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HL Biology - topical sets > Topic 11 > Flashcards

Topic 11 Flashcards

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1
Q

What are some adaptations of desert mammals for osmoregulation [4] (PPQ)

A
  • Longer loops of Henle
  • more ADH released
  • reduced sweat
  • fat stored in humps in camels -> broken down to release metabolic water
  • behavioural adaptations -> nocturnal animals/burrowing
  • large ears -> heat loss
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2
Q

Explain the mechanism that prevents polyspermy

A

cortical reaction;
cortical granules release enzymes;
zona pellucida hardens;
the acrosome enzymes cannot digest hardened outer coat;

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3
Q

explain the propagation of a nerve impulse along the membrane of a neuron [3]

A
  • the depolarisation of one part of the membrane causes depolarisation of the next part
  • local currents
  • Na+ ions from the depolarisation of one part diffuse to the next part of the membrane
  • resting potential reduced
  • sodium channels opened when threshold potential is reached
  • entry of sodium ions causes depolarisation
  • saltatory conduction in myelinated neurons
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4
Q

Describe the process of oogenesis

A
  • oogonia exist in the ovaries
  • oogonia undergo mitosis + growth to produce 1° oocyte
  • 1° oocyte division arrested in P1 till puberty (by granulosa cells surrounding them to form follicles) -> FSH release on a monthly basis stimulates the completion of P1
  • 1 x 1 ° oocyte every month becomes a 2 ° oocyte + polar body (the cytoplasm of one 2 ° oocyte transferred completely to the other)
  • polar body trapped in follicle till it degenerates
  • then it starts to undergo meiosis 2 but it arrested in M2
  • the oocyte is released (surrounded by corona radiata) which gives it nourishment in the oviduct
  • Mei 2 is completed upon fertilisation by a sperm cell -> forms ovum + polar body -> then ovum nucleus and sperm cell nucleus fuse
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5
Q

describe spermatogenesis

A
  • spermatogonia undergo growth and mitosis to form primary s-scytes
  • prim s-cytes undergo mei 1 to form sec. s-cytes
  • sec s-cytes undergo mei 2 to form spermatid
  • spermatid differentiate and are nourished in sertoli cells to form spermatozoa
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6
Q

difference between s genesis and oogenesis

A

S: produces 4 equal size gametes, O produces 1 large gamete and 2-3 smaller polar bodies
S - the spermatozoa is smaller than gonia, O - ovum is larger than gonia
S - begins at puberty, occurs throughout lifespan O - stops at menopause, release starts at puberty, begins in foetus

S - occurs entirely in testes, O - occurs mostly in ovaries
S- uninteruppted O - arrested stages

S- spermatogonia generated from the germline epithelium; O - germline epithelium doesn’t directly contribute to the production of ovum

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7
Q

Where sperm cells produced + qualities

A
  • in seminiferous tubules in testes
  • seminiferous tubules surrounded by basement membrane -> lined with germline epithelium
  • germline epithelium cells divide by mitosis to form the spermatogonia
  • OUTSIDE the tubules -> interstitial/Leydig cells (produce testosterone) and blood capillaries
  • spermatozoa are released into the seminiferous tubules lumen
  • spermatids noursihed by sertoli cells, in the tubule lining
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8
Q

Where oocytes are produced + qualities

A
  • ovaries
  • the primary oocytes are in primordial follicles
  • some of these develop every month into primary and secondary follicles
  • only 1 every month will become a mature/Graafian follicle
  • ruptures to release a sec oocyte -> forms a corpus luteum
  • corpus luteum then becomes corpus albicans
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9
Q

movement of sperm cells in tubule

A
  • production starts at the outer lining of the tubule and moves inwards
  • germ cells divide by meiosis and move towards the inner lining -> released into the lumen
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10
Q

Structure of a sperm cell

A
  • head, midpiece and flagellum
  • Head: has an acrosome cap (contains hydrolytic enzymes that digest the zona pellucida of the egg), HAPLOID nucleus, PAIRED CENTRIOLES (needed by the zygote to divide -> ova release their egg cells in polar bodies)
  • Midpiece: lots of mitochondria (ATP to move)
  • Tail: rotate -> make sperm cells motile -> consists of microtubule structure called acroneme (bends to facilitate movement)
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11
Q

Structure of an egg cell

A
  • Outside: 2 layers -> corona radiata, zona pellucida
    • CR: follicular cells that provide nourishment + support to the egg (CR outermost layer, then ZP)
    • Zone pellucida: jelly coat, glycoprotein matrix that acts as barrier to sperm entry
  • Inside: cortical granules - release contents upon sperm entry to prevent polyspermy in cortical reaction
  • Nucleus: doesn’t exist till after fertilisation as the meiosis 2 is arrested in M2
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12
Q

