen and presents it to T helper cell
  • once antigen has been recognised by T helper cell, immune system is activated to fight agains the antigen
  • triggers production of antibodies and activates macrophages and killer T cells- engulf and destroy the antigen
115
Q

HIV

A
  • human immunodeficiency virus
  • a virus that infects and stops T helper cells functioning
  • infected T helper cells are destroyed by various means- leads to a reduced no. in the body
  • T helper cells are needed to activate B cells to produce antibodies
  • infections w/ HIV causes a loss in ability to produce antibodies, can lead to development of AIDS (acquired immune deficiency syndrome)
  • HIV causes an overall reduction of active lymphocytes in the body, including both T and B cells
  • activated T-cells decrease as infected T helper cells are destroyed
  • activated B cells decreases as there are fewer T helper cells to cause their activation
116
Q

How does HIV work?

A
  • a retrovirus that has RNA as its genetic material
  • once HIV infects a cell, it makes a DNA copy from its RNA w/ help fo reverse transcriptase
  • cDNA that’s produced is inserted into the host cell’s genome
  • nowadays, infection can be slowed down, or even stopped, w/ use of anti-viral drugs specifically targeting reverse transcriptase activity
117
Q

How can HIV be transmitted?

A
  1. Sexual intercourse
    - due to mixing of bodily fluids
    - when abrasions cause bleeding of mucous membranes
  2. Transfusion of infected blood
  3. Sharing of hypodermic needles by drug users
  4. From mother to child during pregnancy, birth or breastfeeding
118
Q

Florey and Chains’s experiment

A
  • infected 8 mice w/ Streptococcus
  • bacterium causes pneumonia in mice
  • 8 mice were kept under identical conditions, but 4/8 were given an injection of penicillin
  • 4 untreated died within 24 hours, but treated mice stayed alive
  • experiment gives a strong indication that penicillin may have played a role in recovery of mice
119
Q

Ventilation

A

No. of breaths, including inhalation and exhalation, taken per minute

  • maintains conc. gradients of oxygen and carbon dioxide between air in alveoli and blood flowing in adjacent capillaries
  • essential to ensure that oxygen continuously diffuses into the blood from the alveoli
  • carbon dioxide diffuses out of the blood into the alveoli
120
Q

Gas exchange

A

exchange of gases that occurs at the alveoli

  • directly dependent on ventilation
  • depends on a conc. gradient
121
Q

Alveoi

A
  • tiny air sacs of the lungs where gas exchange takes place
  • oxygen conc. is higher than conc. in the blood that flows past the alveoli
  • CO2 is a higher conc. in the blood, lower conc. in freshly inhaled air in alveoli
122
Q

What facilitates gas exchange by diffusion?

A
  • concentration gradient between the blood and the air in the alveoli
  • thin walls of the alveoli
  • short distance to the capillaries
123
Q

Two types of alveolar cells

A

The wall of the alveolus is made of 2 types of alveolar cells

  1. Type 1 pneumocytes:
    - extremely thin alveolar cells
    - adapted to carry out gas exchange
  2. Type 2 pneumocytes:
    - secrete a solution containing a surfactant
    - creates moist surface inside the alveoli to prevent sides of alveolus sticking to each other by reducing surface tension
    - moisture also increases speed at which gases dissolve, helps gas exchange
124
Q

Two steps in ventilation

A
  1. Inhalation

2. Exhalation

125
Q

Pressure of a gas

A
  • directly related to no. of molecules that occupy a certain volume
  • flow of gas is always from an area of high pressure to an area of low pressure
126
Q

Gas exchange

A
  • muscles surrounding thorax relax
  • thoracic pressure is lowered, it’s lower than atmospheric pressure
  • causes air to rush into lungs
  • when muscles contract, pressure rises
  • air is forced out of the lung
127
Q

Pathway air follows during ventilation

A
  1. Mouth/nasal passage
  2. Trachea
  3. Two bronchi (one for each lung)
  4. Bronchioles
  5. Alveoli
128
Q

What happens during inhalation?

A
  1. External intercostal muscles contract
  2. Internal intercostal muscles relax
  3. Diaphragm contracts (moves down and in)
  4. Abdominal muscles relax
  5. Pressure in lungs decreases, volume increases
  6. Air enters the lungs
129
Q

What happens during exhalation?

