5.1.1 Communication and Homeostasis Flashcards

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1
Q

What is homeostasis?

A

-maintenance of a constant internal environment in response to changes in external/internal environment
-involves control systems that keep internal environment roughly constant

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2
Q

How do animals respond to the environment?

A
  • respond to changes in their external environment i.e by avoiding harmful environments
    -respond to changes in their internal environment to make sure conditions are optimal for metabolic reactions
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3
Q

Changes to internal environment

A

-internal body temp
-blood glucose levels
-water levels
-pH

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4
Q

Changes to external environment

A

-external temp
-humidity
-light(plants)
-harmful stimuli i.e sudden sounds/pain

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5
Q

Why is homeostasis important?

A

-vital for cells to function normally and stop them being damaged
-allows them to avoid harmful environment / ensure that conditions are optimum for metabolism

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6
Q

Why are receptors and effectors needed?

A

-restore dynamic equilibrium in response to conditions
-receptors trigger and co-ordinate the correct responses
-info from sensory receptors is transmitted to the brain + impulses are sent along motor neurons to effectors(muscles/glands) that react to bring about change in response to stimulus

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7
Q

Why do multicellular organisms need communication systems?

A

-organs, cells and tissues have different functions, are found in different parts of the body and may have different roles to one another
-need to communicate

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8
Q

Short paracrine cell signalling

A

-occurs between cells that are close together i.e neurotransmitters between nerves or muscle cells

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9
Q

Long distance endocrine signalling

A

-involves signalling over long distances
-signalling molecules are transported in the circulatory system

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10
Q

What is a hormone?

A

-a chemical messenger, secreted by glands and found in the endocrine system

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11
Q

similarities between the endocrine + nervous system

A

-both have coordination centres(brain, spinal cord)
-both send signals in the body
-both have receptors to detect stimuli
-both have effectors(muscles/glands) to carry out response

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12
Q

Differences between nervous + endocrine system

A

-chemical messengers vs nerve impulses
-hormones are longer lasting vs nerves are shorter lasting
-nerves work faster than hormones

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13
Q

What do cell surface receptors do?

A

-allow cells to recognise the chemicals involved in cell signalling

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14
Q

What is negative feedback?

A

-control mechanism that elicits response to help restore changed value to norm
-receptors detect when a level is too high/low-}info communicated via nervous/hormonal system –} effectors respond to counteract the change

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15
Q

What happens if the change from normal is too big?

A

-effectors may not be able to counteract it, i.e a huge drop in body temp caused by prolonged exposure to cold

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16
Q

What is positive feedback?

A

-amplifies the change away from normal
-not involved in homeostasis because internal environment isn’t constant
-rapidly activates processes in the body i.e platelets forming blood clots

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17
Q

Why is it important to maintain core body temp?

A
  • temp affects enzyme activity and enzymes control the rate of metabolic reactions
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18
Q

How does high body temp have an effect?

A

-rise in temperature makes the enzyme’s molecules vibrate more
-if temp goes above a certain level, vibration breaks some H bonds in the tertiary structure
-active site changes shape and enzyme + substrate no longer fit together
-enzyme denatures

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19
Q

How does low body temp have an effect?

A

-enzyme activity / RoR
-enzyme-substrate complexes cannot form

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20
Q

Why does body temp fluctuate throughout the day?

A

-it is dependent on the external environment
-respiration is an exothermic reaction, so the temp it works at changes

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21
Q

How are temp changes in the body detected?

A

-the peripheral temp receptors are in the skin + detect changes in the skin surface temp
-temp receptors in the hypothalamus detect temp of blood in the body

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22
Q

What is an ectotherm?

A

-an animal that cannot control their body temp internally via homeostasis
-instead change their behaviour i.e migration

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23
Q

Sources for ectotherms to regulate temp

A

-radiation= absorbing thermal energy
-evaporation
-convection= thermal energy transferred with air/liquids
-conduction= transfer of thermal energy through solid surfaces

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24
Q

What are endotherms?