External fertilisation

A
  • fusion of gametes outside the body of the parent
  • usually in aquatic -> water acts as a medium of transport for the gametes
  • more susceptible to environmental changes (eg - pH, predators) hence more gametes released
  • process of releasing gametes into water: spawning
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12
Q

Internal fertilisation

A
  • fusion of gametes inside the body of the parent
  • gamete usually needs to be introduced into the body of one of the parents -> copulation
  • usually in terrestrials -> protect gamete from exposure/dessication
  • more protection to offspring, potential survival cost to parent
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13
Q

step 1 of fertilisation - capacitation

A
  • uterine chemicals dissolve the cholesterol coat of the sperm cells -> increased motility
  • destabilise the acrosome cap -> necessary for the acrosome reaction when sperm + egg come in contact
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14
Q

step 2 fert - acrosome reaction

A
  • sperm head pushes through the corona radiata cells
  • binds to the jelly coat/zona pellucida
  • acrosome vesicle fuses with the jelly coat and releases hydrolytic enzymes -> soften the jelly coat /glycoprotein matrix
  • pushes through softened jelly coat and reaches egg plasma membrane -> the sperm binds to exposed docking proteins
  • the sperm cell membrane fuses with the egg cell membrane
  • sperm nucleus enters egg
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15
Q

step 3 - cortical reaction

A
  • cotrical granules release enzymes into zp
  • harden the glycoprotein matrix of the zona pellucida
  • destroy the sperm binding sites
  • acrosome enzymes cannot digest the hardened jelly coat
  • prevent polyspermy
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16
Q

Embryo development stages

A

zygote (D0) -> morula (solid ball of cells) (D4) -> blastocyst (D7-8)

  • after fertilisation -> influx of Ca2+ into the egg cell triggers completion of mei. 2 -> zygote forms when nuclei of the 2 gametes fuse
  • zygote undergoes cell division to form morula
  • morula undergoes differentiation and cavitation to form blastocyst

3 parts of blastocyst
- trophoblast -> forms the placenta (surrounding outer layer)
- inner cell mass
- blastocoele (fluid filled cavity)

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17
Q

blastocyst implantation process

A
  • travels from the oviduct towards the uterus
  • in the uterus blastocyst sheds the jelly coat that prevents it from implanting
  • releases enzymes to degrade the endometrial lining. autocrine hormones released which trigger its implantation into the uterine wall. implants itself in the uterine wall
  • embryo develops there -> endometrium provides nutrients and oxygen for its development
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18
Q

hCG

A
  • human chorionic gonadotrophin
  • released by blastocyst when it implants itself in the uterine wall
  • maintains the corpus luteum that secretes oestrogen and progesterone after ovulation
    • oestrogen: inhibits FSH and LH secretion -> prevents development of more follicles
    • prog: maintains uterine lining
  • hCG release for 8-10 weeks -> after this placenta develops -> produces the progesterone to maintain lining
  • hCG levels drop and CL degenerates
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19
Q

Placenta structure

A
  • chorionic villi (containing the foetus’ capillaries)
  • intervillous space (lacunae)
    –> maternal blood pools in the intervillous spaces from open ended maternal arteries
  • placenta is disc-shaped structure -> forms from the development of trophoblast -> invades the uterine wall
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20
Q

placenta material exchange

A
  • chorionic villi contain foetal capillaries (close to the surface)
  • villi extend into the lacunae
  • have microvilli
  • mother to foetus: oxygen, nutrients, vitamins, antibodies, water
  • foetus to mother: hormones, urea, co2
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21
Q

placenta hormonal role

A
  • secretes oestrogen and progesterone
  • O: stimulates mammary gland development + growth pof uterine muscles
  • P: maintains endometrium, prevents maternal immune response, represses contractions
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22
Q

birth af

A

childbirth = parturition
- positive feedback loop -> amplifies a detected change
- growth of baby causes stretching of the uterine walls -> stretch receptor detect -> nerve impulse sent to brain -> oxytocin released from the posterior pituitary gland
- causes the uterine to contract -> lesser space -> more stretching -> more release of oxytocin
- continues till the stimulus is removed