A
  1. Internal intercostal muscles contract
  2. External intercostal muscles relax
  3. Diaphragm relaxes (moves up and out)
  4. Abdominal muscles contract
  5. Pressure in lungs increases, volume decreases
  6. Air leaves the lungs
130
Q

Antagonistic muscles

A

Muscles that work in opposite directions to one another and have opposite effects

eg.
- external and intercostal muscles
- diaphragm and abdominal muscles

131
Q

Tidal volume

A

amount of air that enters or leaves the lungs in a single breath at rest

132
Q

Causes of lung cancer

A
  • asbestos dust particles lodge in the lungs and can’t be broken down
  • smoking (cigarettes, cigars, pipe tobacco)
  • passive smoking
  • air pollution; diesel exhaust fumes contain many carcinogens
  • radon gas: some parts of the world have high conc. of this radioactive gas- it emits alpha particles, causes mutations when inhaled
133
Q

Consequences of lung cancer

A
  • Shortness of breath
  • Cough that doesn’t go away
  • Coughing up blood
  • Pain (chest pain and pain in other areas if cancer spreads)
  • Accumulation of fluid in the chest
  • Spread of cancer to other parts of the body
  • Loss of appetite or weight loss
  • Fatigue
  • Repeated problems with pneumonia or bronchitis
134
Q

Emphysema cause

A

caused by long-term exposure to cigarette smoke and other pollutants

135
Q

What happens in emphysema?

A
  • gives rise to an inflammatory response in the lungs
  • results in narrowing of small airways and breakdown of lung tissue
  • alveoli become less elastic- makes ventilation more difficult
  • furthermore, there’s increased protease activity, which breaks down alveolar wall
  • creates one larger air space instead of many small ones
  • reduces SA of the lungs and results in a smaller amount of oxygen reaching bloodstream
  • normally, proteases are inhibited by alpha-1-antitrypsin, but in emphysema patients, activity of this enzyme inhibitor is reduced

These result in a reduction of oxygen saturation of the blood
- gas exchange can no longer occur in damaged alveoli

136
Q

Consequences of emphysema

A 
Shortness of breath
Persistent cough
Fatigue
Weight loss 
Depression

NB/ some patients need oxygen therapy and perhaps, a lung transplant

137
Q

Neuron

A

a nerve cell

- transmit signals in the form of electrical impulses

138
Q

Nervous system

A

used for communication and higher brain functions

139
Q

Composition of the myelin sheath

A
  • axon of some neurons is coated w/ myelin sheath
  • this fatty layer is made of compacted layers of the Schwann cell membrane
  • Schwann cell membrane is mostly lipid, but also contains several proteins
  • play important roles in maintaining structure and compaction of myelin and adhesion of sheath to the axon
140
Q

What is the myelin sheath?

A

an insulating layer that speeds up transmission of a nerve impulse

141
Q

Node of Ranvier

A

gap between the adjacent Schwann cells

142
Q

Saltatory conduction

A
  • action potential propagated along a myelinated axon moves faster than an non-myelinated one
  • myelin sheath forces nerve signal jump from one node of Ranvier to the next
  • accounts for faster speed of impulse transmission
  • this is the saltatory conduction of nerve impulses
143
Q

Resting potential

A
  • neuron has a gradient of sodium (Na+) and potassium (K+) ions across its membrane
  • When a neuron isn’t transmitting a signal, it has more Na+ ions on the outside of its membrane than the inside
  • has more K+ ions on the inside than the outside
  • also has some proteins w/ a -ve charge located in the neuron
144
Q

Development of negative resting membrane potential

A
  • ion gradient causes an electrical imbalance between inside and outside of the neuron
  • membrane is more permeable to K+ ions than to Na+ ions
  • a Na+/K+ pump transfers Na+ ions out of the cell and pumps K+ ions back in
  • every turn of Na+/K+ pump, 3 Na+ ions are transferred to the outside, 2 K+ ions are pumped back into neuron
  • combination of these factors results in overall loss of +ve ions from the neuron
  • contributes to development of -ve resting membrane potential of -70 mV
145
Q