A

-can control their body temperature internally via homeostasis i.e mammals and birds

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25
Q

Difference in metabolic rate between ectotherms and endotherms

A

-ectotherms don’t have a constant body temp so their metabolic rate varies
–} more active at higher temps and vice versa
-endotherms can keep internal temp constant so they have a constantly high metabolic rate–} largely independent of external temp

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26
Q

Mechanisms to reduce body temp: vasodilation

A

-atertioles near the surface of the skin dilate when temp rises
-vessels that provide a direct connection between the arterioles + the venules constrict
-this forces blood through the capillaries in the surface layers of the skin
-more heat is lost from the skin in radiation +temp is lowered

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27
Q

Mechanisms to reduce body temp:
Sweating

A

-more sweat secreted from sweat glands as core temp increases
-water in sweat evaporates from the surface of the skin + takes heat from the body + cooling the skin

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28
Q

Mechanisms to reduce body temp:
Hairs lie flat

A

-as temp increases, the erector pilli muscles in the skin relax, causing hairs to lie flat
-avoids trapping an insulating layer of air–} skin is less insulated and heat can be lost more easily

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29
Q

Mechanisms to increase body temp:
vasoconstriction

A

-arterioles near me surface of the skin constrict–} less blood flows through the capillary networks close to the surface of the skin
-very little radiation takes place–} the warm blood is kept well below the surface to reduce heat loss

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30
Q

Mechanisms to reduce body temp:
Decreased sweating

A

-less sweat is secreted from sweat glands when it’s cold–} reducing the amount of heat loss
-less evaporation of water from the skin’s surface

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31
Q

Mechanisms to reduce body temp:
Hairs stand up

A

-erector pilli muscles in the skin contract, making the hairs stand up
-traps an insulating layer of air, so reduces cooling through the skin

32
Q

Mechanisms to reduce body temp:
Shivering

A

-muscles contract in spasms–} rapid, involuntary contracting + relaxing of muscles
-metabolic heat from the increased exothermic reactions (respiration) warm up the body

33
Q

Mechanisms to reduce body temp:
Hormones

A

-body releases adrenaline + thyroxine
-increases metabolism + so more heat is produced

34
Q

What is the endocrine system?

A

-made up of endocrine glands–} group of cells which are specialised to secrete hormones
-glands can be stimulated to release hormones by a change in conc of a substance/electrical impulse

35
Q

Hormones

A

-chemical messengers i.e steroids, proteins, glycoproteins, polypeptides, amines etc
-secreted directly into the blood and transported through the body in blood plasma
-then diffuse out of the blood and bind to receptors of membranes on target cells–} stimulate hormone to produce response

36
Q

action of hormones in cell signalling (non-steroid hormones)

A

-primary messenger(hormone) with a complimentary shape binds to the specific receptor on the cell surface membrane of the target cell from the endocrine gland
-this activates an enzyme in the cell membrane which catalyses the production of a secondary messenger–} activates a cascade of reactions inside the cell(to do with protein synthesis/activation) i.e adrenaline

37
Q

action of hormones in cell signalling (steroid hormones)

A

-because they are non-polar + lipid soluble molecules, they can pass through the lipid component of the cell membrane and bind to steroid hormones inside the cell to form a hormone-receptor complex–} acts as a transcription factor which facilitates/inhibits the transcription of a specific gene i.e oestrogen

38
Q

Hormonal vs neuronal communication

A

-communication via hormones vs nerve impulses
-hormone transmission via bloodstream vs nerve transmission is by neurones
-hormones work slow vs nerves work faster
-widespread response in hormones vs localised response in nerves
-slow vs rapid
-long lasting vs short lived
-permanent and irreversible vs temporary and reversible

39
Q

Structure of the adrenal glands

A

-two small endocrine glands located just above the kidney
-produce effects that help prepare the body for the ‘fight or flight’ response
-the cortex= outer region of glands, produce hormones that are vital to life released by the pituitary gland i.e cortisol and aldosterone
-the medulla= inner region of the glands, controlled by the nervous system, produces hormones i.e adrenaline and noradrenaline
-these parts are surrounded by a capsule