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23
Q

birth in more detila

A
  • fully grown baby stretches against the uterine walls -> stress on both mother and foetus
  • mother releases estrogen (estriol in particular)
  • estriol primes smooth uterine muscle for contraction -> increase the sensitivity to oxytocin, also it inhibits progesterone which was reducing contractions
  • brain triggers oxytocin release from posterior pituitary (which also inhibits prog)
  • contractions of uterus -> increased release of oxytocin. foetus also releases prostaglandin -> causes more contractions
  • postive feedback loop -> stops when the birth is complete
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24
Q

Gestation period

A
  • time taken for the foetus to develop -> from fertilisation to birth

factors affecting:
- larger animals tend to have longer gestation periods
- more developed offspring at birth tend to have longer gestation

2 types of offspring:
- altricial: less developed offsrping which need extended rearing at birth
- precocial; more developed, require less rearing at birth

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25
Q

3 frameworks for movement in the body

A
  • Skeletal: consists of bones at act as levers for muscles to pull on
  • Muscular: consists of muscles that deliver force to move bones in relation to one another
  • Nervous: sends signal from the brain to the muscles, causing them to contract and create movement
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26
Q

Exo v endoskeleton

A
  • exo -> connected segments, endo - connected bones
  • both act as levers, moving in response to muscle contraction
  • Bone to Bone connection - ligament
  • Bone to muscle connection - tendon
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27
Q

Joints

A
  • synovial joints -> capsules surrounding the surfaces where 2 bones meet
  • joints enable some movement but not others

Parts of joint:
- cartilage: shock absorber, distributes load, lines the bone surface to allow smoother movement
- synovial fluid: lubricates joint, provides oxygen and nutrients
- joint capsule: seals the joint space and restricts the range of movement -> providing stability

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28
Q

Types of synovial joints (6)

A
  • ball and socket
  • hinge
  • pivot
  • plane
  • saddle
  • condyloid
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29
Q

The three bones in the elbow joint

A
  • humerus (the one above the joint)
  • Radius (higher forearm one -> connected to bicep)
  • ulna (lower forearm one -> connected to tricep)

acronym: RUBUDT (pronounced robot)

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30
Q

Antagonistic muscle roles

A
  • flexor muscle -> brings femur and tibia bones closer together, limb bends
  • extensor muscle -> pushes femur and tibia bones away from each other -> limb extends/becomes straight
  • in grasshopper -> femur, tibia and tarsus -> upper mid and lower legs
  • antagonistic muscle set; extensor tibiae and flexor tibiae

in antagonistic muscles: one contracts, the other relaxes and VV -> they pull the limb in opp. directions

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31
Q

Hierarchy of the parts of muscle

A

sarcomere (single contractile unit) -> myofibrils (tubular and run the length of muscle fibre, responsible for muscle contraction) -> muscle fibres (bundled together) -> muscular bundles -> skeletal muscle

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32
Q

Structure of sarcomere

A
  • HAI
  • H band innermost -> only myosin filament
  • A band where myosin and actin overlap
  • I band -> the Z disc/z lines
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33
Q

Depolarisation and Ca2+ ion release in mus. contraction

A
  • Action potential in motor neurone -> acetylcholine release into the motor end plate
  • acetylcholine release triggers depolarisation of sarcolemma -> spreads though t tubules
  • stimulates ca2+ release from the SR
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34
Q

The power stroke part

A
  • myosin heads bind to actin filament, forming cross bridge
  • ATP binds to the myosin head, cross bridge breaks
  • hydrolysis of ATP causes the myosin head to change config. and bind to next actin binding site
  • myosin head swivels back to OG position
  • z lines pulled closer together as actin and myosin filaments SLIDE OVER each other
  • individual sarcomeres shorten -> causes whole muscle to contract
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35
Q

Msucle contraction questions

A
  • DRAW A SARCOMERE DIAGRAM AND LABEL EVERY. DAMN. THING. (even the dark lines and light lines)
  • myofibrils make up muscle fibres
  • sarcomeres are repeating units that make up myofibrils
  • sarcomeres SHORTEN
  • z lines move closer together/actin filaments pulled towards the centre of sarcomere
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36
Q

Changing length of bands

A
  • A band (dark) -> doesn’t change
  • I band -> shortens upon contraction
  • H band -> shortens upon contraction
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37
Q

Discuss the control of blood glucose levels and consequences if they’ re not maintained