Action potential

A
  • neurons can become depolarised
  • depolarisation is caused by opening of Na+ channels - allows rapid influx of Na+ ions
  • there’s a conc. gradient across neuron membrane (a higher conc. of Na+ ions outside), so change is rapid
  • resting potential of -70 mV changes quickly to +ve value of around +30 mV
  • once an area of neuron is fully depolarised, change in potential causes voltage-gated K+ channels to open
  • so, K+ ions at a higher conc. in the neuron diffuse out and decrease potential = repolarisation - K+ channels remain open until membrane potential becomes as -ve as resting potential
  • often, membrane potential becomes more -ve than resting potential for a brief period = hyperpolarisation
  • because not all K+ channels close immediately after resting potential has been reached
  • right after hyperpolarisation, that part of the neuron enters a refractory period and can’t be depolarised (to generate an action potential) as its Na+ channels are inactivated
146
Q

Threshold potential

A
  • neurons will only fully depolarize (go from -70 mV to +30 mV) if threshold potential (-55mV to -50mV) is reached
  • If a neuron doesn’t reach threshold potential, neuron won’t depolarize
  • if it reaches this threshold, there’s a +ve feedback effect, and adjacent Na+ channels will open to propagate action potential
147
Q

Define depolarisation

A

Na+ channels open, Na+ diffuse to the inside of the neuron.

148
Q

Define repolarisation

A

Na+ channels close and K+ channels open allowing K+ to diffuse out

149
Q

All or nothing principle

A

Neurons need a threshold potential (around -50 mV), otherwise neuron can’t be depolarised

150
Q

Propagation of action potentials along the axon

A
  • Na+ from part of the axon that was depolarised previously diffuse to the right
  • makes membrane potential (there) less negative
  • potential reaches threshold potential; Na+ channels open and allow more Na+ to flow into cytoplasm of the axon and cause depolarisation
  • this disturbs conc. gradient that normally exists
  • establishes 2 new conc. gradients
  • first, on the outside, where more Na+ will diffuse from adjacent area to area which has just been depolarised
  • second, on the inside, where Na+ will diffuse to right hand side of the axon, that’s where Na+ concentration is still lower
  • on the left side of the axon, Na+ channels are inactive (refractory period)
  • once diffusion of Na+ starts, and more Na+ flow to that part of the axon (to the right), it depolarises that part of the axon and creates a new action potential
  • process repeats itself, until the end of the axon is reached
151
Q

Threshold potential

A

minimum level to which a membrane potential must be depolarised to trigger an action potential
- varies between -55 and -40 mV

152
Q

Synapses

A

connections between neurons and other neurons, neurons and glands, neurons and muscles, and neurons and sensory cells

  • synapse consists of a presynaptic neuron and a postsynaptic neuron
  • w/ a gap of about 20 nm between them
  • gap prevents the movement of a nerve signal from one neuron to another
153
Q

Propagation of a nerve signal at a synapse

A
  1. A neurotransmitter is synthesised and stored in vesicles
  2. Action potential reaches presynaptic terminal
  3. Depolarisation of presynaptic terminal causes opening of voltage-gated calcium (Ca2+) channels
  4. Influx of Ca2+ through channels
  5. Ca2+ causes vesicles, w/ neurotransmitter to fuse w/ a presynaptic membrane
  6. Neurotransmitter is released into synaptic cleft via exocytosis
  7. Neurotransmitter binds to receptor molecules on postsynaptic membrane
  8. Opening or closing of postsynaptic channels; if Na+ channels are opened, Na+ ions will enter postsynaptic neuron and initiate an action potential
  9. Postsynaptic current causes excitatory or inhibitory postsynaptic potential
    - changes excitability of the postsynaptic cell
  10. Retrieval of vesicular membrane from plasma membrane
154
Q

Acetylcholine

A
  • a neurotransmitter

- consists of a choline and an acetyl group

155
Q

Acetylcholine and neurotransmission

A
  • acetylcholine is released into synaptic cleft
  • diffuses across to postsynaptic cell
  • it binds for a brief period of time to the receptors
  • Once neurotransmitter is released, acetylcholinesterase breaks down neurotransmitter into choline and acetate
  • choline is reabsorbed by presynaptic cell and used again
156
Q

Why is secretion of acetylcholine important?

A
  • secretion of acetylcholine by neurons at synapses ensures that action potential is propagated to postsynaptic neuron
  • reabsorption of acetylcholine ensures that intensity and duration of signal being sent is controlled
157
Q

How can a nerve signal cross synaptic clefts?