40
Q

Cortex: Cortisol

A

-helps regulate metabolism by stimulating the breakdown of proteins + fats to glucose which increases the amount of energy available so the brain and muscles can form a response
-works with other hormones to suppress the immune system so the body does not attack itself in the fight or flight response

41
Q

Cortex: Aldosterone

A

-helps control blood pressure
-increases blood vol and pressure by increasing the uptake of sodium ions + water by the kidneys

42
Q

Cortex: Androgens

A

-small amounts of male + female sex hormones are released–} small impact but important especially for women after menopause

43
Q

Medulla: Adrenaline and Noradrenaline

A

work together to:
-increase heart rate
-increase breathing rate
-constrict some blood vessels in non-essential organs so blood is diverted to brain and muscles(high bp)
-widening of air passages in the lungs
-convert glycogen to glucose in the liver–}glycogenolysis= increases respiration because more glucose is supplied to muscles, produce more energy

44
Q

Main functions of the pancreas

A

-to secrete hormones into the bloodstream as an endocrine gland
-to secrete enzymes/pancreatic juice and release them via a duct i.e digestive enzymes (amylase, lipase etc) into the digestive system as an exocrine gland

45
Q

3 important digestive enzymes and how they are secreted

A

-amylase: breaks down starch into simple sugars i.e maltose(disaccharide broken down further by maltase into alpha glucose)
-protease: breaks down proteins into amino acids
-lipase: breaks down lipids into fatty acids and glycerol
the digestive enzymes alongside pancreatic juice are delivered to the small intestines via a duct

46
Q

Islets of Langerhans and their role

A

-small regions of endocrine tissue within the exocrine tissue
-found in clusters around the blood capillaries and they secrete insulin and glucagon directly into the bloodstream
-alpha cells secrete glucagon and beta cells secrete insulin–} help to control blood glucose concentration

47
Q

Histology of Islets of Langerhans

A

-lightly stained(differential staining normally used to distinguish alpha cells from beta cells)
-large spherical clusters

48
Q

Histology of exocrine pancreatic tissue

A

-darker stained
-small, berry-like clusters

49
Q

Blood glucose concentration

A

-normal level= 90 mg per 100cm3 of blood
-the body uses glucose to produce ATP during respiration
-high levels after a meal but low levels later
-low levels don’t have enough glucose for respiration

50
Q

Increasing blood glucose concentration: diet

A

-after eating food containing carbohydrates
–} hydrolysed in the digestive system to release glucose into the bloodstream i.e starch=(amylase) maltose= glucose(maltase)

51
Q

Increasing blood glucose concentration: glycogenolysis

A

-glycogen stored in liver + muscle cells is hydrolysed into glucose which is released into the bloodstream

52
Q

Increasing blood glucose concentration: gluconeogenesis

A

-production of glucose from a non-carbohydrate source
-produces glucose from amino acids/ glycerol(from lipids) in the liver

53
Q

Decreasing blood glucose concentration: respiration

A

-glucose is needed as a substrate for respiration
-higher levels needed to generate more energy for muscle cells to contract during exercise

54
Q

Decreasing blood glucose concentration: glycogenesis

A

-formation of glycogen from excess glucose which is stored in the liver when BGC is too high

55
Q

Role of insulin

A

-rise of BGC is detected by the B cells in the islets of Langerhans
-Insulin secreted to lower BGC, which targets liver + most body cells:
-increases the rate of absorption of glucose in liver + muscle cells
-increases rate of respiration in cells(more glucose needed)
-increases rate of glycogenesis(store as glycogen in liver + muscle cells)
-increases rate of glucose to fat conversion
-inhibits release of glucagon from a cells

56
Q

How does insulin enter cells?