A
  • homeostasis maintains a constant internal env
  • pancreas produces hormones that regulate glucose level
  • insulin controls the blood GLUCOSE levels
  • when BG levels increase, detected by pancreas
  • release of insulin from beta cells of pancreas
  • cause uptake of glucose by liver and adipose cells
  • glucose converted to glycogen in liver cells for storage
  • when BG levels too low, alpha pancreas cells release glucagon
  • stimulates the breakdown of glycogen into glucose and its release into the bloodstream -> increase BG levels
  • negative feedback loop created
  • Type 2 diabetes causes other health issues like eye damage
  • when BG levels too high and body becomes resistant to insulin
  • T1 diabetes is from birth -> insulin is not produced by beta cells
  • must be regulated via insulin injections
  • T2 must be regulated via diet and exercise
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38
Q

Causes of T1 v T2 diabetes

A

t1: autoimmune -> the destruction of beta cells in pancreas
t2: the down-regulation of insulin receptors

39
Q

Thyroxin (production, signal, target, function)

A
  • Produced: thyroid gland
  • signals: derived from the hypothalamus
  • target: all cells in the body -> needed to ensure cell differentiation and development
  • function: increase basal metabolic rate (when body at rest) -> by stimulating carb and lipid metabolism via stimulation of glucose/fatty acid metabolism
    => metabolism/respiration releases heat => used to control body temperatures
  • hot body temp -> detected by the hypo. -> thyroxin release from hypothalamus inhibited -> metabolic rate decreased -> reduce heat production
  • low body temp -> hypo. detects -> metabolic rate increased -> heat produced

Iodine deficiency -> thyroid gland doesn’t function properly -> goitre (it swells)

40
Q

Leptin ‘’

A

prod: adipose cells
signals: binds to receptors on the hypothalamus -> cause hypothalamus to suppress appetite
function: suppressing appetite to regulate food intake and regulate fat stores
=> overeating leads to obesity => obesity causes higher stores of fat and adipose tissue => increased leptin production => appetite suppressed
=> starvation periods => adipose tissue decreases => more appetite as less leptin

  • with age -> leptin resistance increases -> potential for weight gain
  • with overeating -> less likely to recognise hunger -> body more desensitised to leptin -> overeat more
41
Q

Leptin mice experiments

A

2 mice bloodstreams were parabiotically fused:
- healthy mouse w mouse that has damaged leptin receptors (obese)
- hm and mouse that doesn’t produce leptin

  • HM and no leptin mouse: HM transferred leptin to obese mouse -> mouse ate less -> became healthy
  • HM and damaged receptor mouse: DR mouse overproduced leptin to account for low receptor sensitivity -> more leptin went into healthy mouse -. emaciated + no diff to DR mouse

Human trials:
- most human obesity caused by low sensitivity, not leptin deficiency
- leptin injections on humans didn’t work v well
- adverse side effects
- so not a good treatment

42
Q

Melatonin

A

prod: pineal gland
signal: light exposure in retina is relayed to the hypothalamus, inhibiting mela secretion. production is suppressed by light (blue in particular) so concentration increases at night
function: controlling the body’s circadian rhythms (responses to the 24 hour day cycle). higher levels promote sleep, and low levels suppress sleep in diurnal animals. converse in nocturnal animals. the production of melatonin can be entrained to anticipate onset of darkness or light

= melatonin levels tend to reduce with age -> differing sleep patterns in the elderly

43
Q

Jet lag

A
  • when circadian rhythms of the body haven’t adjusted to a new time zone after air travel
  • symp: irritability, fatigue, headache
  • melatonin secretion occurs according to the old time zone
  • subsides in a few days as body resynchronises
44
Q

soil and seed theory

A

Aristotle:
- man gives seed (has all the genetic information)
- mixes with womans menstrual blood
- produces embryo

Harvey:
- investigated sexual organs of deer after mating
- couldn’t find embryo till 6-7 weeks
- asserted: menstrual blood didn’t contribute
- incorrect assertion: no mixing of male and female seeds

correct discovery: from light microscopes

45
Q

Y chromosome

A

SRY gene (sex-determining region Y)
- causes embryonic gonads to develop into testes
- if no SRY -> develop into ovaries
- ovaries produce oestrogen and prog
- testes produce testosterone

46
Q

testosterone

A

development of:
- male sex organs + pre-natal development of male genitalia
- secon. characteristics -> facial hair, deepening of voice, muscle mass
- maintains male sex drive
- sperm production

47
Q

oestrogen and prog

A
  • development of sex organs pre-natally
  • role in menstrual cycle
  • development of breasts/body hair (secon. charac)

initially mother’s ovaries and then placenta secrete oestrogen -> in absence of testosterone -> till foetus resproductive organs develop