A

process requires an interaction between a neurotransmitter and a receptor located on cell membrane of the postsynaptic neuron

158
Q

Neonicotinoids

A
  • derivative of nicotine

- can bind to acetylcholine receptors in cholinergic synapses

159
Q

Cholinergic synapses

A

synapses that use acetylcholine as the neurotransmitter

160
Q

Impact of a neonicotinoid on the nervous system

A
  • neonicotinoid enters nervous system
  • it binds irreversibly w/ receptors, preventing acetylcholine from binding
  • additionally, acetyl-cholinesterase can’t break down these compounds
  • effect is that the synaptic transmission is permanently blocked
  • nerve signals can’t be propagated to postsynaptic nerve
  • when this happens in the brain, result can be paralysis or even death

NB/ humans and other mammals are effected less by the binding of these compounds than insects

161
Q

Why are neonicotinoids useful as insecticides?

A
  • most of the cholinergic receptors in insects are located in the brain
  • makes neonicotinoids useful as insecticides
162
Q

Islets of Langerhans

A
  • located in the pancreases
  • insulin and glucagon are produced here
  • insulin and glucagon are responsible for maintaining and controlling blood glucose conc.
163
Q

What happens when blood glucose level is higher than normal?

A
  • Insulin is secreted
  • produced and secreted by β-cells of Islets of Langerhans in the pancreas
  • level of blood glucose fall
  • insulin stimulates glucose uptake into muscles and liver cells, where it’s converted into glycogen
164
Q

What happens when blood glucose level is lower than normal?

A
  • glucagon is secreted
  • produced and secreted by α-cells of Islets of Langerhans in the pancreas
  • level of blood glucose rises
  • glucagon stimulates glycogen hydrolysis to glucose in liver
  • this in turn releases glucose into the blood
165
Q

Pancreas and hormones

A
  • it has both exocrine and endocrine functions
  • as an exocrine gland, it secretes enzymes that help in digestion
  • as an endocrine gland it secretes hormones that regulate blood sugar levels
166
Q

Exocrine vs. endocrine gland

A

Exocrine: a gland associated w/ a duct

Endocrine: a ductless gland

167
Q

Diabetes mellitus

A

a disease where the blood glucose levels are consistently too high
- takes a lot of time for blood glucose level to come back to normal in diabetics

168
Q

Symptoms of diabetes mellitus

A
  • produce urine with elevated glucose levels
  • frequent urination, increased thirst and hunger
  • if untreated, diabetes can lead to long-term complications, eg. heart disease, kidney failure and retinal damage
169
Q

Two types of diabetes

A
  1. Type 1 diabetes

2. Type 2 diabetes

170
Q

Type 1 diabetes

A
  • results from body’s failure to produce insulin
  • referred to as insulin-dependent diabetes mellitus (IDDM) or juvenile diabetes

Treatment:
- involves injecting insulin into the body on a daily basis

171
Q

Type 2 diabetes

A
  • results from insulin resistance- condition where body cells fail to use insulin properly
  • referred to as non insulin-dependent diabetes mellitus (NIDDM), or adult-onset diabetes
  • it often begins later in life

Treatment:

  • may be treated by eating food w/ low levels of carbohydrates
  • eating frequent but small meals
  • doing strenuous exercise
  • losing weight
172
Q

Thyroxine

A
  • main hormone that. regulates metabolism and body temperature
  • produced in the thyroid gland
  • effect of thyroxine is to activate nuclear transcription of larger numbers of genes in all cells of the body
  • hence, thyroxine increases metabolic activities of almost all tissues of the body
173
Q

Effects of thyroxine

A
  1. Increased rate of utilisation of foods for energy
  2. Increased breathing rate to obtain oxygen and get rid of CO2
  3. Increased rate of protein synthesis and protein catabolism
  4. Increased no. and size of mitochondria in most cells of the body
  5. Increased growth rate of children and adolescents
  6. Enhanced carb and fat metabolism
174
Q

Relationship between thyroxine and metabolism

A
  • when body’s metabolic rate increases, rate of cellular respiration also increases producing a large amount of heat
  • so, elevated thyroxine production accounts for increased body temperature
  • relationship is used to help control body temperature
  • eg. when body temperature is above normal, thyroxine level is decreased to reduce heat production
175
Q