A

-most body cells have insulin receptors on cell surface membrane(not RBCs)
-insulin binds to glycoprotein receptor which changes tertiary structure of glucose transport protein channels
-causes channels to open allowing more glucose to enter
-can also activate enzymes(secondary messengers) in some cells to covert glucose to glycogen/fat

57
Q

Regulating insulin secretion

A

-broken down by enzymes in liver cells–} has to be constantly secreted to maintain effect
-when BGC falls below a certain level, B cells reduce insulin secretion= negative feedback

58
Q

Role of glucagon

A

-produced by alpha cells of the Islets of Langerhans after drop in BGC is detected
-target liver + fat cells(highest store of glycogen + lipids)
-Raises BGC levels:
-gluconeogenesis–} increasing conversion of amino acids + glycerol in the liver
-glycogenolysis–} liver breaks down its glycogen store into glucose and releases it back into bloodstream
-reducing the amount of glucose absorbed the liver cells

59
Q

How does glucagon enter cells?

A

-only liver and fat cells have specific glucagon receptors–} only cells that respond to glucagon

60
Q

Negative feedback in glucagon

A

-when BGC rises above a certain level, the a cells reduce glucagon secretion

61
Q

Why is maintaining blood glucose self-regualting?

A

-the level of glucose determines the quantity of insulin and glucagon secreted

62
Q

Membrane potential

A

-generated through an unequal distribution of ions either side of the plasma membrane
-most cells have a resting -70 mv

63
Q

3 things that generate resting potential

A

-permeability
-electrical gradient
-concentration gradient

64
Q

Difference between depolarised and repolarised

A

-mv of membrane closer to 0= depolarising
-mv of membrane further from 0= repolarising

65
Q

Control of insulin secretion by B cells

A

-B cells are at rest with -70 mv(potassium ion channels are open)
-high BGC is detected–} more glucose enters the cell via glucose transporter(facilitated diffusion)
-glucose is metabolised in mitochondria= production of ATP via respiration
-Influx of ATP causes K+ channels to close(binds to ATP sensitive K+ channels)
-K+ conc increases inside of the cell
-potential difference of B cells gets more positive and depolarises(-30mv)
-depolarisation causes voltage gated calcium channels to open–} Ca2+ ions diffuse into the cell
-increase of calcium ions causes insulin vesicles to move to and fuse with the plasma membrane
(cascade of reactions)
-insulin secreted via exocytosis

66
Q

hyperglycaemia vs hypoglycaemia

A

-hyper= high BGC
-hypo= low BGC

67
Q

What is diabetes?

A

-condition where blood glucose concentration cannot be controlled properly

68
Q

Type 1 diabetes

A

-autoimmune disease where the body attacks and destroys B cells in the islets–} no insulin produced
-BGC conc stays high after eating and can result in death if untreated
-normally develops in childhood
-risk slightly increased with family history

69
Q

Treating type 1

A

-regular insulin injections throughout the day
-insulin pump–} delivers insulin via a tube beneath the skin
-regular testing of BGC(normally pricking finger to analyse blood to calculate conc of insulin needed)

70
Q

What happens if a person in injected with too much/little?

A

-too much= may experience hypo and can result in unconsciousness
-too little= hyper= unconsciousness/ death if untreated

71
Q

Type 2 diabetes

A

-when B cells don’t produce enough insulin or body cells don’t respond properly to insulin
-insulin receptors on membranes may not work properly–} cells don’t take up enough glucose
-often linked with obesity
-risk increased from certain ethnic groups + family history

72
Q

Treating type 2

A

-regulating carb intake and matching it to exercise level(diet and excercise)
-medication to stimulate insulin production or slows down rate of glucose absorption from intestine

73
Q

What is synthetic biology?

A

-using other organisms to produce something man-made

74
Q

Potential treatments:
transplants

A

-pancreas transplants–} 80% success rate
-B cell injections–} less than 8% success
-hard to source
-over exhausting immunosuppressants

74
Q

Where did insulin used to get extracted from?

A

-from animal pancreases i.e pigs and cows

75
Q

Potential treatments: Stem cells

A

-totipotent cells could differentiated to B cells which would be implanted into patient
:( embryos have to be destroyed
:) no need to wait for donor, less likelihood of rejection

76
Q

Role of pancreatic acini

A

-produce and secrete digestive enzymes