48
Q

functions of the different parts of the male rep. system

A
  • testes: produce the sperm and testosterone
  • vas deferens: tube via which the sperm travel from the testes to the prostate gland
  • seminal vesicle: produce fluid containing fructose (nourish sperm), prostaglandin (trigger uterine contractions), mucus (protect sperm)
  • epididymis: sperm matures and develops motility (stored here till ejaculation)
  • prostate gland: secrete alkaline fluid to neutralise vaginal acids
  • urethra: conveys sperm from the prostate gland through outside the body through penis
49
Q

functions of diff parts of female rep sys

A

ovary: the oocytes mature prior to release + secrete oestrogen and prog.
fimbriae: fringe of tissue adjacent to the ovary that sweep oocyte into oviduct
oviduct: conducts the occyte from the ovary to the uterus. usually where fertilisation occurs
uterus: zygote implants, foetus develops in uterus
endometrium: uterus lining that provides oxygen and nutrients to developing embryo, thickens in prep for implantation, shed if no implantation
cervix: opening of the uterus
vagina: passage to the cervix -> penis deposits sperm

50
Q

Menstrual cycle

A
  • FSH released from anterior pituitary
  • causes the development/maturation of follicles in the ovary
  • dominant follicle produces oestrogen, which causes the endometrium layer to begin developing + inhibits FSH to prevent other follicles developing
  • around day 12, oestrogen stimulates LH release from the pituitary causing the rupture of the dom follicle -> release the oocyte
  • ruptured follicle becomes a slowly degenerating corpus luteum, dv. stimulated by LH -> secretes progesterone and small amounts of oestrogen
  • these maintain the endometrium + inhibit LH and FSH to prevent more oocytes from being released
  • if the released oocyte is fertilised -> implants in the endometrium -> embryo release hCG to maintain the CL
  • if not, prog and oes levels fall as the corpus luteum degenerates into a CA -> endometrium layer sloughed away and removed via menstruation
51
Q

IVF Procedure

A
  1. down regulation: woman takes drugs via nasal spray to arrest the menstrual cycle. prevents production of FSH, LH and hence oes and prog as well
  2. superovulation: woman takes large FSH doses to stimulate the development of many follicles. hCG also taken to help them mature. oocytes then surgically removed with a needle before follicles rupture
  3. fertilisation: oocytes placed in presence of sperm from donor. microscope used to see if fertilised
  4. implantation: woman takes progesterone to build up the endometrium. zygotes implanted. 2 weeks later -> preg test to see if successful
52
Q

What are neurons

A

specialised cells, transmit nerve impulses within nervous system

53
Q

roles of the 3 different neuron parts

A

dendrite: converts chem signals from other neurons/receptor cells to electrical impulse

axon: elongated cell fibre that transmits an electrical impulses from terminal regions to communicate with other effectors/neurons

soma: cell body containing the nucleus and other organelles -> carry out metabolic processes for the cell’s survival

54
Q

Resting potential

A
  • membrane potential difference when neurone not firing
  • usually ‘-70 mV’
  • the inside of the membrane is more negative than the outside
  • maintained by the sodium potassium pump
  • ATP hydrolysis occurs for this electrochemical gradient to be maintained
  • 3 Na+ ions expelled for every K+ ion brought into the cell
55
Q

Action potential

A
  • threshold potential reached -> the Na ion channels opened in response to signal at dendrite
  • passive influx of na ions
  • positive charge in the cell (+30mv)

repolarisation:
- potassium ion channels open in the membrane
- K+ ions diffuse out passively
- more K+ ions diffuse out -> negative charge

refractory period;
- the Na moved out side and the K+ moved inside -> restore the resting potential via antiport action of Na/K pump

56
Q

nerve impulse transfer along the axon

A
  • depolarisation of one segment of neurone stimulates depolarisation in the next segment
  • ## due to local currents
56
Q

nerve impulse transfer along the axon

A
  • depolarisation of one segment of neurone stimulates depolarisation in the next segment
  • due to local currents
  • Na+ ions from the depolarisation of one part diffuse to the next part of the membrane
  • if the minimum threshold potential is reached, sodium ion channels open
  • sodium ion influx causes depolarisation
  • if myelinated -> saltatory conduction transmits the impulse down the axon
57
Q

Threshold potential

A
  • the minimum electrical stimulus of the dendrites needed to stimulate an action potential -> this stimulus opens voltage gated sodium ion channels
  • if minimum potential reached, an action potential of the same magnitude will be generated
  • TP is usually -55mV
  • movement of ions in one part sufficient to cause depolarisation in the next
58
Q