Goitre

A

an enlargement of the thyroid gland

  • production of thyroxine in thyroid gland requires four atoms of iodine and AA tyrosine
  • goitre is caused when iodine isn’t present in the diet, or in amounts too low to produce sufficient amounts of thyroxine

Treatment: treated by supplying the diet w/ iodine tablets

176
Q

Symptoms of thyroxine deficiency

A
  • Fatigue
  • Depression
  • Forgetfulness
  • Feeling cold
  • Constipation

In young children, can lead to impaired brain development

177
Q

Leptin

A

hormone produced and secreted by cells in adipose tissues that store lipids in your body

  • leptin receptors are found in hypothalamus
  • once leptin binds to these receptors, it causes appetite inhibition
178
Q

Adipose tissue

A

fatty tissues mainly composed of fat cells (adipocytes) that are specialised in synthesis and storage of fat globules

179
Q

Factors that control blood leptin concentration

A
  • food intake

- amount of adipose tissues in the body

180
Q

What happens when fat mass decreases? (leptin)

A
  • when fat mass decreases, level of plasma leptin falls- only a few leptin receptors bind to leptin in hypothalamus
  • appetite is stimulated until fat mass is recovered
  • decrease in body temp. and energy expenditure is suppressed
181
Q

What happens when fat mass increases? (leptin)

A
  • when fat mass increases, level of plasma leptin increases
  • lots of leptin receptors bind to leptin in hypothalamus
  • appetite is suppressed until fat mass is decreased
  • increase in body temp.
  • energy expenditure increases
182
Q

Low leptin production

A

Causes:

  • weight loss
  • just before eating
  • sleep deprivation

Effects:

  • less leptin secreted from fat cells
  • appetite increases
  • energy expenditure decreases
  • temp. decreases
183
Q

High leptin production

A

Causes:

  • weight gain
  • after eating

Effects:

  • more leptin secreted from fat cells
  • appetite decreases
  • energy expenditure increases
184
Q

Leptin injections and. clinical trials

A
  • leptin injections appeared to work in mice- didn’t have same effect when tested on humans
  • small subset of people homozygous for ob allele were tested- these people are frequently obese
  • In a double-blind trial, results showed some participants lost body mass but others gained in mass
  • any loss in mass was quickly regained after trial was stopped
  • obese people have very high leptin levels in their blood
  • implies that receptor cells in hypothalamus may no longer be sensitive and responsive to leptin
  • thus they don’t induce appetite inhibition
185
Q

How does the body keep track of circadian rhythms?

A
  • through the controlled secretion of melatonin from pineal gland
186
Q

Pineal gland

A
  • a small endocrine gland

- found near to the centre of the brain between the 2 hemispheres

187
Q

How does light exposure affect melatonin secretion?

A
  • special receptor cells in retina signal dawn and dusk to pineal gland
  • impulses from retina are channelled to the suprachiasmatic nuclei (SCN)
  • SCN which then pass on information to pineal gland
  • pineal gland then adapts melatonin conc. in the blood to coincide w/ a normal 24-hour cycle
  • melatonin receptors are present on neurons of suprachiasmatic nuclei of most species
  • implies the possible involvement of a negative feedback loop in regulation of melatonin
188
Q

What impacts melatonin secretion?

A
  • melatonin is synthesised from AA tryptophan
  • its production is dictated by light
  • exposure to light has a negative effect on release of melatonin
  • melatonin secretion is generally low when exposed to daylight and high during dark periods
189
Q

How does the body react to melatonin?

A
  • body core temp. drops
  • receptors in the kidney cause decreased urine production
  • increases sleepiness
190
Q

Jet lag

A
  • upsets our normal circadian rhythm forcefully and artificially
  • makes us irritable, gives us headaches, indigestion and makes increases sleepiness during light periods
  • melatonin intake can help people sleep and alleviate some of the symptoms of jet lag
191
Q

Forming a femal embryo

A
  • for all humans, life in the uterus starts out as female
  • oestrogen and progesterone are continually present during pregnancy because mother’s ovaries and placenta keep secreting these two hormones
  • oestrogen and progesterone start embryo on path to becoming a female w/ gonads developing into ovaries
  • if embryo has sex chromosomes XX, development is completed to form female genitalia
  • secondary female sexual characteristics then develop during puberty when there’s a rise in blood concentration of these two hormones
192
Q

Forming a male embryo

A
  • for all humans, life in the uterus starts out as female
  • in males, TDF (Testis Determining Factor), coded for by SRY gene on Y chromosome, triggers development of testis and, indirectly, production of testosterone
  • TDF is a DNA-binding protein that regulates transcription of no. of genes involved in differentiation of gonads into the testis
  • happens around week 8 of pregnancy
  • Once testis have developed they start to produce testosterone
  • triggers development of male genitalia
  • during puberty, testosterone production further increases, giving rise to secondary male sexual characteristics,
193
Q

Secondary female sex characteristics

A
  • development of breasts
  • development of pubic hair
  • broadening of hips
  • start of menses
194
Q

Secondary male sex characteristics

A
  • development of pubic hair
  • enlargement of penis
  • deepening of voice
195
Q

Ovary

A

Produces oestrogen, progesterone and ovum (egg)

196
Q

Oviduct (fallopian tubes)

A

Collects eggs from ovary and carries them to uterus

197
Q

Uterus

A

Place for gestation of embryo and foetus

198
Q

Cervix

A

Blocks entry to uterus during pregnancy and dilates during birth

199
Q

Vagina

A

Receptacle for penis during intercourse and forms birth canal

200
Q

Vulva

A

External parts for protection of internal reproductive system

201
Q

Testis

A

Sperm and testosterone production

202
Q

Epididymis

A

Stores sperm until ejaculation

203
Q

Sperm duct

A

Transfers sperm during ejaculation

204
Q

Seminal vesicles

A

Produce a sugar-rich fluid (fructose) that provides sperm with a source of energy to help them move

205
Q

Prostate gland

A

Produces an alkaline fluid, rich in proteins which together with seminal vesicles’ secretion and sperm makes semen

206
Q

Urethra

A

Transfers semen during ejaculation and the passage of urine during urination

207
Q

Penis

A

Penetrates the vagina to deposit semen close to the cervix

208
Q

Menstrual cycle

A

cyclic and periodic change in ovarian and pituitary hormones that controls when a woman is fertile

  • occurs between onset of puberty and end of menopause
  • can be divided into two phases: follicular and luteal
209
Q

Follicular phase

A
  • refers to formation of follicles in the ovaries

- each follicle contains one egg during its development until ovulation

210
Q

Luteal phase

A

refers to transformation of a follicle into a corpus luteum once ovulation has taken place around day 14

211
Q

Puberty

A
  • period of adolescence when individual reaches sexual maturity and becomes capable of reproducing
  • It’s accompanied by maturation of genital organs, development of secondary sexual characteristics and, in humans and some primates, by first occurrence of menstruation in female
212
Q

Menopause

A

period in a woman’s life (around 45–50 years) when her menses stops

213
Q

Hormones that control the menstrual cycle

A

Secreted by the pituitary gland:

  • luteinising hormone (LH)
  • follicle-stimulating hormone (FSH)

Secreted by the ovaries:

  • oestrogen
  • progesterone

Hormones are produced in sequence of:
FSH –> oestrogen –> LH –> progesterone

214
Q

Negative feedback

A

has a stabilising effect on system or processes

- in this case, product of a process controls rate of its own production

215
Q

Negative feedback in the menstrual cycle

A
  • pituitary gland secretes FSH; stimulates production of oestrogen
  • but, an increased conc. of estrogen feeds back to inhibit production of FSH
  • in this way no more FSH is produced
216
Q

Positive feedback

A

involves enhancing or amplification of a product by its own effect on the process which gives rise to it

217
Q

Follicle stage of menstrual cycle

A
  • FSH causes several follicles in ovary to develop
  • usually, only one matures
  • as follicle develops, it secretes oestrogen
  • oestrogen stimulates uterine lining to thicken w/ mucous and a rich supply of blood vessels
  • these changes last around 10 days
  • prepare uterus for a possible pregnancy
218
Q

Ovulation

A
  • a high level of oestrogen in the blood causes pituitary gland to reduce secretion of FSH (by -ve feedback) and begin secretion of LH (by +ve feedback)
  • decrease in FSH decreases production of oestrogen
  • when conc. of LH in the blood reach a certain level, ovulation occurs
  • one mature follicle (a Graafian follicle) ruptures- releasing a mature egg
  • ovulation usually occurs around the middle of the menstrual cycle
219
Q