Oscilloscope numbers to remember

A
  • RP: - 70 mV
  • TP: -55 mV
  • dep: +30 mV
  • rep: - 80 mV
59
Q

Myelination

A
  • some axons coated with insulating fatty layer called myelin sheath
  • increases the speed of conduction and transfer of the electrical impulse
  • there is no continuous wave of depolarisation, instead depolarisation ‘jumps’ between gaps in myelin sheath called nodes of Ranvier -> saltatory conduction

A: faster transmission of electrical impulse
DA: The neurone takes up more space in enclosed env

60
Q

synaptic transfer

A
  • membrane needed for a nerve impulse to be transmitted
  • the impulse reaches the axon terminal of the neurone -> stimulates the opening of voltage gated Ca 2+ ion channels
  • Ca2+ ions diffuse into the neurone stimulating fusion of neurotransmitter-containing vesicles with the membrane
  • neurotransmitters released into the synapse -> cross the synaptic cleft and bind to receptors on the post-synaptic neurone
  • open ligand gated ion channels -> generating impulse in the post-synaptic neurone
  • if TP reached -> depolarisation of post-synaptic neurone
  • neurotransmitters are either degraded or recycled
61
Q

acetylcholine as a neuotransmitter

A
  • neurotran can either trigger or prevent a response by binding to receptors on post-synaptic neurons
  • common neurotransmitter -> used to stimulate muscle contraction. autonomous nervous system also releases it for parasympathetic responses
  • formed by the binding of acetyl group to a choline group in axon terminal -> vesicles bind to membrane and it is released into the synapse
  • binds to specific receptors on post-synaptic neurone

must be removed from synapse and degraded by enzymes -> overstimulation can cause fatal convulsions and paralysis
=> acetylcholinesterase breaks it down into the acetyl and choline groups
=> choline is taken up again by the pre-synaptic neurone
=> enzyme either released by pre-synaptic neurone or is bound to the membrane of the post-syn neurone

62
Q

Neonicotinoid pesticides

A
  • pesticides binds irreversibly to the nicotinic acetylcholine receptors at CHOLINERGIC synapses of insects -> blocking synaptic transmission
  • low activation of receptors promotes nerve signalling, overstimulation -> convulsions and paralysis
  • acetylcholinesterase can’t break down the neonictinoid
  • insect receptors bind to the neonicotinoid much more strongly -> it doesn’t impact mammals as much (hence good pesticide)

DA:
- reduction in honey bee and bird populations (loss of insect food)

63
Q

graded potentials

A
  • when neurotransmitters bind to the post synaptic neurone, they open the ligan gated ion channels -> cause small changes in mem potential (graded potential)

excitatory neurotrans - open ligand gated Na or Ca ion channels -> depolarisation
inhibitory neurotrans -> open K or Cl channels -> hyperpolarisation

If D > H -> fires
is H> D -> doesn’t

64
Q

Self vs non-self in immune system

A
  • body has the potential to differentiate body cells (self) and foreign cells (non-self)
  • nucleated body cells have self markers -> body recognises them as its own -> major histocompatibility molecules (MHC class 1) on their surfaces
    => doesn’t trigger an immune response
  • any substance that is foreign and capable of triggering an immune response is an antigen
    => antigens are recognised by lymphocytes -> bind to and detect specific exposed portions of the antigen (epitope)
    => adaptive immunity - release antibodies that specifically bind to epitopes via complementary paratopes
65
Q

Antigenic determinants

A

surface markers of cells -> bacteria/fungi/virus
self-markers of other cells -> rejection of transplants
proteins from food, unless broken down into components

66
Q

Blood types

A
  • RBC don’t have nucleus hence don’t have the usual MHC class 1 self marker -> transfusions between different people possible
  • RBC have surface glycoproteins -> A, B, both or non e
  • A -> A glyco + anti-B antibodies
  • O -> both antibodies, no glyco
  • AB -> both glyco, no antibodies

if wrong blood transfusion

67
Q

Blood types

A
  • RBC don’t have nucleus hence don’t have the usual MHC class 1 self marker -> transfusions between different people possible
  • RBC have surface glycoproteins -> A, B, both or non e
  • A -> A glyco + anti-B antibodies
  • O -> both antibodies, no glyco
  • AB -> both glyco, no antibodies

if wrong blood transfusion -> agglutination/clumping

Additional glycoprotein -> Rhesus factor (+/-)

68
Q

Disease, pathogen and illness

A
  • pathogen: any agent that causes a disease
  • illness: deterioration in the normal state of health of an organism
  • disease: a condition that disrupts the normal functioning of an organism

pathogens usually species specific -> certain pathogens infect only humans (syphillis, measles, etc.)

  • some pathogens are zoonotic -> can transfer to humans from animals
69
Q

Ways that diseases are transmitted between humans

A

direct contact: physical contact or exchange of bodily fluids
airborne: coughing/sneezing
vector: through an animal vector that doesn’t display the symptoms themselves
contamination: ingestion of pathogens on or in edible food sources

70
Q

clonal selection

A

the whole reaction where the macrophages ingest the pathogen -> b cells divide into clones -> plasma cells, etc.

one pathogen is likely to have many antigens -> multiple different antibodies released -> polyclonal activation

71
Q

Ways in which antibodies impact pathogens

A
  • agglutination
  • neutralises toxins/pathogenic regions
  • may trigger an inflammatory response in the body
  • complement proteins may perforate membranes -> cause cell lysis
  • precipitation -> soluble pathogens become insoluble
  • opsonisation: constant region of antibodies recognisable by phagocytes -> easier to detect pathogens -. easily engulf and digest pathogens
72
Q

Immunity

A
  • first exposure -> delay in the exposure and production of antibodies -> if too slow
  • memory cells stored for long periods of time in the body
  • produce low levels of circulating antibodies
  • upon secondary exposure, the antibodies are produced much more rapidly -> pathogens do not have time to reproduce sufficiently to cause disease symptoms -> individual is immune
73
Q

allergen

A
  • environmental substance that triggers an immune response despite not being intrinsically harmful
  • allergic reactions usually localised to exposure region -> unless serious -> causes anaphylaxis -> fatal
  • when first encountering the allergen, B lymph produces large amount of antibodies (IgE)
  • IgE binds to mast cells and primes them
  • upon secondary exposure to allergen, the pre-primed mast cells release large amounts of histamine
74
Q

allergic reaction and release of histamine

A
  • inflammation -> increases capillary permeability and vasodilation -> leukocyte mobility to infected regions improved
  • vasodilation causes redness (blood vessels closer to the skin) and heat (transported in the blood)
  • Capillary permeability -> swelling (more fluid leaks from the blood) -> causing pain (swelling = compression of nerves)
75
Q

How vaccinations work

A
  • an incapacitated version of the pathogen with the antigens is introduced to the body
  • antigens may be conjugated to an adjuvant to boost the immune response
  • memory cells produced as a part of the immune response
  • memory cells stored in the body -> the secondary response when exposed to a pathogen is much more rapid and vigorous
  • different memory cells last in the body for diff amounts of time -> booster shots may be required

Herd immunity:
- when people who are not immune to a pathogen are protected due to large proprotions of immune individuals in the population

Vaxx programmes usually to reduce outbreak of certain diseases in areas:
- epidemic: substantially increased occurrence of a certain infection in a given area
- pandemic: large scale spread of epidemic over a wider geographical region (eg continent)

76
Q

Small pox eradication

A

Elimination: when a disease stops circulating in a region
eradication: when disease stops circulating worldwide

smallpox was eradicated via a large scale worldwide vaccination initiative by WHO. why successful:
- smallpox easy to recognise symptoms
- relatively stable virus that didn’t last too long in body and didn’t mutate easily
- worldwide intl cooperation + long term immunity
- only spread through direct contact and didn’t have animal vectors or reservoirs

77
Q

Epidemiology

A

the study of patterns, causes and effects of disease and health conditions in a defined population

78
Q

How monoclonal antibodies produced

A
  • mice infected with antigens
  • they produce lots of B cells which differentiate into plasma cells
  • plasma cells extracted and fused with tumour cells that have unlimited capacity to divide (melanoma)
  • hybridoma cells formed -> continuously and limitlessly produce antibodies
  • large amounts of antibodies harvested
  • antibodies can be injected into individuals
79
Q

Therapeutic uses of monoclonal antibodies

A

Rabies:
- injecting purified antibodies as a potential emergency treatment
- as can be fatal

Cancer cells:
- can be used to target cancer cells that the body cannot recognise as harmful

mice antibodies easier to synthesise -> more likely to be rejected

80
Q

monoclonal antibodies diagnostic use

A

Pregnancy test:
- reaction site: free antibody bound to a dye enzyme (hCG binds to antibody if present in pee)
- test site: fixed antibody + dye substrate -> binds to hCG that is alr attached to the dye enzyme and antibody -> forms hCG sandwich -> dye enzyme and subs brought in close proximity -> dye changes colour
- control site: fixed antibody + dye subs -> traps free antibody + dye enzyme -> colour change as there will be free antibody + dye enzyme whether or not hCG is present