Corpus luteum stage

A
  • after ovulation, LH causes ruptured follicle to fill w/ cells, forming corpus luteum
  • corpus luteum begins to secrete hormone progesterone, which maintains continued growth of uterine lining
  • corpus luteum also produces oestrogen- accounts for rise in this hormone level after ovulation
  • as conc. of oestrogen and progesterone rise to a certain level, they inhibit secretion of FSH and LH (-ve feedback)
  • this stage lasts about 14 days
220
Q

Menstruation

A
  • if fertilisation doesn’t occur, corpus luteum breaks down
  • results in a decrease in level of progesterone and oestrogen
  • w/ drop in progesterone level, thickened lining of uterus can’t be maintained, and it breaks down
  • extra layers of endometrium lining, unfertilised egg, and small amount of blood pass out through the vagina
  • lasts about 3-5 days
  • while menstruation is occurring, amount of oestrogen in blood falls, reduces inhibitory effect of oestrogen on FSH secretion
  • pituitary gland then increases its output of FSH, a new follicle starts maturing, and cycle starts again
221
Q

Role of progesterone (ovary)

A

Rises at the start of the luteal phase

- promotes thickening and maintenance of the endometrium

222
Q

Role of oestrogen (ovary)

A

Rises to a peak towards the end of the follicular phase

- stimulates repair of endometrium and increase in FSH receptors on ovary cells

223
Q

FSH (pituitary)

A

Starts to rise towards the end of the cycle (day 28)

- stimulates development of follicles and production of oestrogen by follicle wall

224
Q

LH (pituitary)

A

Rises to a sudden peak towards the end of the follicular phase

  • stimulates completion of meiosis in the oocyte and thinning of the follicular wall- so ovulation can occur
  • after ovulation, it stimulates development of remaining part of Graafian follicle into corpus luteum
  • this is by causing an increase in no. of follicle cells
  • corpus luteum secretes oestrogen and progesterone
225
Q

IVF

A
  • in vitro fertilisation (artificial fertilisation)

- means that fertilisation takes place in glass

226
Q

Why do couples go for IVF?

A
  • woman w/ blocked fallopian tubes
  • woman can’t produce healthy eggs
  • man doesn’t produce enough sperm for fertilisation to take place
  • man suffers from erection problems
  • genetic predisposition of one parent towards certain health problems
  • couple is unable to conceive normally
227
Q

Process of in vitro fertilisation

A
  1. Woman is given drugs to suppress her natural cycle by suspending her normal secretion of hormones
  2. FSH and LH are injected at higher doses that normal to stimulate production of no. of ova- superovulation
  3. Between 34-48 hours before eggs are due to be collected, woman is given a HCG injection to help eggs mature
    - eggs are then collected from ovary by ultrasound guidance while person is sedated
    - hollow needle is attached to the ultrasound probe and is used to collect eggs from follicles on each ovary
  4. Sperm sample is collected from woman’s partner and checked for viability
  5. Eggs are mixed w/ sperm and cultured in lab for 16-20 hours- then checked for signs of fertilisation
    - fertilised eggs, the embryos, are grown in lab incubator for 6 days
    - development of embryos is monitored- best is chosen to transfer
    - remaining embryos of suitable quality are frozen for future use
  6. If woman is under 40 years, one or two embryos are implanted in uterus
    - if above 40, a maximum of 3 may be used
    - no. of embryos transferred is restricted due to risks associated w/ multiple births
228
Q

Arguments for IVF

A
  • infertile families can have a baby
  • embryos can be screened for genetic and other disorders
  • increases understanding of human reproduction
229
Q

Arguments against IVF

A
  • not all embryos are used, and some are destroyed
  • IVF often results in multiple births- increased risk of mother and babies
  • not considered ‘natural’- frowned upon by religious groups
  • woman may be at risk because of hormonal injections
230
Q

William Harvey and Aristotle

A

Aristotle’s theory: man produces a seed which develops into an egg, which further develops into an embryo w/ help of menstrual blood

Harvey:

  • observed and dissected female deer in mating season
  • to see if small embryos could be found immediately after fertilisation
  • theorised that ‘seed and soil’ theory by Aristotle couldn’t be true because he found no embryos in the uterus of the female deer
  • But, Harvey didn’t conclude that sex resulted in formation of an embryo
  • he couldn’t conclusively determine that fertilisation of an egg by sperm gave rise to an embryo

IB Biology HL (12 decks)

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