81
Q

Excretion + 2 functions

A

removal of the waste products of metabolism from the body

2 functions of excretory system:
- removing nitrogenous waste from breakdown of proteins and nucleotides
- remove excess water to maintain osmolarity in tissues and cells

82
Q

Different animals N waste forms

A

Aquatic:
- ammonia
- highly toxic but soluble
- since in water -> easy to flush out

Mammals:
- urea
- less toxic
- can be stored at higher concentrations

Bords/reptiles/insects:
- uric acid
- non-toxic
- least water needed to flush out
- more energy needed to make

83
Q

Osmoregulators v. conformers

A

regulators: maintain a constant internal osmolarity despite changes in environment. less subject to changes in env -> internal/optimal osmotic conditions always controlled -> more energy required/used to maintain

conformers: conform/match the osmolarity of the environment. less energy needed to maintain but subject to environmental changes

84
Q

Malpighian tubules

A
  • insects don’t have separate digestive and excretory systems like mammals
  • malpighian tubules branch off from the hemolyph (circulating fluid system like blood system) and connect to the digestive tract
  • nitrogenous wastes and water are actively taken up by the malpighian tubles from the hemolymph and sent to the digestive tract
  • in the hindgut water, solutes and salts are reabsorbed
  • uric acid and digested food waste are both excreted together from the anus
85
Q

name of blood capillary network efferent arteriole forms

A

vasa recta
- it reabsorbs components from the filtrate in the nephron

86
Q

Structure of the Bowman’s capsule

A
  • Capillary tuft called glomerulus
  • surrounded by the bowman’s capsule
  • inner surface of the BC has podocytes with cellular extensions (pedicels) -> wrapping around the glomerulus blood vessel
  • between podocytes and glomerulus -> glycoprotein matrix that filters the blood -> basement membrane
  • Glomerulus walls are fenestrated -> allow for the removal of blood through the pores
  • the pedicels have gaps between them -> allows for the passage of materials
  • BM the only filter -> glycoprotein matrix that allows for the passage of urea, solutes, water but not any blood cells, proteins, platelets, etc.
87
Q

Hydrostatic pressure in glomerulus

A
  • afferent arteriole is wider than efferent arteriole
  • blood enters at a faster rate than it can exit
  • high pressure within the glomerulus -> solutes and water are pushed out of the glomerulus by being forced against the BM -> ultrafiltered into the BC
  • glomerulus forms extensive narrow branches -> optimise the filtration
88
Q

Adaptations of the proximal convoluted tubule

A
  • lining consists of cells with tight junctions in between them -> no gaps
  • tubule lining is one cell thick
  • inner surface has microvilli to maximise absorption
  • membrane contains carrier proteins/pumps to transport materials across
  • more mitochondria to produce ATP for active transport
89
Q

selective reabsorption processes

A

substances actively transported across apical membrane (facing inside) + passively diffuse across the basolateral membrane (facing blood)

  • mineral ions and vitamins actively transported via protein pump and carrier proteins resp.
  • water follows mineral ions across membrane passively/osmosis
  • glucose and AAs -> cotransported symport w sodium
90
Q

Loop of Henle details

A
  • ascending limb permeable to salts not water
  • descending limb perm to water not salts
  • increase the hypertonicity of medulla
  • salts and water diffuse out of the loop of H
  • counter current in a vasa recta -> draws salts further down into the medulla -> further establishing the salt gradient
  • lower down in the medulla, it is more hypertonic
91
Q

what detects blood water levels
where is ADH released from

A
  • osmoreceptors in the hypothalamus
  • posterior pituitary
92
Q

Over and dehydration

A

Over:
- blood hypotonic
- excess water enters cells causes them to swell -> cell lysis/tissue damage
- body releases large amounts to clear urine to remove water from body
- swelling can cause headaches and nerve impulse disruption in mild cases
- serious: fatigue, delirium, coma, death

De:
- blood is hypertonic, water leaves cells and they become shrivelled
- reduced release of sweat -> problems cooling
- can cause fatigue, brain seizures, death
- feel thirsty -> small quantities of concentrated urine

93
Q

Diseases detection from urine

A

Glucose: high amounts of blood sugar -> diabetes
proteins: certain diseases (PKU) or hormonal conditions (hCG)
blood cells: wide variety of infections or cancer
drugs: usually pass through urine -> ingestion can be detected by presence in urine

94
Q

How dialysis works

A
  • blood is removed from the body and passed through a dialyzer
  • dialyzer has 2 functions common to cell membranes -> semi-permeable membrane + introduces fresh dialysis fluid and removes wastes -> maintains [] gradient

HL Biology - topical sets (11 decks)

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